Category Archives: Molecular Genetics

SEATTLE--(BUSINESS WIRE)-- NanoString Technologies, Inc. (NASDAQ: NSTG), a leading provider of life science tools for discovery and translational research, today announced a peer-reviewed paper published in Nature Genetics using the GeoMx Human Whole Transcriptome Atlas (WTA) to construct a high-resolution molecular landscape of pancreatic cancer. This paper, along with a tissue image generated using the GeoMx Digital Spatial Profiler (DSP), is featured on the cover of the August 2022 edition of Nature Genetics.

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A tissue image generated using NanoString's GeoMx Digital Spatial Profiler (DSP) is on the cover of Nature Genetics. (Graphic: Business Wire)

The paper, Single-nucleus and spatial transcriptome profiling of pancreatic cancer identifies multicellular dynamics associated with neoadjuvant treatment, was authored by a team led by William L. Hwang, M.D., Ph.D., Assistant Professor at Harvard Medical School and Clinician-Investigator in the Center for Systems Biology, Center for Cancer Research and Department of Radiation Oncology at Massachusetts General Hospital.

Since pancreatic cancer is one of the most challenging malignancies to treat with standard approaches, the research team sought to advance precision oncology strategies by understanding the molecular landscape of the multicellular subtypes and spatial communities of this cancer, including how they are remodeled after treatment.

The researchers used single-nucleus RNA sequencing (snRNA-seq) and digital spatial profiling with the GeoMx WTA to profile the tumors from a cohort of patients before or after neoadjuvant intervention. The snRNA-seq cell type signatures were used to deconvolve the GeoMx spatial profiles, demonstrating the complementarity of the two platforms. Together, the platforms demonstrated that malignant cells following different cellular programs (basal-like vs. classical-like) cluster in distinct immune niches within a tumor. The spatially-resolved transcriptomics analysis supported the hypothesis that basal-like malignant cell programs and classical-like programs drive different degrees of immune infiltration with distinct immune cell compositions and suggests that therapeutic strategies may be more effective if differentially targeted for these specific phenotypes.

Since resistance to cytotoxic therapy is pervasive, there is a critical need to elucidate clinically-relevant gene expression programs and spatial relationships among malignant and stromal cells in the tumor microenvironment, particularly in residual disease, said Hwang. GeoMx spatial technology was critical in achieving this research objective because it allowed us to map our single-nucleus gene expression programs onto the tumor architecture with high fidelity (whole transcriptome) and in a cell-type specific manner (morphology antibody-based segmentation) and was optimized for FFPE samples, which is the specimen format that is most commonly available in the clinic. This unique combination of technological features enabled us to refine our understanding of the molecular taxonomy and spatial organization of PDAC that will ultimately advance precision oncology for this deadly disease.

The high-resolution molecular framework sheds light on pancreatic cancers inter-and intra-tumoral diversity, spatial organization into discrete communities, treatment-associated remodeling, and clinically relevant prognostication. With these findings, researchers can harness this information to augment precision oncology efforts in pancreatic cancer and drive significant breakthroughs in oncology research.

About NanoString Technologies, Inc.

NanoString Technologies is a leading provider of life science tools for discovery and translational research. The company provides three platforms that allow researchers to map the universe of biology. The nCounter Analysis System, cited in more than 6,000 peer-reviewed publications, offers a way to easily profile the expression of hundreds of genes, proteins, miRNAs, or copy number variations, simultaneously with high sensitivity and precision. NanoStrings GeoMx Digital Spatial Profiler enables highly multiplexed spatial profiling of RNA and protein targets in various sample types, including FFPE tissue sections, and has been cited in more than 100 peer-reviewed publications. The CosMx Spatial Molecular Imager, with commercial availability expected in 2022, enables highly sensitive, high-resolution imaging of hundreds to thousands of RNAs or proteins directly from single cells within morphologically intact whole tissue sections. For more information, visit http://www.nanostring.com.

Forward-Looking Statements

This news release contains forward-looking statements within the meaning of Section 27A of the Securities Act of 1933 and Section 21E of the Securities Exchange Act of 1934 and the Private Securities Litigation Reform Act of 1995. These forward-looking statements include statements regarding our products and the anticipated launch of new products and technology. Such statements are based on current assumptions that involve risks and uncertainties that could cause actual outcomes and results to differ materially. These risks and uncertainties, many of which are beyond our control, include market acceptance of our products; the extent and duration of the impact of the COVID-19 pandemic and adverse conditions in the general domestic and global economic markets; the effects of ongoing litigation; the impact of competition; the impact of expanded sales, marketing, product development and clinical activities on operating expenses; delays or other unforeseen problems with respect to manufacturing and product development; as well as the other risks set forth in our filings with the Securities and Exchange Commission. These forward-looking statements speak only as of the date hereof. NanoString Technologies disclaims any obligation to update these forward-looking statements.

NanoString, NanoString Technologies, the NanoString logo, CosMx, GeoMx, and nCounter are trademarks or registered trademarks of NanoString Technologies, Inc. in various jurisdictions.

View source version on businesswire.com: https://www.businesswire.com/news/home/20220809005149/en/

Contacts

Doug Farrell, NanoStringVice President, Investor Relations & Corporate Communicationsdfarrell@nanostring.com Phone: 206-602-1768

Source: NanoString Technologies, Inc.

A tissue image generated using NanoString's GeoMx Digital Spatial Profiler (DSP) is on the cover of Nature Genetics. (Graphic: Business Wire)

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Study Using NanoStrings GeoMx Digital Spatial Profiler Featured on the Cover of Nature Genetics - BioSpace

During the 2021-2022 flu season, influenza activity in the United States was lower than pre-pandemic levels despite increased reporting and testing, possibly owing to COVID-19 precautions, according to a new report from the US Centers for Disease Control and Prevention (CDC).

For the 2022-2023 season, CDC has updated recommendations for the annual vaccine to include a closer antigenic match to the A(H3N2) subclade that predominated in the 2021-2022 US season, the report notes.

"The 2021-22 influenza season was mild," lead author Angiezel Merced-Morales, MPH, and colleagues write in Morbidity and Mortality Weekly Report. "Influenza activity continued from October 2021 through mid-June 2022, with A(H3N2) viruses predominating throughout the season."

"Since SARS-CoV-2 emerged in the United States in early 2020, influenza activity has been lower than that seen before the pandemic," add the authors, from the CDC's Influenza Division of the National Center for Immunization and Respiratory Diseases.

"The adoption of COVID-19-related mitigation measures might have had an impact on the timing or severity of influenza activity," they write.

The US influenza surveillance system involves collaborations between CDC and state, local, and territorial health departments; clinical and public health laboratories; vital statistics offices; healthcare providers; and hospitals, emergency departments, clinics, and long-term care facilities.

CDC used the cumulative rates of influenza-related hospitalizations reported through FluSurv-NET, as well as a mathematical model to estimate the number of people with symptomatic influenza who had a medical visit, were hospitalized for, or died of influenza.

Using data available from early October 2021 through mid-June 2022, CDC estimated that influenza virus infection resulted in 8-13 million symptomatic illnesses, 3.7-6.1 million medical visits, 82,000-170,000 hospitalizations, and 5000-14,000 deaths.

Clinical laboratories tested more than 2.8 million respiratory specimens for influenza virus. Overall, 4.5% specimens tested positive, including 98.6% for influenza A and 1.4% for influenza B. Each week, between 0.1% and 9.9% of the specimens tested positive for influenza.

Of the nearly 900,000 specimens tested in public health laboratories, 2.8% were positive for influenza virus. Of these, 99.5% were positive for influenza A viruses and 0.5% were positive for influenza B viruses.

Among over 19,000 seasonal influenza A virus specimens that were subtyped, 0.1% were influenza A(H1N1)pdm09 and 99.9% were influenza A(H3N2).

Of the A(H3N2) viruses with age data available, the proportions reported were 10% in people aged 0-4 years, 51% in those aged 5-24 years, 28% in those aged 25-64 years, and 11% those aged 65 years or older. The numbers of reported A(H1N1)pdm09, B/Victoria, and B/Yamagata viruses were too low to analyze by age group.

COVID-19 continued to dominate the deaths from pneumonia, influenza, and/or COVID-19 (PIC). According to the National Center for Health Statistics Mortality Surveillance System, the weekly percentage of PIC deaths remained above the epidemic threshold set at 1.645 standard deviations above the seasonal baseline during the entire 2021-2022 season.

Of the 387,112 PIC deaths, 71.6% of death certificates listed COVID-19 as an underlying or contributing cause of death and 0.6% listed influenza. These numbers indicate that PIC-related deaths were due primarily to COVID-19, not to influenza.

All 31 laboratory-confirmed influenza-related pediatric deaths reported to CDC were linked with an influenza A virus infection, and all 13 influenza A viruses with subtyping information were identified as A(H3N2).

All of the influenza viruses collected and tested for antiviral resistance by CDC were susceptible to zanamivir, and over 99% were susceptible to baloxavir, oseltamivir, and peramivir.

The US Food and Drug Administration's Vaccines and Related Biologic Products Advisory Committee has selected the composition of the 2022-2023 influenza vaccines on the basis of the World Health Organization's recommended Northern Hemisphere 2022-2023 influenza vaccine composition.

The committee updated the recommended A(H3N2) component for the 2022-2023 influenza vaccine to one that belongs to the subclade that predominated in the US during the 2021-2022 season, 3C.2a1b.2a.2. They made no changes to the A(H1N1)pdm09 or the B/Yamagata egg-based, cell-based, or recombinant vaccine recommended components.

Kevin McCarthy, PhD

Commenting on the report to Medscape Medical News, Kevin McCarthy, PhD, assistant professor of microbiology and molecular genetics at the University of Pittsburgh Center for Vaccine Research, said that influenza seasons are notoriously unpredictable.

"Behavioral changes brought about by the SARS-CoV-2 pandemic changed long-standing patterns of influenza circulation," he noted in an email. "This year, the peaks of infection were blunted, the overall severity of the season was diminished, and the season was elongated.

"Our vaccines for the 2022-2023 season have been chosen to match viruses currently circulating during the protracted tail end of the 2021-2022 season," he said. "Perhaps this will help us more closely match the circulating and vaccine viruses.

"As we return to something closer to the pre-pandemic world, will influenza return to its long-held trends?" asked McCarthy, who was not involved in developing the report. "Unfortunately, we will only know after next year's report."

"Regardless of what the future holds," he advises, "receiving the 2022-2023 vaccine is the best way to prepare."

The authors agree.

"Receiving a seasonal influenza vaccine each year remains the best way to protect against seasonal influenza and its potentially severe consequences," they write.

Influenza surveillance reports for the US are published online weekly at https://www.cdc.gov/flu/weekly, and more information about influenza viruses, surveillance, vaccines, antiviral medications, and novel influenza A infections is at https://www.cdc.gov/flu.

The authors and McCarthy report no relevant financial relationships.

Morbidity and Mortality Weekly Report. Published online July 22, 2022. Full text HTML and PDF

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CDC Says Recent Flu Season Mild, Maybe Owing to COVID Precautions - Medscape

Although a new virus recently detected in China may not pose an immediate threat of outbreak, experts stress that its appearance is an example of the need for improved global disease surveillance.

Heres what you need to know about the virus

Langya henipavirus (LayV) was identified in 35 patients in China from April 2018 through August 2021. Research about the pathogen was published last week in the New England Journal of Medicine.

In this report, investigators in China identified a new henipavirus associated with a febrile human illness, said the research. This virus was also found in shrews.

Symptoms of LayV include fever, cough and fatigue. It is related to other henipaviruses including the Hendra virus and the Nipah virus, which cause respiratory infections and can be fatal. These viruses belong to the Paramyxoviridae family of viruses that causes measles and mumps, according to the Nature journal.

So far, there have been no fatalities reported in connection to LayV.

Patients in China were recruited into the study of LayV if they had a fever. A 53-year-old woman from the town of Langya in Shandong Province was the first to be diagnosed with the virus.

During the study period, most patients with LayV were farmers and had symptoms ranging from severe pneumonia to a cough. Most also said in a questionnaire that they had been exposed to an animal within a month of their symptoms beginning.

Researchers have not observed any human-to-human transmission of the virus and none of the 35 cases appear to be linked, according to an article in the Nature journal. It said that researchers found LayV antibodies in a handful of goats and dogs, living in the villages of infected patients and identified LayV viral RNA in 27% of 262 sampled shrews, indicating that the animal is a reservoir for the virus.

This means that shrews pass the virus between themselves and are somehow infecting people here and there by chance, according to Emily Gurley, an infectious-diseases epidemiologist at Johns Hopkins University in Baltimore, Md.

It is not clear if patients with LayV were infected by shrews directly or an intermediate animal. Linfa Wang, a virologist at DukeNational University of Singapore Medical School in Singapore said there was limited contact tracing involved in the study and Gurley said more research is needed regarding how the virus spreads.

Why is this virus important?

Researchers believe that humans were infected with LayV by animals, which is referred to as zoonotic spillover.

These sorts of zoonotic spillover events happen all the time, said Edward Holmes, an evolutionary virologist at the University of Sydney in Australia, according to the Nature journal. The world needs to wake up.

According to a 2021 study published in the Genetics and Molecular Biology Journal most human infectious diseases (60-75%) are derived from pathogens that originally circulated in non-human animal species, which demonstrates that spillover has a fundamental role in the emergence of new human infectious diseases.

A white paper released in June by the World Health Organization said shortening the time between a spillover event and disease detection is a major focus of global disease prevention improvement and Health Emergency Preparedness, Response, and Resilience (HEPR) efforts.

Two current outbreaks the COVID-19 pandemic and the monkeypox outbreak have been traced to potential zoonotic spillover events.

The virus that causes COVID-19, SARS-CoV-2, is a zoonotic virus, which means it can spread between people and animals, said a November statement from the U.S. Centers for Disease Control and Prevention. Per the CDC, the virus likely originated in bats and monkeypox was first observed in colonies of monkeys kept for research.

Research into the LayV genome shows it is most closely related to Mojiang henipavirus first isolated in rats in an abandoned mine in the southern Chinese province of Yunnan a decade ago.

There is no particular need to worry about this, but ongoing surveillance is critical, said Holmes of the recent LayV cases. Gurely also said that outbreaks typically occur after false starts.

If we are actively looking for those sparks, then we are in a much better position to stop or to find something early, she said.

Going forward, Taiwans Centers for Disease Control (CDC) said it plans to establish a nucleic acid testing method to identify cases of LayV, according to the Taipei Times.

Link:
New virus detected in China; here's everything you need to know about it - WCCO

Acer Therapeutics Inc.

Orphan designation provides potential for up to 10-year market exclusivity in the EU upon regulatory approval

GENEVA, Switzerland and NEWTON, Mass., Aug. 12, 2022 (GLOBE NEWSWIRE) -- RELIEF THERAPEUTICS Holding SA (SIX: RLF, OTCQB: RLFTF, RLFTY) (Relief), and its collaboration partner, Acer Therapeutics Inc. (Nasdaq: ACER) (Acer), today announced that the European Commission has granted orphan medicinal product designation in the EU to ACER-001 (sodium phenylbutyrate) for the potential treatment of patients with Maple Syrup Urine Disease (MSUD). ACER-001 was granted orphan drug designation by the U.S. Food and Drug Administration (FDA) in the U.S. for MSUD in 2014.

Orphan designation by the European Commission is another important milestone for the ACER-001 program that provides further validation of the important role we believe ACER-001 will play in the potential treatment of multiple rare diseases, stated Raghuram (Ram) Selvaraju, Ph.D., Chairman of the Board of Directors of Relief. We look forward to the continued advancement of ACER-001 in MSUD and Urea Cycle Disorders.

We are very pleased to receive orphan medicinal product designation in both the U.S. and now the EU, underscoring the urgent need for an approved treatment for MSUD, said Adrian Quartel, MD, FFPM, Chief Medical Officer of Acer. Currently, the only treatment option for patients with MSUD is a lifelong, protein-restricted diet, however, they still remain at serious risk for a wide range of life-threatening complications.

Orphan drug designation is granted to medicines that treat or prevent a life-threatening or chronically debilitating rare disease, with a prevalence in the EU of not more than 5 in 10,000, and with either no currently approved method of prevention or treatment, or with significant benefit to those affected by the disease. The designation potentially provides certain benefits to ACER-001, including the potential for up to 10-year EU market exclusivity upon regulatory approval, if received, reductions in EMA application fees, and access to study protocol assistance.

Story continues

Rationale for ACER-001 Treatment in MSUDMultiple investigational trials evaluating sodium phenylbutyrate in urea cycle disorder (UCD) patients suggest treatment with sodium phenylbutyrate is associated with selective reduction in branched chain amino acids (BCAA) despite adequate restricted dietary protein intake.1,2,3,4 Analysis of data from a longitudinal multicenter study of 553 UCD patients treated with sodium phenylbutyrate demonstrated that sodium phenylbutyrate decreased plasma BCAA in patients with UCDs and could serve as a therapy in maple syrup urine disease and other common complex disorders with dysregulation of BCAA metabolism.2

Based on this clinical observation, investigators at Baylor College of Medicine explored the potential of sodium phenylbutyrate treatment to lower BCAA and corresponding branched-chain -ketoacid (BCKA) levels in both healthy subjects and patients with MSUD. The investigators found that sodium phenylbutyrate, when dosed over three days, showed a statistically significant reduction of leucine in all three healthy subjects and in three out of the five MSUD patients who participated in the trial.5

In November 2020, study results evaluating the effect of sodium phenylbutyrate in the management of acute metabolic decompensation in pediatric MSUD patients (n=10) were published by investigators from Istanbul University-Cerrahpasa Medical Faculty in the peer-reviewed Journal of Pediatric Endocrinology and Metabolism showing a significant reduction in leucine levels in MSUD patients experiencing an acute attack.6 The results suggested that sodium phenylbutyrate could be safely administered in combination with emergency protocol using other active pharmaceuticals and supports additional investigation of potential clinical benefit beyond emergency protocol alone.

About MSUDMSUD is a rare inherited disorder caused by a deficiency of branched-chain alpha-keto acid dehydrogenase complex, resulting in elevated blood levels of the (BCAA) leucine, valine, and isoleucine, as well as the associated (BCKA) in a patients blood. Left untreated, this can result in neurological damage, mental disability, coma, or death. The most severe presentation of MSUD, known as classic MSUD, accounts for 80% of cases and can result in neonatal onset with encephalopathy and coma. Although metabolic management of the disease is possible via a highly restrictive diet, the outcome is unpredictable, and a significant portion of affected individuals are mentally impaired or experience neurological complications.

MSUD is typically diagnosed at birth via newborn screening and incidence is estimated at 1 in 185,000 people worldwide and 1 in 220,000 people in the United States.7 The disorder occurs more frequently in the Old Order Mennonite population, with an estimated incidence of about 1 in 380 newborns, and the Ashkenazi Jewish population, with an estimated incidence of 1 in 26,000.8

About ACER-001ACER-001 (sodium phenylbutyrate) is being developed for the treatment of various inborn errors of metabolism, including UCDs and Maple Syrup Urine Disease (MSUD). ACER-001 (sodium phenylbutyrate) is an immediate-release, polymer coated, multi-particulate formulation of sodium phenylbutyrate for oral administration via suspension, that is designed to improve palatability. ACER-001 (sodium phenylbutyrate) has been granted orphan drug designation by the FDA for MSUD. In July 2022, the FDA accepted Acers NDA resubmission (Class 2) and assigned a Prescription Drug User Fee Act (PDUFA) target action date of January 15, 2023. This investigational product candidate has not been approved by FDA, the European Medicines Agency (EMA), or any other regulatory authority. There can be no assurance that the resubmitted ACER-001 NDA for UCDs will be approved by the FDA, or that ACER-001 (sodium phenylbutyrate) will otherwise be approved for any indication.

About RELIEF THERAPEUTICS Holding SARelief is a Swiss, commercial-stage, biopharmaceutical company focused on identification development and commercialization of novel, patent protected products intended for the treatment of metabolic, dermatological and pulmonary rare diseases with a portfolio of clinical and marketed assets that serve unmet patient needs. Relief has a Collaboration and License Agreement with Acer Therapeutics for the worldwide development and commercialization of ACER-001 (sodium phenylbutyrate) for the treatment of various inborn errors of metabolism, including UCDs and Maple Syrup Urine Disease (MSUD). Relief also continues to develop aviptadil for several rare pulmonary indications; Relief's 2021 acquisitions of APR Applied Pharma Research SA and AdVita Lifescience GmbH brought to Relief a diverse pipeline of marketed and development-stage programs.

RELIEF THERAPEUTICS Holding SA is listed on the SIX Swiss Exchange under the symbol RLF and quoted in the U.S. on OTCQB under the symbols RLFTF and RLFTY. For more information, visit http://www.relieftherapeutics.com Follow Relief on LinkedIn.

About Acer Therapeutics Inc.Acer is a pharmaceutical company focused on the acquisition, development and commercialization of therapies for serious rare and life-threatening diseases with significant unmet medical needs. Acers pipeline includes four investigational programs: ACER-001 (sodium phenylbutyrate) for treatment of various inborn errors of metabolism, including urea cycle disorders (UCDs) and Maple Syrup Urine Disease (MSUD); ACER-801 (osanetant) for treatment of induced Vasomotor Symptoms (iVMS); EDSIVO (celiprolol) for treatment of vascular Ehlers-Danlos syndrome (vEDS) in patients with a confirmed type III collagen (COL3A1) mutation; and ACER-2820 (emetine), a host-directed therapy against a variety of viruses, including cytomegalovirus, Zika, dengue, Ebola and COVID-19. For more information, visit http://www.acertx.com.

References

Muelly 2011 Neuropsychiatric and Neurochemical Sequelae of MSUD.

L.C. Burrage, et al., Sodium phenylbutyrate decreases plasma branched-chain amino acids in patients with urea cycle disorders, Mol. Genet. Metab. (2014)

Scaglia F. New insights in nutritional management and amino acid supplementation in urea cycle disorders. Mol Genet Metab. 2010;100 Suppl 1(Suppl 1):S72-6.

Hberle, J., Boddaert, N., Burlina, A. et al. Suggested guidelines for the diagnosis and management of urea cycle disorders. Orphanet J Rare Dis 7, 32 (2012)

Brunetti-Pierri et al. Phenylbutyrate therapy for maple syrup urine disease. Hum Mol Genet. 2011 February 15; 20(4): 631640.

Zubarioglu T, et al. Impact of sodium phenylbutyrate treatment in acute management of maple syrup urine disease attacks: a single-center experience. J Pediatr Endocrinol Metab. 2020 Nov 11;34(1):121-126.

Chapman, K, et al. (2018). Incidence of maple syrup urine disease, propionic acidemia, and methylmalonic aciduria from newborn screening data. Molecular Genetics and Metabolism Reports. 15. 106-109.

Strauss KA, et al. Maple Syrup Urine Disease. In: Pagon RA, Adam MP, Ardinger HH, al. e, eds. GeneReviews [Internet]. https://www.ncbi.nlm.nih.gov/books/NBK1319/: University of Washington, Seattle; 2006. Accessed March 22, 2017

Relief Forward-Looking StatementsThis communication expressly or implicitly contains certain forward-looking statements concerning RELIEF THERAPEUTICS Holding SA and its businesses. Such statements involve certain known and unknown risks, uncertainties and other factors, including (i) whether the FDA will approve Acers NDA for ACER-001 for the treatment of UCDs, (ii) whether RELIEF THERAPEUTICS Holding SA will submit an application for approval of ACER-001 in Europe for the treatment of UCDs and the timing of filing such application, (iii) whether any application submitted to European authorities seeking marketing authorization for ACER-001 for the treatment of patients in Europe with UCDs will be approved, (iv) whether the FDA will approve Acers IND to evaluate ACER-001 for the treatment of MSUDs, (v) the timing of Acers Phase 2b trial evaluating ACER-001 for the treatment of MSUDs, (vi) whether ACER-001s currently proposed trial and any future required trials of ACER-001 for MSUDs will be undertaken and successful, (vii) whether ACER-001 will ever be approved for the treatment of MSUDs in the United States, (viii) whether Relief will ever file the necessary applications in Europe to seek the right to commercialize ACER-001 in Europe for the treatment of MSUDs and whether any such applications filed will be granted, and (ix) those other risks, uncertainties and factors described in RELIEF THERAPEUTICS Holding SAs press releases and filings with the SIX Swiss Exchange and the U.S. Securities and Exchange Commission, all of which could cause the actual results, financial condition, performance or achievements of RELIEF THERAPEUTICS Holding SA to be materially different from any future results, performance or achievements expressed or implied by such forward-looking statements. RELIEF THERAPEUTICS Holding SA is providing this communication as of this date and does not undertake to update any forward-looking statements contained herein as a result of new information, future events or otherwise.

Acer Forward-Looking StatementsThis press release contains forward-looking statements that involve substantial risks and uncertainties for purposes of the safe harbor provided by the Private Securities Litigation Reform Act of 1995. All statements, other than statements of historical facts, included in this press release are forward-looking statements. Examples of such statements include, but are not limited to, statements about the role we believe ACER-001 could play in the potential treatment of multiple rare diseases and its continued advancement in MSUD and Urea Cycle Disorders, potential results of the investigational trial and the potential of ACER-001 to reduce certain amino acids and leucine levels in MSUD patients, the rationale for ACER-001 treatment in MUSD, the potential outcomes of having MUSD, and statements about our resubmission of an ACER-001 NDA for UCDs and potential regulatory approval thereof. Our pipeline products are under investigation and their safety and efficacy have not been established and there is no guarantee that any of our investigational products in development will receive health authority approval or become commercially available for the uses being investigated. We may not actually achieve the plans, carry out the intentions or meet the expectations or projections disclosed in the forward-looking statements and you should not place undue reliance on these forward-looking statements. Such statements are based on managements current expectations and involve risks and uncertainties. Actual results and performance could differ materially from those projected in the forward-looking statements as a result of many factors, including, without limitation, risks related to the drug development and the regulatory approval process, including the timing and requirements of regulatory actions. We disclaim any intent or obligation to update these forward-looking statements to reflect events or circumstances that exist after the date on which they were made. You should review additional disclosures we make in our filings with the Securities and Exchange Commission, including our Annual Report on Form 10-K and Quarterly Reports on Form 10-Q. You may access these documents for no charge athttp://www.sec.gov.

CORPORATE CONTACTSRELIEF THERAPEUTICS Holding SA:Jack WeinsteinChief Financial Officer and Treasurercontact@relieftherapeutics.com

Acer Therapeutics:Jim DeNikeAcer Therapeutics Inc.jdenike@acertx.com+1-844-902-6100

INVESTOR RELATIONS CONTACTSRELIEF THERAPEUTICS Holding SA:Michael MillerRx Communications Group mmiller@rxir.com+1-917-633-6086

Acer Therapeutics:Nick ColangeloGilmartin Groupnick@gilmartinIR.com+1-332-895-3226

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Relief Therapeutics and Acer Therapeutics Announce that the European Commission Has Granted Orphan Drug Designation for ACER-001 in Maple Syrup Urine...

When Mad in America received a notice this past June that Joanna Moncrieff, Mark Horowitz, and colleagues would soon publish a paper concluding that there were no research findings that supported the low-serotonin hypothesis of depression, I initially wondered whether we should bother to report on it. Mad in America readers know well that the low-serotonin theory had long ago been debunked, with numerous articles on our site telling of that fact, and so I quipped to other MIA staff that reviewing the article would be like beating a dead horse.

But such is our little cocoon here at Mad in America. For much of the mainstream media, their paper made for a stunning finding. In print, radio, and television, the paper has been described as a landmark finding, as a game changer and so forth, the media telling of how it has shaken up accepted wisdom about antidepressants and how they work.

This was rather amusing, I thought, as the exclamations of surprise revealed the medias utter failure regarding their reporting on psychiatry for the past decades. Their surprise served as a tacit confession that they had been publishing propaganda for some time.

Then, as psychiatrists publicly commented on the paper, a second confession appeared, this one indeed of landmark importance. Their comments serve as an admission that, for the past several decades, their profession committed medical fraud. And I am using that term in its legal sense.

As Moncrieff and colleagues noted, there is a long line of research that failed to find evidence supporting the low-serotonin theory of depression. What was new about their work was that they performed a comprehensive review of this research, looking at the different types of studies that had been done, and finding that all had failed to produce evidence supporting the theory. In response, a number of prominent psychiatrists in the UK and the United States dismissed the paper as old news. Here is a sampling:

From UK psychiatrists:

The findings from this review are really unsurprising. Depression has lots of different symptoms and I dont think Ive met any serious scientists or psychiatrists who think that all causes of depression are caused by a simple chemical imbalance in serotonin. Michael Bloomfield, University College London (UCL)

This paper does not present any new findings but just reports results which have been published elsewhere and it is certainly not news that depression is not caused by low serotonin levels.' David Curtis, UCL Genetics Institute

From US psychiatrists:

Nothing is new here. And the fuss surrounding the paper reveals much ignorance about psychiatry. The serotonin hypothesis of depression which became popular from the 1990s until now, is false, and has known to be false for a long time, and never was proven to begin with. Nassir Ghaemi, Tufts University School of Medicine

When I was doing research for [my] book, I was reading the same studies that I am sure that Dr. Moncrieff and colleagues read, which were basically saying that theres no direct evidence of a serotonin deficiency. So its not really new. Daniel Carlat, publisher of the Carlat Psychiatry Report

The psychiatrists making these comments are correct. The psychiatric research community has long known that the low-serotonin theory didnt pan out and that, in fact, the field long ago moved on to new theories about the possible pathology that gives rise to depression. Yet, as is easy to show, the American Psychiatric Association, in concert with pharmaceutical companies, promoted the low-serotonin theory to the public long after the low-serotonin theory had been found to be without merit. Scientific advisory councils populated by professors of psychiatry at prestigious medical schools also signed off on such pronouncements by non-profit advocacy associations, and in that manner, share culpability for telling this falsehood to the public.

That fraudulent story-telling worked, in the sense of deluding the public. As Moncrieff and colleagues noted, surveys in recent years found that 85% to 90% of the public believed that low serotonin was the cause of depression, and that antidepressants helped fix that imbalance.

There you have the basis for a class action lawsuit: the psychiatric community long ago knew that the low-serotonin story of depression hadnt panned out, yet the American Psychiatric Association, pharmaceutical companies, and scientific advisory councils told the public otherwise, and this created a societal belief in that false story. The surveys prove that many millions of patients acted upon that falsehood and incorporated it into their sense of self.

In the wake of World War II, the discovery of Nazi medical experiments on Jewish prisoners and the mentally ill led to the principle, codified in law in the United States, of the duty to provide volunteers in research studies with informed consent. Potential study subjects need to be informed about the risks of a study before they can give consent.

In the 1950s and 1960s, this principle of informed consent was extended to ordinary medical care. The principle is grounded in the concept of personal autonomy: the individual has a right to self-determination. A 1972 landmark case in federal court, Canterbury v. Spence, ruled that providing patients with informed consent was not just an ethical obligation, but a legal one. The court wrote:

The patients right of self-decision shapes the boundaries of the duty to reveal. That right can be exercised only if the patient possesses enough information to enable an intelligent choice.

The court also set forth a standard for assessing whether this legal obligation had been met: What would a reasonable patient want to know with respect to the proposed therapy and the dangers that may be inherently or potentially involved?

While it is the physician or medical caregiver who is required to obtain the informed consent of the patient, this legal standard clearly imposes an ethical duty, by proxy, on the medical specialty that provides individual physicians with the information that should be disclosed. The medical specialty must provide physicians with the best possible accounting of the risks and benefits of any proposed therapy, and in its communications to the public, do the same.

The diagnosis of a disease is obviously a first step in obtaining informed consent. What is the illness that needs to be treated? If the presenting symptoms do not lead to a diagnosis with a known pathology, that is okaythe absence of knowledge helps inform the patients decision-making. If it isnt understood why a drug works, that is okay too. Once again, the absence of knowledge helps inform the patients decision-making. At that point, the patient can focus on the risks and benefits of the proposed treatment: what have clinical studies shown?

The chemical imbalance story violated those principles at every step. Patients were informed that they had a known pathology, and that an antidepressant fixed that pathology. That was a story of an antidote to a disease, and thus was a medically necessary treatment. If a patient didnt take the antidepressant, he or she could expect to continue to suffer from depression.

This isnt simply a failure to give patients the information needed to make an informed choice. Instead, from a legal standpoint, this is a case of a patient being told a lie.

Here is how one Arizona law firm describes the legal consequences for a doctor that lies to a patient:

You can sue your doctor for lying, provided certain breaches of duty of care occur. A doctors duty of care is to be truthful about your diagnosis, treatment options, and prognosis. If a doctor has lied about any of this information, it could be proof of a medical malpractice claim. The law considers it medical negligence if a doctor fails to provide the truth for informed consent, which may also bring a battery lawsuit.

Medical malpractice is the charge if the action was due to negligence; medical battery requires the action to be intentional. Here is how a Washington D.C. law firm describes medical battery:

When you visit a doctor and they prescribe a treatment or procedure, an essential element is your consent. You have the right to know what will be done to you, to learn the risk or potential side effects of a procedure, and to be informed of any alternative treatment options available to you . . . Medical battery occurs when the doctor or other medical professional violates your right to decide what kinds of medical treatments you will receive and which you do not wish to receive.

The FDA, of course, approved the prescribing of antidepressants for depression. And it may be that many individual prescribers who told their patients that antidepressants fixed a chemical imbalance thought that was true. They believed they were providing patients with informed consent.

As such, in this instance of the chemical-imbalance story, the medical malpractice and battery can be understood as not necessarily originating in the doctor-patient interaction, but rather in the telling of a false story to the public by the American Psychiatric Association (APA) and pharmaceutical companies that knowingly promoted this falsehood. The academic psychiatrists that served on the scientific advisory boards of non-profit advocacy organizations that peddled this story share in this collective guilt.

As is well-known, the low-serotonin theory of depression had its roots in findings, dating back to the 1960s, that the first generation of antidepressants, tricyclics and monoamine oxidase inhibitors, both prevented the usual removal of neurotransmitters known as monoamines from the synaptic cleft between neurons. This led researchers in the 1965 to hypothesize that a deficit in monamines could be a cause of depression.

Once this hypothesis was floated, researchers then sought to determine whether if patients with depression actually suffered from a monamine deficiency. Its a history of one negative finding after another.

As early as 1974, researchers concluded that all such studies up to that time indicated that the depletion of brain norepinephrine, dopamine, or serotonin is in itself not sufficient to account for the development of the clinical syndrome of depression. This was the first round of findings, and after that there was speculation that a monoamine deficit might be present in a subset of depressed patients (as opposed to being a pathology common to all such patients.) In 1984, the NIMH conducted a study to investigate that possibility. Once more, the bottom-line findings were negative, which led the NIMH researchers to conclude that elevations or decrements in the functioning of serotonergic systems per are not likely to be associated with depression.

At that point, the hypothesis had been around for nearly two decades and found to be wanting. In the research community, there was a sense that the hypothesis had always presented an overly reductive picture of how the brain functioned, and thus it wasnt a surprise that research had failed to support the hypothesis. Even so, after that 1984 report, investigators continued to study whether depressed patients suffered from low serotonin, with this research quickening after Prozac arrived on the market in 1988. Many different investigative methods were tried, but once again, the results were negative. The hypothesis was officially buried by the American Psychiatric Association in 1999, when it published the third edition of its Textbook of Psychiatry. The authors of a section on mood disorders even pointed out the faulty logic that had led to the chemical imbalance theory of depression in the first place. They wrote:

The monoamine hypothesis, which was first proposed in 1965, holds that monoamines such as norepinephrine and 5-HT [serotonin] are deficient in depression and that the action of antidepressants depends on increasing the synaptic availability of these monoamines. The monoamine hypothesis was based on observations that that antidepressants block reuptake inhibition of norepinephrine, 5-HT, and/or dopamine. However, inferring neurotransmitter pathophysiology from an observed action of a class of medications on neurotransmitter availability is similar to concluding that because aspirin causes gastrointestinal bleeding, headaches are caused by too much blood and the therapeutic action of aspirin in headaches involves blood loss. Additional experience has not confirmed the monoamine depletion hypothesis.

Other experts in the field echoed this point in the next few years. In his 2000 textbook Essential Psychopharmacology, psychiatrist Stephen Stahl wrote that there is no clear and convincing evidence that monamine deficiency accounts for depression; that is, there is no real monoamine deficit.

More such confessions appeared in the research literature, and finally, in a 2010 paper, Eric Nestler, famous for his work on the biology of mental disorders, detailed how the many types of inquiries into the low-serotonin theory had all come to the same conclusion:

After more than a decade of PET studies (positioned aptly to quantitatively measure receptor and transporter numbers and occupancy), monoamine depletion studies (which transiently and experimentally reduce brain monoamine levels), as well as genetic association analyses examining polymorphisms in monoaminergic genes, there is little evidence to implicate true deficits in serotonergic, noradrenergic, or dopaminergic neurotransmission in the pathophysiology of depression. This is not surprising, as there is no a priori reason that the mechanism of action of a treatment is the opposite of disease pathophysiology.

This is the research history that psychiatrists today, when asked to comment about Moncrieffs paper, are referring to when they state, there is nothing new here. They are right. The theory was abandoned long ago. In a 2011 blog, Ronald Pies, editor of Psychiatric Times, the trade publication of the American Psychiatric Association, put it this way: In truth, the chemical imbalance notion was always a kind of urban legendnever a theory seriously propounded by well-informed psychiatrists.

From a legal standpoint, the APAs publication of the third edition of its Textbook of Psychiatry in 1999 is the pivotal moment in this history. Up until that time, the argument could be made that while the biology of depression remained unknown, one hypothesis was that it was due to low serotonin, and that there were still efforts to see if that might be true. However, after that date, the APA, the pharmaceutical companies, and the academic psychiatrists that populated the scientific advisory councils had an obligation to inform the public that the low-serotonin theory had not panned out. If instead these three groups informed the public that depressed patients suffered from a chemical imbalance that could be fixed by a drug, they were knowingly telling the public a lie, and thus, by informed consent standards, they were abetting medical malpractice and the medical battery of patients.

And its easy to document that is exactly what the APA, the pharmaceutical companies, and the scientific advisory boards did.

The APAs promotion of the chemical imbalance theory of mental disorders can be traced back to 1980, when it published the third edition of its Diagnostic and Statistical Manual. That publication is regularly characterized as a transformative moment for American psychiatry, as this was when the APA adopted a disease model for diagnosing and treating psychiatric disorders.

There were no scientific findings that spurred this transformation. The scientific impulse that was present arose from the failure of DSM II: the diagnoses in that edition were understood to lack reliability and validity. That led a team of researchers at Washington University in St. Louis to advocate that psychiatry should start fresh: it could develop categories for grouping patients with like symptoms, with the hope that subsequent research would validate the groupings as real diseases. DSM II would be abandoned, and new categories would be drawn up for research purposes.

However, during the 1970s, APA leaders spoke of how, in the face of various criticisms, psychiatry was fighting for its survival. Its diagnostic manual was understood to lack validity; psychologists and counselors were offering talk therapies that appeared to be as effective as psychoanalysis; One Flew Over the Cuckoos Nest depicted staff in mental hospitals as the truly crazy ones; and an antipsychiatry movement described psychiatry as an agency of social control.

The criticism that stung the most was that psychiatrists were not real doctors. There was an obvious solution that beckoned: if they adopted a disease model, they could present themselves as physicians who treated real diseases. This would enable them to don the white coatboth figuratively and literallythat society recognized as the garb of real doctors.

DSM III, said APA president Jack Weinberg in 1977, would clarify to anyone who may be in doubt that we regard psychiatry as a specialty of medicine.

Once DSM III was published, the APA set out to market its new disease model to the public. In 1981, it established a division of publications and marketing to deepen the medical identification of psychiatrists. That same year it established a press to bring psychiatrys best talent and current knowledge before the reading public. It developed a nationwide roster of experts to promote this disease model, and it set up a public affairs institute to run workshops that trained its members in techniques for dealing with radio and television.

This PR effort told of a revolution in psychiatry, with the media informed that researchers were discovering the very molecules that caused psychiatric symptoms. The APA held media days to promote this understanding, with awards given to media that reported on this revolution, and soon newspapers and magazines were writing stories about extraordinary advances that heralded a day when mental disorders could be cured.

The Baltimore Sun, in a seven-part series titled The Mind-Fixers, which won a Pulitzer Prize for expository journalism in 1984, described the revolution in this way:

For a decade and more, research psychiatrists have been working quietly in laboratories, dissecting the brains of mice and men and teasing out the chemical formulas that unlock the secrets of the mind. Now, in the 1980s, their work is paying off. They are rapidly identifying the interlocking molecules that produce human thought and emotion . . . As a result, psychiatry today stands on the threshold of becoming an exact science, as precise and quantifiable as molecular genetics. Ahead lies an era of psychic engineering, and the development of specialized drugs and therapies.

Pharmaceutical companies, of course, were thrilled with the APAs adoption of a disease model, for they understood it would greatly expand the market for their drugs, and they began funneling money to the APA and to psychiatrists at academic medical centers to support this PR effort.

The chemical imbalance story served, in essence, as the soundbite that could best sell this disease model to the public. It was a claim that fit into a larger societal narrative about the march of medicine in the 20th century: insulin as a treatment for diabetes, antibiotics for infectious diseases, a vaccine for polio, and so forth. Now it was psychiatrys turn to take its place at the head of this parade.

The public began hearing this soundbite immediately after DSM III was published. In 1981, an Associated Press article featuring an interview with University of Chicago psychiatrist Herbert Meltzer informed readers that researchers believe clinical depression is caused by a chemical imbalance in the brain, and that there were already two drugs in development that restore the chemical imbalance to normal.

Three years later, Nancy Andreasen, who would soon become editor-in-chief of the American Journal of Psychiatry, published a best-selling book titled The Broken Brain: The Biological Revolution. The new understanding in psychiatry, she wrote, was that the major psychiatric illnesses are diseases, and that each different illness has a different specific cause . . . there are many hints that mental illness is due to chemical imbalances in their brain and that treatment involves correcting these chemical imbalances.

Eli Lilly brought Prozac to market in 1988, and soon the public was hearing that this selective serotonin reuptake inhibitor restored serotonin to normal levels, and thus was like insulin for diabetes. New York magazine featured the pill on its cover: Bye, Bye Blues declared the headline. Newsweeks did as well, with this headline atop the pill: Prozac, A Breakthrough Drug for Depression.

Magazine and newspaper stories told of how patients were feeling better than ever. In the spring of 1990, the New York Times, in an article by Natalie Angier, who arguably was the nations most well-known science writer, informed readers that all antidepressants work by restoring the balance of neurotransmitter activity in the brain, correcting an abnormal excess or inhibition of the electrochemical signals that control mood, thoughts, appetite, pain, and other sensations. This new drug, Dr. Francis Mondimore told Angier, is not like alcohol or Valium. Its like antibiotics.

Television shows weighed in with a similar message, and on 60 Minutes, Lesley Stahl told the inspiring story of a woman, Maria Romero, who, after a decade of horrible depression, had been reborn on Prozac. Somebody, something left my body and another person came in, Romero said. Stahl explained the biological cure that was at work: Most doctors believe that chronic depression like Romeros is caused by a chemical imbalance in the brain. To correct it, the doctors prescribed Prozac.

Sales of Prozac soared, and as other drug companies brought new SSRI antidepressants to marketZoloft, Paxil, Celexa, Lexapro, and so forththey relied on the chemical imbalance soundbite to market their products. The National Alliance on Mental Illness grew in prominence during this period, and its core message was that psychiatric disorders were diseases caused by chemical imbalances in the brain, and that psychiatric drugs fixed those imbalances.

The American population, and populations around the globe, came to understand this story as scientific truth. The new millennium arrived, and although the APAs own textbook had declared the low-serotonin theory dead and buried, the APA publicly doubled-down on the chemical imbalance story, informing the public that it was now proven.

In the last decade, neuroscience and psychiatric research has begun to unleash the brains secrets, wrote APA president Richard Harding, in a 2001 article published in Family Circle. We now know that mental illnessessuch as depression or schizophreniaare not moral weaknesses or imagined, but real diseases caused by abnormalities of brain structure and imbalances of chemicals in the brain.

In the same issue, future APA president Nada Stotland informed readers that antidepressants restore brain chemistry to normal.

And the public believed. On May 4, 2005, the APA issued a press release celebrating the fact that a survey it conducted had found that 75 percent of consumers believe that mental illnesses are usually caused by a chemical imbalance in the brain. This, said APA president Steven Sharfstein, was evidence of good news for [public] understanding of mental health. A psychiatrist, the press release helpfully noted, was a specialist specifically trained to diagnose and treat chemical imbalances.

That same year, the APA published its Lets Talk Facts about Depression brochure, which delivered the same message: Antidepressants may be prescribed to correct imbalances in the levels of chemicals in the brain.

The APAs public education website continued to tell of chemical imbalances for the next 16 years. Finally, in early 2021, Ronald Pies wrote that he had, at last, managed to get the APA to delete that message.

Even so, the APA website still tells the public a limited version of that story. Visitors to a page titled What is Depression learn that brain chemistry may contribute to an individuals depression and may factor into their treatment. For this reason, antidepressants may be prescribed to modify ones brain chemistry.

In the 1980s and 1990s, the pharmaceutical companiesand the American Psychiatric Associationrealized that non-profit advocacy organizations, like the National Alliance on Mental Illness, could help them sell their disease model to the public and inform the public of the effectiveness of psychiatric drugs. Pharmaceutical money flowed to NAMI and other advocacy organizations, and soon the academic psychiatrists that served as industry thought leaders were populating the scientific advisory councils of the non-profit advocacy groups.

In a 2014 blog published on Mad in America, Philip Hickey identified three prominent consumer organizations that informed the public that depression was due to a chemical imbalance, and published the names of the psychiatrists that served on their scientific advisory boards. Here is the list:

Child and Adolescent Bipolar Foundation

Depression and Bipolar Support Alliance

NAMI

The names on the list constituted a whos who of prominent academic psychiatrists at that time, many of whom were known to have been paid hundreds of thousands of dollars for their thought leader services to industry. Theirs was a collective voice informing the American public that depression was due to a chemical imbalance, which could be successfully treated by antidepressants that helped correct that imbalance. Fifteen years after the APA declared the low-serotonin theory dead, antidepressantson these websiteswere still being presented as an antidote to a disease.

While many consumer organizations have now scrubbed such claims from their sites, they have not disappeared altogether. For example, the Child Mind Institute website, on a page titled Medication for Kids with Depression, provides this description of antidepressants:

The founder of the Child Mind Institute is one of the most prominent child psychiatrists in the United States, Harold Koplewicz. He is chair of the Department of Child and Adolescent Psychiatry at NYU School of Medicine and has been editor-in-chief of the Journal of Child and Adolescent Psychopharmacology since 1997. A primary mission of the Child Mind institute, his profile page states, is to educate and empower parents by providing trustworthy information and resources.

As anyone who watched television in the first decade of the new millennium knows, pharmaceutical companies used the chemical imbalance story to sell their antidepressants. Pfizer, for instance, flooded the airways with its Sad Blob ad, and if you pay close attention, youll see that Pfizer knows the chemical imbalance story is unfounded. Yet, it uses the chemical story to sell its drug anyway. It accomplishes this verbal sleight of hand in two brief sentences: While the cause (of depression) is unknown, depression may be related to an imbalance of natural brain chemicals between nerve cells in the brain. Prescription Zoloft works to correct this imbalance.

The ad closes with this reminder: When you know more about what is wrong, you can help make it right.

Such is the trail of fraud that lawyers could present if they mounted a class action lawsuit. They could detail how there is a long line of research, dating back to the 1970s, that failed to find that low serotonin was a cause of depression. They could show that in 1999 the APAs own textbook declared the theory dead and buried. And then they could detail how the APA, scientific advisory boards at advocacy organizations, and pharmaceutical companies continued to promote the chemical imbalance theory after that, with antidepressants presented as drugs that fixed chemical imbalances. That continued promotion is evidence that from 1999 forward these three groups were knowingly promoting a falsehood, which patients could be expected to act upon.

This is evidence of medical fraudand, one might say, societal medical batterycommitted on a grand scale.

While researchers did not discover that people diagnosed with depression had abnormal serotonin systems before they took an antidepressant, they did discover that the compounds induced the very abnormality hypothesized to cause the disorder in the first place.

The basic mechanism of an SSRI is well known. When a presynaptic neuron releases serotonin into the tiny gap between neurons (known as the synapse), the serotonin molecules bind with receptors on the post-synaptic neuron, and then, in a flash, the serotonin is removed from the synapse. An enzyme metabolizes a small amount of the serotonin; the rest is quickly pumped back into the presynaptic neuron, entering via a channel known as SERT. In a 1975 paper, Eli Lilly scientists reported that fluoxetine, the compound that would be marketed as Prozac, blocked this reuptake process, causing a pile-up of serotonin at the synapse.

However, the presynaptic neuron has autoreceptors on its terminal membrane that monitor serotonin levels in the synapse, and with serotonin levels piling up, these autoreceptors begin to scream, as one scientist quipped, turn off the serotonin machine. The presynaptic neurons begin to fire at a lower rate, while the postsynaptic neurons decrease the density of their receptors for serotonin.

In other words, the drug puts down the accelerator on serotonergic transmission, and the brain responds by putting on the brake.

Over time, other changes may kick in. There are feedback loops that connect different neurotransmitter systems to each other, and so this initial response to the drug is likely a prelude to a host of downstream changes that have yet to be identified. However, the initial response to fluoxetine was fleshed out early, and it told of how fluoxetine, rather than normalize serotonergic pathways, induced profound abnormalities in this system.

In 1996, NIMH director Steven Hyman published a paper titled Initiation and Adaptation: A Paradigm for Understanding Psychotropic Drug Action that told of how all psychiatric drugs could be understood to create abnormalities in brain function.

Psychiatric drugs, he wrote, create create perturbations in neurotransmitter function. In response to this perturbation, the brain goes through a series of compensatory adaptations, and in each instance, the immediate adaption is for the brain to oppose the effects of the drug. An antipsychotic blocks dopamine transmission, and in response the brains dopaminergic pathways spring into high gear, at least for a time. An antidepressant ups serotonergic levels in the synapse, and in response, the brain puts a brake on its serotonergic pathways. These compensatory adaptations, Hyman wrote, are rooted in homeostatic mechanisms that exist, presumably, to permit cells to maintain their equilibrium in the face of alterations in the environment or changes in the internal mileu.

Hyman was describing adaptive changes known as oppositional tolerance to a drug. After a period of time, he continued, the chronic administration of the drug causes substantial and long-lasting alterations in neural function. As part of this process, there are changes in intracellular signaling pathways and gene expression. After a few weeks, he concluded, the persons brain is functioning in a manner that is qualitatively as well as quantitatively different from the normal state.

Qualitatively as well as quantitatively different than normal. Indeed, two Eli Lilly scientists, Ray Fuller and David Wong, early on observed that fluoxetine, since it disrupted serotonergic pathways, could be used to study the role of serotonin neurons in various brain functionsbehavior, sleep, regulation of pituitary hormone releases, pain responsiveness and so on. To conduct such experiments, researchers could administer fluoxetine to animals to observe which functions became compromised. They would look for pathologies to appear.

Such was the state of scientific knowledge about antidepressants as a treatment for depression by the end of the 1990s. There was no evidence that depressed patients suffered from low serotonin before they took an antidepressant, but research had shown that once they did, their brain would begin functioning in a manner that was qualitatively as well as quantitatively different from the normal state.

Antidepressants were promoted to the public as normalizing agents, when in fact researchers knew they were abnormalizing agents.

In their responses to Moncrieffs paper, many psychiatrists sounded a no harm, no foul argument. Antidepressants work, they stated, and thus the prescribing of antidepressants was a helpful practice, even if there was some confusion about the cause of depression and what the drugs did.

Here is how Massachusetts psychiatrist Daniel Carlat put it, in his interview on National Public Radios On Point program:

Doctors dont know exactly about how (antidepressants) work. Patients do want to know there is an explanation out there. And there are times when we do have to give them a shorthand explanation, even if it is not entirely accurate.

In terms of harm done by the chemical imbalance lie, whether an antidepressant reduces the patients symptoms over some period of time is beside the point. The chemical imbalance story informs the patient that he or she suffers from a brain pathology, which requires treatment with a drug that treats that pathology. That is a diagnostic story that changes a patients sense of self and understanding of his or her own mind. Moreover, the treatment is designed to change how the individual emotionally responds to the worldthis is an intervention of a most profound sort.

Indeed, the decision to take an antidepressant puts the patient on a different life course. It puts a person on a path of a medicated future, as opposed to the life the person had known before and the life that the person might have if he or she sought some other non-medical form of treatment. In that sense, the decision of whether to take an antidepressant acts as the proverbial fork in the roadtwo different lives stretch ahead.

That is the harm done when the chemical imbalance story was told to patients seeking help for depression: They made a profound decision about their future based on a lie.

The chemical imbalance story also did harm at a societal level. It remade our collective sense of self.

Before Prozac arrived on the market, a NIMH survey found that only 12% of American adults said they would take a pill to treat depression. This was a survey that told of a public that understood, at some level, that to experience periods of suffering was normal, that life had its ups and downs, and that often people could call on an inner resilienceand environmental supportto lead them out of the tunnel of darkness.

But then came the selling of psychiatrys disease model, and in fairly quick order the public came to see human nature in a new light: our moods were directed by a molecule called serotonin, and if a person experienced depression, they had, in the words of Nancy Andreasen, a broken brain.

This is a conception that also stifles political efforts to create a society that better nurtures mental and emotional well-being. The chemical imbalance story placed the cause of depression within the brain of the individual, which fits a neoliberal agenda, but produces a blindness to social conditions that promote suffering and depression: poverty, lack of access to decent housing, poor childcare support, and so on.

As Moncrieff wrote, surveys have found that more than 85% of the public came to believe that depression is caused by low serotonin. That number tells of a conspiracyby a guild, pharmaceutical companies, and academic psychiatriststhat profoundly betrayed our society. They told us a story that their own research had shown to be false, and they did so because it benefitted guild interests and the financial interests of pharmaceutical companies. As for the members of the scientific councils, they were signing off on a story that kept them in good standing as industry thought leaders and further burnished their public reputations as leaders in the field.

From a legal standpoint, it doesnt really matter whether antidepressants work. Lying to patients and to society is a form of medical battery, and any possible therapeutic benefit doesnt excuse that deception. However, when that antidepressants work claim is examined, it can be seen that it is a continuation of the false marketing of these drugs.

When the public is told that a drug works, they are being led to believe that most people who take the drug can expect to receive a benefit. An antibiotic, for instance, is a drug that can be said to work. When penicillin and other antibiotics were introduced in the 1940s, they cured bacterial infections and any number of bacterial illnesses: pneumonia, scarlet fever, diphtheria, and tuberculosis, to name a few. But an antidepressant cannot be said to work in this way.

What can be said is that there are clinical studies that provide information about the possible risks and benefits of antidepressants, both over the short-term and long-term. The relevant information can be grouped into three types.

Read this article:
Psychiatry, Fraud, and the Case for a Class-Action Lawsuit - Mad In America - Mad in America

But scientists have just bypassed 90 percent of this process creating the first synthetic mouse embryos. Heres what you need to know about this bizarre experiment and what scientists are (and arent) saying about its ethical implications.

What happens when you start messing around with the chemical composition of stem cells? This was the question a team of researchers at the Weizmann Institute of Science in Israel recently delved into with startling results. Publishing their work in the scientific journal Cell, they gave their piece the juicy title Post-Gastrulation Synthetic Embryos Generated Ex Utero from Mouse Nave ESCs. Talk about a tongue twister! Despite the rather confusing and somewhat yawn-inducing title, the experiment detailed in the paper is anything but mundane.

The scientists deluged mice stem cells with a chemical treatment, reverting them to a so-called nave state where they remained ripe for transformation into various cell types (e.g., liver, heart, brain, etc.) vital to the assemblage of a mouse fetus. Next, scientists treated roughly 30 percent of the cells to transform them into the yolk sac. And another percentage received stimulation to develop into the placenta.

In a Weizmann Institute of Science study published in Cell, researchers led by Prof. @jacob_hanna have grown synthetic embryo models of mice outside the womb by starting solely with stem cells cultured in a petri dish without the use of fertilized eggs>> https://t.co/MU3TnLGsfT pic.twitter.com/FNQyWaqXL4

Weizmann Institute (@WeizmannScience) August 2, 2022

Biologist Jacob Hanna, who specializes in embryonic stem cells, explains, We gave these two groups of cells a transient push to give rise to extraembryonic tissues that sustain the developing embryo. After these manipulations, the scientists mixed up the three groups of cells (nave cells, placenta cells, and yolk sac cells) and then placed them in an artificial womb to see what would happen.

The mingled cells floated in small beakers in a specially designed bioreactor imitating the conditions of a mouses womb. The beakers contained nutrient-rich liquid to nourish the cells, and they sat within a spinning cylinder that provided constant movement. The movement simulated a mouse wombs atmospheric pressure, as reported by the Weizmann Institute of Science. The spinning motion also mimicked how nutrients and blood flow through the placenta to the fetus.

If youre wondering how the scientists engineered an artificial womb, thats another story for another time. But suffice to say, Nature reported in 2021 on an experiment where natural mouse fetuses were grown in perpetually moving bioreactor beakers for 11 days. Hanna notes, That really showed that mammalian embryos can grow outside the uterus its not really patterning or sending signals to the embryo so much as providing nutritional support.

3/n Our electronically controlled ex utero natural embryo culture device & novel EUCM conditions (our 2021 Nature paper https://t.co/xNw0FNhn4H ), support Synthetic post-gastrulation Whole Embryo formation (with all extra-embryonic compartments) & only by starting from naive ESCs pic.twitter.com/jykZzgrFbF

Jacob () Hanna (@jacob_hanna) August 1, 2022

Now that youre caught up on the fake womb component of the experiment, lets get back to the mingled cells floating in the beakers. Scientists watched in amazement as the cells formed clumps based on cell type. All told, 10,000 cellular clusters formed, but the vast majority did nothing beyond that.

Only in about 50 cases did the clumps keep going, growing into embryo-like structures, includinga little brain, a beating heart, and an intestinal tract, after 8.5 days in the bioreactor. (Thats nearly half the length of a mouses gestation period.) Ominously, the researchers also noted that the proto-embryos contained variations distinguishing them from naturally occurring mouse embryos.

If this is starting to sound like the makings of a horror movie chock full of zombie mice, all we can say is great minds think alike. Theres a stark gap between being able to do something and deciding whether you should in the first place. Anybody familiar with the premise of Jurassic Park gets this. Despite the breakthrough nature of the experiment, the researchers involved have thus far dodged many of these ethical questions. Thats impressive considering the high stakes involved.

via GIPHY

Alex Meissner, a stem cell biologist at the Max Planck Institute for Molecular Genetics, gave this ambivalent analysis, The mouse is a starting point for thinking about how one wants to approach this in humans. Its not necessary to be alarmed or raise any panic, but as we learn, its important to have in parallel the discussion: How far do we want to take it?

Considering some of the other crazy stuff going on in scientific laboratories worldwide, maybe this conversation shouldve happened, like, yesterday. After all, an article in Cell from April 2021 announced the creation of human-monkey embryos that survived in lab dishes for 20 days (via Live Science). Experiments like these make Jurassic Park look like childs play. Worse, they make the dystopian Planet of the Apes increasingly possible. Such experiments beg the question: Okay, but should we?

By Engrid Barnett, contributor for Ripleys.com

FIND AN ATTRACTION NEAR YOU

Source: Scientists Grow Mouse Embryos Without Sperm Or Eggs

by Ripley's Believe It or Not!

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Scientists Grow Mouse Embryos Without Sperm Or Eggs - EverythingGP

Recent research analyzesmathematical models created to deduce conclusions about how evolution works at the level of populations of organisms.

Claudius Ptolemy, an astronomer and mathematician from Alexandria in the second century, had a lofty goal. He wrote the Almagest, a magisterialtreatise that attempts to explain the motion of stars and the motions of planets. Ptolemy devised a sophisticated mathematical universe model that seemed to replicate the motions of the celestial bodies he had been seeing.

Jeffrey Jensen is a researcher in the Biodesign Center for Mechanisms of Evolution at Arizona State University and a professor in the School of Life Sciences with the Center for Evolution & Medicine. Credit: The Biodesign Institute at Arizona State University

Unfortunately, his cosmic plan had a catastrophic weakness at its heart. Ptolemy began his study with the presumption that the Earth was the center of the cosmos, in keeping with the preconceptions of his day. The Ptolemaic universe, which was made up of intricate epicycles to explain the motions of the planets and stars, has long ago been consigned to history books,its conclusions persisted as scientific dogma for more than 1200 years.

No less vulnerable to flawed theoretical methods are the models in the area of evolutionary biology. Evolutionary biology can result in impressive models that fall short of capturing the genuine workings of nature as it develops the bewildering variety of living species on Earth.

A recent study looks at mathematical models created to deduce conclusions about how evolution works at the level of populations of species. The research comes to the conclusion that these models must be built with great caution, avoiding unwarranted starting assumptions, considering the quality of existing knowledge, and staying open to alternative explanations.

Failure to adhere to strict procedures in the construction of null models can result in theories that appear to fit some aspects of the data obtained from DNA sequencing but fall short in accurately elucidating the underlying evolutionary processes, which are frequently extremely complex and multifaceted.

Such theoretical frameworks may offer compelling but ultimately flawed pictures of how evolution actually acts on populations over time, be these populations of bacteria, shoals of fish, or human societies and their various migrations during prehistory.

In the new study, Jeffrey Jensen, a researcher in the Biodesign Center for Mechanisms of Evolution at Arizona State University and professor in the School of Life Sciences with the Center for Evolution & Medicine, leads a group of international luminaries in the field in providing guidance for future research. Together, they describe a range of criteria that can be used to better ensure the accuracy of models that produce statistical inferences in population genomicsa scientific discipline concerned with large-scale comparisons of DNA sequences within and across populations and species.

One of our key messages is the importance of considering the contributions of evolutionary processes certain to be in constant operation (such as purifying selection and genetic drift), before simply relying on hypothesized or rare evolutionary processes as the primary drivers of observed population variation (such as positive selection), Jensen emphasized.

The study was recently published in the journal PLoS Biology.

Population genomics arose as early efforts in the field attempted to reconcile Charles Darwins notion of evolution by means of natural selection with the first inklings of the mechanisms of inheritance, uncovered by the Augustinian monk, Gregor Mendel.

Susanne Pfeifer is a researcher in the Biodesign Center for Mechanisms of Evolution and an assistant professor at the Center for Evolution & Medicine. Credit: The Biodesign Institute at Arizona State University

The synthesis culminated in the 1920s and early 30s, largely thanks to the mathematical work of Fisher, Haldane, and Wright, who were the first to explore how natural selection together with other evolutionary forces would modify the genetic composition of Mendelian populations over time.

Today, studies in population genomics involve the large-scale application of various genomic technologies to explore the genetic composition of biological populations, and how various factors, including natural selection and genetic drift, produce changes in genetic composition over time.

To accomplish this, population geneticists develop mathematical models quantifying the contributions of these evolutionary processes in shaping gene frequencies, use this theory to design statistical inference approaches for estimating the forces producing observed patterns of genetic variation in actual populations, and test their conclusions against accumulated data.

The study of genomic variation focuses on DNA sequence differences among individuals and populations. Some of these variants are critically important for biological function, including mutations responsible for genetic disease, while others have no detectable biological effects.

Such variation in the human genome can take several forms. One common source of variation is known as single nucleotide polymorphisms, or SNPs, where a single DNA letter in the genome is altered. But larger-scale variation in the genome, involving the simultaneous alteration of hundreds or even thousands of base pairs is also possible. Again, some such alterations may play a role in disease risk and survival while many others have no effect.

Natural selection may occur when different variants segregating in a population have a fitness differential relative to one another. By designing and studying mathematical models governing the corresponding gene frequency change and applying those models to empirical data, population geneticists seek to understand the contributing evolutionary processes in a rigorous, quantitative way. Thus, population genetics is often regarded as the theoretical cornerstone of modern Darwinian evolution.

Although the importance of natural selection to the evolutionary process is undeniable, the role of positive selection in increasing the frequency of beneficial variants the potential driver of adaptation is certain to be comparatively rare relative even to other forms of natural selection. For example, purifying selection the removal of deleterious variants from the population is a constantly acting and far more pervasive form of selection.

In addition, there are multiple non-selective evolutionary processes of great importance. For example, genetic drift describes the many stochastic fluctuations inherent to evolution. In large populations, natural selection may act more efficiently in purging deleterious variation and potentially fixing beneficial variation, whereas as populations become smaller genetic drift will be increasingly dominant.

The distinction can be seen in dramatic form when comparing prokaryotic organisms like bacteria with organisms composed of eukaryotic cells, including humans. In the former case, the vast population sizes tend to result in more efficient selection. In contrast, a weaker selection pressure operating in eukaryotes is more permissive to genomic changes, provided that they are not strongly deleterious.

According to the Neutral Theory of Molecular Evolution a new guiding principle of evolutionary theory proposed by the population geneticist Motoo Kimura over 50 years ago most evolutionary changes at the molecular level in real populations are governed not by natural selection, but by genetic drift. The study emphasizes that this critical point is too often missed by evolutionary biologists. As co-author Michael Lynch, director of ASUs Biodesign Center for Mechanisms in Evolution cogently observes, natural selection is just one of several evolutionary mechanisms, and the failure to realize this is probably the most significant impediment to a fruitful integration of evolutionary theory with molecular, cellular, and developmental biology.

The new consensus study further stresses that a failure to consider these alternative evolutionary mechanisms which are certain to be operating, including genetic drift, and incorporate these into models of population genomics, is likely to lead researchers astray. The common overreliance on purely adaptive models to explain genomic variation has led to a raft of interpretations of dubious value, the authors assert.

The study presents a detailed flow chart that can help guide the development of more accurate models used to draw evolutionary inferences, based on genomic data. Biological parameters that vary among species include not only evolutionary variables like population size, mutation rates, recombination rates, and population structure and history but the way the genome itself is structured and life history traits, including mating behavior. All of these factors play a vital role in dictating observed molecular variation and evolution.

While these many considerations may sound daunting for some researchers, it is important to note that many excellent research groups at ASU and around the world are actively improving our understanding of these underlying evolutionary parameters, providing constantly improving inference, for example, of mutation and recombination rates, added co-author Susanne Pfeifer, an Assistant Professor in the Center for Evolution & Medicine and the Biodesign Center for Mechanisms of Evolution.

Where once, theoretical models in population genomics proliferated alongside relatively scant genomic data, today an avalanche of data, enabled by rapid, low-cost DNA sequencing of organisms across the tree of life, has dramatically changed the field. The careful and judicious use of this gold mine of genomic data will help advance the most rigorous models to unlock evolutions many remaining mysteries.

Reference: Recommendations for improving statistical inference in population genomics by Parul Johri, Charles F. Aquadro, Mark Beaumont, Brian Charlesworth, Laurent Excoffier, Adam Eyre-Walker, Peter D. Keightley, Michael Lynch, Gil McVean, Bret A. Payseur, Susanne P. Pfeifer, Wolfgang Stephan and Jeffrey D. Jensen, 31 May 2022, PLoS Biology.DOI: 10.1371/journal.pbio.3001669

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The Pitfalls of Evolutionary Genomics - SciTechDaily

Genomics and DNA testing have been hailed as a window into our medical future that could help us live longer, healthier lives.

The first such consumer test available in Dubai, for Dh999, has been trialled to find out exactly what a spit sample can reveal, and what steps should be taken as a result.

Three weeks after a saliva sample was collected by Emirates Post from my home and processed at Dante Labs' $6 million laboratory in Dubai Silicon Oasis, I received a call from the company that my unique genetic profile was ready.

I was invited to meet Alexandra Fonzi, a genomic and molecular biotechnologist at Dante Labs, to discuss my test results.

A little apprehensive about what revelations may be revealed about how my life may end, I was also eager to understand more about my genetics and why my body reacts in certain ways to exercise and diet.

Genetic screening can answer questions such as how some people put on weight, yet others who eat similar foods do not, and why some healthy people get cancer while other sedentary cigarette smokers live well into old age.

My specific DNA report had a number of different colour codes to indicate analysis.

Green icons showed no area of concern, while yellow markers showed genes that could help in fitness and lifestyle.

The $6 million laboratory opened in January and has the capacity to analyse up to 1,000 samples a week. All photos: Pawan Singh / The National

An orange flag in my report identified a requirement for action, and a predisposition towards certain illnesses and diseases because of my specific genes.

A blood pressure alert was issued to suggest I was potentially at risk of a heart attack or stroke without changes to my diet, despite regularly exercising, because of the genes I carried.

You can reduce salt or do more outdoor activities like running to help reduce blood pressure, said Ms Fonzi, who provides a one-to-one genetic consultation once results are available.

This information can be passed on to a personal trainer and dietitian to help them develop a personalised plan based on this genetic information.

Isometric exercises were recommended as the test showed I had a genetically poor response to muscle building, but I was physiologically suited to high-intensity sports and endurance events.

Without dietary changes, you may experience problems later in life, with high blood pressure you can have issues when you fly for example, said Ms Fonzi.

If you notify a doctor, they can help with medication to reduce blood pressure.

Chief executive Andrea Riposati shows the sequencer machine at Dante Labs, Dubai Silicon Oasis. Pawan Singh / The National

The report is split into two areas, a fitness report showed what injuries I may be predisposed to in my case tennis elbow and lower back problems, as well as metabolism and genetic markers for disease.

A second report focused on nutrition and revealed what foods could trigger inflammation or digestive problems.

Glucose intolerance in metabolism is connected to diet, so there is a predisposition that should be addressed by altering your diet to avoid the chances of diabetes in the future, Ms Fonzi said.

If we have a high level of oxidative stress, as in your case, you can age earlier and your body will respond differently to someone who does not react to this kind of inflammatory process.

A Mediterranean-style diet, with whole grains, low-fat dairy products, more vegetables, fruits and fish oils was recommended as the test showed I had a slow lipid metabolism and glucose intolerance.

It meant without regular exercise, I was more likely to put on weight and potentially be at risk of diabetes, while impaired glucose tolerance is a common risk factor for ischaemic heart disease.

Some genetic traits revealed in the report can help you, with a good response to working out to help you achieve a high level in sport, but you also have a propensity to put on weight if you ceased to exercise, Ms Fonzi said.

I was also told I was more likely to develop certain injuries, such as shoulder injuries, muscle cramps and arthritis later in life, because of my specific genetic profile.

Cramps could be countered by taking drinks with added sodium and potassium, particularly in the heat, while maintaining a healthy weight could avoid stress on joints in older age, I was told.

Lab technicians working in the Dante Labs at Silicon Oasis in Dubai. Pawan Singh / The National

More of a worry was the presence of a specific gene that made me more predisposed to some cancers and cardiovascular disease.

As you have a high disposition to oxidative stress and carry the A allele gene, if you were a smoker you would be at greater risk of cancer and other cardiovascular disease, said Ms Fonzi.

The way your body absorbs HDL cholesterol and fats is also making you at risk of high cholesterol, which is also a hereditary condition in this case as you have an active life.

It is something that needs to be monitored with regular blood analysis.

This is a scientific test to you and will give you information as to how you can make your life better in the future by knowing what food you need to avoid, or what nutrition you need to take.

Genetic testing and profiling of patients to predict future care requirements will become a key component of the healthcare strategy in Abu Dhabi, and elsewhere in the GCC.

Thanks to the latest artificial intelligence, G42 Healthcare in Masdar City is one of the leaders in the region, in this kind of medical technology.

At the companys Biogenix Labs, diagnostic tests or biomarkers help assess high-risk patients and aid in the early detection of diseases, their prognosis, therapy selection, response to treatment, and chances of recurrence.

Thousands of genome sequencing procedures carried out weekly can unlock the possibilities for preventive and precision therapies to transform the UAE healthcare landscape, enabling it to transition from 'sick care' to health care.

G42 Healthcare aims to use the technology to provide insights and facilitate early diagnosis and treatment of cancer, rare and metabolic diseases and other genetic conditions.

As part of our efforts to support the health of future generations and provide better healthcare every day, Biogenix Labs is expanding its clinical genetics offering in the region and reinforcing its reputation as the regional testing provider of choice, said Dr Fahed Al Marzooqi, chief operating officer of G42 Healthcare.

We will soon be expanding this offering to the Kingdom of Saudi Arabia and the wider GCC region as well.

Updated: August 14, 2022, 4:54 AM

Excerpt from:
How a simple home DNA test unravelled the genetic code that could help prolong my life - The National

The University of Western Australia (UWA) is ranked among the top 100 universities in the world and a member of the prestigious Australian Group of Eight research intensive universities. With a strong research track record, vibrant campus and working environments, supported by the freedom to innovate and inspire, there is no better time to join Western Australias top university.

About the team

UWAs Medical School brings together the brightest students, experienced clinicians and committed researchers to unlock the greatest health challenges of our day. Celebrating 60 years in 2017, the Medical School is an infinite source of teaching and learning for individuals who share our goal of delivering better health outcomes today and into the future.

This position is based within the Systems Biology and Genomics Laboratory, led by Professor Alistair Forrest, and is part of the UWA Centre for Medical Research.

The Forrest lab is comprised of molecular, cellular and computational biologists, forming a multi-disciplinary team environment undertaking a diverse range of genomics and cancer single cell research. We are leading the Western Australian Cancer Single Cell initiative which is using single cell, single nuclei and spatial transcriptomic profiling to characterize hundreds of tumour samples kindly donated by patients around Perth.

About the opportunity

You will provide a high level of technical support to researchers with responsibility to perform experimental molecular and cellular biology work in a collaborative research program. You will primarily assist in the processing of tumour samples for spatial transcriptomic profiling.

About you

To be considered for this role, you will demonstrate a relevant degree qualification (preferably a BSc Hons), or an equivalent degree in molecular biology, pathology, lab medicine, biomedical science, genetics, biochemistry, or related fields.

You will also have substantial experience in a tissue sectioning and staining, single cell or spatial transcriptomics, or next generation sequencing, along with competency in standard techniques used in at least one of the following: histopathology, molecular biology or cell biology.

Note: This position requires compliance with Human and Animal Ethics requirements.

About your application

You are required to address the selection criteria in your submission in a separate document. For information to assist you with compiling statements to answer the selection criteria, please visit Addressing the selection criteria.

Closing date: 11:55 PM AWST on Tuesday, 23 August 2022

To learn more about this opportunity, please contact Professor Alistair Forrest on (08) 6151 0780 or at alistair.forrest@perkins.uwa.edu.au.

This position is only open to applicants with relevant rights to work in Australia.

Application Details: Please apply online via the Apply Now button.

Our commitment to inclusion and diversity

UWA is committed to a diverse workforce. We celebrate inclusion and diversity and believe gender equity is fundamental to achieving our goals.

UWA is committed to inclusive recruitment and is happy to adjust the recruitment process for your accessibility requirements. If you have queries in relation to the application process, please contact talent-hr@uwa.edu.aureferencing the 6-digit job reference number and type of communication you prefer, and a member of our team will be in touch to discuss your requirements.

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Graduate Research Officer job with UNIVERSITY OF WESTERN AUSTRALIA | 304277 - Times Higher Education

Faculty and staff

Eugene Parker, professor emeritus of astronomy and astrophysics, died March 15 in Chicago. He was 94. Parker is considered a visionary in the field of heliophysics, which focuses on the sun and other stars. Trained at Michigan State University and Caltech, he joined the UChicago faculty in 1955. He is best known for theorizing the existence of solar wind, a supersonic flow of particles off the suns surface. The theorys confirmation in 1962 reshaped understanding of space and the solar system. He also made important contributions to the study of magnetized shock waves, cosmic rays, and galaxies magnetic fields. His many honors include the US National Medal of Science and the Kyoto Prize. In 2017 NASA announced it would name its landmark solar mission for Parker. Soon after, he became the first person to witness the launch of a spacecraft bearing his name. Parker is survived by his wife, Niesje; a daughter, Joyce Marie Parker, SB77; a son, Eric Glenn Parker, MBA88; a brother; three grandchildren, including Miles Loh, AB10; and two great-grandchildren.

Walter Kaegi Jr., professor emeritus in the Department of History and the Oriental Institute, died February 24 in Chicago. He was 84. Kaegi was noted for his scholarship on the Byzantine and Roman Empires as well as early Islam. With degrees from Haverford College and Harvard, he joined the faculty at UChicago in 1965, where he taught for 52 years. A military historian whose studies of warfare and strategy often drew upon a wide variety of sources, Kaegi demonstrated in his research a detailed knowledge of geography, honed by extensive travel to the regions he studied. Over his career, he authored, coauthored, or edited some 30 books while teaching and mentoring three generations of historians. His iconic Russian fur hat was included in the 1999 Scav Hunt. He is survived by two sons, a sister, and three grandchildren.

Dietrich Mller of Chicago, professor emeritus of physics, died December 22. He was 85. Born and educated in Germany, he spent more than 50 years as an experimental physicist at the University. His research focused on cosmic raysenergetic particles that travel through our solar system from elsewhere in the galaxy, offering a window into astrophysical phenomena and the universe. Mller built instruments that collected data during space shuttle flights and aboard high-altitude balloons above the Arctic and Antarctic. He worked on HEAT (High Energy Antimatter Telescope), which took measurements of the abundances and energy spectra of cosmic-ray positrons and antiprotons. He is survived by his wife, Renate; a daughter, Agnes B. Mller-Goldstein, LAB92; two sons, Georg S. Mller, LAB87, AB91, MBA97, PhD98, and Michael Mller, LAB89; a sister; a brother; and six grandchildren.

James W. Truran, professor emeritus of astronomy and astrophysics, of Olympia Fields, IL, died March 5. He was 81. A leading figure in nuclear astrophysics, he helped explain how stars and stellar explosions produce virtually all the elements of the universe. His research explored the mechanisms of novae and supernovae and the processes by which they produce elements heavier than hydrogen and helium. Educated at Cornell and Yale, Truran spent time at NASA, Caltech, Lawrence Livermore National Laboratory, and Yeshiva Universityand taught at the University of Illinois at Urbana-Champaignbefore joining the UChicago faculty in the early 1990s. His many honors include the American Physical Societys 2021 Hans A. Bethe Prize. He is survived by his wife, Carol; three daughters; four grandchildren; and a great-grandchild.

Vincent L. Scamurra, MBA74, of Chicago, died January 2. He was 78. A graduate of Canisius College and Chicago Booth, he worked in UChicagos Information Technology Services department from 1987 to 2010 as a programmer and software systems engineer. Survivors include three sisters.

Joshua Stampfer, SB42, of Portland, OR, died December 26, 2019. He was 97. As rabbi at Congregation Neveh Shalom from 1954 to 1993, he helped grow Portlands Jewish community. His legacy includes creating Camp Solomon Schechter near Tumwater, WA, establishing the Oregon Holocaust Resource Center and the Institute for Judaic Studies, building the Oregon Jewish Historical Society, and helping found the Oregon Jewish Museum. The son and grandson of rabbis, he was born in what was then Palestine and moved to the United States as a child. While working toward his chemistry degree in the College, he taught Hebrew in a synagogue. He is survived by four children, 20 grandchildren, and 16 great-grandchildren.

Robert G. Frazier, LAB41, PhB43, SB45, MD47, died October 13 in Prospect Heights, IL. He was 98. As executive director of the American Academy of Pediatrics in the 1960s, he testified before Congress on the value of the new Head Start program. A lifelong advocate of the great books, Frazier taught the course Medical Ethics and Literature for Medical Students at Loyola University Chicago. He was an avid woodworker who received a patent for his tetrahedral joint, which required no nails or glue. Survivors include his wife, Ruth Ann (Johnson) Frazier, LAB44, AB49; daughter Carolyn Ruth Frazier, MLA01; a son; and three grandchildren.

Walter Lawrence Jr., PhB44, SB46, MD48, died November 9 in Richmond, VA. He was 96. During the Korean War, he was chief of surgery in a mobile Army surgical hospital (MASH). In 1963, as a surgeon at Memorial Sloan Kettering Cancer Center, Lawrence performed the first renal transplant in New York City. At the Medical College of Virginia (later Virginia Commonwealth University), where he served for some 50 years, he helped establish the first academic division of surgical oncology in the United States. He received the Distinguished Alumni Award from UChicagos Medical and Biological Sciences Alumni Association in 1976. His wife, Susan Shryock Lawrence, PhB44, AM47, EX48, died in 2019. He is survived by a daughter; three sons; eight grandchildren; and brother Arthur Gene Lawrence, SB50, MD52.

Marion (Levin) Swerdlow, SB46, of Highland Park, IL, died December 16. She was 97. After graduating from the College, she worked as a bacteriology technologist at Michael Reese Hospital and in mycology laboratories at the University. Swerdlow also studied classical guitar and played the piano. Her husband, Martin A. Swerdlow, a professor of pathology and associate dean in the Pritzker School of Medicine, died in 2012. She is survived by two sons, Steven H. Swerdlow, LAB67, and Gary Swerdlow, LAB70; two grandchildren; and one great-grandchild.

Donald R. Gerth, AB47, AM51, PhD63, died December 6 in Carmichael, CA. He was 93. Gerth spent 45 years as a professor of political science and leader in the California State University (CSU) system. Born in Chicago, he worked in a steel mill before entering the College at age 16. With his masters in political science, Gerth served in the Air Force during the Korean War and later returned to the University to earn his doctorate. Following appointments at San Francisco State, Chico State, and as president of CSU Dominguez Hills, he became the longest-serving president in the history of Sacramento State University. As president he expanded facilities and academic programs, increased and diversified student enrollment, and defended affirmative action programs. He is survived by his wife, Beverly; two daughters; five grandchildren; and nine great-grandchildren.

Connie (Holubar) Hogarth, PhB47, SB48, died February 11 in Beacon, NY. She was 95. A lifelong activist, she prepared for a medical career and studied dance as a scholarship student in the College. Moving to New York with her first husband, she protested the Rosenberg trial in 1951 at the White House. Hogarth later became involved in Vietnam War protests and in 1973 cofounded the Westchester Peoples Action Coalition. For almost a quarter century as WESPACs executive director, she led protests, lobbying, and educational efforts around issues including nuclear power, South African apartheid, the Iraq War, womens rights, and the environment. After retiring she taught students to become social activists at the Connie Hogarth Center for Social Action at Manhattanville College. She is survived by two sons and a grandson.

Erle M. Korshak, EX47, of San Francisco, died August 26, 2021. He was 97. Korshak, a science fiction editor, publisher, bookseller, and fan, was an early organizer of Worldcon, the World Science Fiction Convention. A World War II Army veteran, Korshak attended the University upon his discharge but left to cofound Shasta Publishers, which issued several seminal science fiction books. After the press closed in 1957, Korshak earned a JD and went on to practice law in California and Nevada. During this time, he and his son, Stephen D. Korshak, LAB69, AB74, began collecting and exhibiting classic science fiction art; in 2009, they revived Shasta Publishers as Shasta-Phoenix. The elder Korshak was inducted into the First Fandom Hall of Fame in 1996 and received the Barry R. Levin Lifetime Collectors Award in 2000. He is survived by his son and four grandchildren. (For more, see Notes.)

Milton A. Levenfeld, PhB47, JD50, died October 21 in Canton, MA. He was 94. Early in his law career, Levenfeld argued a case before the US Supreme Court. In 1963 he cofounded Levenfeld & Kanter (later Levenfeld, Kanter, Baskes & Lippitz), a nationwide tax, trust, and estate law firm. It was later restructured as Levenfeld Pearlstein, a regional general practice law firm in Chicago. He is survived by his wife, Iona Wishner Levenfeld, AB49, AM51; a daughter; two sons, including David M. Levenfeld, AM79; 11 grandchildren; and three great-grandchildren.

Meyer Rubin, SB47, SM49, PhD56, died May 2, 2020, in Manassas, VA. He was 96. Rubin joined the US Army Air Corps in 1943, studying meteorology at the University of Michigan before duty as a field meteorologist in the Pacific theater during World War II. A geochemist, he spent his career at the US Geological Survey in Washington, DC, and made major contributions in radiocarbon dating, mass spectrometry, and climate science. He is survived by three sons, five grandchildren, and six great-grandchildren.

Eve Spiro Jones Bonner, SB48, SM48, PhD53, of Los Angeles, died September 16, 2021. She was 96. Trained as a psychologist, she worked under Bruno Bettelheim at the Sonia Shankman Orthogenic School in the 1950s, providing psychological testing and counseling. She published two parenting books, and her nationally syndicated advice column, Parents World, appeared for over a decade in more than 100 US newspapers. After moving to California, she taught psychology at Los Angeles City College until her retirement in 1992; she also maintained a private practice. An avid rosarian, she competed in rose shows. The University recognized her with an Alumni Service Award in 2001. She is survived by three daughters, one son, a sister, eight grandchildren, and 14 great-grandchildren.

Warner C. White, AM50, of Burlington, VT, died April 16. He was 95. During his graduate studies in English, he met and married Phyllis Cox White, LAB44. Ordained an Episcopal priest in 1953, he served as rector of the Church of St. Paul & the Redeemer in Hyde Park during the 1960s and 70s and took an active role in the civil rights movement. In 1979 he moved to Marshall, MI, where he served at Trinity Episcopal until his retirement in 1991. He and Phyllis, who died in 2007, moved to Vermont in 1999. He is survived by his second wife, Roberta; two daughters; three sons, including Sumner Warner White, SB73; two stepdaughters; a stepson; 16 grandchildren and step-grandchildren; and 17 great-grandchildren.

Mary Elizabeth Molly Felker Lunsford, AB52, AM57, died November 26 in Nashville, TN. She was 90. At UChicago she served as cohead of Linn House in Burton-Judson with her then husband, Terry Farquhar Lunsford, AB51, JD57. She later worked as a budget analyst for the State of Colorado and the University of California; as a community organizer and volunteer in Berkeley, CA; and in volunteer and staff positions in the Peace Corps. Before retiring and moving to Tennessee in 2018, she was a teacher of English as a foreign language and computer lab librarian at Montgomery College in Rockville, MD. Survivors include a son and a granddaughter.

Mary (Deters) ODowd, AB52, died January 22 in Lakewood, NJ. She was 89. She worked most of her career in college and university administration and lived in Chicago and Evanston, IL. An accomplished singer and musician, she sang in several choral and Renaissance music groups, including the Rockefeller Chapel Choir during her College years. She moved to New Jersey in 2017. Survivors include her daughter.

Norman Mages, AB53, MD58, of Kentfield, CA, died November 9. He was 86. After attending Chicago public schools, he entered the College at age 16 and continued to medical school, specializing in psychiatry. Early in his career, he worked with narcotics offenders at a prison hospital in Texas. He later joined the faculty of the University of California, San Francisco, and opened a private practice in psychiatry. He is survived by his wife, Ruth Noel; two daughters; three sons; and two grandchildren.

Marshall J. Hartman, AB54, JD57, of Skokie, IL, died September 21, 2021. He was 87. Hartmans legal career began when he was hired as the only lawyer probation officer at the Juvenile Court of Cook County. Moving to the Law Office of the Cook County Public Defender, he successfully argued three cases before the US Supreme Court. He drafted legislation to create the Illinois Office of the State Appellate Defender, which represents indigent persons in criminal appeals. He later served as chief public defender of Lake County and led OSADs Capital Litigation Division. The Illinois State Bar Association recognized Hartman with a 2017 Laureate Award. Survivors include his wife, Patricia; two daughters; two sons; a sister; and nine grandchildren.

Terrance Sandalow, AB54, JD57, died January 29 in Washington, DC. He was 87. An influential scholar in the fields of constitutional law, federal courts, and local government, he served on the University of Michigan Law School faculty for 34 years and as the schools dean from 1978 to 1986. Early in his career, he clerked for Justice Potter Stewart of the US Supreme Court. A strong supporter of the constitutionality of affirmative action, he authored the brief submitted to the Supreme Court in the 1978 Regents of the University of California v. Bakke case on behalf of the American Association of University Professors. In 1995 UChicago recognized him with a Professional Achievement Alumni Award. His wife, Ina Faye Davis Sandalow, EX58, died in 2020. He is survived by three children; five siblings, including Michael Sandalow, AB62; seven grandchildren; and multiple great-grandchildren.

Stuart O. Zimmerman, AB54, PhD64, died October 2 in Houston. He was 86. After earning a PhD in mathematical biology, he served as a research associate, instructor, and assistant professor at UChicago. In 1967 Zimmerman was appointed chair of the Department of Biomathematics at Houstons MD Anderson Cancer Center, a position he held until his retirement in 2001; he continued in a part-time appointment until 2012. His first wife, Mary Joan (Spiegel) Zimmerman, AB56, AB58, died in 2008. He is survived by his second wife, Judy McConathy; a son; and two grandchildren.

Leona Jacker Peterson, AM55, PhD71, died January 4 in Elmhurst, IL. She was 92. Trained as a nurse, she received her doctorate in education at the University. After working at the US Embassy in Kinshasa, Democratic Republic of the Congo, she taught nursing at Purdue and at the University of Illinois at Chicago. She is survived by her husband, Arthur; two daughters; six grandchildren; and six great-grandchildren.

Johan E. Hille, AM56, of Lake Zurich, IL, died December 3, 2018. He was 88. An educator in suburban Chicago, he taught at Hadley Junior High School in Glen Ellyn and served as principal of Hauser Junior High School in Riverside. He was an Army veteran and active in various volunteer organizations, including the Kiwanis Club. He is survived by a daughter, a son, a sister, and a granddaughter.

Philip M. Phibbs, AM56, PhD57, of Tacoma, WA, died March 21. He was 90. Following his graduate studies in political science, he taught at Wellesley College, where he also served as executive vice president. In 1973 he became the 11th president of the University of Puget Sound, leading the institution until 1992. In retirement Phibbs spent a decade working with artist Dale Chihuly to establish the Museum of Glass in Tacoma. He served on the boards of the Seattle Opera, the Museum of Glass, and the National Association of Schools and Colleges of the United Methodist Church, among others. He is survived by his wife, Gwen; two daughters; a brother; seven grandchildren; and one great-grandchild.

Jean Lani Kwon Herrmann, AB57, died December 3, in Hana, HI. She was 85. Born in Hana, eastern Maui, she was a musician and folklorist. She and Cal C. Herrmann, AB51, SM56, married in 1961. Over her long career she performed at music venues and festivals across the United States and Europe; she also restored traditional instruments and produced books on folk music. Herrmann cofounded the Folklore Society of Greater Washington in 1964 and the farmers market in Richmond, CA, in 1984. She later earned a masters degree in library and information science. She is survived by her husband, a daughter, two sons, and six grandchildren.

Irene M. (Samorajski) Moody, SB57, died June 21, 2021, in Shelburne, MA. She was 86. Born at home on the family farm in Shelburne, she attended Arms Academy before enrolling in the College. With a masters in education from Fitchburg State University, she taught science for 27 years at Montachusett Regional Vocational Technical High School. She also sang with the Nashoba Valley Chorale and the Hundredth Town Chorus. She is survived by a daughter, Lisa Moody, AB86; two sons, including Robert Moody II, MBA99; 10 grandchildren; and a great-grandchild.

James F. ODonnell, PhD57, died September 7, 2021, in Rockville, MD. He was 93. A Korean War veteran, ODonnell spent a decade at the University of Cincinnati conducting research on liver disease. In 1968 he joined the National Institutes of Health, rising to the position of director of extramural affairs by his retirement in 1999. He was selected in 1979 by President Jimmy Carter as a charter member of the federal Senior Executive Service. ODonnell volunteered to participate in a decades-long study on Alzheimers, in honor of family members affected by the disease, and donated his brain to this research as part of his legacy. His wife, Winifred Locke ODonnell, AM54, died in 2011. He is survived by two daughters, a son, two brothers, two grandchildren, and a great-grandchild.

Harriet E. Manelis Klein, AB58, died September 4, 2021, in Briarcliff Manor, NY. She was 84. Growing up in an English- and Yiddish-speaking household in New York City, she studied ancient languages and classics in the College. She later pursued her doctorate at Columbia University, concentrating on indigenous languages in Argentina and Panama. A linguistic anthropologist, she joined the faculty of Montclair State University in 1972. Active in the professional associations of both disciplines, she particularly focused on advancing gender equity. Klein retired to Long Island, NY, and became a visiting scholar in linguistics at Stony Brook University. Survivors include a daughter, two sons, and several grandchildren.

Merton S. Krause, PhD59, of Evanston, IL, died July 23, 2021. He was 90. Krause, who published nearly 100 papers, was a highly regarded expert and critical scholar of research methods and psychometric measurement. One of the earliest members of the Society for Psychotherapy Research, he devised creative ways to measure and evaluate treatment progress. His wife, Carroll Bordelon, AB58, died in 1983. He is survived by his companion, Catharine Jones.

Alvin Platt, AM60, died June 17, 2021, in Palo Alto, CA. He was 86. After studying social sciences at the University, he worked as a teacher and counselor in the Sonia Shankman Orthogenic School and Chicago Public Schools. For more than 25 years he held educational and administrative positions at North Shore Congregation Israel in Glencoe, IL. Later, as executive director of the Jewish Community Federation of the South Peninsula Region in Palo Alto, he helped create what is now the Gideon Hausner Jewish Day School. He served as president and board member of the Palo Alto Humane Society. He is survived by his wife, Barbara; two daughters; three sons; a sister; a brother; and several grandchildren and great-grandchildren.

Walter T. K. Nugent, PhD61, died September 8, 2021, in Seattle. He was 86. A historian whose research focused on western migration in the US, populism, and demography, he taught for 21 years at Indiana UniversityBloomington, also serving as an associate dean, director of study abroad programs, and chair of the history department. In 1984 he joined the University of Notre Dame as its inaugural Andrew V. Tackes Professor of American History. A recipient of a Guggenheim Fellowship and two Fulbright Awards, he authored, coauthored, or edited numerous books, including Color Coded: Party Politics in the American West, 19502016 (2018). He is survived by his wife, Suellen Hoy; six children, including Katherine Nugent Yngve, AM86; a sister; a brother; eight grandchildren; and two great-grandchildren.

Nicholas Snowden Hopkins, AM64, PhD67, died June 9, 2021, in Cairo. He was 82. An anthropologist, he conducted his dissertation fieldwork in a small town in Mali, studying local politics and development. While teaching at New York University in the early 70s, he researched agrarian and social change in northern Tunisia. He joined the faculty of the American University of Cairo in 1975, where he stayed for the remainder of his career. At AUC he served as a department chair and dean of the humanities and social sciences and pursued research on development and social change in Egypt and India. He is survived by his wife, Ferial Ghazoul; two sons; a sister; a brother; and three grandchildren.

Albert E. Dahlberg, LAB54, MD65, PhD68, died March 1 in Providence, RI. He was 83. A professor of molecular genetics and biochemistry at Brown University, he focused on the structure and function of the ribosome. He received 43 years of uninterrupted funding from the National Institutes of Health for his investigations; published widely; and taught and mentored countless students and postdoctoral researchers in his laboratory. He is survived by his wife, Pamela; a daughter; two sons; a sister, Cordelia D. Benedict, LAB53, AM67; a brother, James E. Dahlberg, LAB56, PhD66; and six grandchildren.

Marden D. Paru, AM65, of Sarasota, FL, died September 1, 2021. He was 79. An educator and author, he was the dean and cofounder of the Sarasota Liberal Yeshiva, an adult Jewish studies institute. Trained as a social worker, he served as a Jewish Federation executive and directed other nonprofit organizations. He met his wife, Joan Kemeny Paru, when they were matched by a computer program created on the Harvard-MIT mainframe in 1965; their engagement made the front page of the Chicago Daily News. He is survived by his wife, a daughter, a son, a sister, and two grandchildren.

Thomas W. Cole Jr., PhD66, of Atlanta, died April 14. He was 81. An organic chemist, Cole served as a teacher and administrator at several historically Black colleges and universities throughout his career. He was a professor at Atlanta University Center, later becoming provost and vice president for academic affairs. In the early 1980s he served as president of West Virginia State University. In 1988, as president of Clark College, Cole led its consolidation with Atlanta University; he remained president of Clark Atlanta University for more than a decade. He is survived by his wife, Brenda; a daughter; a son; two grandchildren; and three sisters.

Sandra Jane Kelley Musgrave Harvey, AB67, AM68, of Wilmington, DE, died October 1. She was 76. After studying the humanities and English literature at UChicago, she worked in computer programming and data processing. Moving to Delaware with her family, she embarked on a 24-year career in state government, working as a data center manager and in the information resources management unit of the Department of Health and Social Services. She is survived by a daughter, a son, and a sister.

Maurice Mo D. Levi, AM68, PhD72, died April 28, 2021, in Vancouver, British Columbia. He was 75. An economist, he joined the faculty at the University of British Columbia in 1974. Known for his ability to explain complex ideas to students of all levels, he won eight teaching awards during his career at the UBCs Sauder School of Business. He wrote acclaimed textbooks on international finance and several economics books. Survivors include his wife, Kate; a daughter; and two sons.

James Ryosaku Morita, PhD68, of Lincolnshire, IL, died March 9, 2021. He was 89. Raised in Daianji, Okayama, Japan, he moved to the US in 1958 with his wife, Ichiko, where both pursued graduate studies. He taught at the University of Oregon for three years and for more than 20 years at the Ohio State University. A specialist in tankaa genre of classical Japanese poetryhe published seven books and many scholarly articles. Survivors include his wife, Ichiko T. Morita, AM64; two daughters, including Louise Morita Landry, AB80; a sister; and five grandchildren, including Erik S. Landry, SB13.

Kenning M. Anderson, PhD69, died March 1 in Evanston, IL. He was 88. A biochemist who focused on cancer, he received BA, MSc, and MD degrees at Northwestern University. In the 1960s, he worked as a postdoctoral fellow in UChicagos Ben May Department for Cancer Research, mentored by Nobel laureate Charles B. Huggins. After completing his PhD, Anderson held faculty appointments at the University of Toronto and Rush University. He authored hundreds of publications in oncology. He is survived by his wife, Marion Anderson, CER05; a daughter; two sons; and three grandchildren.

Thomas Jobe, MD69, died March 16 in Chicago. He was 78. A psychiatrist, he taught and practiced at the University of Illinois at Chicago from 1978 to 2005. There he cofounded a neuropsychiatry program, treated patients, and researched and wrote extensively on topics in psychiatry and neurology. His interests also included the history of neuroscience, which he taught at UChicago early in his career. Well into retirement, he pursued longitudinal research with a colleague on the neurological effects of psychotropic drugs, publishing an influential series of articles that called into question the long-term efficacy of psychiatric medications. His wife, Patricia Hawkins Jobe, AM81, died in 2011. Survivors include his life partner, Anna Weaver, and a son.

Jo N. Hays, PhD70, died March 20 in Chicago. He was 83. A professor of history at Loyola University for 37 years, he studied the history of science and disease. His books include The Burdens of Disease: Epidemics and Human Response in Western History (1998) and the coauthored Epidemics and Pandemics: From Ancient Plagues to Modern-Day Threats (2021). In his hometown of Oak Park, IL, he volunteered at the Frank Lloyd Wright Home and Studio and with Reading for the Blind. He is survived by his wife, Rosalind Conklin Hays, AB60, AM61, PhD64; a daughter; a son; and three grandchildren.

Barry Bauman, AM71, died February 5 in Riverside, IL. He was 73. Following his graduate studies in art history, he trained and worked as a conservator at the Art Institute of Chicago and for private clients. In 1983 he launched the Chicago Conservation Center to serve smaller organizations, restoring flood-damaged paintings for the Chicago History Museum and Works Progress Administration murals in Chicago schools. He later created Barry Bauman Conservation to provide pro bono services for nonprofit institutions, donating his labor to restore more than 1,500 paintings. His work made national headlines in 2011, when he identified a portrait of Mary Todd Lincoln as a fake. He is survived by his wife, Mary; two sons; and two sisters.

William Bruce Carney, AB72, of Sitges, Spain, died October 5. He was 71. After graduating from UChicago, he attended Mannes School of Music and became a professional musician. He sang with numerous groups nationally and internationally, including the Gregg Smith Singers, the choir of Saint Thomas Church in New York City, and at Trinity Cathedral and St. Johns in Miami, where he became the director of music. In 2012 he moved to Spain with his husband and partner, Ross Borsody, and founded Sitges Canta!, a choir of singers and instrumentalists who perform throughout Catalonia. He also began a new career as a film actor and taught music at the Institute of Arts Barcelona. He is survived by his husband and a brother.

James Frank Bartusek, MBA73, died January 15 in Prescott, AZ. He was 95. As a University of Illinois at Urbana-Champaign undergraduate, he studied engineering, played football, and ran track. He served with the Navy in the Pacific during the final stages of World War II, returning to Chicago to finish his undergraduate work and begin an engineering career. As plant manager at Argonne National Laboratory, he oversaw roughly 2,000 employees and led several major research and engineering projects, earning his MBA along the way. He was active in the Freemasons and Shriners. He is survived by his wife, Ann; two sons; and three grandchildren.

William S. Cox, AM74, died November 8 in Englewood, CO. He was 73. Cox grew up on the family cattle ranch near Cheyenne, WY. He was an outdoorsman and conservationist whose travels took him to every continent except Antarctica. He was laid to rest with his parents in the family mausoleum at the Wyoming Angus Ranch. Survivors include a sister and a brother.

Elizabeth Libby Eggleston Griffin, AM75, died November 30 in Winter Haven, FL. She was 91. As a graduate student in the Department of Near Eastern Languages and Civilizations, Griffin studied Hittite language and culture. She participated in archaeological digs in Syria and Turkey, publishing her findings in the Journal of Near Eastern Studies. A dedicated family historian, she preserved family letters and photographs from the mid-19th century through the present.

Jean O. Kelly, MST75, of Roseville, CA, died March 3. She was 82. After graduating from Monmouth College and the University, she embarked on a long career as a teacher in public elementary schools and reading programs. In her 20s she traveled around the world, briefly teaching at the Lahore American School in Pakistan. She later taught college-level teacher-training courses and tutored people of all ages with learning disabilities. She is survived by two brothers, including James Kelly, AM56; four step-children; and four grandchildren.

Sidney Roy Lehky, AB75, PhD85, of Montgomery Village, MD, died of cancer November 15. He was 67. With his doctorate in biophysics and theoretical biology, he embarked on a distinguished career in cognitive and computational neuroscience, researching the complexities of the visual cortex. He worked at the National Institute of Mental Health, the Salk Institute, and RIKEN in Japan, collaborating with international scientists to develop neural models of visual processing. Survivors include his wife, Jennifer Schumacher, and two sisters.

Emil Mariani, AB77, died of a brain tumor April 3, 2021, in Manchester, MO. He was 66. As a high school honor student in Gary, IN, he attended the College with an academic scholarship. Along with a successful career in publishing and banking, he contributed to his community as a volunteer. He did computer literacy work with homeless women at a local shelter, which named him its volunteer of the year, and started and ran the computer rehab ministry at Manchester United Methodist Church, reconditioning more than 500 computers that were donated to people without computer access. Survivors include his wife, Karen; a daughter; and a son.

Gary L. McDowell, AM78, of Richmond, VA, died August 6, 2021. He was 72. McDowell served as chief speechwriter for Attorney General Edwin Meese during the Reagan administration and directed the Office of the Bicentennial of the Constitution at the National Endowment of the Humanities. A constitutional law expert, he taught at Harvard Law School, the University of London, and the University of Richmond, where the Gary L. McDowell Institute was named in his honor. McDowell was a lifelong Republican who never let politics interfere with friendship; he enjoyed mentoring and helping liberals as much as fellow conservatives. Survivors include his wife, Brenda, and a sister.

Sheila Anne Williams Boyd, MBA92, of Homewood, IL, died November 6. She was 70. A graduate of Roosevelt University, Boyd was a certified public accountant and certified internal auditor. After more than 15 years at BP Amoco Corporation, she served as chief financial officer at several companies. She later created SAWB Consulting to support nonprofits and small and emerging businesses. A past president of Chicago Booths Executive MBA Program Club, her many honors include being counted among Ebony magazines Promising Women in Corporate America. Survivors include a daughter, three sisters, two brothers, and a granddaughter.

Jonathan Stong Groat, AB94, died November 26, in Royal Oak, MI, after a brief illness. He was 49. A sociology major in the College, he attended law school at the University of Illinois at Urbana-Champaign and spent a decade at the law firm Dickinson Wright PLLC, becoming a partner. He later held senior legal positions at Delta Dental Plan of Michigan, Indiana, and Ohio and at Credit Acceptance Corporation. Known for his kindness and wit, he was passionate about books, music, movies, comic books, travel, and his watch and Lego collections. He is survived by his parents, two sisters, and a brother.

Mark P. Pitts, EX99, of Wilmington, VT, died December 29. He was 64. His career in the US Army included a tour of Korea with the 17th Cavalry Squadron and helicopter search-and-rescue missions in the Alaskan wilderness. After studying Russian at the Defense Language Institute, he worked at Dun & Bradstreet in Russia. A graduate of Indiana University, he attended Chicago Booths Executive MBA Program. Survivors include three daughters, one son, two sisters, and three grandchildren.

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University of Chicago obituaries - University of Chicago