Category Archives: Molecular Medicine

Roswell completed the development and prototyping of the first of its kind molecular-electronic chips, which used all the latest achievements from the fields of semiconductor technology, nanotechnology, biosensors, etc. All this made it possible to create an integrated CMOS chip, which contains a huge number of elements of molecular sensors, which, at a chip price of $ 100, can read information from the entire human genome in just one hour.

In 2019, Roswell Biotechnologies, Inc, whose management managed to attract $ 32 million of investments, completed the development of a number of key technologies necessary for implementing direct, high-speed and accurate reading of genetic data and other information of biological origin.

As mentioned above, Roswells first molecular-electronic chip is designed to quickly read genetic information from DNA. The chips that the company plans to create in the near future will be much more complicated and they will be able to perform more complex functions, such as detecting certain types of proteins, biomarkers of various diseases, which can be used in field infectious medicine, environmental monitoring, or to identify biological samples of various nature.

Currently, the ENDSeq System (Electronic Nano-Device Sequencing) technology, which can reduce the time it takes to read genetic information from a few days to tens of minutes, can become a drastic reduction in the cost of this procedure. This, in turn, can serve as a strong impetus for the further development of the relevant areas of medicine. In addition, on the basis of the new chip, Roswell plans to launch the first device, Data Reader, which will provide high speed information reading using synthetic DNA molecules as an information carrier.

View post:
Roswell Biotechnologies created a chip capable of reading biological information from human DNA - FREE NEWS

Zendesk (NYSE:ZEN) and NantHealth (NASDAQ:NH) are both computer and technology companies, but which is the better investment? We will contrast the two businesses based on the strength of their risk, analyst recommendations, profitability, dividends, valuation, institutional ownership and earnings.

Insider and Institutional Ownership

95.9% of Zendesk shares are held by institutional investors. Comparatively, 2.8% of NantHealth shares are held by institutional investors. 4.6% of Zendesk shares are held by company insiders. Comparatively, 64.5% of NantHealth shares are held by company insiders. Strong institutional ownership is an indication that endowments, large money managers and hedge funds believe a stock is poised for long-term growth.

Risk & Volatility

Zendesk has a beta of 1.22, indicating that its share price is 22% more volatile than the S&P 500. Comparatively, NantHealth has a beta of 1.53, indicating that its share price is 53% more volatile than the S&P 500.

Profitability

This table compares Zendesk and NantHealths net margins, return on equity and return on assets.

Analyst Recommendations

This is a summary of recent recommendations and price targets for Zendesk and NantHealth, as reported by MarketBeat.

Zendesk presently has a consensus target price of $94.94, indicating a potential upside of 21.17%. NantHealth has a consensus target price of $1.00, indicating a potential downside of 1.96%. Given Zendesks higher probable upside, analysts clearly believe Zendesk is more favorable than NantHealth.

Valuation & Earnings

This table compares Zendesk and NantHealths top-line revenue, earnings per share (EPS) and valuation.

Zendesk has higher revenue and earnings than NantHealth. Zendesk is trading at a lower price-to-earnings ratio than NantHealth, indicating that it is currently the more affordable of the two stocks.

Summary

Zendesk beats NantHealth on 10 of the 14 factors compared between the two stocks.

Zendesk Company Profile

Zendesk, Inc., a software development company, provides SaaS products for organizations. Its flagship product is Zendesk Support, a system for tracking, prioritizing, and solving customer support tickets across various channels. The company also offers Zendesk Chat, a live chat software to connect with customers on Websites, applications, and mobile devices; Zendesk Talk, a cloud-based call center software; Zendesk Guide, a knowledge base that powers customer self-service and support agent productivity; Zendesk Sell, a sales force automation software to enhance productivity, processes, and pipeline visibility for sales teams; Zendesk Connect that manages customer communication across channels; and Zendesk Explore, which provides analytics for businesses to measure and enhance the customer experience. In addition, it provides Zendesk Sunshine, a customer relationship management platform; Zendesk Embeddables, which allow developers to embed support, chat, and guide experiences on the Web and within mobile applications; and Zendesk application platform interfaces and Apps. The company has operations in North America, Latin America, Europe, the Middle East, Africa, Australia, Asia, and South America. Zendesk, Inc. was founded in 2007 and is headquartered in San Francisco, California.

NantHealth Company Profile

NantHealth, Inc., together with its subsidiaries, operates as a healthcare technology company in the United States and internationally. The company engages in converging science and technology through an integrated clinical platform to provide health information at the point of care. It develops NantHealth solutions, including molecular profiling solutions, software, and hardware systems infrastructure, which integrates patient data management, bioinformatics, and molecular medicine to enable value-based care and evidence-based clinical practice. The company's products include GPS Cancer, a molecular profile that integrates whole genome sequencing of tumor and normal germline samples, as well as whole transcriptome sequencing; GPS Cancer Report, a GPS cancer solution; GPS in rare diseases and chronic illnesses; Liquid GPS, a blood-based molecular test; and Eviti, a decision support solution. It also provides Web-based and mobile software solutions, such as Device Connectivity Suite, a device connectivity and near real-time biometric software and hardware suite; DeviceConX, a device data normalization software; HBox, an Internet of Medical Things and Internet of Things hardware hub; and VitalsConX, a tablet-optimized application. In addition, NantHealth, Inc. offers NaviNet Open, a payer-provider collaboration platform comprising plan central, eligibility and benefit, claims status inquiry, claims management, referral, authorization, document exchange, and AllPayer services; and cloud-based computing, storage, and transport infrastructure-as-a-service solutions. The company was formerly known as Nant Health, LLC and changed its name to NantHealth, Inc. in June 2016. The company was founded in 2010 and is headquartered in Culver City, California. NantHealth, Inc. is as a subsidiary of NantWorks, LLC.

Receive News & Ratings for Zendesk Daily - Enter your email address below to receive a concise daily summary of the latest news and analysts' ratings for Zendesk and related companies with MarketBeat.com's FREE daily email newsletter.

Read more here:
Head-To-Head Survey: NantHealth (NASDAQ:NH) and Zendesk (NASDAQ:ZEN) - Riverton Roll

Wenxiang Bai,1,2,* Honghua Wang,1,* Hua Bai1,3

1Comprehensive Cancer Center, Xiangshui Peoples Hospital, Xiangshui 224600, Peoples Republic of China; 2Department of Respiratory Medicine, Xiangshui Peoples Hospital, Xiangshui, 224600, Peoples Republic of China; 3Department of Hematology, The Affiliated Drum Tower Hospital of Nanjing University Medical School, Nanjing 210008, Peoples Republic of China

*These authors contributed equally to this work

Correspondence: Hua BaiComprehensive Cancer Center, Xiangshui Peoples Hospital, Xiangshui 224600, Peoples Republic of ChinaEmail baihua92@126.com

Objective: Systemic amyloid light chain (AL) amyloidosis is a rare plasma cell disease. However, the regulatory mechanisms of AL amyloidosis have not been thoroughly uncovered, identification of candidate genes and therapeutic agents for this disease is crucial to provide novel insights into exploring the regulatory mechanisms underlying AL amyloidosis.Methods: The gene expression profile of GSE73040, including 9 specimens from AL amyloidosis patients and 5 specimens from normal control, was downloaded from GEO datasets. Differentially expressed genes (DEGs) were sorted with regard to AL amyloidosis versus normal control group using Limma package. The gene enrichment analyses including GO and KEGG pathway were performed using DAVID website subsequently. Furthermore, the proteinprotein interaction (PPI) network for DEGs was constructed by Cytoscape software and STRING database. DEGs were mapped to the connectivity map datasets to identify potential molecular agents of AL amyloidosis.Results: A total of 1464 DEGs (727 up-regulated, 737 down-regulated) were identified in AL amyloidosis samples versus control samples, these dysregulated genes were associated with the dysfunction of ribosome biogenesis and immune response. PPI network and module analysis uncovered that several crucial genes were defined as candidate genes, including ITGAM, ITGB2, ITGAX, IMP3 and FBL. More importantly, we identified the small molecular agents (AT-9283, Ritonavir and PKC beta-inhibitor) as the potential drugs for AL amyloidosis.Conclusion: Using bioinformatics approach, we have identified candidate genes and pathways in AL amyloidosis, which can extend our understanding of the cause and molecular mechanisms, and these crucial genes and pathways could act as biomarkers and therapeutic targets for AL amyloidosis.

Keywords: light chain amyloidosis, bioinformatics approach, differentially expressed genes, candidate genes, therapeutic agent

This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution - Non Commercial (unported, v3.0) License.By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms.

Read the original here:
Identification of Candidate Genes and Therapeutic Agents for Light Cha | PGPM - Dove Medical Press

Brain imaging of pathological tau-protein tangles reliably predicts the location of future brain atrophy in Alzheimers patients a year or more in advance, according to a new study by scientists at the UC San Francisco Memory and Aging Center. In contrast, the location of amyloid plaques, which have been the focus of Alzheimers research and drug development for decades, was found to be of little utility in predicting how damage would unfold as the disease progressed.

The results, published Jan. 1, 2020, in Science Translational Medicine, support researchers growing recognition that tau drives brain degeneration in Alzheimers disease more directly than amyloid protein, and at the same time demonstrates the potential of recently developed tau-based PET (positron emission tomography) brain imaging technology to accelerate Alzheimers clinical trials and improve individualized patient care.

The match between the spread of tau and what happened to the brain in the following year was really striking, said neurologist Gil Rabinovici, MD, the Edward Fein and Pearl Landrith Distinguished Professor in Memory and Aging and leader of the PET imaging program at the UCSF Memory and Aging Center. Tau PET imaging predicted not only how much atrophy we would see, but also where it would happen. These predictions were much more powerful than anything weve been able to do with other imaging tools, and add to evidence that tau is a major driver of the disease.

Alzheimers researchers have long debated the relative importance of amyloid plaques and tau tangles two kinds of misfolded protein clusters seen in postmortem studies of patients brains, both first identified by Alois Alzheimer in the early 20th century. For decades, the amyloid camp has dominated, leading to multiple high-profile efforts to slow Alzheimers with amyloid-targeting drugs, all with disappointing or mixed results.

Many researchers are now taking a second look at tau protein, once dismissed as simply a tombstone marking dying cells, and investigating whether tau may in fact be an important biological driver of the disease. In contrast to amyloid, which accumulates widely across the brain, sometimes even in people with no symptoms, autopsies of Alzheimers patients have revealed that tau is concentrated precisely where brain atrophy is most severe, and in locations that help explain differences in patients symptoms (in language-related areas vs. memory-related regions, for example).

No one doubts that amyloid plays a role in Alzheimers disease, but more and more tau findings are beginning to shift how people think about what is actually driving the disease, explained Renaud La Joie, PhD, a postdoctoral researcher in Rabinovicis In Vivo Molecular Neuroimaging Lab, and lead author of the new study. Still, just looking at postmortem brain tissue, it has been hard to prove that tau tangles cause brain degeneration and not the other way around. One of our groups key goals has been to develop non-invasive brain imaging tools that would let us see whether the location of tau buildup early in the disease predicts later brain degeneration.

Despite early misgivings that tau might be impossible to measure in the living brain, scientists recently developed an injectable molecule called flortaucipir currently under review by the FDA which binds to misfolded tau in the brain and emits a mild radioactive signal that can be picked up by PET scans.

Rabinovici and collaborator William Jagust, MD, of UC Berkeley and Lawrence Berkeley National Laboratory, have been among the first to adopt tau PET imaging to study the distribution of tau tangles in the normally aging brain and in a smaller cross-sectional study of Alzheimers patients. Their new study represents the first attempt to test whether tau levels in Alzheimers patients can predict future brain degeneration.

La Joie recruited 32 participants with early clinical stage Alzheimers disease through the UCSF Memory and Aging Center, all of whom received PET scans using two different tracers to measure levels of amyloid protein and tau protein in their brains. The participants also received MRI scans to measure their brains structural integrity, both at the start of the study, and again in follow-up visits one to two years later.

The researchers found that overall tau levels in participants brains at the start of the study predicted how much degeneration would occur by the time of their follow up visit (on average 15 months later). Moreover, local patterns of tau buildup predicted subsequent atrophy in the same locations with more than 40 percent accuracy. In contrast, baseline amyloid-PET scans correctly predicted only 3 percent of future brain degeneration.

Seeing that tau buildup predicts where degeneration will occur supports our hypothesis that tau is a key driver of neurodegeneration in Alzheimers disease, La Joie said.

Notably, PET scans revealed that younger study participants had higher overall levels of tau in their brains, as well as a stronger link between baseline tau and subsequent brain atrophy, compared to older participants. This suggests that other factors likely other abnormal proteins or vascular injuries may play a larger role in late-onset Alzheimers, the researchers say.

The results add to hopes that tau-targeting drugs currently under study at the UCSF Memory and Aging Center and elsewhere may provide clinical benefits to patients by blocking this key driver of neurodegeneration in the disease. At the same time, the ability to use tau PET to predict later brain degeneration could enable more personalized dementia care and speed ongoing clinical trials, the authors say.

One of the first things people want to know when they hear a diagnosis of Alzheimers disease is simply what the future holds for themselves or their loved ones. Will it be a long fading of memory, or a quick decline into dementia? How long will the patient be able to live independently? Will they lose the ability to speak or get around on their own? These are questions we cant currently answer, except in the most general terms, Rabinovici said. Now, for the first time, this tool could let us give patients a sense of what to expect by revealing the biological process underlying their disease.

Rabinovici and his team also anticipate that the ability to predict future brain atrophy based on tau PET imaging will allow Alzheimers clinical trials to quickly assess whether an experimental treatment can alter the specific trajectory predicted for an individual patient, which is currently impossible due to the wide variability in how the disease progresses from individual to individual. Such insights could make it possible to adjust dosage or switch to a different experimental compound if the first treatment is not affecting tau levels or altering a patients predicted trajectory of brain atrophy.

Tau PET could be an extremely valuable precision medicine tool for future clinical trials, Rabinovici said. The ability to sensitively track tau accumulation in living patients would for the first time let clinical researchers seek out treatments that can slow down or even prevent the specific pattern of brain atrophy predicted for each patient.

Authors: La Joie is corresponding author on the study; Rabinovici is senior author. Additional authors on the study are Adrienne V. Visani, Jesse A. Brown, Viktoriya Bourakova, Jungho Cha, Kiran Chaudhary, Lauren Edwards, Leonardo Iaccarino, Orit Lesman-Segev, Zachary Miller, David C. Perry, Julie Pham, Julio C. Rojas, Howard J. Rosen, William W. Seeley, Richard M. Tsai, and Bruce L. Miller, all of UCSF; Suzanne L. Baker, Mustafa Janabi, and James P. ONeil, of Lawrence Berkeley National Laboratory (LBNL); and Jagust, of LBNL and UC Berkeley.

Funding: The study was supported by the Alzheimers Association (AARF-16-443577), the National Institute on Aging (NIA) of the US National Institutes of Health (R01-AG045611, P50-AG023501, P01-AG19724), the Tau Consortium, and an Alzheimers Disease Research Center of California grant (04-33516) from the California Department of Health Services.

Disclosures: Rabinovici receives research support from Avid Radiopharmaceuticals, GE Healthcare, and Life Molecular Imaging, and has received consulting fees or speaking honoraria from Axon Neurosciences, Roche, Eisai, Genentech, Merck. La Joie reports no conflicts of interest. See study online for a full list of conflict of interest disclosures.

The University of California, San Francisco (UCSF) is exclusively focused on the health sciences and is dedicated to promoting health worldwide through advanced biomedical research, graduate-level education in the life sciences and health professions, and excellence in patient care.UCSF Health, whichserves as UCSFs primary academic medical center, includestop-ranked specialty hospitalsandother clinical programs,and has affiliations throughout the Bay Area.

Originally posted here:
Alzheimer 'Tau' Protein Far Surpasses Amyloid in Predicting Toll on Brain Tissue - UCSF News Services

A group led by researchers at Baylor College of Medicine has identified significant differences at the epigenetic level the chemical tags in DNA that help regulate gene expression between two clinically distinct forms of acute childhood malnutrition known as edematous severe acute malnutrition (ESAM) and non-edematous SAM (NESAM).

The researchers report in the journal Nature Communications that ESAM, but not NESAM, is characterized by a reduction in methyl chemical tags in DNA and complex changes in gene activity, including both enhanced and reduced gene expression. Some of the genes that lost their methyl tags have been linked to other disorders of nutrition and metabolism, such as abnormal blood sugar and fatty liver disease, conditions that also have been observed in ESAM. The findings support consideration of methyl-group supplementation in ESAM.

Severe acute childhood malnutrition presents in two clinically distinct forms: ESAM and NESAM, said corresponding author Dr. Neil Hanchard, assistant professor of molecular and human genetics and the USDA/ARS Children's Nutrition Research Center at Baylor. ESAM is characterized by body swelling and extensive dysfunction of multiple organs, including liver, blood cells and the gut, as well as skin and hair abnormalities. NESAM, on the other hand, typically presents with weight loss and wasting.

The differences between ESAM and NESAM are still not fully explained despite decades of studies addressing this question. In the current study, Hanchard and his colleagues looked to better understand the conditions by investigating whether there were differences at the molecular level, specifically on DNA methylation.

The decision to look at DNA methylation was partly driven by previous studies looking at biochemical markers in these individuals. In particular, the turnover of a particular amino acid called methionine, said Hanchard.

Previous work has shown that methionine turnover is slower in ESAM than in NESAM. Methionine is a central ingredient of 1-carbon metabolism, a metabolic pathway that is key to DNA methylation. Lower methionine turnover suggested the possibility of alterations in DNA methylation.

First, we conducted a genome-wide analysis of DNA methylation. When we found in children acutely ill with ESAM genes with levels of DNA methylation that were significantly different from those in NESAM patients, the levels were always lower. Of the genes analyzed, 161 showed a highly significant reduced level of methylation in ESAM, when compared to the same genes in NESAM, Hanchard said.

Interestingly, a group of adults who had recovered from having ESAM malnutrition in their childhood did not show the same reduction in DNA methylation the researchers observed in childhood acute cases. This suggested that lower DNA methylation was probably related to acute ESAM.

Knowing that DNA methylation helps regulate gene expression, Hanchard and his colleagues next investigated whether there were differences in gene expression between ESAM and NESAM. They found that reduced overall methylation in ESAM resulted in a complex pattern of gene expression changes. For some genes, having reduced methylation enhanced their expression, while for others it reduced it.

Among the genes that were highly affected by reduced methylation were some of those related to conditions such as blood sugar regulation, fatty liver disease and other metabolic problems, which are also commonly seen more often in ESAM than NESAM.

Our findings contribute to a better understanding of the molecular events that likely result in the differences between ESAM and NESAM, Hanchard said. Although we still dont know why malnutrition leads to ESAM in some children, while it results in NESAM in others, our findings suggest that, once ESAM gets on its way, methylation changes are likely involved in the clinical signs and symptoms of the condition. There is also evidence that individual genetic variation also influences the level of DNA methylation. Furthermore, I am excited about the possibility that altering the molecular outcome of malnutrition with specific interventions could one day help alter the clinical outcome.

Other contributors to this work include first author Katharina V. Schulze, Shanker Swaminathan, Sharon Howell, Aarti Jajoo, Natasha C. Lie, Orgen Brown, Roa Sadat, Nancy Hall, Liang Zhao, Kwesi Marshall, Thaddaeus May, Marvin E. Reid, Carolyn Taylor-Bryan, Xueqing Wang, John W. Belmont, Yongtao Guan, Mark J. Manary, Indi Trehan and Colin A. McKenzie.

See a complete list of author affiliations and financial support for this study.

Follow this link:
Form of severe malnutrition linked to DNA modification - Baylor College of Medicine News

- Presentation Demonstrates Advantages of iBios Recently Launched FastGlycaneering Development Service -

NEW YORK, Dec. 16, 2019 (GLOBE NEWSWIRE) -- iBio, Inc. (NYSE AMERICAN:IBIO) presented results of the application of its new FastGlycaneering Development Serviceto enhance potency of recombinant proteins at last weeks Antibody Engineering & Therapeutics conference in San Diego, CA. Specifically, the presented data demonstrated the ability to deploy iBios glycan engineering technologies and plant-based manufacturing platform to rapidly develop and produce biobetters, such as the biobetter rituximab (iBio Rituximab) product candidate currently being developed in collaboration with CC-Pharming Ltd.

Dr. Sylvain Marcel, iBios Vice President of Protein Expression Sciences, highlighted laboratory results showing how iBios FastGlycaneering Technology enables greater N-linked glycosylation customization and control. In the case of iBio Rituximab, antibody dependent cellular cytotoxicity was increased 30-fold; potency, as measured by half maximal effective concentration, was substantially improved versus the control antibody; and iBios glycan engineering methods were shown to be capable of producing antibodies with more homogeneous and fully human glycosylation patterns.

This study demonstrated that our complementary glycan engineering technology can improve the activity of therapeutic antibodies, which is instrumental in the development of antibodies with higher potency, stated Dr. Marcel. These data represent a very positive development within our collaboration with CC-Pharming and, in addition, highlight iBios ability to produce antibodies with more homogeneous and humanized glycosylation patterns, which can help our other clients and partners achieve their target product profiles.

In addition to joint work on a biobetter rituximab, iBio and CC-Pharming are undertaking joint product assessments in other categories that, in some cases, may reach the commercial stage faster than is possible with therapeutic antibodies. The companies expect to use iBios FastGlycaneering Technology for any glycoproteins selected from the initial candidate pool for advancement to commercial development.

In August 2019, iBio granted to CC-Pharming an exclusive, royalty-bearing commercial license to iBio Rituximab product candidates for the territory of China, as well as a research license to iBios FastPharming System and know-how for the evaluation of multiple product opportunities.

About CC-Pharming Ltd.

CC-Pharming is located in Zhongguancun Biomedical Engineering Transformation Center, Shunyi District, Beijing, China. The company is specialized in plant molecular medicine technology research and product development using proprietary tobacco and lettuce transient expression platforms, focusing on the use of plant bioreactors for the development of animal-free, safe, high-value recombinant protein and peptide product for industrial and clinical applications. The Company develops innovative indoor vertical farming system for efficient plant-based expression systems, and offers therapeutic biomedicine, life science research, cosmetics, and CRO/CMO services to clients in China. Further information is available at http://www.cc-pharming.com.

About iBio

iBio, Inc., is a global leader in plant-based biologics manufacturing. Its FastPharming System combines vertical farming, automated hydroponics, and glycan engineering technologies to rapidly deliver gram quantities of high-quality monoclonal antibodies, vaccines, bioinks and other proteins. The Companys subsidiary, iBio CDMO LLC, provides FastPharming Contract Development and Manufacturing Services via its 130,000 square foot facility in Bryan, Texas. iBio CDMO also enables innovators to use the FastPharming System for insourced manufacturing via its Factory Solutions design-and-build services. iBios FastGlycaneering Development Service includes an array of new glycosylation technologies for engineering high-performance recombinant proteins. Additionally, iBio is developing its own proprietary products which include its lead asset, IBIO-100, for the treatment of fibrotic diseases. For more information, visit http://www.ibioinc.com.

Story continues

FORWARD-LOOKING STATEMENTSSTATEMENTS INCLUDED IN THIS NEWS RELEASE RELATED TO IBIO, INC. MAY CONSTITUTE FORWARD-LOOKING STATEMENTS WITHIN THE MEANING OF THE PRIVATE SECURITIES LITIGATION REFORM ACT OF 1995. SUCH STATEMENTS INVOLVE A NUMBER OF RISKS AND UNCERTAINTIES SUCH AS COMPETITIVE FACTORS, TECHNOLOGICAL DEVELOPMENT, MARKET DEMAND, AND THE COMPANY'S ABILITY TO OBTAIN NEW CONTRACTS AND ACCURATELY ESTIMATE NET REVENUES DUE TO VARIABILITY IN SIZE, SCOPE, AND DURATION OF PROJECTS. FURTHER INFORMATION ON POTENTIAL RISK FACTORS THAT COULD AFFECT THE COMPANY'S FINANCIAL RESULTS CAN BE FOUND IN THE COMPANY'S REPORTS FILED WITH THE SECURITIES AND EXCHANGE COMMISSION.

Contact:

Stephen KilmerInvestor Relations(646) 274-3580 skilmer@ibioinc.com

Visit link:
iBio Reports Progress on its Bio-Better Rituximab Collaboration with CC-Pharming - Yahoo Finance

Atomic-level studies of the architecture of tiny sodium channel proteins, critical to generating electrical signals that start off each beat of the heart, are imparting striking details about their function, malfunctions, disruption by many disease mutations, and response to medication.

This structural information could become the basis for developing better diagnostics and drugs for life-threatening heart rhythm problems, according to the researchers from the University of Washington School of Medicine working in this area.

Their latest findings appear Dec. 19 in Cell in the paper, Structure of the Cardiac Sodium Channel. The senior authors are William Catterall and Ning Zheng, both UW School of Medicine professors of pharmacology. The first authors are Daohau Jiang and Hui Shi, UW postdoctoral fellows in pharmacology.

The cardiac sodium channel not only initiates the heartbeat, mutations in it also cause deadly arrhythmias, and antiarrhythmic drugs act directly on it to control cardiac rhythms, explained Catterall.

The heart is both a plumbing and electrical marvel. For each heartbeat, electrical waves travel across a healthy heart in a pattern that controls its filling and pumping in a tightly coordinated manner. The rate at which the impulse is propagated through the heart tissue relies on actions taking place at the molecular level in tiny protein pores present in cardiac cell membranes.

Sodium ions a type of charged particles -- pass through these protein passageways in the membrane boundary between the outside and inside of the cell.

Pufferfish harbor a toxin that acts on nerve and muscle, but not heart, sodium channels.

The activation and quick inactivation of these voltage-gated sodium channels are part of a series of electrical and physiological events that maintain a steady heartbeat.

Sodium channels operate in concert with calcium channels and potassium channels to drive the heartbeat at a consistent frequency for our entire lives, Zheng noted.

When sodium channels dont work properly, the heart can be in trouble, even to the point of having dangerously fast and uncoordinated contractions that are life-threatening, the researchers explained. Specifically, the NaV (Latin abbreviation for sodium, V for voltage) 1.5 channel has such an indispensable role that certain mutations in those channels can be fatal, because other sodium channels in the heart cannot compensate for their loss. These mutations can cause dangerous arrhythmias in adults and even sudden death in children and young athletes.

Fortunately, many heart rhythm disturbances can be treated with drugs that block cardiac sodium channels. For example, as UW Medicine physician Michael Lenaeus, a UW assistant professor of medicine, Division of General Internal Medicine, and a co-author of the study, noted, atrial fibrillation, or A-fib, is increasingly prevalent among older Americans. This condition can often be treated effectively with the drug flecainide. In their recent study, the researchers sought to learn, among other things, how drugs like flecainide act within the predominant form of sodium channels found in cardiac cells.

To obtain a high-resolution, 3-D map of the channels, the scientists used advanced cryo-electron microscopy at the new Beckman Center for Cryo-EM at the UW. They wanted to explore important structural features of these sodium channels and relate their configuration to their actions in normal physiological function, dysfunction, disease mutations, toxin sensitivity and the pharmacology of antiarrhythmic drugs.

According to the scientists, their experiments provide a blueprint for understanding many various aspects of cardiac sodium channels.

Among the key findings from this work were:

An electrocardiogram record of the electrical activitiry of the heartbeat

In their conclusion, the researchers noted that, overall, the detailed, high-resolution structures they were able to obtain for the cardiac NaV1.5 channel allowed them to elucidate the molecular basis for several

of its specific, distinctive, vital functions and to provide key chemical information for design and development of safer and more effective antiarrhythmic medications.

Our high-resolution cryoEM structure of this iconic sodium channel gives new structure/function insights, reveals the molecular mechanisms of many inherited arrhythmias, and elucidates the exact binding site and blocking mode of the antiarrhythmic drug flecainide, which is used to treat atrial fibrillation, an increasingly prevalent problem in our aging population, Catterall said in summarizing the results.

The research was funded by the National Institutes of Health (R01HL112808) and the Howard Hughes Medical Institute.

More:
An atomic view of the trigger for the heartbeat - UW Medicine Newsroom

NEW YORK, Dec. 17, 2019 /PRNewswire/ -- Hoth Therapeutics,Inc. (NASDAQ: HOTH), ("HOTH" or the "Company"), a biopharmaceutical company focused on developing new generation therapies for dermatological disorders such as atopic dermatitis, chronic wounds, psoriasis and acne, today announcedthe addition of Dr.William Weglicki, M.D. to the Company's Scientific Advisory Board. While serving on the Board, Dr, Weglicki will oversee Hoth's Aprepitant Program under its Scientific Research Agreement with the George Washington University ("GW").

Mr.Robb Knie, CEO of Hoth Therapeutics, commented, "I am pleased to welcome Dr. Weglicki to our Scientific Advisory Board.Dr. Weglicki will be instrumental towards the advancement of our Aprepitant program.Hoth is fortunate to have such well-respected leaders providing their invaluable expertise and insight to each of our significant research and development initiatives."

Dr. Weglicki isProfessor of Biochemistry and Molecular Medicine at the George Washington University School of Medicine.Dr Weglicki is a recipient of the Lifetime Achievement Award in Cardiovascular Science, Medicine and Surgery, The International Academy of Cardiovascular Sciences. After completing a medical residency at Georgetown University Hospital in 1964 he completed a Cardiology fellowship in 1966 at Duke University where he trained in clinical cardiac catheterization and pharmacology basic research. He was then appointed as a research associate at NIH's NICHHD and the McCollum Pratt Institute of the Johns Hopkins University where he studied the cardiac pathobiology of alpha tocopherol deficiency. In 1968 He joined Harvard's Peter Bent Brigham Hospital Department of Medicine's Cardiovascular Research unit, androse from Instructor to Associate Professor in 1975. There he concentrated his research on the role of phospholipases of the heart in the ischemic perturbation of cardiac membrane phospholipids and organelles, which led to several RO1 NIH grant awards. With his research team he moved to the Medical College of Virginia/VCU in 1975 as chairman of the Department of Biophysics and served as a professor of Medicine (Cardiology); there he was active in teaching medical and mentoring graduate students, while publishing a series of manuscripts on cardiac lysosomal activity in myocardial ischemia and the distribution of phospholipases in cardiac mitochondria and sarcolemmal membranes, and overseeing a new NHLBI Training Grant on molecular mechanisms of cardiovascular injury. At the Oklahoma Medical Research Foundation he led their Cardiovascular Research Program. He joined the George Washington University Department of Medicine in 1985 and formed the Division of Experimental Medicine; in 1987 this core group of investigators was awarded a Program Project grant on Molecular Mechanisms of Cardiovascular Injury from the National Heart, Lung, and Blood Institute. This research included identifying free-radical peroxidative injury during myocardial ischemia and the protective antioxidant properties of cardiac beta blocking drugs such as propranolol and carvedilol. At present he is a Professor of Biochemistry and Molecular Medicine and Medicine (Cardiology). He has been a principal investigator of NIH grants for more than thirty years. His ongoing research focuses on preventing neurogenic inflammation and hyomagnesemia effects associated with some anticancer drugs.

About Hoth Therapeutics, Inc.Hoth Therapeutics, Inc. isa clinical-stage biopharmaceutical company focused on developing new generation therapies for dermatological disorders. HOTH's pipeline has the potential to improve the quality of life for patients suffering from indications including atopic dermatitis, chronic wounds, psoriasis, and acne. HOTH has the exclusive worldwide rights to BioLexa, the company's proprietary lead drug candidate topical platform that uniquely combines two FDA approved compounds to fight bacterial infections across multiple indications. HOTH is preparing to launch its clinical trial for the treatment of adolescent subjects, 2-17 years of age, with mild to moderate atopic dermatitis during 2020. To learn more, please visitwww.hoththerapeutics.com.

Forward Looking StatementsThis press release includes "forward-looking statements" within the meaning of the Private Securities Litigation Reform Act of 1995. Forward-looking statements in this press release include, but are not limited to, statements that relate to the advancement and development of the BioLexa Platform, the commencement of clinical trials, the availability of data from clinical trials and other information that is not historical information. When used herein, words such as "anticipate", "being", "will", "plan", "may", "continue", and similar expressions are intended to identify forward-looking statements. In addition, any statements or information that refer to expectations, beliefs, plans, projections, objectives, performance or other characterizations of future events or circumstances, including any underlying assumptions, are forward-looking. All forward-looking statements are based upon Hoth's current expectations and various assumptions. Hoth believes there is a reasonable basis for its expectations and beliefs, but they are inherently uncertain. Hoth may not realize its expectations, and its beliefs may not prove correct. Actual results could differ materially from those described or implied by such forward-looking statements as a result of various important factors, including, without limitation, market conditions and the factors described under the caption "Risk Factors" in Hoth's Form 10K for the period endingDecember 31, 2018, and Hoth's other filings made with the Securities and Exchange Commission. Consequently, forward-looking statements should be regarded solely as Hoth's current plans, estimates and beliefs. Investors should not place undue reliance on forward-looking statements. Hoth cannot guarantee future results, events, levels of activity, performance or achievements. Hoth does not undertake and specifically declines any obligation to update, republish, or revise any forward-looking statements to reflect new information, future events or circumstances or to reflect the occurrences of unanticipated events, except as may be required by law.

ContactsInvestor Relations Contact:Phone: (646) 756-2997Email:investorrelations@hoththerapeutics.comwww.hoththerapeutics.com

KCSA Strategic CommunicationsValter Pinto / Daniela Guerrero(212) 896-1254 / (212) 682-6300Hoth@kcsa.com

View original content to download multimedia:http://www.prnewswire.com/news-releases/hoth-therapeutics-announces-the-appointment-of-dr-william-weglicki-md-to-scientific-advisory-board-300976186.html

SOURCE Hoth Therapeutics, Inc.

See more here:
Hoth Therapeutics Announces the Appointment of Dr. William Weglicki, M.D. to Scientific Advisory Board - P&T Community

By Michelle Morgante, UC Merced

Proteins are miniscule machines inside the body, about 10,000 times smaller than the thickness of human hair. They control all the processes of life like how cells communicate to each other, how the immune system combats infection, how muscles contract, and how oxygen is picked up in the lungs and delivered to those very same muscles.

Proteins can do all of this because they change shape, assemble and interact with other biomolecules in response to specific cues. This general property makes proteins extremely attractive targets for a variety of applications in medicine, environment, food industry and energy. But it also has proven very difficult to harness. Now, bioengineering Professor Victor Muoz has made a key discovery that could allow scientists to engineer adaptive proteins and convert them into powerful technological applications, including smart medicines.

In a paper published Dec. 13 in Nature Communications, Muoz and a team of researchers describe how they were able to engineer proteins to form assemblies, dissociate and change shape in response to signals. The discovery could allow scientists to, for example, use proteins to deliver drugs in a way that is less toxic and more targeted than current practices.

Proteins in their natural state are easily passed through the kidney, meaning they are not in the blood long enough to act as an effective medicine.

But when a protein makes an assembly, Muoz said. It forms structures that are larger and sturdier and dont get secreted out of the kidney. They stay in the blood for a longer time.

Muoz, who is director of UC Merceds Center for Cellular and Bio-Molecular Machines (CCBM-CREST), said research for this project began a decade ago and has involved collaboration from several groups around the world. The work to figure out how to engineer proteins to act as nanomachines has been challenging and tortuous.

They do all these complicated things and are so small. That means their design principles and organization are incredibly sophisticated, he said. People have been able to design proteins that will form particular assemblies of many different shapes, but they have not been able to make them adaptive so they switch their shape and properties in response to stimuli.

"This opens the gate for developing drugs that are based on proteins in a way they could be delivered as inactive assemblies that remain in the blood as needed to then be activated on cue at a given time or in a specific location in the body."

director, Center for Cellular and Bio-Molecular Machines

The discovery may lead to important applications in biosensor research, medicine, diagnostics, vaccines, bioremediation anything you could imagine, Muoz said.

In medical applications, for example, proteins engineered this way could become a new technology for the smart delivery of specific drugs.

This would have enormous advantages over conventional drugs, which are much less specific, more toxic and can cause a range of harmful side-effects. It could also help store an inactive version of the protein in blood for a relatively long time, eliminating the short lifespan curse of current protein pharmaceuticals.

This opens the gate for developing drugs that are based on proteins in a way they could be delivered as inactive assemblies that remain in the blood as needed to then be activated on cue at a given time or in a specific location in the body, Muoz said.

The next step, Muoz said, will be to try the process in other systems and see whether it can be generalized. This was a proof of concept. Next, wed like to target systems that have more interesting applications to exploit the possibility of making this into a real technology thats useful.

View post:
Engineered Protein Assemblies that Respond to Cues Open Path for Smart, Protein-Based Medicines | Newsroom - UC Merced University News

'TIS the season for too much to drink, not enough sleep and increased anxiety.

So it's not surprising blokes are likely to struggle getting - and keeping- an erection over the festive period.

7

Unfortunately, impotence rates have doubled in the last 25 years, according to a new study by Kings College, London - and young men are increasingly affected.

A third blamed tiredness, a third anxiety and a third drinking too much - all factors which increase at this time of year.

But these six surprising Christmas gift ideas might just help perk up your lovers performance.

It might not sound like a sexy stocking filler, but scientists say a tongue-scraper could work wonders for your mans performance.

Thats because using the metal device to remove surface debris from the tongue allows good oral bacteria to flourish, producing chemicals called nitrites, which build up in the saliva.

7

When your lover swallows, the nitrites mix with the acid of his stomach and turn it into nitric oxide, giving a boost to the blood-flow to his manhood.

Dr Nathan Bryan, a specialist in molecular medicine from Baylor College of Medicine, Texas, says: "With enough nitric oxide you can dilate blood vessels, increase blood flow and improve sexual function."

While your man is busy in the bathroom scraping his tongue, get him flossing too.

Several studies have found that men with gum disease are more likely to have problems getting and keeping erections.

Chronic inflammation caused by gum disease can damage the lining of the blood vessels in his penis, reducing healthy blood flow into the organ.

In fact, if a man has serious gum disease, hes more than twice as likely to have problems between the sheets, according to a study of more than 200,000 men aged 20 to 80.

7

Brew up some coffee in the morning, if youd like to see a stronger performance from your man in the bedroom.

Just two or three cups a day could really perk him up, according to researchers at the University of Texas.

After studying the coffee-drinking of 4000 men, they found that those who enjoyed a couple of coffees were 42 per cent less likely to have erectile dysfunction.

Its thought that ingredients in coffee relax the arteries in the penis and allow more blood to flow into it.

7

Many men believe that eating meat is a sign of virility.

But recent research suggests its actually vegans who are likely to perform better in the bedroom.

US urologist Dr Aaron Spitz decided to conduct an experiment. One night, he gave men burritos containing beef, chicken or pork. The next, the burritos contained plant-based meat substitutes.

While they slept, the men wore special devices to monitor penile length and girth.

In the mornings, it was found that that men who ate the plant-based burritos had erections which lasted three to four times longer.

Why? Possibly because diets high in animal fats and rich in cholesterol can clog up the arteries, restricting blood flow to the penis. But plant-based foods boost nitric oxide, increasing blood flow.

Dr Spitz said: "What the scientific studies are showing is that the more meat men eat, the more quickly they lose their manly manhood."

Consultant urological surgeon Mr Vivek Wadhwa, who is based at Birminghams Spire Parkway Hospital, says the strength of your mans erection can be a red flag for future heart problems.

"The small arteries in the penis tend to fur up (with fatty deposits) a good 10 to 15 years earlier than the bigger arteries to the heart and brain.

So it can help for a man to reduce his intake of animal protein and increase plant fibre and antioxidants in the diet when he gets this early warning sign.

7

If your man is a lycra cycling warrior, it might be doing wonders for his physique but not much for his endurance in the bedroom.

Very active male cyclists have twice the rate of erectile dysfunction than non-cyclists, according to a study of 6,751 men by the University of Hamburg.

Certain mens bikes which make the rider lean forward and hold on to dropped handlebars - can press on the artery into the penis - as well as the blood vessels and nerves between the scrotum and anus.

This can cause pain, numbness and damage.

However, the effect can be lessened with padded cycling shorts which reduce pressure.

Or another option could be to buy him a new saddle with grooves in the middle.

A study in the British Journal of Urology International found that this type of seat is less numbing and less likely to cause erection problems.

Mr Wadhwa told The Sun: "I also tell patients that if they change their saddle to something softer theres not so much pressure on the perineum - the area between the scrotum and anus."

7

Baste your Christmas dinner roast potatoes in olive oil, not chicken fat - it could be better than Viagra at reducing impotence as it boosts testosterone.

Researchers from the University of Athens found that eating just nine tablespoons of olive oil a week does the trick.

Study leader, Dr Christina Chrysohoou, said diet and exercise were key to improving a mens sexual performance.

Men who follow a Mediterranean diet particularly consuming lots of olive oil see their risk of impotence reduced by up to 40 per cent in older age."

7

YULE HOUSE Pregnant mum-of-21 Sue Radford gives kids' rooms a Christmas makeover

NOW HEIR THIS Kate & William to make big announcement over Christmas, says royal expert

HAPPY MEAL-TIMEs Dad shares genius tip for giving daughter a McDonalds Happy Meal at home

RING THE CHANGES Can YOU tell the difference between a 21,400 ring and its 100 dupe?

FAMILY AFFAIR Mistress whos bedded over 100 married men says cheating is in your genes

PIC PERFECT Macho Wills and dominant Kate - what their Xmas cards really say about them

Go here to read the rest:
Six surprising Christmas gifts to give your man a boost in the bedroom from a vegan cookbook to a - The Sun