Category Archives: Molecular Medicine

DUBLIN, Feb. 14, 2020 /PRNewswire/ -- The "Global In-Silico Drug Discovery Market: Focus on Products, Technologies, Workflow, End Users, Country Data (17 Countries), and Competitive Landscape - Analysis and Forecast, 2018-2029" report has been added to ResearchAndMarkets.com's offering.

The in-silico drug discovery industry analysis projects the market to grow at a significant CAGR of 12.92% during the forecast period, 2019-2029. The in-silico drug discovery market generated $2,094.5 million in revenue in 2018, in terms of value.

The global in-silico drug discovery market growth has been primarily attributed to the major drivers in this market such as an emphasis on the reduction in medical errors and readmission rates, growth in the biomarker identification market and advancements in In-silico drug discovery techniques, and computational technological advancements in the field of computational biology.

However, there are significant challenges that are restraining the market growth. These challenges include the high cost of methods and expensive procedures and their applications in medical treatments.

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North America is the leading contributor to the in-silico drug discovery market and contributed approximately 41.65% to the global market value in 2018. This region is anticipated to grow at a significant CAGR during the forecast period 2019-2029 and continue dominating the global market in 2029. However, the Asia-Pacific region is expected to grow at the highest CAGR of 13.29% during the forecast period. In addition, the region of Europe also contributed a significant share of 28.40% to the global market in 2018.

Scope of the Market Intelligence

The in-silico drug discovery research provides a holistic view of the market in terms of various factors influencing it, including regulatory reforms, and technological advancements.

The scope of this report is centered upon conducting a detailed study of the products and manufacturers allied with the service market. In addition, the study also includes exhaustive information on the unmet needs, perception of the new products, competitive landscape, market share of leading manufacturers, the growth potential of each underlying sub-segment, and company, as well as other vital information with respect to the global in-silico drug discovery market.

Key Companies in the Market

The key manufacturers who have been contributing significantly to the global in-silico drug discovery market include Albany Molecular Research Inc., Certara USA, Inc., Charles River, Chemical Computing Group ULC, Collaborative Drug Discovery Inc., Dassault System (Biovia), Evotec A.G., GVK Biosciences Private Limited, ICAGEN, INC., Novo Informatics Pvt. Ltd., Numerate Inc., PerkinElmer Inc, Schrdinger, LLC, Selvita, Simulation Plus, and WuXi AppTec, among others.

Key Questions Answered in the Report

Key Topics Covered

1 Product Definition1.1 Inclusion and Exclusion

2 Research Scope2.1 Scope of the Study2.2 Key Questions Answered in the Report

3 Research Methodology3.1 Global In-Silico Drug Discovery Market: Research Methodology3.2 Primary Data Sources3.3 Secondary Data Sources3.4 Market Estimation Model

4 Industry Analysis4.1 Regulatory Framework4.1.1 Regulatory Framework in North America4.1.2 Regulatory Framework in Europe4.1.3 Regulatory Framework in Asia-Pacific

5 Competitive Landscape5.1 Mergers and Acquisitions5.2 Product Launches and Product Updates5.3 Synergistic Activities5.4 Business Expansion Activities and Others5.5 Market Share Analysis

6 Market Dynamics6.1 Overview6.2 Impact Analysis6.3 Market Drivers6.3.1 Emphasis on Reduction in Medical Errors and Readmission Rates6.3.2 Growth in the Biomarker Identification Market and Advancements in In-Silico Drug Discovery Techniques6.3.3 Technological Advancements in the Field of Computational Biology6.4 Market Restraints6.4.1 Lack of High Complexity Testing Centers6.4.2 Expensive Procedures and Their Applications in Medical Treatments6.4.3 High Capital Requirement Hampering the Expansion of Global Reach6.5 Market Opportunities6.5.1 Massive Scope for Adoption of In-Silico Drug Discovery in Developing Nations6.5.2 Integration of Blockchain Technology in Interoperability6.5.3 Collaborations With Precision Medicine Providers

7 In-Silico Drug Discovery: Overview7.1 Introduction7.2 Market Availability for In-Silico Drug Discovery7.3 In-Silico Drug Discovery Market Technology Trends

8 Global In-Silico Drug Discovery Market (by Workflow)8.1 Overview8.2 Discovery8.2.1 Target Identification8.2.1.1 Bioinformatics8.2.1.2 Reverse Docking8.2.1.3 Protein Structure Prediction8.2.2 Target Validation8.2.3 Lead Discovery8.2.3.1 Library Design8.2.3.2 Pharmacophore8.3 Pre-Clinical Tests8.4 Clinical Trials

9 Global In-Silico Drug Discovery Market (by Product)9.1 Software9.2 Software as-a-Service (Cloud)9.3 Consultancy as-a-Service

10 Global In-Silico Drug Discovery Market (by Software Type)10.1 Molecular Modeling and de Novo Drug Design Software10.2 Pharmacophore Modeling Software

11 Global In-Silico Drug Discovery Market (by End-user)11.1 Contract Research Organizations11.2 Pharmaceutical Industry11.3 Academic and Research Institutes11.4 Other End-users (Hospitals and Other Care Facilities)

12 Global In-Silico Drug Discovery Market, by Region12.1 Overview12.2 North America12.2.1 U.S.12.2.2 Canada12.3 Europe12.3.1 Germany12.3.2 France12.3.3 U.K.12.3.4 Italy12.3.5 Spain12.3.6 Russia12.3.7 Rest-of-Europe12.4 Asia-Pacific12.4.1 China12.4.2 Japan12.4.3 Australia12.4.4 India12.4.5 South Korea12.4.6 Rest-of-APAC12.5 Latin America12.5.1 Brazil12.5.2 Mexico12.6 Rest-of-the-World

13 Company Profiles13.1 Overview13.2 Albany Molecular Research Inc.13.2.1 Company Overview13.2.2 Role of Albany Molecular Research in the Global In-Silico Drug Discovery Market13.2.3 SWOT Analysis13.3 Certara USA Inc.13.4 Charles River13.5 Chemical Computing Group ULC13.6 Collaborative Drug Discovery Inc.13.7 Dassault System (Biovia)13.8 Evotec AG13.9 GVK Biosciences Private Limited13.10 ICAGEN Inc.13.11 Novo Informatics Pvt. Ltd.13.12 Numerate Inc.13.13 PerkinElmer Inc.13.14 Schrdinger LLC13.15 Selvita13.16 Simulation Plus13.17 WuXi AppTec13.18 e-therapeutics plc (Snapshot)

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Human urinary bladder cancer is one of the most common cancers worldwide with the mortality rate of approximately 165,000 people annually. The modulation of extracellular matrix is a crucial event in the metastatic spread, among others in angiogenesis. It is initiated and prolonged by the cascade of matrix metalloproteinases. MMP-14 and MMP-15 are associated with a high degree of malignancy, aggressiveness, and survival prognosis by the activation of other matrix metalloproteinases (MMPs). This study was aimed at evaluating the expression and the activity of selected transmembrane metalloproteinases at different stages of human urinary bladder cancer.

Western blot and enzyme linked immunosorbent assay (ELISA) method were used to evaluate the expression and content of MMPs and TIMP-1. The activity of studied enzymes was determined with fluorometric method.

Both transmembrane metalloproteinases are found in healthy or cancerous tissue in high molecular complexes of human urinary bladder. MMP-14 dominates over MMP-15, particularly in high-grade urinary bladder cancer. Their contents significantly change with the grade of bladder tumor. The amount of MMP-14 increases with increasing grade of tumor. MMP-15 content decreases in high-grade bladder cancer. With increasing grade of urinary bladder cancer their actual activity (per kg of total protein content) is varying in different ways. In all examined tissues, the specific activity of MMP-15 (per kg of the enzyme content) is much higher in comparison to MMP-14. Human urinary bladder cancer contains higher TIMP-1 amounts than control tissue but with the decrease with an increase in tumor grade.

Comparison of investigated enzymes' activity and the inhibitor content suggests it opposite effects, higher suppression of MMP-14 than MMP-15 activity in low-grade bladder cancer and reverse TIMP-1 action in high-grade cancer. The MMP-14 activity determination in urinary bladder cancer tissue may be used as a predictor of a risk of metastasis.

Medicine. 2020 Feb [Epub]

Jacek Kudelski, Grzegorz Mynarczyk, Barbara Darewicz, Marta Bruczko-Goralewska, Lech Romanowicz

Department of Urology, Medical University of Biaystok, Poland., Department of Medical Biochemistry.

PubMed http://www.ncbi.nlm.nih.gov/pubmed/32049862

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Dominative role of MMP-14 over MMP-15 in human urinary bladder carcinoma on the basis of its enhanced specific activity. - UroToday

NEW YORK, Jan. 16, 2020 (GLOBE NEWSWIRE) -- Progenics Pharmaceuticals, Inc. (Nasdaq:PGNX), an oncology company developing innovative targeted medicines and artificial intelligence to find, fight and follow cancer, today announced that an abstract highlighting data from its PSMA AI program has been selected for a moderated poster presentation at the 2020 Society for Nuclear and Molecular Medicine (SNMMI) Mid-Winter Meeting, which will be held from January 23 25, 2020 in Tampa, FL.

Date & Time:January 23, 2020 from 12:15 p.m. to 1:15 p.m. Eastern TimeTitle:Deep Learning-Enabled Automated Hotspot Detection from 18F-DCFPyL (PyL-PSMA) PET/CT in Metastatic Prostate Cancer

About PyL for PET Imaging of Prostate CancerPyL (also known as 18F-DCFPyL) is a fluorinated PSMA-targeted positron emission tomography (PET) imaging agent that enables visualization of both bone and soft tissue metastases to determine the presence or absence of recurrent and/or metastatic prostate cancer.

About PROGENICS

Progenics is an oncology company focused on the development and commercialization of innovative targeted medicines and artificial intelligence to find, fight and follow cancer, including: therapeutic agents designed to treat cancer (AZEDRA, 1095, and PSMA TTC); prostate-specific membrane antigen (PSMA) targeted imaging agents for prostate cancer (PyL and 1404); and imaging analysis technology (aBSI and PSMA AI). Progenics has three commercial products, AZEDRA, for the treatment of patients with unresectable, locally advanced or metastatic pheochromocytoma or paraganglioma (rare neuroendocrine tumors of neural crest origin) who require systemic anticancer therapy; and oral and subcutaneous formulations of RELISTOR (methylnaltrexone bromide) for the treatment of opioid-induced constipation, which are partnered with Bausch Health Companies Inc.

Forward Looking StatementsThis press release contains projections and other forward-looking statements regarding future events. Statements contained in this communication that refer to Progenics estimated or anticipated future results or other non-historical facts are forward-looking statements that reflect Progenics current perspective of existing trends and information as of the date of this communication and include statements regarding Progenics strategic and operational plans and delivering value for shareholders. Forward looking statements generally will be accompanied by words such as anticipate, believe, plan, could, should, estimate, expect, forecast, outlook, guidance, intend, may, might, will, possible, potential, predict, project, or other similar words, phrases or expressions. Such statements are predictions only and are subject to risks and uncertainties that could cause actual events or results to differ materially. These risks and uncertainties include, among others: risks associated with the proposed merger transaction with Lantheus Holdings, Inc.; market acceptance for approved products; the risk that the commercial launch of AZEDRA may not meet revenue and income expectations; the cost, timing and unpredictability of results of clinical trials and other development activities and collaborations; the unpredictability of the duration and results of regulatory review of New Drug Applications (NDA) and Investigational NDAs; the inherent uncertainty of outcomes in the intellectual property disputes such as the dispute with the University of Heidelberg regarding PSMA-617; our ability to successfully develop and commercialize products that incorporate licensed intellectual property; the effectiveness of the efforts of our partners to market and sell products on which we collaborate and the royalty revenue generated thereby; generic and other competition; the possible impairment of, inability to obtain and costs of obtaining intellectual property rights; possible product safety or efficacy concerns, general business, financial, regulatory and accounting matters, litigation and other risks; and risks related to changes in the composition of our Board of Directors following the delivery of shareholder consents in response to the recent consent solicitation conducted by one of our shareholders. More information concerning Progenics and such risks and uncertainties is available on its website, and in its press releases and reports it files with the Securities and Exchange Commission (the SEC), including those risk factors included in its Annual Report on Form 10-K for the year ended December 31, 2018, as updated in its subsequent Quarterly Reports on Form 10-Q. Progenics is providing the information in this press release as of its date and, except as expressly required by law, Progenics disclaims any intent or obligation to update or revise any forward-looking statements, whether as a result of new information, future events or circumstances or otherwise.

Additional information concerning Progenics and its business may be available in press releases or other public announcements and public filings made after this press release. For more information, please visit http://www.progenics.com. Information on or accessed through our website or social media sites is not included in the companys SEC filings.

ContactMelissa DownsInvestor Relations(646) 975-2533mdowns@progenics.com

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Progenics Pharmaceuticals Announces Presentation at the 2020 SNMMI Mid-Winter Meeting - BioSpace

Food is more than the energy that fuels our bodies it is preventive medicine. Maybe not a cheesy chimichanga, but the type of food that is loaded with vitamins and proteins can maximize the benefits to the human body.

We need to look at the functional properties of food more closely so we can achieve the desired outcome, said Justin Siegel, associate professor of chemistry, biochemistry and molecular medicine, and faculty director for the Innovation Institute for Food and Health. Instead of focusing on the quantity of food which is a legitimate long-term concern globally lets hone in on creating quality food that possesses more active nutritional ingredients that deliver greater health benefits with every serving.

Siegel has a vision to transform the greater Sacramento region into the incubator pipeline for food science innovations. The initiative, dubbed Food Valley, would accelerate the commercialization of game-changing ideas across the food system by tapping into research, industry and policy. It would also prepare tomorrows food innovators and entrepreneurs through experiential learning programs.

Food Valley aims to patent its food innovations through developing technologies. These concepts can be grown into companies and potentially be a launchpad for Aggie entrepreneurs.

Siegel became interested in biotechnology as a kid. More recently, he thought about the possibilities of using biotech to disrupt the food systems industry. He co-founded PVP Biologics, a food biotech company, in 2016. PVP created a pill called KumaMax, which could help those who have celiac disease. KumaMax is currently in clinical trials, awaiting FDA approval.

Food Valley is about letting people experience freedom in what they are able to eat especially as it pertains to food allergies and restrictions, Siegel said. With modern technology we can both see the exact molecules that make up our food and manipulate those molecules to change how they interact with someones body.

No centralized hub for food innovations exists yet. Siegel said he believes UCDavis has the right ingredients to emerge as the leader.

Twenty years ago, this was science fiction, he said. Now we can do things we never thought possible. There is going to be a hub for food innovation, and UCDavis should be the place it happens.

This is one of several Big Ideas, forward-thinking, interdisciplinary programs and projects that will build upon the strengths of UCDavis to positively impact the world for generations to come. Learn more at bigideas.ucdavis.edu.

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The Future of Food - UC Davis

06 September 2019, Berlin: After a group music therapy session in a dementia residential community ... [+] in Berlin-Neuklln, which is looked after by the Unionhilfswerk, one resident holds hands. In Germany, the number of people suffering from dementia is increasing. Although the sick forget more and more, music can reawaken certain memories - at least for a moment. (to dpa "Dit one does not forget" - with music memories awaken) Photo: Christoph Soeder/dpa (Photo by Christoph Soeder/picture alliance via Getty Images)

Alzheimers is a devastating diagnosis for people suffering from the disease, as well as their families, but a group of researchers feels that they are one step closer to finding a cure.

Alzheimer's disease (AD) affects about 5.7 million people in the US and is the leading cause of age-related dementia today. Many people suffering from AD face a myriad of challenges including the lack of effective treatments, reliable biomarkers, or preventive strategies. Unfortunately, several promising drug candidates in the past have failed in clinical trials so researchers are still searching for new preventions or therapies to combat the development of AD. But there seems to be hope with a new vaccine that may proceed to clinical trials after successful animal testing.

A new paper in the journalAlzheimer's Research & Therapyis opening the door for further research in 2020, with medical researchers at the Institute for Molecular Medicine and University of California, Irvine (UCI) working with a successful vaccine formulated on adjuvants(1) developed by Flinders University Professor Nikolai Petrovsky in South Australia.

The causes of AD, in part, are believed to be tied to the role two proteins in the brain;

It is these two proteins that the US-led research team is looking to develop effective immunotherapy for via a new vaccine to remove brain plaques and tau protein tangles.

As explained in the research teams report, Alzheimer disease (AD) is characterised by the accumulation of beta-amyloid (A) plaques and neurofibrillary tangles composed of hyperphosphorylated(2) tau, which together lead to neurodegeneration and cognitive decline, continuing that, Current therapeutic approaches have primarily aimed to reduce pathological aggregates of either A or tau, yet phase 3 clinical trials of these approaches have thus far failed to delay disease progression in humans. The researchers contend that combinatorial therapies that concurrently target both A and tau might be needed for effective disease modification.

The research teams claims that recent success in their tests with mice supports progression to human trials in years to come, sparking hope in he field. "Our approach is looking to cover all bases and get past previous roadblocks in finding a therapy to slow the accumulation of A/tau molecules and delay AD progression in a the rising number of people around the world," says Professor Petrovsky.

However, one downside of the potential vaccine is thatit could not currently be used as a preventive measure in healthy subjects due to the need for frequent (monthly) administration of high concentrations of immunotherapeutic drugs, which are a class of drugs targeting the immune system to either kickstart or suppress immune function.

However, if future human trials are successful, the new paper concludes that the new combined vaccination approach could potentially be used to induce strong immune responses to both of the hallmark pathologies of AD in a broad population base of vaccinated subjects with high MHC (major histocompatibility complex(3)) class II gene polymorphisms, stating that, This synergistic model suggests that combinatorial/multi-target therapies directed at the accumulation of both amyloid and tau pathologies may be more effective in the treatment of AD than previously tested unimodal approaches.

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We May Be One Step Closer To A Vaccine Against Alzheimers Disease - Forbes

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Researchers may have found a way to prevent Duchenne muscular dystrophy-related heart disease, the leading cause of death in patients living with the disease.

The study examines the role of Connexin-43 (Cx43), a protein that regulates heart function. The researchers found that Cx43 was dysfunctional in both human and mouse Duchenne muscular dystrophy (DMD) hearts, so they modified the Cx43 protein in the hopes of alleviating heart disease.

They discovered that altering the Cx43 protein through a process called phosphorylation protected DMD mice against irregular heart beat and late-stage failure.

DMD, a genetic disorder characterized by progressive muscle degeneration, is the most common type of muscular dystrophy, affecting about one in 5,000 males and typically beginning at about age 4. The average life expectancy is 26.

For many DMD patients, the heart muscles gradually break down, leading to death. Our findings may help give hope to millions of patients, says study coauthor Diego Fraidenraich, an assistant professor of cell biology and molecular medicine at Rutgers University New Jersey Medical School.

Medical advances have managed to slow down the disease progression in most muscles in the body, but there are yet to be any discoveries that target or prevent deterioration of the DMD heart, which remains the number one killer among these patients, says coauthor Eric Himelman, a PhD candidate. Therapies based on our finding may help prolong the lives of muscular dystrophy and other heart disease patients.

Next steps include developing drugs that directly target Cx43 in DMD hearts, with a goal of potentially introducing clinical trials using Cx43 modification as a therapy for DMD patients.

The study appears in the Journal of Clinical Investigation. Another study in JCI Insight also examined Cx43 activity in the heart.

The National Institutes of Health, the Muscular Dystrophy Association, and the American Heart Association funded the work.

Additional researchers are from Rutgers, the Fred Hutchinson Cancer Research Center, New York University, and Baylor College of Medicine.

Source: Rutgers University

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Research focuses on precisely how the disease develops in the brain

Anne Fagan, PhD, supervises staff scientist Matthew R. Amos as he analyzes samples for molecular signs of Alzheimer's disease. Fagan leads one arm of a long-running, international Alzheimers study aimed at understanding how the disease develops and progresses. Researchers at Washington University School of Medicine in St. Louis have received $29 million to continue the study known as the Dominantly Inherited Alzheimer Network for another five years.

For more than a decade, Washington University School of Medicine in St. Louis has led an international effort to better understand Alzheimers disease by studying people with rare genetic mutations that cause the disease to develop in their 50s, 40s or even 30s. The researchers have shown that the disease begins developing two decades or more before peoples memories begin to fade, as damaging proteins silently accumulate in the brain.

Now, the National Institute on Aging of the National Institutes of Health (NIH) has committed $29 million to support the effort known as the Dominantly Inherited Alzheimer Network (DIAN) for another five years, pending availability of funds. With the new funding, the network will add three new research initiatives to investigate more closely the changes that occur in the brain as the disease develops, which could lead to new ways to diagnose or treat Alzheimers.

The extraordinary accomplishments of the DIAN investigators and participants over the past decade have set the stage to understand the molecular changes that can cause Alzheimers disease, said DIAN director Randall J. Bateman, MD, the Charles F. and Joanne Knight Distinguished Professor of Neurology. The three new scientific projects will provide deep insights into how Alzheimers disease begins and progresses to dementia.

DIAN follows families with genetic mutations that all but guarantee that those who inherit the mutations will develop Alzheimers disease at young ages. While devastating for families, this genetic form of Alzheimers disease creates a rare opportunity for researchers to look for brain changes long before symptoms appear in people who carry such mutations, compared with their relatives who dont have the mutation.

Although the study follows only people with a rare genetic form of Alzheimers, its findings could apply to the millions of people living with the much more common late-onset Alzheimers, which appears after age 65. The brain changes that lead to memory loss and confusion are thought to be much the same in early- and late-onset Alzheimers.

Since the network was established in 2008, DIAN researchers have established 19 sites in eight countries representing North and South America, Europe, Asia and Australia with another five sites in four Latin American countries in the works. People from families with genetic forms of Alzheimers take part in observational studies to track changes to their brains over time. The network also has established a clinical trials unit to test investigational therapies to prevent or treat the disease.

Participants undergo assessments of their memory and thinking skills, provide DNA for genetic analysis, undergo brain scans, and give blood and cerebrospinal fluid so researchers can look for molecular signs of Alzheimers disease. With the help of such participants, researchers have begun to piece together a timeline of the brain changes that culminate in cognitive decline and dementia. First, the protein amyloid beta starts forming plaques in the brain up to two decades before symptoms arise. Later, tangles of tau protein form, and the brain begins to shrink. Only then do signs of confusion and forgetfulness appear.

In addition to supporting ongoing research efforts, the grant funds three new projects:

The study described in this press release is supported by the National Institute on Aging of the National Institutes of Health (NIH) under award number U19AG032438. The grant from the National Institute on Aging provides 95.4% of the funding for this study, with the remainder provided by the Alzheimers Association (3.3%) and a consortium of pharmaceutical companies (1.3%). The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.

Washington University School of Medicines 1,500 faculty physicians also are the medical staff of Barnes-Jewish and St. Louis Childrens hospitals. The School of Medicine is a leader in medical research, teaching and patient care, ranking among the top 10 medical schools in the nation by U.S. News & World Report. Through its affiliations with Barnes-Jewish and St. Louis Childrens hospitals, the School of Medicine is linked to BJC HealthCare.

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$29 million for new phase of international Alzheimer's study Washington University School of Medicine in St. Louis - Washington University School of...

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Culprit identified in bone loss from cancer therapy

Red and green lines represent new bone in this image of a normal mouse bone. Exposure to chemotherapy and radiation during cancer treatment leads to bone loss and increases the risk of osteoporosis and fractures. A new study from Washington University School of Medicine in St. Louis identifies the trigger for this bone loss and suggests ways to prevent it.

Bone loss that can lead to osteoporosis and fractures is a major problem for cancer patients who receive chemotherapy and radiation. Since the hormone estrogen plays an important role in maintaining bone health, bone loss is especially pronounced among postmenopausal women with breast cancer who are treated using therapies aimed at eliminating estrogen.

Men and children treated for other cancers also experience bone loss, suggesting that eliminating estrogen is not the only trigger leading to bone degeneration.

Studying mice, researchers from Washington University School of Medicine in St. Louis have found a driver of bone loss related to cancer treatment. They have shown that radiation and chemotherapy can halt cell division in bone, which results in a stress response referred to as senescence. According to the new study, cell senescence drives bone loss in female mice beyond that seen from the absence of estrogen alone. The researchers further found that this process occurs in males and females and is independent of cancer type. And perhaps most importantly, the researchers showed that such bone loss can be stopped by treating the mice with either of two investigational drugs already being evaluated in clinical trials.

The study appears Jan. 13 in Cancer Research, a journal of the American Association for Cancer Research.

Researchers have understood that this bone loss has to be due to more than just hormone loss, said senior author Sheila A. Stewart, PhD, a professor of cell biology & physiology. Cancer patients who receive chemotherapy and radiation lose a lot more bone than women with breast cancer treated with aromatase inhibitors, which eliminate estrogen. And children who have not yet gone through puberty, and arent making much estrogen, also lose bone. We wanted to understand what causes bone loss beyond a lack of estrogen and whether we can do anything to stop it.

Stopping bone loss could improve quality of life for cancer patients. Bone loss leads to an increased risk of fractures that continues many years after treatment. This loss of bone density makes it much more likely that patients will develop fractures in the pelvis, hips and spine, which affect mobility and increase the risk of death.

The researchers studied bone loss in mice treated with two common chemotherapy drugs doxorubicin and paclitaxel as well as in mice that received radiation to one limb, to understand whether the bone loss effects were similar in different types of cancer therapies. In all situations, the treatments induced the process of cellular senescence.

Senescence is a chronic stress response in a cell that stops it from dividing and also results in the release of many molecules, some of which we showed drive bone loss, said Stewart, who is also the associate director for basic sciences at Siteman Cancer Center at Barnes-Jewish Hospital and Washington University School of Medicine.

The cells in mouse bones that were most affected by the cancer therapies included those responsible for bone remodeling. These are sets of cells that strike a vital balance between dismantling old bone and building new bone in its place. This balance is disturbed in conditions such as osteoporosis, in which the bone-building cells can no longer keep up with the bone-dismantling cells. The new study suggests that the balance is even more off-kilter following cancer therapy: Bone-building cell activity slows down, and the activity of cells that remove old bone actually accelerates.

The researchers showed they could prevent bone loss in the mice if they took steps to remove the cells that are no longer dividing, thus eliminating the molecular signals that the cells produce that drive bone loss. Toward possible therapies, Stewart and her colleagues then showed they could achieve a similar effect with two different types of compounds that block these molecular signals.

The investigational drugs, a p38MAPK inhibitor and a MK2 inhibitor, block different parts of the same pathway leading to bone loss. Stewart and her colleagues also published a study in 2018 showing that the two inhibitors slowed the growth of metastatic breast cancer in mice. The p38MAPK inhibitor is being tested in U.S. clinical trials for inflammatory diseases, such as chronic obstructive pulmonary disease (COPD). And the MK2 inhibitor is about to be evaluated as atherapy for rheumatoid arthritis.

Cancer patients at risk of bone loss often are treated with drugs for osteoporosis, including bisphosphonates and denosumab. Both have some undesirable side effects, such as muscle and bone pain and, because of the way they work, they may be less desirable for children whose bones are still growing.

The inhibitors we studied have extremely low toxicity, so we are interested in exploring whether they could be an improved option to stop bone loss in children receiving cancer therapy, Stewart said. Were also interested in pursuing a clinical trial to evaluate these drugs in women with metastatic breast cancer to see if we can slow metastatic growth and also preserve bone health in these patients.

This work was supported by the National Institutes of Health (NIH), grant numbers P30 AR074992, NS086741 and P30 CA91842; Washington University School of Medicine; and The Childrens Discovery Institute of Washington University and St. Louis Childrens Hospital, grant number CDI-CORE-2015-505.

Yao Z, Murali B, Ren Q, Luo X, Faget DV, Cole T, Ricci B, Thotala D, Monahan JB, van Deursen J, Baker D, Faccio R, Schwarz J, Stewart SA. Therapy-induced senescence drives bone loss. Cancer Research. Jan. 13, 2020.

Washington University School of Medicines 1,500 faculty physicians also are the medical staff of Barnes-Jewish and St. Louis Childrens hospitals. The School of Medicine is a leader in medical research, teaching and patient care, ranking among the top 10 medical schools in the nation by U.S. News & World Report. Through its affiliations with Barnes-Jewish and St. Louis Childrens hospitals, the School of Medicine is linked to BJC HealthCare.

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Investigational drugs block bone loss in mice receiving chemotherapy - Washington University School of Medicine in St. Louis

Scientists from the University of Zurich and the Max Planck Institute for Molecular Genetics, as well as the Icahn School of Medicine at Mount Sinai have come together to summarize recent evidence has challenged our working theory on the origin of life. Previously, scientists thought early life may have arisen from proteins or other chemical reactions important for life reacting in the hot soup of early Earth before there were actually cells. Then, it has been thought that these chemical reactions may have later been taken over by early cells.

However, long ago, after discovering large amounts of amino acids, DNA, and RNA on meteorites in our cosmic neighborhood, researchers again had to shift their train of thought. This paper explained that experiments that mimicked the temperature, acidity, pressure, and energy of an Early earth provided evidence that life may have come from random assortments of RNA and other small molecules. Then, the authors continued, a hypothesis was developed that RNA may have been the primordial first lifeform which took shape on our planet and may have already formed on others. The authors claim that this led to this most recent and widely accepted theory: our world may have been a RNA world at one point in its development; one in which life was composed of a few self-reproducing RNA molecules that worked to spread information as rapidly as possible and combined with amino acids to make proteins which could assist it. The problem with this idea is that researchers are still struggling to engineer RNA molecules that create themselves; a necessary condition if RNA is to reproduce and be able to evolve. Enter the viroid viroids are, essentially, a piece of RNA that can copy itself. Viroids can also insert themselves into a hosts DNA using normal cell processes.

A study highlighted in this article attempted to imitate RNA. Researchers showed that, in solutions of rich in salts and sugars, RNA can spontaneously regrow quite rapidly. These molecules were able to reproduce across 74 generations. From looking at how the sequences changed over these generations, it was determined that viroids replicated fast and continually became smaller and smaller strands of RNA.

The authors conclude that, given what we know about viroids, the idea of a viroid-first origin-of-life theory should be seriously considered, though there is not yet enough evidence to be confident. The good news is that detecting small organic molecules and viroid particles in the depths of space and below the surface of other planets is a lot easier to do than finding evidence to support other origin of life theories, since this theory uses techniques and science that are already familiar to biologists. Genetic engineers are still struggling to create self-copying RNA outside of a viroid-like model and proteins and metabolic chemicals havent turned up in our observations of the space beyond our solar system.

Evidence of organic molecules such as pieces of RNA, DNA, and proteins have been found on recent meteorites. This demonstrates that space already has the conditions to allow for these chemical reactions to take place beyond Earth. The authors suggest that the beginning of life must have been simple, and the search for signatures of viruses, viroids, and small RNA and the modeling of these life forms may be where we need to turn our attention next to answer the questions about life in our Universe.

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How Colds Are Unlocking Secrets About Life on Other Planets - Sciworthy

Espanol Version

January 4, 2020 -Most viral respiratory infections, like the common cold, usually come and go within a few days, with no lasting effects. But influenza (flu) is a disease that can cause serious health problems and can result in hospitalization or death.

You can fight back by adopting healthy habits and by using medicines and vaccines approved by the U.S. Food and Drug Administration to combat and help prevent the flu.If you are generally healthy, heres how to tell if you have a cold or the flu, and when to seek medical care.

Flu and cold viruses spread mainly by droplets, when infected people cough, sneeze, or talk. You also can get infected by touching a surface or object that has flu viruses on it, such as a door handle, and then touching your eyes, nose, or mouth. Flu season in the United States may begin as early as October and can last as late as May, and generally peaks between December and February.

Colds:Symptoms of colds usually are a stuffy or runny nose and sneezing. Other symptoms include coughing, a scratchy throat, and watery eyes. There is no vaccine to prevent colds, which come on gradually and often spread through everyday contact.

Flu:Symptoms of the flu come on suddenly and can include fever, headache, chills, dry cough, sore throat, body or muscle aches, tiredness, and feeling generally miserable. Like the viruses that cause a cold, flu viruses can cause a stuffy or runny nose, sneezing, and watery eyes. Young children also may experience nausea and vomiting.

Check with your health care provider promptly if you are at high risk for flu-related complications and you have flu symptoms or if you have flu symptoms that do not improve.People at high riskinclude:

Some health care providers can give you an FDA-cleared rapid flu test. There are 17 rapid flu tests (11 antigen-based and six molecular-based) on the market with updated performance criteria that the FDA created to provide reasonable assurance that the test is accurate, reliable, and clinically valid.

According to the Centers for Disease Control and Preventions flu testing guidelines, you dont need testing or to await test results before your health care provider can prescribe antiviral medication. Your health care provider will decide what to prescribe based on the signs and symptoms you have.

Colds usually run their course. When youre sick, limit exposing yourself to other people. Cover your mouth and nose when you cough or sneeze. Also, stay hydrated and rested. Avoid alcohol and caffeinated products.

There are FDA-approved prescription medications called antivirals for treating flu. Also, a cold or flu may lead to a bacterial infection (such as bronchitis, sinusitis, ear infections, and pneumonia) that could require antibiotics.

Most people with the flu who aren't at high risk have mild illness and do not need medical care or antiviral drugs. Still, your symptoms may last up to two weeks.

Read medicine labels carefully and follow the directions.People with certain health conditions, such as high blood pressure or diabetes, should check with a doctor or pharmacist before taking a new cough or cold medicine.

Choose the right over-the-counter (OTC, or non-prescription) medicines for your symptoms.

Check the medicines side effects.Medications can cause drowsiness and interact with food, alcohol, dietary supplements, and other medicines. Tell your doctor and pharmacist about every medical product and supplement you are taking.

Check with a health care professional before giving medicine to children.

Get vaccinated against the flu.The best way to prevent the flu is by getting vaccinated every year. The vaccine changes each year and contains flu virus strains that are expected to be prevalent during the upcoming flu season. The protection from the previous years vaccine will diminish over time and may be too low to protect you into the next year, even if the flu virus strains circulating the next year are the same as those contained in the previous years vaccine.

With rare exceptions, the CDC recommends that everyone ages 6 months and older should be vaccinated against flu. The flu vaccine provides protection from the flu and its potential complications, which can result in hospitalization and sometimes death.

Annual vaccination is especially important for people at high risk for developing serious complications from flu: health care workers, and anyone who lives with or cares for people at high risk for serious flu-related complications.

Although children younger than 6 months are too young to be vaccinated, they have the highest risk for being hospitalized because of flu and flu-related complications compared to children of other ages. Therefore, the CDC recommends that parents, grandparents, caregivers, and all household members 6 months or older should be vaccinated because they will be less likely to get the flu and spread it to the unvaccinated child. If possible, keep infants away from crowds for the first few months of life.

Wash your hands often.Teach children to do the same. Both colds and flu can be passed through contaminated surfaces, including the hands. Wash hands with warm water and soap for at least 20 seconds. Try not to touch your eyes, nose, or mouth. Clean and disinfect frequently touched surfaces, especially when someone is ill.

Limit exposure to infected people.Cover your nose and mouth with a tissue when you cough or sneeze. Throw the tissue in the trash after you use it.Source: FDA

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FDA: Is It a Cold or the Flu? Prevention, Symptoms, Treatments - Sierra Sun Times