N95 respirators offer the best protection against wildfire smoke and other types of air pollution, performing better than synthetic, cotton and surgical masks.
Researchers performed lab experiments to investigate the ability of different face masks and respirators to filter out particles in a range of sizes found in smoke and air pollution. They placed the different mask materials over a pipe that “breathes” in air and particles inside a plastic box.
N95s were so effective in the lab experiments that the researchers estimate their widespread use could reduce hospital visits attributable to wildfire smoke by 22% to 39%. The study’s findings can provide evidence-based recommendations to help people protect themselves during wildfire season.
The new study was published in GeoHealth, AGU’s journal investigating the intersection of human and planetary health for a sustainable future.
Climate change has made wildfires more frequent and intense in the Western U.S., and the resulting smoke exposure is taking a toll on people’s health. Wildfire smoke contains tiny particles smaller than 2.5 microns in diameter (PM2.5) — about the size of a single bacterium — that enter the lungs and are linked to multiple health problems, including a higher risk of asthma, respiratory infections and chronic obstructive pulmonary disease (COPD).
Face coverings have become second nature to many people during the coronavirus pandemic, making some wonder if masks and respirators could also protect against smoke and pollution. By definition, respirators are tight-fitting protective equipment that seal around the nose and mouth to filter the air coming in and out. Surgical-style face masks are designed to capture the droplets and particles produced by the wearer to prevent the spread of disease.

Addictive psychostimulants, from nicotine in cigarettes to illicit drugs like methamphetamine and cocaine, affect different regions of the brain. The same is believed true during withdrawal; finding a common brain pathway has proved elusive.
In a new paper, publishing September 27, 2021 in the journal eNeuro, a multi-institution team of researchers describe how withdrawal from nicotine, methamphetamine and cocaine altered the functional architecture and patterns in the brains of mice, compared to control animals.
They found that each drug produced a unique pattern of activity in the brain, but that mouse brains in withdrawal shared similar features. Perhaps more notably, the researchers said all psychostimulants shared a common link: Reduced modularity.
“All brains are organized into semiautonomous groups of neurons with specific functions, such as the cortex, amygdala and thalamus. Each region, however, is connected and interacts with other regions performing similar functions, creating a functional unit called a module,” said senior author Olivier George, PhD, professor in Department of Psychiatry at University of California San Diego School of Medicine. “Think of it as many different work stations, one station is in control of your mood, another takes care of your needs, and many other stations takes care of your goals, memories, motivations, sensation, et cetera. The brain needs many modules to take care of all of these processes at the same time.
“We found that in withdrawal, there was a dramatic decrease in the number of modules compared to control mice. It’s like the whole brain was dedicated to the effect of the lack of drugs, all of the work stations doing the same thing.”
That decreased modularity, the authors said, resulted in a complete restructuring of the brain networks. Reduced modularity has been shown in several brain disorders in humans, including traumatic brain injury and dementia. It may also be the common link between drugs of abuse.
To conduct their studies, the scientists implanted osmotic mini-pumps in mice that contained either nicotine, cocaine, methamphetamine or saline. The pumps remained in place for one week, with sufficient dosing and time to create a state of dependence. After the pumps were removed, the brains of mice were examined using single-cell whole-brain imaging at the peak of withdrawal symptoms, about eight to 12 hours post-pump removal.
“We found that cocaine, methamphetamine and nicotine withdrawal all produced a major shuffling of brain regions with major increases in functional connectivity throughout the brain compared to control (saline) mice,” said George, “with a decrease in modular structuring of the brain most strongly with methamphetamine and cocaine, then nicotine.”
The brains of methamphetamine and cocaine dependent mice were also very similar, consistent with their shared pharmacology, targeting the dopaminergic system.
This reduced modularity was associated with a shift of networks being controlled by the higher-level cortex to sub-cortical networks. The effect, said researchers, has been documented in humans after abstaining from alcohol dependence and in persons suffering from dementia and traumatic brain injury. Reduced modularity is associated with cognitive deficits and inflexible behavior which may explain the obsession and compulsion for the drug in people with substance use disorder.
George said the commonality of this kind of restructuring during withdrawal from psychostimulants helps explain why these drugs are so addictive. His team is currently using this approach to test experimental medications that may reverse and normalize brain network modularity.
Co-authors include: Adam Kimbrough, UC San Diego and Purdue University; Marsida Kallupi, UC San Diego; Lauren C. Smith and Sierra Simpson, UC San Diego and The Scripps Research Institute; and Andres Collazo, California Institute of Technology.

A commentary by Mayo Clinic Cancer Center researchers published in the Journal of Clinical Oncology Practice suggests that advances in breast cancer prevention research have resulted in new and innovative opportunities to modify breast cancer risk and potentially reduce breast cancer incidence and mortality.
“It is prudent for health care providers to be knowledgeable about the benefits of assessing individual breast cancer risk, and counsel and implement risk-reducing strategies with their patients, says Sandhya Pruthi, M.D., a Mayo Clinic internist and author of the commentary.
Dr. Pruthi says evidence-based, risk-reducing strategies include lifestyle modification, preventive anti-estrogen medications, surveillance breast imaging and genetic testing. Women at high risk of harboring a hereditary breast cancer mutation should consider prophylactic surgery to reduce risk.
“Physicians should be recommending individualized risk assessments for their patients and counseling them on interventions that range from lifestyle modifications to the use of preventive (anti-estrogen) medications or conjugated equine estrogen,” says Dr. Pruthi.
She says these strategies may be beneficial in reducing hormone-sensitive breast cancer tumors that have a good prognosis, and they also may be beneficial in preventing tumors that are not hormone-sensitive and have a poor prognosis.
“For many years, breast cancer prevention research has primarily focused on the use of anti-estrogen medications to reduce the incidence of favorable, hormone-sensitive breast cancers, but it is critical that we reexamine and implement other risk-reducing strategies to prevent unfavorable breast cancers, known as triple-negative tumors,” says Dr. Pruthi.
She encourages women and their health care providers to consider a comprehensive approach to breast cancer prevention that includes risk assessment; awareness of modifiable lifestyle factors, including low-fat dietary interventions; and use of medications that reduce the risk of dying from breast cancer.
Dr. Pruthi says her commentary was based on research conducted in two large randomized clinical trials: the Women’s Health Initiative Dietary Modification trial and the Women’s Health Initiative randomized trial with conjugated equine estrogen in women with prior hysterectomy. She says both clinical trials demonstrated a reduction in death from breast cancer.
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Materials provided by Mayo Clinic. Original written by Joe Dangor. Note: Content may be edited for style and length.

A type of drug already used to treat obesity and Type 2 diabetes, when taken six months prior to the diagnosis of COVID-19, was associated with a decreased risk of hospitalization, respiratory complications and death in COVID-19 patients with Type 2 diabetes, according to researchers at Penn State College of Medicine. The team, which analyzed electronic medical records of patients with type 2 diabetes, concludes that the drugs, called glucagon-like peptide-1 receptor (GLP-1R) agonists, should be further evaluated for potential protective effects against COVID-19 complications.
“Our results are very promising as GLP-1R agonist treatment appears to be highly protective, but more research is needed to establish a causal relationship between the use of these drugs and decreased risk for severe COVID-19 outcomes in patients with Type 2 diabetes,” said Patricia “Sue” Grigson, professor and chair of the Department of Neural and Behavioral Sciences.
According to the researchers, even though vaccines remain the most effective protection against hospitalization and death from COVID-19, additional effective therapies are needed to improve outcomes for patients with rare, severe breakthrough infections.
Patients living with pre-existing conditions like diabetes are at increased risk of severe COVID-19 complications, including death. A recent study from England reported that close to a third of COVID-19-related deaths in the country were among patients living with Type 2 diabetes.
“Vaccines have been shown to reduce hospitalization and death from COVID-19,” said Jennifer Nyland, assistant professor of neural and behavioral sciences and co-author of the study. “But the scientific community continues to search for treatments that may complement vaccination by further reducing the risk of hospitalization, respiratory complications and death from COVID-19 in at-risk patients with pre-existing conditions like diabetes.”
Nyland, Grigson and co-author Dr. Nazia Raja-Khan, associate professor of medicine and endocrinologist at Penn State Health Milton S. Hershey Medical Center, are studying how GLP-1R agonists could be used to treat substance use disorders. They hypothesized that patients with Type 2 diabetes who are taking these same medications, which they estimate to be less than 15% of Type 2 diabetes patients in the U.S., might have some level of protection from severe COVID-19 outcomes based on their anti-inflammatory properties. Patients with Type 2 diabetes often struggle with dysregulated inflammation, or swelling of body tissues. Overactive inflammatory responses have been implicated in severe COVID-19 cases and deaths.

One example of a complex autoimmune disease is systemic lupus erythematosus (SLE), which predominantly affects women. As the disease progresses, the body’s own immune system attacks the skin, blood vessels and internal organs such as the kidneys. Early intervention is important to prevent severe organ damage. Treatment options include suppressing the body’s immune system as well as more targeted therapies, such as removing autoreactive cells. However, until now it has remained unclear how the timing of the various types of treatment would affect the later progression of the disease.
A team of researchers led by Dr. Anja Werner from the Chair of Genetics at FAU has now investigated this question in more detail. ‘Our aim was to target the misguided immune response as accurately and as early on as possible,’ explains Dr. Werner. ‘Many autoimmune diseases are characterised by a loss of self-tolerance years before the actual onset of the disease, for example with autoantibodies being produced which may then attack and destroy organs at a later, active stage of the disease.’ Until now, only limited research has been conducted into whether this early and in some cases temporary loss of self-tolerance may act as a possible biomarker for the later disease, thereby allowing treatment to be commenced at an extremely early stage. Dr. Werner and her team have now demonstrated that targeting and temporarily removing B cells, which are not only involved in producing autoantibodies but can also influence other cells by presenting self-antigens or using messenger substances, has a major impact on how the disease progresses.
‘We were very surprised to see that early and temporary intervention using a well-established method of treatment could have such a dramatic impact on the later progression of the autoimmune disease,’ says Prof. Falk Nimmerjahn, Chair of Genetics. ‘It really seems as if the intervention served to reset the immune system in the treated animals, not only suppressing the production of autoantibodies but also by preventing or significantly delaying severe organ damage.’
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Materials provided by Friedrich-Alexander-Universität Erlangen-Nürnberg. Note: Content may be edited for style and length.

If the suspicion of Alzheimer’s disease creeps up, those affected must prepare themselves for lengthy and complex procedures until the case is clear. A team from Empa and the Cantonal Hospital of St. Gallen is now in the process of developing a blood test that will enable a reliable diagnosis using atomic force microscopy (AFM). The researchers have recently published their first results of a successful pilot study in the journal Science Advances.
A deep look into the molecular universe
In the beginning, physicist Peter Nirmalraj wanted to understand the molecular pathogenesis of Alzheimer’s in order to enable new approaches in diagnostics and therapy. One step further would be to decipher the exact role of beta-amyloid peptides and tau proteins associated with the neurodegenerative disease. Nirmalraj therefore set out not only to detect the mere presence of the suspicious proteins, but also to determine their variable shape and form as well as their amounts.
Current methods allow the determination of the total amount of both proteins in body fluids. However, these techniques do not allow the visualization of differences in the shape and condition of protein accumulations. The researcher is therefore working on technologies that allow nanometer-scale observations in blood and yet do not destroy the structure and morphology of the proteins.
Together with neurologists at the Cantonal Hospital in St. Gallen, Nirmalraj has now successfully completed an initial study. For their pilot study, he examined blood samples from 50 patients and 16 healthy subjects. Using AFM technology, the Empa researcher analyzed the surface of around 1000 red blood cells per person without knowing anything about their state of health. “This was the only way to make sure the interpretation of the data remained objective,” says Nirmalraj.
Protein fibers as an indicator
The Empa researcher measured the size, structure and texture of protein accumulations found on the blood cells. After thousands of red blood cells, the team eagerly awaited the comparison of the results from Nirmalraj’s counts with the clinical data from the neurologists. And indeed, the researchers were able to discern a pattern that matched the patients’ disease stage: People who had Alzheimer’s disease had large amounts of protein fibers made up of beta-amyloid peptides and tau proteins. The proteins were able to assemble into fibers several hundred nanometers long. In healthy individuals or those with incipient brain disorders, however, Nirmalraj counted only few fibers.
This proves the feasibility of blood analysis using AFM technology, the Empa researcher says: “If a reliable blood test can be developed based on this method, people with suspected Alzheimer’s would be spared the unpleasant puncture of the spinal canal in order to be able to diagnose the disease reliably.”
However, there is still a long way to go before a simple blood test is available in hospitals. The team’s next step is to corroborate the data by studying a larger number of subjects at different stages of the disease using AFM and chemical analysis.
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Materials provided by Swiss Federal Laboratories for Materials Science and Technology (EMPA). Note: Content may be edited for style and length.

A version of SARS-CoV-2, the virus that causes COVID-19 disease, has been successfully modified to glow brightly in cells and animal tissues, providing a real-time way to track the spread and intensity of viral infection as it happens in animal models, researchers at Texas Biomedical Research Institute (Texas Biomed) report in the journal The Proceedings of the National Academy of Sciences (PNAS).
“Now we can track where the virus goes in animal models for COVID-19,” said virologist Luis Martinez-Sobrido, Ph.D., a Professor at Texas Biomed, and senior paper author. “Being able to see how the virus progresses, and which organs and cell types it specifically targets, will be a big help for understanding the virus and optimizing anti-viral drugs and vaccines.”
In addition to tracking the virus, Martinez-Sobrido and his collaborators have already begun using the reporter viruses to screen how well neutralizing antibodies work against different variants of concern, as recently reported in the Journal of Virology.
Turning up the lights
To make the reporter virus, Martinez-Sobrido and his team combined several advanced molecular biology tools to add the genetic sequence for the fluorescent or bioluminescent “reporter” proteins to the virus genetic code. As the virus’s code is replicated and transcribed, so too is the code for the glowing proteins.
In an earlier study, the team replaced one of the virus’s genes with the gene for the glowing proteins, but this resulted in a very dim signal — the gene was not expressed enough to be easily detected in animals. To turn up the brightness, the researchers had to figure out how to get the virus to produce larger quantities of the reporter proteins.

A team of international researchers, including McGill Professor Stéphane Laporte, have discovered the working mechanism of potential drug targets for various diseases such as cancer, rheumatoid arthritis, and even COVID-19. The findings published in Molecular Cell uncover the inner workings of cell receptors that are involved in cancer progression and inflammatory diseases.
“The complement system is an integral part of our body’s defense mechanism against pathogenic attacks including viruses. When bacteria or viruses enter our body, the complement system is activated including two different membrane receptors called C5aR1 and C5aR2,” says Arun Shukla, the Joy Gill Chair Professor at IIT Kanpur who spearheaded the study. “While activation of the complement system is essential to combat harmful pathogens, excessive and sustained activation leads to inflammation, even life-threatening conditions like the ones responsible for severe complications in COVID-19.”
Using cutting-edge technologies such as CRISPR and cryogenic electron microscopy, the researchers unraveled the inner workings of C5aR2, providing an additional opportunity for therapeutic targeting for COVID-19. “To treat COVID-19, some scientists are already trying to block the activation of the C5aR1 receptor and clinical trials are already underway for Avdoralimab in patients with COVID-19 induced sever pneumonia. Our study opens up the possibility of targeting C5aR2 by designing new drug molecules that can bind to this receptor and block its activation and inflammation response,” says Stéphane Laporte, a Professor in the Faculty of Medicine and Health Sciences.
Cells in the human body are surrounded by receptors that are important drug targets where medicines produce their beneficial effects. These receptors work as messengers because they receive and transmit signals that allow the cells to trigger physiological processes in our body, the researchers explain.
“We are very excited to decipher the finer details of these receptors using cutting-edge technologies. Such information should enhance our fundamental knowledge about cellular signaling and allow us to translate our findings into novel drug discovery,” concludes Arun Shukla.
About this study
“Intrinsic bias at non-canonical, β-arrestin-coupled seven transmembrane receptors” by Shubhi Pandey, Punita Kumari, Mithu Baidya, Ryoji Kise, Yubo Cao, Hemlata Dwivedi-Agnihotri, Ramanuj Banerjee, Xaria X. Li, Cedric S. Cui, John D. Lee, Kouki Kawakami, Jagannath Maharana, Ashutosh Ranjan, Madhu Chaturvedi, Gagan Deep Jhingan, Stéphane A. Laporte, Trent M. Woodruff, Asuka Inoue and Arun K. Shukla was published in Molecular Cell.
This research was supported by the DBT Wellcome Trust India Alliance, Department of Science and Technology (DST), Science and Engineering Research Board (SERB), Council of Scientific and Industrial Research (CSIR), Lady Tata Memorial Trust, and the Canadian Institutes of Health Research.
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Materials provided by McGill University. Note: Content may be edited for style and length.

A protein — measuring just a few nanometers in size — acts as a molecular switch with a crucial role in determining whether we feel hungry or full. By determining of the protein’s 3D structure, researchers from Charité — Universitätsmedizin Berlin were able to visualize the molecular structures of the hormones with which this protein — melanocortin 4 receptor (MC4R) — interacts. Writing in Cell Research, the researchers report that this enabled them to describe the molecular mechanisms involved in the receptor’s activation and inhibition. These new findings could stimulate the development of optimized drugs to treat patients with severe overweight and obesity patients.
Studies exploring the nature of weight control ‘switches’ are more important than ever. We need to be able to treat genetic disorders that result in an inability to feel satiety after eating and which, even in young sufferers, cause severe and difficult-to-treat obesity. At the same time, obesity is one of the most pressing global challenges. Estimates suggest that 1.6 billion adults and 650 million children worldwide are classified as overweight or obese. The condition is associated with an increased risk of comorbidities such as cardiovascular disease and diabetes mellitus. Steadily increasing incidence rates and long-term consequences are driving global research efforts to decipher the mechanisms of appetite regulation at the molecular and ultimately at the atomic level. In addition to exploring the impact of genetic defects on appetite and hunger, research efforts also focus on finding potential targets for drug interventions.
In their recently published study, the team led by Dr. Patrick Scheerer, Head of Protein X-ray Crystallography and Signal Transduction (Scheerer Lab) at Charité’s Institute of Medical Physics and Biophysics, focused on one of the key players in hunger (and therefore weight) control in humans: the melanocortin 4 receptor (MC4R). Primarily found in the brain, this receptor protein is controlled by hormones that produce important satiety signals by binding to it. Activation of MC4R by stimulating hormones (α-/-MSH) results in the feeling of satiety. Conversely, inhibition by the hormone’s natural antagonist, known as Agouti-related protein (AgRP), results in increased hunger feeling. Genetic defects resulting in the functional impairment of this protein ‘switch’ often led to mild or even severe obesity in humans. Prof. Dr. Peter Kühnen, physician-scientist at the Institute of Experimental Pediatric Endocrinology, specializes in the treatment of patients with genetically induced impairments in the transduction of satiety signals. As part of his search for new treatment options for these types of obesity, the endocrinology specialist has devoted extensive efforts to studying the signaling pathways underlying human body weight regulation. He has also explored mutations in the genes encoding the relevant cellular messengers and receptors and analyzed the potential of drugs that might be able to replace individual messengers.
The drug-based treatment of pathologically increased appetite continues to face the same challenge: “To date, all of these pharmacological interventions have been dogged by side effects. These range from abnormal darkening of the skin — the hormone melanocortin also being responsible for skin and hair pigmentation — to cardiovascular events,” says Prof. Kühnen, who was also involved in the current study and whose work supporting the development of new, low-side-effect drugs was awarded the Paul-Martini Prize in 2020. “The reason for these undesirable side effects lies in the nature of the currently available drugs,” explains study lead Dr. Scheerer. He adds: “Instead of addressing a single target, they are usually directed at a range of receptors from the same family which, unfortunately, play different roles in our bodies. The more we know about the interactions between the components involved, the easier it will be to target interventions.” The teams led by Dr. Scheerer and Prof. Kühnen work closely together. In addition to sharing a common interest in the translation of research findings into clinical practice, their endeavors also complement the work of the DFG-funded Collaborative Research Center ‘Structural Dynamics of GPCR Activation and Signaling’ at Leipzig University. Charité is involved in four of the Collaborative Research Center’s subprojects.
As part of the current study, the researchers were able to elucidate and visualize the 3D molecular structure of the hormone receptor MC4R, a member of the G-protein-coupled receptor (GPCR) family. Given that the protein’s tiny size is expressed in nanoscale dimensions, conventional optical methods were inadequate for the task. “Using a state-of-the art imaging technology known as cryo-electron microscopy, we were able to visualize the receptor’s three-dimensional structure at a resolution of around 0.26 nanometers” says the study’s first author, Nicolas Heyder, a researcher at the Institute of Medical Physics and Biophysics. “We visualized the structures of two receptor-effector complexes, both of which contain the G-protein which is coupled to the receptor inside the cell. The differences between the two complexes are due to their being bound to two different hormones, namely setmelanotide and NDP-α-MSH. Both received their marketing authorization in the past two years, and both are stabilized by a calcium ion in the hormone binding pocket of MC4R.” In addition, the researchers found that the two receptor structures showed minor yet important differences in the way they bound both the drugs and the G-protein. “These molecular details provide important information on why and how various ligands — i.e., messenger molecules — exert specific effects on different MC4R signaling pathways. For a pharmacological intervention, this is of major importance,” says Nicolas Heyder.
This essential groundwork regarding the nature of the tiniest cell components would not have been possible without cryo-electron microscopy and many years of experience in establishing cell culture-based protein production. Both have been subject to ongoing optimization at Charité, thanks to collaborations with world-leading laboratories and experts, including Chemistry Nobel Laureate Prof. Dr. Brian Kobilka, a Stanford professor and an Einstein Visiting Fellow at the Berlin Institute of Health (BIH) at Charité.
In their study results, the researchers describe previously unknown details regarding the mechanisms underlying melanocortin 4 receptor function: how it is activated, how it is blocked, and how the interaction between a hormone and the receptor protein produces a signal inside the cell. “We are now able to identify the smallest differences in the interactions between receptors and hormones. These could prove important for the continued refinement of new drugs which would previously have been associated with side effects,” says Dr. Scheerer. He adds: “Now that the precise structure of the hormone-binding pocket is known, it can be targeted directly.” This is key to the translational use of knowledge on both the endocrinological aspects (in this case hormone regulation) and structural characteristics of interacting proteins.
The research team was able to show that how a previously known receptor-deactivator — or antagonist — binds to the receptor almost identical to the receptor-activating agonist, with only one significant difference. “This difference pinpoints the precise site that blocks the receptor, and which contains a sensitive switch that is responsible for activating the protein,” explains Dr. Scheerer. The researchers hope that additional research to improve their understanding of the MC4R signaling system will enable them to identify potential sites for targeted interventions. As a next step, the researchers hope to understand how additional factors might be controlling the receptor at the molecular level. Some of the directly interacting factors have already been identified. Their impact, however, remains to be elucidated.
About this study This research was made possible thanks to funding provided by the German Research Foundation (DFG) through the Collaborative Research Center 1423 (CRC 1423) ‘Structural Dynamics of GPCR Activation and Signaling’. The research received additional support through the Excellence Cluster ‘Unifying Systems in Catalysis (UniSysCat)’, the Collaborative Research Center ‘CRC 1365’ (DFG) and the Berlin Institute of Health (BIH) at Charité.

Today’s genetic engineers have a plethora of resources at their disposal: an ever-increasing number of massive datasets available online, highly precise gene editing tools like CRISPR, and cheap gene sequencing methods. But the proliferation of new technologies has not come with a clear roadmap to help researchers figure out which genes to target, which tools to use, and how to interpret their results. So, a team of scientists and engineers at Harvard’s Wyss Institute for Biologically Inspired Engineering, Harvard Medical School (HMS), and the MIT Media Lab decided to make one.
The Wyss team has created an integrated pipeline for performing genetic screening studies, encompassing every step of the process from identifying target genes of interest to cloning and screening them quickly and efficiently. The protocol, called Sequencing-based Target Ascertainment and Modular Perturbation Screening (STAMPScreen), is described in Cell Reports Methods, and the associated open-source algorithms are available on GitHub.
“STAMPScreen is a streamlined workflow that makes it easy for researchers to identify genes of interest and perform genetic screens without having to guess which tool to use or what experiments to perform to get the results they want,” said corresponding author Pranam Chatterjee, Ph.D., a former graduate student at the MIT Media Lab who is now the Carlos M. Varsavsky Research Fellow at HMS and the Wyss Institute. “It is fully compatible with many existing databases and systems, and we hope that many scientists are able to take advantage of STAMPScreen to save themselves time and improve the quality of their results.”
Frustration is the mother of invention
Chatterjee and Christian Kramme, a co-first author of the paper, were frustrated. The two scientists were trying to explore the genetic underpinnings of different aspects of biology — like fertility, aging, and immunity — by combining the strengths of digital methods (think algorithms) and genetic engineering (think gene sequencing). But they kept running into problems with the various tools and protocols they were using, which are commonplace in science labs.
The algorithms that purported to sift through an organism’s genes to identify those with a significant impact on a given biological process could tell when a gene’s expression pattern changed, but didn’t provide any insight into the cause of that change. When they wanted to test a list of candidate genes in living cells, it wasn’t immediately clear what type of experiment they should run. And many of the tools available to insert genes into cells and screen them were expensive, time-consuming, and inflexible.