Month: September 2022

Categories : Cardiovascular DiseaseTags :

Coffee Extends Life as Well as Consciousness

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Coffee cup and beans
Photo by Mike Kenneally on Unsplash

Coffee lovers have another thing to rejoice about: drinking two to three cups of coffee a day is linked with a longer lifespan and lower risk of cardiovascular disease (CVD) compared with avoiding coffee, according to a study in the European Journal of Preventive Cardiology. The association was strongest with drinking ground coffee, though instant and decaffeinated preparations also showed this benefit.

“In this large, observational study, ground, instant and decaffeinated coffee were associated with equivalent reductions in the incidence of cardiovascular disease and death from cardiovascular disease or any cause,” said study author Professor Peter Kistler of the Baker Heart and Diabetes Research Institute, Melbourne. “The results suggest that mild to moderate intake of ground, instant and decaffeinated coffee should be considered part of a healthy lifestyle.”

There is little information on the impact of different coffee preparations on heart health and survival. This study examined the associations between types of coffee and incident arrhythmias, CVD and death using data from the UK Biobank, with participants aged 40–69. CVD was comprised of coronary heart disease, congestive heart failure and ischaemic stroke.

The study included 449 563 participants free of arrhythmias or other CVD at baseline. The median age was 58 years and 55.3% were women. Participants completed a questionnaire asking how many cups of coffee they drank each day and whether they usually drank instant, ground (such as cappuccino or filtered coffee), or decaffeinated coffee. They were then grouped into six daily intake categories, consisting of none, less than one, one, two to three, four to five, and more than five cups per day. The usual coffee type was instant in 198 062 (44.1%) participants, ground in 82 575 (18.4%), and decaffeinated in 68 416 (15.2%). A comparator group of 100 510 (22.4%) non-coffee drinkers was included.

Coffee drinkers were compared to non-drinkers for the incidence of arrhythmias, cardiovascular disease and death, after adjusting for age, sex, ethnicity, obesity, hypertension, diabetes, obstructive sleep apnoea, smoking status, and tea and alcohol consumption. Outcome information was obtained from medical records and death records. The median follow up was 12.5 years.

A total of 27 809 (6.2%) participants died during follow up. All types of coffee were linked with a reduction in death from any cause. The greatest risk reduction seen with two to three cups per day, which compared to no coffee drinking was associated with a 14%, 27% and 11% lower likelihood of death for decaffeinated, ground, and instant preparations, respectively.

CVD was diagnosed in 43 173 (9.6%) participants during follow up. All coffee subtypes were associated with a reduction in incident cardiovascular disease. Again, the lowest risk was observed with two to three cups a day, which compared to abstinence from coffee was associated with a 6%, 20%, and 9% reduced likelihood of cardiovascular disease for decaffeinated, ground, instant coffee, respectively.

During follow up, an arrhythmia was diagnosed in 30 100 (6.7%) participants. Ground and instant coffee, but not decaffeinated, was associated with a reduction in arrhythmias including atrial fibrillation. Compared with non-drinkers, the lowest risks were observed with four to five cups a day for ground coffee and two to three cups a day for instant coffee, with 17% and 12% reduced risks, respectively.

Professor Kistler said: “Caffeine is the most well-known constituent in coffee, but the beverage contains more than 100 biologically active components. It is likely that the non-caffeinated compounds were responsible for the positive relationships observed between coffee drinking, cardiovascular disease and survival. Our findings indicate that drinking modest amounts of coffee of all types should not be discouraged but can be enjoyed as a heart healthy behaviour.”

Source: European Society of Cardiology

Categories : COVIDTags :

SARS-CoV-2 Can also Impact the Colon

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Anatomy of the gut
Source: Pixabay CC0

Although SARS-CoV-2 infections mainly attack the lungs, in many cases they can also damage other organs, such as the colon: around 60% of patients experienced digestive tract impacts. A study published in the International Journal of Molecular Sciences analysed the manifestations of COVID in the lungs and colon, identifying the differences at a molecular level.

Their findings serve as the basis for the identification of novel biomarkers and the development of new treatment strategies.

The University of Vienna scientific team, led by Diana Mechtcheriakova, studied the singularities and commonalities in the impact of COVID on the lungs and other organs. Using complex dataset analyses, the researchers recognised that a different molecular mechanism is at work in pulmonary and gastrointestinal manifestations. While SARS-CoV-2 infections of the lungs evoke classic immune system responses, in the gastrointestinal tract they evoke responses related to liver and lipid metabolism.

The fact that SARS-CoV-2 infections not only manifest in the lungs but frequently also manifest in other organs, such as the heart, kidneys, skin or gut, can be attributed to the particular structure of the virus. During the course of COVID, up to 60% of patients experience gastrointestinal symptoms, which may be associated with a longer duration of disease and/or a worse outcome. The results of this study will add to our understanding of the organ- and tissue-specific molecular processes triggered by SARS-CoV-2.

“Our findings can advance the identification of new biomarkers and treatment strategies for COVID, taking account of the specific responses in manifestations outside the lung,” said Diana Mechtcheriakova, Head of the Molecular Systems Biology and Pathophysiology Research Group at MedUni Vienna, holding out the prospect of promising follow-up studies.

Source: Medical University of Vienna

Categories : Medical Research & TechnologyTags :

Microscopic Robots Kill Pneumonia Bacteria in Lungs

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Pseudomonas
Scanning Electron Micrograph of Pseudomonas aeruginosa. Credit: CDC/Janice Carr

Nanoengineers have developed microscopic robots, called microrobots, that can swim around in the lungs, deliver medication and be used to clear up life-threatening cases of bacterial pneumonia.

In mice, the microrobots safely eliminated Pseudomonas aeruginosa in the lungs of infected mice, resulting in a 100% survival rate. By contrast, untreated mice all died within three days after infection. The scientists describe the technology in Nature Materials.

The microrobots are not actually made of metal and plastic: instead they are algae cells armed with antibiotic-filled nanoparticles on their surfaces. The algae provide movement, which allows the microrobots to swim around and deliver antibiotics directly to more bacteria in the lungs. The nanoparticles are also coated with the neutrophil cell membranes, which absorb and neutralise inflammatory molecules produced by bacteria and the body’s immune system. This gives the microrobots a powerful anti-inflammatory tool, and the algae are biodegradable in the body, leaving no toxic traces.

The work is a joint effort between the labs of nanoengineering professors Joseph Wang and Liangfang Zhang, both at the UC San Diego Jacobs School of Engineering, both world leaders in nanoengineering.

“Our goal is to do targeted drug delivery into more challenging parts of the body, like the lungs. And we want to do it in a way that is safe, easy, biocompatible and long lasting,” said Prof Zhang. “That is what we’ve demonstrated in this work.”

The team used the microrobots to treat mice with an acute and potentially fatal form of pneumonia caused by P. aeruginosa. This is commonly seen in mechanically ventilated ICU patients. The researchers administered the microrobots to the lungs of the mice through a tube inserted in the windpipe. The infections fully cleared up after one week. All mice treated with the microrobots survived past 30 days, while untreated mice died within three days.

The microrobots enabled targeted drug delivery of only 500 nanograms of antibiotics per mouse, while an IV injection provided 1.644 milligrams of antibiotics per mouse.

“These results show how targeted drug delivery combined with active movement from the microalgae improves therapeutic efficacy,” said Wang.

“With an IV injection, sometimes only a very small fraction of antibiotics will get into the lungs. That’s why many current antibiotic treatments for pneumonia don’t work as well as needed, leading to very high mortality rates in the sickest patients,” said Professor Victor Nizet, co-author on the study and a physician-scientist collaborator of Profs Wang and Zhang. “Based on these mouse data, we see that the microrobots could potentially improve antibiotic penetration to kill bacterial pathogens and save more patients’ lives.”

The work is still at the proof-of-concept stage. The team plans to do more basic research to understand exactly how the microrobots interact with the immune system. Next steps also include studies to validate the microrobot treatment and scaling it up before testing it in larger animals and eventually, in humans.

“We’re pushing the boundary further in the field of targeted drug delivery,” said Zhang.

Source: University of California – San Diego

Categories : Medical IndustryTags : 1 Comment

The Same Medications for Humans are Pricier than for Pets

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Photo by Pauline Loroy on Unsplash

In a research letter published in JAMA Internal Medicine, researchers compared the prices of 120 medications commonly used in humans and pets. The authors found human medication prices were typically higher than the price of pet medications – with the same ingredients at common human-equivalent doses.

While some medications are common to both pets and humans, but price differences can be extreme. In 1991, levamisole (introduced in the 1960s as a veterinary antiparasitic) demonstrated efficacy in treating human colon cancer. The introductory human price of Janssen’s Ergamisol (brand-name levamisole; $5 per 50mg tablet) was 100 times the then veterinary price (approximately $0.05 for an equivalent amount). With the COVID pandemic, a misinformation-driven demand for ivermectin as a COVID treatment led to people seeking veterinary formulations of the drug, increasing the price 15-fold over a month ($6 to $92 for 3 tubes). In this cross-sectional study, the researchers sought to compare prices of commonly prescribed medications used to treat both humans and pets.

The researchers from the University of Minnesota found that retail price for human medications was on average 5.5 times higher than pet medications. For more than 60% of medications, even discounted prices for humans were higher than pet prices. On average, discounted prices were 1.5 times higher for human medications than for pet medications.

‘’A 10-day supply of the same medication costs $2 for a pet dog, $10 for a person with a discount coupon, and $100 for a person without a coupon,” said Arjun Gupta, MBBS, assistant professor at the U of M Medical School and oncologist with M Health Fairview. He is also a member of the Masonic Cancer Center. “With many humans and pets uninsured or underinsured, it is important that cash prices for medications are affordable and that pricing is not exploitative.”

Human prices were also higher than pet prices for drugs such as antibiotics. Researchers warn this may promote humans sourcing antibiotics for their own use from pet sources, especially since human antibiotic use is more regulated.

Exactly why there is such a significant price difference is unclear. One possibility may be drug manufacturers engaging in price discrimination by charging consumers different prices in different markets for the same product, the researchers suggest. Additionally, price differences could reflect variations in medication effectiveness, willingness to pay, and manufacturing, storage, and regulatory standards.

Further research is suggested to explore the causes of price differences.

Source: University of Minnesota Medical School

Categories : Medical Research & TechnologyTags :

Long-standing Theory of Hearing Turned on its Ear

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The sensory cells of hearing, outer and inner hair cells, are located in the cochlea, where the arrival sound waves cause the ‘hairs’ of the inner hair cells to bend, sending a signal through the nerves to the brain, which interprets the sound we hear.

For the past century, scientific belief was that each sensory cell has its own ‘optimal frequency’, to which the hair cell responds most strongly. This idea means that a sensory cell with an optimal frequency of 1000Hz would be much less responsive to sounds of slightly lower or higher frequency. It has also been assumed that all parts of the cochlea work in the same way. Now, however, researchers have discovered that this is not so for sensory cells that process sound with frequencies under 1000Hz, considered to be low-frequency sound, where the vowel sounds in human speech lie.

“Our study shows that many cells in the inner ear react simultaneously to low-frequency sound. We believe that this makes it easier to experience low-frequency sounds than would otherwise be the case, since the brain receives information from many sensory cells at the same time,” said Professor Anders Fridberger at Linköping University, senior author of the study published in Science Advances.

The scientists believe that this construction of our hearing system makes it more robust. If some sensory cells are damaged, many others remain that can send nerve impulses to the brain.

As well as the vowel sounds of human speech, many of the sounds that go to make up music also lie in this low-frequency area. Middle C on a piano, for example, has a frequency of 262Hz.

These results may eventually be significant for people with severe hearing impairments. The most successful treatment currently available in such cases is a cochlear implant, in which electrodes are placed into the cochlea.

“The design of current cochlear implants is based on the assumption that each electrode should only give nerve stimulation at certain frequencies, in a way that tries to copy what was believed about the function of our hearing system. We suggest that changing the stimulation method at low frequencies will be more similar to the natural stimulation, and the hearing experience of the user should in this way be improved,” says Anders Fridberger.

The researchers now plan to examine how their new knowledge can be applied in practice. One of the projects they are investigating concerns new methods to stimulate the low-frequency parts of the cochlea.

These results come from experiments on the cochlea of guinea pigs, whose hearing in the low-frequency region is similar to that of humans.

Source: Linköping University

Categories : Diseases, Syndromes and ConditionsTags :

Viruses may ‘Watch’ for the Right Moment to Strike

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Lassa virus scanning electron micrograph
Scanning electron micrograph of Lassa virus budding off a Vero cell. Image credit: National Institute of Allergy and Infectious Diseases, NIH

Scientists have found that viruses lurking inside cells may be on the ‘watch’ for information from their environment to choose when to multiply and burst out. The work, published in Frontiers in Microbiology, has implications for antiviral drug development.

A virus’s ability to sense its environment, including elements produced by its host, adds “another layer of complexity to the viral-host interaction,” said senior author Ivan Erill, professor of biological sciences. Currently, viruses use that ability to their benefit. But in the future, he says, “we could exploit it to their detriment.”

Not a coincidence

The new study focused on bacteriophages, viruses which infect bacteria – also known as ‘phages.’ The phages in the study can only infect their hosts when the bacterial cells have special appendages, called pili and flagella, that help the bacteria move and mate. The bacteria produce a protein called CtrA that controls when they generate these appendages. The new paper shows that many appendage-dependent phages have patterns in their DNA where the CtrA protein can attach, called binding sites. A phage having a binding site for a protein produced by its host is unusual, explained Prof Erill.

Even more surprising, Erill and the paper’s first author Elia Mascolo, a PhD student in Erill’s lab, found through detailed genomic analysis that these binding sites were not unique to a single phage, or even a single group of phages. Many different types of phages had CtrA binding sites – but they all needed their hosts to have pili and/or flagella to infect them. It couldn’t be a coincidence, they decided.

The ability to monitor CtrA levels “has been invented multiple times throughout evolution by different phages that infect different bacteria,” Prof Erill said. This convergent evolution indicates that the trait is useful.

Timing is everything

Another wrinkle in the story: The first phage in which the research team identified CtrA binding sites infects a particular group of bacteria called Caulobacterales. Caulobacterales are an especially well-studied group of bacteria, because they exist in two forms: a free-swimming ‘swarmer’ form which has pili/flagella, and a ‘stalked’ form that attaches to a surface and lacks those appendages. In these bacteria, CtrA also regulates the cell cycle, determining whether a cell will divide evenly into two more of the same cell type, or divide asymmetrically to produce one swarmer and one stalk cell.

Because the phages can only infect swarmer cells, it’s in their best interest only to burst out of their host when there are many swarmer cells available to infect. Generally, Caulobacterales live in nutrient-poor environments, and they are very spread out. “But when they find a good pocket of microhabitat, they become stalked cells and proliferate,” Prof Erill said, eventually producing large quantities of swarmer cells.

“We hypothesise the phages are monitoring CtrA levels, which go up and down during the life cycle of the cells, to figure out when the swarmer cell is becoming a stalk cell and becoming a factory of swarmers,” Prof Erill said, “and at that point, they burst the cell, because there are going to be many swarmers nearby to infect.”

Listening in

Unfortunately, the method to prove this hypothesis is labour-intensive and extremely difficult, so that wasn’t part of this latest paper — although Erill and colleagues hope to tackle that question in the future. However, the research team sees no other plausible explanation for the proliferation of CtrA binding sites on so many different phages, all of which require pili/flagella to infect their hosts. Even more interesting, they note, are the implications for viruses that infect humans.

“Everything that we know about phages, every single evolutionary strategy they have developed, has been shown to translate to viruses that infect plants and animals,” he said. “It’s almost a given. So if phages are listening in on their hosts, the viruses that affect humans are bound to be doing the same.”

There are a few other documented examples of phages monitoring their environment in interesting ways, but none include so many different phages employing the same strategy against so many bacterial hosts.

Prof Erill predicts that more examples of this will be found, and his lab is already discovering more.

New therapeutic avenues

The key takeaway from this research is that “the virus is using cellular intel to make decisions,” Erill says, “and if it’s happening in bacteria, it’s almost certainly happening in plants and animals, because if it’s an evolutionary strategy that makes sense, evolution will discover it and exploit it.”

For example, to optimize its strategy for survival and replication, an animal virus might want to know what kind of tissue it is in, or how robust the host’s immune response is to its infection. While it might be unsettling to think about all the information viruses could gather and possibly use to make us sicker, these discoveries also open up avenues for new therapies.

“If you are developing an antiviral drug, and you know the virus is listening in on a particular signal, then maybe you can fool the virus,” Erill said. “We are just starting to realise how actively viruses have eyes on us – how they are monitoring what’s going on around them and making decisions based on that. “It’s fascinating.”

Source: University of Maryland Baltimore County

Categories : Cardiovascular Disease Diet and NutritionTags :

Milk Risky for CVD Patients – but Perhaps not Cheese

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Source: Pixabay CC0

For people with established cardiovascular disease (CVD), consuming more dairy products was linked to worse health outcomes, according to a study in the European Journal of Preventive Cardiology. However, the type of dairy product appeared to make a difference, with the outcomes for cheese remaining unclear.

In patients with stable angina, significant associations with stroke, cardiovascular mortality, and all-cause mortality were seen with increasing daily intakes of total dairy and milk over follow-up of 5 to 14 years.

While acute myocardial infarction (MI) had no clear linear relationship with total dairy intake or milk consumption, a risk increase was seen for butter consumption of more than 2g per 1000kcal of daily intake.

Data were also inconclusive when it came to cheese consumption and CVD risk, with no significant associations between greater cheese consumption with acute MI, stroke, CVD mortality, or all-cause mortality.

Thus, the study draws a more complicated picture of dairy’s risks that supports other observational data suggesting that different dairy products may have different effects. “We can speculate that at least part of the differential associations seen for milk, butter, and cheese may be because cheese contains intact MFGM [milk fat globule membrane], while milk and butter does [sic] not,” the researchers wrote.

Dairy is “probably harmful” overall, the verdict on cheese is unclear, and some of the fermented dairy products may be less dangerous if dairy is to be consumed at all, commented Andrew Freeman, MD, a cardiologist at National Jewish Health in Denver, who was not involved with the study.

Even without a randomised trial, Dr Freeman said in an interview, “there’s enough signal in the noise to draw the conclusion that higher-fat dairy products, the number one source of saturated fat in our diet, are probably not going to be helpful to human health, and heart health in particular.”

He nevertheless cautioned that there may be worldwide variation in the effects of dairy products, which may be different between countries that place more restrictions on raising cattle with chemicals such as growth hormones.

Nevertheless, the global PURE study of people around the world consistently found the best outcomes from eating a balanced diet including lots of fruits and vegetables and a modest amount of dairy, unprocessed red meat, and nuts and legumes. The PURE investigators had also reported that at least two servings of dairy per day was linked with less CVD and mortality, compared with no dairy.

“Dairy is a heterogenous food group with divergent health effects and dairy products should therefore be investigated individually,” the researchers maintained.

Their data was drawn from 1929 patients with stable angina (80% men, mean age 62 years) from the Western Norway B Vitamin Intervention Trial.

All had undergone coronary angiography due to suspected coronary artery disease or aortic stenosis in 1999–2004. Use of preventive medications was high and included aspirin (90%), statins (90%), and beta-blockers (77%).

Participants self-reported dietary habits on a food frequency questionnaire. Average dairy intake was 169g/1000 kcal; mostly milk (133g/1000 kcal).

Bias and confounding were possible due to the observational nature of the study: people who ate more dairy already tended to eat less meat, vegetables, fruit and berries, fish, and potatoes. These individuals also got more calories from protein and less from fats (except saturated fats).

Further limitations include the lack of additional dietary evaluations over years of follow-up and the potential for participants to mischaracterize their diets on a survey.

Source: MedPage Today

Categories : Immune System Metabolic DisordersTags :

A Theory Behind Autoimmunity in Type 1 Diabetes

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A 3D map of the islets in the human pancreas. Source: Wikimedia

The autoimmune destruction of the pancreatic beta-cells in type 1 diabetes (T1D) has been studied extensively, yet the mystery of what causes autoimmunity is unknown. In a new study, researchers present a testable hypothesis to explain the initiation of autoimmunity – which, if validated, this would allow early detection and possible prevention of T1D in susceptible individuals. This hypothesis is discussed in the journal Diabetes.

“Previous studies have focused on the triggers, genes and proteins that differentiate individuals with T1D from those without diabetes with a focus on the b-cell (b-cells create antibodies) as a target of immune destruction and blood glucose as the main abnormality. Our focus is on metabolic communication as an early instigator with the b-cell as an active participant together with the immune cells,” explained corresponding author Barbara Corkey, PhD, professor at Boston University School of Medicine.

Prof Corkey’s research led her to hypothesise that autoimmunity induction results from one or more major inflammatory events in individuals with susceptible human leukocyte antigens phenotypes plus elevated sensitivity to cytokines and free fatty acids (FFA).

“Illnesses or environmental agents that dramatically increase cytokine production and/or elevate FFA initiate autoimmune destruction in individuals with specific genetic features. Thus, early prevention should be aimed at decreasing elevated lipids and diminishing excessive simultaneous elevation of cytokines or cytokine- and lipid-induced immune cell proliferation,” she said.

Prof Corkey believes that the characteristics that make individuals susceptible to autoimmune destruction could also apply to other autoimmune diseases such as toxic shock syndrome and possibly long COVID.

Source: Boston University School of Medicine

Categories : AllergiesTags :

New Guideline to Tackle Incorrect Penicillin Allergy Labelling

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Photo by MedicAlert UK on Unsplash

A new guideline published in Clinical & Experimental Allergy will help non-allergist clinicians evaluate and test patients for potential penicillin allergies.

Penicillin allergy labels are carried by 5.6% of the general population, with a seemingly higher incidence in hospitalised patients. About 95% of penicillin allergy labels are incorrect when tested.

Over the past 10 years, the clinical ramifications of a label of ‘penicillin allergy’ have been clearly defined. A diagnosis of penicillin allergy increases the risk of MRSA, Clostriodes difficile or VRE infections and death; presumably through increased use of alternatives to beta-lactam antibiotics. It also increases the duration of hospital admissions and has significant implications for the cost of health care. Several studies have shown the healthcare costs of the label and the economic benefits of removing incorrect labels.

Despite widespread evidence of its harms, resources are not available in the NHS for penicillin allergy testing, prompting the development of this guideline.

The guideline was developed by the Standards of Care Committee of the British Society for Allergy and Clinical Immunology (BSACI) along with a committee of experts and key stakeholders.

The aim of this guideline is to provide a framework for the set-up and delivery of penicillin allergy de-labelling services by non-allergists by using drug provocation testing. The intended users are non-allergists with an interest in clarifying the penicillin allergy status of their patients. The target population is adult and children with an untested label of penicillin allergy. 

There are separate recommendations for adults and children within the guideline.

“The intended users are non-allergists with an interest in clarifying the penicillin allergy status of their patients. The guideline details appropriate patient selection, risk stratification, minimum safety standards, conduct of a drug provocation test, and the degree of oversight required from allergy or immunology specialists,” the authors wrote. “The guideline will be reviewed 5 years from original publication date.”

Source: Wiley

Categories : Uncategorized

Protecting the Lungs from Neutrophil Overactivation

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Anatomical model of lungs
Photo by Robina Weermeijer on Unsplash

Neutrophils are the body’s first line of defence against infection, which can be activated when foreign pathogens stress the body. When overactivated, neutrophils can damage the body’s own tissues. Lung tissue is saturated with blood vessels, making them very susceptible to neutrophil attacks. If severe enough, acute lung injuries can lead to acute respiratory distress syndrome (ARDS), the leading cause of death due to COVID.

Reporting in JCI Insight, Cold Spring Harbor Laboratory (CSHL) researchers have found a drug candidate that can prevent lethal lung inflammation in mice by inhibiting a protein called PTP1B. Their discovery may help develop better treatments for severe inflammatory conditions like sepsis and COVID.

“When you think about COVID, acute lung injury and ARDS underlie the fatal aspects of the disease,” leader researcher Nicholas Tonks, professor of cancer research says. “And so, when the pandemic took hold, we were wondering whether there was anything we could do to help, to provide an understanding of this aspect of the disease and suggest ways it could be treated.”

Tonks’ graduate student Dongyan Song investigated whether using a PTP1B inhibitor drug candidate could dampen the lethal consequences of overactive neutrophils in mice. She found that pretreating mice with the PTP1B inhibitor reduced lung tissue damage. When untreated, less than half of the mice survived acute lung injuries and ARDS. But when pretreated, they all survived.

The researchers exploited a natural process, called neutrophil aging, that the body uses to control the immune cell’s lifespan. As they age, neutrophils become less dangerous. Tonks’ team discovered PTP1B inhibition speeds up neutrophil aging. “An aged neutrophil is like a soldier without a weapon,” Song explains. “So regardless of how many neutrophils flood an area, they won’t be able to do serious damage.”

Going forward, he and Song are working to increase the understanding of how PTP1B inhibitors affect the immune system. Tonks hopes his lab’s continued research leads to new treatments and preventative measures for various inflammatory diseases.

Tonks’ lab studies signal transduction, the process that controls how cells respond to signals from their environment. In particular, they focus on the PTP protein family, which Tonks discovered over 30 years ago. Since then, he’s sought to develop small molecule drug candidates that target these proteins, which can provide new approaches for treating major human diseases including cancer and metabolic and neurodegenerative diseases.

Source: Cold Spring Harbor Laboratory