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Cancer biologists identify new drug combo

Cancer biologists identify new drug combo

When it comes to killing cancer cells, two drugs are often better than one. Some drug combinations offer a one-two punch that kills cells more effectively, requires lower doses of each drug, and can help to prevent drug resistance.

MIT biologists have now found that by combining two existing classes of drugs, both of which target cancer cells’ ability to divide, they can dramatically boost the drugs’ killing power. This drug combination also appears to largely spare normal cells, because cancer cells divide differently than healthy cells, the researchers say. They hope a clinical trial of this combination can be started within a year or two.

“This is a combination of one class of drugs that a lot of people are already using, with another type of drug that multiple companies have been developing,” says Michael Yaffe, a David H. Koch Professor of Science and the director of the MIT Center for Precision Cancer Medicine. “I think this opens up the possibility of rapid translation of these findings in patients.”

The discovery was enabled by a new software program the researchers developed, which revealed that one of the drugs had a previously unknown mechanism of action that strongly enhances the effect of the other drug.

Yaffe, who is also a member of the Koch Institute for Integrative Cancer Research, is the senior author of the study, which appears in the July 10 issue of Cell Systems. Koch Institute research scientists Jesse Patterson and Brian Joughin are the first authors of the paper.

Unexpected synergy

Yaffe’s lab has a longstanding interest in analyzing cellular pathways that are active in cancer cells, to find how these pathways work together in signaling networks to create disease-specific vulnerabilities that can be targeted with multiple drugs. When the researchers began this study, they were looking for a drug that would amplify the effects of a type of drug known as a PLK1 inhibitor. Several PLK1 inhibitors, which interfere with cell division, have been developed, and some are now in phase 2 clinical trials.

Based on their previous work, the researchers knew that PLK1 inhibitors also produce a type of DNA and protein damage known as oxidation. They hypothesized that pairing PLK1 inhibitors with a drug that prevents cells from repairing oxidative damage could make them work even better.

To explore that possibility, the researchers tested a PLK1 inhibitor along with a drug called TH588, which blocks MTH1, an enzyme that helps cells counteract oxidative damage. This combination worked extremely well against many types of human cancer cells. In some cases, the researchers could use one-tenth of the original doses of each drug, given together, and achieve the same rates of cell death of either drug given on its own.

“It’s really striking,” Joughin says. “It’s more synergy than you generally see from a rationally designed combination.”

However, they soon realized that this synergy had nothing to do with oxidative damage. When the researchers treated cancer cells missing the gene for MTH1, which they thought was TH588’s target, they found that the drug combination still killed cancer cells at the same high rates.

“Then we were really stuck, because we had a good combination, but we didn’t know why it worked,” Yaffe says.

To solve the mystery, they developed a new software program that allowed them to identify the cellular networks most affected by the drugs. The researchers tested the drug combination in 29 different types of human cancer cells, then fed the data into the software, which compared the results to gene expression data for those cell lines. This allowed them to discover patterns of gene expression that were linked with higher or lower levels of synergy between the two drugs.

This analysis suggested that both drugs were targeting the mitotic spindle, a structure that forms when chromosomes align in the center of a cell as it prepares to divide. Experiments in the lab confirmed that this was correct. The researchers had already known that PLK1 inhibitors target the mitotic spindle, but they were surprised to see that TH588 affected the same structure.

“This combination that we found was very nonobvious,” Yaffe says. “I would never have given two drugs that both targeted the same process and expected anything better than just additive effects.”

“This is an exciting paper for two reasons,” says David Pellman, associate director for basic science at Dana-Farber/Harvard Cancer Center, who was not involved in the study. “First, Yaffe and colleagues make an important advance for the rational design of drug therapy combinations. Second, if you like scientific mysteries, this is a riveting example of molecular sleuthing. A drug that was thought to act in one way is unmasked to work through an entirely different mechanism.”

Disrupting mitosis

The researchers found that while both of the drugs they tested disrupt mitosis, they appear to do so in different ways. TH588 binds to microtubules, which form the mitotic spindle, and slows their assembly. Many similar microtubule inhibitors are already used clinically to treat cancer. The researchers showed that some of those microtubule inhibitors also synergize with PLK1 inhibitors, and they believe those would likely be more readily available for rapid use in patients than TH588, the drug they originally tested.

While the PLK1 protein is involved in multiple aspects of cell division and spindle formation, it’s not known exactly how PLK1 inhibitors interfere with the mitotic spindle to produce this synergy. Yaffe said he suspects they may block a motor protein that is necessary for chromosomes to travel along the spindle.

One potential benefit of this drug combination is that the synergistic effects appear to specifically target cancer cell division and not normal cell division. The researchers believe this could be because cancer cells are forced to rely on alternative strategies for cell division because they often have too many or too few chromosomes, a state known as aneuploidy.

“Based on the work we have done, we propose that this drug combination targets something fundamentally different about the way cancer cells divide, such as altered cell division checkpoints, chromosome number and structure, or other structural differences in cancer cells,” Patterson says.

The researchers are now working on identifying biomarkers that could help them to predict which patients would respond best to this drug combination. They are also trying to determine the exact function of PLK1 that is responsible for this synergy, in hopes of finding additional drugs that would block that interaction.

Materials provided by Massachusetts Institute of Technology

Mosca Fly Diptera

Researchers find more than 90 percent of flying insects in hospitals carry harmful bacteria

Flies in hospitals may be more dangerous than their irritating buzzing. A study carried out in seven hospitals in England found out that 90 percent of the flying insects had potential harming bacteria with them. The study was published in the Journal of Medical Entomology.

More than half of the bacterial strains which were identified were ‘superbugs‘. It means that these bacteria were resistant to a minimum of one class of antibiotics. Additionally, it was found that 20 percent of the bacteria were resistant to several classes of antibiotics. Penicillin was least effective against the bacteria which were found.

Federica Boiocchi, the principal author of the study and a Ph.D. student at Aston University said in a university press release that the results of the microbiological analysis demonstrate a variety of insects flying in the hospitals of United Kingdom harbor a wide range of harmful bacteria belonging to several species. It is quite interesting that a large sample of the bacteria in this study is resistant to several antibiotics. This shows that the overuse of antibiotics in the treatment of patients is making it even more difficult while treating infections.

Nearly eighty-six bacterial strains were found in the insects among which E.Coli and Salmonella were the most common as they were found in 41 percent of the strains. In twenty-four percent of the strains, the food poisoning bacteria B. cereus was found while 19 percent of the strains contained the microbes causing skin infections and respiratory problems.

More than 20,000 flying insects were collected by the scientists in a period of 18 months with the help of devices such as ultraviolet-light flytraps, electric fly killers. Out of these insects, more than 75 percent were flies and included house flies and ants, bees, moths. When any of these insects lands on food items such as fruits, the bacterial cells are released on to the foods. It may not be infectious immediately as there are a fewer number of microbes but with the passing of time, proliferation of bacteria can cause infections in the person eating the food.

Anthony Hilton, a co-author and professor of applied microbiology said that the National Health Service(NHS) hospitals of the UK are very clean with highly hygienic conditions. Hence the risk of infections in the patients through these bacteria is less. However, the main goal of the study is to bring to notice that even clean environments can contain pathological bacteria, so adequate steps have to be taken to improve the situation to a greater extent. The NHS hospitals will be implementing steps to adhere to this and bring an improvement in hygiene.

MIT Nanoemulsions

“Nanoemulsion” gels offer new way to deliver drugs through the skin

MIT chemical engineers have devised a new way to create very tiny droplets of one liquid suspended within another liquid, known as nanoemulsion. Such emulsions are similar to the mixture that forms when you shake an oil-and-vinegar salad dressing, but with much smaller droplets. Their tiny size allows them to remain stable for relatively long periods of time.

The researchers also found a way to easily convert the liquid nanoemulsion to a gel when they reach body temperature (37 degrees Celsius), which could be useful for developing materials that can deliver medication when rubbed on the skin or injected into the body.

“The pharmaceutical industry is hugely interested in nanoemulsions as a way of delivering small molecule therapeutics. That could be topically, through ingestion, or by spraying into the nose, because once you start getting into the size range of hundreds of nanometers you can permeate much more effectively into the skin,” says Patrick Doyle, the Robert T. Haslam Professor of Chemical Engineering and the senior author of the study.

In their new study, which appears in the June 21 issue of Nature Communications, the researchers created nanoemulsions that were stable for more than a year. To demonstrate the emulsions’ potential usefulness for delivering drugs, the researchers showed that they could incorporate ibuprofen into the droplets.

Seyed Meysam Hashemnejad, a former MIT postdoc, is the first author of the study. Other authors include former postdoc Abu Zayed Badruddoza, L’Oréal senior scientist Brady Zarket, and former MIT summer research intern Carlos Ricardo Castaneda.

Energy reduction

One of the easiest ways to create an emulsion is to add energy — by shaking your salad dressing, for example, or using a homogenizer to break down fat globules in milk. The more energy that goes in, the smaller the droplets, and the more stable they are.

Nanoemulsions, which contain droplets with a diameter 200 nanometers or smaller, are desirable not only because they are more stable, but they also have a higher ratio of surface area to volume, which allows them to carry larger payloads of active ingredients such as drugs or sunscreens.

Over the past few years, Doyle’s lab has been working on lower-energy strategies for making nanoemulsions, which could make the process easier to adapt for large-scale industrial manufacturing.

Detergent-like chemicals called surfactants can speed up the formation of emulsions, but many of the surfactants that have previously been used for creating nanoemulsions are not FDA-approved for use in humans. Doyle and his students chose two surfactants that are uncharged, which makes them less likely to irritate the skin, and are already FDA-approved as food or cosmetic additives. They also added a small amount of polyethylene glycol (PEG), a biocompatible polymer used for drug delivery that helps the solution to form even smaller droplets, down to about 50 nanometers in diameter.

“With this approach, you don’t have to put in much energy at all,” Doyle says. “In fact, a slow stirring bar almost spontaneously creates these super small emulsions.”

Active ingredients can be mixed into the oil phase before the emulsion is formed, so they end up loaded into the droplets of the emulsion.

Once they had developed a low-energy way to create nanoemulsions, using nontoxic ingredients, the researchers added a step that would allow the emulsions to be easily converted to gels when they reach body temperature. They achieved this by incorporating heat-sensitive polymers called poloxamers, or Pluronics, which are already FDA-approved and used in some drugs and cosmetics.

Pluronics contain three “blocks” of polymers: The outer two regions are hydrophilic, while the middle region is slightly hydrophobic. At room temperature, these molecules dissolve in water but do not interact much with the droplets that form the emulsion. However, when heated, the hydrophobic regions attach to the droplets, forcing them to pack together more tightly and creating a jelly-like solid. This process happens within seconds of heating the emulsion to the necessary temperature.

MIT chemical engineers have devised a way to convert liquid nanoemulsions into solid gels. These gels (red) form almost instantaneously when drops of the liquid emulsion enter warm water.

MIT chemical engineers have devised a way to convert liquid nanoemulsions into solid gels. These gels (red) form almost instantaneously when drops of the liquid emulsion enter warm water.

Tunable properties

The researchers found that they could tune the properties of the gels, including the temperature at which the material becomes a gel, by changing the size of the emulsion droplets and the concentration and structure of the Pluronics that they added to the emulsion. They can also alter traits such as elasticity and yield stress, which is a measure of how much force is needed to spread the gel.

Doyle is now exploring ways to incorporate a variety of active pharmaceutical ingredients into this type of gel. Such products could be useful for delivering topical medications to help heal burns or other types of injuries, or could be injected to form a “drug depot” that would solidify inside the body and release drugs over an extended period of time. These droplets could also be made small enough that they could be used in nasal sprays for delivering inhalable drugs, Doyle says.

For cosmetic applications, this approach could be used to create moisturizers or other products that are more shelf-stable and feel smoother on the skin.

Materials provided by Massachusetts Institute of Technology

CRISPR Cas9

Using human genome, scientists build CRISPR for RNA to open pathways for medicine

Less than a decade ago, biology underwent one of those once-in-a-generation events that shakes up a scientific field, when the discovery of gene editing technology called CRISPR/Cas-9 made it possible to precisely alter the sequence of DNA in a living being.

But while DNA may be the raw blueprints for life, RNA is the architect—translating those ideas into reality for the cell through proteins and regulation. While CRISPR systems that target RNA have recently been discovered, none offers a single clear solution.

A group of scientists from the University of Chicago has announced a breakthrough method to alter RNA—and instead of using a protein from bacteria, like CRISPR, the new system is built out of parts from the human genome. Announced June 20 in Cell, the discovery could open new pathways for treating diseases or injuries by temporarily altering how the genetic template is carried out in the cell.

“People had delayed targeting RNA for a long time because it’s so complex in how it works,” said study author Bryan Dickinson, an associate professor of chemistry at UChicago. “But I think now we’re realizing that complexity is an opportunity to figure out how to exploit and change those pathways. In principle, you could make even more dramatic changes to the cell than with DNA, and now we finally have the tools to do so.”

Even as DNA-targeting CRISPR methods begin their initial clinical trials in humans, scientists have become increasingly interested in equivalent systems for RNA. An RNA-targeting method that can safely be applied to humans would be a valuable complement to CRISPR, Dickinson said.

“If you imagine the universe of diseases that CRISPR is going to correct, it’ll be really important ones, but only those that are based off of one single mutation in your DNA,” said Dickinson, whose work tries to create functional molecules that lead to biological breakthroughs. “There are many more diseases out there with multiple causes in the cell, which may be much more difficult to understand—and there will also be those where the risks associated with changing someone’s DNA permanently are just too high.”

Because the effects of RNA alteration are temporary rather than permanent, an RNA-CRISPR is inherently less risky, because doctors can simply stop the treatment if there are intolerable side effects. It could also be used for things like briefly boosting a person’s system to accelerate wound healing: “We know what to do for that—you would encourage processes for cell growth and proliferation,” Dickinson said. “But those are the same things that cause cancer, so you could never do that at the DNA level.”

But translating these microbial systems into therapeutics is going to be challenging, he said. “RNA-targeting drugs need to be continually administered, so the foreign nature of CRISPR/Cas systems it going to create an immune backlash when applied to humans.”

This presents key roadblocks for natural CRISPR systems, which Dickinson’s team realized it had an opportunity to correct by reengineering the whole system from scratch.

“In principle, you could make even more dramatic changes to the cell than with DNA, and now we finally have the tools to do so.”

—Assoc. Prof. Bryan Dickinson on targeting RNA

Because it’s a very large protein, CRISPR is generally too big to use the most common delivery system to insert genetic material into cells—“phages,” which originate from tiny viruses. This is a problem, especially if you need to deliver them continually. More critically, because CRISPR comes from a microbe, there are significant concerns about the human immune system reacting to it.

Instead, the team broke down CRISPR into its components based on what each part does, and looked for human versions of those proteins that did equivalent tasks. Then they cobbled those together into a cohesive whole—which is smaller than CRISPR, and made out of human material.

“Although there’s still a lot of work to do, the crazy thing is it actually works,” Dickinson said.

Their system succeeded in altering RNA in tests in the lab. The scientists plan to improve the system at a few points where the performance is not as good as CRISPR, they said, but they’re encouraged by the early results.

“As we learn more, you could imagine targeting multiple RNAs in different ways, and doing more complex reprogramming of the cell at the RNA level,” Dickinson said. “It’s a really exciting field right now.”

The first author was graduate student Simone Rauch; other co-authors were visiting scholar Michael Srienc, postdoctoral fellow Huiqing Zhou, high school student Emily He and graduate student Zijie Zhang.

The scientists are working with the Polsky Center for Entrepreneurship and Innovation at the University of Chicago to advance this discovery.

Materials provided by University of Chicago

Researchers develop new sensor to help detect early-stage cancer

Researchers develop new sensor to help detect early-stage cancer

A new device that can detect very low concentrations of cancer markers in blood tests could one day help doctors diagnose cancer at its earliest stages, researchers say.

A group of chemists from UNSW Sydney’s Australian Centre for NanoMedicine (ACN) and biologists from UNSW’s Lowy Cancer Research Centre have created an early version of the first “nanopore blockade sensor” that can analyse disease biomarkers at a rapid, single molecule level.

Cancer biomarkers – or tumour markers – are substances, often proteins, that are produced by the body in response to cancer growth.

UNSW Scientia Professor Justin Gooding, who developed the technology with a team of scientists, said a key approach to reducing deaths from life-threatening cancers was to diagnose cancers as early as possible, when treatments were far more effective.

“Developing ultrasensitive cancer marker sensors is critical because it allows for very early detection after the cancer has occurred but before any symptoms start appearing,” said Professor Gooding, from the School of Chemistry at UNSW Science. “The best way to cure cancer is to detect and diagnose it early. What this sensor can do is detect biomarkers and single molecules at much lower levels than current blood tests can, and we can get results in several minutes.”

The nanopore blockade sensors work by using magnetic particles to capture biomarkers and bring them to one of many small pores drilled through a silicon membrane. If a magnetic nanoparticle has captured the biomarker, it will block the pore. By counting which pores are blocked the biomarkers can be counted, one molecule at a time. Importantly, the device can be used on whole blood samples regularly taken at pathology labs.

‘This sensor can detect biomarkers and single molecules at much lower levels than current blood tests can, and we can get results in several minutes.’

The technology is about five to 10 years away from being available to patients and needs to go through rigorous further research and trials now, said Professor Gooding. “This is a really hot area in cancer research, especially as it could potentially have a substantial impact as an effective means to estimate how effective treatment will be and assess how likely it is for cancer to reoccur.”

The research and development of the sensor is funded by the Australian Research Council through the ARC Centre of Excellence in Convergent Bio-Nano Science and Technology and an ARC Australian Laureate Fellowship.

Materials provided by the University of New South Wales

Situs Inversus Totalis

Bizarre case study reveals man with his body organs on the wrong side

A medical emergency room with the patient turned into a tale of an unexpected tale in the case of a 66-year-old man who turned up at the hospital with coughs and chest pains. Only for the doctors to realize that the internal organs of the patients were on the wrong side of the body like the heart was on the right, liver on the left, etc. The report was published in the New England Journal of Medicine.

This condition is named as Situs inversus totalis and it is not life changing as it sounds. This was discovered due to modern medical scanning tools and many people had lived their lives without any diagnosis. The doctors have said that the patient was migrated to the United States after being in a refugee camp for 20 years. The findings as shown by the chest radiograph were dextrocardia in which the heart is situated on the right rather than on the left and a mirror image transposition for the abdominal organs. The symptoms of the man included chest pain, congestion and coughing and a little pain on the left of the abdomen as seen on the medical reports.

This case is very rare but not unheard. Donny Osmond is a well-known case of Situs Inversus Totalis where all internal organs are flipped like a mirror image and this common type affects close to 1 in 10,000 people. Such people are generally seen wearing a bracelet that declares and signals the doctor of this disorder in case of an emergency surgery where the doctor might mistakenly open the wrong part of the body. The heart is the part where most of the complication occurs in the case of Situs Inversus and dextrocardia in which the key important arteries can end up lying in parallel rather than crisscrossing which makes the heart surgery and transplants very difficult to operate.

The name of this abnormality was coined by Matthew Baillie in 1788 which is “location” and “opposite” in Latin and this terminology is continued by doctors and scientists even today. One recent case was reported of Rose Marie Bentley who lived up to the age of 99 years and no one knew about this abnormal condition until her death report came. Her heart was on the correct side of the body which makes Situs Inversus much more dangerous.

Situs Inversus is often dismissed as an X-ray error after the reports when the baby is born and is the reason why people aren’t diagnosed until many years later.

Turmeric can prevent cancer

Timed release of turmeric stops cancer cell growth

A Washington State University research team has developed a drug delivery system using curcumin, the main ingredient in the spice turmeric, that successfully inhibits bone cancer cells while promoting the growth of healthy bone cells.

The work could lead to better post‑operative treatments for people with osteosarcoma, the second most prevalent cause of cancer death in children.

The researchers, including Susmita Bose, Herman and Brita Lindholm Endowed Chair Professor in the School of Mechanical and Materials Engineering, and graduate student Naboneeta Sarkar, report on their work in the journal, ACS Applied Materials and Interfaces.

Young patients with bone cancer are often treated with high doses of chemotherapy before and after surgery, many of which have harmful side effects. Researchers would like to develop gentler treatment options, especially after surgery when patients are trying to recover from bone damage at the same time that they are taking harsh drugs to suppress tumor growth.

Turmeric has been used in cooking and as medicine for centuries in Asian countries, and its active ingredient, curcumin has been shown to have anti‑oxidant, anti‑inflammatory and bone‑building capabilities. It has also been shown to prevent various forms of cancers.

“I want people to know the beneficial effects of these natural compounds,” said Bose. “Natural biomolecules derived from these plant‑based products are inexpensive and a safer alternative to synthetic drugs.”

However, when taken orally as medicine, the compound can’t be absorbed well in the body. It is metabolized and eliminated too quickly.

Closeup of Bose in laboratory.
Susmita Bose

In their study, the researchers used 3D printing to build support scaffolds out of calcium phosphate. While most implants are currently made of metal, such ceramic scaffolds, which are more like real bone, could someday be used as a graft material after bone cancer surgery. The researchers incorporated curcumin, encapsulated in a vesicle of fat molecules into the scaffolds, allowing for the gradual release of the chemical.

The researchers found that their system inhibited the growth of osteosarcoma cells by 96 percent after 11 days as compared to untreated samples. The system also promoted healthy bone cell growth.

“This study introduces a new era of integration – where modern 3D printing technology is coupled with the safe and effective use of alternative medicine, which may provide a better tool for bone tissue engineering,” said Bose.

The researchers are continuing the unique area of research, studying the benefits of integrating other natural compounds in biomedical technology. The work was funded by the National Institutes of Health.

Materials provided by Washington State University

Testing Blood Sugar Levels or Diabetes

UBC study holds promise for novel and safe treatment for Type 2 diabetes

Reducing a specific protein in the fat cells of mice not only prevents onset of Type 2 diabetes but also appears to reverse the disease in the animals, researchers at the University of British Columbia and Sweden’s Karolinska Institute have found.

Researchers also found that levels of the protein, called CD248, were higher in the fat cells of people with diabetes, no matter their shape or size. When obesity-associated diabetes was reversed through weight loss, CD248 levels decreased to normal range, they found. 

The findings, published today in EBioMedicine, a journal of The Lancet, hold promise for the development of a new and safe treatment for Type 2 diabetes.

Type 2 diabetes is a chronic inflammatory condition that affects how the body metabolizes sugar. Obesity, smoking and a lack of physical activity are major risk factors for developing Type 2 diabetes, in which the body either resists the effects of insulin—a hormone that regulates the movement of sugar into cells—or doesn’t produce enough insulin to maintain normal glucose levels. Complications of Type 2 diabetes are common and include heart and blood vessel disease, stroke, kidney damage, poor skin wound healing, increased risk of infections and a higher incidence of some types of cancer.“It’s early days but modifying the amount or function of CD248, in fat cells seems to be a promising new treatment strategy, an approach that may be eventually used by itself or with other drugs,” said co-senior author Dr. Edward Conway, professor in the faculty of medicine at UBC, director of the Centre for Blood Research and recipient of a Canada Research Chair in Endothelial Cell Biology. “With more than 60 million adults diagnosed in North America and Europe and many more with pre-diabetes, the number of people with Type 2 diabetes is staggering. And as the incidence of obesity increases, more effective treatments for Type 2 diabetes are urgently needed.”

For the study, UBC researchers collaborated with a renowned diabetes research group at the Karolinska Institute, led by the co-senior investigator Dr. Mikael Rydén, a professor and senior consultant, unit of endocrinology and lipid laboratory. Rydén and his PhD student, Paul Petrus, used human genetic approaches to study fat biopsies of patients who were thin, obese, diabetic and not diabetic.

Their findings showed that CD248 protein levels in the fat might provide a better marker compared to current measures of how sensitive a person is to insulin, which may be used to better predict those who are at risk of developing Type 2 diabetes and to measure the effectiveness of treatments.

“The levels of CD248 in human fat are strongly associated with clinical measures of Type 2 diabetes risk. This, together with experiments in which we reduced the CD248 gene in human fat cells, suggested that this approach improved fat tissue function, which could be relevant in future treatments of Type 2 diabetes,” said Rydén. “We then contacted Dr. Conway, who had studied the effects of CD248 gene knock-out in mice, focusing on its role in tissues other than fat.”

To gain a better understanding of how CD248 works, the UBC researchers used genetically modified mice that lack CD248 only in the fat cells. They found that the lack of this protein in those cells protected the animals from developing Type 2 diabetes, even when fed high-fat diets that made them obese. Having no CD248 in their fat cells did not appear to be associated with negative health outcomes, suggesting that therapies that reduce CD248 to treat diabetes are likely to be safe.

“A most interesting finding was that the insulin sensitivity of mice that already have diabetes can be improved by reducing CD248 levels in the fat cells, even while they remain obese,” said Conway. “While these discoveries are exciting, we are still some distance from a new treatment. To reach that goal, our immediate goals are to understand how CD248 works so that safe and effective drugs that reduce the protein’s levels or that interfere with its function can be designed.”

The study was co-authored by scientists from the University of Turku in Finland, the Université de Sherbrooke in Quebec and members of the diabetes research group at UBC. It was supported by grants from the Canadian Institutes of Health Research, the Natural Sciences and Engineering Research Council of Canada, a Killam Scholarship, Morphotek Inc., along with funding from the Swedish Research Council, Novo Nordisk Foundation, Swedish Diabetes Foundation and the Diabetes Research Program at the Karolinska Institute.

Materials provided by the University of British Columbia

Dodgeball

Study finds out dodgeball to be a tool for oppression

According to a group of Canadian scientists, one of the most played games in gym classes, dodgeball is used as a tool for “oppression“. Professors from Canadian universities presented before the Congress of the Humanities and Social Sciences, Vancouver their paper on this subject where they mention that dodgeball is used to teach the students how to harm others.

Joy Butler, a professor of pedagogy and curriculum development at the University of British Columbia told over a phone interview that when an environment is created where students are told that it is alright to use the softball and hit whomever one likes, then the intention to harm others is present although subtle. Students are told it is okay to do it and this acts as an outlet for their inner aggression. He added that the classes of physical education should be a platform for students to have control over their anger, move beyond it rather than expressing it. Teachers should be telling students methods to control their aggression, not the opposite.

Scientists interviewed students of middle-schools regarding various physical education courses but they learnt repeatedly from some students that they hated dodgeball. They asked further and then matched the answers against the ideas given in Five Faces of Oppression, an article in Justice and the Politics of Difference authored by Iris Marion Young.

Here, Young says that the faces of oppression are, using benefits of other’s work for oneself, pushing a section of the society to a corner, taking away independence from that section of society, making the preferences of the ruling class as norm and making known to the marginalized section that they may be hurt. These points matched with the answers that the researchers got in the interviews.

Scientists found that the athletic students of the class formed their own groups to dominate over the rest of the class and whimsically created their rules. The true definition of competition is where evenly matched teams compete and all the students derive enjoyment from that. When asked in the class for creating a new game using the same ball and two goals, these same set of students developed their version without consulting their friends. This established that the dominating culture spilt to other sections of the physical education class.

Canadian schools are making positive changes in improving P.E classes. Teachers are taking steps to prevent girls from dropping out of their classes. Thus they should also focus in this area and make the curriculum holistic for all. This includes removing dodgeball.

Person looking at smartphone in the dark

Hitting the snooze button to get some extra sleep may not be a good idea

Every morning it is a fight to wake up early for many of us. Whether to snooze the alarm or to sleep for some more time is a decision we make every morning. Snoozing the alarm might seem harmless to us but it is not. Snoozing the alarm is a habit which is acquired early on in life. Snoozing the alarm has been associated with poor health, and poor sleep can cause various mental issues like high blood pressure, a gain in weight and memory problems.

A facial pain specialist who has analyzed the relation between sleep and facial pain has identified that patients who suffer from chronic pain also suffer from sleep disorders. Our body has a natural body clock with which it regulates the cycles in the body. Mental, physical and behavioral changes take place every day in these daily cycles. Adults require seven to eight hours of good sleep.

There are two types of stages in sleep, one is non-rapid eye movement sleep (NREM) and rapid eye movement sleep (REM). Our body changes its state from NREM to REM almost four to six times per night. Generally, NREM is the first portion of sleep and REM is the last stage of sleep. If this cycle having these stages is disturbed abruptly then we tend to wake up feeling tired in the morning. A well-structured sleep is very important for having a good day. Sleep quality diminishes with the use of electronic gadgets, tobacco or alcohol consumption in the evening and also eating heavy food very close to bedtime. If a person does not breathe well during sleep he may end up snoring and will disturb the normal sequence of cycles.

The teenage is the age when the use of snooze buttons plays a key role and teenagers tend to use this button very often due to the alteration of circadian rhythms which causes teenagers to sleep up till late morning and stay up till late night. The five minutes of time the snooze button offers does not give us good restorative sleep and in turn confuses the brain as to whether to start the process to secrete more neurochemicals that cause more sleep. These predictions are made possible by some hypothesis. The best way to stay physically fit and mentally healthy is to get a good sleep which is best when you set up an alarm for a specific time and follow the time.