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05/03/2018

If you live with anxiety, you're probably familiar with the vicious circle of being anxious about being anxious. A helpful way to break the cycle may be to remind yourself of the benefits of being anxious. New research highlights such a benefit, as anxiety raises the chances of survival after heart attack.
People with anxiety disorder — and women in particular — may recover more quickly after a heart attack, suggests new research.
Anyone living with anxiety knows how terrible it is to worry about worrying, and how this can send you spiraling into a full-blown anxiety attack.
During such times, some people — including myself — may find it useful to focus on the benefits of anxiety.
Trust me, there are benefits to being anxiety-prone; at least from an evolutionary standpoint, anxiety may have evolved as a useful response to that predator hiding in the bushes.
Some previous studies have suggested that anxiety can help people to make better decisions, perform better under stressful circumstances, and even lead a more healthful lifestyle overall.
New research adds to this list, as those who are extremely anxious about their health are found to seek medical help more promptly after a heart attack , thus drastically improving their outlook. The findings were published in the journal Clinical Research in Cardiology.
None of this, however, is to say that living with anxiety is a walk in the park, or that the condition isn't serious.
Often debilitating, generalized anxiety disorder (GAD) is a psychiatric condition that affects almost 7 million people across the United States, many of whom are
reluctant to seek help because they feel that their condition isn't "real" if it doesn't have any physical symptoms.
However, if you're prone to anxiety and tend to berate yourself for it, the next time you're in a dark moment, you may benefit from remembering that your anxiety can sometimes be your friend.
Anxiety may protect you after a heart attack
The new research — led by Prof. Karl-Heinz Ladwig, from the Technical University of Munich in Germany — used data from the Munich Examination of Delay in Patients Experiencing Acute Myocardial Infarction (MEDEA) study.
The team examined the information on the 619 heart attack patients, all of whom were interviewed as part of MEDEA, considering things such as the time they arrived at the hospital and how their condition unfolded.
Of the 619 patients included in the study, 12 percent also had GAD. These individuals, the study has revealed, reacted more promptly to their heart attacks and got to the hospital much sooner.
In fact, women with anxiety disorder got to the hospital 112 minutes, on average, following heart attack onset, whereas it took women without the condition 2 hours longer to seek medical help.
For men, the beneficial effect of anxiety was also noticeable, although not as marked as it was for women. Men with anxiety disorder received treatment 48 minutes sooner, on average.
As Prof. Ladwig explains, every half an hour is vital for survival after a heart attack. That being said, ironically, having anxiety may also increase a person's risk of having cardiovascular disease in the first place.
"Individuals with anxiety disorder are at greater risk of having a heart attack but are more likely to survive it," says Prof. Ladwig. "Our data revealed an important factor. Individuals with anxiety disorder often react more sensitively to their health needs."
"Doctors should always take their concern very seriously. Such patients are also mor decisive when it comes to accepting help. In this way, one illness can help protect against another serious illness."
Prof. Karl-Heinz Ladwig

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05/03/2018

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04/03/2018

New insights from research on how insulin exits the bloodstream to metabolize glucose in cells could lead to new treatments for insulin resistance, a condition that usually precedes type 2 diabetes.
Tracking insulin's journey through the bloodstream could yield new treatments for insulin resistance and type 2 diabetes.
In a paper that was published in The Journal of Clinical Investigation , scientists at Vanderbilt University in Nashville, TN, report how they used a new microscopy technique alongside mathematical models to directly measure and characterize the movement of insulin as it traversed blood vessel walls into skeletal muscle cells in live mice.
Their findings suggest that the mechanism of insulin transport as it leaves the tiny blood vessels, or capillaries, in muscle tissue is different to that suggested by previous studies.
"Defining how insulin leaves the capillary," explains senior study author David H. Wasserman, a professor in molecular physiology and biophysics, "is essential to understanding and treating insulin resistance ."
Insulin resistance can lead to type 2 diabetes
Insulin resistance develops when the cells that make up the tissues of the liver, fat, and muscles do not respond effectively to insulin, the hormone that helps them to convert glucose into energy. The pancreas compensates by making more insulin to keep glucose at the correct level.
But as time goes on, pancreatic cells cannot keep up, glucose levels rise, and prediabetes and type 2 diabetes develop. The majority of people with diabetes have type 2 diabetes.
More than 30 million adults in the United States have
diabetes, including more than 7 million who are undiagnosed. Another 84 million have prediabetes.
It is not clear exactly what causes insulin resistance, but scientists suggest that being physically inactive and carrying too much weight are major contributors.
Understanding insulin's movements
Prof. Wasserman and his colleagues note that the "ability of insulin to stimulate glucose uptake" in muscle cells "depends on the rate at which insulin gets through the endothelium," which is the thin layer of tissue that lines the blood vessels and controls movement of substances in and out of the bloodstream.
They also note that there is evidence that impairment in the delivery of insulin to muscle cells is a feature of "diet-induced insulin resistance."
Thus, characterizing the mechanism that controls the movement of insulin through the endothelium "is critical to understanding the progression of insulin resistance," they argue, as they set out the objective of their study.
Insulin moves by 'fluid-phase transport'
Some studies suggest that the mechanism of insulin transport is "saturable" — that is, that the rate drops off with increasing levels of insulin, and that it depends on the presence of insulin receptors on the cells of the endothelium.
"In contrast," the study authors note that their findings "convincingly demonstrate that insulin movement across the endothelium is nonsaturable and does not require the insulin receptor."
With the help of the technique that they developed to track, image, and model the movement of insulin as it exits the capillaries in live mice, they concluded that the mechanism works by "fluid-phase transport."
This mode of transport "may be accomplished by either convective movement of insulin" through the junctions between cells in the endothelium, or "a nonspecific vesicular process, or a combination of both," they explain.
The findings could lead to new treatments
The scientists suggest that one of the main reasons for the difference between their findings and those of earlier studies is that they were able to directly measure the movement of insulin across the endothelium in live animals, as opposed to using "cultured monolayers" of endothelial cells.
Improving our understanding at the cellular and molecular level of how insulin exits the capillaries could lead to new ways to reverse insulin resistance, including drugs based on small molecules that boost insulin delivery and new synthetic versions of insulin that reach muscle cells more effectively.
Prof. Wasserman is of the opinion that the fluorescence tracing and microscopy technique that they have developed for use in live animals could also be used to study how drugs and other hormones exit the bloodstream to enter target tissues.
"The muscle capillary wall is a formidable barrier to insulin's action on muscles. It is the rate-limiting step for muscle insulin action and a potential site of regulation."
Prof. David H. Wasserman

04/03/2018

How far has cancer research come?
The World Health Organization (WHO) note that, worldwide, nearly 1 in 6 deaths are down to cancer .
In the United States alone, the National Cancer Institute (NCI) estimated 1,688,780 new cancer cases and 600,920 cancer-related deaths in 2017.
Currently, the most common types of cancer treatment are chemotherapy, radiotherapy , tumor surgery, and — in the case prostate cancer and breast cancer — hormonal therapy.
However, other types of treatment are beginning to pick up steam: therapies that — on their own or in combination with other treatments — are meant to help defeat cancer more efficiently and, ideally, have fewer side effects.
Innovations in cancer treatment aim to address a set of issues that will typically face healthcare providers and patients, including aggressive treatment accompanied by unwanted side effects, tumor recurrence after treatment, surgery, or both, and aggressive cancers that are resilient to widely utilized treatments.
Below, we review some of the most recent cancer research breakthroughs that give us renewed hope that better therapies and prevention strategies will soon follow suit.
Boosting the immune system's 'arsenal'
One type of therapy that has attracted a lot of attention recently is immunotherapy , which aims to reinforce our own bodies' existing arsenal against foreign bodies and harmful cells: our immune system's response to the spread of cancer tumors.
But many types of cancer cell are so dangerous because they have ways of "duping" the immune system — either into ignoring them altogether or else into giving them a "helping hand .
Therefore, some types of aggressive cancer are able to spread more easily and become resistant to chemotherapy or radiotherapy.
However, thanks to in vitro and in vivo experiments, researchers are now learning how they might be able to "deactivate" the cancer cells' protective systems. A
study published last year in Nature Immunology found that macrophages, or white blood cells, that are normally tasked with "eating up" cellular debris and other harmful foreign "objects" failed to obliterate the super-aggressive cancer cells.
That was because, in their interaction with the cancer cells, the macrophages read not one but two signals meant to repel their "cleansing" action.
This knowledge, however, also showed the scientists the way forward: by blocking the two relevant signaling pathways, they re-enabled the white blood cells to do their work.
Therapeutic viruses and innovative 'vaccines'
A surprising weapon in the fight against cancer could be
therapeutic viruses , as revealed by a team from the United Kingdom earlier this year. In their experiments, they managed to use a reovirus to attack brain cancer cells while leaving healthy cells alone.
"This is the first time it has been shown that a therapeutic virus is able to pass through the brain-blood barrier," explained the study authors, which "opens up the possibility [that] this type of immunotherapy could be used to treat more people with aggressive brain cancers."
Another area for improvement in immunotherapy is "dendritic vaccines," a strategy wherein dendritic cells (which play a key role in the body's immune response) are collected from a person's body, "armed" with tumor-specific antigens — which will teach them to "hunt" and destroy relevant cancer cells — and injected back into the body to boost the immune system.
In a new study, researchers in Switzerland identified a way to improve the action of these dendritic vaccines by creating artificial receptors able to recognize and "abduct" tiny vesicles that have been linked to cancer tumors' spread in the body.
By attaching these artificial receptors to the dendritic cells in the "vaccines," the therapeutic cells are enabled to recognize harmful cancer cells with more accuracy.
Importantly, recent studies have shown that immunotherapy may work best if delivered in tandem with chemotherapy — specifically, if the chemotherapy drugs are delivered first, and they are followed up with immunotherapy.
But this approach does have some pitfalls; it is difficult to control the effects of this combined method, so sometimes, healthy tissue may be attacked alongside cancer tumors.
However, scientists from two institutions in North Carolina have developed a substance that, once injected into the body, becomes gel-like: a " bioresponsive scaffold system ." The scaffold can hold both chemotherapy and immunotherapy drugs at once, releasing them systematically into primary tumors.
This method allows for a better control of both therapies, ensuring that the drugs act on the targeted tumor alone.
The nanoparticle revolution
Speaking of specially developed tools for delivering drugs straight to the tumor and hunting down micro tumors with accuracy and efficiency, the past couple of years have seen a "boom" in nanotechnology and nanoparticle developments for cancer treatments.
Nanoparticles could be 'a game-changer' in cancer treatment.
Nanoparticles are microscopic particles that have garnered so much attention in clinical research, among other fields, because they bring us the chance to develop precise, less invasive methods of tackling disease.
Vitally, they can target cancer cells or cancer tumors without harming healthy cells in the surrounding environment.
Some nanoparticles have now been created to provide very focused hyperthermic treatment, which is a type of therapy that uses hot temperatures to make cancer tumors shrink.
Last year, scientists from China and the U.K. managed to come up with a type of " self-regulating " nanoparticle that was able to expose tumors to heat while avoiding contact with healthy tissue.
"This could potentially be a game-changer in the way we treat people who have cancer," said one of the researchers in charge of this project.
These tiny vehicles can also be used to target cancer stem-like cells , which are undifferentiated cells that have been linked to the resilience of certain types of cancer in the face of traditional treatments such as chemotherapy.
Thus, nanoparticles can be "loaded" with drugs and set to "hunt down" cancer stem cells to prevent the growth or recurrence of tumors. Scientists have experimented with drug-filled nanoparticles in the treatment of various types of cancer, including breast cancer and endometrial cancer .
No less importantly, minuscule vehicles called "nanoprobes " can be used to detect the presence of micrometastases, which are secondary tumors so tiny that they cannot be seen using traditional methods.
Dr. Steven K. Libutti, director of the Rutgers Cancer Institute of New Jersey in New Brunswick, calls micrometastases "the Achilles' heel of surgical management for cancer" and argues that nanoprobes "go a long way to solving [such] problems."
Tumor 'starvation' strategies
Another type of strategy that researchers have been investigating of late is that of "starving" tumors of the nutrients they need to grow and spread. This, scientists point out, could be a saving grace in the case of aggressive, resilient cancers that cannot effectively be eradicated otherwise.
One novel method of 'attacking' cancer is by 'starving' cancer cells to death.
Three different studies — whose results were all published in January this year — looked at ways of cutting off cancers' nutritional supplies.
One of these studies looked at ways of stopping glutamine , a naturally occurring amino acid, from feeding cancer cells.
Certain cancers, such as breast, lung, and colon, are known to use this amino acid to support their growth.
By blocking cancer cells' access to glutamine, the researchers managed to maximize the impact of oxidative stress , a process that eventually induces cell death, on these cells.
Some aggressive types of breast cancer may be halted by stopping the cells from "feeding" on a particular enzyme that helps them to produce the energy they need to thrive.
Another way of depleting cancer cells of energy is by blocking their access to vitamin B-2 , as researchers from the University of Salford in the U.K. have observed.
As one study author says, "This is hopefully the beginning of an alternative approach to halting cancer stem cells." This strategy could help individuals receiving cancer treatment to avoid the toxic side effects of chemotherapy.
Cancer treatments and epigenetics
Epigenetics refers to the changes caused in our bodies by alterations in gene expression, which dictate whether certain characteristics appear or if certain "actions" are affected at a biological level.
According to research that addressed the impact of such changes, many cancers, as well as the behaviors of cancer cells, are determined by epigenetic factors .
"Recent advances in the field of epigenetics have shown that human cancer cells harbor global epigenetic abnormalities, in addition to numerous genetic alterations."
These genetic and epigenetic alterations interact at all stages of cancer development, working together to promot cancer progression."
Thus, it is crucial for specialists to understand when and where to intervene and the expression of which genes they may need to switch on or off, depending on their role in the development of cancer.
One study , for instance, found that the gene responsible for the advent of Huntington's disease produces a set of molecules whose action may actually prevent cancer from occurring.
Now, the researchers' challenge is to channel the therapeutic potential of this process without triggering Huntington's disease. However, the scientists are hopeful.
"We believe a short-term treatment cancer therapy for a few weeks might be possible," says the study's senior author.
Another recent study was able to establish that estrogen-receptor positive breast cancers that become resistant to chemotherapy gain their resilience through
genetic mutations that "confer a metastatic advantage to the tumor."
But this knowledge also gave researchers the "break" that they needed to come up with an improved treatment for such stubborn tumors: a combination therapy that delivers the chemotherapeutic drug fulvestrant alongside an experimental enzyme inhibitor.
What does this all mean?
Cancer research is running at full speed, taking advantage of all the technological advances that science has achieved over recent years. But what does that mean in terms of coming up with a cure for cancer?
Whether or not there will ever be a cure for all cancer types is currently a matter of strong debate; although promising studies are published and covered by the media almost every day, cancer types vary immensely.
This makes it very difficult to say that an approach that works for one type will be adaptable to all.
Also, while there is much emerging research promising more effective treatments, most of these projects are still in their early stages, having conducted in vitro and in vivo experiments. Some potential treatments still have a long way to go before clinical trials in human patients.
Still, that doesn't mean we should lose all hope. Some researchers explain that these efforts should make us optimistic; while we may not be at the stage where we can claim that cancer can easily be eradicated, our furthered knowledge and ever more precise tools keep us ahead of the game and improve our odds in the fight against this disease.

03/03/2018

Researchers say that diabetes should be categorized into five types, rather than two.
The research was led by Prof. Leif Groop, of the Lund University Diabetes Centre in Sweden and the Institute for Molecular Medicine Finland in Helsinki.
In the United States alone, around 30.3 million people are living with diabetes.
Excluding gestational diabetes — diabetes that develops during pregnancy — there are two main types: type 1 and type 2.
In type 1 diabetes, the beta cells of the pancreas — which produce insulin , the hormone that regulates blood sugar levels — are mistakingly attacked and destroyed by the immune system.
Type 2 diabetes is the most common form, accounting for around 90–95 percent of all cases. This occurs when the body's cells stop responding to insulin, or the beta cells are unable to produce sufficient amounts of the hormone.
In both forms of the condition, blood sugar levels can become too high — a condition known as hyperglycemia. Unless controlled, this can lead to a number of complications, including kidney disease, cardiovascular disease, and nerve damage.
The heterogeneity of diabetes
A diabetes diagnosis is normally made using the fasting plasma glucose (FPG) test or the A1C test. The FPG test assesses a person's blood glucose level at a single time point, while the A1C test measures average blood glucose levels over the previous 3 months.
When it comes to determining which type of diabetes a person has, healthcare professionals might look for diabetes-related autoantibodies in the blood. These are proteins produced by the immune system that can attack the body's own cells.
The presence of such autoantibodies is an indicator of type 1 diabetes. If a person does not have these autoantibodies, they are considered to have type 2 diabetes.
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But, as Prof. Groop and colleagues note, the classification guidelines for diabetes have not been updated for 20 years — despite increasing evidence that diabetes has high heterogeneity.
"Diabetes is a group of chronic metabolic disorders," says Dr. Rob Sladek, of the McGill University and Génome Québec Innovation Centre in Canada, in an editorial linked to the study, "that share the common feature of hyperglycemia, meaning that, in principle, diabetes can be diagnosed via measurement of a single blood component."
"However, elevations in blood glucose can be caused by a number of genetic and acquired factors that reduce the circulating concentrations of insulin or decrease its effectiveness, leading to heterogeneity in the clinical presentation and progression of the disease."
Prof. Groop and his team say that a "refined classification" of diabetes based on its heterogeneity could help healthcare professionals better predict which individuals are most likely to develop complications and allow a more personalized approach to treatment.
In their study, the researchers propose that diabetes should no longer be categorized as two types. Instead, they say that the condition should be classified into five distinct types.
The five 'clusters' of diabetes
The researchers came to their proposal by analyzing the data of four study cohorts. These included a total of 14,775 adults from Sweden and Finland, all of whom had been newly diagnosed with diabetes.
As part of the analysis, the scientists looked at six measures in each subject that each represent different features of diabetes.
These measures were: body mass index ( BMI); age at diabetes diagnosis; hemoglobin A1C (HbA1C), a measure of long-term blood sugar control; beta cell functioning; insulin resistance; and the presence of diabetes-related autoantibodies.
As well as conducting genetic analyses of the participants, the researchers also compared their disease progression, complications, and treatment.
The study revealed five distinct forms of diabetes, three of which were severe and two that were mild. The team categorized these as follows:
Cluster 1 : severe autoimmune diabetes (currently known as type 1 diabetes), characterized by insulin deficiency and the presence of autoantibodies. This was identifi in 6–15 percent of subjects.
Cluster 2 : severe insulin-deficient diabetes, characterized by younger age, insulin deficie and poor metabolic control, but no autoantibodies. This was identified in 9–20 percent of subjects.
Cluster 3 : severe insulin-resistant diabetes, characterized by severe insulin resistance an significantly higher risk of kidney disease. Th was identified in 11–17 percent of subjects.
Cluster 4 : mild obesity-related diabetes, mos common in obese individuals. This affected23 percent of subjects.
Cluster 5 : mild age-related diabetes, most common in elderly individuals. This was the common form, affecting 39–47 percent of subjects.
The researchers note that each of these five types "were also genetically distinct," meaning that there were no genetic mutations that were shared across all five clusters.
A 'step toward precision medicine'
When the researchers assessed the treatment received by adults in each of the five clusters, they noticed that some were being treated inappropriately.
As an example, the team points out that just 42 percent of patients in cluster 1 and 29 percent of patients in cluster 2 received insulin therapy from the point of disease onset.
They say that this indicates that the current classifications of diabetes fail to target the underlying features of the disease.
As such, Prof. Groop and colleagues propose that diabetes should be categorized into five distinct types.
While further research is required to refine these five clusters — by using biomarkers and genetic risk scores, for example — the team believes that this study is a great stride toward tailored treatments for diabetes.
"Existing treatment guidelines," concludes Prof. Groop, "are limited by the fact they respond to poor metabolic control when it has developed, but do not have the means to predict which patients will need intensified treatment."
"This study moves us towards a more clinically useful diagnosis, and represents an important step towards precision medicine in diabetes."
Prof. Leif Groop

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