All posts by Johnathan Flint

Fat can also accumulate in the lungs

Already in the past, several studies have linked being overweight or obesity to respiratory problems such as asthma or wheezing and something very close to confirming this connection came from a new study published in the European Respiratory Journal.

The researchers examined lung tissue samples taken from 52 cadavers stored in a respiratory tissue biobank. Of the 52 people to whom the corpses belonged, 16 had died from asthma. By analyzing the structure of the lungs, the researchers quantified the adipose tissue also comparing it with the body mass index of each person when he was alive.

The researchers say they have identified, for the first time, that adipose tissue can also accumulate in the airway walls of the lungs. The researchers suggest that this increase in fat may alter the normal functioning of the lung’s airways leading to inflammation of the latter and favoring diseases such as asthma. John Elliot, one of the authors of the study and a researcher at the Sir Charles Gairdner Hospital in Perth, says: “By observing lung samples, we identified adipose tissue that had accumulated in the airway walls. We wanted to see if this accumulation was related to body weight.”

According to the other main research author, Peter Noble, an associate professor at the University of Western Australia in Perth, being overweight or being obese in the past had been linked to an increased risk of asthma but this connection had never been fully explained. This research shows that excess fat can also occur in the lungs, especially in the airway walls.

These can, in fact, be different in thickness and this can limit the flow of air both in and out, which in turn increases the risk of asthma. This would also explain why those who are overweight or obese tend to need to breathe more when doing physical activity, which increases the ventilatory load. Now the researchers want to find out if with a slimming effect it is possible not only to lower body weight but also to counteract these respiratory diseases.

Schizophrenia: 10 new genes identified

In what is defined as one of the largest DNA sequencing studies related to schizophrenia, a group of researchers led by Tarjinder Singh has discovered 10 new genes implicated in the development of this pathology with a method called “whole-exome sequencing.” The researchers used genetic data from more than 125,000 people to obtain various information regarding the genetic basis of schizophrenia itself. The results of the research were then presented at the annual meeting of the American Society of Human Genetics 2019 in Houston.

One of the reasons that led researchers to use DNA sequencing to obtain information on schizophrenia is that for this disease, in the last fifty years, there has been quite limited progress regarding the development of new drugs. However, the use of new genetic techniques is proving very useful, in recent years, in many fields and the same researchers believe that useful results can also be obtained to discover mechanisms underlying schizophrenia.

The latter is one of the psychiatric disorders not yet fully understood. It is believed, however, that its development can be accelerated by disorders concerning some genes that encode certain proteins. Because these are rare genetic changes, the researchers used a very large set of people. Of the 125,000 people analyzed, 25,000 of them had been diagnosed with schizophrenia. People came from all five continents.

Following the analyzes, the researchers identified 10 genes that, once they stopped their functions, caused an increased risk of schizophrenia, as Singh himself stated in the press release. Two of these 10 genes encoded glutamate receptors, indicating that these receptors could potentially be a target for future therapies against schizophrenia.

Diabetes: scientists discover new possible therapy to limit insulin collateral damage

A protein that can act as a regulator of blood sugar and lipids under certain conditions has been identified by a group of researchers at the University of Geneva (UNIGE). The protein, called S100A9, could counteract the side effects of insulin given to diabetics.

The study, published in Nature Communications, mentions what could be a new treatment for diabetes and in general to significantly improve the quality of daily life of tens of millions of people. In fact, millions of people have to use insulin injections for both type 1 and type 2 diabetes. Any overdose can trigger hypoglycemia, the drop in blood glucose levels, while an overdose can lead to hyperglycemia.

By performing experiments on mice, the scientists found that by administering doses of S100A9 to diabetic deficient insulin-deficient rats, improved glucose management and better ketone and lipid control were achieved. They then discovered that this protein appears to work only when there is TLR4, a receptor placed on the membrane of certain cells, including adipocytes and cells of the immune system.

Now Roberto Coppari, one of the authors of the study together with Giorgio Ramadori, intends to understand with his team how the S100A9 protein works. In this regard, they are devising a new treatment that combines low doses of insulin and S100A9 to determine whether glucose and ketones can be better controlled and limit the same negative side effect as insulin.

“We also want to decipher the exact role of TLR4 in order to offer a therapeutic strategy that achieves the delicate balance between optimal blood glucose, ketones and lipid control,” explains Coppari himself.

Birth weight related to the risk of childhood allergies, according to study

According to a study produced by researcher Kathy Gatford of the Robinson Research Institute of the University of Adelaide, the greater the weight of the child at birth compared to the gestational period, the greater the risk of food allergies and eczema.

To reach this conclusion, the researchers analyzed 15,000 previous studies mostly from European countries. This is data related to millions of allergic people and researchers have focused mostly on data on children. Specifically, Gatford and colleagues analyzed the links between birth weight and the incidence of allergic diseases in children and adults.

According to the researcher, for every pound of weight gain at birth there was a 44% increase in the child’s risk of incurring food allergies and a 17% increase in incurring eczema. There were no connections with hay fever.

According to the doctor, those children who showed limited intrauterine growth seemed to be protected, once born, from the development of allergic responses. However, these same children saw their risks of developing other diseases later in life increase.

“It is increasingly clear that genetics alone does not explain the risks of developing allergies and that environmental exposures before and around birth can plan people for an increase or a reduction in the risk of allergies”, explains the researcher who adds: “We do not want small children, but we would like to understand how much less or slower growth before birth is protective against allergies.”

Researchers reverse important symptom of schizophrenia in mice by manipulating genes

This is an announcement of no small importance that appeared on the Columbia University website. The researchers say they have reversed one of the most important symptoms of schizophrenia in mice by reversing the SETD1A gene mutation, a gene already known and previously linked by other studies to schizophrenia. Specifically, the researchers reversed the impairment of spatial working memory.

For schizophrenia, there are currently no real treatments. This pathology, which influences the functioning of the brain as well as behavior and mood, must be linked to a sort of cognitive impairment. However, the drugs that exist today for schizophrenia mostly control the psychotic symptoms and not the cognitive ones. This new study shows that it is possible, in a sense, to repair brain cells made dysfunctional by schizophrenia, at least in mice, bringing their level of working memory back to a pre-existing state.

The study, published in Neuron, therefore shows what Joseph Gogos, a researcher at Columbia’s Brain Behavior Institute and senior author of the study, defines as a “promising path” to treat schizophrenia, particularly damage to working memory, not always treated with antipsychotic drugs. An inoperative working memory makes it difficult to maintain any kind of relationship and even damages everyday life by literally putting on by people with schizophrenia who can no longer interact with other people.

The researchers worked on the SETD1A gene. The latter produces a protein that can influence the activity of other important genes. The researchers worked on a group of memory-deficient mice, mice that had some difficulty, for example, in moving into a simple maze. These mice presented neurons from the different prefrontal cortex of normal mice. Specifically, mice lacking SETD1A had short and poorly developed neuronal branches.

This prevented them from establishing the necessary connections with other groups of brain neurons, as Jun Mukai, the study’s first author and former researcher in the Gogos laboratory, explains. By manipulating the SETD1A gene they discovered that it was linked to another gene, called LSD1. By inhibiting the latter, the memory of the mice greatly improved so that their axons began to grow again, becoming similar to those of healthy mice.

Researchers say SETD1A influences a number of other genes and proteins that, combined, can cause memory deficits. This finding could be useful, according to the researchers, to make personalized drugs for people with SETD1A gene mutations and, in a broader view, even to treat schizophrenia itself.

Oral anticoagulant drug retards progression of Alzheimer’s disease in mice

A group of researchers has discovered that the use of a particular drug that acts as an oral anticoagulant, dabigatran, can delay the appearance of Alzheimer’s disease in mice. The research was carried out by scientists from the Centro Nacional de Investigaciones Cardiovasculares (CNIC) and the Rockfeller University of New York while the study was published in the Journal of the American College of Cardiology .

According to the researchers, long-term anticoagulation with dabigatran effectively slowed the progression of Alzheimer’s disease in mice during experiments. Marta Cort├ęs Canteli, a researcher at the CNIC and one of the authors of the study, speaks of an “important progress” regarding effective treatments for Alzheimer’s disease.

To defeat this disease, according to the researcher, there will be a need for personalized therapies aimed at various and different processes that can contribute to the progression of the disease. Among the objectives there is, according to the researcher, cerebral circulation and precisely to treat the latter an oral anticoagulant such as dabigatran can have an effective approach for those Alzheimer’s patients who have a tendency to coagulation.

According to the researcher, in addition to other studies that will have to certify the beneficial action of this drug, there will also be a need to create new diagnostic tools to identify Alzheimer’s patients with a tendency to coagulation with greater precision and efficiency, and precisely this “will be an important research line in the coming years.”