Oral vitamin D spray as effective as tablets according to a new study

In an attempt to understand the efficacy of oral vitamin sprays, a research group from the University of Sheffield performed a clinical study on various subjects. The study, published later in the European Journal of Clinical Nutrition, concludes that the spray method for taking vitamin D is as effective as the ingestion of a tablet.

During the experiments, the volunteers took vitamin D for six weeks. All achieved adequate levels of vitamin D after only three weeks of using the oral spray, even those patients who were most lacking, as specified by Bernard Corfe, professor of molecular gastroenterology and lead author of the study.

“There is now a greater awareness of the need for people to integrate their vitamin D level, but only about 40% of adults in the UK have sufficient levels. So this research is an opportunity to highlight the importance of this vitamin, which is essential in supporting general health and providing a valuable alternative source for those who may have difficulty or prefer not to take tablets,” says the researcher in the press release that presents research.

Taking vitamins through an oral spray can be very useful for those people who have problems with swallowing, problems that can arise even for medical conditions, and that cannot swallow various tablets. There are also children among those who may find problems taking tablets. This study shows that oral spray is just as effective for raising levels of vitamin D.

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.”

Chronic pain strongly involves a protein called RGS4

An important finding regarding chronic pain was made by a group of researchers from the Icahn School of Medicine at Mount Sinai. In their study, published in the Journal of Neuroscience, the researchers explain that they discovered a protein called RGS4 (Regulator of G protein Signaling 4) that plays a very important role in maintaining chronic pain.

The transition from acute pain to chronic pain occurs through adaptations in the immune cells, in the glial and in the neuronal ones, changes that at the moment are not completely understood. It is precisely this lack of understanding that underlies the failure of many chronic pain medications which can also cause side effects. The only drugs that seem to actually work are opioids but these can cause serious long-term side effects.

This new discovery, which the researchers themselves refer to as “exciting”, could instead be very useful for creating new drugs that target this protein to stop chronic pain. As Venetia Zachariou, a professor at Mount Sinai explains, the RGS4 protein appears to strongly contribute to the transition from acute to pathologic/chronic pain.

The experiments, in this case, were carried out on mice: the researchers used genetically modified mice in which the action of the RGS4 protein was deactivated. This deactivation did not affect acute pain or the induction of chronic pain itself but the mice themselves recovered within three weeks.

The researchers also tried to reduce the expression of RGS4 in a particular area of ​​the brain and this caused recovery from mechanical and cold allodynia. Now researchers are trying to study the influence of RGS4 also in other areas of the body such as the spinal cord or in other areas of the brain that regulate mood.

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.

Scientists discover that Valium does not work alone and needs the help of a gene

A group of researchers has discovered a particular gene, called Shisa7, which plays an important role with regard to the regulation of inhibitory neural circuits and the sedative effects of certain anxiolytics based on benzodiazepines.

This means that the classic Valium, for example, used to treat things like anxiety, muscle spasms or even sleep disorders, does not work alone to calm the nerves but needs the important contribution of a gene that is defined in the press release as “sticky.”

In fact, prior to this study, it was thought that the benzodiazepines essentially worked by themselves to trigger the calming responses of the A GABA type receptors (GABAA). Experiments that Ling Gang Wu, senior researcher at the National Institute for Neurological Disorders and the Ictus (NINDS), and Ronald S. Petralia, of the National Institute of Deafness and Other Communication Disorders (NIDCD), showed that Shisa7 attaches directly to GABAA receptors accelerating responses and increasing their effectiveness in the presence of Valium.

“These results suggest that Shisa7 directly models inhibitory synaptic responses in a variety of conditions, including the presence of benzodiazepines,” reports Chris J. McBain, a researcher at the Enice Kennedy Shriver National Institute of Child Health and Human Development (NICHD). The researchers carried out experiments on modified mice from which the Shisa7 gene was eliminated. These mice, after undergoing Valium injections, were not affected by any calming effect compared to the control group mice.

Furthermore, in other experiments, the researchers discovered that Shisa7 could also influence sleepiness levels and the hypnotic effects of benzodiazepines. Such discoveries could help in the development of new drugs or treatments aimed at GABAA receptors.

Human cells that produce testosterone grown in the laboratory

One way to grow human cells to produce testosterone in the laboratory was developed by a group of researchers at the University of Southern California Pharmacy School.

The researchers hope that with this method it will be possible to arrive at treatments to counteract low levels of testosterone in the body by using special personalized replacement cells, as reported by Vassilios Papadopoulos, a researcher who led the study.

The researchers transformed induced pluripotent stem cells, derived from human skin or blood, into Leydig cells, which are the cells present in human testes that produce the male sex hormone.
According to the researchers, Leydig’s cells grown in the laboratory looked the same as their real counterparts.

The low level of testosterone in men, also known as hypogonadism, can lead to fertility problems and to sexual function in general and can affect mood as well as conditions such as bone density and obesity.

The level of testosterone in the body is lowered naturally in the course of the age, however more or less sudden lowering can also be caused by infections such as mumps or by treatments for cancer during childhood or adolescence.

The main therapy is that which sees the intake of testosterone which can be applied as a gel or can be taken orally or injected.

“Leydig’s human cell transplant is just a few years away,” the researcher said.

Health News And Research