Preeclampsia and CD74 protein linked – Underlying cause revealed
Categories Medical news

Preeclampsia and CD74 protein linked – Underlying cause revealed

A new study, lead by Dr. Florian Herse, has demonstrated that preeclamptic women contain lower levels of placenta’s immune protein CD74 and higher levels of certain inflammatory factors, which is responsible for abnormal placenta formation during pregnancy. The fetus receives nourishment from mother through the placenta. Preeclampsia happens when there is disrupted placental growth and is manifested as high blood pressure, water retention and protein in urine. It can also affect fetal growth and development.

Preeclampsia has been nicknamed “the disease of theories” as its exact cause is yet unclear. Published in the Circulation, the study performed translational research using human subjects, cell cultures and animal models; applied comprehensive methodology to get robust results and provided solid evidence of correlation between CD74 receptor protein of immune cells and preeclampsia. The CD74 receptors are found on active large phagocytic cells (macrophages) in the placenta, which interact with and stimulate other placental cells (trophoblasts). Scientists, in preparatory research, identified fewer than expected CD74 receptors on placental macrophages in preeclamptic women. Researchers then went in depth and restrained CD74 receptor production on placental macrophages in cell cultures and observed that the cells produced pro-inflammatory factors in response.

Further, the structures of placentas in mice without CD74 receptor protein were disrupted and less functional than in control mice. Based on this finding, the study emphasizes that interrupted macrophage-trophoblast interaction is the underlying cause of inflammation and abnormal placental growth and that this interaction should be perfect during pregnancy to avert the occurrence of preeclampsia.

Inheritance of the Risk Gene THADA from the Mother Poses Increased Risk of Type 2 Diabetes in the Child
Categories Medical news

Inheritance of the Risk Gene THADA from the Mother Poses Increased Risk of Type 2 Diabetes in the Child

The causes of type 2 diabetes are a combination of heredity and environment. Lund University in Sweden has exclusively analyzed the reason as to why type 2 diabetes is inherited to a greater extent from an individual’s mother. In the new study, the researchers used data from previous investigations and DNA gathered from 2000 families in which one parent and a child suffer from type 2 diabetes.

The results unveiled that the variations in two previously identified risk genes for type 2 diabetes, KCNQ1 and THADA, cause an increased risk of acquiring the disease in the child if they are inherited from the mother whereas inheritance from the father had less or no effect. The fact that the genes inherited from the mother affect the risk of disease probably depended on the genes from the father being silenced in a process known as imprinting.

Thus the lifestyle of the mother, with factors such as stress, diet, illness etc., probably affects the future risk of disease in the foetus. Prof. Leif Groop, the Lund University, responsible for this new study conveyed that exposure of foetus for a longer time in utero and breast-feeding could explain why heredity from the mother has a greater effect on the child’s genome.

Antimicrobial Agent Triclosan
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Is the Antimicrobial Agent Triclosan a Double-edged Sword?

Triclosan an antimicrobial and antifungal agent commonly used in most of the consumer products like shampoos, deodorants, toothpastes, etc. can disrupt bacterial communities found in the gut says a new study from Oregon State University. Triclosan continues to be used in medical settings, and can be easily absorbed through the skin. The research was published in PLOS ONE. The study was done in zebrafish, which is believed to be an important animal model to help determine possible human biological and health impacts of triclosan.

The study unveiled that triclosan exposure caused rapid changes in both the diversity and composition of the microbiome in the laboratory animals. Some bacteria (family Enterobacteriaceae) were more susceptible to the impact of triclosan and others were more resilient (genus Pseudomonas). However, implication on animal or human health is unclear. The gut-associated microbiome performs vital functions for human health, prevents colonization with pathogens, stimulates the development of the immune system, and produces micronutrients needed by the host. It is believed that compromising of the bacteria in the intestinal tract may contribute to the development or severity of disease.

According to scientists, part of the strength of the present study is developing improved ways, through rapid screening of zebrafish, to more easily determine which compounds may be acceptable and which are toxic. This study showed triclosan was quickly associated with shifts in the microbial community structure and can alter the abundance of specific taxa.

Loss of Y chromosomes
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Could `Loss of Y’ in Men Lead to Alzheimer’s Disease?

An inquisitive study has suggested that lose of Y chromosomes from the blood cells of elderly men may elevate the risk of developing Alzheimer’s disease. The study of more than 3,200 European elderly men established that those who already had Alzheimer’s were nearly three times more likely to show a loss of the Y chromosome in some of their blood cells. Overall, 17 percent had a detectable loss of Y. Men missing the chromosome from around 35% of their blood cells were more likely to develop Alzheimer’s than those with loss of Y in 10% of their cells.

In accordance to a study carried out by the co-author Lars Forsberg (researcher at Uppsala University, Sweden) loss of Y has been linked to cancer risk in elderly men. Dr. Luca Giliberto (neurologist and researcher with the Feinstein Institute for Medical Research, NY) noted the loss of Y in certain autoimmune diseases which may affect Alzheimer’s risk. However, the workings of Y have not been fully understood and the reasons for the link are unclear. According to experts the study does not prove that loss of the Y chromosome directly contributes to Alzheimer’s disease. But it adds to evidence tying loss of Y to disease risk. The findings were reported online May 2016 in the American Journal of Human Genetics.