White Blood Cells Aid

You probably already know how important it is to keep blood sugar levels within the recommended range if you or a loved one has diabetes. Major, long-term health issues like vision loss, heart disease, and renal disease can be avoided or delayed with proper management of blood sugar, HbA1c, cholesterol levels, and blood pressure. Diabetes can have a serious negative impact on the eyes, which can result in blindness or visual impairment. This is due to the fact that high blood sugar can destroy the capillaries in the eye's most delicate tissues, which transmit signals to the brain and enable clear vision. A permanent loss of vision may result from this retinal damage brought on by high blood pressure. However, there is hope. One can avoid major eye damage by monitoring and regulating the blood sugar levels as per their doctor's recommendation. The following five actions can help safeguard vision during diabetes. Understand Numbers When blood sugar levels rise, the delicate blood vessels that nourish the most delicate areas of the eyes are often the first to sustain damage. High blood sugar specifically harms the retina. The thin tissue that makes up around 65 per cent of the back of the eye is called the retina. Many light-sensitive cells reside there, allowing the eyes to communicate visual information to the brain via the optic nerve. The blood vessels that supply the retina are harmed when blood sugar levels rise. Vision blurring may result from this, either temporarily or permanently. Diabetic retinopathy, glaucoma, and cataracts are three distinct eye conditions that are quite common in people with diabetes. Timely detection and interventions can minimize such complications. By keeping track of the blood sugar levels one can reduce the risk for these sight-stealing conditions. Stop Smoking Every physiological system is harmed by smoking, but diabetics are particularly vulnerable. Smoking harms the veins, arteries, and capillaries in the body, aggravating diabetes-related eye damage already present. Whether you're a smoker and have tried to quit, or want to quit for the first time, don't give up. Talk to your doctor about your options. Moving It Exercise benefits all physical systems in the same way that smoking does, so get moving! After lunch, go for a couple laps around the block. Take a few extra steps and park at the far end of the parking lot. Regular exercise can reduce your risk of developing diabetic eye disease since it lowers blood sugar levels. Put it on your calendar each week to remind you to make time for this appointment with yourself that will improve your life. Before beginning any workout regimen, discuss it with your doctor to find out the exercises they advise. Focus on Eating Healthily You are what you eat, we've all been told since we were young. Healthy eating leads to healthy eyes. Eat a diet that is well-balanced and contains meals that provide your body with good nutrients to safeguard diabetic eyes. Vitamins A, C, E, beta-carotene, lutein, omega-3 fatty acids, zinc, and zeaxanthin are some of them. Consuming a diet high in leafy greens, fatty fish like salmon, tuna, or mackerel, nuts like walnuts and almonds, beans, lentils, and mushrooms will help you reach this goal. Maintaining a low glycemic diet is important to manage blood sugar levels. Yearly Dilated Eye Examination The finest tip is reserved for last: get a full dilated eye exam from your ophthalmologist once a year, or more frequently if advised, to make sure that your efforts to control blood sugar are aiding in maintaining the health of your eyesight. A screening for cataracts, glaucoma, and diabetic retinopathy may be performed at this visit. Your pupils enlarge as your eyes dilate, allowing your ophthalmologist to inspect the retina, macula, and optic nerve up close. Your doctor can identify diabetic retinopathy in its early stages long before you have any symptoms by looking at these sensitive tissues. (Dr. Kuldeep Dole, Medical Director - PBMA's H.V. Desai Eye Hospital An Orbis Partner Hospital)    

The SARS-CoV-2 virus can directly infect a specialised type of kidney cell, explaining why acute kidney injury is one of the main complications observed in patients with severe Covid-19, finds a study. Primarily known to infect cells in the respiratory tract, physicians were surprised to see that many patients, especially those with severe Covid, were also developing injuries to their kidneys. "It was shocking to hear doctors describe how patients who were healthy suddenly developed kidney injury and needed to go on dialysis after contracting SARS-CoV-2," said Samira Musah, assistant professor of biomedical engineering and medicine at Duke University. "It was clear that the virus was doing something to the kidneys, but it was so early in the pandemic that nobody was sure what was going on," she added. For the new study, described in the journal Frontiers in Cell and Developmental Biology, the team worked worked with a pseudovirus version of SARS-CoV-2 on a previously developed model of podocyte cell, a specific type of kidney cell that helps control the removal of toxins and waste from the blood. When the pseudovirus was introduced to the podocyte cell model, the team discovered that the spike protein of the virus could directly bind to numerous receptors on the surface of podocytes. "We found that the virus was especially adept at binding to two key receptors on the surface of the podocytes, and these receptors are abundant in these kidney cells," explained Titilola Kalejaiye, a postdoctoral fellow at Duke. "There was a strong uptake of the virus initially, and we also found that when you increased the dose of the virus, the uptake would increase even further. The virus seemed to have a strong affinity for these kidney cells." Further, the team tested their podocyte model with the real SARS-CoV-2 virus. Just like with the pseudovirus, the team observed that the live version of the virus had a strong affinity for podocytes. Once the virus infected the cells, it damaged the podocytes, causing their long, finger-like structures, which help filter blood, to retract and shrivel. If the injuries to the cells were too severe, the podocytes would die. "Beyond the structural damage, we saw that the virus could hijack the machinery of the podocytes to produce additional viral particles that could spread to infect additional cells," said Maria Blasi, Assistant Professor of medicine at Duke. Now the team hopes to expand their work to study how the different variants of SARS-CoV-2 behave in kidney cells. Read More► Omicron Ups Risk of Upper Airway Infections, Cardiac Arrest in Small Kids

London: Increased levels of blood fats, also known as lipids, in people with Type 2 diabetes and obesity are more harmful than previously thought, a new study has found. In patients with metabolic diseases, elevated fat levels in the blood create stress in muscle cells -- a reaction to changes outside the cell which damage their structure and function. The study, published in the journal Nature Communications showed that these stressed-out cells give off a signal which can be passed on to other cells. The signals, known as ceramides, may have a protective benefit in the short-term, because they are part of a mechanism designed to reduce stress in the cell. But in metabolic diseases, which are long term conditions, the signals can kill the cells, make symptoms more severe, and worsen the illness, said researchers at University of Leeds in the UK. Increased fat in the blood has long been known to damage tissues and organs, contributing to the development of cardiovascular and metabolic diseases including Type 2 diabetes. The condition can be caused by obesity, rates of which have nearly tripled worldwide between 1975 and 2020. "This research gives us a novel perspective on how stress develops in the cells of individuals with obesity, and provides new pathways to consider when looking to develop new treatments for metabolic diseases," said Lee Roberts, Professor of Molecular Physiology and Metabolism in the University's School of Medicine. "With obesity an ever-increasing epidemic, the burden of associated chronic disease such as Type 2 diabetes necessitates new treatments. We hope the results of our research here open a new avenue for research to help address this growing concern," he added. In the lab, the team replicated the blood fat levels observed in humans with metabolic disease by exposing skeletal muscle cells to a fatty acid called palmitate. The cells began to transmit the ceramide signal. When these cells were mixed with others which had not been previously exposed to fats, the researchers found that they communicated with each other, transporting the signal in packages called extracellular vesicles. The experiment was reproduced in human volunteers with metabolic diseases and gave comparable results. The findings provide a completely new angle on how cells respond to stress, with important consequences for our understanding of certain metabolic diseases including obesity.  (Agency) Read More► Genetic Inflammation Linked to Neuropsychiatric Illness

Tokyo: Mycobacteria, a group of pathogenic bacteria that cause diseases like leprosy and tuberculosis in humans, are associated with red blood cells at lung infection sites. M. tuberculosis and other mycobacteria implicated in lung disease are now known to live in macrophages - white blood cells that engulf and kill pathogens. Mycobacteria turn up in blood and sputum coughed up by sick patients. Red blood cells, although also found in the sputum of tuberculosis patients, have not yet been specifically studied in disease progression. But, "our research will change the conventional common sense that mycobacteria grow intracellularly", said Yukiko Nishiuchi, Associate Professor at Hiroshima University in Japan. The team obtained lung tissue samples from five mice infected with two species of Mycobacteria - M. avium and M. intracellulare - as well as from a human patient infected with Mycobacterium avium subsp. hominissuis (MAH). Microscopic examination revealed red blood cells were co-located with mycobacteria in both the capillary vessels and granulomas (clumps of immune cells) of mice and human lung tissues. To assess the relationship of the mycobacteria to human red blood cells, the team monitored their growth with and without the blood cells. They found that MAH grew more in the presence of red blood cells, multiplying at a rate dependent on blood cell concentration. Their exponential growth was even faster than the growth of MAH inside macrophages - typically targeted as parasitic hosts by mycobacteria. The findings, published in the journal Microbiology Spectrum, showed that pathogenic mycobacteria attach to human red blood cells, then capitalise on the relationship to multiply. Mycobacteria had previously been found outside macrophages at infection sites; the new findings suggest that the presence of those extracellular mycobacteria may be a result of the relationship with red blood cells. While red blood cells are best known for their role in transporting oxygen between lungs and tissues, they also play two roles in mycobacterial infections. They play a defensive role against infections by capturing pathogens and transferring them to macrophages in the liver and spleen to eliminate them. Nishiuchi said the study shows that red blood cells may also get targeted as host cells for mycobacteria. However, how these roles play out might determine the outcome of an infection. If the red blood cells' defense role is going well, the TB or other mycobacterial disease is controlled. But red blood cells overwhelmed by an attack of mycobacteria may help spread them throughout the body, Nishiuchi noted. (Agency) Read More► Commonly Used Anti-Nausea Drugs May Triple Stroke Risk