Shield Eyes From Infection During Monsoon

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While enjoying the rainy season, don’t forget to take care of your eyes as the climate also encourages infective microorganisms to thrive. Avoid infections like conjunctivitis, sties, dry eyes and corneal ulcers by using clean towels and more, say experts.

Uma Singh, Medical Consultant at Ozone Group, Gowri Kulkarni, Head of Medical Operations, DocsApp and Shailja Mittal, Creative Head at Zapyle, have listed ways to avoid eye problems:

* Most eye diseases are transmitted by hand-to-eye contact. Therefore, wash your hands before touching your eyes in order to reduce or prevent infection.

* Avoid rubbing your eyes as that only increases the chances of spreading the infection. Instead, use disposable tissues to wipe off the overflowing discharge or tears.

* Avoid getting wet in the rain. Always wear adequately protective rain gear.

* Be careful of dirty water, muck and dampness during the monsoon season.

* Do not use contact lenses if you have eye-irritation, red eye or any form of abnormal discharge.

* Be careful about using expired make-up around your eyes, and if using contact lenses, make sure you never share your solution or container with someone else.

* Don’t share personal products with others. Items like handkerchiefs, sunglasses and contact lenses should not be shared with others because they can carry highly contagious infections.


Why HIV Infection Ups Tuberculosis Risk

Why HIV Infection Ups Tuberculosis Risk

LONDON: Researchers have found that the HIV virus increases the potency of the tuberculosis bacterium (Mtb) by affecting a central function of the immune system.

In most people who are exposed to tuberculosis infection, the immune defence deals with the bacteria by enclosing them in a special scar tissue. In this condition the tuberculosis is said to be “latent”. Around 10 per cent of those with latent tuberculosis go on to develop active disease.

“The risk of infection progressing to active tuberculosis is around 30 times higher for people who are HIV-positive. But the reason for this has not been known at the cellular level,” said lead researcher Robert Blomgran from Linkoping University in Sweden.

The new study, published in the American Journal of Pathology, describes how the researchers looked in more detail at what happens in one particular type of immune cell, known as dendritic cells.

These play an important role in the immune defence. Dendritic cells break down tuberculosis bacteria and other foreign microorganisms, and display the bacteria fragments at the cell surface.

Other cells of the immune system, in particular T-cells, recognise the fragments and bind to them.
The dendritic cell then activates the T-cell such that it can kill the tuberculosis bacteria efficiently.

In this way, dendritic cells act as a communication link between the innate immune defence and the specific immune defence, of which the T-cells are part.

The researchers infected human dendritic cells with both Mtb and the HIV virus. They showed that co-infection reduced the ability of the dendritic cells to present foreign molecules to the immune defence.

They also had a lower capacity to activate tuberculosis-specific T-cells than was the case when the dendritic cells were infected with Mtb alone.

“We have now shown that HIV has a clear effect also on the innate immune defence, in particular the dendritic cells, which link the innate and the adaptive immune defences,” Blomgran said.

Antibiotic History Of A Hospital Bed May Increase A Patient’s Risk Of Infection: Study

Antibiotic History Of A Hospital Bed May Increase A Patient's Risk Of Infection: Study

If the previous occupant of a hospital bed received antibiotics, the next patient who uses that bed may be at higher risk for a severe form of infectious diarrhea, according to a new study.

Clostridium difficile (C. diff) diarrhea causes 27,000 deaths each year in the US Hospital patients taking antibiotics are particularly at risk for it, say the authors of the study. Antibiotics disturb the normal healthy bacteria of the gut so a C. diff infection can take hold.

The new study shows that “antibiotics given to one patient may alter the local microenvironment to influence a different patient’s risk” for C. diff infection, the researchers wrote in JAMA Internal Medicine.

“Other studies have also demonstrated that antibiotics can have a ‘herd’ effect – in other words, that antibiotics can affect people who do not themselves receive the antibiotics,” said lead author Dr. Daniel Freedberg of Columbia University Medical Center in New York.

Freedberg and his colleagues studied more than 100,000 pairs of patients who sequentially occupied a given hospital bed in four institutions between 2010 and 2015, not including those who had recent C. diff infection or whose prior bed occupant was in the bed for less than 24 hours.

More than 500 patients, or less than 1 per cent of the total group, developed a C. diff infection as the second bed occupant.

The infections were 22 per cent more likely when then previous occupant had received antibiotics.

Other factors about the previous bed occupant were not associated with C. diff risk.

People can be carrying C. diff organisms without having any symptoms, Freedberg told Reuters Health by email. When these colonized patients receive antibiotics, C. diff may expand within their gut microbiome and start shedding more spores, which means more spores on the bed, the bedside table, the floor, and other areas, he said.
“The next patient who enters the room is thus more likely to be exposed to C. diff spores,” he said. “It’s not easy to sterilize the room/bed between patients because C. diff spores are extremely hardy. To be killed, they need to be soaked in a bleach-containing cleaning agent for an adequate amount of time.”

About half of patients in acute care facilities take antibiotics on any given day, said Kevin Brown of the University of Toronto Dalla Lana School of Public Health, who was not part of the new study.

“That’s a huge portion of patients that could be involved in spreading the infection,” Brown told Reuters Health by email.

But the increased risk is modest, Freedberg added.

“There was a 22 percent relative increase in risk for C. diff with the prior patient’s antibiotics but there was a four-fold increase in risk related to the antibiotics received by the patient him- or herself,” he said.

Other patients, such as other antibiotic user patients within the ward, could have contributed increased risk as well, Brown said.

“Doctors (and patients) should avoid antibiotics in situations where they are not necessary,” Freedberg said. “Too often, antibiotics are prescribed without clear indications.”

“I think this evidence needs to be taken just as an association that needs further exploration,” said Jack A. Gilbert of Argonne National Laboratory in Argonne, Illinois, who was not part of the new study.

“While it would be tempting to use these results to change policy, there are so many uncertainties here that such a move would not be advisable.”


New blood cells fight mind infection

Hyperactivity of our immune system can cause a state of chronic irritation. If continual, the inflammationwill have an effect on our frame and result in ailment. inside the devastating disease more than onesclerosis, hyperactivity of immune cells called T-cells set off continual infection and degeneration of thebrain. Researchers at BRIC, the college of Copenhagen, have diagnosed a brand new form of regulatory blood cells that can combat such hyperactive T-cells in blood from sufferers with multiple sclerosis. bystimulating the regulatory blood cells, the researchers appreciably decreased the extent of braininflammation and disorder in a organic version. The outcomes are posted in the magazine Naturemedicinal drug.

Molecule activate 07b031025f5f96dfa8443f843db463b6 blood cells

the brand new blood cells belong to the organization of our white blood cells known as lymphocytes. The cells specific a molecule referred to as FoxA1 that the researchers observed is chargeable for the cells’development and suppressive features.

“We knew that a few unidentified blood cells have been able to inhibit more than one sclerosis-like ailmentin mice and through gene analysis we determined out, that these cells are a subset of our lymphocytes expressing the gene FoxA1. Importantly, whilst placing FoxA1 into normal lymphocytes with gene remedy, we ought to alternate them to actively modify infection and inhibit multiple sclerosis, explains relatedprofessor Yawei Liu leading the experimental research.

Activating personal blood cells for remedy of disease

FoxA1 expressing lymphocytes were no longer recognised until now, and that is the first documentation of their importance in controlling a couple of sclerosis. The variety of human beings residing with this devastating disease round the arena has increased by means of 10 percentage in the beyond five yearsto 2.3 million. It affects women two times more than guys and no curing remedy exists. The studiesorganization headed through professor Shohreh Issazadeh-Navikas from BRIC tested blood of patients withmore than one sclerosis, before and after years of remedy with the drug interferon-beta. They observedthat sufferers who enjoy the remedy growth the wide variety of this new blood cell type, which fightsickness.

“From a healing standpoint, our findings are surely exciting and we are hoping that they could helpfinding new treatment alternatives for patients no longer cashing in on current capsules, mainly extrapersistent and revolutionary a couple of sclerosis patients. In our model, we could set off lymphocyteswith the aid of chemical stimulation and gene remedy, and we are curios whether this may be a brand new treatment method,” says professor Shohreh Issazadeh-Navikas.

And that is precisely what the research organization will recognition on at subsequent degree in theirresearch. they’ve already started to check whether the new FoxA1-lymphocytes can save you degradation of the nerve mobile‘s myelin layer and brain degeneration in a model of modern more than one sclerosis.besides more than one sclerosis, knowledge on a way to save you persistent inflammation can also betreasured for different autoimmune sicknesses like type 1 diabetes, anti inflammatory bowel ailment and rheumatoid arthritis, in which infection is a main reason of the sickness.

Scientists unpack how Toxoplasma infection is linked to neurodegenerative disease

Toxoplasma gondii, a protozoan parasite about 5 microns lengthy, infects a third of the world‘s population. Ingested via undercooked meat or unwashed veggies, the parasite infects 15-30 percent of the united states population. In France and Brazil, up to 80 percentage of the populace has the contamination.

particularly dangerous throughout being pregnantinfection in pregnant ladies can reason criticalcongenital defects or even demise of the fetus — this persistent infection has two components: the unicellular parasite, and inflammation of tissues it reasons.

working on mice (like all mammals, a herbal host for this parasite), a college of California, Riverside groupof biomedical scientists reports inside the magazine PLOS Pathogens that Toxoplasma infection ends in a disruption of neurotransmitters inside the mind and postulates that it triggers neurological disorder in the ones already predisposed to this kind of disorder.

They notice that Toxoplasma infection results in a extensive increase in glutamate — the number one andmaximum critical neurotransmitter within the mind, which transmits excitatory indicators among neurons. This glutamate boom is “extracellular,” that means out of doors the cell, and is precisely managed by using specialized cells inside the primary apprehensive system (mind and spinal cord), known asastrocytes. Glutamate buildup is visible in disturbing mind damage in addition to especially pathological and neurodegenerating diseases inclusive of epilepsy, multiple sclerosis and amyotrophic lateral sclerosis (ALS).

One position astrocytes play is to cast off extracellular glutamate, lest it growth to pathological ranges that would harm neurons. that is commonly done using a glutamate transporter, called GLT-1, tasked with regulating extracellular glutamate. GLT-1 soaks up glutamate released by means of neurons and converts itreturned into the more secure substance glutamine, which could then be utilized by cells for strength.

whilst a neuron fires it releases glutamate into the gap among itself and a close-by neuron,” defined lead researcher Emma H. Wilson, an partner professor within the department of Biomedical Sciences in thefaculty of medicine, who has worked on toxoplasmosis for greater than 15 years. “The nearby neuron detects this glutamate which triggers a firing of the neuron. If the glutamate is not cleared by way of GLT-1 then the neurons can not fireplace well the following time and they start to die.”

Wilson and her crew discovered that in toxoplasma infection, astrocytes swell and are not capable ofmodify extracellular glutamate concentrations. similarly, GLT-1 isn’t always expressed nicely. This ends ina buildup of the glutamate launched from neurons and the neurons misfire.

those effects recommend that during assessment to assuming chronic Toxoplasma infection as quiescent and benign, we need to be aware of the ability threat to regular neurological pathways andchanges in mind chemistry,” Wilson said.

when the researchers treated the infected mice with ceftriaxone, an antibiotic regarded to supplybeneficial consequences in mouse models of ALS as well as neuroprotection in an expansion of primaryanxious device accidents, they found that GLT-1 turned into upregulated. This recovery of GLT-1 expression appreciably decreased extracellular glutamate from pathological to ordinary concentrations, returning neuronal feature to a normal country.

we have shown for the primary time the direct disruption of a prime neurotransmitter in the brain as a consequence of this contamination,” Wilson stated. “more direct and mechanistic research needs to becompleted to apprehend the realities of this very commonplace pathogen.”

subsequent, Wilson and her colleagues will research what initiates the downregulation of GLT-1 at some stage in persistent Toxoplasma infection.

in spite of the significance of this transporter to retaining glutamate homeostasis, there may be littleinformation of the mechanism that governs its expression,” Wilson stated. “we’d want to understand how cells, which include peripheral immune cells, control the parasite in the brain. Toxoplasma contaminationconsequences in the lifelong presence of parasitic cysts inside the neurons inside the mind. we mightlike to similarly develop a challenge targeted on killing the cysts, that’s where the parasite hides from the immune response for the rest of the inflamed person‘s life. putting off the cyst gets rid of the threat of reactivation of the parasite and the danger of encephalitis even as additionally allowing us to limitchronic inflammation within the brain.”

Mysteriously, the parasite that causes toxoplasmosis can sexually reproduce simplest in cats. Asexually, it could reflect and stay in any mammalian cellular that has a nucleus. indeed, the parasite has beendetermined in each mammal ever examined.

put upcontamination, a equipped immune machine is needed to save you parasite reactivation and encephalitis. inflamed people with compromised immune systems need to be on prophylactic pills forlifestyles. otherwise they’re susceptible to cyst reactivation and death. The parasite lives in areas of thebrain which have the capacity to disrupt positive behaviors including dangerin search of (infected mice will run closer to cat urine instead of far from it).

The parasite isn’t always as latent or dormant as researchers once concept. cases of congenital infectionand retinal toxoplasmosis are on the upward push (the brain and retina are closely connected). peoplewho’ve schizophrenia are much more likely to be inflamed with Toxoplasma. infection shows a fewcorrelation with Alzheimer’s disorder, Parkinson’s disease and epilepsy.

although, Wilson notes that infection is no reason for principal fear.

“We have been living with this parasite for a long term,” she stated. “It does no longer want to kill its host and lose its home. The nice manner to save you infection is to cook your meat and wash your palms andveggies. And in case you are pregnant, do not trade the cat muddle.”



What ingredients can help combat the threat of continual infection?

a new study by means of the college of Liverpool’s Institute of ageing and persistent disease has diagnosedmeals stuffs that could help save you persistent irritation that contributes to many leading reasons of death.

inflammation takes place evidently inside the frame but whilst it is going incorrect or goes on too long, it is able to trigger sickness tactics. out of control infection plays a role in lots of most important sicknesses,which includes cancer, heart disorder, diabetes and Alzheimer’s disorder.

Diets rich in culmination and vegetables, which contain polyphenols, shield in opposition to age-relatedinflammation and chronic sicknesses.

cellular-to-cellular conversation

Polyphenols are plentiful micronutrients in our eating regimen, and evidence for their function in theprevention of degenerative diseases inclusive of most cancers and cardiovascular illnesses is alreadyemerging. The health outcomes of polyphenols rely on the amount ate up and on their bioavailability.

T-cells, or T-lymphocytes, are a kind of white blood cell that circulate around our bodies, scanning for cellularabnormalities and infections. They contribute to cellular signalling molecules (cytokines) that resourcemobile-to-mobile communique in immune responses and stimulate the movement of cells towards sites ofirritation, contamination and trauma. Cytokines are modulated with the aid of fruit and vegetable intake.

Little is known approximately the relative potency of various (poly)phenols in modulating cytokine release by means of lymphocytes.

seasoned-inflammatory mediators

The take a look at, carried out by using Sian Richardson and Dr Chris Ford from the university‘s Institute ofgetting old and continual disorder, tested the one-of-a-kind potencies of the polyphenols.

Sian Richardson, said: “The outcomes of our have a look at propose that (poly)phenols derived from onions, turmeric, crimson grapes, inexperienced tea and a├žai berries may additionally help lessen the release ofpro-inflammatory mediators in humans susceptible to chronic inflammation.

“Older human beings are greater susceptible to continual irritation and as such they will benefit from supplementing their diets with isorhamnetin, resveratrol, curcumin and vanillic acid or with meals resourcesthat yield these bioactive molecules.”