Antibiotics linked to higher death rate

A common antibiotic used to treat infections could be deadly for heart disease patients years after taking the drug. Clarithromycin, sold under the brand name Biaxin, is used to treat many skin, ear, sinus and lung infections.

People suffering from heart disease that took a two-week course of it had a significantly higher risk of heart attack or sudden death a year or more after they were treated for infection.

Clarithromycin belongs to a family of antibiotics called macrolides, which fight infections by blocking protein production in bacteria. Both clarithromycin and azithromycin-another common drug in the same family, sold as Z-Pak-are broad-spectrum antibiotics.

Respiratory infections have been shown, in some studies, to raise the risk of heart attack by as much as 17 percent, so it is key that heart disease patients get effective treatment for them quickly, but the FDA's trial suggests that clarithromycin could pose a similar risk to infection.
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Using smartphone app for detecting bacteria in food

Researchers have developed a smartphone app that alerts users of bacteria in their food using only a microscope attachment. There are very few methods for preventing food poisoning in part because testing for harmful bacteria such as E.Coli and salmonella requires specialized equipment and can take up to two days to show results.

 New technology from researchers at the University of Massachusetts Amherst changes that, delivering bacteria results in minutes using a smartphone app. Current methods for identifying bacteria associated with food poisoning are time-consuming because it is challenging to collect enough material.

The most common method involves rinsing potentially risky food, collecting small amounts of bacteria from the water and giving it 24 hours to multiply so there's enough to test.The tool developed at UMass uses a chemically-coated chip that binds to even the smallest amounts of bacteria. The university created a video showing how the prototype works: They rinse a potentially contaminated product with water and then place the chip into the water. Within half an hour, the microscope, which can attach to any type of smartphone camera, reveals the bacteria on the screen.

If you don't have the app, you can prevent food poisoning by: keeping the cooking area and your hands clean. Avoiding cross-contamination-raw meat, poultry, seafood and eggs can spread germs to ready-to-eat foods if not kept separate. Use separate cutting boards and plates when handling different foods. To cook food safely, the internal temperature must be high to kill the germs that could cause food poisoning-use a food thermometer.

Store foods properly-storing food properly is essential to combating harmful bacteria, expiration dates may not be accurate for some foods-strange smell or color may indicate that the food is not safe, frozen foods should be thawed in the refrigerator, in cold water, or in the microwave.
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Technology for accelerated wound healing

Researchers at Uppsala University and SLU have found a new way of accelerating wound healing. The technology involves using lactic acid bacteria as vectors to produce and deliver a human chemokine on site in the wounds. The research group is the first in the world to have developed the concept for topical use and the technology could turn out to be disruptive to the field of biologic drugs.

Treatment of large and chronic wounds are a high cost burden to the health care system since effective tools to accelerate healing are lacking. Wound care is today limited to mechanical debridement, use of different dressings and significant amounts of antibiotics preventing or treating wound infections. With the aging population, occurrence of chronic diseases such as diabetes and the alarming global spread of antibiotic resistance, a treatment that kick-starts and accelerates wound healing will have a significant impact.

There have been many attempts to solve the problem of chronic wounds that have failed. Drug candidates currently in late stage clinical trials comprise of growth factors, which are traditional protein-based biological drugs associated with high costs, and some trials have been prematurely terminated.

Researcher have developed a drug candidate, a next-generation biologic medical product, and are now publishing the fantastic results from the preclinical part where wound healing was strongly accelerated in mice," says Mia Phillipson, Professor at the Department of Medical Cell Biology, Division of Integrative Physiology, Uppsala University.

The acceleration of the healing process occurs due to changes in the microenvironment in the wound, which change the behaviour of specific immune cells. With the newly developed technology, the researchers can increase the level of a chemokine, CXCL12, for a sufficient time period through continuous delivery directly to the wound surface.

Bioavailability of CXCL12 is synergistically increased within the wound as the bacterial produced lactic acid causes a slight pH drop that inhibits degradation. The chemokine, CXCL12, is endogenously upregulated in injured tissue and by increasing the levels further, more immune cells are recruited and are more specialised to heal the wound, which accelerates the whole process.

The potent effect on acceleration of wound healing is demonstrated in healthy mice but also in two models of diabetes, one model of peripheral ischemia as well as in a model using human skin biopsies. There were clear differences in the composition of immune cells in the wounds and the immune cells present produced higher levels of TGFß at earlier time points. The treatment was local without systemic exposure.
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Roles of bacteria in colon cancer

Patients with an inherited form of colon cancer harbor two bacterial species that lead to development of the disease, and the same species have been found in people who develop a sporadic form of colon cancer, a study led by a Johns Hopkins Bloomberg~Kimmel Institute for Cancer Immunotherapy research team finds.

A second study by the same researchers shows a possible mechanism behind how one of these species spurs a specific type of immune response, promoting-instead of inhibiting the formation of malignant tumors. Together, these findings could lead to new ways to more effectively screen for and ultimately prevent colon cancer.

The Science findings describe a process in which these bacteria invade the protective mucus layer of the colon and collude to create a microenvironment-complete with nutrients and everything the bacteria need to survive that induces chronic inflammation and subsequent DNA damage that supports tumor formation.

These findings suggest a change in the standard of care for people who carry both types of bacteria. "More frequent colon cancer screening than the currently recommended once every 10 years should be considered," says Drew Pardoll, M.D., Ph.D., director of the Bloomberg~Kimmel Institute for Cancer Immunotherapy. Ultimately, once better understood, administering drugs or vaccines to prevent colonization of the bacteria in the colon, and potentially even probiotics to chase the bugs from the colon, are preventive measures that could be explored to interrupt the cancer-promoting process.

These new findings shows that particular strains of bacteria can invade the colon mucus in some patients who get colon cancer but who have no inherited predisposition for the disease. Unlike most bacteria, which do not make it past the colon's protective mucus layer, these communities of bacteria that invade the mucus form a sticky biofilm right next to the colon epithelial cells that line the colon, where colon cancer usually originates.

About 5 percent of colon cancers are caused by a hereditary syndrome called familial adenomatous polyposis (FAP), in which an inherited mutation launches a series of genetic changes that develop over time and eventually prompt the epithelial cells to turn malignant. However, it was unclear whether ETBF or other bacteria played a role in the progression to colon cancer in FAP patients.

To investigate the relationship between the bacteria-caused biofilms and cancer formation, researchers examined colon tissue removed from six FAP patients. Tests showed patchy sections of biofilms distributed along the colon's length in about 70 percent of the patients. The researchers used gene probes to identify the particular bacterial species and found that the biofilms consisted mainly of two types, Bacteroides fragilis and Escherichia coli, a surprising finding since the colon contains at least 500 different types of bacteria.

Tests on 25 additional colon samples from FAP patients showed that the B. fragilis strain was a subtype, called ETBF, which makes a toxin that triggers certain oncogenic, or cancer-promoting, pathways in colon epithelial cells and causes colon inflammation. The E. coli strain produced a substance called colibactin (synthesized by a set of genes in the bacterial genome called the PKS island), which causes DNA mutations.

FAP is a devastating disease that ultimately results in surgical removal of the colon, a Currently, using colonoscopy to monitor for the formation of precancerous tumors, called polyps, is the standard of care. Using a mouse model of colon cancer, the researchers found that animals whose colons were colonized with just one of these species developed few or no tumors. However, when their colons were colonized with both species simultaneously, they developed many tumors, suggesting a synergy between the two types of bacteria.

An earlier study suggested a unique type of immune response producing an inflammatory protein called IL-17-was key to ETBF-induced tumor formation. In order to prove the importance of IL-17 in the cancer-promoting effects of the bacterial combination, they used a mouse model in which the IL-17 gene was genetically deleted so it could not make IL-17, and colonized the mice with both ETBF and PKS+E. coli. Unlike animals that readily made IL-17, the genetically altered mice didn't form colon tumors, confirming the importance of this protein in bacterial-driven colon cancer.

However, in addition to IL-17, the studies showed that ETBF digested the mucus layer, enabling the PKS+ E. coli to adhere in larger numbers to the colon mucosa where together the bacteria induced increased DNA damage, a step preceding the gene mutations that underlie colon tumor formation. The complementary findings in Cell Host & Microbe demonstrate how ETBF's toxin prompts colon cancer to develop. Using a different mouse model of colon cancer, the researchers colonized the animals' colons with ETBF and then performed a series of tests to monitor the resulting cellular and molecular changes.

Their results revealed that ETBF's toxin spurs a cascade of events that promote colon inflammation that feeds back to act on the colon epithelial cells. First, the toxin triggers colon immune cells to produce IL-17. This inflammatory molecule then acts directly on the colon epithelial cells to trigger activation of a protein complex involved in promoting further inflammation, known as NFkappaB. NFkappaB in turn induces the colon epithelial cells to produce several signaling molecules that recruit more immune cells, called myeloid cells, to the colon.

These immune cells are involved in the inflammatory response and are known to support tumor growth. This process culminates in tumors forming in the colon. Additional experiments showed that a protein known as STAT3, which was previously shown to play a role in regulating cancer and inflammatory genes, is also necessary for tumor formation.
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Antibiotics with narrower targets for respiratory infections

Researchers who studied pediatric treatment practices in patients with earaches, strep throat and other common infections found that narrow-spectrum antibiotics, which act against a smaller range of bacteria, had fewer adverse effects than broad-spectrum antibiotics, which target a broader variety of bacteria. When judged by both practical and clinical outcomes, narrow-spectrum antibiotics performed equally well or better than broad-spectrum ones, with fewer disruptions to family routines.

The study reflects an "antimicrobial stewardship" approach, guiding healthcare providers to prescribe the most appropriate antibiotic for a patient's specific type of infection, with the aim of improving individual outcomes and reducing the overall risk of antibiotic resistance in which disease-causing microorganisms develop resistance to commonly used antibiotics.

Many children unnecessarily receive broad-spectrum antibiotics for common infections, which can lead to antibiotic resistance and unnecessary side effects," said study leader Jeffrey Gerber, MD, PhD, associate director for Inpatient Research Activities in the Center for Pediatric Clinical Effectiveness at Children's Hospital of Philadelphia (CHOP). "This study showed that inappropriate prescribing of antibiotics also affects families.

The study team performed two complementary studies in 31 primary care practices in CHOP's pediatric network in Pennsylvania and New Jersey, between January 2015 and April 2016. They drew on electronic health records of infants and children up to age 12 diagnosed with an acute respiratory tract infection (ARTI) and prescribed an oral antibiotic. In a retrospective cohort of approximately 30,000 patients, 14 percent received broad-spectrum drugs and 86 percent received narrow-spectrum drugs.

The ARTIs in the analysis were acute otitis media (earache), Group A streptococcal pharyngitis (strep throat) and sinusitis (sinus infection). ARTIs account for the majority of antibiotic exposures in children. In addition to assessing clinical outcomes in a retrospective cohort of 30,000 children, the researchers studied a prospective cohort of 2,472 children, doing telephone interviews with caregivers to measure outcomes that parents had identified as their highest concerns: adverse drug effects.

The study team found a significantly higher risk of adverse events for broad-spectrum antibiotics compared to narrow-spectrum antibiotics (3.7 percent vs. 2.7 percent as documented by clinicians, and 35.6 percent vs. 25.1 percent, as reported by patients and families). The rates of treatment failure were not significantly different between both types of antibiotics. Research tells us that antibiotic stewardship programs not only reduce the overall burden of antibiotic resistance, but also improve patient outcomes.
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Bacteria in milk linked to rheumatoid arthritis

A strain of bacteria found in milk and beef may be a trigger for developing rheumatoid arthritis in people who are at risk, according to a new study from the University of Central Florida. A team of UCF College of Medicine researchers has discovered a link between rheumatoid arthritis and Mycobacterium avium subspecies paratuberculosis, known as MAP, a bacteria found in about half the cows in the United States. The bacteria can be spread to humans through the consumption of infected milk, beef and produce fertilized by cow manure.

For the study, researchers recruited 100 of her patients who volunteered clinical samples for testing. Seventy-eight percent of the patients with rheumatoid arthritis were found to have a mutation in the PTPN2/22 gene, the same genetic mutation found in Crohn's patients, and 40 percent of that number tested positive for MAP. People born with this genetic mutation and who are later exposed to MAP through consuming contaminated milk or meat from infected cattle are at a higher risk of developing rheumatoid arthritis.

Rheumatoid arthritis is an autoimmune and inflammatory disease that causes the immune system to attack a person's joints, muscles, bones and organs. Patients suffer from pain and deformities mostly in the hands and feet. It can occur at any age but the most common onset is between 40 and 60 years old and is three times more prevalent in women. Some RA patients suffer from Crohn's disease and vice versa, the researchers say a national study needs to investigate the incidence of the two diseases in the same patients.
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Links between colonoscopy and appendicitis

Colonoscopy is the examination of the colon- the large intestine by a gastroenterologist. It is is associated with increased risk of appendicitis, there is an evidence to suggest that colonoscopy can cause appendicitis up to one week after colonoscopy in some patients. The rate of appendicitis and appendectomy in the first week after a colonoscopy is high.

The colon must be completely cleaned before colonoscopy, if bacteria within the colon are altered as the bowel is prepared prior to colonoscopy in ways that increase the likelihood of inflammation, or if the increased air pressure caused by colonoscopy, it may have effects on the colonic mucosa that can predispose people to appendicitis.

Appendicitis is a condition when the appendix becomes inflamed and filled with pus, colonoscopy is valuable and the appendicitis rate is still very low, right-lower abdominal pain after colonoscopy may be a sign of appendicitis.
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Broccoli can prevent colorectal cancer

Colorectal cancer is one of the most common cancers in the world, A team of researchers in the NUS Medicine lab of Associate Professor Matthew Chang have found a way to turn a humble bacteria and vegetables into a targeted system that seeks out and kills colorectal cancer cells. The study, which was led by Dr Chun-Loong Ho, will be published online today and in the current issue of Nature Biomedical Engineering.

At the heart of this cancer-targeting system is an engineered form of E. coli Nissle, a harmless type of bacteria found in the gut. Using genetic techniques, the team engineered the bacteria into a probiotic that attached to the surface of colorectal cancer cells and secreted an enzyme to convert a substance found in cruciferous vegetables (like broccoli) into a potent anticancer agent.

The idea was for the cancer cells in the vicinity to take up this anticancer agent and be killed. Normal cells cannot do this conversion, nor are they affected by the toxin, thus the system should be targeted only to colorectal cancer cells. True enough, the mixture of engineered probiotics with a broccoli extract or water containing the dietary substance killed more than 95% of colorectal cancer cells in a dish.

 Moreover, the mixture had no effect on cells from other types of cancer such as breast and stomach cancer. Strikingly, the probiotics-veggie combination reduced tumour numbers by 75% in mice with colorectal cancer. Also, the tumours that were detected in these mice were 3 times smaller than those in control mice which were not fed with the mixture.

These probiotics could be used in two ways: as prevention, to clean up the cancer cells remaining after surgical removal of tumours. Colorectal cancer patients may be able to take the probiotics as a dietary supplement along with their broccoli to prevent colorectal cancer or to reduce recurrence after cancer surgery.
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Gene therapy may kill HIV

Gene therapy may have the potential to eradicate HIV in people infected with the virus, new animal research suggests. The science centers around the use of "chimeric antigen receptor" (CAR) genes. In laboratory work with monkeys, these engineered cells have destroyed HIV-infected cells for more than two years, scientists reported.

T-cells are the cells that are largely responsible for human ability to fight off pathogens and get rid of infections in the body. Every T-cell has a unique receptor, or molecule, on it. That receptor allows the cell to recognize a specific target-a bacteria, or fungus or virus. And when it recognizes that target, it's called into duty to clear it from the body. Taking artificial receptors- CAR that can go on to these cells and allow them to recognize what we want them to recognize," he noted. "In this case that's HIV."

First, the team genetically engineered CAR to find and bind to simian/human immunodeficiency virus (SHIV), a lab-engineered HIV hybrid composed of human virus and monkey virus. Then the researchers modified the DNA of certain blood-forming stem cells so they would carry SHIV-killing CAR. The resulting cells were introduced into the bloodstream of four male juvenile SHIV-infected macaque monkeys.

The engineered cells successfully took up residence in each monkey's bone marrow. The cells moved widely throughout the body, targeting and killing SHIV-infected cells, without producing any notable adverse side effects. The advantage of the stem cell-based approach is that once these cells are grafted into the body, they continuously produce new T-cells that have this gene in them that can target HIV cells.

Plans are underway for a human trial, this study shows both that these cells will respond to HIV and that it's safe. This strategy is unlikely to fully work on its own, CAR will most likely need to be used with antiretroviral therapy. CAR therapy is already leading to impressive results in cancer and holds promise for HIV eradication.
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Bacteria obtain resistance from competitor

Bacteria not only develop resistance to antibiotics, they also can pick it up from their rivals. In a recent publication in Cell Reports, Researchers from the Biozentrum of the University of Basel have demonstrated that some bacteria inject a toxic cocktail into their competitors causing cell lysis and death. Then, by integrating the released genetic material, which may also carry drug resistance genes, the predator cell can acquire antibiotic resistance.

The frequent and sometimes careless use of antibiotics leads to an increasingly rapid spread of resistance. Hospitals are a particular hot spot for this. Patients not only introduce a wide variety of pathogens, which may already be resistant but also, due to the use of antibiotics to combat infections, hospitals may be a place where anti-microbial resistance can develop and be transferred from pathogen to pathogen. One of these typical hospital germs is the bacterium Acinetobacter baumannii. It is also known as the "Iraq bug" because multidrug-resistant bacteria of this species caused severe wound infections in American soldiers during the Iraq war.

The emergence and spread of multidrug resistance could be attributed, among other things, to the special skills of certain bacteria: Firstly, they combat their competitors by injecting them with a cocktail of toxic proteins, so-called effectors, using the type VI secretion system (T6SS), a poison syringe. They are able to uptake and reuse the released genetic material. In the model organism Acinetobacter baylyi, a close relative of the Iraq bug, Prof. Marek Basler's team at the Biozentrum of the University of Basel, has now identified five differently acting effectors. Some of these toxic proteins kill the bacterial competition very effectively, but do not destroy the cells.

The predator bacteria take up the released DNA fragments. If these fragments carry certain drug resistance genes, the specific resistance can be conferred upon the new owner. As a result, the antibiotic is no longer effective and the bacterium can reproduce largely undisturbed. Pathogens with such abilities are a major problem in hospitals, as through contact with other resistant bacteria they may accumulate resistance to many antibiotics -- the bacteria become multidrug-resistant. In the worst case, antibiotic treatments are no longer effective, thus nosocomial infections with multidrug-resistant pathogens become a deadly threat to patients.

The T6SS, as well as a set of different effectors, can also be found in other pathogens such as those which cause pneumonia or cholera. Interestingly, not all effectors are sufficient to kill the target cell, as many bacteria have developed or acquired antitoxins -- so-called immunity proteins. Antibiotics and anti-microbial resistance have existed for a long time. They developed through the coexistence of microorganisms and enabled bacteria to defend themselves against enemies or to eliminate competitors. This is one of the ways in which bacteria can conquer and colonize new environmental niches. With the use of antibiotics in medicine, however, the natural ability to develop resistance has become a problem. This faces researchers with the challenge of continually developing new antibiotics and slowing down the spread of drug resistance.
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Don't urinate before sex

New York City urologist David Kaufman explained the idea females should pee before intercourse is one of the biggest misconceptions he has to address with patients in his clinic. He stresses that urinating after sex is important, but warns going to the bathroom beforehand is not advisable. Urinating and consequently having enough urine stored up to create a strong stream, increases the odds of pushing bacteria out after sex.

Holding on will ensure full bladder to produce a stream strong enough to clear any bacteria in the urethra. Without any urine in the bladder, the bacteria can cause an infection. Not urinating after sex  can make cause bacterial to make its way into the bladder and develop into an infection. Women are far more susceptible to UTIs than men because of their anatomy. The female urethra is separated from the vagina and anus by just a small distance, making it easy for bacteria from either the vagina or bottom to reach it.

According to the NHS, using a diaphragm as contraception can increase your risk of getting a UTI, as the diaphragm may press on the bladder and prevent it emptying completely. You can do this to prevent UTI. Avoiding perfumed bubble bath, soap or talcum powder around your genitals-use plain, unperfumed varieties, and have a shower rather than a bath.

Going to the toilet as soon as you need to pee and always emptying your bladder fully. Staying hydrated,wiping your bottom from front to back when you go to the toilet, emptying your bladder as soon as possible after having sex,  not using a contraceptive diaphragm or condoms with spermicidal lubricant on them.Wearing underwear made from cotton, rather than synthetic material such as nylon, and avoiding tight jeans and trousers
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How to cure a burned mouth

Burns on the tongue heal faster than on the roof of the mouth, since the tongue has the most blood vessel supply in the entire body.

However, the pain can be searing since the skin here is more sensitive than other parts of the body, and it doesn't have any fat between the skin and the bones. As a result, it usually lingers two to three days.

Burned mouth can be healed quickly by sticking to a soft diet like yogurt and sushi, avoiding spice,noodles,soup, iced drink and hot foods eat lukewarm food - room temperature.

Coffee, wine and soda should all be off the menu for days. These foods are acidic, they will irritate skin as it's healing, potentially delaying the healing process.

Bacteria in an open wound can lead to infection and prevent healing. After a burn, brush your teeth thoroughly, use mouthwash, and drink plenty of water to wash out any built-up food or bacteria from your mouth.
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Viruses share gene with some organisms

A new study finds that viruses share some genes exclusively with cells that are not their hosts, viruses swap genes with a variety of cellular organisms and are agents of diversity. The study looked at protein structures in viruses and across all domains of life: from the single-celled microbes known as bacteria and archaea, to eukaryotes, a group that includes animals, plants, fungi and all other living things.

Viruses that infect archaea and bacteria, for example, are not known to infect eukarya. However, they may still interact in non harmful ways with organisms they do not infect. The team used a bioinformatics approach to analyze the genomes of organisms and the viruses that infect them. Rather than focusing on genetic sequences, which can change over the generations, the team examined the functional components of proteins, which they call folds.

 There are more than 1,400 of folds across all domains of life-has a unique 3-D structure that performs a specific operation. Because folds are critical to protein function, they remain stable even as the sequences that code for them change as a result of mutations or other processes.This makes protein folds reliable markers of evolutionary changes over vast time periods, especially for viruses that mutate notoriously fast.

The researchers found hundreds of folds that are present across all domaind of life and in all types of viruses, which suggests that they came from an ancient ancestor of all life forms. Some folds, however, occur only within a single domain and the viruses that infect it, suggesting a transfer of genetic material only between that group of viruses and their hosts. Out of a total of about 2,000 superfamilies of folds, the team found one that was exclusive to archaea and the viruses that infect archaea, 29 shared only by bacteria and the viruses that infect them, and 37 that are exclusive to eukaryotes and their viruses.

The data also point to other, as yet unknown, mechanisms that allow viruses to exchange genetic material with cells, many virus-hallmark genes in cellular organisms those viruses are not known to infect. People tend to think only about viruses that infect and kill their hosts, we have known for decades that a virus will sometimes enter into a cell and incorporate its genetic material into the cell without killing it. In the case of single-celled organisms, those genes are sometimes passed along to future generations. Human DNA, too, contains remnants of viruses.

Some retroelements and transposons are believed to have originated in ancient viruses. Retroelements are sequences copied from RNA viruses into DNA and inserted into the genomes of nonviral organisms. Transposons, also known as "jumping genes," can move from one part of the genome to another.The team also discovered a large subset of virus-specific protein folds that were not present in any cellular genomes. This suggests that viruses can create new genes and, potentially, transfer those genes to cellular organisms.
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Traumatic brain injury causes intestinal damage

Researchers has found a two-way link between traumatic brain injury (TBI) and intestinal changes. These interactions may contribute to increased infections and may worsen chronic brain damage. This is the first study to find that TBI in mice can trigger delayed, long-term changes in the colon and that subsequent bacterial infections in the gastrointestinal system can increase post traumatic brain inflammation and associated tissue loss.

These results indicate strong two-way interactions between the brain and the gut that may help explain the increased incidence of systemic infections after brain trauma and allow new treatment approaches. TBI has significant effects on the gastrointestinal tract, brain trauma can make the colon more permeable, potentially allowing harmful microbes to migrate from the intestine to other areas of the body, causing infection.

People are 12 times more likely to die from blood poisoning after TBI, which is often caused by bacteria, and 2.5 times more likely to die of a digestive system problem, compared with those without such injury.In this study, the researchers examined mice that received an experimental TBI. They found that the intestinal wall of the colon became more permeable after trauma. It is not clear how TBI causes these gut changes.

A key factor in the process may be enteric glial cells (EGCs), a class of cells that exist in the gut. These cells are similar to brain astroglial cells, and both types of glial cells are activated after TBI. After TBI, such activation is associated with brain inflammation that contributes to delayed tissue damage in the brain. Researchers don't know whether activation of ECGs after TBI contributes to intestinal injury or is instead an attempt to compensate for the injury.

The researchers also focused on the two-way nature of the process: how gut dysfunction may worsen brain inflammation and tissue loss after TBI. They infected the mice with Citrobacter rodentium, a species of bacteria that is the rodent equivalent of E. coli, which infects humans. In mice with a TBI who were infected with the bacteria, brain inflammation worsened.

Furthermore, in the hippocampus, a key region for memory, the mice who had TBI and were then infected lost more neurons than animals without infection. This suggests that TBI may trigger a vicious cycle, in which brain injury causes gut dysfunction, which then has the potential to worsen the original brain injury.
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Gum disease increases the risk of breast cancer

Gum disease increases women's risk of breast cancer up to three times. This is thought to be due to the bacteria that causes inflammation in the mouth entering the circulation via the gums and going into breast tissue, which can result in cancer.

Severe gum disease, known as periodontitis, can affect the bones in people's jaws and cause teeth to fall out. Higher levels of certain bacteria that are linked to gum disease increase an individual's likelihood of developing the condition.

It is unclear whether it is the bacteria themselves or gum disease that leads to foodpipe tumors. Researchers argue their findings highlight the importance of good oral hygiene, including brushing teeth twice a day and regular dentist visits, to maintain people's dental health, as well as avoiding other complications.

 Researchers examined women visiting gynecology, some of the participants had breast cancer. The cases and controls were matched according to smoking status and alcohol intake. All of the participants were assessed for gum inflammation at six sites per tooth.

 Gum disease increases the risk of breast cancer by up to three times Results reveal women with severe gum disease are up to three times more likely to have breast cancer. There is no link between tooth loss and developing the disease. Severe gum disease is associated with instances of breast cancer and this may be through spread of infection and inflammation starting in the mouth.
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Managing antibiotics can not reverse the resistance

Researchers have discovered that reducing the use of antibiotics will not be enough to reverse the growing prevalence of antibiotic resistance for some types of bacteria. Besides passing along the genes bestowing antibiotic resistance to their offspring, many bacteria can also swap genes among themselves through a process called conjugation.

The bacteria tested by researchers have fast conjugation rate, even if you don't use antibiotics the resistance can be maintained. Most resistance to antibiotics arises and spreads through natural selection. Some bacteria have genes that help them survive around of antibiotics, they quickly parent the next generation and pass on those genes.

Many of these genes, however, come at a cost. For example, a mutation may allow a bacterium to build a thicker membrane to survive a particular antibiotic, but that mutation might also make it more difficult for the cell to reproduce. Without the selective pressure of antibiotics killing off the competition, bacteria with this mutation should disappear over time.

The results indicate that for bacteria that swap resistance genes simply managing the amount of antibiotics being used will not turn the tide on the growing problem of resistance. To make any headway, drugs will also be needed that stop the sharing of genes and decrease the rate at which they are passed on through reproduction. One of the drugs is a benign natural product and FDA-approved antipsychotic.
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The secrets of Ebola

In a comprehensive and complex molecular study of blood samples from Ebola patients in Sierra Leone. Conducting a sweeping analysis of everything from enzymes to lipids to immune-system-associated molecules, the teamfound 11 biomarkers that distinguish fatal infections from nonfatal ones and two that, when screened for early symptom onset, accurately predict which patients are likely to die.

Health workers collected blood samples from patients after they were diagnosed with Ebola and at multiple points thereafter.They obtained 29 blood samples from 11 patients who ultimately survived and nine blood samples from nine patients who died from the virus. For comparison, the research team also obtained blood samples from 10 healthy volunteers with no exposure to Ebola virus.
"Our team studied thousands of molecular clues in each of these samples, sifting through extensive data on the activity of genes, proteins and other molecules to identify those of most interest.

The team found that survivors had higher levels of some immune-related molecules, and lower levels of others compared to those who died. Plasma cytokines, which are involved in immunity and stress response, were higher in the blood of people who perished. Fatal cases had unique metabolic responses compared to survivors, higher levels of virus, changes to plasma lipids involved in
processes like blood coagulation, and more pronounced activation of some types of immune cells.

Pancreatic enzymes also leaked into the blood of patients who died, suggesting that damage from these enzymes contributes to the tissue damage characteristic of fatal Ebola virus disease. The study showed that levels of two biomarkers, known as L-threonine (an amino acid) and vitamin D binding protein, may accurately predict which patients live and which die. Both were present at lower levels at the time of admission in the patients who ultimately perished.

When Ebola virus leads to death, experts believe it is because of overwhelming viral replication. Symptoms of infection include severe hemorrhaging, vomiting and diarrhea, fever and more. In the current Ebola study, the team found that many of the molecular signals present in the
blood of sick, infected patients overlap with sepsis, a condition in which the body in response to infection by bacteria or other pathogens mounts a damaging inflammatory reaction.
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Gut bacteria may change after severe injury

After a severe traumatic injury, the composition of a patient's intestinal bacteria changes and this could affects patient's prognosis. The gut microbiome experiences a depletion in the presence of some bacteria and an increase in the presence of others came from a small investigation, involving critically injured adults.

Stool samples were collected from each person three times: when they were admitted to the hospital, and then 24 and 72 hours later. The samples were compared with those from 10 other patients who had not sustained traumatic injury.

Samples taken at the time of admission were similar in both groups. But within 24 hours, differences started to show, the investigators found. By 72 hours, three types of bacteria were depleted in the traumatic injury group, relative to the non-injury group, and the levels of two other types of bacteria had risen.

Rapid alterations in intestinal microbiota represent a critical and unrecognized phenomenon that may influence clinical course and outcomes after severe trauma. The intestinal bacterial composition could in some way be critical to patient outcomes after a traumatic injury. This could create the way towards interventions, such as administering probiotic regimens that might improve patient outcomes after injury.
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Exposing children to germs and pets reduces the risk of asthma

Asthma is a chronic disease that frequently aggravates and narrows the airways, leading to wheezing, coughing, breathlessness and a tight chest.

According to National Institute of Health, contact with cats, dogs, mice and cockroach at three months lowers chance of having asthma by age seven. Exposure to certain bacteria in house dust during infancy was also associated with a reduce risk.

According to a study, exposing children to pets and germs early reduces their risk of developing asthma. Exposure to allergens early in life, before asthma develops, has a preventive effect.

Early-life environment can influence the development of certain health conditions, preventing asthma before it develops is the best method of preventing it. Exposure to different indoor allergens, bacteria and bacterial products early in life may reduce the risk of developing asthma.

Researchers discovered that higher concentrations of cockroach, mouse and cat allergens present in dust samples collected from the children's homes at three months were linked to a lower risk of asthma by age seven.
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Aspiring could reverse tooth decay

Tooth decay occurs when acid in the mouth dissolves the enamel and dentine of the teeth causing formation of holes or cavities. The acid is produced by bacteria that are found within the plaque and thin film that builds up on the teeth.

Aspirin could reverse the effects of tooth decay by triggering teeth to self-reported, reducing the need for filling.
The drug can form new dentine, the hard tooth structure that is usually damaged by decay.

When we eat sugar it interacts with the bacteria within the plaque to produce the destructive acid. If the plaque is allowed to build up, the acid can begin to break down the surface of tooth, causing holes.

After the damage, the cavity begins to eat away at the second level of tooth material that lies beneath the enamel: the dentin. Tooth decay can lead to tooth abscesses, which may result in the tooth having to be removed.

A filling can be used to stop the bacteria in order to prevent the cavity from reaching the tooth's pulp. Fillings may fail and may need to be replaced many times during the life time of the tooth.

Low dose of aspirin increased the rebuilding of minerals which restores strength and function of the tooth, it also stimulated existing stem cells in the tooth to regenerate the damaged tooth structure.
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