Common antibiotic may be the answer to many multidrug-resistant bacterial infections

Common antibiotic may be the answer to many multidrug-resistant bacterial infections (Neat, because the assumptions of the medical mob, proved not so correct for a long period of time, and until somebody bothered to say 'Really, let's test that!' Sounds a lot like D3 fears of overdose, or apylori?? the gut bacteria that causes ulcers....until somebody asked if it was a bacteriologic infection not do to acid indigestion) Contrary to current medical dogma, researchers at University of California, San Diego School of Medicine and Skaggs School of Pharmacy and Pharmaceutical Sciences report that the common antibiotic azithromycin kills many multidrug-resistant bacteria very effectively -- when tested under conditions that closely resemble the human body and its natural antimicrobial factors. The researchers believe the finding, published June 10 by EBioMedicine, could prompt an immediate review of the current standard of care for patients with certain so-called "superbug" infections. Azithromycin is the most often prescribed antibiotic in the United States, where short courses can cure common bacterial infections such as strep throat and sinusitis. But azithromycin, also sold commercially as Zithromax Z-Pak, is never given to patients with some of the most nefarious multidrug-resistant bacterial infections. That's because years of testing in standard laboratory media -- the nutrient broth that helps bacteria grow -- concluded that azithromycin doesn't kill these types of bacteria. "Unquestioning adherence to a single standardized lab practice may be keeping doctors from considering potentially life-saving antibiotics -- therapies that are proven safe and readily available in any hospital or pharmacy," said senior author Victor Nizet, MD, professor of pediatrics and pharmacy. "While bacterial agars and testing media are useful in providing consistency for hospital laboratories around the world, the actual infection is taking place in the blood and tissues of the patient, and we know the action and potency of drugs can change quite dramatically in different surroundings." The bacteria at the center of this study are Gram-negative rods, so-called due to their cell wall structure (they appear "negative" in a classic typing test known as the Gram stain) and their shape. Nizet's team studied extremely antibiotic-resistant strains of three medically important Gram-negative rods:Pseudomonas aeruginosa, Klebsiella pneumoniae and Acinetobacter baumannii. These opportunistic pathogens rarely infect healthy people but instead strike debilitated patients in hospitals, such as those with weakened immune systems, or following trauma or surgery, sometimes with deadly consequences. The Centers for Disease Control and World Health Organization have warned that resistance is rapidly spreading in these species, and no new antibiotic candidates are on the horizon. In this study, Nizet's team found that simply growing these Gram-negative rod bacteria in mammalian tissue culture media -- the same stuff used to sustain human cells in the lab -- instead of standard bacteriologic media made a huge difference in their sensitivity to azithromycin. Even more striking, the drug-resistant superbugs were completely wiped out when azithromycin was paired with the antibiotic colistin or with antimicrobial peptides produced naturally by the human body during infection. To test these promising laboratory results in a live infection system, Nizet and team moved the experiment into a mouse model of multidrug-resistantA. baumannii pneumonia. They treated the mice with a single injected dose of azithromycin at a concentration that mimics the amount typically given by IV to human patients. Twenty-four hours after infection, azithromycin-treated mice had 99 percent fewer bacteria in their lungs than untreated mice. Similarly, in mouse models of multidrug-resistant P. aeruginosa and K. pneumoniae infections, a single dose of azithromycin reduced bacterial counts by more than 10-fold. According to the authors, the study suggests that the general effectiveness of antibiotics in the decades since the discovery of penicillin has led to complacency in our approach to antibiotic evaluation. In the current era of ever-increasing antibiotic resistance, they recommend a more holistic approach that considers both the bug and the patient's immune system. "If something this simple could be overlooked for so many years, what else might we be missing?" Nizet said. Story Source: The above story is based on materials provided by University of California, San Diego Health Sciences. The original article was written by Heather Buschman. Note: Materials may be edited for content and length.

Get Your solid Eight. (Even if you have to exercise to relax enough!)

A new study suggests that one night of partial sleep deprivation promotes biological aging in older adults. Results show that one night of partial sleep deprivation activates gene expression patterns in peripheral blood mononuclear cells (PBMCs) consistent with increasing accumulation of damage that initiates cell cycle arrest and increases susceptibility to senescence. These findings causally link sleep deprivation to the etiology of biological aging, and further supports the hypothesis that sleep deprivation may be associated with elevated disease risk because it promotes molecular processes involved in biological aging. "Our data support the hypothesis that one night of not getting enough sleep in older adults activates important biological pathways that promote biological aging," said lead author Judith Carroll, PhD, assistant professor of psychiatry and biobehavioral science at the UCLA Cousins Center for Psychoneuroimmunology in Los Angeles, Calif. The research abstract was published recently in an online supplement of the journal Sleep and will be presented June 10, in Seattle, Washington, at SLEEP 2015, the 29th annual meeting of the Associated Professional Sleep Societies LLC. The study group comprised 29 community-dwelling older adults. They were age 61-86 years and 48 percent were male. Participants underwent an experimental partial sleep deprivation protocol over four nights, including adaptation, an uninterrupted night of sleep, partial sleep deprivation (restricted 3 a.m. -- 7 a.m.) and another uninterrupted night of sleep (recovery). Blood samples were obtained each morning to assess PBMC gene expression using Illumina HT-12 arrays. Story Source: The above story is based on materials provided by American Academy of Sleep Medicine. Note: Materials may be edited for content and length.

Heart attack risk increases 16-21% with use of common antacid

Heart attack risk increases 16-21% with use of common antacid

[[Personal Experience: The Doctors screwed-up my mother's stomach with all kinds of pills, gave her a proton pump inhibitor to cure the reflux, and, then shook their heads sadly when she died of a heart attack. Think about what it is they feed you to cure you!]]

Adults who use proton pump inhibitors are between 16 and 21 percent more likely to experience a heart attack than people who don't use the commonly prescribed antacid drugs, according to a massive new study by Houston Methodist and Stanford University scientists.

An examination of 16 million clinical documents representing 2.9 million patients also showed that patients who use a different type of antacid drug called an H2 blocker have no increased heart attack risk. The findings, reported in PLOS ONE, follow aCirculation report in 2013 in which scientists showed how -- at a molecular level -- PPIs might cause long-term cardiovascular disease and increase a patient's heart attack risk.

"Our earlier work identified that the PPIs can adversely affect the endothelium, the Teflon-like lining of the blood vessels," said John Cooke, M.D., Ph.D., a senior author of the PLOS ONE report. "That observation led us to hypothesize that anyone taking PPIs may be at greater risk for heart attack. Accordingly, in two large populations of patients, we asked what happened to people that were on PPIs versus other medications for the stomach."

The PLOS ONE study's principal investigator was Stanford vascular medicine specialist Nicholas J. Leeper, M.D.

In the present study, the researchers found a clear and significant association between exposure to PPIs and the occurrences of heart attack.

"By looking at data from people who were given PPI drugs primarily for acid reflux and had no prior history of heart disease, our data-mining pipeline signals an association with a higher rate of heart attacks," said the PLOS ONE report's lead author, Nigam H. Shah, M.B.B.S., Ph.D., an assistant professor of biomedical informatics at Stanford, where the work was done. "Our results demonstrate that PPIs appear to be associated with elevated risk of heart attack in the general population, and H2 blockers show no such association."

The estimated increase of heart attack risk ranges from 16 to 21 percent, because of uncertainty in the estimation process, Shah said.

The FDA estimates about 1 in 14 Americans has used proton pump inhibitors. In 2009, PPIs were the third-most taken type of drug in the U.S., and are believed to account for $13 billion in annual global sales. Doctors prescribe PPIs to treat a wide range of disorders, including gastro-esophageal reflux disease, or GERD, infection by the ulcer-causing bacteriumHelicobacter pylori, Zollinger-Ellison syndrome, and Barrett's esophagus. The drugs can also be purchased over the counter. PPIs come in a variety of slightly different chemical forms, always ending with the suffix "-prazole," for example, omeprazole or lansoprazole. Brand examples of PPIs are Nexium, Prilosec, and PrevAcid.

H2 blockers are another type of antacid drug. They are not believed to be associated with increased risk of heart attack or cardiovascular disease. Examples of the drug are cimetidine and ranitidine. Brand examples of H2 blockers are Zantac and Tagamet.

The researchers collected data from two repositories -- STRIDE (Stanford Translational Research Integrated Database Environment), which contains information about 1.8 million Stanford hospital and clinic patients, and a subset of information for 1.1 million patients from the Web-based electronic medical records company Practice Fusion, Inc. Both sources of patient information were anonymized before the researchers accessed the data.

The group scanned the databases for patients who were prescribed proton pump inhibitors or other drugs, such as H2 blockers, and also looked to see if a given patient had a mention of having experienced a major cardiovascular event, such as myocardial infarction (heart attack), in their medical record.

Patients who had used PPIs were found to be at 1.16-1.21-fold-increased risk of heart attack.

Scrutiny of PPIs has only increased with time. Initially it was believed PPIs only posed a risk to a very narrow subset of patients -- those with coronary artery disease who were using the anti-platelet drug clopidogrel to prevent future heart attacks.

"Investigators originally assumed this was due to a drug-drug interaction between these compounds, and the FDA went so far as to release a warning about their concomitant use," said Nicholas Leeper.

A 2013 report to Circulation by several of the present report's coauthors, including Cooke, raised the possibility that PPIs could lead to cardiovascular disease in the general population.

"This led us to use powerful 'big-data' approaches to try to determine whether PPIs might in fact be associated with risk in 'all comers,' Leeper said. "Our report raises concerns that these drugs -- which are available over the counter and are among the most commonly prescribed drugs in the world -- may not be as safe as we previously assumed."

In the future, the researchers say they hope to conduct a large, prospective, randomized trial to determine whether PPIs are harmful to a broader population of patients.


Story Source:

The above story is based on materials provided by Houston Methodist.Note: Materials may be edited for content and length.