Edmund’s Blog

When you’re doing your spring cleaning, don’t forget your nose.

Nasal irrigation is a cheap and easy way for people with spring allergies, nasal congestion, stuffy noses and post-nasal drip to get relief, says Dr. Melissa Pynnonen, co-director of the Michigan Sinus Center and an assistant professor in the University of Michigan’s department of otolaryngology.

Nasal irrigation involves rinsing the nose and nasal passages with a solution made with a quarter-teaspoon of kosher salt, eight ounces of warm tap water and a quarter-teaspoon of baking soda.

There are a number of ways to administer the solution. For people who’ve never done nasal irrigation, Pynnonen recommended using an eight-ounce squeeze bottle and squirting four ounces of the solution into each nostril. The solutions exits through the opposite nostril. Opening your mouth and making a “K” sound will prevent the solution from coming out of your mouth.

Some people use a neti-pot, which looks like a miniature teapot. When using a neti-pot, the solution is poured, rather than squeezed, into the nose. Turkey basters or syringes like those used to suction a baby’s nose also work.

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Penicillin, one of the safest and most effective drugs for the treatment of community-acquired pneumonia caused by Streptococcus pneumoniae, is back in the armamentarium following action by the Food and Drug Administration (FDA) and pressure from IDSA and several key members.

FDA has raised the concentration at which S. pneumoniae is considered susceptible to penicillin, according to an amended package insert for Baxter Healthcare Corporation’s penicillin G approved by FDA and obtained by IDSA. The breakpoint changes are:

The susceptible breakpoint for meningitis caused by S. pneumoniae remains unchanged (0.06 mcg/mL). The package insert is available online from FDA’s website.

Evidence has been mounting for years that penicillin is effective against pneumococcal pneumonia at concentrations that would fail for meningitis or otitis media. Victor L. Yu, MD, FIDSA, co-authored one significant study in Clinical Infectious Diseases in 2003 looking at patients with pneumococcal bacteremia who were initially treated with penicillin before laboratory tests came back resistant. “It turned out they uniformly did fine,” Dr. Yu said. The study won IDSA’s Emmanuel Wolinsky Award in 2003. Since then, several other studies have been published showing penicillin is effective against pneumococcal pneumonia at concentrations that would fail for other diseases.

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Botulinum neurotoxin — responsible for the deadly food poisoning disease botulism and for the beneficial effects of smoothing out facial wrinkles - can also be used as a dreaded biological weapon. When ingested or inhaled, less than a billionth of an ounce can cause muscle paralysis and eventual death. Although experimental vaccines administered prior to exposure can inhibit the destructive action of this neurotoxin - the most deadly protein known to humans — no effective pharmacological treatment exists.
Swaminathan, Kumaran, and Rawat.

Reviewing their data are (from left) Brookhaven Lab researchers Subramanyam Swaminathan, Desigan Kumaran and Richa Rawat. (Click on the image to download a high-resolution version.)

Now, scientists at the U.S. Department of Energy’s Brookhaven National Laboratory and the U.S. Army Medical Research Institute of Infectious Diseases (USAMRIID) have taken the first step toward designing an effective antidote to the most potent form of the toxin. They have found that they can trick the toxin to bypass its normal binding protein, thereby blocking its deadly action. The results of their research are reported in the April 22, 2008 online issue of the Journal of Biological Chemistry.

“We have found a highly efficient inhibitor of botulinum neurotoxin type A - the most potent of seven neurotoxins produced by the bacterium Clostridium botulinum. This finding can lead to a very effective drug to stop the devastating effects of the toxin,” said Brookhaven Lab biologist Subramanyam Swaminathan, the study’s co-principal investigator. “We intend to do further research to tailor the inhibitor for the best results.”

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A natural compound extracted from the milk of coconuts has proven effective in curbing the uncontrolled growth of certain cancer tumors, according to researchers at Mayo Clinic.

A recently published study by Drs. A. Keith Stewart and Rodger E. Tiedemann of the Mayo Clinic Cancer Center indicates that a substance called kinetin riboside, prevents new cell growth in tumors controlled by cyclin D proteins. (Cyclin D proteins are members of the cyclin family of proteins related to cell division.) Kinetin riboside is found in minute quantities in coconut milk and other natural plants and is related to the hormones that govern root growth in plants.

The results of the study were published in the May 1, 2008, issue of the Journal of Clinical Investigation. The journal is published by the American Society for Clinical Investigation, founded in 1908 to recognize important advances in medical research. “Cyclin D is like the gas pedal for cell progression,” Stewart said. “In cancer cells, too much cyclin is produced and overwhelms the cell, causing it to grow too quickly. Kinetin riboside appears to switch that process off.”

Three closely related proteins called cyclin D1, D2 and D3 are found in all proliferating cell types and collectively control the progression of cells through their cell cycle. Since D-cyclin proteins are essential to cell division, they are implicated in certain types of cancer.

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When a form of cancer that begins in the milk ducts of the breast invades neighboring tissue to spread to other parts of the body, the cause lies not in the tumor cells themselves but in a group of abnormal surrounding cells that cause the walls of the duct to deteriorate like a rusty pipe, according to a new study led by Dana-Farber Cancer Institute researchers.

The discovery, reported in the May 6 issue of Cancer Cell, may lead to screening tests to determine whether the disease — known as ductal carcinoma in situ, or DCIS — is likely to spread beyond the ducts, based on genetic abnormalities in cells in the ducts’ lining. And it sets the stage for treatments that, by targeting these abnormalities, shore up the duct walls and keep the cancer contained.

“Women whose DCIS has invaded the ducts are known to have a greater chance of metastasis, or spreading disease. But it hasn’t been clear what causes the transition from a localized cancer to invasive disease,” according to the study’s senior author, Kornelia Polyak, MD, PhD, of Dana-Farber. “This study demonstrates that in DCIS of the breast, and potentially in other cancers that originate in duct tissues, the answer may lie in the tumor’s microenvironment — the cells and tissue that surround the cancer.”

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Millions of American teens report experiencing weeks of hopelessness and loss of interest in normal daily activities and many of these depressed teens are using marijuana and other drugs, making their situation worse, according to a new White House report released today. The report, from the White House Office of National Drug Control Policy (ONDCP), reveals that marijuana use can worsen depression and lead to more serious mental disorders, such as schizophrenia, anxiety, and even suicide.

Research shows that some teens are using drugs to alleviate feelings of depression (”self-medicating”), when in fact, using marijuana can compound the problem. The report, released to coincide with May’s Mental Health Awareness Month, shows a staggering two million teens felt depressed at some point during the past year, and depressed teens are more than twice as likely as non-depressed teens to have used marijuana during that same period. Depressed teens are also almost twice as likely to have used illicit drugs as non-depressed teens. They are also more than twice as likely as their peers to abuse or become dependent on marijuana. Marijuana use is associated with depression, suicidal thoughts, and suicide attempts.

“Marijuana is not the answer. Too many young people are making a bad situation worse by using marijuana in a misguided effort to relieve their symptoms of depression,” said John P. Walters, Director, National Drug Control Policy. “Parents must not dismiss teen moodiness as a passing phase. Look closely at your teen’s behavior because it could be a sign of something more serious.”

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When most people discover mold on their bread, they immediately throw it out. Others see a world of possibilities in the tiny fungus. A University of Missouri scientist, along with a collaborative research team, has examined a new mechanism in the reproductive cycle of a certain species of mold. This mechanism protects the organism from genetic abnormalities by “silencing” unmatched genes during meiosis (sexual reproduction). The finding could have implications for higher organisms and may lead to precise “targeting” of unwanted genes, such as those from the HIV virus.

“Meiotic silencing also occurs in worms, mice and human beings,” said Patrick Shiu, assistant professor of biological sciences in the MU College of Arts and Science. “It’s unlikely that all share the same mechanism, but the principle of targeting unpaired DNA for silencing seems to be found in both simple and complex organisms. Knowing the process of how DNA in molds is targeted for silencing could be important for silencing genes you don’t want to be expressed, like disease-causing genes.”

Shiu and his colleagues discovered that each sexual cell in mold has an internal mechanism that “scans” paired chromosomes for anomalies. The researchers found that when one chromosome in a pair carries an extra copy of a gene not found in its partner chromosome, it is a good indication of an intruder and the fungus will “turn off” all copies of that gene during meiosis. The researchers call this process “meiotic silencing by unpaired DNA,” or MSUD.

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A group of USC School of Dentistry researchers said it has identified the slimy culprits killing the jawbones of some people taking drugs that treat osteoporosis.

Microbial biofilms, a mix of bacteria and sticky extracellular material, are causing jaw tissue infections in patients taking bisphosphonate drugs, said Parish Sedghizadeh, lead researcher and assistant clinical professor at the school.

Sold under brand names such as Fosamax, Boniva and Actonel, bisphosphonates are prescribed to millions of patients to combat osteoporosis, a bone-wasting disease that increases the risk of fractures.

Sedghizadeh said there have been increasing reports of osteonecrosis (bone death) of the jaw in patients who have been taking the drugs for osteoporosis or for treatment from the bone-wasting effects of cancer.

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A team led by Dr. Xue-Hai Tan from the Beijing Genomics Institute has determined that the antifibrotic function of Chinese herbal extract Cpd 861 is mediated by both downregulating the synthesis of collagens and upregulating the degradation of collagens. This effect is evidently different from that of Western antifibrogenic drugs and could allow for the development of effective antifibrogenic drugs from Chinese medicinal herbs.

In human hepatic stellate cells, the key cells involved in both the synthesis and degradation of matrix proteins (mainly collagens) in the liver, the plant extract Cpd 861 can regulate the expression levels of collagen synthesis and degradation-related genes, thus demonstrating an antifibrotic effect.

Hepatic fibrosis, which can lead to portal hypertension or cirrhosis, is a wound-healing response to chronic liver injuries due to a variety of insults. The altered balance between the synthesis and degradation of matrix proteins (mainly collagens) is the major pathogenic feature in the hepatic fibrosis process. Although remarkable progress has been made recently in understanding the mechanisms of hepatic fibrosis and while numerous agents have been studied, very few effective antifibrogenic drugs have been approved for use in humans.

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University of Florida researchers have identified a drug compound that dramatically lowers blood pressure, improves heart function and — in a remarkable finding — prevents damage to the heart and kidneys in rats with persistent hypertension.

The findings, which appear in today’s (May 1) edition of the American Heart Association journal Hypertension, could lead to a new class of antihypertensive drugs designed to address two major problems associated with cardiovascular disease: high blood pressure and the tissue damage associated with it, known as fibrosis.

“When people have heart attacks (or suffer from hypertension) the blood vessels get more rigid,” said study author David Ostrov, Ph.D., an assistant professor in the UF College of Medicine’s department of pathology, immunology and laboratory medicine. “We discovered a compound that reverses the fibrosis that makes the blood vessels more rigid.”

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