Lung health , tuberculosis and neurons in the mucosal tissue that detect infection


Image shows Amish people.


Researchers have identified a genetic mutation in an extended Amish family that allow them to live 10 percent longer and have 10 percent longer telomeres than other Amish kindred members who do not have the mutation. People with this mutation also have a lower diabetes risk and lower vascular aging, researchers note. READ MORE…
Image shows a small child with chickenpox.


Researchers at Aarhus University have identified a mutation in an immune system sensor that can result in chicken pox infection becoming fatal. According to the study, immune cells in those with extreme reaction to VZV neither detected the virus nor activated the immune system. The findings shed light on why some people are more susceptible to infections than others.  READ MORE…

WHO | Tuberculosis (TB) – World Health Organization

26 January 2018 – Countries and partners at the 142nd World Health Organization (WHO) Executive Board (EB), adopted a Resolution yesterday in support of the upcoming UN General Assembly high-level meeting (UNHLM) on tuberculosis (TB). The Resolution included a request to WHO to work with key stakeholders to …

Tuberculosis | TB | TB Test| MedlinePlus › Health Topics

Feb 21, 2018 – Tuberculosis (TB) is a disease caused by bacteria called Mycobacterium tuberculosis. The bacteria usually attack the lungs, but they can also damage other parts of the body. TB spreads through the air when a person with TB of the lungs or throat coughs, sneezes, or talks.

Supercharged Tuberculosis, Made in India – Scientific American

Many of these patients, like 19-year-old Nisha, an engineering student from the central state of Madhya Pradesh, have tuberculosis (TB). Nisha, who asked that her real name be withheld, has been treated for lung problems for more than a year, only to learn that inaccurate diagnoses and prescription errors …

Tuberculosis | Nature Reviews Disease Primers

Tuberculosis (TB) is an airborne infectious disease caused by organisms of the Mycobacteriumtuberculosis complex. Although primarily a pulmonary pathogen, M. tuberculosis can cause disease in almost any part of the body. Infection with M. tuberculosis can evolve from containment in the host, in which …

The Danger of Ignoring Tuberculosis – The Atlantic

Tuberculosis remains a major killer. As antibiotic-resistant strains of the disease spread across the globe, it’s getting harder to wipe out. In the next three decades, drug-resistant strains of the bacteria could drive up tuberculosis deaths by 2.4 million per year—to some 4 million fatalities annually—according …

Those with Alzheimer’s disease gene face sharper weight loss after age 70

Image shows a fat mouse and a thin mouse.


According to a new study, your sense of smell could be responsible for weight gain. Using mice, researchers noticed that those who lost their sense of smell also lost weight, while those mice with a super sense of smell gained more weight on a high fat diet than mice with a regular sense of smell. Findings suggest odor may play an important role in calorie burning processes; if you can’t smell your food, you may burn it rather than store it. READ MORE…

Addictive Nut’s Derivatives Could Help Smokers Break the Nicotine Habit

Addictive Nut’s Derivatives Could Help Smokers Break the Nicotine Habit

Summary: Compound derived from the areca nut could help people to quit smoking, a new study reports.

Source: ACS.

As many as 600 million people in Southeast Asia chew areca nuts with betel leaves, sometimes adding tobacco leaves. Many users are addicted to this harmful “betel quid” preparation, which can create a sense of euphoria and alertness. Yet researchers have now discovered that compounds derived from the nut could help cigarette smokers — as well as betel quid chewers — kick their habits.

The researchers will present their work today at the 253rd National Meeting & Exposition of the American Chemical Society (ACS). ACS, the world’s largest scientific society, is holding the meeting here through Thursday. It features more than 14,000 presentations on a wide range of science topics.

“There’s a commonality to the two addictions, so we thought we could develop drugs that target both,” says Roger L. Papke, Ph.D., one of the lead researchers on the project. Fellow lead researcher Nicole A. Horenstein, Ph.D., and Papke, along with Clare Stokes and Marta Quadri, Ph.D., are studying compounds from the areca nut to make new molecules that might work better than existing smoking cessation drugs such as Chantix® (varenicline).

More than 480,000 people die each year in the U.S. from the effects of cigarette smoking, according to the U.S. Centers for Disease Control and Prevention. Prescription smoking cessation drugs currently on the market can work well but can also cause harmful side effects. For example, some patients taking the drug varenicline report having suicidal thoughts, sleepwalking and having cardiovascular problems.

Because of varenicline’s side effects, researchers such as Papke and Horenstein are working on alternatives at the University of Florida. Varenicline reduces nicotine cravings by binding to the same receptors that attach nicotine molecules to brain cells, but it activates those receptors to a lesser degree. Undesirable effects occur because the drug also binds to other nicotine receptors that aren’t involved in addiction, Papke explains. “The molecules that we’re developing are more specific — they do not target those other receptors at all, so our compounds should be safer,” he says.

The idea to study the areca nut came when Papke obtained a headhunter’s sword from Borneo. He learned that the peculiar carvings on its hilt might have been made by someone using betel quid. Quids are prepared by mixing sliced areca nuts with slaked lime (calcium hydroxide), spices or sweets, and in some cases tobacco, and wrapping the concoction in leaves from the betel vine. Quid chewing turns users’ teeth bright red and forces them to spit out a lot of red saliva, which discolors local sidewalks and buildings. Worse, quid use is addictive and leads to serious health effects including oral cancer and cardiovascular issues.

Image shows the nut.

In prior work, Papke and Horenstein studied arecoline, one of the psychoactive alkaloids in the areca nut. They discovered that arecoline stimulates the same brain cell receptors responsible for nicotine addiction but doesn’t stimulate the other types of nicotine receptors.

Now, Horenstein is synthesizing a range of compounds with structures that are slightly different from arecoline. The researchers have found that some of these new compounds also bind to the addiction-related receptors, while leaving the other receptors alone. That means these arecoline analogs may be able to treat addiction to cigarettes or to betel quids without side effects. The next step for Horenstein and Papke is to seek funding so they can test these potential new drugs in animal trials.


Funding: The researchers acknowledge funding from the U.S. National Institutes of Health.

Source: Katie Cottingham – ACS 
Image Source: image is credited to Roger Papke, Ph.D.
Original Research: The study will be presented at American Chemical Society 253rd National Meeting & Exposition.

ACS “Addictive Nut’s Derivatives Could Help Smokers Break the Nicotine Habit.” NeuroscienceNews. NeuroscienceNews, 5 April 2017.

e-cigarettes, nicotine should not be the norm

Since 2010, the Food and Drug Administration has been debating how to regulate the sale of e-cigarettes. The FDA should hurry up. These battery-powered devices, which heat a nicotine solution and create an inhalable vapor, are exploding in popularity – driven mostly by a tobacco industry in search of new addicts.

Addiction itself does lie at the heart of the FDA’s dilemma about regulating e-cigarettes. Should the agency assume that millions of Americans choose to be nicotine addicts, with the federal role simply to make the use of electronic cigarettes as safe as possible? Or should the FDA see this powerful addiction as inherently wrong, both for individuals and society, with the government helping people avoid or overcome it?

Several countries already ban the sale of e-cigarettes, a wise course for the FDA. They see the electronic devices as delivering a drug with no use, even if it does not have all the effects of regular smoking. Indeed, the tobacco industry does not claim e-cigarettes are a temporary tool for ending tobacco addiction. Most likely, e-cigarettes are being heavily promoted to attract people to take up smoking. Yearly sales of e-cigarettes are already approaching $1 billion.

Any benefit of e-cigarettes remains unproven while a few toxins have been found in the device’s vapors. At least three American cities ban their use indoors. And, according to one study, quitting e-cigarettes may be as difficult as for tobacco smoking.

In taking any action, the FDA must assume people do not want to become addicts to nicotine. Government already takes that approach inherently with increasing restrictions on the sale and use of tobacco products. The result has been a welcome decline in public smoking and smoking in general. People tempted to take up smoking now face difficult choices – in costs, inconvenience, and social stigma.

The opposite approach of tolerance toward e-cigarettes would be similar to the way states, once faced with criminal activities associated with illegal gambling, decided that people everywhere want to gamble and government might as well join in by offering lotteries. Now millions of mainly poor people can’t get enough of this daily gambling fix. And states are addicted to the revenues.

Simply curbing the sale of e-cigarettes to minors should not be the FDA’s final decision. The agency, and indeed much of government, can help persuade people that nicotine addiction is not “cool” and can be easily avoidable. The agency should do more than prevent harm. It can also assert that each individual has a right to be free of addiction.

Connie’s comments: My dad died of lung cancer at age 64. He started smoking at age 19. He stopped smoking 15 yrs before he died by cold turkey, just determination. He worked in copper and nickle mines and as car mechanic. In 2001, when he was diagnosed in San Jose, California in last stage of lung cancer, we did not choose radiation or chemotherapy. He lived for 9 months more with juicing of green papaya and green apples.


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Effect of Nicotine on the Pharmacokinetics of Levodopa, anti-parkinsons med

The study found that nicotine reduced plasma levodopa concentration in some healthy subjects but with no alteration of gastric emptying rate. In vitro, nicotine inhibited levodopa transport by Caco-2 cell monolayers in an α-methyl amino isobutyric acid-independent, 2-amino-norbornanecarboxylic acid-dependent manner. These results suggest that nicotine may inhibit the transport of levodopa by the system L-amino acid transporter.

Some patients with Parkinson disease improved their symptoms on treatment with nicotine patch or gum. Nicotine has also been studied for its antidyskinetic effect on levodopa-induced dyskinesia. We determined the effects of nicotine on levodopa pharmacokinetics and gastric emptying in healthy subjects and on levodopa transport in Caco-2 monolayers in vitro.

Healthy subjects received transdermal nicotine patch application followed by oral levodopa/benserazide, 100/25 mg, in a fasting state and with enteral nutrition. Levodopa pharmacokinetics was determined, and gastric emptying was evaluated by carbon 13 (13C)-labeled acetic acid breath testing. In vitro studies using intestinal Caco-2 cell monolayers evaluated whether the intestinal transport of levodopa was affected by nicotine and its metabolite, cotinine.

Nicotine did not increase mean plasma concentration significantly during fasting or with enteral nutrition, although the extent of levodopa absorption was reduced by 34% to 60% in some individuals and the mean plasma concentration of levodopa was statistically decreased by nicotine in subjects who received enteral nutrition. However, gastric parameters were not significantly affected by nicotine. Nicotine and cotinine at 0.1 μmol/L significantly reduced levodopa uptake by Caco-2 cells.

Kyaw, Win Thiri; Nagai, Masahiro; Kaneta, Mika; Kubo, Madoka; Nishikawa, Noriko; Tsujii, Tomoaki; Iwaki, Hirotaka; Nomoto, Masahiro. CLINICAL NEUROPHARMACOLOGY, 20130362-5664


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