In his most recent study, Angelos Halaris, MD, PhD, and colleagues found that an inflammatory biomarker, interleukin-6, was significantly higher in the blood of 48 patients diagnosed with major depression than it was in 20 healthy controls. Interleukin-6 has been associated with cardiovascular disease. Halaris presented findings at a joint congress of the World Psychiatric Association and International Neuropsychiatric Association in Athens, Greece. At the congress, Halaris formally proposed creation of a new Psychocardiology subspecialty.

Forty to 60 percent of heart disease patients suffer clinical depression and 30 to 50 percent of patients who suffer clinical depression are at risk of developing cardiovascular disease, Halaris said.

Stress is the key to understanding the association between depression and heart disease. Stress can lead to depression, and depression, in turn, can become stressful.

The body’s immune system fights stress as it would fight a disease or infection. In response to stress, the immune system produces proteins called cytokines, including interleukin-6. Initially, this inflammatory response protects against stress. But over time, a chronic inflammatory response can lead to arteriosclerosis (hardening of the arteries) and cardiovascular disease.

It’s a vicious cycle: depression triggers a chronic inflammation, which leads to heart disease, which causes depression, which leads to more heart disease.

Clinical depression typically begins in young adults. “Treating depression expertly and vigorously in young age can help prevent cardiovascular disease later on,” Halaris said.

Physicians often work in isolation, with psychiatrists treating depression, and cardiologists treating cardiovascular disease. Halaris is proposing that psychiatrists and cardiologists work together in a multidisciplinary Psychocardiology subspecialty.

A Psychocardiology subspecialty would raise awareness among physicians and the public. It would forge closer working relationships between psychiatrists and cardiologists. It would formalize multidisciplinary teams with the requisite training and expertise to enable early detection of cardiovascular disease risk in psychiatric patients and psychiatric problems in heart disease patients. And it would provide continuing education to physicians in the safe and correct use of medications in cardiac patients who have psychiatric disorders.

“It is only through the cohesive interaction of such multidisciplinary teams that we can succeed in unravelling the complex relationships among mental stress, inflammation, immune responses and depression, cardiovascular disease and stroke,” Halaris said.

Halaris is Medical Director of Adult Psychiatry and a Professor in the Department of Psychiatry and Behavioral Neurosciences at Loyola University Chicago Stritch School of Medicine.

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A drug currently approved to treat mouth ulcers has shown promise in animal studies for being a contender in pharmaceutical weight loss. Amlexanox was found by University of Michigan researchers to produce weight loss in obese mice without any change in diet or exercise habits.

For the study, mice fed a high calorie diet until they became obese were injected with amlexanox. The animals lost weight, despite consuming the same amount of calories. The researchers also noted a loss in overall body fat, a decrease in fatty liver, and a reversal of obesity-induced type 2 diabetes. Once taken off the amlexanox injections, however, the mice experienced weight gain.

Amlexanox may work by changing the action of genes that control metabolism versus working as an appetite suppressant.

When the drug was injected in mice, the drug worked by increasing metabolism, not by suppressing appetite.

"One of the reasons that diets are so ineffective in producing weight loss for some people is that their bodies adjust to the reduced calories by also reducing their metabolism, so that they are 'defending' their body weight," says Dr. Alan Saltiel, the lead researcher at the University of Michigan.

 "Amlexanox seems to tweak the metabolic response to excessive calorie storage in mice."

The findings were published Sunday in the journal Nature Medicine. Clinical trials are expected to begin later this year to test the drug's effectiveness in humans.

Cancer drugs of the new, molecular generation destroy malignant breast tumors in a targeted manner: They block characteristic molecules on tumor cells - receptors for the hormones estrogen or progesterone, or a co-receptor, called HER2, that binds to many growth factors. But about one in every six breast tumors has none of these receptors. Such cancers, called triple-negative, are particularly aggressive and notoriously difficult to treat.
Some of these therapy-resistant cancers have a potential molecular target for cancer drugs, a growth-factor receptor called EGFR, but an EGFR-blocking drug has proved ineffective in treating them. In a study published recently in the Proceedings of the National Academy of Sciences, Weizmann Institute researchers propose a potential solution: to simultaneously treat triple-negative breast cancer with two EGFR-blocking antibodies instead of one. In a study in mice, the scientists showed that a certain combination of two antibodies indeed prevented the growth and spread of triple-negative tumors. The research team, led by Prof. Yosef Yarden of the Biological Regulation Department and Prof. Michael Sela of the Immunology Department, included Drs. Daniela Ferraro, Nade`ge Gaborit, Ruth Maron, Hadas Cohen-Dvashi, Ziv Porat, Fresia Pareja, and Sara Lavi, Dr. Moshit Lindzen and Nir Ben-Chetrit.
Of the different combinations they tried, the scientists found that the approach worked when the two antibodies bound to different parts of the EGFR molecule. The combined action of the antibodies was stronger than would have been expected by simply adding up the separate effects of each. Apparently, the use of the two antibodies created an entirely new anti-cancer mechanism: In addition to blocking the EGFR and recruiting the help of immune cells, the antibodies probably overwhelmed the EGFR by their sheer weight, causing it to collapse inward from the membrane into the tumor cell.
Deprived of EGFR on its surface, the cells were no longer receiving the growth signals, preventing the growth of the tumor. This approach resembles the natural functioning of the immune system, which tends to block essential antigens at several sites by targeting them with multiple antibodies. If supported by further studies, the two-antibody approach, in combination with chemotherapy, might in the future be developed into an effective treatment for triple-negative breast cancer.

Smoking tobacco might be bad for your health, but a genetically altered version of the plant might provide a relatively inexpensive cure for the deadly rabies virus. In a new research report appearing in The FASEB Journal, scientists produced a monoclonal antibody in transgenic tobacco plants that was shown to neutralize the rabies virus. This new antibody works by preventing the virus from attaching to nerve endings around the bite site and keeps the virus from traveling to the brain.
"Rabies continues to kill many thousands of people throughout the developing world every year and can also affect international travelers," said Leonard Both, M.Sc., a researcher involved in the work from the Hotung Molecular Immunology Unit at St. George's, University of London, in the United Kingdom. "An untreated rabies infection is nearly 100 percent fatal and is usually seen as a death sentence. Producing an inexpensive antibody in transgenic plants opens the prospect of adequate rabies prevention for low-income families in developing countries."
To make this advance, Both and colleagues "humanized" the sequences for the antibody so people could tolerate it. Then, the antibody was produced using transgenic tobacco plants as an inexpensive production platform. The antibody was purified from the plant leaves and characterized with regards to its protein and sugar composition. The antibody was also shown to be active in neutralizing a broad panel of rabies viruses, and the exact antibody docking site on the viral envelope was identified using certain chimeric rabies viruses.
"Although treatable by antibodies if caught in time, rabies is bad news," said Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal. "This is especially true for people in the developing world where manufacturing costs lead to treatment shortages. Being able to grow safe, humanized antibodies in genetically modified tobacco should reduce costs to make treatments more accessible, and save more lives."