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Archive - Jun 14, 2015

Harvard Scientists Transplant “Biological Clock” from Cyanobacteria to E. coli, Which Normally Does Not Have Circadian Rhythm; “Circadian” E. coli May Ultimately Be Used in Creation of Precisely-Timed Drug Release Medications and Jet Lag Prevention

Often referred to as the "body clock," circadian rhythm controls what time of day people are most alert, hungry, tired, or physically primed due to a complex biological process that is not unique to humans. Circadian rhythms, which oscillate over a roughly 24-hour cycle in adaptation to the Earth's rotation, have been observed in most of the planet's plants, animals, fungi, and cyanobacteria, and are responsible for regulating many aspects of organisms' physiological, behavioral and metabolic functions. Now, scientists, led by the pioneering Harvard synthetic biologist Pamela Silver, Ph.D., have harnessed the circadian mechanism found in cyanobacteria to transplant the circadian wiring into a common species of bacteria that is naturally non-circadian. The novel work, which for the first time demonstrates the transplant of a circadian rhythm, is described in an open-access article published online on June 12, 2015 in Science Advances. "By looking at systems in nature as modular, we think like engineers to manipulate and use biological circuits in a predictable, programmable way," said Dr. Silver, who is a Core Faculty member at the Wyss Institute for Biologically Inspired Engineering at Harvard University and a Professor in the Department of Systems Biology at Harvard Medical School. Dr. Silver's team used this methodology to successfully transplant a circadian rhythm into the bacterial species E. coli, which is widely used as a "workhorse" cell species by biologists due to how well it is understood and the ease with which E. coli can be genetically altered. The genetically engineered circadian E.

Possibly Effective Drug Treatment to Halt Progression of, or Reverse, Pulmonary Fibrosis & Pulmonary Hypertension, Two Rapidly Fatal Lung Diseases; Triciribine Drug Inhibits Production of Akt1 Protein and Halts or Reverses These Diseases in Mouse Models

Researchers at the University of Georgia have discovered that the drug triciribine may reverse or halt the progression of pulmonary fibrosis (image) and pulmonary hypertension, two respiratory diseases that are almost invariably fatal. The scientitst published their findings online on May 29, 2015 in the British Journal of Pharmacology. The article is titled “Akt Inhibitor, Triciribine, Ameliorates Chronic Hypoxia-Induced Vascular Pruning and TGFβ-Induced Pulmonary fFbrosis.” Pulmonary fibrosis occurs when lung tissue becomes scarred, leading to loss of lung function and reduced oxygen supply to the blood. Pulmonary hypertension involves an increase of blood pressure in the arteries of the lung that can lead to heart failure. Although no definitive cause for the disease has been identified, pulmonary fibrosis affects nearly 130,000 people in the U.S., with about 48,000 new cases diagnosed annually, according to the Coalition for Pulmonary Fibrosis. Pulmonary hypertension is rare--with only about 15 to 50 cases per million people--but the total number of deaths attributed to the disease increased by more than 40 percent in the U.S. between 1980 and 2002, according to the Centers for Disease Control and Prevention. "The average life expectancy for people with these diseases is only about five years after diagnosis, and while the drug treatments we currently have may help improve quality of life, they don't reduce mortality," said Dr. Somanath Shenoy, co-author of the paper and associate professor in UGA's College of Pharmacy.