A recent study in PNAS linked social isolation to an increased mortality rate.  They found the increased risk of death to be equivalent to smoking 15 cigarettes per day!  They postulate that social contact helps people deal with the negative effects of stress. The other postulate is that having social interactions helps curtain negative habits.  I wonder if oxytocin may have something to do with it.  Regardless of the cause, the effect is clear and for this classical Jungian introvert, making me rethink the amount of time forming social interactions.  

A recent paper in the Journal of the American Medical Society has taken a look at insurance company data and found a link between people who take drugs that target this pathway and hospitalizations for pancreatitis. In general this is not good.  The endocrine society has countered taking a dim view of the statistics in the paper.  

There are two classes of drugs that target this pathway.  The GLP-1 like peptides, and the DPP4 inhibitors.  There already have been concerns with respect to cardiovascular effects of these drugs, so one more piece of bad news is a problem.  For what its worth, my gut feeling is that it's a sampling error in the statistics.  We are looking at a weak signal and humans being, the variable large omnivorous mammals that we are, require larger sample sizes to really compute meaningful result.  If you look at the pre-selection criteria, these people were already quite ill with the host of complaints that plague those with diabetes. I would wait for more information before panic

Researchers at Boston University and USAAMRID published a set of molecules today, which appear to inhibit viral transcription in cells. The research was carried out on Nonsegmented Negative-Strand RNA viruses including Ebola. These aren't the most drug like compounds I've seen. It's also important to remember it's still in vitro studies. There is still  a long way to go, but hey! it's a start!

The newly discovered corona virus hCoV-EMC (human corona virus-Erasmus Medical Center) which have been causing severe, sometimes fatal lower respiratory infections, is using a protein CD26, which is also called dipeptidyl-peptidease 4, to gain entry to cells. The virus is highly similar in terms of sequence to one found in bats.  This paper shows expression of the human and bat CD26 receptor in nonsensitive cells, enables infection. This suggests a therapeutic target.