The Synaptic Leap

Hi all,

I would like to introduce my open-source project at Stanford, GemIdent:

http://www.gemident.com

http://en.wikipedia.org/wiki/GemIdent

GemIdent specializes in color image segmentation using supervised machine learning. For example, you can use it to locate and count cells in microscopic images:

GemIdent in action identifying cancer cells in a IHC-stained lymphnode image

I am a biochemist i have a good background on molecular biology. i would like to joint a research team to complete my PhD thesis.According to my accademic profile, i am able to work on many research areas like genetic diversity of schistosoma, efficacity of praziquantel, vaccine development against schistosoma spp. and so one.

There's a new database from WHO for tracking new targets for drug discovery for neglected diseases. Not much there yet, but it's sure to grow.

Mat

XDR tuberculosis is resistant to the first-line anti-TB drugs and at least 3 out of 6 of the second line anti-TB drugs. It has an estimated 85% mortality rate. Clearly we're talking about a monster.

I am happy to report that my group in collaboration with Scott Franzblau from the Institute for Tuberculosis Research at U. Illinois-Chicago has published our anti-TB work (see attachment). We explored the quaternized promazine derivatives as antitubercular agents, and found that the most potent thus far are 4- and 3-chlorophenyl derivatives of triflupromazine, both nontoxic in vitro against Vero cells. In our unpublished studies, we have also discovered that both of these actives are bacteriocidal against M. tuberculosis and that the 4-chlorobenzyl derivative is as bacteriocidal as rifampin, the most potent clinically prescribed antitubercular drug. So we're quite happy!

Dear TSL Members,

You are invited to the first annual QB3-UCSF-CDD developing world disease research community meeting scheduled for March 5^th 2007 at the UCSF Mission Bay Campus (details below and attached).  The collaborative community includes leading experts on developing world infectious disease research from Stanford, UCSF, UC Berkeley, UCLA, UW, SBRI, St. Jude CRH, U. Penn, Univ. of Sydney, and industry too.  

Collaborative Drug Discovery
First Annual Community Meeting

Monday, March 5^th 2007 1:00-6:00 pm; Auditorium: J. David Gladstone Institute (1^st Floor)

Hosted by Gladstone Institute and QB3 at the UCSF, Mission Bay Campus

Two major themes of this event are:

1)      Public-Private-Partnerships for Global Health Issues
2)      “Open” concepts for Collaborative Drug Discovery

Confirmed Speakers:
 

• Dr. Christopher Lipinski, Pfizer, retired. (Keynote presentation)
  
• Jim McKerrow, Professor, Dept. of Pathology, QB3 - UCSF
  
• Matt Bogyo, Professor, Dept. of Pathology, Stanford Medical School
  
• Andrej Sali, Professor, Dept of Biopharmaceutical Sciences, QB3 - UCSF
  
• Dr. Anang Shelat, St. Jude Children’s Research Hospital
  
• David Roos, Biology Professor, Univ. of Penn tentatively confirmed (Director, Penn Genomics Institute).

Symposium – Coffee/Snacks – Demos – Posters – Networking – Wine Reception

Registration is free. To register contact/RSVP to: kgregory@collaborativedrug.com.

I've just joined Synaptic Leap.  I'm a medicinal chemist who is involved in synthesis and computational design of NCEs and I'd like to participate in the discussions.

This is a call for creating a tuberculosis research community.

Background

Tuberculosis (TB), the disease caused by Mycobacterium tuberculosis (Mtb), infects approximately two billion people. The World Health Organization estimates that about two million people die each year from TB due to the lack of and inability to afford proper health care.¹ Overcrowding and ill-nourishment of poor people living in large cities leads to a high incidence of the disease due to the ease at which the infection can be transferred.² This contributes to the accelerated speed at which TB spreads in underdeveloped countries. There is also an alarming increase in cases of TB caused by multidrug-resistant strains of Mycobacterium tuberculosis (Mtb), due in part to inadequate drug therapy as a result of incorrectly selected medications or suboptimal drug dosing.³ Thus, there is a need for new drugs targeting enzymes essential to mycobacterial survival.

Research Focus 

My lab is focusing on the inhibition of type II NADH-menaquinone dehydrogenase (ndh-2). By inhibiting ndh-2, the electron transport chain in Mtb becomes blocked and shuts down. Ndh-2 is the only NADH dehydrogenase enzyme expressed in Mtb and is thus vital to its survival.⁴ Ndh-2 is also found in a number of other bacteria such as Staphylococcus aureus and Enterococcus faecalis but is not expressed in humans.⁵ Humans rely only on type I NADH dehydrogenase (ndh-1) and thus minimal toxicity in humans is predicted with ndh-2 inhibitors.