April 6, 2014

ruinedchildhood:

original post

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April 6, 2014

Actually love this movie

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March 18, 2014
New Therapeutic Target Discovered for Alzheimer’s Disease

ucsdhealthsciences:

A team of scientists from the University of California, San Diego School of Medicine, the Medical University of South Carolina and San Diego-based American Life Science Pharmaceuticals, Inc., report that cathepsin B gene knockout or its reduction by an enzyme inhibitor blocks creation of key neurotoxic pGlu-Aβ peptides linked to Alzheimer’s disease (AD). Moreover, the candidate inhibitor drug has been shown to be safe in humans.

The findings, based on AD mouse models and published online in the Journal of Alzheimer’s Disease, support continued development of cysteine protease inhibitors as a new drug target class for AD. “No other therapeutic program is investigating cysteine protease inhibitors for treating AD,” said collaborator Vivian Hook, PhD, professor in the UC San Diego Skaggs School of Pharmacy and Pharmaceutical Sciences and in the UC San Diego School of Medicine.  

Current AD drugs treat some symptoms of the devastating neurological disorder, but none actually slow its progress, prevent or cure it. No new AD drug has been approved in more than a decade.

The researchers focused on cathepsin B production of N-truncated pGlu-Aβ, a peptide or short chain of amino acids, and the blockade of cathepsin B by E64d, a compound shown to inhibit cysteine proteases, a type of enzyme. AD is characterized by accumulation of a variety of Aβ peptides as oligomers and amyloid plaques in the brain, factors involved in neuronal loss and memory deficits over time. These neurotoxic Aβ peptides are created when enzymes cleave a large protein called amyloid precursor protein (APP) into smaller Aβ peptides of varying toxicity. N-truncated pGlu-Aβ has been shown to be among the most neurotoxic of multiple forms of Aβ peptides.

Much AD research has focused on the APP-cutting enzyme BACE1 β-secretase, but its role in producing pGlu-Aβ was unknown. Cathepsin B is an alternative β-secretase which cleaves the wild-type β-secretase site of APP, which is expressed in the major sporadic and many familial forms of AD. Hook and colleagues looked at what happened after gene knockout of BACE1 or cathepsin B. They found that cathepsin B, but not BACE1, produced the highly toxic pGlu-Aβ.

Perhaps most interestingly, the scientists found that E64d, an enzyme inhibitor of cathepsin B, reduced production of pGlu-Aβ and other AD-associated Aβ peptides. Key was the finding that E64d and cathepsin B gene knock out resulted in improved memory deficits in a mouse model of AD.

“This is an exciting finding,” said Hook. “It addresses a new target – cathepsin B – and an effective, safe small molecule, E64d, to reduce the pGlu-Aβ that initiates development of the disease’s neurotoxicity. No other work in the field has addressed protease inhibition for reducing pGlu-Aβ of AD.”

Hook noted that E64d has already been shown to be safe in clinical trials of patients with muscular dystrophy and would, therefore, likely prove safe for treating AD as well. She hopes to launch Phase 1 human clinical trials in the near future with a modified version of the drug candidate.

!!!

March 18, 2014

thebrockway:

sorenbowie:

"Because, Kevin, no one else has boots or gloves."

Good news: He was burning hot for the first two minutes. Bad news: He was cold and soggy for the next 58. 

(Source: copyranter.blogspot.com)

March 17, 2014
ME AFTER A NIGHT AT THE LIBRARY

howdoiputthisgently:

March 16, 2014

(Source: idiotsonfb, via jordanjfelix)

March 16, 2014

ucsdhealthsciences:

sdzsafaripark:

Imani’s baby girl underwent a procedure on Friday to fix a collapsed lung. Thanks to the expertise of our staff, aided by a human neonatal specialist and an anesthesiologist from UC San Diego Health System, the procedure was a success and she is breathing better on her own. More info.

Our very own Dr. Dawn Reeves, neonatologist, helped deliver Imani’s baby by emergency C-section.  

March 15, 2014
Doctor: I think you'll need a shot
Me: AYYYYY
Doctor: AYYYYY *brings out tequila*
March 7, 2014
Anti-psychotic Medications Offer New Hope in the Battle Against Glioblastoma

ucsdhealthsciences:

Researchers at the University of California, San Diego School of Medicine have discovered that FDA-approved anti-psychotic drugs possess tumor-killing activity against the most aggressive form of primary brain cancer, glioblastoma. The finding was published in this week’s online edition of Oncotarget.

The team of scientists, led by principal investigator, Clark C. Chen, MD, PhD, vice-chairman, UC San Diego, School of Medicine, division of neurosurgery, used a technology platform called shRNA to test how each gene in the human genome contributed to glioblastoma growth.  The discovery that led to the shRNA technology won the Nobel Prize in Physiology/Medicine in 2006.

“ShRNAs are invaluable tools in the study of what genes do. They function like molecular erasers,” said Chen. “We can design these ‘erasers’ against every gene in the human genome. These shRNAs can then be packaged into viruses and introduced into cancer cells. If a gene is required for glioblastoma growth and the shRNA erases the function of that gene, then the cancer cell will either stop growing or die.”

Chen said that one surprising finding is that many genes required for glioblastoma growth are also required for dopamine receptor function. Dopamine is a small molecule that is released by nerve cells and binds to the dopamine receptor in surrounding nerve cells, enabling cell communication.

Abnormal dopamine regulation is associated with Parkinson’s disease, schizophrenia, and Attention Deficit Hyperactivity Disorder. Because of the importance of dopamine in these diseases, drugs have been developed to neutralize the effect of dopamine, called dopamine antagonists. 

Following clues unveiled by their shRNA study, Chen and his team tested the effects of dopamine antagonists against glioblastoma and found that these drugs exert significant anti-tumor effects both in cultured cells and mouse models. These effects are synergistic when combined with other anti-glioblastoma drugs in terms of halting tumor growth.

“The anti-glioblastoma effects of these drugs are completely unexpected and were only uncovered because we carried out an unbiased genetic screen,” said Chen.

“On the clinical front, the finding is important for two reasons,” said Bob Carter, MD, PhD, chairman of UC San Diego, School of Medicine, division of neurosurgery. “First, these drugs are already FDA-cleared for human use in the treatment of other diseases, so it is possible these drugs may be re-purposed for glioblastoma treatment, thereby bypassing years of pre-clinical testing. Second, these drugs have been shown to cross the blood-brain barrier, a barrier that prevents more than 90 percent of drugs from entry into the brain.”

Chen is now working with the UC San Diego Moores Cancer Center Neuro-Oncology team to translate his findings into a clinical trial.

Huge news in the fight against arguably the worst cancer you could possibly get. This guy lectured in my class a few weeks ago. Frickin cool.

March 6, 2014
martymcflyinthefuture:

Today is the day that Marty McFly goes to the future!

martymcflyinthefuture:

Today is the day that Marty McFly goes to the future!

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