This blog is not affiliated or endorsed, by Nassau OTB, a public benefit corporation, subject to the New York Freedom
of Information Law, NY Pub Off Law Sec 84 et seq.
Thursday, June 18, 2015
Tricks to learn from a girl in the lab when time is not
On you side.
If you think that the girl has a point act on it and do not wait for her to grind it out while the system grinds her and you.
Girl in point, faustmanlab.org
Bcg works, as per the proof of concept paper. Girl is correct. System beats girl.
What to do if you have autoimmune disease. Shot Bcg.
How do you know how much to shoot how often.
Girl will not or has not said.
Start with vaccination dose. Observe. Plaque psoriasis abates. Girl is smart as her paper explains why this occurs. Girl grinds on and leaves this idea for another day in the distant future.
A girl's good ideas are retarded by the system even when someone takes one girl 's good ideas and convinces another of their validity.
the system retards the app,I action of useful science and art and crushes many into mindless know everything about nothings.
See also clinicaltrials.gov faustman
PLoS One. 2012;7(8):e41756. doi: 10.1371/journal.pone.0041756. Epub 2012 Aug 8.
Proof-of-concept, randomized, controlled clinical trial of Bacillus-Calmette-Guerin for treatment of long-term type 1 diabetes.
No targeted immunotherapies reverse type 1 diabetes in humans. However, in a rodent model of type 1 diabetes, Bacillus Calmette-Guerin (BCG) reverses disease by restoring insulin secretion. Specifically, it stimulates innate immunity by inducing the host to produce tumor necrosis factor (TNF), which, in turn, kills disease-causing autoimmune cells and restores pancreatic beta-cell function through regeneration.
METHODOLOGY/PRINCIPAL FINDINGS:
Translating these findings to humans, we administered BCG, a generic vaccine, in a proof-of-principle, double-blind, placebo-controlled trial of adults with long-term type 1 diabetes (mean: 15.3 years) at one clinical center in North America. Six subjects were randomly assigned to BCG or placebo and compared to self, healthy paired controls (n = 6) or reference subjects with (n = 57) or without (n = 16) type 1 diabetes, depending upon the outcome measure. We monitored weekly blood samples for 20 weeks for insulin-autoreactive T cells, regulatory T cells (Tregs), glutamic acid decarboxylase (GAD) and other autoantibodies, and C-peptide, a marker of insulin secretion. BCG-treated patients and one placebo-treated patient who, after enrollment, unexpectedly developed acute Epstein-Barr virus infection, a known TNF inducer, exclusively showed increases in dead insulin-autoreactive T cells and induction of Tregs. C-peptide levels (pmol/L) significantly rose transiently in two BCG-treated subjects (means: 3.49 pmol/L [95% CI 2.95-3.8], 2.57 [95% CI 1.65-3.49]) and the EBV-infected subject (3.16 [95% CI 2.54-3.69]) vs.1.65 [95% CI 1.55-3.2] in reference diabetic subjects. BCG-treated subjects each had more than 50% of their C-peptide values above the 95(th) percentile of the reference subjects. The EBV-infected subject had 18% of C-peptide values above this level.
CONCLUSIONS/SIGNIFICANCE:
We conclude that BCG treatment or EBV infection transiently modified the autoimmunity that underlies type 1 diabetes by stimulating the host innate immune response. This suggests that BCG or other stimulators of host innate immunity may have value in the treatment of long-term diabetes.
Excess levels of tumor necrosis factor-alpha (TNF-alpha) have been associated with certain autoimmune diseases. Under the rationale that elevated TNF-alpha levels are deleterious, several anti-TNF-alpha therapies are now available to block the action of TNF-alpha in patients with autoimmune diseases with a chronic inflammatory component to the destructive process. TNF-alpha antagonists have provided clinical benefit to many patients, but their use also is accompanied by new or aggravated forms of autoimmunity. Here we propose a mechanistically based hypothesis for the adverse events observed with TNF-alpha antagonists, and argue for the opposite therapeutic strategy: to boost or restore TNF-alpha activity as a treatment for some forms of autoimmunity. Activation defects in the transcription factor nuclear factor kappaB leave autoreactive T cells sensitive to TNF-alpha-induced apoptosis. Treatment with TNF-alpha, by destroying autoreactive T cells, appears to be a highly targeted strategy to interrupt the pathogenesis of type 1 diabetes, lupus and certain forms of autoimmunity.
IT’S 7 p.m. on a Friday night, and I’m still in the lab. Earlier in the day, as I was looking through old data, I unexpectedly found the answer to a question that I’d been trying to address for a year. It was one of those rare “eureka” moments in science. But it’s not as though in an instant a spotlight fell on the pictures of cells I’d been staring at, clearing up all mystery.
No, this is the beginning of a new mystery, and I have to repeat months worth of experiments. The other postdoctoral fellow in our group is also here late, the lights over our work area the only ones illuminating the floor. He offers to share his data and some research tools; I gratefully accept.
Would the Nobel laureate Tim Hunt argue that this scene is likely to be charged with sexual tension? After all, I am female, and Dr. Hunt, a biochemist, said at a conference earlier this month that his “trouble with girls” in laboratories is that “you fall in love with them, they fall in love with you and when you criticize them, they cry.” Certainly, then, he must have feared the possibility that two scientists might find themselves alone late one evening, with the aphrodisiacal power of scientific revelation unloosing their inhibitions.
PubMed Commons