Tracking a Serial Killer: Ebola virus mutating rapidly as it spreads.
Why we need to terminate Ebola 2014 before the virus learns too much about us.
Biochemistry and Molecular Biology Slide 2
This theme is Bloggerized by Dr. Shreekrishna Maharjan.
Biochemistry and Molecular Biology Slide 3
This theme is Bloggerized by Dr. Shreekrishna Maharjan.
Biochemistry and Molecular Biology Slide 4
This theme is Bloggerized by Dr. Shreekrishna Maharjan.
Biochemistry and Molecular Biology Slide 5
This theme is Bloggerized by Dr. Shreekrishna Maharjan.
Biochemistry and Molecular Biology Slide 6
This theme is Bloggerized by Dr. Shreekrishna Maharjan.
Biochemistry and Molecular Biology Slide 7
This theme is Bloggerized by Dr. Shreekrishna Maharjan.
Thursday, November 20, 2014
Gene Test May Spot Which Kidney Transplants More Likely to Fail
MicroRNAs in kidney physiology and disease
Abstract
Key points
- MicroRNAs (miRNAs) are key players in kidney development and physiology
- Transforming growth factor β1 is a major regulator of kidney fibrosis; its signalling is finely regulated by miRNAs
- miRNAs contribute to both the induction and progression of chronic kidney disease (CKD)
- Current translational research on miRNAs in kidney disease is mainly focused on developing reliable biomarkers for diagnosis and prognosis of CKD and renal transplantation
- miRNAs represent novel therapeutic targets for CKD, but delivery and safety issues must be taken into account before translation into clinical practice
Introduction
Biogenesis and function of miRNAs
Conclusions
Mother’s Microbes Protect Baby’s Brain
Tags
Cystic fibrosis genetics: from molecular understanding to clinical application
Abstract
Key points
- Investigation of disease-causing variants such as F508del is resolving the mechanisms underlying cystic fibrosis transmembrane conductance regulator (CFTR) folding and will inform rational design of compounds to correct the folding of mutant CFTR.
- New tissue culture methods will facilitate the evaluation of molecular targeted therapy for a wide array of CFTR genotypes, and new animal models should enable assessment of treatment at the earliest stages of the disease.
- Analyses of affected twin and sibling pairs have quantified the contribution of genetic and non-genetic modifiers to variation in key features of cystic fibrosis.
- Candidate and genome-wide approaches have identified biologically plausible gene modifiers of lung disease severity, neonatal intestinal obstruction and diabetes in cystic fibrosis.
- Annotation of variants in CFTR will increase the utility of genetic testing in newborn screening, carrier testing and diagnostic settings. Assignment of variants as disease-causing will validate efforts to target variants for molecular therapies.
- Small-molecule therapy for cystic fibrosis has been successful for patients carrying a subset of CFTR variants. Grouping of variants according to responses in cell-based assays (that is, theratypes) could expedite treatment of affected individuals with rare CFTR genotypes.