Institution
University of Texas Health Science Center at Houston
Education•Houston, Texas, United States•
About: University of Texas Health Science Center at Houston is a education organization based out in Houston, Texas, United States. It is known for research contribution in the topics: Population & Poison control. The organization has 27309 authors who have published 42520 publications receiving 2151596 citations. The organization is also known as: UTHealth & The UT Health Science Center at Houston.
Topics: Population, Poison control, Cancer, Stroke, Health care
Papers published on a yearly basis
Papers
More filters
••
TL;DR: A “micro-electrospray” ionization source has been developed that markedly increases the sensitivity of the conventional electrosprays source by optimization of the source to accommodate nanoliter flow rates from 300 to 800-nL/min spraying directly from a capillary needle that contained C18 liquid chromatography packing as an integrated concentration-desalting device.
495 citations
••
TL;DR: The results show that deadenylation is the key first step that triggers decay of both wild-type stable and nonsense codon–containing unstable β-globin mRNAs in mouse NIH3T3 fibroblasts.
Abstract: In mammalian cells, the enzymatic pathways involved in cytoplasmic mRNA decay are incompletely defined. In this study, we have used two approaches to disrupt activities of deadenylating and/or decapping enzymes to monitor effects on mRNA decay kinetics and trap decay intermediates. Our results show that deadenylation is the key first step that triggers decay of both wild-type stable and nonsense codon–containing unstable β-globin mRNAs in mouse NIH3T3 fibroblasts. PAN2 and CCR4 are the major poly(A) nucleases active in cytoplasmic deadenylation that have biphasic kinetics, with PAN2 initiating deadenylation followed by CCR4-mediated poly(A) shortening. DCP2-mediated decapping takes place after deadenylation and may serve as a backup mechanism for triggering mRNA decay when initial deadenylation by PAN2 is compromised. Our findings reveal a functional link between deadenylation and decapping and help to define in vivo pathways for mammalian cytoplasmic mRNA decay.
494 citations
••
TL;DR: A global effort is needed to safely translate laboratory innovation to the clinic and seven priority areas have been identified for this endeavour.
Abstract: Nanomedicine offers new opportunities to fight diseases but a global effort is needed to safely translate laboratory innovation to the clinic Seven priority areas have been identified for this endeavour
493 citations
••
TL;DR: Bipolar disorder has a strong relationship to a history of suicide attempts relative to unipolar disorder and other Axis I disorders.
492 citations
••
TL;DR: It is suggested that curcumin has high anticancer efficacy in vitro and in vivo by inducing autophagy and warrant further investigation toward possible clinical application in patients with malignant glioma.
Abstract: Autophagy is a response of cancer cells to various anticancer therapies. It is designated as programmed cell death type II and characterized by the formation of autophagic vacuoles in the cytoplasm. The Akt/mammalian target of rapamycin (mTOR)/p70 ribosomal protein S6 kinase (p70S6K) and the extracellular signal-regulated kinases 1/2 (ERK1/2) pathways are two major pathways that regulate autophagy induced by nutrient starvation. These pathways are also frequently associated with oncogenesis in a variety of cancer cell types, including malignant gliomas. However, few studies have examined both of these signal pathways in the context of anticancer therapy-induced autophagy in cancer cells, and the effect of autophagy on cell death remains unclear. Here, we examined the anticancer efficacy and mechanisms of curcumin, a natural compound with low toxicity in normal cells, in U87-MG and U373-MG malignant glioma cells. Curcumin induced G(2)/M arrest and nonapoptotic autophagic cell death in both cell types. It inhibited the Akt/mTOR/p70S6K pathway and activated the ERK1/2 pathway, resulting in induction of autophagy. It is interesting that activation of the Akt pathway inhibited curcumin-induced autophagy and cytotoxicity, whereas inhibition of the ERK1/2 pathway inhibited curcumin-induced autophagy and induced apoptosis, thus resulting in enhanced cytotoxicity. These results imply that the effect of autophagy on cell death may be pathway-specific. In the subcutaneous xenograft model of U87-MG cells, curcumin inhibited tumor growth significantly (P < 0.05) and induced autophagy. These results suggest that curcumin has high anticancer efficacy in vitro and in vivo by inducing autophagy and warrant further investigation toward possible clinical application in patients with malignant glioma.
492 citations
Authors
Showing all 27450 results
Name | H-index | Papers | Citations |
---|---|---|---|
Paul M. Ridker | 233 | 1242 | 245097 |
Eugene Braunwald | 230 | 1711 | 264576 |
Eric N. Olson | 206 | 814 | 144586 |
Hagop M. Kantarjian | 204 | 3708 | 210208 |
André G. Uitterlinden | 199 | 1229 | 156747 |
Gordon B. Mills | 187 | 1273 | 186451 |
Eric Boerwinkle | 183 | 1321 | 170971 |
Bruce M. Psaty | 181 | 1205 | 138244 |
Aaron R. Folsom | 181 | 1118 | 134044 |
Daniel R. Weinberger | 177 | 879 | 128450 |
Bharat B. Aggarwal | 175 | 706 | 116213 |
Richard A. Gibbs | 172 | 889 | 249708 |
Russel J. Reiter | 169 | 1646 | 121010 |
James F. Sallis | 169 | 825 | 144836 |
Steven N. Blair | 165 | 879 | 132929 |