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Institution

University of Tennessee Health Science Center

EducationMemphis, Tennessee, United States
About: University of Tennessee Health Science Center is a education organization based out in Memphis, Tennessee, United States. It is known for research contribution in the topics: Population & Transplantation. The organization has 15716 authors who have published 26884 publications receiving 1176697 citations.


Papers
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Journal ArticleDOI
TL;DR: The literature is faced with difficulties regarding the definitions and classifications used to categorize hypertension in pregnant women, and a broad spectrum of conditions in which blood pressure varies widely are described.
Abstract: Hypertensive disorders are the most common medical complications of pregnancy and are an important cause of maternal and perinatal morbidity and mortality worldwide.1 During normal pregnancy, systolic pressure changes little; however, diastolic pressure decreases by an average of 10 mm Hg early in gestation (13 to 20 weeks) and rises again to prepregnancy levels in the third trimester. The term “hypertension in pregnancy” describes a broad spectrum of conditions in which blood pressure varies widely. In reviewing the literature on this subject, one is faced with difficulties regarding the definitions and classifications used to categorize hypertension in pregnant women,2– . . .

349 citations

Journal ArticleDOI
TL;DR: It is revealed that the majority of zebrafish CYP genes are expressed in embryos, with waves of expression of different sets of genes over the course of development, which provides a foundation for the use ofZebrafish as a model in toxicological, pharmacological and chemical disease research.
Abstract: Increasing use of zebrafish in drug discovery and mechanistic toxicology demands knowledge of cytochrome P450 (CYP) gene regulation and function. CYP enzymes catalyze oxidative transformation leading to activation or inactivation of many endogenous and exogenous chemicals, with consequences for normal physiology and disease processes. Many CYPs potentially have roles in developmental specification, and many chemicals that cause developmental abnormalities are substrates for CYPs. Here we identify and annotate the full suite of CYP genes in zebrafish, compare these to the human CYP gene complement, and determine the expression of CYP genes during normal development. Zebrafish have a total of 94 CYP genes, distributed among 18 gene families found also in mammals. There are 32 genes in CYP families 5 to 51, most of which are direct orthologs of human CYPs that are involved in endogenous functions including synthesis or inactivation of regulatory molecules. The high degree of sequence similarity suggests conservation of enzyme activities for these CYPs, confirmed in reports for some steroidogenic enzymes (e.g. CYP19, aromatase; CYP11A, P450scc; CYP17, steroid 17a-hydroxylase), and the CYP26 retinoic acid hydroxylases. Complexity is much greater in gene families 1, 2, and 3, which include CYPs prominent in metabolism of drugs and pollutants, as well as of endogenous substrates. There are orthologous relationships for some CYP1 s and some CYP3 s between zebrafish and human. In contrast, zebrafish have 47 CYP2 genes, compared to 16 in human, with only two (CYP2R1 and CYP2U1) recognized as orthologous based on sequence. Analysis of shared synteny identified CYP2 gene clusters evolutionarily related to mammalian CYP2 s, as well as unique clusters. Transcript profiling by microarray and quantitative PCR revealed that the majority of zebrafish CYP genes are expressed in embryos, with waves of expression of different sets of genes over the course of development. Transcripts of some CYP occur also in oocytes. The results provide a foundation for the use of zebrafish as a model in toxicological, pharmacological and chemical disease research.

349 citations

Journal ArticleDOI
18 Aug 2005-Nature
TL;DR: Results show thatRNAi is activated during VSV infection and that RNAi is a genuine antiviral immune defence mechanism in the worm.
Abstract: The nematode Caenorhabditis elegans is an ideal model for the study of many aspects of cell biology, including the hot topic of RNA interference (RNAi). But there was a problem in using the worm to study antiviral RNAi responses: C. elegans seemed not to support viral replication. But now the insect pathogen Flock house virus and the mammalian pathogen vesicular stomatitis virus are both shown to infect the worm, and to provoke a strong RNAi-based antiviral defence. So this important genetic model is now available for the study of host–virus interactions, and the antiviral effect of RNAi. RNA interference (RNAi) is an evolutionarily conserved sequence-specific post-transcriptional gene silencing mechanism that is well defined genetically in Caenorhabditis elegans1,2,3,4. RNAi has been postulated to function as an adaptive antiviral immune mechanism in the worm, but there is no experimental evidence for this. Part of the limitation is that there are no known natural viral pathogens of C. elegans. Here we describe an infection model in C. elegans using the mammalian pathogen vesicular stomatitis virus (VSV) to study the role of RNAi in antiviral immunity. VSV infection is potentiated in cells derived from RNAi-defective worm mutants (rde-1; rde-4), leading to the production of infectious progeny virus, and is inhibited in mutants with an enhanced RNAi response (rrf-3; eri-1). Because the RNAi response occurs in the absence of exogenously added VSV small interfering RNAs, these results show that RNAi is activated during VSV infection and that RNAi is a genuine antiviral immune defence mechanism in the worm.

349 citations

Journal ArticleDOI
TL;DR: Projections from the basolateral nucleus of the amygdala to the frontal cortex and the striatum were studied by using Phaseolus vulgaris‐leucoagglutinin (PHA‐L) anterograde tracing technique in the rat.
Abstract: Projections from the basolateral nucleus of the amygdala (BLA) to the frontal cortex and the striatum were studied by using Phaseolus vulgaris-leucoagglutinin (PHA-L) anterograde tracing technique in the rat. PHA-L injections into the rostral part of the BLA resulted in a dense labeling of fibers with boutons in the dorsal bank of the rhinal fissure and in the lateral and the medial agranular cortex. PHA-L injections into the caudal part of the BLA produced a dense labeling of fibers in the medial surface of the frontal cortex. In most of the cortical regions, labeled fibers were predominantly distributed in two bands: one in the deep part of layers I and II and the other, heavier band, in layers V and VI. PHA-L injections into the rostral BLA resulted in a dense labeling of fibers with boutons in the olfactory tubercle, the rostral and caudolateral portion of the nucleus accumbens, and a large region of the caudate-putamen. The labeled area of the caudate-putamen included the rostroventral area, the central area, and the area caudal to the anterior commissure and dorsal and lateral to the globus pallidus. PHA-L injections into the caudal BLA produced fiber labeling in the most rostromedial area of the caudate-putamen facing the lateral ventricle, the medial portion of the nucleus accumbens, and the lateral septum. In the rostroventral striatum, PHA-L-labeled fibers selectively innervated the matrix compartment that contains abundant somatostatin-immunoreactive fibers. Compartmental segregation was less clear in the caudodorsolateral caudate-putamen and in the nucleus accumbens. Electron microscopy revealed that PHA-L-labeled boutons in the striatum contained abundant, small, round vesicles. These boutons formed asymmetrical synapses with dendritic spines of striatal neurons.

348 citations

Journal ArticleDOI
TL;DR: The available evidence for the regulation of Na+ channels by phosphorylation, its molecular mechanism, and the possible ways in which it affects neuronal function is reviewed.
Abstract: Voltage-gated Na+ channels set the threshold for action potential generation and are therefore good candidates to mediate forms of plasticity that affect the entire neuronal output Although early studies led to the idea that Na+ channels were not subject to modulation, we now know that Na+ channel function is affected by phosphorylation Furthermore, Na+ channel modulation is implicated in the control of input-output relationships in several types of neuron and seems to be involved in phenomena as varied as cocaine withdrawal, hyperalgesia and light adaptation Here we review the available evidence for the regulation of Na+ channels by phosphorylation, its molecular mechanism, and the possible ways in which it affects neuronal function

348 citations


Authors

Showing all 15827 results

NameH-indexPapersCitations
George P. Chrousos1691612120752
Steven N. Blair165879132929
Bruce L. Miller1631153115975
Ralph A. DeFronzo160759132993
Frank J. Gonzalez160114496971
Robert G. Webster15884390776
Anne B. Newman15090299255
Ching-Hon Pui14580572146
Barton F. Haynes14491179014
Yoshihiro Kawaoka13988375087
Seth M. Steinberg13793680148
Richard J. Johnson13788072201
Kristine Yaffe13679472250
Leslie L. Robison13185464373
Gerardo Heiss12862369393
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
202338
2022194
20211,699
20201,503
20191,401
20181,292