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71.
Comparison of the effects of parasympathetic nervous stimulation on cat submaxillary gland saliva 总被引:1,自引:0,他引:1
72.
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74.
Ariana M. Chao Thomas A. Wadden Robert I. Berkowitz George Blackburn Paula Bolin Jeanne M. Clark Mace Coday Jeffrey M. Curtis Linda M. Delahanty Gareth R. Dutton Mary Evans Linda J. Ewing John P. Foreyt Linda J. Gay Edward W. Gregg Helen P. Hazuda James O. Hill Edward S. Horton Denise K. Houston John M. Jakicic Robert W. Jeffery Karen C. Johnson Steven E. Kahn William C. Knowler Anne Kure Katherine L. Michalski Maria G. Montez Rebecca H. Neiberg Jennifer Patricio Anne Peters Xavier Pi‐Sunyer Henry Pownall David Reboussin Bruce Redmon W. Jack Rejeski Helmut Steinburg Martha Walker Donald A. Williamson Rena R. Wing Holly Wyatt Susan Z. Yanovski Ping Zhang 《Obesity (Silver Spring, Md.)》2020,28(5):893-901
75.
Edmond M. Linossi Jeffrey J. Babon Douglas J. Hilton Sandra E. Nicholson 《Cytokine & growth factor reviews》2013,24(3):241-248
The discovery of the Suppressor of Cytokine Signaling (SOCS) family of proteins has resulted in a significant body of research dedicated to dissecting their biological functions and the molecular mechanisms by which they achieve potent and specific inhibition of cytokine and growth factor signaling. The Australian contribution to this field has been substantial, with the initial discovery of SOCS1 by Hilton, Starr and colleagues (discovered concurrently by two other groups) and the following work, providing a new perspective on the regulation of JAK/STAT signaling. In this review, we reflect on the critical discoveries that have lead to our current understanding of how SOCS proteins function and discuss what we see as important questions for future research. 相似文献
76.
Meredith Mealer John Kittelson B. Taylor Thompson Arthur P. Wheeler John C. Magee Ronald J. Sokol Marc Moss Michael G. Kahn 《PloS one》2013,8(12)
Objective
Barriers to executing large-scale randomized controlled trials include costs, complexity, and regulatory requirements. We hypothesized that source document verification (SDV) via remote electronic monitoring is feasible.Methods
Five hospitals from two NIH sponsored networks provided remote electronic access to study monitors. We evaluated pre-visit remote SDV compared to traditional on-site SDV using a randomized convenience sample of all study subjects due for a monitoring visit. The number of data values verified and the time to perform remote and on-site SDV was collected.Results
Thirty-two study subjects were randomized to either remote SDV (N=16) or traditional on-site SDV (N=16). Technical capabilities, remote access policies and regulatory requirements varied widely across sites. In the adult network, only 14 of 2965 data values (0.47%) could not be located remotely. In the traditional on-site SDV arm, 3 of 2608 data values (0.12%) required coordinator help. In the pediatric network, all 198 data values in the remote SDV arm and all 183 data values in the on-site SDV arm were located. Although not statistically significant there was a consistent trend for more time consumed per data value (minutes +/- SD): Adult 0.50 +/- 0.17 min vs. 0.39 +/- 0.10 min (two-tailed t-test p=0.11); Pediatric 0.99 +/- 1.07 min vs. 0.56 +/- 0.61 min (p=0.37) and time per case report form: Adult: 4.60 +/- 1.42 min vs. 3.60 +/- 0.96 min (p=0.10); Pediatric: 11.64 +/- 7.54 min vs. 6.07 +/- 3.18 min (p=0.10) using remote SDV.Conclusions
Because each site had different policies, requirements, and technologies, a common approach to assimilating monitors into the access management system could not be implemented. Despite substantial technology differences, more than 99% of data values were successfully monitored remotely. This pilot study demonstrates the feasibility of remote monitoring and the need to develop consistent access policies for remote study monitoring. 相似文献77.
Samuel J. Clark Kathleen Kahn Brian Houle Adriane Arteche Mark A. Collinson Stephen M. Tollman Alan Stein 《PLoS medicine》2013,10(3)
Background
There is evidence that a young child''s risk of dying increases following the mother''s death, but little is known about the risk when the mother becomes very ill prior to her death. We hypothesized that children would be more likely to die during the period several months before their mother''s death, as well as for several months after her death. Therefore we investigated the relationship between young children''s likelihood of dying and the timing of their mother''s death and, in particular, the existence of a critical period of increased risk.Methods and Findings
Data from a health and socio-demographic surveillance system in rural South Africa were collected on children 0–5 y of age from 1 January 1994 to 31 December 2008. Discrete time survival analysis was used to estimate children''s probability of dying before and after their mother''s death, accounting for moderators. 1,244 children (3% of sample) died from 1994 to 2008. The probability of child death began to rise 6–11 mo prior to the mother''s death and increased markedly during the 2 mo immediately before the month of her death (odds ratio [OR] 7.1 [95% CI 3.9–12.7]), in the month of her death (OR 12.6 [6.2–25.3]), and during the 2 mo following her death (OR 7.0 [3.2–15.6]). This increase in the probability of dying was more pronounced for children whose mothers died of AIDS or tuberculosis compared to other causes of death, but the pattern remained for causes unrelated to AIDS/tuberculosis. Infants aged 0–6 mo at the time of their mother''s death were nine times more likely to die than children aged 2–5 y. The limitations of the study included the lack of knowledge about precisely when a very ill mother will die, a lack of information about child nutrition and care, and the diagnosis of AIDS deaths by verbal autopsy rather than serostatus.Conclusions
Young children in lower income settings are more likely to die not only after their mother''s death but also in the months before, when she is seriously ill. Interventions are urgently needed to support families both when the mother becomes very ill and after her death. Please see later in the article for the Editors'' Summary 相似文献78.
Thomas J. Jaworek Elodie M. Richard Anna A. Ivanova Arnaud P. J. Giese Daniel I. Choo Shaheen N. Khan Sheikh Riazuddin Richard A. Kahn Saima Riazuddin 《PLoS genetics》2013,9(9)
Exome sequencing coupled with homozygosity mapping was used to identify a transition mutation (c.794T>C; p.Leu265Ser) in ELMOD3 at the DFNB88 locus that is associated with nonsyndromic deafness in a large Pakistani family, PKDF468. The affected individuals of this family exhibited pre-lingual, severe-to-profound degrees of mixed hearing loss. ELMOD3 belongs to the engulfment and cell motility (ELMO) family, which consists of six paralogs in mammals. Several members of the ELMO family have been shown to regulate a subset of GTPases within the Ras superfamily. However, ELMOD3 is a largely uncharacterized protein that has no previously known biochemical activities. We found that in rodents, within the sensory epithelia of the inner ear, ELMOD3 appears most pronounced in the stereocilia of cochlear hair cells. Fluorescently tagged ELMOD3 co-localized with the actin cytoskeleton in MDCK cells and actin-based microvilli of LLC-PK1-CL4 epithelial cells. The p.Leu265Ser mutation in the ELMO domain impaired each of these activities. Super-resolution imaging revealed instances of close association of ELMOD3 with actin at the plasma membrane of MDCK cells. Furthermore, recombinant human GST-ELMOD3 exhibited GTPase activating protein (GAP) activity against the Arl2 GTPase, which was completely abolished by the p.Leu265Ser mutation. Collectively, our data provide the first insights into the expression and biochemical properties of ELMOD3 and highlight its functional links to sound perception and actin cytoskeleton. 相似文献
79.
Kishan?Kumar Chudasama Jonathon Winnay Stefan Johansson Tor Claudi Rainer K?nig Ingfrid Haldorsen Bente Johansson Ju?Rang Woo Dagfinn Aarskog J?rn?V. Sagen C.?Ronald Kahn Anders Molven P?l?Rasmus Nj?lstad 《American journal of human genetics》2013,93(1):150-157
The phosphatidylinositol 3 kinase (PI3K) pathway regulates fundamental cellular processes such as metabolism, proliferation, and survival. A central component in this pathway is the p85α regulatory subunit, encoded by PIK3R1. Using whole-exome sequencing, we identified a heterozygous PIK3R1 mutation (c.1945C>T [p.Arg649Trp]) in two unrelated families affected by partial lipodystrophy, low body mass index, short stature, progeroid face, and Rieger anomaly (SHORT syndrome). This mutation led to impaired interaction between p85α and IRS-1 and reduced AKT-mediated insulin signaling in fibroblasts from affected subjects and in reconstituted Pik3r1-knockout preadipocytes. Normal PI3K activity is critical for adipose differentiation and insulin signaling; the mutated PIK3R1 therefore provides a unique link among lipodystrophy, growth, and insulin signaling. 相似文献
80.
Marie-Paule?VassonEmail author Marie-Chantal?Farges Nicolas?Goncalves-Mendes Jérémie?Talvas Josep?Ribalta Brigitte?Winklhofer-Roob Edmond?Rock Adrien?Rossary 《Immunity & ageing : I & A》2013,10(1):38