Institution
Medical University of South Carolina
Education•Charleston, South Carolina, United States•
About: Medical University of South Carolina is a education organization based out in Charleston, South Carolina, United States. It is known for research contribution in the topics: Population & Poison control. The organization has 23436 authors who have published 45440 publications receiving 1769397 citations. The organization is also known as: MUSC & Medical College of the State of South Carolina.
Topics: Population, Poison control, Medicine, Cancer, Stroke
Papers published on a yearly basis
Papers
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TL;DR: In this paper, the authors investigated the role of Cortico-striatal glutamate transmission in both the initiation and expression of addiction related behaviors, such as locomotor sensitization and drug-seeking.
347 citations
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TL;DR: Stimulation of all three prefrontal regions, but not the occipital or cerebellar regions, was associated with increases in serum thyroid-stimulating hormone and there was no effect on serum prolactin.
Abstract: Rapid-rate transcranial magnetic stimulation (rTMS) was administered to 10 healthy volunteers on different days over the right or left prefrontal cortex, midfrontal cortex, occipital cortex, or cerebellum. Mood (self-rated), reaction time, and hormone levels were serially measured. Consistent with a previous study, comparison of hemispheres revealed significant associations with decreased happiness after left prefrontal rTMS and decreased sadness after right prefrontal rTMS. Stimulation of all three prefrontal regions, but not the occipital or cerebellar regions, was associated with increases in serum thyroid-stimulating hormone. There was no effect on serum prolactin. rTMS applied to prefrontal cortex is safe and well tolerated and produces regionally and laterally specific changes in mood and neuroendocrine measures in healthy adults. rTMS is a promising tool for investigating prefrontal cortex functions.
347 citations
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29 Aug 2019TL;DR: The past 15 years have brought a remarkable improvement in the clinical outcome of patients with valvular heart disease, and it is impossible to attribute the change to any single advance in the field as mentioned in this paper.
Abstract: The past 15 years have brought a remarkable improvement in the clinical outcome of patients with valvular heart disease. It is impossible to attribute the change to any single advance in the field. However, it is likely that more effective noninvasive monitoring of ventricular function, improvement in prosthetic valves, advances in valve-reconstruction techniques, and the development of useful guidelines for choosing the proper timing of surgical intervention have all worked in concert to improve prognosis. Moreover, advances in minimally invasive surgical techniques may make valve procedures more easily tolerated by the patient.1 All valvular heart diseases place a hemodynamic burden . . .
346 citations
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TL;DR: A mouse model of ethanol dependence and repeated withdrawals that demonstrates sensitization of seizures and other symptoms of withdrawal may be useful in studying the mechanisms and conditions in which chronic ethanol treatment influences motivation to resume drinking after a period of abstinence (relapse).
Abstract: Background: The development of dependence may have significant motivational consequences regarding continued use and abuse of ethanol. We have developed a mouse model of ethanol dependence and repeated withdrawals that demonstrates sensitization of seizures and other symptoms of withdrawal. It is unclear whether such experience influences ethanol drinking behavior. The present series of experiments were designed to examine whether repeated cycles of chronic ethanol exposure and withdrawal has an impact on subsequent motivation to voluntarily self-administer ethanol.
Methods: With the use of a modified sucrose-fading procedure, adult male C57BL/6J mice were trained to drink 15% (v/v) ethanol in a limited access procedure (2 hr/day). The animals were not food or water deprived at any time during the experiments. Once stable baseline intake was established, mice were exposed to four cycles of 16 hr of ethanol vapor (or air) in inhalation chambers separated by 8-hr periods of withdrawal. At 32 hr after the last cycle of ethanol exposure, all mice were tested for ethanol intake under limited access conditions for 5 consecutive days. The animals then received a second series of chronic ethanol exposure and withdrawal followed by another 5-day test period for ethanol drinking.
Results: Stable daily baseline intake was established in mice that drank 15% ethanol combined with 5% sucrose (experiment 1), 15% ethanol alone (experiment 2), 5% sucrose alone (experiment 3), or 15% ethanol when presented as a choice with water (experiment 4). After repeated cycles of chronic ethanol exposure and withdrawal experience, consumption of ethanol solutions increased over baseline levels and in comparison with control (air-exposed) groups. However, sucrose consumption did not change in mice that were trained to drink 5% sucrose. The increase in ethanol consumption after chronic ethanol exposure and withdrawal experience resulted in a significant increase in resultant blood ethanol levels.
Conclusions: Once the positive reinforcing properties of ethanol were established, chronic ethanol exposure and withdrawal experience resulted in a significant increase in voluntary ethanol drinking that yielded a >2-fold increase in resultant blood ethanol levels. This increase in ethanol intake occurred whether ethanol was presented in combination with sucrose, alone (unadulterated), or as a choice with tap water. Furthermore, this effect seems to be selective for ethanol in that animals that were trained to drink a sucrose solution did not exhibit a change in their intake after similar chronic ethanol exposure. As such, this model may be useful in studying the mechanisms and conditions in which chronic ethanol treatment influences motivation to resume drinking after a period of abstinence (relapse).
346 citations
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TL;DR: First-degree relatives of African Americans with AD have a higher cumulative risk of dementia than do those of whites with AD, and the patterns of risk among first-degree biological relatives stratified by APOE genotype of the probands were similar in white families and African American families.
Abstract: ContextEvidence exists that the incidence of Alzheimer disease (AD), as well
as risk attributable to specific genetic factors such as apolipoprotein E
(APOE) genotype, may vary considerably among ethnic
groups. Family studies of probands with AD offer an opportunity to evaluate
lifetime risk of dementia among relatives of these probands.ObjectiveTo compare lifetime dementia risk estimates among relatives of white
and African American probands with probable or definite AD.Design and SettingRisk analysis using data collected by questionnaire and supplemental
records between May 1991 and March 2001 at 17 medical centers contributing
to the Multi-Institutional Research in Alzheimer's Genetic Epidemiology Study.ParticipantsA total of 17 639 first-degree biological relatives and 2474 spouses
of 2339 white AD probands, and 2281 first-degree biological relatives and
257 spouses of 255 African American AD probands.Main Outcome MeasuresCumulative risk of dementia by age 85 years, stratified by ethnicity
and sex of relatives and by APOE genotype of probands.ResultsCumulative risk of dementia in first-degree biological relatives of
African American AD probands by age 85 years was 43.7% (SE, 3.1%), and the
corresponding risk in first-degree biological relatives of white AD probands
was 26.9% (SE, 0.8%), yielding a relative risk (RR) of 1.6 (95% confidence
interval [CI], 1.4-1.9; P<.001). The risk in spouses
of African American AD probands of 18.5% (SE, 8.4%) was also higher than the
risk in white spouses of 10.4% (SE, 1.7%) but did not reach statistical significance
(RR, 1.8; 95% CI, 0.5-6.0; P = .34), likely due to
the smaller sample size of African Americans. The proportional increase in
risk of dementia among white first-degree biological relatives compared with
white spouses of 2.6 (95% CI, 2.1-3.2) was similar to that of 2.4 (95% CI,
1.3-4.4) in African American first-degree biological relatives compared with
African American spouses. Female first-degree biological relatives of probands
had a higher risk of developing dementia than did their male counterparts,
among whites (31.2% vs 20.4%; RR, 1.5; 95% CI, 1.3-1.7; P<.001) as well as among African Americans, although this was not
significant among African Americans (46.7% vs 40.1%; RR, 1.2; 95% CI, 0.9-1.7, P = .30). The patterns of risk among first-degree biological
relatives stratified by APOE genotype of the probands
were similar in white families and African American families.ConclusionFirst-degree relatives of African Americans with AD have a higher cumulative
risk of dementia than do those of whites with AD. However, in this study,
the additional risk of dementia conferred by being a first-degree relative,
by being female, or by the probability of having an APOE ∊4 allele appeared similar in African American and white families.
These data provide estimates of dementia risk that can be used to offer counseling
to family members of patients with AD.
346 citations
Authors
Showing all 23601 results
Name | H-index | Papers | Citations |
---|---|---|---|
Edward Giovannucci | 206 | 1671 | 179875 |
Ronald Klein | 194 | 1305 | 149140 |
Peter W.F. Wilson | 181 | 680 | 139852 |
Yusuke Nakamura | 179 | 2076 | 160313 |
John J.V. McMurray | 178 | 1389 | 184502 |
Nora D. Volkow | 165 | 958 | 107463 |
L. Joseph Melton | 161 | 531 | 97861 |
Gregg C. Fonarow | 161 | 1676 | 126516 |
Michael Boehnke | 152 | 511 | 136681 |
Charles B. Nemeroff | 149 | 979 | 90426 |
Deepak L. Bhatt | 149 | 1973 | 114652 |
Clifford R. Jack | 140 | 965 | 94814 |
Scott D. Solomon | 137 | 1145 | 103041 |
Karl Swedberg | 136 | 706 | 111214 |
Charles J. Yeo | 136 | 672 | 76424 |