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Institution

Medical University of South Carolina

EducationCharleston, South Carolina, United States
About: Medical University of South Carolina is a(n) education organization based out in Charleston, South Carolina, United States. It is known for research contribution in the topic(s): Population & Poison control. The organization has 23436 authors who have published 45440 publication(s) receiving 1769397 citation(s). The organization is also known as: MUSC & Medical College of the State of South Carolina.


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Journal ArticleDOI
05 Feb 2014-JAMA
TL;DR: Although this guideline provides evidence-based recommendations for the management of high BP and should meet the clinical needs of most patients, these recommendations are not a substitute for clinical judgment, and decisions about care must carefully consider and incorporate the clinical characteristics and circumstances of each individual patient.
Abstract: Hypertension is the most common condition seen in primary care and leads to myocardial infarction, stroke, renal failure, and death if not detected early and treated appropriately. Patients want to be assured that blood pressure (BP) treatment will reduce their disease burden, while clinicians want guidance on hypertension management using the best scientific evidence. This report takes a rigorous, evidence-based approach to recommend treatment thresholds, goals, and medications in the management of hypertension in adults. Evidence was drawn from randomized controlled trials, which represent the gold standard for determining efficacy and effectiveness. Evidence quality and recommendations were graded based on their effect on important outcomes. There is strong evidence to support treating hypertensive persons aged 60 years or older to a BP goal of less than 150/90 mm Hg and hypertensive persons 30 through 59 years of age to a diastolic goal of less than 90 mm Hg; however, there is insufficient evidence in hypertensive persons younger than 60 years for a systolic goal, or in those younger than 30 years for a diastolic goal, so the panel recommends a BP of less than 140/90 mm Hg for those groups based on expert opinion. The same thresholds and goals are recommended for hypertensive adults with diabetes or nondiabetic chronic kidney disease (CKD) as for the general hypertensive population younger than 60 years. There is moderate evidence to support initiating drug treatment with an angiotensin-converting enzyme inhibitor, angiotensin receptor blocker, calcium channel blocker, or thiazide-type diuretic in the nonblack hypertensive population, including those with diabetes. In the black hypertensive population, including those with diabetes, a calcium channel blocker or thiazide-type diuretic is recommended as initial therapy. There is moderate evidence to support initial or add-on antihypertensive therapy with an angiotensin-converting enzyme inhibitor or angiotensin receptor blocker in persons with CKD to improve kidney outcomes. Although this guideline provides evidence-based recommendations for the management of high BP and should meet the clinical needs of most patients, these recommendations are not a substitute for clinical judgment, and decisions about care must carefully consider and incorporate the clinical characteristics and circumstances of each individual patient.

6,388 citations

Journal ArticleDOI
Daniel J. Klionsky1, Kotb Abdelmohsen2, Akihisa Abe3, Joynal Abedin4  +2519 moreInstitutions (695)
Abstract: In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes. For example, a key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process versus those that measure flux through the autophagy pathway (i.e., the complete process including the amount and rate of cargo sequestered and degraded). In particular, a block in macroautophagy that results in autophagosome accumulation must be differentiated from stimuli that increase autophagic activity, defined as increased autophagy induction coupled with increased delivery to, and degradation within, lysosomes (in most higher eukaryotes and some protists such as Dictyostelium) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the field understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in many cases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. It is worth emphasizing here that lysosomal digestion is a stage of autophagy and evaluating its competence is a crucial part of the evaluation of autophagic flux, or complete autophagy. Here, we present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes. These guidelines are not meant to be a formulaic set of rules, because the appropriate assays depend in part on the question being asked and the system being used. In addition, we emphasize that no individual assay is guaranteed to be the most appropriate one in every situation, and we strongly recommend the use of multiple assays to monitor autophagy. Along these lines, because of the potential for pleiotropic effects due to blocking autophagy through genetic manipulation, it is imperative to target by gene knockout or RNA interference more than one autophagy-related protein. In addition, some individual Atg proteins, or groups of proteins, are involved in other cellular pathways implying that not all Atg proteins can be used as a specific marker for an autophagic process. In these guidelines, we consider these various methods of assessing autophagy and what information can, or cannot, be obtained from them. Finally, by discussing the merits and limits of particular assays, we hope to encourage technical innovation in the field.

4,756 citations

Journal ArticleDOI
TL;DR: These guidelines are presented for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
Abstract: In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes. A key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process vs. those that measure flux through the autophagy pathway (i.e., the complete process); thus, a block in macroautophagy that results in autophagosome accumulation needs to be differentiated from stimuli that result in increased autophagic activity, defined as increased autophagy induction coupled with increased delivery to, and degradation within, lysosomes (in most higher eukaryotes and some protists such as Dictyostelium) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the field understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in many cases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. Here, we present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes. These guidelines are not meant to be a formulaic set of rules, because the appropriate assays depend in part on the question being asked and the system being used. In addition, we emphasize that no individual assay is guaranteed to be the most appropriate one in every situation, and we strongly recommend the use of multiple assays to monitor autophagy. In these guidelines, we consider these various methods of assessing autophagy and what information can, or cannot, be obtained from them. Finally, by discussing the merits and limits of particular autophagy assays, we hope to encourage technical innovation in the field.

3,426 citations

Journal ArticleDOI
Christopher G. Goetz1, Barbara C. Tilley2, Stephanie R. Shaftman2, Glenn T. Stebbins1, Stanley Fahn3, Pablo Martinez-Martin, Werner Poewe4, Cristina Sampaio5, Matthew B. Stern6, Richard Dodel7, Bruno Dubois8, Robert G. Holloway9, Joseph Jankovic10, Jaime Kulisevsky11, Anthony E. Lang12, Andrew J. Lees13, Sue Leurgans1, Peter A. LeWitt14, David L. Nyenhuis15, C. Warren Olanow16, Olivier Rascol17, Anette Schrag13, Jeanne A. Teresi3, Jacobus J. van Hilten18, Nancy R. LaPelle19, Pinky Agarwal, Saima Athar, Yvette Bordelan, Helen Bronte-Stewart, Richard Camicioli, Kelvin L. Chou, Wendy Cole, Arif Dalvi, Holly Delgado, Alan Diamond, Jeremy P.R. Dick, John E. Duda, Rodger J. Elble, Carol Evans, V. G. H. Evidente, Hubert H. Fernandez, Susan H. Fox, Joseph H. Friedman, Robin D. Fross, David A. Gallagher, Deborah A. Hall, Neal Hermanowicz, Vanessa K. Hinson, Stacy Horn, Howard I. Hurtig, Un Jung Kang, Galit Kleiner-Fisman, Olga Klepitskaya, Katie Kompoliti, Eugene C. Lai, Maureen L. Leehey, Iracema Leroi, Kelly E. Lyons, Terry McClain, Steven W. Metzer, Janis M. Miyasaki, John C. Morgan, Martha Nance, Joanne Nemeth, Rajesh Pahwa, Sotirios A. Parashos, Jay S. Schneider, Kapil D. Sethi, Lisa M. Shulman, Andrew Siderowf, Monty Silverdale, Tanya Simuni, Mark Stacy, Robert Malcolm Stewart, Kelly L. Sullivan, David M. Swope, Pettaruse M. Wadia, Richard Walker, Ruth H. Walker, William J. Weiner, Jill Wiener, Jayne R. Wilkinson, Joanna M. Wojcieszek, Summer C. Wolfrath, Frederick Wooten, Allen Wu, Theresa A. Zesiewicz, Richard M. Zweig 
TL;DR: The combined clinimetric results of this study support the validity of the MDS‐UPDRS for rating PD.
Abstract: We present a clinimetric assessment of the Movement Disorder Society (MDS)-sponsored revision of the Unified Parkinson's Disease Rating Scale (MDS-UPDRS). The MDS-UDPRS Task Force revised and expanded the UPDRS using recommendations from a published critique. The MDS-UPDRS has four parts, namely, I: Non-motor Experiences of Daily Living; II: Motor Experiences of Daily Living; III: Motor Examination; IV: Motor Complications. Twenty questions are completed by the patient/caregiver. Item-specific instructions and an appendix of complementary additional scales are provided. Movement disorder specialists and study coordinators administered the UPDRS (55 items) and MDS-UPDRS (65 items) to 877 English speaking (78% non-Latino Caucasian) patients with Parkinson's disease from 39 sites. We compared the two scales using correlative techniques and factor analysis. The MDS-UPDRS showed high internal consistency (Cronbach's alpha = 0.79-0.93 across parts) and correlated with the original UPDRS (rho = 0.96). MDS-UPDRS across-part correlations ranged from 0.22 to 0.66. Reliable factor structures for each part were obtained (comparative fit index > 0.90 for each part), which support the use of sum scores for each part in preference to a total score of all parts. The combined clinimetric results of this study support the validity of the MDS-UPDRS for rating PD.

3,385 citations


Authors

Showing all 23436 results

NameH-indexPapersCitations
Edward Giovannucci2061671179875
Ronald Klein1941305149140
Peter W.F. Wilson181680139852
Yusuke Nakamura1792076160313
John J.V. McMurray1781389184502
Nora D. Volkow165958107463
L. Joseph Melton16153197861
Gregg C. Fonarow1611676126516
Michael Boehnke152511136681
Charles B. Nemeroff14997990426
Deepak L. Bhatt1491973114652
Clifford R. Jack14096594814
Scott D. Solomon1371145103041
Karl Swedberg136706111214
Charles J. Yeo13667276424
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
202223
20212,652
20202,486
20192,343
20182,094
20172,332