Institution
Johns Hopkins University School of Medicine
Healthcare•Baltimore, Maryland, United States•
About: Johns Hopkins University School of Medicine is a healthcare organization based out in Baltimore, Maryland, United States. It is known for research contribution in the topics: Population & Medicine. The organization has 44277 authors who have published 79222 publications receiving 4788882 citations.
Topics: Population, Medicine, Cancer, Transplantation, Gene
Papers published on a yearly basis
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TL;DR: Impotence after radical prostatectomy results from injury to the pelvic nerve plexus that provides autonomic innervation to the corpora cavernosa, and refinements in surgical technique, especially during ligation of the lateral pedicle and apical dissection, can prevent this complication.
1,401 citations
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TL;DR: This work has reported the involvement of a 'parallel' but distinct kinase cascade leading to the activation of p38 MAPK, which might control distinct forms of synaptic plasticity in the adult brain.
Abstract: The mitogen-activated protein kinase (MAPK) cascade that leads to the activation of extracellular signal-regulated kinases-1 and -2 (ERK1 and ERK2) has a key role in the differentiation of some cell types and the proliferation of others. However, several recent reports implicate this cascade in the control of synaptic plasticity in the adult brain. ERK signalling seems to be essential for characterized neuronal transcriptional events, and might also regulate synaptic targets to control plasticity. Another recently emerging story is the involvement of a 'parallel' but distinct kinase cascade leading to the activation of p38 MAPK, which might control distinct forms of synaptic plasticity.
1,396 citations
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TL;DR: Online Mendelian Inheritance In Man is a public database of bibliographic information about human genes and genetic disorders that is increasingly becoming a major gateway for clinicians, students, and basic researchers to the ever‐growing literature and resources of human genetics.
Abstract: Online Mendelian Inheritance In Man (OMIM) is a public database of bibliographic information about human genes and genetic disorders. Begun by Dr. Victor McKusick as the authoritative reference Mendelian Inheritance in Man, it is now distributed electronically by the National Center for Biotechnology Information (NCBI). Material in OMIM is derived from the biomedical literature and is written by Dr. McKusick and his colleagues at Johns Hopkins University and elsewhere. Each OMIM entry has a full text summary of a genetic phenotype and/or gene and has copious links to other genetic resources such as DNA and protein sequence, PubMed references, mutation databases, approved gene nomenclature, and more. In addition, NCBI's neighboring feature allows users to identify related articles from PubMed selected on the basis of key words in the OMIM entry. Through its many features, OMIM is increasingly becoming a major gateway for clinicians, students, and basic researchers to the ever-growing literature and resources of human genetics.
1,396 citations
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TL;DR: Through 144 weeks, the combination of tenofovir DF, lamivudine, and efavirenz was highly effective and comparable with stavudine for antiretroviral-naive patients and appeared to be associated with better lipid profiles and less lipodystrophy.
Abstract: ContextTenofovir disoproxil fumarate (DF) is a once-daily nucleotide analogue
reverse transcriptase inhibitor.ObjectiveTo evaluate the efficacy and safety of tenofovir DF compared with stavudine
in antiretroviral-naive patients.Design, Setting, and ParticipantsA prospective, randomized, double-blind study conducted at 81 centers
in the United States, South America, and Europe from June 9, 2000, to January
30, 2004. A total of 753 patients infected with HIV who were antiretroviral
naive were screened and 602 patients entered the study.InterventionPatients were randomized to receive either tenofovir DF (n = 299) or
stavudine (n = 303), with placebo, in combination with lamivudine and efavirenz.Main Outcome MeasureProportion of patients with HIV RNA levels of less than 400 copies/mL
at week 48.ResultsIn the primary intent-to-treat analysis in which patients with missing
data or who added or switched antiretroviral medications before week 48 were
considered as failures, the proportion of patients with HIV RNA of less than
400 copies/mL at week 48 was 239 (80%) of 299 in patients receiving tenofovir
DF and 253 (84%) of 301 in patients receiving stavudine (95% confidence interval,
−10.4% to 1.5%), exceeding the predefined −10% limit for equivalence.
However, equivalence was demonstrated in the secondary analyses (HIV RNA <50
copies/mL) at week 48 and through 144 weeks. Virologic failure was associated
most frequently with efavirenz and lamivudine resistance. Through 144 weeks,
the K65R mutation emerged in 8 and 2 patients in the tenofovir DF and stavudine
groups, respectively (P = .06). A more favorable
mean change from baseline in fasting lipid profile was noted in the tenofovir
DF group at week 144: for triglyceride levels (+1 mg/dL for tenofovir DF [n
= 170] vs +134 mg/dL for stavudine [n = 162], P<.001),
total cholesterol (+30 mg/dL [n = 170] vs +58 mg/dL [n = 162], P<.001), direct low-density lipoprotein cholesterol (+14 mg/dL [n
= 169] vs +26 mg/dL [n = 161], P<.001), and high-density
lipoprotein cholesterol (+9 mg/dL [n = 168] vs +6 mg/dL [n = 154], P = .003). Investigator-reported lipodystrophy was less common in the
tenofovir DF group compared with the stavudine group (9 [3%] of 299 vs 58
[19%] of 301, P<.001). The number of bone fractures
and the renal safety profile were similar between the 2 groups.ConclusionsThrough 144 weeks, the combination of tenofovir DF, lamivudine, and
efavirenz was highly effective and comparable with stavudine, lamivudine,
and efavirenz in antiretroviral-naive patients. However, tenofovir DF appeared
to be associated with better lipid profiles and less lipodystrophy.
1,394 citations
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TL;DR: Predictive genetic testing and findings of neuroimaging studies show that Huntington's disease is emerging as a model for strategies to develop therapeutic interventions, not only to slow progression of manifest disease but also to delay, or ideally prevent, its onset.
Abstract: Huntington's disease is a progressive, fatal, neurodegenerative disorder caused by an expanded CAG repeat in the huntingtin gene, which encodes an abnormally long polyglutamine repeat in the huntingtin protein. Huntington's disease has served as a model for the study of other more common neurodegenerative disorders, such as Alzheimer's disease and Parkinson's disease. These disorders all share features including: delayed onset; selective neuronal vulnerability, despite widespread expression of disease-related proteins during the whole lifetime; abnormal protein processing and aggregation; and cellular toxic effects involving both cell autonomous and cell-cell interaction mechanisms. Pathogenic pathways of Huntington's disease are beginning to be unravelled, offering targets for treatments. Additionally, predictive genetic testing and findings of neuroimaging studies show that, as in some other neurodegenerative disorders, neurodegeneration in affected individuals begins many years before onset of diagnosable signs and symptoms of Huntington's disease, and it is accompanied by subtle cognitive, motor, and psychiatric changes (so-called prodromal disease). Thus, Huntington's disease is also emerging as a model for strategies to develop therapeutic interventions, not only to slow progression of manifest disease but also to delay, or ideally prevent, its onset.
1,394 citations
Authors
Showing all 44754 results
Name | H-index | Papers | Citations |
---|---|---|---|
Robert Langer | 281 | 2324 | 326306 |
Bert Vogelstein | 247 | 757 | 332094 |
Solomon H. Snyder | 232 | 1222 | 200444 |
Steven A. Rosenberg | 218 | 1204 | 199262 |
Kenneth W. Kinzler | 215 | 640 | 243944 |
Hagop M. Kantarjian | 204 | 3708 | 210208 |
Mark P. Mattson | 200 | 980 | 138033 |
Stuart H. Orkin | 186 | 715 | 112182 |
Paul G. Richardson | 183 | 1533 | 155912 |
Aaron R. Folsom | 181 | 1118 | 134044 |
Gonçalo R. Abecasis | 179 | 595 | 230323 |
Jie Zhang | 178 | 4857 | 221720 |
Daniel R. Weinberger | 177 | 879 | 128450 |
David Baker | 173 | 1226 | 109377 |
Eliezer Masliah | 170 | 982 | 127818 |