Institution
University of Maryland Medical System
Healthcare•Baltimore, Maryland, United States•
About: University of Maryland Medical System is a healthcare organization based out in Baltimore, Maryland, United States. It is known for research contribution in the topics: Transplantation & Health care. The organization has 1104 authors who have published 958 publications receiving 29507 citations. The organization is also known as: UMMS & University of Maryland Medical System Corporation.
Topics: Transplantation, Health care, Poison control, Population, Medicine
Papers published on a yearly basis
Papers
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TL;DR: The usefulness of base-line levels of cardiac troponin T and CK-MB and the electrocardiographic category assigned at admission and the presence of confounding factors that impair the detection of ischemia were assessed to assess the usefulness of outcome.
Abstract: Background The prognosis of patients hospitalized with acute myocardial ischemia is quite variable. We examined the value of serum levels of cardiac troponin T, serum creatine kinase MB (CK-MB) levels, and electrocardiographic abnormalities for risk stratification in patients with acute myocardial ischemia. Methods We studied 855 patients within 12 hours of the onset of symptoms. Cardiac troponin T levels, CK-MB levels, and electrocardiograms were analyzed in a blinded fashion at the core laboratory. We used logistic regression to assess the usefulness of base-line levels of cardiac troponin T and CK-MB and the electrocardiographic category assigned at admission — ST-segment elevation, ST-segment depression, T-wave inversion, or the presence of confounding factors that impair the detection of ischemia (bundle-branch block and paced rhythms) — in predicting outcome. Results On admission, 289 of 801 patients with base-line serum samples had elevated troponin T levels (>0.1 ng per milliliter). Mortality with...
1,064 citations
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TL;DR: In this article, the efficacy of continuous intravenous infusion of prostacyclin (epoprostenol) in primary pulmonary hypertension was evaluated in a randomized trial with 8-week treatment periods and nonrandomized treatment for up to 18 months.
Abstract: Study objective To determine the efficacy of continuous intravenous infusion of prostacyclin (epoprostenol) in primary pulmonary hypertension. Design Randomized trial with 8-week treatment periods and nonrandomized treatment for up to 18 months. Setting Four referral centers. Patients Sequential sample of 24 patients with primary pulmonary hypertension. Nineteen patients completed the study. Four patients died and one left the study because of adverse effects (pulmonary edema). Interventions Continuous intravenous prostacyclin administered by portable infusion pump at doses determined by acute responses during baseline catheterization in ten patients. Nine patients were treated with anticoagulants, oral vasodilators, and diuretics. Measurements and main results Starting with a baseline value for total pulmonary resistance of 21.6 units, there was a decrease of 7.9 units (95% CI, -13.1 to -2.2; P = 0.022) in the prostacyclin-treated group after 8 weeks; there was virtually no change in the conventional therapy group (from 20.6 to 20.4 units, not significant). Six of ten prostacyclin-treated patients who completed the 8-week study period had reductions in mean pulmonary artery pressure of greater than 10 mm Hg, whereas only one of nine in the conventional treatment group had a similar response (P = 0.057). Nine patients receiving prostacyclin for up to 18 months have persistent hemodynamic effects, although dose requirements have increased with time. Complications have been attributable to the drug delivery system. Conclusions Prostacyclin produces substantial and sustained hemodynamic and symptomatic responses in severe primary pulmonary hypertension and may be useful in the management of some patients with this disease.
623 citations
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TL;DR: It is concluded that CRP has limited utility in the emergency department and may be a useful adjunct to serial examinations in equivocal presentations of appendicitis in those centers without ready access to computed tomography (CT) scan.
Abstract: C-reactive protein (CRP) was identified in 1930 and was subsequently considered to be an "acute phase protein," an early indicator of infectious or inflammatory conditions. Since its discovery, CRP has been studied as a screening device for inflammation, a marker for disease activity, and as a diagnostic adjunct. Improved methods of quantifying CRP have led to increased application to clinical medicine. In the emergency department (ED), CRP must be interpreted in the clinical context; no single value can be used to rule in or rule out a specific diagnosis. We conclude that CRP has limited utility in the ED. It may be a useful adjunct to serial examinations in equivocal presentations of appendicitis in those centers without ready access to computed tomography (CT) scan. It may be elevated with complications or treatment failures in patients with pneumonia, pancreatitis, pelvic inflammatory disease (PID), and urinary tract infections. In patients with meningitis, neonatal sepsis, and occult bacteremia, CRP is usually elevated. However, CRP has no role in diagnosing these clinical entities, and a normal CRP level should never delay antibiotic coverage.
569 citations
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TL;DR: The data suggest that homozygous CCR5-2 is an HIV-1 resistance factor in Caucasians with complete penetrance, and that heterozygously CCR 5-2 slows the rate of disease progression in infected Caucasian homosexuals.
Abstract: CC chemokine receptor 5 (CCR5) is a cell entry cofactor for macrophage-tropic isolates of human immunodeficiency virus-1 (HIV-1). Recently, an inactive CCR5 allele (designated here as CCR5-2) was identified that confers resistance to HIV-1 infection in homozygotes and slows the rate of progression to AIDS in heterozygotes. The reports conflict on the effect of heterozygous CCR5-2 on HIV-1 susceptibility, and race and risk levels have not yet been fully analyzed. Here we report our independent identification of CCR5-2 and test its effects on HIV-1 pathogenesis in individuals with contrasting clinical outcomes, defined race, and quantified risk. Mutant CCR5 alleles were sought by directed heteroduplex analysis of genomic DNA from random blood donors. Genotypic frequencies were then determined in (1) random blood donors from North America, Asia, and Africa; (2) HIV-1 + individuals; and (3) highly exposed-seronegative homosexuals with quantified risk. CCR5-2 was the only mutant allele found. It was common in Caucasians, less common in other North American racial groups, and not detected in West Africans or Tamil Indians. Homozygous CCR5-2 frequencies differed reciprocally in highly exposed-seronegative (4.5%, n = 111) and HIV-1-seropositive (0%, n = 614) Caucasians relative to Caucasian random blood donors (0.8%, n = 387). This difference was highly significant (p < 0.0001). By contrast, heterozygous CCR5-2 frequencies did not differ significantly in the same three groups (21.6, 22.6, and 21.7%, respectively). A 55% increase in the frequency of heterozygous CCR5-2 was observed in both of two cohorts of Caucasian homosexual male, long-term nonprogressors compared with other HIV-1+ Caucasian homosexuals (p = 0.006) and compared with Caucasian random blood donors. Moreover, Kaplan-Meier estimates indicated that CCR5-2 heterozygous seroconvertors had a 52.6% lower risk of developing AIDS than homozygous wild-type seroconvertors. The data suggest that homozygous CCR5-2 is an HIV-1 resistance factor in Caucasians with complete penetrance, and that heterozygous CCR5-2 slows the rate of disease progression in infected Caucasian homosexuals. Since the majority (∼96%) of highly exposed-seronegative individuals tested are not homozygous for CCR5-2, other resistance factors must exist. Since CCR5-2 homozygotes have no obvious clinical problems, CCR5 may be a good target for the development of novel antiretroviral therapy.
441 citations
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TL;DR: The molecular mechanisms that promote the survival of MM cells are examined and a key role is identified for myeloid cell factor-1 (Mcl-1), an antiapoptotic member of the Bcl-2 family, which is likely to be the labile factor governing MM cell survival.
358 citations
Authors
Showing all 1110 results
Name | H-index | Papers | Citations |
---|---|---|---|
Robert J. Mayer | 111 | 414 | 47589 |
Lewis J. Rubin | 101 | 370 | 57044 |
Thomas M. Scalea | 94 | 742 | 31851 |
David J. Sugarbaker | 86 | 348 | 32299 |
Patrick T. O'Gara | 84 | 345 | 62175 |
Norihiro Sadato | 83 | 430 | 24793 |
Matthew R. Weir | 83 | 679 | 26727 |
Allen P. Burke | 81 | 339 | 38011 |
Mandeep R. Mehra | 80 | 644 | 31939 |
Robert H. Christenson | 77 | 441 | 23846 |
Paul A. Gurbel | 77 | 589 | 28852 |
Ellen K. Silbergeld | 75 | 298 | 17669 |
Mortimer J. Buckley | 65 | 223 | 12154 |
Paul C. Kuo | 64 | 389 | 13445 |
Cinthia B. Drachenberg | 62 | 282 | 18252 |