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Biomedical subjects

R Groves

Publications and source records attributed to R Groves.

At least 19 recordsLinked to original sources
PubMed2003

Calcium homeostasis remains unaffected after 12 weeks' therapy with calcitriol 3 microg/g ointment; no correlation with extent of psoriasis.

OBJECTIVE: To assess the systemic safety of calcitriol 3 microg/g ointment (Silkis) ointment) in relation to body surface area (BSA) affected by chronic plaque psoriasis. METHODS: In this open-label, multicentre study, patients were divided into three parallel groups: 5% to <15% (n=23), 15% to <25% (n=18), 25% to 35% (n=18) based on BSA involvement. Ointment was applied topically twice daily for 12 weeks; patients were followed up for a further 8 weeks. RESULTS: There was no alteration of calcium homeostasis: the mean values of albumin-adjusted serum total calcium, as well as 24-hour urinary calcium and serum calcitriol levels, remained within normal ranges throughout treatment. No changes in calcium or phosphate homeostasis related to the area of psoriasis being treated with calcitriol ointment were detected. CONCLUSIONS: Reductions in the global severity score and BSA involvement, as well as results of the assessment of improvement, attested to the clinical efficacy of calcitriol 3 microg/g ointment in psoriasis. The study confirms the systemic safety of calcitriol 3 microg/g in psoriatic patients with 5-35% BSA involvement.

Administration, Cutaneous↗
PubMed1998

Randomized, double-blind study comparing saruplase with streptokinase therapy in acute myocardial infarction: the COMPASS Equivalence Trial. Comparison Trial of Saruplase and Streptokinase (COMASS) Investigators.

OBJECTIVES: This study sought to demonstrate the equivalence of saruplase and streptokinase in terms of 30-day mortality. BACKGROUND: The use of thrombolytic agents in the treatment of acute myocardial infarction is well established and has been shown to substantially reduce post-myocardial infarction mortality. METHODS: Three thousand eighty-nine patients with symptoms compatible with those of acute myocardial infarction for < 6 h entered the study at a total of 104 centers and were randomized to receive streptokinase (1.5-MU infusion over 60 min) or saruplase (20-mg bolus and 60-mg infusion over 60 min). In the saruplase group, a bolus of heparin (5,000 IU) was administered before saruplase, and a corresponding blinded double-dummy placebo bolus was administered before streptokinase. All patients received intravenous heparin infusions for > or = 24 h starting 30 min after the end of the thrombolytic infusions; the infusions were titrated to maintain an activated partial thromboplastin time at 1.5 to 2.5 times that of normal. RESULTS: Death of any cause up to 30 days after randomization occurred in 88 (5.7%) of 1,542 patients randomized to receive saruplase and 104 (6.7%) of 1,547 patients randomized to receive streptokinase (odds ratio 0.84, p < 0.01 for equivalence). Hemorrhagic strokes occurred more often in patients receiving saruplase (0.9% vs. 0.3%), whereas thromboembolic strokes were more prevalent in the streptokinase-treated patients (0.5% vs. 1.0%). The rate of bleeding was similar in the two treatment groups (10.4% vs. 10.9%). Hypotension and cardiogenic shock occurred less frequently in the saruplase group. Reinfarction rates were similar. CONCLUSIONS: Saruplase is a clinically safe and effective thrombolytic medication. This profile ranks saruplase favorably among the currently available thrombolytic agents.

Aged↗
PubMed1998

Cutaneous infection with Alternaria alternata complicating immunosuppression: successful treatment with itraconazole.

We report an immunosuppressed patient who presented with unusual leg ulceration caused by Alternaria alternata infection. Alternaria is a common saprophyte that is not usually pathogenic in humans. However, infections have previously been documented. Most cases occur in immunocompromised patients and the skin manifestations may vary considerably. The diagnosis is often missed initially as it is not frequently suspected. The treatment is controversial both in choice of agent used and in duration of therapy.

Aged↗
PubMed1996

Cell-cycle regulation of B-Myb protein expression: specific phosphorylation during the S phase of the cell cycle.

Previous studies revealed that transcription of B-Myb, which encodes a transcription factor related to the c-Myb proto-oncoprotein, is cell-cycle regulated by an E2F transcription factor-mediated repression mechanism operating in G0/G1. To begin to determine the consequences of transcriptional regulation on B-Myb function, we report here further studies of B-Myb protein expression in the cell cycle. We found that G0-arrest of serum-deprived mouse fibroblasts was achieved without significant reduction in B-Myb levels, moreover, over-expression of B-Myb in stably transfected cells did not prevent their entry into G0. Following serum-induction of arrested fibroblasts, B-Myb abundance increased as cells entered S phase to levels significantly greater than found in cycling cells. This was accompanied by the appearance of a novel phosphorylated form of B-Myb (112 kDa) of distinctly lower electrophoretic mobility than B-Myb present in G1 (110 kDa). The 112 kDa species was S phase-specific even in transfected cells overexpressing B-Myb. Consistent with modification in the S phase of the cell cycle, preliminary evidence suggested that a cyclin A/cdk2, but not cyclin E/cdk2 or cyclin D1/cdk4, complex could induce a similar electrophoretic mobility change in baculovirus-specified B-Myb. These findings show that B-Myb expression may be subject to two levels of control during the cell cycle, transcription and protein phosphorylation.

3T3 Cells↗
PubMed1993

The effect of taprostene in patients with acute myocardial infarction treated with thrombolytic therapy: results of the START study. Saruplase Taprostene Acute Reocclusion Trial.

Taprostene is a prostacyclin analogue that inhibits platelet aggregation and thus might be a useful adjuvant to thrombolytic agents in acute myocardial infarction. In a placebo-controlled dose rising study, taprostene or placebo was intravenously infused in 80 patients treated with the thrombolytic agent saruplase (rscu-PA) for acute myocardial infarction. Three doses of taprostene were used: 6.25; 12.5; or 25.0 ng.kg-1 x min-1. Taprostene or placebo was infused for 48 h, followed by a 24 h tapering period. All 80 patients had short symptom-to-treatment delay and marked ST segment elevation. Patency at 90 min was documented in 58/78 patients (two patients had no angiography). Success rate varied from 67-82% in the four treatment arms (P = 0.33). Patency after rescue PTCA was seen in 10 out of 13 patients. Of the 58 patients having a patent artery at 90 min, none of the 43 taprostene patients and one of the 15 placebo patients had a re-occluded artery at the second angiography at 32-48 h (5/58 patients had no recatheterization). Conversely, of nine patients who had successful rescue PTCA, three of four placebo patients had a re-occluded artery at the second angiography compared to one of five taprostene patients (one placebo patient had no recatheterization) (P = 0.33). Safety evaluation revealed no major difference between the placebo plus saruplase and the taprostene plus saruplase groups. Taprostene was well tolerated up to 25 ng.kg-1 x min-1. Although taprostene did not affect 90 min patency, there was a trend to better maintenance of patency after rescue PTCA.

Angioplasty, Balloon, Coronary↗
PubMed1992

Lichen planus associated with chenodeoxycholic acid and ursodeoxycholic acid for gallstone dissolution.

A patient who developed lichen planus while receiving chenodeoxycholic acid and ursodeoxycholic acid therapy for gallstones is described. Skin biopsy was performed and histological examination suggested a drug etiology. An association between lichen planus and liver disease is recognized, but this patient exhibited no clinical or biochemical evidence of liver disease and the rash disappeared after cessation of the bile acid therapy. Bile acids may cause lichen planus. The mechanism is unknown.

Aged↗
PubMed1990

Human orf.

Explore the source record for details and available documents.

Biopsy↗
PubMed1989

Evolution and stability of chromosomal DNA coamplified with the CAD gene.

We have compared clones of Syrian hamster cells selected for the first amplification of the CAD gene with clones selected for further amplification. The large domain amplified initially was not reamplified as an intact unit. Instead, subregions were reamplified preferentially, and parts of the initial array were often lost. These events reduced the average amount of coamplified DNA accompanying each copy of the selected gene. The degree of amplification was small in the first step (about three extra copies of CAD per cell), but second-step amplifications to a high copy number (up to 60 extra copies per cell) occurred frequently. After several separate steps of amplification, highly condensed arrays that brought many CAD genes close together were formed. In striking contrast to the stability of these highly amplified arrays, the low-copy chromosomal arrays formed early were quite unstable and were often lost completely within 1 or 2 months of growth without selection. The results suggest that different mechanisms may be involved in the first step of amplification and in the later evolution of an already amplified array.

Amidohydrolases↗
PubMed1989

Additional myocardial salvage by coadministration of the epoprostenol analog taprostene to recombinant single-chain urokinase-type plasminogen activator in a canine coronary thrombosis model.

In open chest dogs myocardial ischemia was induced by formation of an occlusive thrombus in the left anterior circumflex artery (LCX). Reperfusion of the LCX was achieved by infusion of the fibrin specific recombinant single-chain urokinase-type plasminogen activator (r-scu-PA). The myocardial salvage by r-scu-PA alone and in combination with the epoprostenol (prostacyclin) analog taprostene (CG 4203) was compared. There were four experimental groups: group 1 (n = 4) did not receive any treatment after LCX thrombosis; in group 2 (n = 9) at 100 min after LCX thrombosis r-scu-PA (20 micrograms.kg-1.min-1 i.v. for 30 min) was infused; in groups 3 and 4 treatment with taprostene started concomitantly with r-scu-PA infusion. The taprostene infusions lasted for 120 min and the doses were 0.1 microgram.kg-1.min-1 in group 3 (n = 6) and 0.215 microgram.kg-1.min-1 in group 4 (n = 6). Time to r-scu-PA-induced recanalisation ranged from 18-22 min with no significant difference between groups 2-4. Percent of left ventricle at risk did not differ between the groups. Infarct size as percent of the risk zone was 48.3 +/- 7.7 in group 1, 25.3 +/- 3.7 in group 2, 21.3 +/- 6.5 in group 3 and 17.1 +/- 3.5 in group 4 (p less than 0.05 groups 2-4 vs group 1). Incidence of ectopic beats increased after r-scu-PA-induced reperfusion in groups 2-4, but was significantly reduced by taprostene.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗