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Biomedical subjects

J E Roepke

Publications and source records attributed to J E Roepke.

9 recordsLinked to original sources
PubMed1999

Primary anaplastic large cell lymphoma of the small intestine.

We describe the clinicopathologic, immunophenotypic, and molecular findings in 4 cases of anaplastic large cell lymphoma (ALCL) arising in the small intestine. All patients were men with acute symptoms of gastrointestinal tract obstruction. The clinical preoperative diagnosis was gastrointestinal carcinoma in 3 cases, and pancreatic carcinoma in 1 case. Histologic examination revealed cohesive aggregates of neoplastic cells, with multiple vesicular nuclei, prominent nucleoli, and abundant amphophilic cytoplasm. There was no clinical or histopathologic evidence of enteropathy. All cases were CD30+, and all showed evidence of T-cell lineage with cytotoxic potential by expression of CD3, CD43, or CD45RO; T-cell intracellular antigen-1; or perforin. One tumor showed p80 and anaplastic lymphoma kinase (ALK) overexpression corroborated by the presence of the t(2:5). One tumor expressed Epstein-Barr virus latent membrane protein. In all cases, the tumor cells were negative for CD20, CD15, CD56, and cytokeratin. Polymerase chain reaction revealed clonal rearrangements of the T-cell receptor gamma-chain gene, without evidence of immunoglobulin heavy-chain gene rearrangement. The diagnosis of primary bowel ALCL is facilitated by immunophenotypic and molecular studies. With 24 months of clinical follow-up, only the patient with the t(2:5)-positive tumor is alive and free of disease, suggesting that p80/ALK overexpression may be a good prognostic indicator.

Adult↗
PubMed1998

Myosin isoform shifts and decreased reactivity in hypoxia-induced hypertensive pulmonary arterial muscle.

The principal stimulus that evokes pulmonary hypertension is chronic alveolar hypoxia. Pulmonary hypertension is associated with remodeling of the vessel walls, involving hypertrophy and hyperplasia of pulmonary arterial smooth muscle (PASM) and a concomitant increase in the deposition of connective tissue, resulting in increased wall thickness. The purpose of the present study was to determine the effect of hypoxia-induced hypertension on the structure and function of PASM. Experiments were designed to determine whether hypoxia-induced pulmonary hypertension is associated with alterations in PASM: 1) reactivity to a variety of agonists, 2) contractile protein proportions and isoforms, and 3) structural properties. Young adult male rats were made hypoxic by lowering the fraction of inspired O2 (10%) for 14 days. Pulmonary arterial segments were isolated and dose-response curves to various agonists (high K+, norepinephrine, serotonin, angiotensin II, and adenosine) were generated. Gel electrophoresis was used to measure changes in the relative amounts of actin or myosin and of myosin heavy chain (MHC) isoforms. Structural changes were correlated with the pharmacological and biochemical data. Hypoxia-induced pulmonary hypertension caused a general decreased reactivity, an increase in the proportion of nonmuscle to muscle MHC isoforms in PASM, and an increase in arterial wall thickness with PASM hypertrophy or hyperplasia.

Adenosine↗
PubMed1997

Rat tendon morphologic and functional changes resulting from soft tissue mobilization.

Augmented Soft Tissue Mobilization (ASTM) is a new non-invasive soft tissue mobilization technique which has been used successfully to treat a variety of musculoskeletal disorders. The purpose of this study was to determine the effects of ASTM therapy on the morphological and functional characteristics of enzyme induced injured rat Achilles tendons. Four groups of five rats were allocated as follows: (A) control, (B) tendinitis, (C) tendinitis plus ASTM, and (D) ASTM alone. Collagenase injury was induced, and the surgical site was allowed to heal for 3 wk. ASTM was performed on the Achilles tendon of groups C and D for 3 min on postoperative days 21, 25, 29, and 33 for a total of four treatments. Gait data were gathered prior to each treatment. The Achilles tendons of each group were harvested 1 wk after the last treatment. Specimens were prepared for light and electron microscopy, and immunostaining for type I and type III collagen and fibronectin was performed. Light microscopy showed increased fibroblast proliferation in the tendinitis plus ASTM treatment group. Although healing in rats may not translate directly to healing in humans, the findings of this study suggest that ASTM may promote healing via increased fibroblast recruitment.

Achilles Tendon↗
PubMed1987

Loss of sexual differentiation of rat hepatocytes in short-term culture.

We investigated the maintenance of alcohol dehydrogenase (ADH) and estrogen receptors in primary cultures of rat hepatocytes. Female hepatocytes partially lose ADH activity and completely lose estrogen receptors during 4 days in culture. Growth hormone, which induces both the enzyme and receptor in vivo, did not induce either in vitro.

Alcohol Dehydrogenase↗
PubMedDate not supplied

Response of perfused lung and isolated pulmonary artery to adenosine.

Adenosine (AD) has been reported to induce both pulmonary arterial constriction and dilation. We investigated the effect of AD using two complementary techniques. The isolated rat lung perfused with Earle's balanced salt solution containing albumin was used to measure pulmonary arterial (Ppa), venous, and double occlusion (microvascular; Pmv) pressure, and resistance changes. AD alone had no effect on Ppa, Pmv, or resistance at any dose tested (5 x 10(-7) through 10(-3) M). However, when Ppa was elevated by pretreatment with 5 x 10(-7) M norepinephrine (NE), then 10(-4) M AD lowered Ppa by 19.5 +/- 3.2% and Pmv by 6.0 +/- 6.1% and attenuated the increase in upstream resistance caused by NE. Higher doses of AD (10(-3) M) resulted in greater relaxation. In isolated segments from rat and guinea pig pulmonary lobar arteries, isometric force production in response to AD was measured as a percentage of the active isometric force produced in response to 10(-5) M NE (% NE contraction). No response was observed in rat pulmonary arterial rings for doses of AD less than 10(-6) M. In vessels with intact endothelium, 10(-6) M AD caused a slight increase in isometric tension (2.3 +/- 1.2% NE contraction; p less than 0.05), but 10(-4) M AD caused relaxation (-17.2 +/- 2.2% NE contraction; p less than 0.05), and 10(-3) M caused further relaxation (-61.5 +/- 5.0% NE contraction; p less than 0.05). In vessels without endothelium, only relaxation was observed. Isolated guinea pig arterial rings responded to AD with vasodilation similar to the results in the rat arterial rings. Results of this study show that AD primarily causes a direct dose-dependent relaxation of pulmonary arterial smooth muscle in both the isolated perfused lung and isolated arterial ring preparation.

Adenosine↗