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Biomedical subjects

R Breuer

Publications and source records attributed to R Breuer.

101 records · Page 6Linked to original sources
PubMed1981

Hypertransaminasemia with subcutaneous heparin therapy.

An elevation of serum aspartate aminotransferase (GOT) and alanine aminotransferase (GPT) may be produced in patients treated with i.v. full-dose HEPARIN. We studied the influence of low-dose s.c. HEPARIN (5,000 IU X 2) in 34 patients with acute myocardial infarction (AMI) and in 7 with cerebrovascular accidents or calf thrombophlebitis. Twelve patients (all males) with AMI showed a secondary elevation of GOT and GPT at about the sixth or seventh day after the commencement of therapy that persisted throughout the period of treatment. Four patients (two males and two females) with cerebrovascular accidents or thrombophlebitis showed similar increases of GOT and GPT.

Alanine Transaminase↗
PubMed1978

[In vitro incubation of lenses. Model for testing substrate utilization of substances of the energy metabolism, demonstrated with bencyclane-hydrogen-fumarate (author's transl)].

When bovine lens homogenate was treated with bencyclane-hydrogen-fumarate, the carbohydrate metabolism was activated. This may chiefly be due to the fumarate part of the substance. A 24 H In vitro incubation of whole bovine lenses in TC-199 with and without bencyclane-hydrogen-fumarate did not show the above effect. On the model of former investigations by J.E. Harris et al. we modified the test procedure by selecting the medium and the time of incubation so that the endogenous carbohydrates of the lens were consumed, thus creating new metabolic balances. This metabolic condition allows investigations intended to activate metabolic processes and to restore the steady state of metabolic parameters. We investigated the effect of bencyclane-hydrogen-fumarate using the same method and found that given certain conditions the lens recovers when incubated for 2 h in TC-199 (containing 1 g glucose/1) with addition of a 10(-4) M solution of bencyclane-hydrogen-fumarate. The ATP-content of these lenses in particular gives proof of this result. As already observed in former investigations on homogenates, this effect is probably due to metabolization of the fumarate part of the bencyclane-hydrogen-fumarate by the citric acid cycle. The method used explains the differences observed when using lens homogenates or whole lenses under the same experimental conditions.

Adenine Nucleotides↗
PubMedDate not supplied

Lymphokines in bleomycin-induced lung injury in bleomycin-sensitive C57BL/6 and -resistant BALB/c mice.

To study the pattern of lymphokines in bleomycin-induced lung injury, T cells were isolated from lung interstitial tissue (LIL), peribronchial lymphatic tissue (PBLT), and bronchoalveolar lavage (BAL) fluid of bleomycin-"sensitive" C57Bl/6 and bleomycin-"resistant" BALB/c mice at 3, 6, and 14 days following intratracheal instillation of bleomycin or saline. After 48 hours in culture, conditioned media were collected and assayed with specific enzyme-linked immunosorbent assay (ELISA) for interferon (IFN)-gamma, interleukin (IL)-2, IL-4 and IL-5. In bleomycin-treated C57B1/6 mice, IFN-gamma production was increased up to 20-fold at 3 and 6 days in LIL, and at 3 days in PBLT lymphocytes. IL-4 production was slightly decreased in LIL and PBLT lymphocytes at 14 days. IL-2 and IL-5 were not changed by bleomycin. In BALB/c mice, IFN-gamma production was increased 5-fold at 14 days, and IL-2 production at 6 days, in LIL but not PBLT. IL-4 and IL-5 were not significantly changed. The increase in IFN-gamma may play a role in the pathogenesis of bleomycin-induced lung injury. Differences in the cytokine pattern between the strains of mice may contribute to the variable strain susceptibility in bleomycin-induced lung injury.

Animals↗
PubMedDate not supplied

Subcutaneous mycosis in a cat due to Staphylotrichum coccosporum.

A 5.5-year-old, male, feline leucosis virus-positive cat developed a concurrent dermatophytosis due to Microsporum canis and a subcutaneous infection due to Staphylotrichum coccosporum. St. coccosporum caused mycetoma-like lesions. The fungal elements revealed features like those seen in phaeohyphomycosis. Until now St. coccosporum has been described to be non-pathogenic. The pathogenicity of St. coccosporum was corroborated by experimental infection.

Animals↗
PubMedDate not supplied

Resistance of hamster bronchiolar epithelium to neutrophil elastase: investigation by cell surface lectin cytochemistry.

An intratracheal instillation of human neutrophil elastase (HNE) causes accumulation of an excess number of secretory granules in the epithelial secretory cells lining the hamster bronchus. This chronic lesion, which we refer to as secretory cell metaplasia (SCM), is not seen in the trachea or bronchioles. Because luminal cell surface lectin binding is much higher in the trachea than in the bronchus, we concluded that tracheal resistance may be due to a protective glycoconjugate coat. In the present ultrastructural study, we analyzed the lectin-binding capability of bronchiolar epithelial cells to determine whether their luminal cell surface glycoconjugate layer is similar to tracheal epithelial cells. None of the six ferritin-conjugated lectins showed higher binding in bronchioles compared to the bronchus, suggesting that a high level of surface oligosaccharides is not necessary for resistance to the metaplastic effects of HNE. HNE caused a significant reduction in bronchiolar surface binding of the gold-labeled, secretory cell-specific lectin, Helix pomatia agglutinin. The principal granulated secretory cell type in bronchioles was ultrastructurally similar to a form of bronchial Clara cell that converts to a mucous cell phenotype in response to HNE. The results suggest that absence of bronchiolar SCM is not attributable to a protective layer of cell surface oligosaccharides, a lack of cellular contact by HNE, or the presence of a morphologically distinct population of epithelial cells in bronchioles.

Animals↗
PubMedDate not supplied

Elastase causes secretory discharge in bronchi of hamsters with elastase-induced secretory cell metaplasia.

A single intratracheal instillation of human neutrophil elastase (HNE) into hamsters causes granule discharge from bronchial secretory cells followed by marked accumulation of granules, visible by light microscopy at 21 days and persisting through 18 months. To determine whether persistence of this secretory cell metaplasia (SCM) is due to inability of the metaplastic secretory cells to secrete their granules, hamsters having HNE-induced SCM were challenged with the potent secretagogue HNE. Four groups of 10 hamsters each received 300 micrograms HNE intratracheally. Twenty-one days later, hamsters were intratracheally treated with HNE or saline; the groups were designated HNE-HNE and HNE-SAL, respectively. Hamsters were killed 2 h or 21 days following the second treatment. Using light microscopy, nucleated epithelial cells were counted in plastic sections of the left main intrapulmonary bronchus. Cells were classified as ciliated (C), basal (B), indeterminate (IN), or secretory. Secretory cells were subcategorized as S0 (0 granules), S1 (1-4 granules), S2 (> or = 5 granules with intervening cytoplasm), and S3 (abundant granules completely filling the cytoplasm). At 2 h, S3 cell frequency in the HNE-HNE group was 13.0 +/- 2.2 (% mean +/- SE), significantly lower than in the 2 h HNE-SAL group (31.1 +/- 4.5). Concomitantly, higher cell frequencies were seen in the other secretory categories of the HNE-HNE group compared to the HNE-SAL group; S2 17.1 +/- 1.9 compared to 9.4 +/- 1.9, S1 2.4 +/- 0.4 compared to 1.1 +/- 0.5, and S0 2.4 +/- 0.5 compared to 1.1 +/- 0.5, respectively. The S3 cell frequency of the 21-day HNE-HNE group was 25.4 +/- 4.7, increased significantly compared to the 2 h HNE-HNE group; this change was concomitant with significant decrease in the frequency of the S0 secretory cells. Cell frequencies of C, B, and IN were not affected by treatment or time. It is concluded that metaplastic secretory cells discharge their granules in response to HNE; SCM returns to its original state after HNE rechallenge; persistent SCM is not due to the inability of metaplastic secretory cells to discharge their granules.

Animals↗
PubMedDate not supplied

Amelioration of bleomycin-induced pulmonary injury by cyclosporin A.

This study evaluated the effect of cyclosporin-A (CyA), a potent immunosuppressive drug, on Bleomycin (Bleo)-induced pulmonary inflammation in hamsters. Pulmonary injury was induced by a single intratracheal (i.t.) instillation of Bleo. Four groups of 10 male Syrian hamsters each received one of four treatments: (1) i.t. Bleo and daily intraperitoneal (i.p.) injections of CyA starting 1 day before i.t. instillation of Bleo (Bleo-CyA); (2) i.t. Bleo and i.p. injections of saline (Bleo-Sal); (3) i.t. saline and i.p. CyA (Sal-CyA); (4) i.t. saline and i.p. saline (Sal-Sal). Animals were sacrificed 14 days after i.t. treatment. Lung injury was evaluated histologically, biochemically, and by analysis of bronchoalveolar lavage (BAL) fluid. Treatment of hamsters with CyA significantly ameliorated the Bleo-induced lung injury, as determined by a semiquantitative morphological index that assesses the severity and extent of the injury on a scale of 0-3. Lung hydroxyproline measurements were lower in Bleo-CyA compared to Bleo-Sal, comparable to Sal-Sal and Sal-CyA controls. The percentage of neutrophils, eosinophils, and lymphocytes in BAL fluid was higher in Bleo-Sal and Bleo-CyA animals when compared with control Sal-CyA or Sal-Sal animals. A further increase in percentage of eosinophils was observed in Bleo-CyA compared with Bleo-Sal animals (13.3 +/- 6.6% [mean +/- SE] and 3.7 +/- 2.1%, respectively, p = .0007). BAL fluid protein content was higher in Bleo-Sal compared to Sal-Sal animals, but BAL fluid protein content from Bleo-CyA was not significantly different from that of Bleo-Sal animals. These results indicate that CyA ameliorates the Bleo-induced inflammation but does not prevent leakage of plasma protein or cells into the airspaces. The increased eosinophil numbers in Bleo-CyA-treated hamsters suggests enhanced production of interleukin-4 and -5.

Animals↗
PubMedDate not supplied

Effect of interleukin-2 and interleukin-4 on lymphocytes from peribronchial lymphatic tissue.

Lymphocyte activation in spleen and peribronchial lymphatic tissue (PBLT) following stimulation with T-cell mitogens and lymphokines was investigated in the hamster. Optimal mitogen-induced cell proliferation was achieved after culturing for 6 days in vitro. Interleukin-2 (IL-2) and interleukin-4 (IL-4) did not induce DNA synthesis in resting T-cells from either spleen or PBLT.IL-2 or IL-4 in combination with concanavalin A promoted splenic T-cell proliferation. In contrast, in PBLT, IL-2-but not IL-4-enhanced cell proliferation (p < .001). The findings indicate that PBLT represents an independent compartment of the immune system. Furthermore, in the hamster PBLT cells consist predominantly of IL-2-responsive cells, i.e., are of the Th1 type. Immunological pathogenesis of lung injury can therefore be studied by functional analysis of PBLT lymphocytes.

Animals↗
PubMedDate not supplied

Abnormal mucous cell phenotype induced by neutrophil elastase in hamster bronchi.

Bronchial mucous cell metaplasia (MCM) is a histologic component of chronic mucus hypersecretion. The hamster model of elastase-induced MCM appears to involve an irreversible conversion of Clara cells to mucous cells. The present study questioned whether the mucous cells seen in hamster bronchi exposed to neutrophil elastase produce and maintain a form of glycoconjugate secretory product different from that normally found in mucous cells or Clara cells. Ultrastructural cytochemistry using the gold-labeled lectin HPA revealed a difference in the cell surface and stored secretory granules of elastase-derived mucous cells compared to normal mucous cells and Clara cells at 3 weeks and 4 months following exposure. The results suggest that elastase irreversibly alters the glycoconjugate character of the Clara cells normally present so that they produce an abnormal form of mucus. Because secreted glycoconjugates can affect the rate of mucociliary clearance and receptor-mediated binding of microorganisms, this change in phenotype may be involved in the pathogenesis of diseases associated with chronic mucus hypersecretion in humans.

Animals↗