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L Bruch

Publications and source records attributed to L Bruch.

26 records · Page 2Linked to original sources
PubMed1988

[Quantitative histological studies of lamina V and lamina III pyramidal neurons in the motor cortex of the rat. The question of laterality].

Laterality of several brain functions has been demonstrated in the human brain cortex as well as in several animal species indicating an evolutionary genesis of the brain's asymmetry. To get some morphological data, we investigated Golgi impregnated pyramidal neurons in lamina III of regio precentralis agranularis of the major cortex from adult rats. The spine number and density and the length of the dendrites forming a basal or apical single dendritic field (SDF = EDF) of these neurons were estimated. The statistical significance of the data was proved by comparing the neuronal parameters obtained from the right or left hemisphere of the same animal (individual laterality), as well as by testing the mean values from right or left cortex of several animals (species laterality). However, in both cases no statistical significance could be obtained. From these results two conclusions should be drawn: Firstly, the parameters in a single dendritic field of cortical pyramidal neurons of both brain sides are statistically equivalent and not asymmetrical developed. Secondly, the single dendritic field of cortical pyramidal neurons can not serve as a morphological counterpart for functional asymmetries in the rat brain. Here, further interdisciplinary research is necessary.

Animals↗
PubMed1985

Infection with HTLV-III/LAV and transfusion-associated acquired immunodeficiency syndrome. Serologic evidence of an association.

We studied patients with transfusion-associated acquired immunodeficiency syndrome (AIDS) and their blood donors for serologic evidence of infection with human T-cell lymphotropic virus type III/lymphadenopathy-associated virus with two enzyme-linked immunosorbent assays and a Western blot assay. All 19 patients with AIDS were seropositive by at least one test. In all 28 donor sets containing "high-risk" donors, at least one donor was seropositive by one or more tests. Of 255 donors not considered high risk, two (0.8%) were seropositive by all three tests. When 30 seropositive high-risk donors were evaluated a median of 29 months after donation, four (13%) had developed AIDS and eight (27%) had lymphadenopathy. Our findings support the hypothesis that human T-cell lymphotropic virus type III/lymphadenopathy-associated virus causes AIDS and indicate that seropositive high-risk donors may be at relatively high risk for developing AIDS or related conditions themselves.

Acquired Immunodeficiency Syndrome↗
PubMed1985

Immunological properties of the Gag protein p24 of the acquired immunodeficiency syndrome retrovirus (human T-cell leukemia virus type III).

Antigenic cross-reactivity of human T-cell leukemia virus type III (HTLV-III) with HTLV-I and HTLV-II and other retroviruses was measured by using a stringent homologous competition radioimmunoassay for the Gag protein p24 and a less stringent electrophoretic transfer blot assay. In the competition radioimmunoassay only minimal cross-reactivities were detected between HTLV-III p24 and both HTLV-I and HTLV-II. No cross-reactivity was detected with any other retrovirus. In the electrophoretic transfer blot system using rabbit antibody to HTLV-I, HTLV-II, and HTLV-III, low-level cross-reaction was detected between HTLV-I and HTLV-III and between HTLV-II and HTLV-III. Unlike the cross-reactivity between HTLV-I p24 and HTLV-III p24, which was bidirectional, the one between HTLV-II and HTLV-III was only a one-way reactivity. Antiserum to HTLV-II recognized HTLV-III p24, but the antiserum to HTLV-III did not recognize HTLV-II p24. The results indicate that HTLV-III is a unique retrovirus with a limited homology with HTLV-I and HTLV-II but unrelated to most other retroviruses.

Acquired Immunodeficiency Syndrome↗
PubMed1984

Antibodies reactive with human T-lymphotropic retroviruses (HTLV-III) in the serum of patients with AIDS.

In cats, infection with T-lymphotropic retroviruses can cause T-cell proliferation and leukemia or T-cell depletion and immunosuppression. In humans, some highly T4 tropic retroviruses called HTLV-I can cause T-cell proliferation and leukemia. The subgroup HTLV-II also induces T-cell proliferation in vitro, but its role in disease is unclear. Viruses of a third subgroup of human T-lymphotropic retroviruses, collectively designated HTLV-III, have been isolated from cultured cells of 48 patients with acquired immunodeficiency syndrome (AIDS). The biological properties of HTLV-III and immunological analyses of its proteins show that this virus is a member of the HTLV family, and that it is more closely related to HTLV-II than to HTLV-I. Serum samples from 88 percent of patients with AIDS and from 79 percent of homosexual men with signs and symptoms that frequently precede AIDS, but from less than 1 percent of heterosexual subjects, have antibodies reactive against antigens of HTLV-III. The major immune reactivity appears to be directed against p41, the presumed envelope antigen of the virus.

Acquired Immunodeficiency Syndrome↗
PubMed1984

HTLV-III: the etiologic agent of AIDS.

A retrovirus belonging to the family of human T-cell leukemia/lymphoma virus (HTLV) was isolated from several patients with acquired immunodeficiency syndrome (AIDS), AIDS-related complex (ARC) and asymptomatic homosexual males at increased risk of developing AIDS. This new virus was designated HTLV-III. A serological screening procedure incorporating an enzyme-linked immunosorbent assay (ELISA) and a radioimmunoassay using a Western blot technique was developed employing disrupted HTLV-III as the antigen source. These assays identified serum antibodies to HTLV-III antigens in almost all patients with AIDS, greater than 90% patients with ARC and about 40% of homosexual males at risk for developing AIDS. In a study of transfusion associated AIDS (TA-AIDS) all 19 of the TA-AIDS cases had antibodies to HTLV-III. Similarly 31 of 35 high risk donors who donated to cases of TA-AIDS had antibodies to HTLV-III. All four of the antibody negative high risk donors donated to cases that received blood from at least one other high risk donor. In contrast only 2 of 255 other donors were antibody positive. The data clearly indicate that TA-AIDS cases developed the disease as a result of transmission of HTLV-III through contaminated blood and that HTLV-III is the primary etiologic agent of AIDS.

Acquired Immunodeficiency Syndrome↗
PubMed1982

Superoxide dismutase activity in the intestine of the streptozotocin-diabetic rat.

Insulin stimulates the production of superoxide and hydrogen peroxide in various tissues. Hydrogen peroxide has been proposed to be an intracellular second messenger for insulin and a moderator of cellular proliferation and differentiation. We previously found that cell proliferation is increased in small intestinal mucosa of streptozotocin-diabetic rats. The current study was undertaken to determine if superoxide dismutase (SOD), the enzyme that converts superoxide to hydrogen peroxide, is altered in the mucosa of the alimentary tract and renal cortex of the diabetic rat, and if so, whether SOD responds to insulin treatment. Total SOD and cyanide-insensitive [manganese-containing SOD (Mn SOD)] SOD were measured by the nitroblue tetrazolium inhibition assay. We studied ad libitum fed animals, where diabetics are hyperphagic and pair-fed animals, where hyperphagia is not present. Since cyclic nucleotides appear to control cell proliferation in some tissues, we also measured cAMP and cGMP in mucosa of the small intestine. In ad libitum fed animals, total SOD was depressed in the mucosa of duodenum, jejunum, and ileum, but not in the cecum or colon of the streptozotocin-diabetic rats. The level of Mn-SOD was not affected by diabetes or insulin treatment, but the cyanide-sensitive [copper- and zinc containing SOD (Cu-Zn SOD] SOD was depressed in the small intestine and colon of diabetic rats. Insulin treatment restored total and Cu-Zn SOD activity in the small intestine to normal and increased Cu-Zn SOD activity in the colon to normal. Pair-fed animals showed the same changes in the SOD activity of jejunal mucosa that were found in ad libitum fed animals. In renal cortex, diabetes did not alter total SOD, but increased Mn SOD and decreased Cu-Zn SOD. Both responses were reversed by insulin treatment. Cyclic nucleotide concentrations were not affected by diabetes. We conclude that SOD enzymes re altered in diabetes, at least in proliferating tissues. Responses are tissue specific. The mucosa of the small intestine and colon show decreased Cu-Zn SOD, the SOD of the cecum is unaffected, and the kidney shows increased Mn SOD and decreased Cu-Zn SOD. The SOD responses of diabetics are reversed by insulin treatment.

Animals↗
PubMedDate not supplied

Pituitary adenylate-cyclase-activating peptides relax human coronary arteries by activating K(ATP) and K(Ca) channels in smooth muscle cells.

Pituitary adenylate-cyclase-activating peptides (PACAPs) are potent dilators of arteries, including human coronary arteries. We tested the importance of specific K+ channel regulatory mechanisms in human arterial smooth muscle relaxation induced by PACAPs, using contraction and patch clamp measurements on human coronary artery vascular smooth muscle cells. PACAP27 and PACAP38 produced dose-dependent relaxations of 5 microM PGF2alpha-preconstricted rings, with half-maximal relaxations at 1.0 nM and 2.0 nM, respectively. Both peptides induced complete relaxation at 100 nM. Pretreatment of the vessels with the ATP-dependent K+ (K(ATP)) channel blocker glibenclamide (1 microM) or with the Ca2+-activated K+ (K(Ca)) channel blocker iberiotoxin (100 nM) inhibited PACAP27-induced relaxation in an additive manner. Moreover, in the patch clamp experiments on freshly isolated cells from human coronary arteries, PACAP27 (100 nM) induced a large, nonrectifying, outward (I(K)(ATP)) K+ current in a proportion of cells and a voltage-dependent outward (I(K)(Ca)) K+ current in other cells. The PACAP27-induced I(K)(ATP) was blocked by glibenclamide (3 microM), while the PACAP27-stimulated I(K)(Ca) was blocked by iberiotoxin (100 nM). These findings provide the first evidence that relaxation of arterial smooth muscle cells by PACAPs is mediated by opening of K(ATP) and K(Ca) channels. The data indicate that both K(ATP) and K(Ca) channels in vascular smooth muscle cells may serve as final common pathway to induce vasorelaxation by endogenous vasoactive signals in man.

Coronary Vessels↗