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M L Berger

Publications and source records attributed to M L Berger.

65 records · Page 4Linked to original sources
PubMed1982

Immunologic requirements for the adoptive transfer of ectromelia virus meningitis.

Intracerebral infection with the Hampstead egg strain of ectromelia virus in mice produced a meningitis with clinical signs and death. A single injection of cyclophosphamide three days after infection delayed the onset of pathology and clinical signs. Adoptive transfer of immune spleen cells into preinfected recipients could induce the meningitis earlier. These donor-immune cells were virus-specific in their action. The Ig- population, deficient in B lymphocytes, could transfer meningitis; but donor-immune cells depleted of T lymphocytes by anti-theta treatment or the Ig+ population, deficient in T-cells, were unsuccessful. Studies with labeled cells showed a preferential accumulation of labeled donor cells in cerebrospinal fluid in the first 24 hours post-transfer, whereas labeled recipient cells accumulated between 24 and 48 hours. The results demonstrated that the adoptive transfer of ectromelia virus meningitis was a cell-mediated inflammatory process.

Animals↗
PubMed1982

The role of the major histocompatibility complex in the adoptive transfer of ectromelia virus meningitis.

Adoptive transfer of ectromelia virus meningitis was most efficient when donor-immune spleen cells and recipients were compatible in the K region of the H-2 gene complex. Weak responses could be obtained with H-2D region compatibility, but none occurred with H-2I region compatibility. Spleen cells used in adoptive transfers and cells found in cerebrospinal fluid from infected mice were found to have identical H-2-imposed restriction in their in vitro cytotoxic activity. This suggests a significant role for the major histocompatibility complex in the generation of virus-specific T lymphocytes and the recognition of virus-infected tissue in the central nervous system by these cells.

Animals↗
PubMed1981

Flow cytometric analysis of DNA content of mouse liver cells following in vivo infection by human adenovirus type 5.

Human adenovirus type 5 caused acute hepatocellular damage when injected intravenously into C57B1/6 mice. Early protein (P) and late virus protein (V) antigen staining by immunofluorescence was located principally, if not exclusively, in hepatocytes. Autoradiography following incorporation of tritiated thymidine into Ad5-infected liver cells in vivo indicated that DNA synthesis was initiated in hepatocytes. Flow cytometry showed that cells with a 4n DNA content prior to infection were highly susceptible to infection, with 75% being lost from the liver cell population by 5 days post-infection. This observation was correlated with the observed pathology during the course of the infection.

Adenoviridae Infections↗
PubMed1980

Humoral and cell-mediated immune mechanisms in the production of pathology in avirulent Semliki Forest virus encephalitis.

Seven days after peripheral inoculation with an avirulent strain of Semliki Forest virus, the brains of CBA and nude mice exhibited a mononuclear inflammation and spongiform degeneration. Mice that had received cyclophosphamide (150 mg/kg) 24 h after infection showed no pathology until day 11. However, immunofluorescence studies of the brains of immunosuppressed, infected mice demonstrated viral antigen within the soma and processes of neurons at earlier periods. The brain lesions could be reconstituted on day 7 in immunosuppressed, infected recipients with 6-day immune spleen cells. Immune spleen cells depleted of T lymphocytes, the non-immunoglobulin-bearing population deficient in B lymphocytes, or immune sera plus nonimmune bone marrow cells could also reconstitute the lesions. However, inflammation and spongiform changes were reduced when donor immune cells were depleted of either T or B lymphocytes. When both T and B lymphocytes were removed from the donor immune population, recipient brains did not show pathology. The results demonstrate that either antibody or immune T cells can trigger pathology, but there is also participation of nonimmune bone marrow-derived mononuclear cells, probably of the monocyte-macrophage lineage.

Animals↗
PubMed1976

Effect of mannitol on phosphate transport in intact and acutely thyroparathyroidectomized rats.

Clearance experiments were performed in male Sprague-Dawley rats to determine the effect of mannitol on phosphate (Pi) transport. Solutions of 10 per cent mannitol or normal saline were infused at progressively increasing flow rates with or without parathyroid extract (PTE) infusion into the following animals: Group I: Intact Rats-Mannitol Infusion: A--Intact, hypocalcemic; B--Intact, normocalcemic, normomagnesemic; Group II: TPTX Rats: A--Mannitol infusion; B--Mannitol + PTE infusion; C--Hydropenia + PTE infusion; and D--Saline + PTE infusion. In contrast to previous reports, mannitol increased Pi excretion in intact rats. When Ca + Mg were maintained constant in intact rats or after TPTX, mannitol failed to increase Pi excretion. In TPTX rats receiving mannitol + PTE, increased Pi excretion was again noted. Comparison of Pi excretion during PTE infusion during hydropenia and volume expansion with mannitol or saline in TPTX rats revealed significantly higher Pi excretion with volume expansion. Pi excretion paralleled Na excretion in intact mannitol-loaded and PTE-infused TPTX animals undergoing a mannitol or saline diuresis. Pi and Na excretions, however, were dissociated in mannitol-loaded TPTX rats, intact animals receiving simultaneous Ca and Mg infusion, and TPTX hydropenic animals receiving PTE. These studies indicate that (1) mannitol increases Pi excretion in intact rat, (2) the phosphaturia is PTH-mediated, (3) Pi and Na excretions can be dissociated, and (4) volume expansion with either mannitol or saline enhances the effect of PTH on Pi transport in the renal tubule.

Animals↗
PubMed1975

Zinc distribution in mouse brain subsequent to hippocampal lesions.

The role of zinc in central nervous system metabolism remains obscure but it has been shown in animals that diphenylthiocarbazone (Dithizone) selectively colors intravitally the hippocampus and adnexa, parts affected in human temporal lobe epilepsy. To examine the effect of experimental cerebral lesions on zinc storage in that region, 80 mice were divided into two operative and two control groups. The operative groups had unilateral lesions placed in the hippocampus or frontal lobe. One control group and both lesion groups were injected subcutaneously with zinc lactate daily for ten days before intravenous injection of diphenylthiocarbazone. The other control group was used to determine if zinc storage occurs as a result of its increased systemic availability. Hippocampal lesion mice showed more extensive staining of lethal amygdala and associated cortex on the side of the lesion. Frontal lesions remained unstained and frontal lesions did not alter the staining of hippocampus and related parts. Lack of difference between controls shows that greater availability of systemic zinc does not increase its content in the hippocampal-lateral amygdalar region. Increased zinc uptake in this instance appears to be a local phenomenon.

Adenosine Triphosphatases↗
PubMedDate not supplied

CCl4-induced toxicity in isolated hepatocytes: the importance of direct solvent injury.

CCl4 is proposed to induce cellular injury through its metabolites that are generated by a cytochrome P-450 dependent step. These free radical products can interact with membrane structures, thereby generating lipid peroxides. The latter process has been implicated as a major mechanism of CCl4 hepatoxicity, although this relationship has been difficult to demonstrate when using isolated hepatocyte preparations. This report demonstrates that there are at least two mechanisms by which CCl4 induces injury in isolated hepatocytes. One occurs within minutes of exposure to CCl4 and is characterized by modest malondialdehyde formation and no decline in cellular-reduced glutathione. SKF 525A, metyrapone and promethazine did not protect against this early damage. A second phase of damage, evident particularly after 3 hr, is characterized by a marked increase in malondialdehyde formation, a fall in cellular glutathione and substantial further cellular damage. These changes could be moderated by the cytochrome P-450 inhibitors and promethazine, and antioxidant. Further examination of the initial phase of damage reveals an immediate dose-related inhibition of O2 consumption. This could not be prevented by SKF 525A or metyrapone and was associated with loss of ability to stimulate mitochondrial respiration with dinitrophenol. Rapid recovery to initial O2 consumption rates occurred with time as CCl4 evaporated from the incubation system. This was associated with a partial return of dinitrophenol stimulation of mitochondrial O2 consumption despite significant glutamate dehydrogenase release. A portion of this recovery could be inhibited by SKF 525A, suggesting that some O2 consumption was due to CCl4 metabolism and ensuing lipid peroxidation. These data suggest that early CCl4 toxicity is a direct consequence of its solvent properties and is partially reversible; subsequent damage may be mediated by lipid peroxidation. This solvent injury has not been previously recognized and may have relevance not only to a reversible toxicity as demonstrated with isolated hepatocytes but also in vivo as well.

Animals↗