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Biomedical subjects

M J Levin

Publications and source records attributed to M J Levin.

At least 163 records · Page 9Linked to original sources
PubMed1984

How many Samoans? An evaluation of the 1980 census count of Samoans in the United States.

"This paper reports the results of applying demographic methods, in combination with assumptions about vital rates and migration, to estimate the total Samoan population of the United States in 1980." The authors conclude that the most plausible estimate of the Samoan population in the United States in 1980 is between 46,600 and 50,800. These estimates are 10 to 17.5 percent higher than the census count.

American Samoa↗
PubMed1983

An outbreak of rotavirus-associated neonatal necrotizing enterocolitis.

An outbreak of necrotizing enterocolitis and hemorrhagic gastroenteritis occurred in two nurseries during 25 days in August 1982. Eleven of the 40 patients in these nurseries during that time developed disease (attack rate 27.5%). In seven of the 10 patients with gastrointestinal disease, stool samples tested for human rotavirus were positive by ELISA, whereas in 20 unaffected infants, no stools tested demonstrated HRV (P = 0.0001). Eleven staff members had serologic evidence of recent HRV infection. Comparison of risk factors traditionally associated with the development of NEC between the affected and unaffected infants revealed no significant differences. Rotavirus infection was the only finding that was highly correlated with this epidemic.

Cross Infection↗
PubMed1983

Evaluation of varicella-zoster immune globulin: protection of immunosuppressed children after household exposure to varicella.

Varicella-zoster immune globulin (VZIG), an immunoglobulin prepared from normal donor plasma selected for high titer of antibody to varicella-zoster virus (VZV), and zoster immune globulin (ZIG), prepared from the plasma of donors convalescing from herpes zoster, were compared in a double-blind, randomized clinical trial to determine their relative efficacy in protecting immunosuppressed children from severe varicella. VZV infection occurred in 49 (60.4%) of 81 recipients of VZIG and in 57 (68.6%) of 83 recipients of ZIG. These rates and the clinical severity of varicella were not significantly different; however, the subclinical infection rate was significantly higher in ZIG recipients (31.3% vs. 16.0%). This difference was accounted for by a subgroup of patients receiving immunosuppressive therapy for nonneoplastic diseases. Doubling the dose of VZIG administered reduced the rate of subclinical infection. These data indicate that VZIG can be used to protect immunosuppressed children from severe chicken pox.

Chickenpox↗
PubMed1983

Absence of functional messenger RNA for glycogen phosphorylase in the muscle of two patients with McArdle's disease.

(1) Two unrelated cases of McArdle's disease (glycogen storage disease type V, deficiency in muscle-type glycogen phosphorylase, EC.2.4.1.1) with no detectable inactive protein, and two heterozygous relatives of one patient, have been investigated for the presence or absence of functional messenger RNA. Methods were developed and scaled down to be compatible with clinical-size biopsies. (2) Total muscle RNA was prepared and translated in a rabbit reticulocyte cell-free system. Neosynthesized products were isolated by immunoaffinity microchromatography. Phosphorylase was compared with control enzymes neosynthesized and purified under the same conditions. (3) No functional mRNA for phosphorylase could be detected in the muscles of the two patients. A decreased amount of messenger for phosphorylase, compared with the control enzymes, was found in the muscles of the two heterozygotes. (4) Exploration of functional messenger RNA in clinical enzymopathies should be readily adaptable to a number of enzymatic diseases.

Adolescent↗
PubMed1983

Prevention of cytomegalovirus infection by cytomegalovirus immune globulin after marrow transplantation.

In an effort to prevent cytomegalovirus infection among seronegative patients having marrow transplants, a globulin with high antibody levels against cytomegalovirus was given before and for 11 weeks after transplantation in a randomized trial. Among 36 patients who received no prophylactic granulocyte transfusions, globulin recipients had significantly fewer infections than controls (2 of 17 versus 8 of 19, p = 0.05 by Fisher's exact test and p = 0.03 by Mantel-Cox test). Conversely, infection rates were high and unchanged by globulin use among patients who received granulocytes from seropositive donors (7 of 8 recipients versus 6 of 7 controls). The lack of effect of the globulin among patients receiving transfusions of granulocytes from seropositive donors may suggest that the dose of antibody was insufficient or that antibody is ineffective against virus transmitted in granulocytes. We conclude that cytomegalovirus infection can be prevented by immunoprophylaxis in seronegative patients having marrow transplants who are not given granulocyte transfusions.

Adolescent↗
PubMed1983

Genetic and epigenetic control of the pyruvate kinase isozymes in mammals.

In man, patients with hereditary red cell pyruvate kinase (PK) deficiency have their enzyme concomitantly affected in both red cells and liver (PK-L), such that red cell L' and liver L PK subunits appear to be encoded by the same structural gene. Very recently, a mutant M1 PK has been described in muscle from a special mouse strain in which the M2 PK was concomitantly modified. Thus, it has been suggested that the M1 and M2 PK subunits are also encoded by the same structural gene, a gene distinct from that encoding L' and L. In this paper, we show that synthesis of each of the four PK subunits is specified by a different specific mRNA. Two structural genes, but at least four different mRNAs seem therefore to control synthesis of the PK isozymes. Genetic and epigenetic mechanisms responsible for generation of this diversity at the RNA level are discussed. In addition to these mechanisms of PK diversity, some PK subunits can be modified by post-translational events. In red cells, for instance, cell aging is associated with a progressive, partial proteolysis of the C-terminal extremities of L' subunits, ultimately resulting in cleavage of the phosphorylatable site.

Animals↗
PubMed1982

Two different species of messenger RNAs specify synthesis of M1 and M2 pyruvate kinase subunits.

A study was performed to determine whether M1 and M2 pyruvate kinases were synthesized under the direction of one or two messenger RNAs. We compared M1 and M2 pyruvate kinases purified from fresh tissues with those neosynthesized under the direction of messenger RNAs from tissues synthesizing either M1 or M2. RNA was isolated from rat muscle, lung, spleen and kidney by ethanol precipitation in 7 M guanidium chloride, translated in rabbit reticulocyte system and newly-synthesized pyruvate kinase subunits were purified by microimmunoaffinity chromatography. Pyruvate kinase from fresh muscle and spleen was purified in one step by a similar process. Muscle and spleen RNA directed the synthesis of M subunits with molecular weights of approx. 61000 and 62000, respectively, the same as those of the corresponding fresh tissue monomers. In addition, peptide maps obtained by partial digestion of neosynthesized M1 and M2 with V8 protease from Staphylococcus aureus confirmed that these polypeptides were clearly different.

Animals↗
PubMed1982

Multicenter collaborative trial of intravenous acyclovir for treatment of mucocutaneous herpes simplex virus infection in the immunocompromised host.

Intravenous acyclovir was evaluated in the treatment of 97 immunocompromised patients with mucocutaneous herpes simplex virus infection in a randomized, double-blind, placebo-controlled trial. Acyclovir recipients had significantly shorter periods of virus shedding (p less than 0.0002) and lesion pain (p less than 0.01), and more rapid lesion scabbing (p less than 0.004) and lesion healing (p less than 0.04). The most common adverse reaction was a low incidence of peripheral vein irritation; no serious toxicity could be definitely attributed to acyclovir treatment even in these seriously ill patients. Intravenous acyclovir offers both safe and effective treatment for mucocutaneous herpes simplex virus infection in the immunocompromised host.

Acyclovir↗
PubMed1982

Drug-resistant herpes simplex virus in vitro and after acyclovir treatment in an immunocompromised patient.

An acyclovir-resistant herpes simplex virus (HSV) has been isolated from an immunocompromised patient during treatment for severe orofacial HSV infections with acyclovir. The resistant virus is deficient in expression of the HSV thymidine kinase (TK). Emergence of acyclovir resistance during clinical use appears to parallel the in vitro observations of selection for TK-deficient, acyclovir-resistant viruses following serial passage in the presence of the drug. The clinical importance of drug-resistant HSV in unclear, and further investigations are required to determine whether it will be an impediment to successful therapy of HSV infections.

Acyclovir↗
PubMed1982

Effect of acyclovir and interferon on human hematopoietic progenitor cells.

Continuous in vitro exposure of human bone marrow cells to acyclovir (approximately 200 microM) or human leukocyte interferon (approximately 250 U/ml) caused 50% inhibition of granulocyte colony-forming cell differentiation. Colonies expressed in the presence of either agent were reduced both in size and number. Erythroid progenitors were more resistant than granulocyte progenitors to the antiproliferative effects of acyclovir. Progenitor cells of patients recovering from cytotoxic chemotherapy were no more sensitive to the effects of acyclovir or interferon than were cells obtained from patients before chemotherapy.

Acyclovir↗
PubMed1982

Gamma interferon production by combinations of human peripheral blood lymphocytes, monocytes, and cultured macrophages.

Mitogen-induced interferon (IFN) production was studied using human peripheral blood mononuclear cells and subpopulations of lymphocytes, monocytes, and cultured macrophages. Cell populations were prepared in suspension to permit quantitative analysis of the interactions among different cell types. After stimulation by staphylococcal enterotoxin A, nylon column-purified lymphocytes produced only 5% as much IFN as the peripheral blood mononuclear cells from which they were prepared. When lymphocytes were supplemented with as little as 2% monocytes, IFN production increased two- to eightfold; with the addition of up to 20% monocytes, IFN production increased further, to levels approximating those of peripheral blood mononuclear cells. Monocytes alone produced no or very little IFN. Macrophages were derived from monocytes by culturing in vitro for 7 days. The addition of 2 to 5% autologous macrophages augmented IFN production to the same extent as 2 to 5% monocytes. However, more macrophages consistently resulted in less, rather than more, IFN, so that lymphocytes with 20% monocytes produced three- to eightfold more IFN than did lymphocytes with 20% macrophages. Thus, whereas the addition of monocytes over a broad dose-response range (2 to 20%) progressively augmented IFN production, macrophages showed an optimal effect at 2 to 5%, with higher percentages being inhibitory. The IFN induced by stimulation with staphylococcal enterotoxin A was characterized as IFN-gamma by its resistance to neutralization by antibody to IFN- alpha and its inability to induce antiviral protection in embryonic bovine trachea cells.

Cell Communication↗
PubMed1982

Infection of human peripheral blood mononuclear cells by varicella-zoster virus.

The infection of human peripheral blood leukocytes by varicella-zoster virus (VZV) was studied using an infectious center assay, indirect immunofluorescence and electron microscopy. Subsets of freshly isolated leukocytes were prepared, including granulocytes, mononuclear cells from Ficoll-Hypaque gradients, lymphocytes, and glass-adherent monocytes. When each of these populations was inoculated with VZV (MOI = 0.1), there was no evidence of effective infection. However, when monocytes were cultured in vitro for 7 days, they differentiated into macrophages that were productively infected with VZV. Peak percentages of infectious macrophages were detected 8-24 h after inoculation (mean 17.5%; range 10.2-30.4%). Using indirect immunofluorescence, viral antigens were detected in the cytoplasm and at the nuclear membranes of infected macrophages between 24 and 72 h after infection. Electron microscopy demonstrated the appearance of viral particles in the nucleus by 24 h. Large numbers of virions, often collected in tubules or vacuoles, were present in the cytoplasm at 48 h. The difference between the infection of fresh monocytes and cultured macrophages by VZV might reflect differences in their metabolic or differentiation state. The possible significance of these observations to VZV infection of immunocompromised hosts is discussed.

Antigens, Viral↗
PubMed1981

Inhibition of human herpesviruses by combination of acyclovir and human leukocyte interferon.

Human leukocytes interferon in low concentrations (1 to 5 U/ml) enhanced the antiviral effect of acyclovir against herpes simplex virus, varicella-zoster virus, and cytomegalovirus grown in human fibroblasts. This occurred without additive inhibition of the division of human fibroblasts or proliferation of peripheral blood mononuclear cells. The combined antiviral effect was additive against clinical isolates of cytomegalovirus and was synergistic against clinical isolates of the other two viruses. The magnitude of the effect with cytomegalovirus was the same when laboratory and wild-type virus were compared. The persistence of varicella-zoster virus in the presence of acyclovir in infected human cells was also reduced by the addition of interferon.

Acyclovir↗
PubMed1980

Effect of acyclovir on the proliferation of human fibroblasts and peripheral blood mononuclear cells.

The effect of acyclovir on human cells was measured. A concentration of 50 to 100 microM inhibited the division of fibroblasts to a variable extent, depending on the experimental design and the confluency of the monolayer. The magnitude of this effect was less than that caused by human leukocyte interferon when these antiviral agents were compared at clinically relevant concentrations. Acyclovir also inhibited thymidine incorporation by peripheral blood mononuclear cells stimulated by either phytohemagglutinin or three different herpesvirus antigens. A linear dose-response curve was observed with these cells, and their proliferation was inhibited 50% by 100 microM acyclovir. Inhibition was exerted on T-cell proliferation without apparent effect on the release of lymphokines or on monocyte function.

Acyclovir↗