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V Peterson

Publications and source records attributed to V Peterson.

At least 19 recordsLinked to original sources
PubMed1996

Associations among PH and SH3 domain-containing proteins and Rho-type GTPases in Yeast.

The src homology region 3 (SH3) domain-bearing protein Bem1p and the Rho-type GTPase Cdc42p are important for bud emergence in Saccharomyces cervisiae. Here, we present evidence that through its second SH3 domain, Bem1p binds to the structurally and functionally similar proteins Boi1p and Boi2p, each of which contain an SH3 and pleckstrin homology (PH) domain. Deletion of BOI1 and BO12 together leads to impaired morphogenesis and poor ability. A PH domain-bearing segment of Boi1p that lacks the Bem1p-binding site is necessary and sufficient for function. This segment of Boi1p displays a two-hybrid interaction with Cdc42p, suggesting that Boi1p either binds directly to or is part of a larger complex that contains Cdc42p. Consistent with these possibilities, overexpression of Boi1p inhibits bud emergence, but this inhibition is counteracted by cooverexpression of Cdc42p. Increased expression of the Rho-type GTPase Rho3p, which is implicated in bud growth defects of boil boi2 mutants, suggesting that Boi1p and Boi2p may also play roles in the activation or function of Rho3p. These findings provide an example of a tight coupling in function between PH domain-bearing proteins and both Rho-type GTPases and SH3 domain-containing proteins, and they raise the possibility that Boi1p and Boi2 play a role in linking the actions of Cdc42p and Rho3p.

Adaptor Proteins, Signal Transducing↗
PubMed1992

Survival in Hodgkin's disease by stage and age.

Patterns of care for Hodgkin's disease in the United States were surveyed through voluntary audits of hospitals with cancer programs nonapproved and approved by the Cancer Commission of the American College of Surgeons. Four hundred and seventy-three hospitals reported 6,345 patients diagnosed immediately preceding December 31, 1975. The survival rates varied with age, being better at younger ages and worse in the elderly. By pathologic stage, the younger patients faired better than the elderly in each stage grouping. Histologic type was not a factor in this poor prognosis. Hodgkin's disease in elderly patients has a different biologic behavior than in younger patients.

Adolescent↗
PubMed1985

Prevention of suppressed cell-mediated immunity in burned mice with histamine-2 receptor antagonist drugs.

Thermal injury has been shown to suppress many aspects of both specific and nonspecific immune responses. We investigated the effect of two histamine H-2 antagonist drugs on cell-mediated immunity in burned mice, utilizing a method of quantitating the degree of contact sensitivity elicited to the antigen. 2,4-dinitrofluorobenzene (DNFB). Following sensitization by painting the abdomen with DNFB, animals were challenged 5 days later by painting the ears; subsequent ear swelling is a sensitive and reproducible measure of cell-mediated immunity. We have previously demonstrated that burned mice are maximally immunosuppressed 10 to 14 days following burn injury. In the present study we found that daily intraperitoneal administration of appropriate doses of the H-2 antagonists cimetidine (2 and 10 mg/kg/day) and ranitidine (2 and 10 mg/kg/day) resulted in maintenance of normal cell-mediated immunity in burned animals. Neither a lower dose of ranitidine (0.2 mg/kg/day) nor higher doses of cimetidine (20 and 50 mg/kg/day) restored immunity, and diphenhydramine, an H-1 antagonist, had no effect. There was no augmentation of contact sensitivity in unburned mice treated with cimetidine. The immunorestorative effect is probably secondary to antagonism of histamine H-2 receptors on suppressor T lymphocytes, and may reflect increased suppressor cell activity in burned mice; however, other mechanisms may be involved.

Animals↗
PubMed1984

Characterization of the immunosuppressive effect of burned tissue in an animal model.

The immunosuppressive effect of burned tissue was studied using a mouse burn model. To evaluate the immunologic status an in vivo measure of cell-mediated immunity (CMI) involving contact sensitization of mice by painting the skin with dinitrofluorobenzene was used; mice were challenged 5 days later by painting the ear with the same antigen. Ear swelling in response to antigenic challenge was used as a quantitative measure of CMI; diminution in ear swelling in treatment mice compared to sensitized, unburned control mice indicated the degree of immunosuppression. A full-thickness steam burn covering 20% body surface ares (BSA) was profoundly immunosuppressive as reflected by ear swelling of 45 to 60% of that found in normal mice; partial thickness burns and burns of 10% BSA extent were not significantly immunosuppressive. Transfer into unburned mice of burned skin equivalent in size to a 20% BSA burn eschar resulted in marked immunosuppression, but transfer of smaller amounts of burned skin, or of larger amounts of unburned skin and normal and burned liver tissue, did not produce immunosuppression. Mice receiving a very high-temperature (300 degrees C), dry burn were only slightly more suppressed than mice receiving a standard steam burn. Normal immunity was preserved in burned mice which received daily application of cerium nitrate to the wound for 7 days, but application of other topical agents commonly used in burn treatment did not preserve immunity. Postburn immunosuppression thus appears related quantitatively to toxic factors in burned skin, and these toxic factors can be abrogated in burned mice by the topical application of cerium nitrate.

Animals↗
PubMed1984

The haematopoietic response to burning: studies in an animal model.

Changes in haematopoiesis which occur in humans after burning injury may have important effects on morbidity and mortality. Because of the heterogeneity of burn patients we studied the regulation of blood cell formation which occurs in an animal using an established mouse model. Mice received a 20 per cent third degree scald injury on the back. Serial studies of a variety of haematopoietic parameters including stem cell, bone marrow and peripheral blood findings were done post burn. Although anaemia occurred frequently after injury red blood cell survival studies and examination of the stool for occult blood showed that neither haemolysis nor blood loss were primary causes of the anaemia. Bone marrow erythroid stem cells fell markedly post burn and this was associated with the development of a substance in serum capable of inhibiting red cell colony formation but not white cell colony formation of normal marrow cells. Reticulocytosis occurred but was mild and the anaemia was primarily of the aregenerative type. Partial compensation for the depressed marrow erythropoiesis occurred in the spleen with an increase in erythroid colony-forming cells and erythroblasts. Marked granulocytosis occurred in the peripheral blood and bone marrow. There was an increase in splenic granulocytic stem cells post burn. Megakaryocytosis was striking in the bone marrow and spleen and there was an increase in peripheral blood platelet count. Evidence of immune stimulation included an increase in the size of the spleen and an increase in peripheral blood and splenic lymphocytes. Correlations of many of these findings suggested that the events were not occurring at random but that the changes in haematopoiesis were linked together. We speculate that the anaemia was the result of the increase in granulopoietic and thrombopoietic effort seen post burn.

Anemia↗
PubMed1984

Postburn immunosuppression in an animal model. II. Restoration of cell-mediated immunity by immunomodulating drugs.

We used a model of full-thickness burn injury in the mouse and quantitated cell-mediated immunity (CMI) by measuring the degree of sensitization to the contact antigen, 2,4-dinitrofluorobenzene (DNFB). Our previous studies have shown that CMI in the burned mouse is severely suppressed. Using this immunosuppression model, we were able to significantly restore CMI by treating animals following the burn injury either with one of the nonsteroidal anti-inflammatory drugs ibuprofen or indomethacin or with the cytotoxic alkylating agent cyclophosphamide. These drugs probably restore CMI by inhibiting generation of suppressor T lymphocytes in the burned host.

Animals↗
PubMed1983

Regulation of granulopoiesis following severe thermal injury.

Neutropenia often accompanies septicemia in burned patients. This paradox suggests a defect in the regulation of granulopoiesis. Colony stimulating factor (CSF) produced by the monocyte-macrophage system is an important regulator of granulocyte production. We followed serial serum CSF levels and peripheral blood leukocyte differential counts in 22 patients with greater than 30% burns. Six patients (mean burn, 58%) developed Gram-negative septicemia and died (Group I). Sixteen patients (mean burn, 38%) had no fatal septicemias (Group II). Nonsurvivors had initially low levels of CSF and developed persistent monocytopenia. Survivors, in contrast, had prompt rises in CSF and developed monocytosis. The presence of monocytopenia and low CSF levels in Group I suggests an abnormality in the stimulatory arm regulating granulopoiesis. Such a defect may play a role in the development of fatal septicemia following severe thermal injury.

Adult↗
PubMed1983

Postburn immunosuppression in an animal model: monocyte dysfunction induced by burned tissue.

We studied cell-mediated immunity (CMI) in burned mice using an assay that involves the induction of contact sensitivity to dinitrofluorobenzene (DNFB). Subsequent painting of the ears with DNFB and measurement of ear swelling with calipers is a sensitive and quantifiable assay for CMI. Results may be expressed as mean ear swelling (MS) in units of 10(-4) inches +/- 2 standard errors of the mean. CMI was severely depressed in burned mice over a 2-week period following burn (control MS 48.3 +/- 1.0, 14 days after burn 29.0 +/- 1.0, P less than 0.01). Immediate postburn eschar removal resulted in avoidance of immunosuppression (MS 41.5 +/- 1.0, P less than 0.01) while transfer of burned tissue subcutaneously into unburned mice resulted in severe immunosuppression (MS 33.2 +/- 2.6, P less than 0.01). CMI was restored by intravenous infusion of peritoneal macrophages from unburned mice (MS 41.4 +/- 2.2), but not by infusion of lymphocytes or of macrophages taken from burned mice. This model should prove useful for further study of burn injury-induced immunosuppression.

Animals↗
PubMed1979

Abnormalities of bone marrow simulating histiocytic medullary reticulosis in a patient with gastric carcinoma.

In the proper clinical setting, phagocytosis by bone marrow histiocytes of erythrocytes, granulocytes, and platelets (panphagocytosis) is generally accepted as the morphologic hallmark of histiocytic medullary reticulosis. A patient with clinical manifestations that suggested histiocytic medullary reticulosis was found also to have histiocytic panphagocytosis in the bone marrow. Biopsy of the liver, however, revealed metastatic adenocarcinoma. In addition, postmortem examination demonstrated a gastric adenocarcinoma with massive hepatic involvement and absence of lymphadenopathy, splenomegaly, or evidence of generalized histiocytic proliferation. Therefore, histiocytic panphagocytosis is probably not specific for histiocytic medullary reticulosis, and may be a nonspecific feature of a variety of diseases.

Bone Marrow↗
PubMed1979

Cytoplasmic fragments causing spurious platelet counts in the leukemic phase of poorly differentiated lymphocytic lymphoma.

A patient with a leukemic phase of poorly differentiated lymphocytic lymphoma had a spuriously high automated platelet count because of cytoplasmic fragments. The number and relative percentage of cytoplasmic fragments increased during chemotherapy. The cytoplasmic fragments did not interfere with platelet aggregation using adenosine diphosphate, collagen, and epinephrine even though they were found in platelet-rich plasma. The ultrastructure of the cytoplasmic fragments is discussed. Cytoplasmic fragments as a cause of spuriously high automated platelet counts should be considered in cases of leukemic patients.

Adult↗
PubMed1973

Deletion mapping of the lambda REX gene.

Deletion mapping has been used to order 12 lambda rex(-) mutants. Correlation of recombination data with physically-determined positions of deletion end-points (Szybalski 1971; Blattneret al. 1972) suggests that the left-most rex(-) mutation, rex209, is located about 260-300 nucleotide pairs from the p(L) mutation sex1 and about 475 nucleotide pairs from the left end-point of the region of nonhomology with lambdaimm434.

Chromosome Mapping↗
PubMed1972

Isolation and properties of rex - mutants of bacteriophage lambda.

Twenty-five rex(-) mutants of phage lambda have been isolated. Three of the mutants, including one amber mutant, map at three distinct sites within the rex region of the lambda genetic map. The existence of the amber mutant provides further evidence that rex and cI are distinct genes, since it seems to be identical to wild-type lambda in its ability to establish or maintain lysogeny.

Coliphages↗
PubMed1971

Single-sample diagnosis of recent rubella by fractionation of antibody on Sephadex G-200 column.

To facilitate the diagnosis of recent rubella infection, rubella haemagglutination inhibiting antibody has been determined in four fractions obtained by Sephadex G-200 gel filtration of samples of serum. All the 21 samples collected at the convalescent stage of the disease had varying proportions of haemagglutination inhibiting antibody in fraction 1, representing the major portion of IgM antibody whereas all but three out of 22 sera from persons with no history of recent rubella had negative titres in this fraction. The haemagglutination inhibiting titres in the three positive sera in the second group was very low as compared to the other fractions. Fractionation of sera on a Sephadex G-200 column coupled with the rubella haemagglutination inhibition test can, therefore, be used to diagnose recent rubella infection.

Adult↗