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Biomedical subjects

A Johnson

Publications and source records attributed to A Johnson.

At least 523 records · Page 29Linked to original sources
PubMed1986

Psychological aspects of recurrences of genital herpes.

Fifty-seven patients presenting with virologically confirmed first attacks of genital herpes were assessed for risk factors for time to the first recurrence. These factors included demographic details, personality traits, recent life events, herpes simplex biotype, frequency of orogenital intercourse and psychiatric illness as measured by the General Health Questionnaire (GHQ). This and our similar previous study (58 patients) were analysed separately and combined using a novel statistical technique (Cox's proportional hazards model). In the previous study there was a significant association only for GHQ score (p less than 0.02). For the present study age was the only statistical significant factor (the younger the patient the more likely a recurrence sooner (p less than 0.05), although there was a trend for high GHQ scorers to have recurrences sooner than low scorers. Data of the two studies combined showed that the only significant association with time to recurrence was the GHQ (p less than 0.02). These data support the notion that there is an association between psychiatric illness and recurrence of genital herpes.

Adaptation, Psychological↗
PubMed1986

Exonuclease III and endonuclease IV remove 3' blocks from DNA synthesis primers in H2O2-damaged Escherichia coli.

Escherichia coli deficient in exonuclease III (xth gene mutants) are known to be hypersensitive to hydrogen peroxide. We now show that such mutants accumulate many more DNA single-strand breaks than do wild-type bacteria upon exposure to H2O2. DNA isolated from H2O2-treated xth- cells contains strand breaks that do not efficiently support synthesis by E. coli DNA polymerase I, indicating the presence of blocking groups at the DNA 3' termini. Purified E. coli exonuclease III activates this blocked DNA to allow substantial synthesis by polymerase I in vitro. Another E. coli enzyme, endonuclease IV, also activates primers for DNA polymerase. Exonuclease III accounts for greater than 95% of the total activity in E. coli crude extracts for removal of 3'-terminal phosphoglycolaldehyde esters from model DNA substrates. Purified exonuclease III and endonuclease IV can each efficiently remove 3'-terminal phosphoglycolaldehyde in vitro. An important physiological function for exonuclease III is thus the activation of blocked 3' ends for DNA repair synthesis. Endonuclease IV can also initiate the repair of ruptured 3'-deoxyribose in DNA.

DNA Damage↗
PubMed1986

Beta-adrenergic modulation of pulmonary transvascular fluid and protein exchange.

We determined in anesthetized sheep whether isoproterenol, a beta-adrenergic agonist, prevents the increases in pulmonary fluid and protein exchange produced by thrombin-induced intravascular coagulation. Seven sheep were infused intravenously with 0.05 micrograms X kg-1 X min-1 isoproterenol before infusion of alpha-thrombin, and six sheep were infused with alpha-thrombin only and served as control subjects. The marked increases in pulmonary lymph flow and lymph protein clearance in the control thrombin group were attenuated (P less than 0.05) in the isoproterenol group in association with a higher pulmonary blood flow (P less than 0.05) and a lower pulmonary vascular resistance (P less than 0.05) in the isoproterenol group and with similar increases in pulmonary arterial and pulmonary arterial wedge pressures in both groups. The decreases in fluid and protein fluxes produced by isoproterenol are related to its beta-adrenergic properties because propranolol, a beta-adrenergic antagonist, blocked the protective effects of isoproterenol in a second group of sheep infused with propranolol, isoproterenol, and thrombin. Raising left atrial pressure to test for changes in vascular permeability increased protein flux to a much greater extent in the thrombin control group than in the isoproterenol group challenged with thrombin. The data suggest that isoproterenol attenuated the increase in fluid and protein fluxes produced by thrombin-induced intravascular coagulation by a permeability-decreasing mechanism.

Adrenergic beta-Agonists↗
PubMed1986

Effect of complement activation with cobra venom factor on pulmonary vascular permeability.

We examined the effect of acute complement activation on lung vascular permeability to proteins in awake sheep prepared with lung lymph fistulas. Complement was activated by cobra venom factor (CVF) infusion (400 U/kg for 1 h iv). Studies were made in two groups of sheep: 1) infusion of CVF containing the endogenous phospholipase A2 (PLA2) (n = 6); and 2) infusion of CVF pretreated with bromophenacyl bromide to inhibit PLA2 activity (n = 5). Intravascular complement activation transiently increased mean pulmonary arterial pressure (Ppa) and pulmonary vascular resistance (PVR) in both groups. Pulmonary lymph flow (Qlym) and lymph protein clearance (Qlym X lymph-to-plasma protein concentration ratio) were also transiently increased in both groups. Pulmonary vascular permeability to proteins was assessed by raising left atrial pressure and determining the lymph-to-plasma protein concentration ratio (L/P) at maximal Qlym. In both groups the L/P at maximal Qlym was not different from normal. In a separate group (n = 4), CVF-induced complement activation was associated with 111In-oxine granulocyte sequestration in the lungs. In vitro plasma from CVF-treated animals aggregated neutrophils but did not stimulate neutrophils to produce superoxide anion generation. Therefore, CVF-induced complement activation results in pulmonary neutrophil sequestration and in increases in PVR and lymph protein clearance. The increase in lymph protein clearance is due to increased pulmonary microvascular pressure and not increased vascular permeability to proteins.

Animals↗
PubMed1986

Superoxide dismutase prevents the thrombin-induced increase in lung vascular permeability: role of superoxide in mediating the alterations in lung fluid balance.

We investigated the effects of superoxide dismutase (SOD) and SOD linked to Ficoll (mol. wt = 400,000) on the changes in pulmonary transvascular fluid and protein exchange following pulmonary microembolism induced with alpha-thrombin. Studies were made in chronically prepared unanesthetized sheep with lung lymph fistulas. Control thrombin challenged sheep (n = 5) were compared to animals infused with SOD (the SOD-thrombin group, n = 5) or animals infused with SOD linked to high molecular weight Ficoll (the Ficoll-SOD-thrombin group, n = 6). The Ficoll-SOD-thrombin animals were also compared to animals infused with Ficoll alone (the Ficoll-thrombin group, n = 4). In the control-thrombin group, thrombin induced sustained increases in the pulmonary transvascular protein clearance (pulmonary lymph flow X lymph/plasma protein concentration ratio) and pulmonary vascular resistance (PVR). In the SOD-thrombin group, thrombin initially increased both pulmonary transvascular protein clearance and PVR; however, the later increases in protein clearance and PVR were blunted. The pulmonary reflection coefficients for total protein (sigma), a measure of vascular permeability to protein, decreased from a value of 0.70 +/- 0.03 in normal sheep to 0.60 +/- 0.01 following thrombin challenge (p less than 0.05) indicating an increase in lung vascular permeability. The sigma value in the SOD-treated animals was 0.70 +/- 0.02, indicating a protective effect of SOD. The infusion of the Ficoll-SOD complex also attenuated the increases in pulmonary transvascular protein clearance and PVR after thrombin. However, the infusion of Ficoll alone induced a similar protection. The lymph from the SOD-thrombin and Ficoll-SOD-thrombin groups prevented the reduction of ferricytochrome C by xanthine/xanthine oxidase, whereas, the lymph from the Ficoll-thrombin animals did not have this effect, indicating SOD activity was present in the animals receiving the enzyme but not in the group infused with Ficoll alone. Differences in the degree of intravascular coagulation could not explain the response to Ficoll since the decreases in fibrinogen concentration following the thrombin were similar in all the groups. Since Ficoll and related dextrans may modify neutrophil function, in particular neutrophil adherence to the endothelium, we examined the effects of Ficoll on neutrophil adherence. The results indicated that when Ficoll was added to the endothelial medium Ficoll reduced the increase adherence of neutrophils to the endothelial cell monolayer. Therefore, Ficoll as a carrier for SOD may provide a direct protection in models of lung vascular injury that are dependent on neutrophils.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1986

The competitive impact of health maintenance organizations on hospital finances: an exploratory study.

In this study we explore whether HMO-induced competition has contained expenditures in Minneapolis/St. Paul hospitals. Specifically, we assessed the impact of HMOs on revenue, cost, and net income per admission in Twin Cities hospitals from 1979 to 1981. Some HMOs have obtained negotiated discounts from hospitals. We found that hospitals which gave larger discounts did not have lower costs per admission. This finding suggest that discounts do not force hospitals to operate more efficiently. In addition, hospitals with a large share of patients from HMOs or government Medicare and Medicaid programs did not have lower costs per admission than other hospitals during the years from 1979 to 1981. This finding casts doubt on the claim that discounts are justified by lower costs for HMO or government patients. Finally, neither HMO market share nor discounts had an adverse effect on hospital profits. During the three years studied, hospital profits in the Twin Cities showed an upward trend. This study concludes that if competition is to succeed it must encompass more than HMOs. HMOs may be important, but they are only one agent in the market. Thus, public policy created to induce competition must go beyond the simple stimulus of HMO growth.

Blue Cross Blue Shield Insurance Plans↗
PubMed1986

Stromal cells in myeloid and lymphoid long-term bone marrow cultures can support multiple hemopoietic lineages and modulate their production of hemopoietic growth factors.

Hemopoiesis in long-term bone marrow cultures (LTBMC) is dependent on adherent stromal cells that form an in vitro hemopoietic microenvironment. Myeloid bone marrow cultures (MBMC) are optimal for myelopoiesis, while lymphoid bone marrow cultures (LBMC) only support B lymphopoiesis. The experiments reported here have made a comparative analysis of the two cultures to determine whether the stromal cells that establish in vitro are restricted to the support of myelopoiesis or lymphopoiesis, respectively, and to examine how the different culture conditions affect stromal cell physiology. In order to facilitate this analysis, purified populations of MBMC and LBMC stroma were prepared by treating the LTBMC with the antibiotic mycophenolic acid; this results in the elimination of hemopoietic cells while retaining purified populations of functional stroma. Stromal cell cultures prepared and maintained under MBMC conditions secreted myeloid growth factors that stimulated the growth of granulocyte-macrophage colonies, while no such activity was detected from purified LBMC stromal cultures. However, this was not due to the inability of LBMC stroma to mediate this function. Transfer of LBMC stromal cultures to MBMC conditions resulted in an induction of myeloid growth factor secretion. When seeded under these conditions with stromal cell-depleted populations of hemopoietic cells, obtained by passing marrow through nylon wool columns, the LBMC stromal cells could support long-term myelopoiesis. Conversely, transfer of MBMC stroma to LBMC conditions resulted in a cessation of myeloid growth factor secretion; on seeding these cultures with nylon wool-passed marrow, B lymphopoiesis, but not myelopoiesis, initiated. These findings indicate that the stroma in the different LTBMC are not restricted in their hemopoietic support capacity but are sensitive to culture conditions in a manner that may affect the type of microenvironment formed.

Animals↗
PubMed1986

Leukocytes are required for the trypsin-induced increase in lung vascular permeability.

The authors examined the role of leukocytes in mediating the increase in lung vascular permeability induced by trypsin infusion in the sheep lung lymph preparation. One group of sheep was challenged with an intravenous infusion of trypsin (4.5 mg/kg/hr). A second group was depleted of 80% of circulating granulocytes and of 48% of circulating lymphocytes by repeated injections of hydroxyurea several days prior to the trypsin infusion. Pulmonary lymph flow and transvascular protein clearance increased twofold without changes in pulmonary vascular pressures in the control group, suggesting that trypsin resulted in an increase in pulmonary vascular permeability. The hydroxyurea-induced leukopenia prevented the increases in pulmonary lymph flow and protein clearance after the trypsin infusion, indicating that leukocytes are required for increase in lung vascular permeability. Because neutrophil activation may mediate the trypsin-induced increase in lung vascular permeability, we assessed the effect of trypsin on superoxide anion (O2-) generation by isolated neutrophils. Trypsin (0.09 mg/ml) added to isolated sheep neutrophils did not increase O2- generation more than neutrophils in buffer. The supernatant obtained after incubation of trypsin with citrated whole blood increased O2- generation from isolated neutrophils, this response was greater than with trypsin alone. Therefore, neutrophil activation occurs as a result of the action of trypsin on whole blood. Neutrophil activation may contribute to the leukocyte-dependent increase in lung vascular permeability after trypsin.

Animals↗
PubMed1986

Variability of erythrocyte size and hemoglobin content observed in man and four selected mammals.

A new measurement technique employing light scattering at different angles has been developed for analysis of blood cells. This method which is part of the Technicon H*1 system, a hematology analyzer designed for routine processing of human blood samples, allows the independent measurement of cell volume and hemoglobin content of isovolumetrically sphered red blood cells. Analysis with this instrument of the blood of humans, dogs, rabbits, rats and mice demonstrates that in addition to the expected differences in hematologic parameters, the intrasample distribution of cell hemoglobin is species dependent. In general, cell hemoglobin content is more tightly controlled for the other mammals when compared to humans. In particular, the dogs tested showed the least variability in cell hemoglobin content both within species and within sample.

Animals↗
PubMed1985

Fibrin degradation products increase lung transvascular fluid filtration after thrombin-induced pulmonary microembolism.

The effect of fibrin degradation products (FDP) on pulmonary transvascular fluid and protein exchange was examined in the sheep lung lymph fistula preparation. The pulmonary lymph was used to assess changes in pulmonary lymph flow (Qlym) (a measure of net transvascular fluid filtration rate) and the lymph/plasma protein concentration ratio (L/P) (a measure of protein seiving across the microvascular barrier). Studies were made in 3 groups: Control-Thrombin (n = 7) received 96.9 +/- 9.4 U/kg of alpha-thrombin, Control-FDP (n = 6) received infusion of FDP prepared by plasmin digestion of fibrin, and Thrombin-FDP (n = 5) received thrombin (102.0 +/- 7.5 U/kg) and then an FDP infusion was begun at 60 min after the thrombin. In the Control-Thrombin animals, Qlym increased without a change in the L/P after thrombin, indicating an increase in vascular permeability to proteins. In the Control-FDP group, infusion of FDP had no effect on Qlym and L/P. In the Thrombin-FDP group, thrombin increased Qlym with no change in the L/P and the subsequent infusion of FDP further increased Qlym but slightly decreased the L/P, an effect not seen in the Control-FDR group. The results indicate that FDP infusion alone does not alter pulmonary transvascular fluid and protein exchange. However, in the presence of thrombin-induced pulmonary microembolization FDP infusion enhances the net transvascular fluid filtration rate, probably by increasing the capillary hydrostatic pressure.

Animals↗