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Biomedical subjects

M Vogt

Publications and source records attributed to M Vogt.

At least 181 records · Page 10Linked to original sources
PubMed1986

Autocrine growth and progression of murine X-ray-induced T cell lymphomas.

Primary tumors of X-ray-induced murine T cell lymphomas comprise autocrine, growth factor-dependent cells. We have grown cell lines from primary X-ray-induced thymic lymphomas (PXTLs) under conditions which minimize the progression of the cells from factor dependence to factor independence. All (22) PXTL lines grown secrete a growth factor which supports their own growth and which we will call lymphoma growth factor LGF. LGF-dependent cells are non-tumorigenic or poorly tumorigenic, do not clone in soft agar, have no detectable rearrangements in the c-myc or Pim-1 region and possess near diploid or pseudodiploid karyotypes without evidence for trisomy of chromosomes nos. 15 or 17. PXTL-secreted LGF has no interleukin 1, 2, or 3 activity nor do LGF-secreting cells synthesize detectable IL-1, -2, or -3 mRNA. LGF contains no detectable interferon or GM-CSF activity in specific bioassays. Purified EGF, TGF beta, and interleukin preparations are inactive on LGF-dependent PXTL cells. Thus LGF appears to be a new growth factor that is required for the proliferation of non-progressed T lymphoma cells. Upon progression PXTL cells become growth factor independent, are highly tumorigenic in vivo, clone in soft agar, and assume a near triploid karyotype containing numerous chromosomal aberrations. Thus in X-ray-induced lymphomagenesis an autocrine, LGF-dependent phase precedes the progressed phase characterized by rearrangements in the myc and/or Pim-1 regions as well as by many chromosomal aberrations visible in the karyotype.

Animals↗
PubMed1986

Significance of physical exercise in hypertension. Influence of water temperature and beta-blockade on blood pressure, degree of cardiac hypertrophy and cardiac function in swimming training of spontaneously hypertensive rats.

In previous studies swimming training (ST) of spontaneously hypertensive rats (SHR) at 36 degrees water temperature (WT) led to a decrease in blood pressure (BP). A similar effect of ST has not been described in human hypertension. Our purpose was to investigate the influence of WT on this training effect, the influence of ST on LV hypertrophy and the involvement of adrenergic stimuli in the latter. Male SHR (20 weeks old) were divided randomly into 4 groups. 1) SHR sedentary 2) SHR ST 36 degrees 3) SHR ST 26 degrees 4) SHR ST 36 degrees + atenolol (50 mg/kg/die). ST was performed 2 X 90 min/day for 31 days and then reduced to 2 X 60 min/day. After 7 weeks of ST BP was lower in all ST groups compared with SHR sedentary (p less than 0.001). BP was higher in ST 26 degrees than in ST 36 degrees (p less than 0.05). No additional effect of atenolol on BP was observed. The increase in the degree of LV hypertrophy during ST (ST 36 degrees: +15%; ST 26 degrees: +26%) could be prevented by atenolol (ST 36 degrees + atenolol: -1.5%). ST 36 degrees led to improved ventricular and myocardial performance with decreased LV wall stress ("luxury hypertrophy"), while in ST 26 degrees ventricular dilatation occurred with increased systolic wall stress and elevated LVEDP. It was uncertain whether this should be interpreted as a state of LV pre-insufficiency in ST 26 degrees in spite of no indications of impaired myocardial contractile capability. Peripheral vascular resistance (PVR) was significantly reduced by ST. The reduction was more evident in ST 26 degrees, but was partially compensated for by an increased cardiac output. The weights of adrenal glands increased (p less than 0.001), most markedly for ST 26 degrees. The level of thyroid hormones (T3 and fT3) was increased in ST 26 degrees. In summary, ST proved to be effective in lowering BP of SHR. WT had great influence with respect to cardiovascular adaptation and mechanisms involved in ST of SHR. Cardioadrenergic drive was of great significance for the process of hypertrophy during ST in SHR.

Animals↗
PubMed1986

Pathophysiological mechanisms in cardiac insufficiency induced by chronic pressure overload--an attempt to analyze specific factors in animal experiment.

Experimental results obtained from studies on Goldblatt rats and spontaneously hypertensive rats as well as theoretical considerations render possible an approximate analysis and evaluation of the relative significance of specific factors at different levels of the heart for the manifestation of cardiac failure under chronic pressure overload. In our experimental models congestive failure was never observed independently of structural dilatation. Thus, as a rule dilatation had already set in before symptoms of heart failure became manifest. However, at moderate dilatation of the ventricle, e.g., at double the end-diastolic volume, the geometrical state per se cannot be the cause of hydropic decompensation whereas extreme dilatation would, in principle, cause cardiac pumping failure even in the absence of any impairment of myocardial "contractility". Generally, a more or less marked impairment of myocardial contractile capability was found, which exceeded the effects due to the altered isoenzyme pattern of myosin. As a rule, a reduction in myocardial "contractility" could be ascertained before a marked degree of dilatation was reached. Diffuse fibrosis impairs the contractile capability of the myocardium and certainly contributes to the manifestation of heart insufficiency; although, as a rule, it should not be the main cause. The adaptive transformation of myocardium towards a slower muscle (isoenzyme pattern of myosin; sarcoplasmatic reticulum) as such does not lead to resting insufficiency, not even under persisting pressure load. Further investigations on processes of excitation-mechanical coupling in the advanced stage of cardiac overload are indicated. The absence of sympathetic support to the heart, e.g., following blockade of beta-adrenergic receptors can, in the advanced stage, elicit a transition from the stage of pre-insufficiency to manifest failure. However, this was only observed when dilatation had already occurred. A network of factors are responsible for cardiac insufficiency due to pressure overloading, whereby the respective significance of each component varies, depending on the experimental model used.

Animals↗
PubMed1986

Coinfection with viruses carrying the v-Ha-ras and v-myc oncogenes leads to growth factor independence by an indirect mechanism.

The concomitant expression of certain oncogenes can transform normal diploid rodent cells into transplantable tumorigenic cells. The mechanism by which these oncogenes collaborate is unclear. Recent findings (M. Oshimura, T. M. Gilmer, and J. C. Barrett, Nature [London] 316:636-639, 1985) raise the possibility that karyotypic changes, including monosomy for chromosome 15, are required to induce tumorigenicity in Syrian hamster embryo cells transfected in vitro with v-Ha-ras and v-myc DNAs. We studied the effect of the oncogenes v-Ha-ras and v-myc, introduced by viral infection, on murine hematopoietic cells. The induction of growth factor independence by the two oncogenes was used as an in vitro correlate of tumorigenicity. After a period of reduced growth rate reminiscent of the growth rate of cells in crisis, the doubly infected cells became growth factor independent. These cells showed a great variability in their karyotypes.

Animals↗
PubMed1986

[Gastrointestinal involvement in acquired immunologic deficiency syndrome (AIDS)].

The gastrointestinal tract is a major target organ of the acquired immunodeficiency syndrome. Opportunistic infections or Kaposi's sarcoma within the gastrointestinal tract are the two most frequent lesions. Diarrhoea, weight loss or odynophagy may be the presenting symptoms or signs for which a gastroenterological consultation is sought. In this report we present our own observations of patients with AIDS. Diagnostic and therapeutic aspects of this new syndrome are discussed.

Acquired Immunodeficiency Syndrome↗
PubMed1986

Myocardial and ventricular mechanics as influenced by disopyramide.

The effects of disopyramide (D) on the mechanics of isolated myocardium as well as on the whole ventricle were examined in the rat model. Moreover bipolar leads of the apex and an area at the base of the left ventricle were set up to get indications for changes in the spread of excitation. D in concentrations of 10(-8) to 10(-4) mol/l did not affect the diastolic elastic properties of isolated myocardium. Isometric contraction amplitude was nearly unaltered, while rate of isometric contraction and relaxation were slightly increased. In the whole ventricle in situ D (2 to 10 mg/kg b.w. administered i.v.) induced a dose-dependent decrease in left ventricular isovolumetric peak pressure (16%), max.pos. dP/dt (40%) and max.neg. dP/dt (30%; for highest doses respectively), while time to peak pressure and relaxation time 90% were prolonged. Therapeutic dose of D (2 mg/kg b.w.i.v.) induced no decrease in essential systolic parameters of the whole ventricle under auxotonic conditions. Left ventricular pressure, dP/dt max.pos. and neg., left ventricular end-diastolic pressure and cardiac output were nearly unaltered. Heart rate showed a tendency to decrease, while total time of contraction and left ventricular ejection time increased. Higher doses of D led to marked cardiac depressant effects. The time interval between the excitation of the apex and an area at the base of the heart was increased. It was concluded that the negative dromotropic effect of D and thereby an altered pattern of left ventricular contraction are essential components in the elimination of the pressure gradient between left ventricle and aorta, observed in patients with muscular subaortic stenosis, and are presumably involved in the cardiac depressant effect of the drug in over-therapeutic doses.

Animals↗
PubMed1985

Intra-blood-brain-barrier synthesis of HTLV-III-specific IgG in patients with neurologic symptoms associated with AIDS or AIDS-related complex.

Intra-blood-brain-barrier production of virus-specific antibody is good evidence of infection within the blood-brain barrier. Patients with the acquired immuno-deficiency syndrome (AIDS) have an increased incidence of neurologic abnormalities--i.e., unexplained, diffuse encephalopathy manifested clinically as chronic progressive dementia. To define the role of human T-cell lymphotropic virus Type III (HTLV-III), the etiologic agent of AIDS, in the pathogenesis of neurologic dysfunction, we compared cerebrospinal fluid and serum from patients with neurologic symptoms associated with AIDS and the AIDS-related complex for the presence of antibodies directed against HTLV-III. Antibodies directed against HTLV-III antigens were detected by four immunologic tests: a fixed-cell immunofluorescence assay, an enzyme-linked immunosorbent assay, immunoblots of viral lysates, and immunoprecipitation of cellular lysates. All patients were seropositive, and 22 of 23 (96 per cent) had HTLV-III-specific antibodies in their cerebrospinal fluid. Unique oligoclonal IgG bands were detected in the cerebrospinal fluid, and the rate of IgG synthesis within the blood-brain barrier was elevated. In eight of nine patients tested, the enzyme-linked immunosorbent assay showed that the percentage of HTLV-III-specific IgG in cerebrospinal fluid was higher than in serum, suggesting that HTLV-III infection of neurologic tissue occurs in the majority of patients with neurologic disease associated with AIDS or its related complex.

Acquired Immunodeficiency Syndrome↗
PubMed1985

[HTLV-III antibodies and risk factors for healthy homosexuals in Zurich].

Sera of 100 healthy homosexual men were tested for antibodies to AIDS virus HTLV-III. Significant differences were found between 45 seropositive and 55 seronegative men, such as a higher number of sexual partners per year, more contacts with AIDS patients, positive serological markers for syphilis, and reduced skin reaction after intradermal application of 7 recall antigens.

Adult↗
PubMed1985

[Heterosexual transmission of the acquired immunodeficiency syndrome (AIDS)].

A man who, only in 1979 and on a few occasions, had homosexual contacts, transmitted AIDS virus HTLV-III in 1980 and 1981 to two previously healthy women who did not belong to any AIDS risk group. One of them now has an early form of AIDS, while the other died of AIDS in its full form and her child, born in 1983, has fairly far progressed early symptoms of AIDS. Serum antibodies against HTLV-III were demonstrated in all four subjects.

Acquired Immunodeficiency Syndrome↗
PubMed1985

[Prevalence of antibodies against HTLV-III in various regions in Switzerland].

Acquired immune deficiency syndrome (AIDS) has been etiologically linked with the human T-cell lymphotropic virus HTLV-III. In a study on the prevalence of antibodies to this virus in Switzerland, sera from 941 individuals were collected in 5 major urban areas (Basel, Berne, Geneva, Lausanne and Zurich) in 1983 and 1984. All sera were tested by ELISA and the majority also by Western blot. We found an antibody prevalence of 100% among 22 cases of AIDS, of 94% among 48 cases of AIDS-related complex (ARC), and of 57% among 14 homosexual contacts of AIDS patients. Among 55 sera collected from i.v. drug addicts in 1984, 53% were positive, whereas the rate had been 36% among 103 sera collected in 1983. The rate was 19% among 227 sera collected from asymptomatic active homosexuals in 1984, against 10% among 40 sera collected in 1983. 8% positives were found among 98 patients with various types of viral hepatitis. In addition, 4% of 84 sera of individuals from Equatorial Africa were positive. No positives were found among 15 sera of individuals from other African regions, among 32 sera of persons from various regions of Asia, and among 203 Swiss blood donors. These results demonstrate the high and increasing rate of HTLV-III infection among groups at risk for AIDS, and suggest that HTLV-III-related diseases will be a serious problem in the years ahead.

Acquired Immunodeficiency Syndrome↗
PubMed1985

Oncogene expression in murine splenic T cells and in murine T-cell neoplasms.

The differential expression of a series of proto-oncogenes has been examined in a group of cultured murine T-cell lymphomas that were induced following virus inoculation into, or X irradiation of, C57BL/6 mice. Two classes of T lymphoma cell lines were studied: growth factor-dependent (autocrine) cells, and growth factor-independent T lymphoma cells. Cell lines that were established from X-irradiation-induced T lymphomas were growth factor dependent, whereas T lymphoma lines grown from virus-induced tumors were generally growth factor independent. Of 18 cellular proto-oncogenes studied, five (c-myc, c-myb, c-abl, c-rasHa, c-rasKi) were consistently expressed in all cell lines tested. Thirteen other proto-oncogenes (c-mos, c-sis, c-rel, c-yes, c-fes3, c-fes4, c-fos, c-fms, c-src, c-erbA, c-erbB, int-1, Pim-1) were not expressed in any of the T lymphoma cells tested. Concanavalin A-stimulated spleen cells, representative of replicating T cells, expressed c-myc, c-abl, and Pim-1, suggesting that the products of these proto-oncogenes are involved in T-cell proliferation. The results indicate no qualitative differences (albeit some quantitative differences) in proto-oncogene expression between the growth factor-dependent and growth factor-independent cells. This suggests that expression of the five proto-oncogenes is in itself not sufficient to induce the progression of the growth factor-dependent cells to their fully growth factor-independent counterparts. Changes in the regulation of one or more of the five active proto-oncogenes, i.e., from an inducible to a constitutive state, and/or additional changes in the expression of other cellular genes may be required to induce the transformation of neoplastic T cells from growth factor dependence to growth factor independence.

Animals↗
PubMed1985

Prevention of gram-negative shock and death in surgical patients by antibody to endotoxin core glycolipid.

The prophylactic effect of antibody to endotoxin core glycolipid was studied in surgical patients at high risk of gram-negative infection. At randomisation (on admission to intensive care unit), every 5 days thereafter, and at onset of septic shock, patients received plasma taken from donors before (control) or after immunisation with Escherichia coli J5, a mutant with only core determinants in its endotoxin. Gram-negative shock occurred in 15 of 136 controls and 6 of 126 J5 antibody recipients and related deaths in 9 of 136 and 2 of 126, respectively. J5 antibody was most effective in abdominal surgery patients, in whom shock occurred in 13 of 83 controls and 2 of 71 antibody recipients. Although antibody prophylaxis did not lower the infection rate, it prevented the serious consequences of gram-negative infections and thus improved the overall prognosis.

Bacterial Infections↗
PubMed1985

[Acquired immunodeficiency syndrome (AIDS). An update after 4 years].

At the end of December 1984, 8246 AIDS cases had been reported in the United States, and 762 cases in Europe. The main risk groups are homosexual and bisexual men (73%), heterosexual i.v. drug addicts (17%) and Haitians (4%). AIDS is diagnosed in patients meeting the clinical criteria of the CDC surveillance definition (opportunistic infections and/or Kaposi's sarcoma). The prevalence of HTLV-III antibodies in risk groups is high, its prognostic significance still controversial. Laboratory methods to determine the more relevant circulating viral proteins or the whole virus are now being developed. Limited studies to evaluate the possibility of reconstituting the immune system of AIDS patients with interleukin-2 and gamma-interferon have proved unsuccessful. successful. Several new drugs with possible antiviral properties are now being evaluated in first clinical trials.

Acquired Immunodeficiency Syndrome↗
PubMed1985

Antibodies to HTLV-III in Swiss patients with AIDS and pre-AIDS and in groups at risk for AIDS.

We tested serum samples from Swiss subjects by three different assays based on enzyme-linked immunosorbent assay (ELISA) and Western blot techniques for antibodies to proteins associated with the recently discovered human T-cell leukemia/lymphoma virus HTLV-III, the putative etiologic agent for the acquired immunodeficiency syndrome (AIDS). Of 10 patients with AIDS and 10 with pre-AIDS, all were antibody-positive. Furthermore, 37 of 103 intravenous-drug addicts (36 per cent), 4 of 40 healthy homosexual men (10 per cent), 7 of 83 patients with various types of hepatitis (8.4 per cent), but none of 83 healthy blood donors or 10 other controls were antibody-positive. Antibodies to the major viral protein p24 were found consistently and at high titers in the seropositive members of the groups at risk and in those with pre-AIDS but were dramatically reduced in patients with AIDS. In contrast, antibodies to another virus-associated protein, p41, were present in all cases of AIDS and pre-AIDS but were absent in nearly 10 per cent of seropositive persons at risk. Whereas p41 and p24 thus appear to be the targets of choice for future screening tests, the ELISA test that is currently available is a useful screening tool.

Acquired Immunodeficiency Syndrome↗
PubMed1985

[Immunologic laboratory tests in acquired immunodeficiency syndrome (AIDS) and suspected AIDS].

Since AIDS-specific laboratory tests are not yet commercially available, laboratory diagnoses of AIDS or of the AIDS-related complex (ARC) are based on "surrogate markers". While single tests are of limited diagnostic value, test combinations are of greater help. However, these tests should be applied restrictively and stepwise. The following parameters were analyzed in respect of their diagnostic and differential-diagnostic value: absolute number of lymphocytes, delayed type hypersensitivity skin tests to seven recall antigens, beta-2-microglobulin, serum-neopterin, C-reactive protein, complement factor B, circulating immune complexes, immunoglobulins, hepatitis B markers, and the ratio of T helper to T suppressor cells. 14 AIDS patients, 11 ARC patients, 23 healthy homosexuals, 6 iv drug users, 6 hemophiliacs and 35 patients with various other disorders were investigated. To analyse the value of a given test or of test combinations in the diagnosis of AIDS and ARC, a discrimination index was introduced and defined as the difference between the percentage of pathological values in one patient group compared to the percentage of pathological values in the other group. A discrimination index of 100 means that a given test is pathologic in all members of one group and negative in all members of the other group. A discrimination index of 60 may mean 80% of pathological values in one group versus 20% in the other. To distinguish AIDS patients from ARC patients the test combination yielding the highest mean discrimination index included serum neopterin, complement factor B and C-reactive protein.(ABSTRACT TRUNCATED AT 250 WORDS)

Acquired Immunodeficiency Syndrome↗
PubMed1985

Progressive diffuse leukoencephalopathy in patients with acquired immune deficiency syndrome (AIDS).

Two adult patients with acquired immune deficiency syndrome (AIDS) presented with psycho-organic symptoms produced by an extensive cerebral and cerebellar leukoencephalopathy. Diffuse loss of myelin and axons with reactive astrocytosis and distinctive multinucleated giant cells were prominent in the deep white matter, but less so in the subcortical white matter and in compact myelinated pathways. Bilateral involvement of the centrum semiovale produced distal Wallerian degeneration of the descending pyramidal tracts, which in one patient correlated with progressive paraparesis and bladder dysfunction. Although there were morphological indications of cytomegalovirus infection and immunohistochemical evidence of papovavirus antigens, the neuropathology did not resemble that usually associated with infection by these opportunistic agents. The possibility is entertained that the progressive diffuse leukoencephalopathy (PDL) in these patients was directly related to infection with human T-cell lymphotropic virus (HTLV-III/LAV), the etiologic agent of AIDS.

Acquired Immunodeficiency Syndrome↗