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Biomedical subjects

H Persson

Publications and source records attributed to H Persson.

At least 307 records · Page 17Linked to original sources
PubMed1985

Thyroid hormones in conditions of chronic malnutrition. A study with special reference to cancer cachexia.

Circulating levels of thyroid hormones (T4, free T4, T3) and reverse tri-iodo thyronine (rT3) and thyroid-hormone binding globulin were related to the nutritional state of patients with cancer cachexia, patients with malnutrition due to other reasons and to well-nourished patients with acute illness. Hospitalized weight-stable and well-nourished patients served as controls. Malnourished patients with or without cancer and acutely ill patients had a low T3 syndrome involving both peripheral metabolism of thyroid hormones and the hypothalamus-pituitary-thyroid gland axis. T3 levels were correlated to altered protein metabolism and protein nutritional state. There were pronounced elevations of circulating rT3 concentrations in patients with serum albumin concentration less than 35 g/l irrespective of diagnosis. The results indicate that the low T3 syndrome in our patients is secondary to insufficient caloric intake. It seems to be maintained by the abnormal nutritional state and is related closely to protein metabolism. The authors found no differences between the low T3 syndrome in cancer patients suffering from cachexia compared with that of patients with malnutrition caused by other factors.

Acute Disease↗
PubMed1984

Antibodies to human c-myc oncogene product: evidence of an evolutionarily conserved protein induced during cell proliferation.

Antisera to a synthetic c-myc peptide and to c-myc antigens synthesized from various portions of the human gene expressed in Escherichia coli were used in order to characterize the protein product of the human c-myc oncogene. Although the deduced molecular weight of the human c-myc protein is 49,000, these antisera precipitate a protein from human cells that migrates in sodium dodecyl sulfate-polyacrylamide gel as if its molecular weight were 65,000. In addition, the mouse c-myc protein, whether synthesized in cells or in a cell-free system directed by pure, synthetic messenger RNA, has analogous properties and is immunoprecipitated by the antiserum to the human c-myc protein. Similar proteins are immunoprecipitated from monkey, rat, hamster, and frog cells, suggesting evolutionary conservation of antigenic structure of the c-myc protein among vertebrates. In addition, and in a manner consistent with the behavior of its messenger RNA, the immunoprecipitable c-myc protein is sharply induced by the action of mitogens on resting human T cells.

Amino Acid Sequence↗
PubMed1984

Is there any evidence of beta 1-adrenoceptors mediating relaxation of guinea-pig lung parenchyma?

We tried to find functional evidence for the existence of beta 1- and beta 2-adrenoceptors in the isolated guinea-pig lung parenchymal strip preparation, using potent and selective beta 1- and beta 2-adrenoceptor stimulation. To obtain potent beta 1-adrenoceptor stimulation the nonselective beta-adrenoceptor agonist isoprenaline was combined with a highly selective beta 2-adrenoceptor antagonist--ICI 118,551. Potent beta 2-adrenoceptor stimulation was obtained by procaterol. Practolol (beta 1-adrenoceptor antagonist) and ICI 118,551 were used as antagonists. ICI 118,551, 10(-7) mol/l, shifted the concentration response (C/R) curve of isoprenaline to a higher concentration range. The C/R curve of procaterol was shifted in the same way and to the same degree by this concentration of ICI 118,551. The C/R curve of isoprenaline was not further shifted after blockade with a combination of ICI 118,551, 10(-7) mol/l, and practolol, 10(-6). However, in the trachea preparation, a tissue containing both beta 1- and beta 2-adrenoceptors, there was a further shift of the C/R curve of isoprenaline to a higher concentration range after blockade with a combination of ICI 118,551 and practolol in the concentrations given above. In this preparation the shift of the C/R curve of procaterol was ten times greater than that of isoprenaline after blockade with ICI 118,551, 10(-7) mol/l. We conclude that it is possible to characterize small fractions of beta 1-adrenoceptors coexisting with beta 2-adrenoceptors with the technique used. Furthermore there is still no functional evidence of the existence of beta 1-adrenoceptors in the lung parenchyma.

Adrenergic beta-Antagonists↗
PubMed1984

Lymphokine-like activity of a strain of Mycoplasma arginini.

A Mycoplasma arginini strain, found to contaminate a T-T hybridoma designated TUH-14, was the source of a lymphokine-like activity with an ability to stimulate B-blasts to proliferate. Maturation to immunoglobulin secretion induced by the mycoplasma alone was low compared with induction by lipopolysaccharide (LPS), but could reach the same levels achieved with LPS by the addition of a B-cell maturation factor obtained from lectin-activated EL-4 thymoma cells. The mitogenic effect on B-cells was found only in the strain isolated from TUS-14; three other M. arginini strains were negative. Both mitogenic and nonmitogenic mycoplasma membrane preparations displayed higher affinity for B-cells than for T-blasts. However, membranes from the mitogenic strain, the TUH-14 isolate, bound better to activated blasts than to small resting cells, in contrast to the nonmitogenic strain G-230.

Adhesiveness↗
PubMed1984

Clinical experience of blood transfusion in renal transplantation.

A positive effect on survival of renal grafts of pretransplant blood transfusions have been reported from several centers. The aim of this study was to study if the described graft-protecting effect of blood transfusion was present in the Gothenburg material of transplanted patients, and if this effect could be achieved by deliberately transfusing previously non-transfused patients with two units of leukocyte-reduced blood. The effect on graft survival (GS) of the number and timing of transfusions to recipients, transfusions to the cadaveric donors, HLA-A, B matching, lymphocytotoxic antibodies and pretransplant hemodialysis was also studied. The study includes 844 recipients of primary renal grafts from living related and cadaveric donors (LRD, CD) and 70 patients waiting for transplantation. In the retrospective part of the study the GS of previously transfused and non-transfused non-transfused patients was compared. In the prospective part of the study a protocol with two deliberate transfusions (DT) to previously non-transfused patients was introduced. The GS of the DT group was compared to that for patients transfused for strictly medical reasons (MT) and non-transfused patients (NT). Survival of patients and grafts was calculated according to the life table method. In the retrospective part of study one year GS in LRD transplantation was 86.6% for transfused and 38.4% for non-transfused patients (P less than 0.01). In the first period one year GS in CD transplantation was 62.1% for transfused and 35.1% for non-transfused patients (P less than 0.01). The corresponding figures in the second period were 68.1% and 39.5%, respectively (P less than 0.001). In transfused recipients receiving kidneys from transfused and non-transfused cadaveric donors, the GS was 76.3% and 55.4%, respectively (P less than 0.05). In the prospective part of study the one year GS after LRD transplantation was 85.0% in both the DT and MT groups. In CD transplantation the one year GS was 73.4% and 75.7% of the DT and MT groups, respectively. The GS of each of these two groups was significantly better than that of 20.8% for the NT group (P less than 0.01). Lymphocytotoxic antibodies were detected in 5.0% of the DT group and 23.0% of the MT group (P less than 0.001). Foreign HLA-B series antigens had a negative influence on GS in the first period of the retrospective CD study. Later, no influence on GS was noted of HLA-A, B matching. Hemodialysis prior to transplantation did not influence GS.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1984

Aspects on antidote therapy in acute poisoning affecting the nervous system.

The number of toxic substances affecting the nervous system through acute or chronic exposure is overwhelming. This survey will elucidate the possibilities of antidote therapy in some acute cases of poisoning, caused by nervous system toxicants. Antidotes exert their therapeutic effects through a variety of mechanisms: Adsorption, formation of inert complexes, inhibited conversion to toxic metabolites, enhancement of endogenous detoxification, interference at receptor sites, and physiological antagonism. The application of these principles in treating some poisonings caused by important nervous system toxicants will be considered. This survey is by no means comprehensive, but rather gives some relevant examples and deals only with acute poisoning.

Acute Disease↗
PubMed1983

Beta 2-adrenoceptors in guinea-pig atria.

The occurrence of beta 2-adrenoceptors in the isolated, spontaneously beating right atrium and the electrically driven left atrium of the guinea-pig was studied. Isoprenaline was used as reference compound and procaterol as selective beta 2-agonist. Cumulative concentration response (C/R) curves were obtained with the agonists. The C/R curve of procaterol was biphasic in both preparations. Compared with isoprenaline, procaterol was a partial agonist, with a mean maximum response of 0.78 +/- 0.04 in the right atrium and 0.29 +/- 0.05 in the left atrium. The beta 2-selective antagonist ICI 118,551, 10(-7) mol litre-1, caused a small but significant shift of the C/R curve of isoprenaline to a higher concentration range in both preparations. The same concentration of the beta 2-blocker changed the shape of the C/R curve of procaterol from biphasic to monophasic by blocking the responses to low concentrations of procaterol. Practolol, a beta 1-selective antagonist, 10(-6) mol litre-1, gave a highly significant shift of the C/R curve of isoprenaline to a higher concentration range in both preparations but had no effect on the responses to low concentrations of procaterol. The effect of practolol on the responses to high concentrations of procaterol is discussed. We conclude that the guinea-pig atria may contain beta 2-adrenoceptors mediating positive chronotropic and inotropic effects.

Animals↗
PubMed1983

Control of adenovirus gene expression: cellular gene products restrict expression of adenovirus host range mutants in nonpermissive cells.

Adenovirus type 5 (Ad5) host range mutants dl312 and hr-1, with lesions in region E1A (0 to 4.5 map units) of the viral genome, fail to accumulate virus-specific early RNA during infection in HeLa cells. In a recent report, we showed that the addition of anisomycin, a stringent inhibitor of protein synthesis, at 1 h after infection of HeLa cells with hr-1 virus resulted in the accumulation of properly spliced and translatable mRNA from all early regions (M. G. Katze, H. Persson, and L. Philipson, Mol. Cell. Biol. 1:807-813, 1981). Based on these results we proposed a model in which expression of early mutant RNA was achieved through inactivation of a cellular protein normally causing a reduction in the amount of viral RNA. These studies have been extended in the present report, which shows that early viral proteins can be detected in Ad5 dl312- and Ad5 hr-1-infected HeLa cells which have been treated for several hours with anisomycin either shortly after infection or before infection. A pulse of drug treatment also resulted in expression of substantial amounts of adenovirus structural proteins after infection with both Ad5 hr-1 and Ad5 dl312, whereas in drug-free controls no late proteins were detected. The Ad5 hr-1 virus previously reported to be DNA replication negative in nonpermissive HeLa cells was found to replicate its DNA, albeit at low levels, when anisomycin was present either from 1 to 5 h postinfection or for 5 h before infection. When infectious virus production was examined in mutant-infected cells the titer of Ad5 dl312 virus was found to increase at least 500-fold in anisomycin-treated HeLa cells. Taken together, these and our previous results suggest that the block in gene expression characteristic for complementation group I Ad5 host range mutants in HeLa cells can be overcome by inactivating cellular gene products serving as negative regulators of viral gene expression.

Adenoviruses, Human↗
PubMed1983

Beta-adrenoceptor blocker intoxication: epidemiological data. Prenalterol as an alternative in the treatment of cardiac dysfunction.

1 During the three years 1978--1980 the Swedish Poison Information Centre received reports of 184 patients hospitalized due to beta-adrenoceptor blocker overdosage. Of the 35 patients who developed signs of severe cardiac dysfunction (HR less than 50 beats/min, systolic blood pressure less than 80 mm Hg), 23 had ingested propranolol, 10 metoprolol and 2 alprenolol. 2 The mean value of the defined daily doses (DDD) per 1000 inhabitants per day in Sweden during these years were 11.97 for propranolol, 8.02 for alprenolol and 7.74 for metoprolol. The incidence of severe poisoning due to alprenolol overdosage is lower than expected according to DDD. 3 During 1979 19 persons died from overdosage with beta-adrenoceptor blockers in Sweden: 15 due to propranolol (non-selective, lacks intrinsic sympathomimetic activity), 2 to metoprolol (cardioselective, lacks intrinsic sympathomimetic activity). These findings indicate that severe and even fatal poisoning may occur regardless of the type of beta-blocking agent. 4 The usefulness of prenalterol, a cardioselective beta-adrenoceptor partial agonist, in reversing unwanted cardiac effects of beta-adrenoceptor blocking agents is illustrated by two cases of massive propranolol intoxication (maximal plasma concentrations of propranolol 7.2 and 7.8 mumol/l respectively). Prenalterol in high doses (130 and 280 mg/24 h respectively) restored cardiac function.

Adrenergic beta-Antagonists↗
PubMed1982

An adenovirus glycoprotein binds heavy chains of class I transplantation antigens from man and mouse.

The successful killing of virus-infected cells by cytotoxic T lymphocytes (CTL) is dependent on the recognition of both a viral product and class I antigens of the major histocompatibility complex (MHC) on the infected cell surface. Whether these two entities are found independently on the cell surface and therefore recognized by two different CTL receptors, or whether they are associated together and can therefore be recognized by a single receptor is not known. The association between an adenovirus-encoded glycoprotein expressed on the cell surface early after infection and class I antigens has been investigated and it has been found that antisera against class I antigens can co-precipitate the antigen and the viral glycoprotein from an adenovirus-transformed cell line from the Hooded-Lister rat strain. We show here by in vitro affinity chromatography and in vivo immunoprecipitation that the viral glycoprotein specifically binds to the heavy chain of class I antigens in both man and mouse.

Adenoviridae↗