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Biomedical subjects

A Lochner

Publications and source records attributed to A Lochner.

At least 91 records · Page 5Linked to original sources
PubMed1983

Evaluation of the circulating and splenic lymphocyte subpopulations in patients with non-Hodgkin lymphomas and Hodgkin's disease using monoclonal antibodies.

The number of B lymphocytes, T lymphocytes and their helper/inducer, cytotoxic/suppressor and NK/K subpopulations was measured in peripheral blood and spleen cell suspensions from patients with Hodgkin's disease (HD) in the active stage of the disease and in remission status, as well as in Non-Hodgkin lymphomas (NHL) in active stage of the disease. B lymphocytes were determined by direct immunofluorescence and T lymphocytes with the E rosette technique. Helper/inducer, cytotoxic/suppressor, and NK/K T lymphocytes were determined by indirect immunofluorescence with the monoclonal antibodies OKT4, OKT8 and Leu 7 (HNK1). In the same way, Lyt3 was used for determination of the total T lymphocytes. Whereas in peripheral blood of the NHL group an increase of B lymphocytes and a slight reduction of T lymphocytes could be observed, with normal distribution of the subpopulations, in patients with active HD as well as in those in remission, a marked absolute and relative decrease of T helper/inducer cells was found with normal cytotoxic/suppressor and NK/K proportion. In contrast to this, a significant increase of helper/inducer T lymphocytes with decreased cytotoxic/suppressor T proportion was found in spleen cell suspensions of patients with HD.

Adult↗
PubMed1983

Normothermic ischaemic cardiac arrest and reperfusion of the isolated working heart: effect of chlorpromazine on functional, metabolic and morphological recovery.

The effects of chlorpromazine, an inhibitor of both Ca2+ flux and phospholipase activity, on myocardial ultrastructure, function and metabolism were assessed during normothermic ischaemic cardiac arrest and reperfusion of the isolated working rat heart. Normothermic ischaemic cardiac arrest produced significant changes in myocardial ultrastructure, high energy phosphate contents and mitochondrial oxidative phosphorylation within 20 min. Reperfusion of untreated hearts subjected to 20 and 25 min ischaemia failed to restore mitochondrial function, mechanical activity and ATP content to control, pre-ischaemic levels. Morphological signs of ischaemic injury regressed, especially in the subendocardial layer. Pretreatment of hearts with chlorpromazine did not prevent the ischaemia-induced changes in myocardial ultrastructure and mitochondrial function. However, during reperfusion the chlorpromazine-treated, totally ischaemic heats (20 to 25 min) exhibited improved coronary flow rates, and ultrastructural and mechanical recovery. The mitochondrial oxidative phosphorylation process and tissue high energy phosphate contents were not affected by the drug.

Adenosine Triphosphate↗
PubMed1983

Dual expression of T and B cell markers in human B cell neoplasias.

Macrophage- and T-cell-depleted mononuclear cells from 36 patients with B cell lymphoma and 12 healthy individuals were investigated by indirect immunofluorescence with the monoclonal antibodies NEI-011 (7.2) and NEI-015 (10.2). The monoclonal antibody NEI-011 (7.2) recognized the Ia antigen and identified almost all B cells in the peripheral blood of healthy individuals. Furthermore, neoplastic B cells from all patients except those with plasma cell proliferation were found to react with this antibody. NEI-015 (10.2), a monoclonal antibody known to react with both T cells and B-CLL cells, did not react with normal circulating B cells. However, this antibody did identify neoplastic B cells except in cases of plasma cell proliferation and lymphoblastic lymphoma.

Antibodies, Monoclonal↗
PubMed1983

Normothermic ischemic cardiac arrest of the isolated working rat heart. Effects of time and reperfusion on myocardial ultrastructure, mitochondrial oxidative function, and mechanical recovery.

The ischemic state of the myocardium of the isolated working rat heart after induction of normothermic ischemic cardiac arrest was assessed by the interrelationship among changes in myocardial ultrastructure, mitochondrial oxidative phosphorylation, and tissue high energy phosphate contents. At all time intervals (10-40 minutes) studied, the ultrastructural changes were more severe in the subendocardium than in the subepicardium. After 25-40 minutes of normothermic ischemic cardiac arrest, the mitochondrial oxygen uptake (state 3) became increasingly depressed, particularly in mitochondria isolated from the subendocardium. Mitochondrial oxidative function, as measured in vitro, did not correlate well with mitochondrial ultrastructural damage. In addition, the effects of coronary reperfusion on the ability of the ischemic heart to recover in terms of ultrastructure, mechanical, and metabolic function were evaluated. Hearts subjected to 10-40 minutes of normothermic ischemic cardiac arrest showed almost complete ultrastructural recovery of the subepicardium upon reperfusion; regression of ultrastructural changes occurred to a lesser extent in the subendocardium. Reperfusion for 30 minutes did not alleviate the depression in mitochondrial oxidative function, while tissue ATP levels did not return to control, preischemic levels. After 20 minutes of normothermic ischemic cardiac arrest, the mechanical performance of the working heart during reperfusion was significantly depressed, compared with pre-ischemic control values. Normal ultrastructure of the subendocardium always accompanied mechanical recovery, while improvement of mitochondrial oxidative function was not essential.

Adenosine Triphosphate↗
PubMed1982

Normothermic ischaemic cardiac arrest of isolated working rat heart: effects of reserpine and propranolol on functional, metabolic and morphological recovery.

The ability to preserve myocardial structural and functional integrity during extended periods of total ischaemia has practical clinical significance. The role of endogenous catecholamines in the onset of irreversible damage in global ischaemia of the isolated rat heart was assessed by beta-blockade or catecholamine depletion. The effects of propranolol and reserpine pretreatment on myocardial ultrastructure, function and metabolism were studied during normothermic ischaemic arrest (NICA) and reperfusion of the isolated working rat heart. beta-Blockade as well as catecholamine depletion resulted in an increase in the percentage of totally ischaemic hearts which recovered mechanically upon reperfusion. In these studies mechanical recovery during reperfusion was associated with reversal of ultrastructural ischaemic alterations, but without an improvement in mitochondrial function. These findings support the concept that failure of mitochondria to recover functionally upon reperfusion is not the cause of either irreversible mechanical failure or ultrastructural damage of the ischaemic myocardium.

Animals↗
PubMed1982

Imbalance of T cell subpopulations in patients with chronic lymphocytic leukaemia of the B cell type.

T cell enriched mononuclear cells from the peripheral blood of 20 patients with histologically and immunologically defined chronic lymphocytic leukaemia of the B cell type (B-CLL) and 20 healthy individuals of various ages were investigated with T cell-specific monoclonal antibodies (OKT 4 and OKT 8) with regard to their subpopulation distribution. In B-CLL, a significant increase of lymphocytes reacting with OKT 8 could be demonstrated. Whereas there was a ratio of OKT 4 to OKT 8 of 1 X 72 in the control group, an OKT 4 to OKT 8 ratio of 0 X 67 was found in the B-CLL as a whole. With increasing clinical stage in accordance with the Rai scheme (Rai et al., 1975), a further displacement of this ratio in favour of OKT 8 positive cells was found. These results clearly show that, in peripheral blood of patients with B-CLL, an abnormal distribution pattern of circulating T cell subpopulations is present and that this also has prognostic relevance.

Antibodies, Monoclonal↗
PubMed1981

A study of a family with inherited disease of cardiac and skeletal muscle. Part III. Genealogical considerations and associations with low intelligence.

A family with inherited cardiac and skeletal muscle disease was also found to have members with low intelligence. The effects of social and environmental conditions upon the behaviour of family members are described, with particular attention to the sociomedical problems created by the combination of a hereditary disease and low intelligence.

Adolescent↗
PubMed1981

A study of a family with inherited disease of cardiac and skeletal muscle. Part II. Skeletal muscle morphology and mitochondrial oxidative phosphorylation.

Skeletal muscle morphology and mitochondrial oxidative phosphorylation capacity were examined in a family whose members showed very combinations of mental subnormality, cardiomyopathy and muscle weakness. Light and electron microscopic findings suggested a neuropathic process, while tests of mitochondrial function indicated a state of tight coupling of oxidative phosphorylation, a feature in marked contrast to those in biochemical studies so far reported.

Adenosine Triphosphate↗
PubMed1981

A study of a family with inherited disease of cardiac and skeletal muscle. Part I. Clinical, electrocardiographic, echocardiographic, haemodynamic, electrophysiological and electron microscopic studies.

A family consisting of parents and their 6 sons were investigated to elucidate the relationship between a hypertrophic cardiomyopathy, musculoskeletal abnormalities and mental subnormality. The proband was diagnosed as having definite hypertrophic obstructive cardiomyopathy and the remaining family members were shown to have a spectrum of hypertropic non-obstructive cardiomyopathy. Mild muscle weakness was present in 3 sons. All the subjects except for 1 son showed definite signs of electromyographic abnormality, whereas sensory and motor conduction velocities were normal. All the EEGs except for that of the proband were normal. Testicular hypoplasia was present in 3 sons. The inheritance pattern appears to be polygenic autosomal recessive in type. Definite evidence of linkage between hypertrophic cardiomyopathy and HLA awaits further data.

Adolescent↗
PubMed1979

Mitochondrial function and free fatty acid levels in rats after portacaval shunt.

The effects of portacaval shunting on the oxidative phosphorylation process of mitochondria isolated from rat liver and skeletal muscle were evaluated and correlated with mitochondria free fatty acid (FFA) contents. ADP/O ratios, respiratory control index and QO2 values were significantly depressed in liver mitochondria from portacaval-shunted rats; these changes were associated with decreased mitochondrial FFA contents. The mitochondrial function of skeletal muscle was unaltered.

Animals↗
PubMed1975

Mitochondrial metabolism in infarcting myocardium.

The isolation medium plays an important part in the assessment of mitochondrial damage following coronary artery ligation. Albumin added to either isolation or incubation medium can protect. A depression of oxygen uptake is found only after prolonged ischemia or in a simple incubation medium. Hence mitochondrial oxygen wastage probably occurs in the infarction process.

Animals↗