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Biomedical subjects

D Meyer

Publications and source records attributed to D Meyer.

At least 505 records · Page 28Linked to original sources
PubMed1978

Work load management system ensures stable nurse-patient ratio.

The concept of adjusting work load to staffing is the reverse of most currently accepted practices. However, that is precisely how this management and measurement system works. Patient care units (PCU'S) are estimated for all incoming admissions, and patients are assigned to the units that have the lowest PCU count, the goal being an even distribution of work load among nursing units.

Efficiency↗
PubMed1978

Isolation of human antibodies to factor VIII.

It has been claimed that human anti-VIII:C antibodies do not form stable complexes with factor VIII and this fact has hampered in the past the isolation of such antibodies. In this study the purification of human anti-VIII:C antibodies appearing in haemophiliac patients following replacment therapy has been achieved using two different systems. In a liquid phase system, purified human factor VIII was mixed with IgG from a haemophilic patient with a high titre antibody. Specific anti-VIII:C antibodies were recovered following filtration of the antigen-antibody complexes on Biogel A-5m, dissociation of complexes at pH 3.5 and final isolation by filtration on Sephadex G-200. In a solid phase system, the same IgG fraction was specifically bound to insolubilized human factor VIII. Purified anti-VIII:C antibodies were subsequently recovered by elution of antigen-antibody complexes with magnesium chloride. The results demonstrated that stable complexes from between anti-VIII:C antibodies and either the whole factor VIII molecule, or VIII:C dissociated by previous interaction with the antibodies. It is postulated that, in vivo, similar antigen-antibody complexes may form following replacement therapy in haemophilic patients with antibody.

Antibodies↗
PubMed1977

[Double controlled regulation of renin release by the sympathetic nervous system. Stimulation via beta receptors and inhibition via alpha receptors].

The beta-sympathomimetic amine isoprenaline increases the plasma renin concentration by a stimulation of beta-receptors which control renin release. Isoprenaline also lowers systemic blood pressure and causes a reflex-mediated activation of the sympathetic nervous system. In these investigations it has been tested to see whether the catecholamines released by this activation modulate renin release by stimulation of certain alpha-receptors. Pretreatment of rats with reserpine or with the ganglionic blocking agent Trimethidinium enhanced the increase in plasma renin concentration induced by isoprenaline. So did pretreatment with the irreversible alpha-receptor antagonist phenoxybenzamine. Renal denervation also increased the effect of isoprenaline on plasma renin concentration. It is concluded that catecholamines released from the sympathetic nervous system can decrease renin secretion by an activation of certain alpha-receptors. The sympathetic nervous system may thus exert control of renin release by beta-receptors which stimulate and by alpha-receptors which diminish renin secretion.

Animals↗
PubMed1977

Immunological evidence that human factor VIII is composed of two linked moieties.

The relationship between the three measurable components of the factor VIII complex, procoagulant activity (VIII:C), Ristocetin cofactor (VIIIR:WF) and factor VIII related antigen (VIIR:AG), has been investigated using a solid phase immunoadsorption system in which homologous antibodies specific for VIII:C are insolubilized onto Sepharose beads. The VIII:C component of partially purified factor VIII can be completely separated from the Willebrand factor (VIIIR:WF/VIIIR:AG) by this technique. The loss of VIII:C has no detectable effect on the molecular size, antigenicity or electrophoretic mobility of the original molecule. The Willebrand factor (WF) recovered from these immunoadsorption columns was used to absorb heterologous antisera to factor VIII. A specific heterologous antiserum to VIII:C, which no longer neutralized VIIIR:WF nor precipitated VIIIR:AG, was obtained. Heterologous antisera to WF were prepared which potently neutralized VIIR:WF and precipitated with VIIIR:AG, but also weakly neutralized VIII:C (titre I u/ml). This study is compatible with the theory that VIII:C and VIIIR:WF/VIIIR:AG are two different but linked entities.

Antibodies↗
PubMed1977

[Von Willebrand's syndrome (author's transl)].

The biological syndrome in von Willebrand's disease is presently defined by four parameters: bleeding time, factor VIII coagulant activity (VIII:C), Willebrand factor activity (VIIR:WF) and factor VIII related antigen (VIIR:AG). The study of 48 patients from 25 families confirms the heterogeneity of the von Willebrand's syndrome including both quantitative as well as qualitative defects. Classical von Willebrand's disease results from the quantitative decrease of a plasma protein named "Willebrand factor" which is the primary gene-product of an altosomal chromosome. Both severe and moderate forms can be observed. In very severe forms, the apparent lack of the VIIIR:AG as measured by an immunoradiometric assay suggest the possibility that some patients are homozygous. "Variants" of von Willebrand's disease have been recently described in some patients, based on the discrepancy between the observed subnormal levels of VIIIR:AG and low levels of VIIIR:WF. The qualitative abnormality of the factor VIII/Willebrand protein can be assessed by different methods such as double cross immuno-electrophoresis, or immunoradiometric assay.

Antigens↗
PubMed1977

Heterogeneity of von Willebrand's disease: study of 40 Iranian cases.

Forty Iranian patients with von Willebrand's disease were tested for bleeding time, platelet retention to glass beads, ristocetin-induced platelet aggregation, and assay of factor VIII procoagulant activity (VIII:C), Willebrand factor activity (VIIIR:WF), and factor VIII-related antigen (VIIIR:AG) by two methods (Laurell and immunoradiometric assay). In 22 cases from 11 families, levels of VIII:C, VIIIR:WF and VIIIR:AG (Laurell) were below 5% and the immunoradiometric assay showed total lack of VIIIR:AG in all cases (sensitivity of the method 0.01%). In 10 of these families, the parents were related, raising th;e possibility that these patients are homozygous. The occurrence of precipitating antibodies to factor VIII was demonstrated in one of these severe patients. In seven cases from five families the anomaly was less severe, with results of VIII:C between 5 and 17%. In 11 cases from six families VIII:C was normal or moderately decreased, contrasting with lower levels of VIIIR:WF and VIIIR:AG. The presence of an abnormal factor VIII/von Willebrand factor protein was assessed by double-cross immunoelectrophoresis and gel filtration.

Adolescent↗
PubMed1976

The morphological and clinical course of the different forms of glomerulonephritis.

From repeat biopsies of 291 patients with glomerulonephritis, the clinical and morphological course of the individual forms of glomerulonephritis were compared with one another. From these results we concluded that: 1. Every form of glomerulonephritis has in all probability its individual course and prognosis, which can only be very slightly influenced by therapy. 2. The prognosis is considerably worsened, when either hypertension develops or tubular lesions in the morphological sense of an acute renal failure.

Acute Disease↗
PubMed1976

Primary malignant nephrosclerosis.

1. As proposed by Schürmann & MacMahon (1933), we suggest that two types of malignant nephrosclerosis exist. 2. In the type called primary malignant nephrosclerosis, renal vascular lesions precede hypertension. 3. In the second type, called secondary malignant nephrosclerosis, renal vascular lesions are considered to be the consequence of malignant hypertension.

Basement Membrane↗