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Biomedical subjects

M Rozenblat

Publications and source records attributed to M Rozenblat.

5 recordsLinked to original sources

Extensor tendon impingement in a gymnast.

Wrist injuries in the gymnast are due to the transformation of the upper extremity into a weight bearing entity. Gymnast wrist pain presents a difficult diagnostic and therapeutic challenge. Here, we present a new case of extensor tendon impingement in an elite gymnast. To our knowledge, there is no similar report in the literature.

Adult↗

Sex differences in the expression of haemorheological determinants in individuals with atherothrombotic risk factors and in apparently healthy people.

BACKGROUND: Increased red cell aggregation can be detrimental, leading to slow capillary blood flow and tissue hypoxaemia. Sex differences in the degree of erythrocyte adhesiveness/aggregation in the peripheral blood have not been clearly shown. OBJECTIVES: To determine whether there are sex differences in the expression of erythrocyte adhesiveness/aggregation in the peripheral blood in individuals with atherothrombotic risk factors and in apparently healthy people. METHODS: From a cohort of 965 participants in the Tel Aviv Medical Centre inflammation survey, 192 pairs of different sex were matched for age, body mass index, hip and waist circumferences, cardiovascular risk factors, and the intake of active cardiovascular drugs. RESULTS: Women had an enhanced degree of red cell aggregation (p < 0.0005) as well as increased concentrations of inflammation sensitive proteins including fibrinogen and C reactive protein. Women had a lower haemoglobin concentration than men, but this did not affect the degree of erythrocyte adhesiveness/aggregation. CONCLUSIONS: The significant increase in red blood cell adhesiveness/aggregation in the peripheral blood of women with atherothrombosis could be relevant to the more eventful course that some women experience during and following acute ischaemic disease.

Anemia↗

Serum lipids as minor determinants of the degree of erythrocyte adhesiveness/aggregation in the peripheral blood of individuals with low grade inflammation and moderately increased serum lipids.

Both lipids and inflammation sensitive proteins have been reported to affect the aggregation of red blood cells yet their relative importance in this regard have not been determined. We have included high sensitive C-reactive protein, erythrocyte sedimentation, fibrinogen concentrations as well as various serum lipid concentrations and the degree of erythrocyte adhesiveness/aggregation in the peripheral blood in a linear regression analysis. Partial Pearson correlation coefficients were included as well. In a group of 674 individuals with various atherosclerotic risk factors, low grade inflammation and moderately increased serum lipids, a relatively low correlation was noted between red blood cell adhesiveness/aggregation and triglycerides concentrations. A negative correlation was noted for HDL cholesterol. None of the lipid variables turned significant in the regression analysis. In a group of individuals with atherosclerotic risk factors, low grade inflammation and moderately increased serum lipids, the degree of erythrocyte adhesiveness/aggregation in the peripheral blood correlates much better with the presence of inflammation sensitive proteins than with the presence of increased lipid concentrations.

Adult↗

Significant dominance of fibrinogen over immunoglobulins, C-reactive protein, cholesterol and triglycerides in maintaining increased red blood cell adhesiveness/aggregation in the peripheral venous blood: a model in hypercholesterolaemic patients.

BACKGROUND: It is not clear what is the relative importance of fibrinogen, immunoglobulins, highly sensitive C-reactive protein (hs-CRP), cholesterol and triglyceride concentrations on the appearance of aggregated red blood cells in the peripheral blood. DESIGN: Six hypercholesterolaemic patients undergoing regular LDL apheresis that were examined repeatedly before and following the procedure. RESULTS: We determined the degree of erythrocyte adhesiveness/aggregation in relation to the concentration of the above-mentioned macromolecules in 80 samples. In a linear logistic regression the respective R2 values for fibrinogen, total cholesterol, triglycerides, hs-CRP, IgG, IgM and IgA were 0.45 (P<0.0001), 0.2 (P<0.0001), 0.02 (P=0.02), 0.001 (P=NS) and 0.002 (P=NS), respectively. We further analyzed the potential of ApoA, ApoB and Lpa to participate in red cell adhesiveness/aggregation and found them to be not significant. CONCLUSIONS: In a milieu of adhesive macromolecules, lipids and inflammation-sensitive proteins including fibrinogen, total cholesterol, triglycerides, hs-CRP and immunoglobins G, M and A, fibrinogen has a dominant role in maintaining the red blood cell adhesiveness/aggregation in the peripheral venous blood. These findings are relevant for the research directed at finding new apheretic modalities to reduce the degree of red blood cell adhesiveness/aggregation in the peripheral blood.

Blood Component Removal↗

Stimulation of Jun N-terminal kinase (JNK) by gonadotropin-releasing hormone in pituitary alpha T3-1 cell line is mediated by protein kinase C, c-Src, and CDC42.

The signaling of ligands operating via heterotrimeric G proteins is mediated by a complex network that involves sequential phosphorylation events. Signaling by the G protein-coupled receptor GnRH was shown to include elevation of Ca2+ and activation of phospholipases, protein kinase C (PKC) and extra-cellular signal-regulated kinase (ERK). In this study, GnRH was shown to activate Jun N-Terminal Kinase (JNK)/SAPK in alpha T3-1 cells in a PKC- and tyrosine kinase-dependent manner. GnRH as well as tumor-promoting agent (TPA) also increased c-Src activity, which peaked at 2 min after GnRH stimulation and was sensitive both to PKC and to tyrosine kinase inhibitors. Coexpression of Csk, which serves as a Src-dominant interfering kinase, and constitutively active forms of Src, together with JNK, confirmed the involvement of c-Src downstream of PKC in the GnRH-JNK pathway. Coexpression of dominant negative and constitutively active forms of CDC42, Rac1, Ras, MEKK1, and MEK1 with JNK indicated that JNK activation by GnRH and TPA is mediated by CDC42 and MEKK1. Ras and MEK1, which are involved in a related mitogen-activated protein kinase (MAPK) pathway, did not affect JNK activation in alpha T3-1 cells. Taken together, our results suggest that GnRH stimulation of JNK activity is mediated by a unique pathway that includes sequential activation of PKC, c-Src, CDC42, and probably also MEKK1.

Animals↗