CCR5 genotype and mother-to-child HIV transmission.
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Female↗
Biomedical subjects
H Rascoff
Publications and source records attributed to H Rascoff.
Fibrin regulates neutrophil migration in response to interleukin 8, leukotriene B4, tumor necrosis factor, and formyl-methionyl-leucyl-phenylalanine.
We have examined the capacity of four different chemoattractants/cytokines to promote directed migration of polymorphonuclear leukocytes (PMN) through three-dimensional gels composed of extracellular matrix proteins. About 20% of PMN migrated through fibrin gels and plasma clots in response to a gradient of interleukin 8 (IL-8) or leukotriene B4 (LTB4). In contrast, < 0.3% of PMN migrated through fibrin gels in response to a gradient of tumor necrosis factor alpha (TNF) or formyl-methionyl-leucyl-phenylalanine (FMLP). All four chemoattractants stimulated PMN to migrate through gels composed of collagen IV or of basement membrane proteins (Matrigel), or through filters to which fibronectin or fibrinogen had been adsorbed. PMN stimulated with TNF or FMLP adhered and formed zones of close apposition to fibrin, as measured by the exclusion of a 10-kD rhodamine-polyethylene glycol probe from the contact zones between PMN and the underlying fibrin gel. By this measure, IL-8- or LTB4-treated PMN adhered loosely to fibrin, since 10 kD rhodamine-polyethylene glycol permeated into the contact zones between these cells and the underlying fibrin gel. PMN stimulated with FMLP and IL-8, or FMLP and LTB4, exhibited very little migration through fibrin gels, and three times as many of these cells excluded 10 kD rhodamine-polyethylene glycol from their zones of contact with fibrin as PMN stimulated with IL-8 or LTB4 alone. These results show that PMN chemotaxis is regulated by both the nature of the chemoattractant and the composition of the extracellular matrix; they suggest that certain combinations of chemoattractants and matrix proteins may limit leukocyte movements and promote their localization in specific tissues in vivo.
Adult↗
Syncope in childhood.
The records of 108 children, ages 2 to 19 years (mean age 11.3 years), who were referred to the pediatric neurology and pediatric cardiology clinics for syncope, were reviewed. Sixty-six cases were identified retrospectively, and 42 prospectively. Syncope was defined as transient and complete loss of consciousness with no etiology determined at the time of presentation. The mean follow-up was 2.0 years. In 27 cases (25%), an etiology for syncope was found, including migraines in 12 cases (11%), seizures in 9 cases (8%), and cardiac arrhythmias in 6 cases (6%). All other cases were classified as vasovagal (neurocardiogenic). The past medical history, family history, clinical features of each syncopal episode, and diagnostic tests of each subject were correlated to final diagnosis. No clinical or historical features reliably distinguished children with vasovagal syncope from those with other etiologies. Children referred for the evaluation of syncope have a significant incidence of serious but treatable disorders, which should be actively sought.
Adolescent↗