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Biomedical subjects

P Baker

Publications and source records attributed to P Baker.

158 records · Page 9Linked to original sources
PubMedDate not supplied

Modulation of immune responses by surface polysaccharides of Candida albicans.

Fungal polysaccharides, especially those from the cell wall of the nonpathogenic yeast Saccharomyces cerevisiae, have been investigated as modulators of immune function for many years. More recently, because surface-associated components are known to be elaborated and circulate during serious episodes of candidiasis, investigators have taken interest in the opportunistic fungus Candida albicans. This review emphasizes the immunomodulatory activities of mannan and cell wall-derived glycoproteins from C. albicans. Mannan extracted with hot citrate buffer has been shown in an antibody-forming cell assay to be a heterogeneous mixture with components capable of enhancing or suppressing antibody responses when administered to mice at or near the time of immunization with type III pneumococcal polysaccharide (SSS-III), a T helper cell-independent antigen, or with sheep erythrocytes (SRBC), a T helper cell-dependent antigen. The components responsible for these opposing effects have been separated on the basis of size or charge by column chromatography. Two similar cell wall glycoproteins, removed from isolated cell walls by different procedures, induced enhancement only of the immune response to SSS-III and SRBC. The mechanism(s) by which these polysaccharides effect modulatory activity has not been elucidated. The enhancing property does not appear related to a direct mitogenic effect on lymphocytes or to stimulation of the production of B cell growth factors or interleukin 2.

Animals↗
PubMedDate not supplied

Preeclampsia: the endothelium, circulating factor(s) and vascular endothelial growth factor.

It has been proposed that endothelial cell activation is the primary event in the multisystem disorder of preeclampsia. Evidence for endothelial involvement in this condition abounds. The best-characterized morphologic abnormality of this syndrome, glomerular endotheliosis, involves endothelial cells. Also associated with preeclampsia is a loss of endothelial cell integrity, with the consequent increase in vascular permeability, and an increase in the circulating levels of the endothelial cell markers, fibronectin, von Willebrand factor, tissue plasminogen activator, and plasminogen activator inhibitor-1. It is now well documented that endothelial activation contributes to the coagulation abnormalities observed in this disease. There is much evidence that the endothelial alterations in preeclampsia result from one or more circulating factors. The incubation of cultured endothelial cells with serum or plasma samples, taken from normal pregnant women and women with preeclampsia, results in marked alterations in cell behavior and metabolic processes. More recently, experiments employing myographic techniques have demonstrated convincingly the effects of a circulating factor(s) on the function of endothelial cells of resistance arteries. Vascular endothelial growth factor (VEGF) possesses many of the characteristics required of a candidate circulating factor. It contains a hydrophobic secretory signal sequence, exerts in vitro effects specific to vascular endothelial cell, and promotes endothelial expression of procoagulant activity. Circulating VEGF concentrations are elevated in women with preeclampsia, and VEGF increases microvascular endothelial cell prostacyclin production in a dose-dependent manner, analogous to the acute effects of plasma from patients with preeclampsia. Similarly, in myographic studies, when myometrial resistance arteries are incubated with VEGF, there are dose-dependent alterations in endothelium-dependent behavior, mirroring those found after incubation with plasma from patients with preeclampsia.

Endothelial Growth Factors↗
PubMedDate not supplied

Septo-optic dysplasia and dentato-olivary dysplasia in a case of 18q deletion/3p trisomy.

The brain of an 1 8q deletion/3p trisomy patient is described. The findings revealed septo-optic dysplasia, dentato-olivary dysplasia, deficiency of myelination and disordered neuronal migration. Many of these pathological changes overlap the findings previously described in 18q deletion. An understanding of the pathological changes in the brain of these individuals provides the basis for therapeutic management of their symptoms.

Abnormalities, Multiple↗
PubMedDate not supplied

Estimates of normal binding of a human recombinant alpha interferon to peripheral blood mononuclear cells from a study matching healthy subjects to subjects with insulin dependent diabetes.

This study compares the binding of a human recombinant alpha-interferon to peripheral blood mononuclear cells (PBMC) from patients with insulin dependent diabetes (IDDM) mellitus and control subjects. Diurnal and longer term of variation, feeding, fasting and haemoglobin glycosylation were examinated for their influence on interferon binding to PBMC. No gross differences in binding were demonstrated, in particular no effect of glucose levels was seen on the binding of interferon alpha-2 to PBMC.

Blood Glucose↗