Pancreatic schwannoma.
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Biomedical subjects
Publications and source records attributed to S David.
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During tooth development, enamel organ epithelial cells express a tissue-specific gene product (amelogenin) which presumably functions to control calcium hydroxyapatite crystal growth patterns during enamel biomineralization. The present studies were designed to test the hypothesis that amelogenin as a supramolecular aggregate regulates crystal growth during enamel biomineralization. Antisense oligodeoxynucleotide strategy was used in a simple organ culture system to inhibit amelogenin translation. Under these experimental conditions, antisense treatment prior to and during amelogenin expression resulted in inhibition of amelogenin translation products within immunoprecipitated [35S]methionine metabolically labeled proteins. To determine the efficiency of antisense treatment in this model system, digoxigenin-labeled oligodeoxynucleotides were observed to diffuse throughout the tooth explants including the target ameloblast cells within 24 hours. Ultrastructural analyses of amelogenin supramolecular assembly as electron-dense stippled materials in antisense treated cultures demonstrated dysmorphology of the extracellular enamel matrix with a significant reduction in crystal length and width. We conclude that secreted extracellular proteins form a supramolecular aggregate, which controls both the orientation and dimensions of enamel crystal formation during tooth development.
Fieldwork conducted in Kpelle village in north-central Liberia revealed that health-care expenses constitute a major part of domestic spending. The actual transactions for major health-care expenditures are handled by men, typically using income that jointly belongs to the couple in addition to the husband's personal income. Women are likely to spend their personal incomes on minor health expenses for themselves and their children. Women's health expenditure, as well as their income handling arrangements, seem to differ according to the type of conjugal union they are in. Although Kpelle wives have input in most financial decisions, they tend to defer to men on issues which are associated with the Western world, namely Western health care, educational and tax expenditures.
The response of enteric vasculature to endotoxin was examined at the ultrastructural level using a murine model of endotoxin-induced acute diarrhoea. Morphological changes indicative of endothelial damage were evident as early as 15 minutes following endotoxin challenge. These changes, characterized by widening of intercellular spaces, increased microvillous projections and the appearance of stress fibres, preceded the leucocytic response. Endothelial damage increased with time, being associated with progressive degenerative changes in the plasma membrane, cytoplasm and organelles, ultimately leading to desquamation. These latter changes were temporally associated with margination of neutrophils and platelet adhesion to the denuded subendothelium. The venules were the primary site of these changes while the capillaries were the least affected. The arterioles were markedly constricted with minimal endothelial damage. These changes suggest that the enteric vascular endothelium may be an important target organ, and the resultant endothelial injury may have implications in host responses to endotoxin.
In the present study we evaluated spontaneous and stimulated adherence of human monocytes to regenerated cellulose and polyacrylonitrile (AN69) membranes. Spontaneous adherence at 60 min was significantly higher for regenerated cellulose (28 +/- 2%, P < 0.001) than for AN69 (11 +/- 2) membranes. Stimuli such as bacterial lipopolysaccharide, TNF alpha, interleukin-1 and -6 as well as platelet-activating factor, but not IL-4, significantly enhanced adherence at 60 min to AN69 (28 to 30%). In contrast, adherence was not further inducible in the presence of regenerated cellulose. Both spontaneous and cytokine/bacterial lipopolysaccharide-stimulated adherence were significantly reduced by SDZ-63072, a specific platelet-activating factor receptor antagonist. This difference in sensitivity of monocyte adherence reflects probably the intrinsic ability of regenerated cellulose to provide maximal spontaneous monocyte adhesion. These data suggest that PAF may act as an adherence mediator. This is in line with the ability of regenerated cellulose to directly stimulate monocytes to synthesize platelet-activating factor and with the ability of cytokines and bacterial lipopolysaccharide to stimulate its synthesis. Although AN69 has a low adherence potential, bacterial lipopolysaccharide or cytokines may blunt the biocompatibility of this membrane.
A complex array of inflammatory mediators are generated as a consequence of blood contact with hemodialysis (HD) membranes. Beside complement activation, other mediators are involved in cell activation, and are thought possibly to be responsible for early and long-term multiple changes in immunity infection, hypercatabolism, beta 2-microglobulin generation and hemostatic mechanisms. Previous studies from our laboratories have established platelet activating factor (PAF) as one of the mediators generated by complement-dependent or independent mechanisms of cell interaction with hemodialysis membranes. Recent studies on the production of PAF from endotoxin-primed polymorphonuclear neutrophils in a closed miniaturized circuit, and on the effect of PAF in mediating endotoxin- and cytokine-induced leukocyte adherence to HD membranes, highlight so far undescribed new roles of this mediator in biocompatibility.
SN2-type reaction of 3-O-(1-imidazyl)sulfonyl-1,2:5,6-di-O-isopropylidene-alpha-D-gluco furanose with benzoate gave the 3-O-benzoyl-alpha-D-allo derivative 2, which was hydrolysed to give the 5,6-diol 3. Compound 3 was converted into the 6-deoxy-6-iodo derivative 4 which was reduced with tributylstannane, and then position 5 was protected by benzyloxymethylation, to give 3-O-benzoyl-5-O-benzyloxymethyl-6-deoxy-1,2-O-isopropylidene-alpha -D- allofuranose (6). Debenzoylation of 6 gave 7, (1-imidazyl)sulfonylation gave 8, and azide displacement gave 3-azido-5-O-benzyloxymethyl-3,6-dideoxy- 1,2-O-isopropylidene-alpha-D-glucofuranose (9, 85%). Acetolysis of 9 gave 1,2,4-tri-O-acetyl-3-azido-3,6-dideoxy-alpha,beta-D-glucopyranose (10 and 11). Selective hydrolysis of AcO-1 in the mixture of 10 and 11 with hydrazine acetate (----12), followed by conversion into the pyranosyl chloride 13, treatment with N,N-dimethylformamide dimethyl acetal in the presence of tetrabutylammonium bromide, and benzylation gave 3-azido-4-O-benzyl-3,6-dideoxy-1,2-O-(1-methoxyethylidene)-alpha-D -glucopyranose (15). Treatment of 15 with dry acetic acid gave 1,2-di-O-acetyl-3-azido-4-O-benzyl-3,6-dideoxy-beta-D-glucopyranose (16, 86% yield) that was an excellent glycosyl donor in the presence of trimethylsilyl triflate, allowing the synthesis of cyclohexyl 2-O-acetyl-3-azido-4-O-benzyl-3,6-dideoxy-beta-D-glucopyranoside (17, 90%).(ABSTRACT TRUNCATED AT 250 WORDS)
In earlier studies, the minimum structure which inhibited the binding of anti-i to an i-active glycoprotein was the linear trisaccharide, beta-D-Galp-(1----4)-beta-D-GlcpNAc-(1----3)-D-Gal. There was an increasing hierarchy of inhibitory activities in the linear tetrasaccharide, beta-D-Galp-(1----4)-beta-D-GlcpNAc-(1----3)-beta-D-Galp-(1----4)-beta-D -GlcNAc , its methyl beta-glycoside, and in the methyl beta-glycoside of the hexasaccharide. The linear octasaccharide methyl beta-glycoside in this series is approximately only half as active as the hexasaccharide methyl beta-glycoside. Analyses by high resolution 1H-n.m.r. of these two oligosaccharides indicated that they have similar conformations in solution, and there is no evidence for the occurrence of inter-molecular interactions which might partially hinder the binding of anti-i to the octasaccharide methyl beta-glycoside. These results are consistent with the size of the i antigen being in the region of a hexasaccharide. It is proposed that the methyl aglycon group of the hexasaccharide methyl beta-glycoside confers an above normal activity by presenting a hydrophobic area for additional contact in the vicinity of the antibody-combining site.
A 16-kb BamHI fragment of the lactose plasmid pNZ63 from Leuconostoc lactis NZ6009 was cloned in Escherichia coli MC1061 by using pACYC184 and was found to express a functional beta-galactosidase. Deletion and complementation analysis showed that the coding region for beta-galactosidase was located on a 5.8-kb SalI-BamHI fragment. Nucleotide sequence analysis demonstrated that this fragment contained two partially overlapping genes, lacL (1,878 bp) and lacM (963 bp), that could encode proteins with calculated sizes of 72,113 and 35,389 Da, respectively. The L. lactis beta-galactosidase was overproduced in E. coli by using a lambda pL expression system. Two new proteins with M(r)s of 75,000 and 36,000 appeared upon induction of PL. The N-terminal sequences of these proteins corresponded to those deduced from the lacL and lacM gene sequences. Mutation and deletion analysis showed that lacL expression is essential for LacM production and that both the lacL and lacM genes are required for the production of a functional beta-galactosidase in E. coli. The deduced amino acid sequences of the LacL and LacM proteins showed considerable identity with the sequences of the N- and C-terminal parts, respectively, of beta-galactosidases from other lactic acid bacteria or E. coli. DNA and protein sequence alignments suggest that the L. lactis lacL and lacM genes have been generated by an internal deletion in an ancestral beta-galactosidase gene.
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This is an initial report of spontaneous retrograde gastroesophageal intussusception in an adult. The patient is a 72-yr-old women with a history of ovarian cancer and hiatal hernia, who presented with symptoms of upper gastrointestinal obstruction. Retrograde intussusception was diagnosed endoscopically and confirmed radiographically with an upper gastrointestinal series. Heightened awareness of this entity may lead to its more frequent diagnosis.
Olfactory epithelial neurons in mammals are unique in that they continue to differentiate from precursor cells in the adult. These neurons extend long axons into the olfactory bulb. Previous attempts to grow these cells in dissociated cell cultures at low density, have not been entirely satisfactory. We report that when plated at very low density, rat olfactory epithelial neurons will differentiate morphologically and biochemically when cultured on astrocytes, but not on non-cellular substrata, such as polylysine, laminin or fibronectin. We demonstrate with antibodies, that these olfactory epithelial neurons require N-CAM, N-cadherin and L1 for neurite extension. Furthermore, synthetic cadherin-peptides containing the tripeptide HAV which is found in the first extracellular domain of N-cadherin, as well as the amino acids flanking this region, appear to be important in cadherin-mediated neurite growth on astrocytes. Astrocytes also appear to enhance the survival and differentiation of olfactory epithelial neurons from embryonic day 15 and 4-5 week post-natal rats, but this effect is not sustained beyond 5 days in cultures of postnatal epithelium.
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Five renal transplant recipients developed Pneumocystis carinii pneumonia (PCP) over a 22-month period, while no cases had been observed over a 5-year period in 114 transplanted patients treated with the same immunosuppressive protocol. All patients were HIV-negative, and no modification in diagnostic techniques for P. carinii could account for this observation. All five patients developed PCP within 2 months of an acute graft rejection episode. All of them attended the same outpatient facility as AIDS patients attending the hospital, where they shared the waiting and treatment rooms. Comparison of cases with matched controls was possible in three instances and revealed that the cases had had more outpatient clinic encounters with AIDS patients who had presented, or subsequently developed, PCP. This observation suggests that AIDS patients developing PCP may transmit the infection to other immunosuppressed patients.
This study utilized a vital bleaching agent as well as an enamel microabrasion compound with low hydrochloric acid concentration to remove intrinsic stains on the facial surfaces of anterior teeth. In addition, scanning electron microscopic analyses of enamel from extracted teeth compared the etching pattern of the commercial compound used in this study to 18% hydrochloric acid. Type 1 and Type 2 etch patterns were observed with 18% hydrochloric acid after 5 and 20 seconds, respectively. Milder and more diffuse etch patterns were observed with the enamel microabrasion compound. A conservative form of treatment to remove intrinsic stains would employ the use of a vital bleaching agent, followed by an enamel microabrasion compound.