Practices suffered growing pains.
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Biomedical subjects
Publications and source records attributed to H Scott.
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Tissue sections of ethanol-fixed, paraffin-embedded specimens from human kidney, placenta and umbilical cord were studied by indirect immunofluorescence with a rabbit antiserum to HLA--DR antigens from B lymphocytes. Capillary walls in the kidney showed specific staining both in glomeruli and around tubuli. Conversely, HLA--DR-like antigens were not detected in the walls of larger vessels, in tubular cells, or in the epithelium of Bowman's capsule. HLA-DR-like antigens of kidney elements thus seemed to be restricted to capillary endothelial cells. In specimens from umbilical cord and placenta, HLA--DR-like antigens were not detected in the walls of capillaries or larger vessels. Isolated endothelial cells from the umbilical vein were likewise negative.
By conventional light microscopy, a reduced number of Paneth cells per intestinal crypt was found in the jejunal mucosa of patients with untreated or gluten-challenged coeliac disease as compared with histologically normal control specimens. A much better detection sensitivity was obtained when Paneth cells were counted by fluorescence microscopy after immunostaining for lysozyme with a rhodamine-labelled rabbit IgG conjugate. This method showed that there was no numerical reduction of Paneth cells in coeliac disease, but that the proportion of cells with a low lysozyme content was increased. Most of these cells were probably missed by conventional microscopy in which identification of Paneth cells is principally based on a substantial cellular complement of acidophilic granules. A reduced number of lysozyme-containing granules in coeliac disease may reflect increased discharge enhanced secretory activity, or a raised turnover of the Paneth cells.
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HLA-DR-like antigens and secretory component (SC) were localized immunohistochemically in adjacent tissue sections of ethanol-fixed paraffin-embedded jejunal mucosa from control subjects and patients with coeliac disease (CD) or dermatitis herpetiformis (DH). HLA-DR-like antigens were found in a patchy distribution apically in the columnar epithelial cells facing the gut lumen and in the upper part of the crypt epithelium. The staining pattern was similar in controls and patients with CD or DH. SC was normally most abundant in the crypt epithelium but the concentration of SC in the surface epithelium increased with increasing villous atrophy both in CD and DH patients. Despite this sign of immaturity, the surface cells retained their capacity to express HLA-DR-like antigens in the pathological mucosa.
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Sections of ethanol-fixed, paraffin-embedded tissue specimens from different parts of the human gastrointestinal tract were stained by an indirect immunofluorescence method with a rabbit antiserum to HLA-DR-antigens from B lymphocytes. A specific staining reaction was seen in a patchy pattern apically in the columnar cells of the normal small intestine, decreasing in intensity from the top of the villi towards the crypts. No HLA-DR-like antigens could be detected in colon or stomach epithelium, whereas cells with the morphology of lymphocytes and histiocytes in the lamina propria and also capillary walls were specifically stained throughout the gastrointestinal tract.
The jejunal Ig-producing cell populations in a group of 12 children with established coeliac disease (CD) in remission on a gluten-free diet were compared with those of a group of 10 patients in clinical relapse after gluten challenge. Quantification of the various immunocyte classes was performed by paired immunofluorescence staining in an individually defined mucosal tissue unit constituting a 6-micron-thick and 500-micron-wide block of tissue, including the mucosa at full height from the muscularis mucosae. In the treated group the percentage IgA/IgM/IgG cell ratios were, on the average, 82.6:12.9:4.5. There were no differences in these ratios or in the absolute immunocyte numbers when compared with a group of six control patients without CD. After gluten challenge the corresponding ratios were 77.2:17.2:5.6. The median cell number per mucosal tissue unit in the IgA, IgM, and IgG class was raised 2.1, 3.8 and 2.9 times, respectively. These increases were statistically significant. Moreover, there was a significant negative correlation between the time to clinical relapse and the number of IgG cells per tissue unit after challenge. This finding indicates that locally produced antibodies of the IgG class are especially involved in the pathogenesis of CD.
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The aim of this study was to establish the outcome of very severe birth asphyxia in a group of babies intensively resuscitated at birth. 48 infants, born between 1966 and 1971 inclusive, were selected; 15 were apparently stillborn and 33 had not established spontaneous respirations by 20 minutes after birth. One-half of them died, but 3 to 7 years later three-quarters of the survivors are apparently normal. Later handicap was associated with factors leading to prolonged partial intrapartum asphyxia, while acute periods of more complete asphyxia were not necessarily harmful.
Members of four generations of a family had a defect of serum opsonization for yeast phagocytosis consistent with dominant inheritance. 2 were healthy, one had chronic osteomyelitis, and the fourth developed a fatal illness in infancy characterized by exfoliative dermatitis, diarrhoea, multiple bacterial infections, and failure to thrive, which resembled the two prevously reported cases with this opsonization defect. At necropsy the infant also had lymphoid depletion, which was possibly secondary, and massive histiocytic infiltration.
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