Biomedical subjects
Publications and source records attributed to M Vanderwee.
Mucous within the urinary bladder appears to play a protective role in shielding the uroepithelium against pathogens. This present study employs specific anti-mucous, antisera stabilization techniques to visualize a thin, continuous layer of mucous closely adherent to the human bladder uroepithelium, in both scanning and transmission electron microscopic analyses.
Sucralfate protects the stomach against a number of experimental damaging agents and is efficacious in the treatment of peptic ulcer disease. It binds with acidity to the base of an ulcer to form a protective barrier. Sucralfate also enhances prostaglandin synthesis and release in the mucosa. In this study, the rat stomach was examined to determine sucralfate's interaction with gastric mucus. Mucus in the rat stomach forms a distinct and continuous blanket. In snap-frozen samples, pretreatment with phosphate-buffered saline as a control shows a layer of mucus of homogeneous structure thinner than the homogeneous layer after pretreatment with antibodies developed against rat gastric mucus. Pretreatment with the surface protective agent sucralfate shows some increase in the thickness of mucus with a thin dense sublayer adjacent to the epithelium and a less dense-appearing outer zone of variable thickness. Analysis of x-rays generated by the electron beam on windows of mucus and epithelium showed the expected gradients of sodium, potassium, chloride, and sulfur. The percentage of aluminum and sulfur in the mucus was higher in sucralfate-treated samples than in controls. Interaction between sucralfate and gastric mucus needs further investigation.
A retrospective survey was undertaken of 228 resected Meckel's diverticula to determine if there was any evidence of Campylobacter pylori infection in diverticula containing gastric mucosa. Among the 65 diverticula with gastric mucosa one was heavily infected with organisms having the morphological appearances of C pylori. The specimen had been removed from a six year old Samoan boy who had been admitted with small bowel obstruction. Infection and associated mucosal inflammatory infiltrate were limited to areas of gastric mucosa only. The detection of the organism at this site remote from the gastroduodenal environment suggests the organism may be transmitted by the orofaecal route.
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The purpose of this study was to investigate unusual irregularities observed on the surface of kidneys from rats which had been treated with seven 'clinically effective doses' (25 or 50 mg/kg) of cyclosporin A (CsA). Surface corrugations were obvious on gross examination and were a universal finding in our study which involved greater than 50 rats. Examination by scanning electron microscopy (SEM) showed that the surface irregularities resulted from swollen peritubular capillaries adjacent to vacuolized and partially collapsed tubules at the cortical surface. The enlarged capillaries were associated with vascular congestion, and although peritubular capillary congestion has been recognized in CsA-treated patients, it has been difficult to determine whether this reaction is associated with drug toxicity or graft rejection. Our findings, indicating that peritubular capillary congestion in addition to vacuolization and collapse of subcapsular tubules is a drug-associated phenomenon, may help give a more accurate assessment of biopsy and autopsy material from CsA-treated patients and laboratory animals.
Mucus in the urinary bladder may act as an important intrinsic defence mechanism by shielding the epithelial layer from pathogens. Visualization of any such layer of mucus using electron microscopy has not been possible, as preparative procedures in current use result in the loss or distortion of mucus. We evaluated methods reported to stabilize polysaccharide layers and demonstrated that pretreatment of rat bladder tissue with anti-mucus antiserum, minimized the collapse of the mucus that normally occurred during dehydration of the tissue for electron microscopic examination. Under these conditions, mucus was stabilized as a layer closely adherent to the epithelium.
Peptic ulcer disease occurs when there is an imbalance between aggressive factors and mucosal resistance. Mucus plays a key role in mucosal resistance. The mucus layer is relatively resistant to peptic digestion, it provides a layer through which there is a movement of hydrogen ions from the parietal cell to the lumen but a resistance to back-diffusion of hydrogen ions in the opposite direction. It maintains a pH gradient by 'sequestering' secreted bicarbonate and by its resistance to H+ back-diffusion. Colloidal bismuth subcitrate (De-Nol) binds to mucus to stabilize the mucous layer and increase the resistance to back-diffusion of hydrogen ions without significantly modifying the ion-exchange properties of mucus.
The aortic walls of patients with abdominal aortic aneurysms (AAA) and of healthy controls were examined for elastin, collagen I and III, and the intermediate filament proteins desmin and vimentin by immunohistochemical, enzyme histochemical, and routine histological techniques. The morphology of the aneurysmatic walls varied considerably from case to case, but many pathological changes were seen in all cases, e.g., extensive atherosclerotic plaques in the intima, prominent alterations in amount and organization of the elastic lamellae in the media, and an increase of connective tissue. Both collagen I and III were present in all the aneurysmatic walls. The smooth muscle cells in all the aortic walls showed a marked heterogeneity with respect to the morphological appearance, the enzyme histochemical features, and the content of desmin and vimentin. Vimentin occurred in some intimal, medial muscle, and adventitial cells of both the controls and the AAA patients. Desmin occurred in some of the intimal, medial, and adventitial muscle cells of both the controls and the AAA patients. All the cells with desmin in the intima and media also contained vimentin. Thus, smooth muscle cells in the walls of both the normal human abdominal aorta and aneurysms contained either vimentin, desmin, or both. This variability may be explained by the presence of different phenotypes of smooth muscle cells and could be of significance for the development of atherosclerosis and aneurysms. Of special interest was the finding that 5 of the 24 AAA patients studied had blood relatives with the same disease, suggesting a hereditary influence. However, no systematic differences between the morphological appearance of the aneurysmatic walls in familial and nonfamilial AAA could be detected.