Staples in the specimen.
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Biomedical subjects
Publications and source records attributed to S B Coghill.
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The examination of excised, non-palpable mammographic lesions in breast biopsies is a recognized problem for the pathologist. There may be difficulties in identifying the lesion macroscopically and in subsequent sampling. This paper describes a simple method for resolving these problems. The breast biopsy is attached to a perspex grid and then radiographed. Use of the grid co-ordinates assists appropriate sampling of the specimen. Advantages over previously described methods are discussed.
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A newborn girl presented with generalized mild dysmorphic features. She later developed heart failure and hydrocephalus, and died aged 5 months. Chromosome analysis revealed an unbalanced reciprocal translocation (with partial trisomy for half of the long arm of 7 and partial monosomy for the short arm of chromosome 9) and normal but inappropriate sex chromosomes (XY). The karyotype (46,XY,-9, +der(9),t(7;9)(q31.1;p23)pat) was inferred from her father who was a balanced carrier: 46, XY,(7;9)(q31.1;p23). The evidence of the present case, when considered with that of previous reports, suggests that deletion of genes on the 9p may have caused the feminization and therefore that the 9p region may contain genes which are important in the normal process of testis formation.
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Tripotassium dicitrato-bismuthate (TDB) has a topical action in the upper gastrointestinal tract. Absorption is minimal and the blood levels are therefore irrelevant to the assessment of bioavailability. TDB is however detectable in the stomach and duodenum by conventional electron microscopy. Following oral administration of two different formulations of TDB tables to patients attending a gastroscopy clinic, duodenal biopsies were obtained and examined by electron microscopy. The amount of electron dense drug precipitate was quantified. No difference could be detected between the two formulations.
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Tripotassium dicitrato bismuthate (TDB), De-Nol, heals peptic ulcers with an efficacy similar to the H2 antagonists. Tripotassium dicitrato bismuthate may also be effective in decreasing relapse rates. Its mode of action is unknown, but it was recently observed that TDB rapidly increased the number of macrophages in experimental ulcers. This might accelerate reparative processes, accounting for the drug's action. Using more sophisticated techniques we could not demonstrate any macrophage influx in response to single, or multiple, doses of TDB. Electron micrographs did demonstrate that monocytes, the precursors of macrophages, could internalize TDB. This process occurred rapidly in the presence of plasma where an avid TDB-protein interaction was observed. It has been suggested that such an interaction upon the ulcer may form a protective layer allowing mucosal regeneration to occur unhindered beneath. We believe our electron micrographs support this theory.
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The binding and uptake of lead by the jejunal, colonic and gallbladder epithelium of guinea pig has been investigated by electron microscopy. Binding occurred rapidly, the most marked by the microvilli was by the jejunum, followed by colon and gallbladder. The tracer was subsequently internalised in small membrane bound vesicles and smooth endoplasmic reticulum. By 30 min, it appeared in multivesicular bodies at all three sites.
Intracardiac injection sites were traced at necropsy on 18 patients who died after unsuccessful cardiopulmonary resuscitation. In only 13 patients (72%) was the heart punctured. Of the 46 injections carried out, 5 (11%) pierced the left ventricle and 13 (28%) the right ventricle. Other structures punctured included the pulmonary trunk, the aorta, and the lung. The fourth intercostal space just lateral to the sternal edge was the commonest injection site, and only 5 injections were subxiphoid. Post-mortem injections on a further 20 cadavers confirmed that the right ventricle is the most frequent puncture site whichever approach is used.
Horseradish peroxidase (HRP) was injected into the emptied gallbladder of guinea pigs at laparotomy. The fate of the HRP was observed by light and electron microscopy over the following 2 hr. Within 5 min. HRP appeared in pits and apical vesicles either as a rim of increased electron density or more evenly distributed throughout the pit or vesicle. The pits and vesicles were more frequently seen at the edge of the cell apex. From 15 min. HRP was identified in the basolateral cell space in increasing quantities with spill over through the basement membrane into the lamina propria: by 30 min. and 2 hr, little further change was observed. The quantity of nonspecific electron density in epithelial cell multivesicular bodies and residual bodies made the assessment of intracellular handling of the HRP impossible. Dilution of the HRP in the lamina propria made the identification of the eventual fate of the HRP difficult to determine.
In the presence of hydrochloric acid, tripotassium dicitrato-bismuthate forms a particulate precipitate which is electron dense. In upper gastrointestinal tract endoscopic biopsies, following a single oral dose, precipitate was detected between superficial oesophageal epithelial cells and also lining lipid droplets within oesophageal cells. The precipitate does not appear to penetrate the thick mucus barrier in the normal stomach but reaches the epithelial cell surface in the duodenum and proximal jejunum. Small particles of bismuth complex are endocytosed by the enterocyte and enter multivesicular bodies. A similar series of events was observed in rodents and an approximate time course for adsorption and endocytosis was estimated.