Abstract Loss of genetic material, corresponding to chromosomal deletions, has been detected in a wide range of tumours and may indicate the position of a tumour suppressor gene. In order to identify the position of such a gene more precisely, many tumour samples must be studied until a minimum consensus deletion is characterized. This process is particularly necessary for lung tumours in which the deletion in chromosome 3, seen with such high frequencies in all histological subtypes, is almost always large. We have recently described the use of the polymerase chain reaction (PCR) for restriction fragment length polymorphism (RFLP) analysis of DNA isolated from small bronchial biopsies of lung tumours. In this study we adapted this technique to allow genotyping of DNA isolated from paraffin wax‐embedded material (PWEM) microdissected from glass slides. We have investigated 12 lung tumours at polymorphic loci on chromosome 3 and showed allelic loss in all samples. In adapting PCR–RFLP analysis for DNA isolated from PWEM, we have concentrated on those approaches which might be adaptable to routine clinical practice. Somatic genetic changes are now being identified in many tumour types, and this information is expected to be of diagnostic and prognostic significance.
The parathyroids from ten consecutive cases of chronic renal failure coming to operation in a period of seven years were studied by light and electron microscopy. The clinical and biochemical data as well as the levels of immunoreactive parathormone (iPTH) were reviewed. For the sake of comparison adenomata from two cases of primary hyperparathyroidism were studied. In the cases of chronic ;renal failure there were six cases of tertiary hyperparathyroidism with adenoma formation, surrounded by dense fibrous tissue and compression of adjacent parathyroid cell amidst a background of hyperplasia. Two cases showed secondary parathyroid hyperplasia and the remaining two cases were adenomata which clinically affected only one gland. Neither the biochemical data nor levels of iPTH allowed the cases with secondary hyperplasia to be separated from those with tertiary hyperparathyroidism. Similarly electron microscopy showed no distinct differences between these two groups of adenomata from cases of primary hyperparathyroidism. The diagnosis of tertiary hyperparathyroidism is made on a combination of clinical, biochemical and histological features, the histological features being most important. It is concluded that tertiary hyperparathyroidism is part of a histological spectrum in response to chronic renal failure and autonomous glands are related to the mass of parathyroid tissue present.
Metastatic disease is a complex and multistep process that continues to be one of the most significant problems in cancer medicine. Metastatic cancer cells are unique given their ability to leave the site of the primary tumor, enter the circulation, resist phagocytosis, and grow at distant sites. At distant sites, metastatic tumor cells not only survive, but thrive in the new novel microenvironment co-opting existing blood vessels or inducing neovascularization. These factors lead to the growth of clinically significant metastases.
Adult respiratory distress syndrome (ARDS) represents a common pathway of damage to the lungs by a wide variety of different agents. The important aetiological factors and mechanisms of lung injury are considered. Electron microscopic features as well as light microscopy are described. Factors that may modify the pathological picture are discussed. Probably the most important of these is oxygen. This gas is said to produce interstitial pulmonary fibrosis but this concept is once again questioned.
Abstract Asbestosis is defined as diffuse pulmonary fibrosis caused by the inhalation of excessive amounts of asbestos fibers. Pathologically, both pulmonary fibrosis of a particular pattern and evidence of excess asbestos in the lungs must be present. Clinically, the disease usually progresses slowly, with a typical latent period of more than 20 years from first exposure to onset of symptoms. Differential Diagnosis: Idiopathic Pulmonary Fibrosis The pulmonary fibrosis of asbestosis is interstitial and has a basal subpleural distribution, similar to that seen in idiopathic pulmonary fibrosis, which is the principal differential diagnosis. However, there are differences between the 2 diseases apart from the presence or absence of asbestos. First, the interstitial fibrosis of asbestosis is accompanied by very little inflammation, which, although not marked, is better developed in idiopathic pulmonary fibrosis. Second, in keeping with the slow tempo of the disease, the fibroblastic foci that characterize idiopathic pulmonary fibrosis are infrequent in asbestosis. Third, asbestosis is almost always accompanied by mild fibrosis of the visceral pleura, a feature that is rare in idiopathic pulmonary fibrosis. Differential Diagnosis: Respiratory Bronchiolitis Asbestosis is believed to start in the region of the respiratory bronchiole and gradually extends outward to involve more and more of the lung acinus, until the separate foci of fibrosis link, resulting in the characteristically diffuse pattern of the disease. These early stages of the disease are diagnostically problematic because similar centriacinar fibrosis is often seen in cigarette smokers and is characteristic of mixed-dust pneumoconiosis. Fibrosis limited to the walls of the bronchioles does not represent asbestosis. Role of Asbestos Bodies Histologic evidence of asbestos inhalation is provided by the identification of asbestos bodies either lying freely in the air spaces or embedded in the interstitial fibrosis. Asbestos bodies are distinguished from other ferruginous bodies by their thin, transparent core. Two or more asbestos bodies per square centimeter of a 5-μm-thick lung section, in combination with interstitial fibrosis of the appropriate pattern, are indicative of asbestosis. Fewer asbestos bodies do not necessarily exclude a diagnosis of asbestosis, but evidence of excess asbestos would then require quantitative studies performed on lung digests. Role of Fiber Analysis Quantification of asbestos load may be performed on lung digests or bronchoalveolar lavage material, employing either light microscopy, scanning electron microscopy, or transmission electron microscopy. Whichever technique is employed, the results are only dependable if the laboratory is well practiced in the method chosen, frequently performs such analyses, and the results are compared with those obtained by the same laboratory applying the same technique to a control population.
Mankind is afflicted with hundreds of parasitic diseases that affect every organ, including the upper and lower respiratory tracts. For some infections, man is the definitive host, i.e., the sexual or reproductive part of the parasite's life cycle takes place within the human body. For others, man is accidentally infected, i.e., humans interrupt another animal's parasitic life cycle. This latter scenario represents a dead end for the parasite, since reproduction is not possible.
A case of multiple endocrine neoplasia syndrome (MEN) in a 57‐year‐old woman with multiple endocrine tumours involving the pancreas, parathyroid and thyroid glands is reported. An unusual feature was the presence of collision tumours in the pituitary and adrenal. In the pituitary there were adenomas and a meningioma whereas in the adrenal there was a carcinoma along with a myelolipoma. Such collision tumours in the pituitary and adrenal as components of MEN syndrome have not been previously described.
Journal Article Biochemical investigation of possible lesions in human aorta that predispose to dissecting aneurysms: pyridinoline crosslinks Get access M ANNE WHITTLE, M ANNE WHITTLE ** From the Department of Biochemistry, University of Manchester Medical School, Manchester Address for correspondence and reprints: Dr J C Anderson, Department of Biochemistry, University of Manchester Medical School, Oxford Road, Manchester M13 9PT. Search for other works by this author on: Oxford Academic PubMed Google Scholar SIMON P ROBINS, SIMON P ROBINS † From the Rowett Research Institute, Aberdeen Search for other works by this author on: Oxford Academic PubMed Google Scholar PHILIP S HASLETON, PHILIP S HASLETON ‡ From the Department of Histopathology, Wythenshawe Hospital, Manchester Search for other works by this author on: Oxford Academic PubMed Google Scholar JOHN C ANDERSON JOHN C ANDERSON ** From the Department of Biochemistry, University of Manchester Medical School, Manchester Search for other works by this author on: Oxford Academic PubMed Google Scholar Cardiovascular Research, Volume 21, Issue 3, March 1987, Pages 161–168, https://doi.org/10.1093/cvr/21.3.161 Published: 01 March 1987 Article history Received: 12 May 1986 Accepted: 22 July 1986 Published: 01 March 1987
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