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Biomedical subjects

D J deSa

Publications and source records attributed to D J deSa.

At least 19 recordsLinked to original sources
PubMed1998

Choline acetyltransferase (ChAT) immunoreactivity in paraffin sections of normal and diseased intestines.

There is increasing interest in localizing nerves in the intestine, especially specific populations of nerves. At present, the usual histochemical marker for cholinergic nerves in tissue sections is acetylcholinesterase activity. However, such techniques are applicable only to frozen sections and have uncertain specificity. Choline acetyltransferase (ChAT) is also present in cholinergic nerves, and we therefore aimed to establish a paraffin section immunocytochemical technique using an anti-ChAT antibody. Monoclonal anti-choline acetyltransferase (1.B3.9B3) and a biotin-streptavidin detection system were used to study the distribution of ChAT immunoreactivity (ChAT IR) in paraffin-embedded normal and diseased gastrointestinal tracts from both rats and humans. Optimal staining was seen after 6-24 hr of fixation in neutral buffered formalin and overnight incubation in 1 microgram/ml of 1.B3.9B3, with a similar distribution to that seen in frozen sections. In the rat diaphragm (used as a positive control), axons and motor endplates were ChAT IR. Proportions of ganglion cells and nerve fibers in the intramural plexi of both human and rat gastrointestinal tracts were also ChAT IR, as well as extrinsic nerve bundles in aganglionic segments of Hirschsprung's disease. Mucosal cholinergic nerves, however, were not visualized. In addition, non-neuronal cells such as endothelium, epithelium, and inflammatory cells were ChAT IR. We were able to localize ChAT to nerves in formalin-fixed, paraffin-embedded sections. The presence of ChAT IR in non-neuronal cells indicates that this method should be used in conjunction with other antibodies. Nevertheless, it proves to be a useful technique for studying cholinergic neuronal distinction in normal tissues and pathological disorders.

Animals↗
PubMed1988

Myocardial failure and shock in iron poisoning.

Shock is a well-known complication of iron poisoning. Its aetiology is multifactorial with hypovolaemia due to gastrointestinal blood loss and myocardial depression due to systemic acidosis contributing to its genesis. Primary myocardial dysfunction has not been considered to play a role. Our clinical experiences and autopsy findings in three fatal cases of iron poisoning support myocardial dysfunction and damage as contributing factors to their cardiovascular collapse. The three patients, all female, were 3 1/2, 16 and 28-years-old. Onset of shock occurred at 1, 2 and 5 days post-ingestion. There was no response to vigorous fluid replacement therapy and aggressive catecholamine infusions. Central venous pressures were elevated. Microscopic examination of postmortem tissue showed myocardial damage and the presence of stainable iron. It is speculated that the myocardial depression is mediated by lipid peroxidation of myocyte organelle membranes due to iron catalysed free radical generation. The presence of myocardial dysfunction has therapeutic implications. Patients with severe iron poisoning require early and serial measurements of arterial blood pressure, central venous pressure and cardiac output. If primary myocardial dysfunction is documented then fluid replacement, inotropic support and afterload reduction should be considered.

Adolescent↗
PubMed1987

Demonstration of Epstein-Barr virus in immunoblastic sarcoma of B-cells arising in a child with primary immunodeficiency disease.

The subject of this investigation was an 11-month-old infant girl who presented with a pathological fracture of the right femur due to a metastasis from an abdominal immunoblastic sarcoma. Her past history included recurrent, intractable bacterial and fungal infections. Investigations of her immune status revealed low numbers of T-lymphocytes, a reversed T-helper (TH)/T-suppressor (TS) cell ratio, no response of her peripheral blood lymphocytes to pokeweed mitogen, phytohemagglutinin, concanavalin A, and Candida albicans, and an inability of her cells to react in a mixed lymphocyte culture. Serum levels of IgG, IgM, and IgA were all below normal. No thymic shadow was visible on the chest radiograph. There was no evidence of adenosine deaminase or nucleoside phosphorylase deficiencies. The tumor cells exhibited both surface IgM and IgG, and many of the cells contained large amounts of cytoplasmic IgM. Light chain specificity was restricted to lambda chain for both surface and cytoplasmic immunoglobulin. Ultrastructural study of the tumor cells revealed the presence of both intranuclear and cytoplasmic virions in roughly 1% of the tumor cells. These viral particles strongly resembled herpes viruses. DNA-hybridization studies on the neoplasm revealed the presence of 7-10 genome equivalents of Epstein-Barr virus-DNA per tumor cell.

Abdominal Neoplasms↗
PubMed1986

Structures mimicking sex cord-stromal tumours and gonadoblastomas in the ovaries of normal infants and children.

A chance finding of structures resembling gonadoblastomas in the ovaries of a child with lissencephaly prompted a detailed review of all ovarian histology obtained at autopsy over a 12 month period. Fifty-five stillbirths, infants and children were studied ranging from 20 weeks gestational age to 2.5 years post-natal age. In 19 infants structures mimicking gonadoblastomas and sex cord tumours with annular tubules were seen. In all but one case these structures were found in association with follicular cysts and they closely resembled the atretic follicles often seen in the stroma surrounding the follicular cysts. They differed from the atretic follicles only by virtue of their being larger. In addition, in several infants structures resembling Sertoli cell tubules or clusters of Leydig cells were found. When present, these structures always co-existed with sex cord tumours with annular tubules and gonadoblastoma-like lesions. The abnormal stromal lesions and follicular cysts were found most frequently at the stage of development when a massive 'physiological' reduction of oocytes occurs. It is suggested that the 'abnormal' structures identified in this report represent the 'first hit' of oncogenesis and could serve as the precursor of many of the sex cord-stromal tumours, and possibly germ cell neoplasms, seen in childhood.

Autopsy↗
PubMed1985

Isolated myocarditis in the first year.

Over a period of nearly 40 years, 20 cases of isolated myocarditis were traced from 3086 necropsies. Seventeen occurred in infants less than 12 months of age, often with no antecedent clinical signs (sudden deaths) or with a short clinical history of less than 24 hours' duration.

Age Factors↗
PubMed1983

45,X/46,XX mosaicism in discordant monozygotic twins.

Monozygotic twins discordant for Turner's syndrome were both mosaic for 45,X/46,XX in the blood with the same low frequency of 2% to 3% 45,X cells. However, the fibroblasts of the abnormal girl were all uniformly 45,X whereas her normal twin had only 46,XX cells. Monozygosity was confirmed by genetic markers, chromosome variants, and a single monochorionic placenta with a shared vascular circulation. The mechanism by which this disparate pair developed from a single zygote is suggested.

Dermatoglyphics↗
PubMed1981

Adriamycin cardiotoxicity: report of an unusual case with features resembling endomyocardial fibrosis.

We report on a case of adriamycin cardiotoxicity occurring in a five-year-old boy treated for rhabdomyosarcoma. In addition to the usual features of myofibrillary degeneration associated with adriamycin, extreme endocardial fibrosis and mural thrombosis affecting the apical segments of both ventricles but particularly the left ventricle was seen at necropsy. The changes resembled classical endomyocardial fibrosis.

Cardiomyopathies↗
PubMed1981

Placental involvement in congenital neuroblastoma.

We describe two cases of congenital neuroblastoma involving the placenta and review previously reported cases. The placentae in congenital neuroblastoma have a bulky, hydropic appearance, and contain tumour cells which are confined to the fetal circulation. The tumour emboli are not macroscopically identifiable. Pathophysiological mechanisms of placental involvement by fetal and maternal malignancies are considered. The rarity of this lesion may be artefactual, and may result from failure to examine grossly enlarged placentae in cases of stillbirth and hydrops fetalis. Congenital malignancy must be considered in the differential diagnosis of an abnormally large placenta.

Adrenal Gland Neoplasms↗
PubMed1980

Bronchopulmonary dysplasia. A radiologic-pathologic correlation.

In 26 deaths from the neonatal unit with a histologic diagnosis of bronchopulmonary dysplasia (BPD), the histologic stage was compared to the radiologic stage according to the criteria described by Northway and Rosan. In 18 patients (69%), the histologic stage corresponded exactly to the radiologic stage. In the remaining eight patients (31%), there was a difference of one stage. If the 14 cases of Stages I and II were taken together there would be a discrepancy of one stage between the histologic and radiologic stages in 50%. However, with Stages III and IV the discrepancy was only 8.3%. There appears to be better correlation as the severity of BPD increases.

Diagnosis, Differential↗
PubMed1976

Thromboatheromatous complications of umbilical arterial catheterization in the newborn period. Clinicopathological study.

Severe catheter-related thromboatheromatous lesions were found at necropsy in 33 of 56 infants who had umbilical arterial catheters passed during life. In infants dying within 8 days of insertion of the catheter, varying degrees of thrombosis of the aorta and its major branches were seen. With increasing thrombosis and aging of the thrombus, fatty deposits were seen first within the thrombus, and then in the intima and media. In addition there was evidence of proliferation of medial smooth muscle cells and of disruption of the medial architecture below the thrombus, characterized by the presence of abundant mucopolysaccharide. In infants who survived longer, varying degrees of organization of the thrombus could be traced, leading eventually to raised fibrous plaques with lipid and occasionally calcification. The lesions in the older infants were similar in many respects to experimental thromboatheromatous lesions produced in rabbits, and to some lesions of artheroma occurring spontaneously in humans. A wide variety of embolic phenomena were found, with features suggesting asynchrony of embolic episodes. The presence of thrombotic lesions could not be related to birthweight, Apgar scores at 1 and 5 minutes, age at catheterization, duration of catheterization, underlying disease process, age at death or the presence of hypothermia, acidosis, or anomalies in coagulation tests. There is a need for less hazardous methods of monitoring arterial oxygen tension.

Aorta↗
PubMed1975

Follicular ovarian cysts in stillbirths and neonates.

A review of the histology of 332 ovaries from stillbirths and neonatal deaths within the first 28 days of life showed that follicular cysts, lined by granulosa epithelium and having a diameter greater than 1 mm on a microscopical section, were present in 113 infants. In 48 cases multiple cysts were present, while in 65 only a single cyst satisfying the criteria was found. There was an excess number of infants of low birthweight score among those with multiple cysts and the results were highly significant. Cysts, whether single or multiple in distribution, were commoner with increasing gestation, and possibly occurred more commonly in the infants of diabetic mothers and in infants where pregnancy had been complicated by rhesus isoimmunization. The nature of the changes seen in the granulosa lining and theca internal layer surrounding the cysts suggested that these cysts were not some degenerative phenomenon but occured in response to stimulation. It is suggested that homologous changes may occur in the testis of the dysmature male. The possible significance of these findings with regard to hormonal imbalance in the growth-retarded infant is considered, and the need for closer attention to endocrine function in these infants stressed.

Autopsy↗
PubMedDate not supplied

Isolated myocarditis as a cause of sudden death in the first year of life.

A series of three cases of isolated myocarditis, presenting as sudden death in infancy, occurred over a period of 3 months. This prompted a review of the autopsy records of the Children's Hospital of Winnipeg. Over a period of 40 years, 24 cases of isolated myocarditis were traced from 3196 autopsies. Most (21 of 24) cases of isolated myocarditis occurred in infants less than 12 months of age. In 16 of the infants there were either no antecedent clinical signs (sudden deaths), or a short clinical history of less than 24 h duration. Heart weights, however, were greater than the 99th percentile of published normals in three infants and above the 95th percentile in a further 16 infants. Areas of hypertrophied fibres were seen even in infants with a short history. These latter findings suggest that a latent phase of myocarditis may exist. The responsible pathogens were identified very rarely, due to a lack of suspicion of the existence of myocarditis, and it is suggested that samples of myocardium should be submitted for virologic examination in all cases of sudden death in the first year of life.

Coxsackievirus Infections↗
PubMedDate not supplied

Hypothesis: pathogenesis of skip areas in long-segment Hirschsprung's disease.

The existence of skip areas in a subset of patients with long-segment Hirschsprung's disease (LSHD) is a rare phenomenon that poses practical and theoretical challenges. In this paper, three new cases are described and compared with preceding reports in the medical literature. In addition, an analogous distribution of ganglion cell precursors is reported in the developing large intestines of murine embryos, homozygous for the lethal spotted (ls) allele. In ls/ls embryos, which were destined to have "classic" short-segment aganglionosis coli, a transient phase was observed in which ganglion cells were present in the middle colon, but absent from the cecum and distal large intestine. This "skip area" is attributed to an extramural phase of neuroblast migration which is unique to the colon. Persistence of an abnormal pattern of neuroblast migration, similar to that observed transiently in ls/ls embryos, is invoked as an explanation for skip areas in humans with LSHD.

Animals↗