PubMed Health⌕ Search

Biomedical subjects

D K Dastur

Publications and source records attributed to D K Dastur.

At least 19 recordsLinked to original sources
PubMed1992

Histopathology and fine structure of the brain in six cases of Creutzfeldt-Jakob disease from western India.

Light and electronmicroscopic changes in 5 formalin-fixed brains, and one glutaraldehyde-fixed brain biopsy, from patients with Creutzfeldt-Jakob disease in the age range of 45 to 65 years, are described. These 6 patients (out of 7 reported clinically earlier and 2 unreported) had classical manifestations with progressive dementia, pyramidal signs and myoclonic jerks. Light microscopy showed neuronal and nerve fibre loss, moderate or severe spongiform change, astrocytic proliferation and absence of inflammatory reaction. Electronmicroscopy confirmed the characteristic membranous profiles of the 'cysts' and 'daughter cysts' constituting the spongiform change. The membranes were generally dark and thin, either concentrically arranged or splitting and with stray pale broad segments. The one glutaraldehyde-fixed brain biopsy specimen showed cisterns of RER in close proximity to these 'cysts', suggesting the source of proteinous material of these membranes. Though mainly in the neurones and dendrites of the cortex, at times they were seen in the myelinated fibres also, a few of which showed dystrophic axons bearing dense bodies. One of the 6 patients had cerebellar signs also, and a total duration of the neurological illness of 36 months, as against 2-8 months in the 5 other patients. The histopathological examination of her brain revealed less spongiform change, and many cerebral cortical glial whorls, the centre of which showed PAS-positive and congo-red-positive material representing amyloid. Fine structural examination confirmed the glial whorls, and the filamentous nature of amyloid in the plaques, which resembled Kuru plaques. All brains also showed more or less intraneuronal lipofuscin.

Amyloid↗
PubMed1992

The lung in tropical eosinophilia compared to that in pulmonary hypertension. Fine structural basis of respiratory disability.

Light and electronmicroscopic changes in lung biopsies were studied in six patients with tropical pulmonary eosinophilia, aged 20 to 37 years, of varying duration, and with severe haematologic (blood eosinophil count of 3,600 to 18,200 per mm3), and respiratory changes. On light microscopy the main pathologic reaction consisted of large mononuclear cells and eosinophils in and around the alveoli and blood vessels, and proliferated reticulin. Fine structural changes probably being described for the first time, included the presence of many alveolar macrophages characterised by abundant cytoplasm, irregular or stunted microvilli, increased phagolysosomes with ingested debris, and depletion of other organelles. Eosinophils bearing typical old and young granules, were encountered in and around the alveoli and blood vessels in all case, and collagenosis around alveolar cells in a few. Subacute pneumonitis producing compression and disorganisation of alveoli and blood vessels, and lack of normal apposition of air and blood spaces, appear responsible for the respiratory disability. The detection of mycobacteria, cocci or chlamydia-like bodies in two specimens and of intranuclear virus-like particles in another, could either indicate secondary infection or have an immunogenic significance, in the absence of detection of filarial elements in any of the specimens. Lung biopsies from two additional patients (aged 13 & 32) who had mitral stenosis probably due to rheumatic heart disease, and secondary pulmonary hypertension, were studied as "control" specimens. Both at light and electronmicroscopy these specimens did not show any eosinophils or neutrophils, and fewer macrophages in the lung parenchyma. In contrast to tropical eosinophilia and, as expected, there was considerably more fibrosis of the lung parenchyma, especially in the alveolar subepithelial region and in the vessel walls. This, together with fibroblasts full of endoplasmic cisterns, noted particularly in the younger patient with shorter duration, probably represented an earlier change in this condition.

Adolescent↗
PubMed1990

Neuropathology & pathogenesis of experimental fenfluramine toxicity in young rodents.

The anorectic compound fenfluramine hydrochloride was injected into young Holtzman strain rats (from days 6 to 40 of life), at the dose of 75 mg/kg body weight. Intralysosomal lamellar bodies (LBs) were seen in the endothelial cells, pericytes, the perivascular astrocyte processes and occasionally in the lumen. The pathology of myelinated fibres varied from thinning of myelin to complete demyelination and, at times, presence of dense bodies in the axons, the changes perhaps being a result of the oligodendroglia damage. A small group of adult mice was administered three oral doses each of Ponderax equivalent to 5 mg of fenfluramine. The brain stem and cerebellar neurons of these mice showed abnormal dark cytoplasm, without lamellar bodies. Even in this short-term experiment, there was formation of a few LBs in the neuropil, the prominence of dark glial cells, probably oligodendroglia, and some perivascular intracytoplasmic oedema. The earliest detection of dense bodies in the undistended astrocyte processes before they were observed in the cell perikarya, both in the younger rats and the adult mice, suggested the perivascular astrocyte to be the first CNS constituent to come in contact with the toxic agent as it passes the blood-brain barrier. On the basis of our observations, it also appears that the 'myelinosomes' or lamellar phagolysosomes developing due to failure of degradation of drug-phospholipid interaction product, accumulate in different cells of the CNS.

Aging↗
PubMed1989

Brain tumours in childhood in Bombay: I: Histopathology showing changing patterns; II: Tissue culture with light and electronmicroscopy, stressing ingestion & degradation of bacteria by glial cells in vitro.

The pathological pattern of 86 brain 'tumours' in childhood during the years 1981-85 (out of a total of 586 for all ages), showed a higher proportion of neoplasms and a much lower of tuberculomas compared to the preceding three decades. A large number of histologically unusual cases was revealed. Through tissue culture of brain tumours we carried out morphological, histochemical and fine structural study of the tumour cells in vitro. The abundant presence of lysosomal acid phosphatase, in outgrowing cells, correlated with the detection of lysosomal dense bodies and vacuoles in araldite sections, by light and electronmicroscopy. In view of the phagocytic propensity of schwann cells for M. leprae as the important factor in leprous neuritis, TC preparations of gliomas, (in addition to acoustic schwannomas and meningiomas), were inoculated with two mycobacteria, M. scrofulaceum and the ICRC bacillus. There was a pronounced intracytoplasmic uptake, i.e. endocytosis, of acid-fast bacilli by the growing cells of these tumours. This was confirmed by electronmicroscopy which showed intact and degrading bacilli in various stages, in such cells of a typical cerebral astrocytoma used as an illustrative case in this paper. Ingestion and Digestion appear to be an inherent property of growing tumour cells in vitro. Fine structural examination of in vitro growth of an unusual subependymal giant cell astrocytoma, not inoculated with bacilli, served as a control. Cells of both tumours showed copious autophagic activity and cytoskeletal features of developing microtubules and filaments.

Adolescent↗
PubMed1989

Light and electronmicroscopy of the bowel in an unusual form of Hirschsprung's disease.

In a histological and histochemical study of multiple biopsies of unaffected segments of the bowel from 15 patients with Hirschsprung's Disease (H.D.), the AChE or non-specific esterase and the NADPH tetrazolium reductase enzyme reactions proved to be useful in identification of myenteric plexus islands; and acid phosphatase for the delineation of individual neurones. In the affected segment (usually aganglionic), this myenteric plexus tissue was not reactive for esterase, but individual nerve fibres among muscle fibres of the two muscle coats showed the enzyme product in a third of the cases. Fine structural study of biopsies from a typical case of H.D., showed normal looking axons and Schwann cytoplasm with terminals bearing both andrenergic and cholinergic vesicles in the unaffected colon, smooth muscle fibres with normal fine structure in all parts of the bowel, and loss of neurons with myenteric plexus replaced by nerve fibre groups in the affected rectosigmoid. One patient clinically presenting as a case of severe H.D., with histologically and histochemically normal myenteric and submucous ganglion cells, and not responding to resection of the bowel, showed degeneration of the unmyelinated axons with prominent Schwann cytoplasm, depleted cholinergic but persistent adrenergic vesicles, and markedly thinned and degenerating smooth muscle fibres and myofilaments, suggesting either a primary disorder of muscle tissue of the colon or, less likely, a denervation atrophy with secondary degeneration of the smooth muscle fibres.

Acetylcholinesterase↗
PubMed1989

Histomorphology of Wilms' tumour.

Eleven cases of Wilms' tumour received at Banglore Medical College, Bangalore are being studied focussing on the histopathological appearance of these tumours. One case exhibiting neuronal and glial differentiation, which is a rare observation, was noticed and is reported. The clinicopathological features and a brief review of literature are being presented.

Child↗
PubMed1989

Human rabies: clinical features, diagnosis, complications, and management.

A case of rabies was treated with intensive medical support. This led to a prolongation of life to 25 days. The neurologic progression of the disease was monitored clinically and with serial EEG. This prolonged course enabled us to witness and manage a wide variety of unusual complications including the adult respiratory distress syndrome, hypothermia, myocarditis, and diabetes insipidus. This report documents the clinical features, diagnostic problems, complications, and management.

Coma↗
PubMed1986

The pathology and pathogenesis of tuberculous encephalopathy and myeloradiculopathy: a comparison with allergic encephalomyelitis.

The pathology and pathogenesis of tuberculous encephalopathy are reviewed. They confirm the findings in a smaller series previously published. The main features were: diffuse brain edema and myelin pallor in the majority of specimens; microvascular distension or necrosis with perivascular macrophage reaction and greater demyelination; focal glial nodules in the white matter; less frequently, hemorrhagic lesions in the presence of mild-to-moderate tuberculous meningitis (TM), but in the virtual absence of the commoner brain-damaging mechanisms. Focal demyelinating lesions in the nerve roots are now added to the above pathology in the brain in some of the cases of spinal tuberculous meningitis. In addition, a picture similar to that in human postinfectious allergic or experimental allergic encephalomyelitis (EAE) has emerged. The spinal cords from one case of the former condition and from four animals with EAE are described to illustrate this similarity. The pathogenesis of tuberculous encephalopathy and myeloradiculopathy is believed, as before, to be due to delayed hypersensitivity, i.e., cell-mediated immunity (CMI) to tuberculoprotein. Experimental confirmation of this demyelination as a nonspecific consequence of CMI to various forms of tubercle bacillus proteins has recently been published. In a proportion of our cases, where two episodes of TM had occurred, the possibility of a hypersensitivity reaction to the brain's own myelin protein is also considered.

Adolescent↗
PubMed1986

Pleomorphism of fine structure of rabies virus in human and experimental brain.

Identification of the Negri bodies in the brain of an 8-year-old boy who died 8 days after a paralytic illness and 20 days after a dog bite, and who had received 9 injections of Semple's anti-rabies vaccine, provided evidence that he died of acute rabies encephalitis and not of post-vaccinal allergic encephalomyelitis. The Negri bodies in the human subject and those seen in the inoculated mouse differed in their morphological structure: the former consisted of a matrix of very fine granular material bearing larger granules or strands of higher electron-density resembling nucleic acids and representing products of host cell-virus interaction; and the latter showed better defined areas of granular matrix containing tubular, bullet-shaped and elongated forms of viral structures, and nucleocapsids or capsule-deficient cores, representing the virions, emerging from them. Fine structural examination of the patient's brain and of the inoculated mouse has provided evidence of the pleomorphism of the Negri bodies and the various stages of formation of viral material and virions in them, the animal alone showing the mature virions of rabies, and proving the infectivity of the Negri bodies of the human brain.

Animals↗
PubMed1986

Fine structure of cellular and vascular reaction in brain tuberculomas: a model for phagocytosis in the CNS.

The fine structure of cells of the mononuclear phagocyte series (MPS) and a few other cells with phagocytic capacity, has been critically evaluated, mainly from an electronmicroscopic examination of the reactive border zone of 11 human brain tuberculomas, which provide ideal material for the study of macrophages. Most of them appeared to be blood monocyte-derived epithelioid cells of various forms and stages. The cytoplasm of these cells showed either more rough ER representing protein synthesising activity; or more frequently, phagosomes, phagolysosomes, dense bodies or empty vacuoles, representing various stages of ingestion and digestion of necrotic material. Often such material, which was more or less osmiophilic, was seen abundantly between the cells. These actively phagocytic cells occasionally undergoing, mitosis, are referred to as "epithelioid macrophages" and were morphologically similar to the "activated microglia" described in other conditions. They also showed a tendency to be closely adjacent to each other and occasionally fuse to form giant cells. There were also a number of lymphocytes and plasma cells. The latter showed various stages of active and granular or depleted and distended rough ER tubules, phagocytic activity and tendency to fuse. Expected vasculitis and small vessel necrosis formed part of this granulomatous reaction. Constituents of oedematous or necrosed brain tissue were seen immediately around the reactive zone of these tuberculomas, the most frequent being reactive astrocytes, many of which showed membrane-bound vacuoles. It is conceivable that the excessive pleomorphic cellular, vascular and necrotic reaction in these brain tuberculomas could have resulted from a delayed type of hypersensitivity to a very small quentity of antigenic tuberculoprotein, which probably initiates the chain of immunologic responses.

Adolescent↗
PubMed1985

Experimental neurotoxicity of the anorectic fenfluramine. I. A fine structural model for cerebral lysosomal storage and neuroglial reaction.

Fenfluramine, an amphophilic compound which is a halogenated derivative of amphetamine, is still used as an anorectic agent for weight reduction, as it acts on the satiety center of the hypothalamus. Holtzman strain rats aged 6 days were daily injected s.c. fenfluramine hydrochloride at the dose of 75 mg/kg body weight. The animals were killed at different time intervals between days 7 and 40, and different parts of the brain were examined by light and electron microscopy. About half of the animals showed intralysosomal membrano-cytoplasmic bodies in the oligodendroglia, neurons, and neuropil, maximally in the animals receiving 8-19 injections. They were seen as concentrically arranged, single-layered lamellae; small dense bodies; or larger heterogeneous bodies. The mechanism of production of such inclusions could be the formation of complexes of this amphophilic compound with tissue phospholipids, or some enzyme-inhibiting action. A marked prominence of dark cells, predominantly oligodendroglia, was also noticed in the brains of experimental animals. Some of these cells appeared to be dark neurons, probably resulting from the serotonin-depleting effect of fenfluramine. A few dark cells were identified as resting microglial cells, while macrophagic "reactive microglia" were detected in the brains of very young animals. Fenfluramine appears to provide a model for studying neuroglial reactions.

Animals↗
PubMed1985

Changes in atrial biopsies in chronic rheumatic heart disease. I: Cellulo-vascular and mesenchymal reaction.

The cellular, vascular and connective tissue changes were studied in 32 atrial biopsy specimens from patients with chronic rheumatic heart disease (RHD). 15 of these 32 specimens showed some inflammatory reaction, 7 with small mononuclear cells only and 8 with macrophage reaction amidst increased but necrotic collagen, especially in the subepicardial and subendocardial regions. Most cellulonecrotic foci were histologically consistent with a stage of Aschoff nodule. Acid phosphatase activity in frozen sections was seen in the cytoplasm of the macrophages. Fine structural examination showed membrane-bound vacuoles and lipofuscin bodies rather than ingested material in the macrophages. By light and electronmicroscopy, these macrophages were not different from those encountered in other granulomatous or necrotic conditions. There was moderate proliferation of blood vessels, with prominence of endothelial cells and pinocytotic vesicles, or fibrosis of media, or proliferation of basal laminae. The presence of Aschoff nodules in the right atrium, the least affected chamber in RHD, suggests a diffuse and smouldering pathology on the basis of a persistent subclinical cell-mediated immune (CMI) reaction.

Adolescent↗
PubMed1985

Changes in atrial biopsies in chronic rheumatic heart disease. II: Muscle fibre reaction.

Myocardial fibres were studied in the right atrial biopsies from 32 patients with chronic rheumatic heart disease (RHD). Paraffin and, particularly, araldite sections showed many muscle fibres well preserved, and others with large hyperchromatic nuclei, or with depleted myofibrils and increased mitochondria. With the SDH and ATPase reactions, there was no type difference in the myocardial fibres, and the former showed the reaction predominantly in the centre while the latter showed it mainly at the periphery of the fibres. At electronmicroscopy, fibres with intact myofibrils were found close to "degenerating" fibres with variable degrees of myofibrillar and myofilament disorganisation and loss, mitochondrial proliferation, occasionally with degeneration of cristae, and accumulation of lipofuscin in varying amounts, and irregularly tortuous or loosened intercellular junctions. This study has revealed more severe muscle changes than expected, even in the clinically less affected right atrial chamber in chronic RHD. It is speculated that this might be due to subclinical involvement of the tricuspid valve, known to be frequent in Indian patients, and the resulting "back pressure" on the right atrium might lead to changes in its myofibres.

Adolescent↗
PubMed1985

Cerebral blood flow and metabolism in normal human aging, pathological aging, and senile dementia.

A review and a reappraisal are presented of earlier data on cerebral circulatory and metabolic studies in normal active elderly men (Group I) of mean age 71 years, compared with normal young subjects of mean age 21 years, conducted at the National Institutes of Health, Bethesda, MD, U.S.A., during 1956-1958. There was no significant difference in the mean CBF and cerebral metabolic rate for oxygen (CMRO2) values between the two populations; i.e., these important parameters did not fall with chronological aging per se. There was significant depression in the mean cerebral metabolic rate for glucose (CMRG) value (by approximately 23%) in the aged compared with the young. Newer methods using positron emission tomography and appropriate isotopes have confirmed these findings in normal aging in human subjects and experimental animals. As expected, MABP and cerebral vascular resistance (CVR) were significantly elevated in the normal aged. MABP was even more elevated in elderly hypertensive subjects, and the CVR more elevated in the subjects with arteriosclerosis (Group II), who also showed a small but significant fall in CBF and in internal jugular venous PO2. The CBF showed a more pronounced fall in senile aged patients with chronic brain syndrome (Group III), in whom the CMRO2 also showed a marked drop (by approximately 22%); the CMRG fell still further (approximately 40% of that in the young). Of the few aged subjects followed up after a lapse of 11 years by a repeat estimation of the same physiological and psychological parameters and of the EEG, most showed clear worsening, together with a fall in overall physical and intellectual performance, probably related to a rise in CVR and an increase in atherosclerosis with aging.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗