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Biomedical subjects

D K Dastur

Publications and source records attributed to D K Dastur.

At least 55 records · Page 3Linked to original sources
PubMed1981

CNS involvement in malignant atrophic papulosis (Kohlmeier-Degos disease): vasculopathy and coagulopathy.

The clinical features in a 42 year old man with malignant atrophic papulosis with CNS involvement are described. They included mental dysfunction, paraesthesiae, weakness of left limbs, with pyramidal tract signs, bilateral ptosis, progressing to total ophthalmoplegia and obtundation. There were two crops of characteristic papular lesions on trunk and limbs, with terminal evidence of a coagulopathy and bruises, resulting in death in six months. Papular biopsy revealed multiple microinfarcts in the dermal collagen. The brain showed multiple small haemorrhagic infarcts of both hemispheres, the lower mid-brain, pons and a cerebellar peduncle. Microscopy showed fibrin exudation in the leptomeninges, various stages of thrombosis of small arteries without inflammatory reaction, and corresponding acute and subacute microinfarcts. The pathogenetic basis of the disease appeared to be a combined vasculopathy and coagulopathy.

Adult↗
PubMed1980

Ultrastructural changes in the embryonic cells of the frog Microhyla ornata after cytochalasin H treatment.

Biological effects of cytochalasin H (CH), a newly isolated mould metabolite, have been found to bring about disaggregation of embryonic cells and to inhibit cytokinesis. Disaggregation is known to be a phenomenon related to the cell surface. (The cells are held together by a mucopolysaccharide glycoprotein complex.) In the present work the fact that the mucopolysaccharide glycoprotein surface coat gets affected by CH treatment is confirmed by electron microscopy with the help of Lanthanum, a specific marker, which gets selectively absorbed to the cell surface material and renders it electron dense. The ultrastructural observations indicated the reduction of the cell surface material in treated embryos as compared to the controls. The reappearance of lanthanum-bound cell surface material in the recovered embryos was also observed. However, the exact mechanism of the action of CH on the cell surface remains to be clarified.

Animals↗
PubMed1980

Striated muscle in four categories of leprosy. II. Fine structural changes.

Fine structural changes are described in 21 muscle biopsy specimens from patients with early and established tuberculoid or treated and untreated lepromatous leprosy. The predominant light microscopic finding on paraffin sections of atrophy of the muscle fiber was confirmed in semithin araldite sections, which also revealed considerable degenerative changes in a few or more fibers. These were more clearly seen in ultrathin sections, especially in the lepromatous muscle specimens. The degeneration was in the form of severe loss or disorganization of the myofibrillar elements and in the most affected muscle fiber, a loss of all sarcoplasmic constituents, with occasional accumulation of lipofuscin in lysosome-like bodies. Only 3 of the lepromatous specimens showed 1 and 2 bacilli each, only 1 being within a muscle fiber. There were also mural changes in the small intramuscular blood vessels with proliferation of their basement membrane and pericytes. The mean serum IgG level in lepromatous patients was significantly elevated. This, together with the vascular change, might perhaps be responsible for the degenerative change in the muscle fiber despite a paucity of M. leprae in the muscle.

Atrophy↗
PubMed1979

Lepromatous leprosy as a model of Schwann cell pathology and lysosomal activity.

A brief illustrated account is presented of the light microscopic pathology, histochemistry of lysosomal enzymes, and fine structural changes in the nerves of patients with untreated or treated lepromatous leprosy. Predominant bacillation of the Schwann cells of unmyelinated fibres, degeneration of their axons, prominence of phagolysosomes, and disappearance of these cells with endoneurial collagenosis were observed on electronmicroscopic examination of the index branch of the radial cutaneous nerve. Although there were changes in the blood vessels and proliferation of perineurium, bacillation of endothelial or perineurial cells was much less conspicuous. Intact and degenerating forms of M. leprae were found in both treated and untreated patients, fragmenting or crumpled forms being more frequent in the treated. Both groups of patients also showed increased lysosomal enzyme activity, evidenced by single or paired paranodal spots of acid phosphatase and beta-glucuronidase in Schwann cells in histochemical preparations of the nerve. There was lesser activity, and activity in fewer cells, in the case of beta-glucuronidase than of acid phosphatase. Diffuse beta-glucuronidase activity was found in the wall of empty-looking oval chambers in the Schwann cells, and acid-fast bacilli were seen in these chambers. In teased fibre preparations, both axonal degeneration and segmental demyelination were found. In semi-thin araldite sections, the myelinated fibre density was either preserved or reduced; large diameter fibres were more frequently depleted, with tall peaks of smaller fibres seen on plotting diameter spectra.

Axons↗
PubMed1979

Aspects of cuprogenic disorder in Wilson's Disease in India.

A brief account is given of some aspects of Wilson's disease in India, studied during the periods 1959 to 1967 and 1970 to 1978, with emphasis on disordered parameters of copper metabolism. Among the latter, serum copper oxidase (representing caeruloplasmin) was found to be the most constant laboratory evidence of Wilson's disease. It wad drastically lowered in all patients in both periods (25 and 44 patients respectively), when compared to its level in the parents and siblings of the patients, in other neurological patients and in normal subjects serving as controls. The other constantly involved parameter was direct-reacting serum copper which was highly significantly elevated in the patients compared to the other groups. Most of the patients presented with a predominantly neurological form of the disease, smaller groups presenting with predominantly osseomuscular or hepatic forms. The mean age of patients in both periods was approximately 13 years.

Adolescent↗
PubMed1979

Pathology and pathogenesis of chronic myelopathy in atlanto-axial dislocation, with operative or postoperative haematomyelia or other cord complications.

Pathological features are described, and clinico-pathological correlations are made, in 11 patients presenting the unusual combination of chronic compressive myelopathy of the upper cervical cord due to congenital atlanto-axial dislocation, and sudden haematomyelia and respiratory arrest developing at open surgery for release of pressure on the medullospinal tissues, or as a postoperative catstrophe. Necropsy and histological examination confirmed that the neuropathological substrate of intermittent or progressive quadriplegia and sensory changes (mainly deep sensory loss) was degeneration of the lateral and posterior columns. Loss of anterior horn cells of the lower cervical and upper dorsal cord led to weakness of hand and arm muscles. Acute paracentral haemorrhages occurring at the C1 to C2 or medullospinal level, in the territory of distribution of the sulcal branches of the spinal artery (due to sudden release of pressure at operation) were responsible for postoperative paralysis and sensory loss below C2 segment. In terms of the bony anomaly (dissected at necropsy), the cases fell into 2 sibgroups: a) The majority with the odontoid attached to the body of the axis, but short and ill developed, at times accompanied by other bony anomalies and a poorly formed transverse ligament. This tended to produce a fixed type of dislocation with a higher level (medullospinal) and more severe compression of the CNS. b) Fewer cases with a well formed but detached odontoid, producing a less severe myelopathy at a lower level (C1-C2), and generally more readily reducible on extension.

Adolescent↗
PubMed1977

Ultrastructural basis of the vasculopathy in and around brain tuberculomas. Possible significance of altered basement membrane.

The fine structure of small blood vessels in and around ten brain tuberculomas was examined. In the peripheral reactive zone of the tuberculomas, examination of 1-mu-thick survey sections established the chronic inflammatory process and the vasculitis characterized by infiltration of the vasomurium (vessel wall) by large and small mononuclear cells. This reaction was typical of chronic epithelioid cell granuloma. Electron microscopic examination of the reactive zone confirmed the vascular proliferation and vasculitis, the venule being the most frequently involved type of blood vessel. It showed the infiltrating cells to lie amidst osmiophilic, concentrically proliferated basement membrane laminae, which formed the greater part of the thickened vessel wall, generally surrounding the endothelial cells directly, the pericytes having disappeared. This appearance, together with the results of Gomori's reticulin stain on paraffin sections, suggested that the altered basement membrane material was reticulin. The possibility is discussed that the altered basement membrane material could be antigenic and that it might be responsible for perpetuating the necrotic vascular and perivascular reaction in tuberculous meningitis and tuberculomas. The above change in the basement membrane was not encountered in the blood vessels of the surrounding edematous brain. The endothelial cells and tight junctions were relatively well-preserved. Intact arterioles could be recognized even in severely edematous brain tissue. At both sites the fine structure of the blood vessels was typical of that expected in the central nervous system. Fenestrated vessels were not seen. The perivascular astrocytic end-feet were destroyed in the reactive zone and either distended or ruptured in the overtly edematous brain tissue also. In the central caseous part of the tuberculoma, there were few blood vessels, and they were in a state of advanced necrosis, but ghost outlines of proliferated basement membrane could be seen.

Adolescent↗
PubMed1976

Eales' disease with neurological involvement Part 1. Clinical features in 9 patients.

Nine patients with characteristic changes of Eales' disease in the eye in whom there was neurological involvement, have been described. The characteristic neurological picture comprised an acute or subacute myelopathy occurring at an interval of a few weeks to a few years after the eye episode; in only 1 patient was there cerebral involvement without any evidence of myelopathy. Besides the involvement of spinal cord at the dorsal level in the 8 patients, there was evidence of additional lesions in the brain stem in 1 patient and in the cervical cord in another.

Acute Disease↗
PubMed1976

Eales' disease with neurological involvement. Part 2. Pathology and pathogenesis.

Detailed neuropathologic examination was carried out on 1 case of Eales' disease with CNS involvement, in the form of retinal vasculopathy, followed first by signs of brain stem and cerebellar disease and then by a myelopathy, with death 4 years later from retinal infection. There was mild chronic inflammation in the retina, and sub-total demyelination of one optic nerve. The brain stem and cerebellum showed extensive vasculopathy, with various stages of venous change extending from proliferation and dilatation to haemorrhage, or to thickening with hyalinisation. The perivenular brain tissue, particularly of the cerebellum, often showed demyelination, with relative axon preservation, but no inflammation. Similar, but less pronounced venopathy was seen in the dorsal cord. There was ascending degeneration of Goll's columns and descending degeneration of the lateral columns.

Adult↗
PubMed1976

The B-vitamins in malnutrition with alcoholism. A model of intervitamin relationships.

1. The B-vitamin status of fifty-nine patients, mainly from the lower socio-economic classes in Bombay, with a history of chronic malnutrition, and of alcoholism of 1-5-20 years' duration, was studied before and during treatment, and in relation to their clinical, especially neurological, condition. These patients were divided into two neurological categories: (I) those with peripheral neuropathy (mainly sensory and distal) alone, (2) those with mental changes (mainly confusion and disorientation) also. Both categories frequently showed pellagrous pigmentation and mucocutaneous signs of B-vitamin deficiency. 2. Thiamin and erythrocyte transketolase (EC 2.2.1.1) activity, riboflavin, nicotinic acid, pantothenic acid, total and pyridoxal fraction of vitamin B6, folate and total vitamin B12 were estimated in the blood and the cerebrospinal fluid (CSF) of these patients, and also in the blood of sixty-nine control subjects and in the CSF of some of them. The concentrations of all the vitamins, except vitamin B12, were highly significantly lower in the blood of patients of category I compared to the controls, and erythrocyte transketolase activity and pyridoxal concentration in patients of category 2 were significantly lower than those of category I patients. Blood pantothenic acid and folate concentrations were reduced less consistently. 3. Serum vitamin B12 concentration was significantly increased (though within normal range) in the patients compared to the control group, probably because of the moderate hepatic insufficiency (as assessed by liver function tests) in the former. 4. The concentrations of thiamin, riboflavin, nicotinic acid and total vitamin B6 were also highly significantly lower in the CSF in patients of category I compared with controls. Furthermore, thiamin, nicotinic acid and total vitamin B6 concentrations were significantly lower in patients of category 2 than those of category I patients, indicating that CSF levels reflect better the neurological status of these patients. 5. There was a moderate increase in the blood concentration of all the vitamins tested, after a relatively poor hospital diet alone. There was a concurrent increase in the blood levels of thiamin, riboflavin, nicotinic acid and pantothenic acid after parenteral treatment with either thiamin or nicotinic acid. The administration of pyridoxine resulted in a significant increase in the blood levels of riboflavin and the pyridoxal fraction of vitamin B6.

Adult↗