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Biomedical subjects

V Malhotra

Publications and source records attributed to V Malhotra.

At least 91 records · Page 5Linked to original sources
PubMed1994

Infantile histiocytoid cardiomyopathy: three cases and literature review.

A review is presented of the clinical and cardiac morphologic findings in 50 previously reported and 3 new patients with histiocytoid cardiomyopathy. This disorder occurs in infants and small children and is characterized clinically by severe and often fatal arrhythmias and morphologically by focal collections of altered myocytes that are roundshaped and resemble histiocytes. Sixteen patients had yellowish nodules on the endocardium, epicardium, and/or valves; the other 37 had foci of abnormal myocytes throughout the myocardium. These cells were remarkably similar in all patients and had poorly developed or absent intercellular junctions, few or no contractile elements, and markedly increased numbers of mitochondria, which imparted a granular or vacuolated appearance to the cytoplasm. There was a high prevalence of anomalies involving the nervous system and eyes and of oncocytic cells in various glands. Evidence is presented to exclude the possibilities that the disorder represents a developmental anomaly of the atrioventricular conduction system, a multifocal tumor of Purkinje cells, a developmental arrest of cardiac myocytes, and a diffuse type of mitochondrial cardiomyopathy. Histiocytoid cardiomyopathy is considered to be the result of hamartoma-like aggregations of cardiac myocytes with features similar to those of oncocytes. This syndrome is likely caused by prenatal myocardial or systemic (viral?) injury. Surgical excision of nodules of histiocytoid cells can result in clinical remission.

Cardiomyopathies↗
PubMed1994

Golgi spectrin: identification of an erythroid beta-spectrin homolog associated with the Golgi complex.

Spectrin is a major component of a membrane-associated cytoskeleton involved in the maintenance of membrane structural integrity and the generation of functionally distinct membrane protein domains. Here, we show that a homolog of erythrocyte beta-spectrin (beta I sigma*) co-localizes with markers of the Golgi complex in a variety of cell types, and that microinjected beta-spectrin codistributes with elements of the Golgi complex. Significantly, we show a dynamic relationship between beta-spectrin and the structural and functional organization of the Golgi complex. Disruption of both Golgi structure and function, either in mitotic cells or following addition of brefeldin A, is accompanied by loss of beta-spectrin from Golgi membranes and dispersal in the cytoplasm. In contrast, perturbation of Golgi structure without a loss of function, by the addition of nocodazole, results in retention of beta-spectrin with the dispersed Golgi elements. These results indicate that the association of beta-spectrin with Golgi membranes is coupled to Golgi organization and function.

Animals↗
PubMed1994

Human giardiasis. A morphometric study of duodenal biopsy specimens in relation to the trophozoite count in the duodenal aspirate.

We present a morphometric analysis of findings from a histopathologic study of duodenal giardiasis in relation to the trophozoite count in the duodenal aspirate. Of 30 patients with giardiasis whose conditions were studied, a mean trophozoite count of 10(3)/mL or greater was found in 21, and a mean trophozoite count of less than 10(3)/mL was found in nine--these two types of trophozoite counts in these 30 patients represented the acute phase (group 1) and the clearance phase (group 2) of giardiasis, respectively. Group 1 patients had a low mean villus height that was significantly less than that found in the control subjects. Group 2 patients had a high mean crypt depth that was significantly greater than that found in the control subjects. Partial villus atrophy was seen in only seven of the group 1 patients, including five with villus epithelial cell lesions. Groups 1 and 2 showed minor differences of an inflammatory response that was significantly greater than that shown in the control subjects.

Adult↗
PubMed1993

Role of alpha 1-adrenergic receptors in the intermediolateral column in mediating the pressor responses elicited by the stimulation of ventrolateral medullary pressor area.

Microinjections of alpha 1-adrenergic receptor agonists into the intermediolateral cell column of the spinal cord (IML) elicit sympathoexcitatory responses. This observation, together with the identification of projections of epinephrine-containing cells in the rostral ventrolateral medullary pressor area (VLPA) to the IML, has prompted speculation that epinephrine may mediate pressor responses to the stimulation of the VLPA. This hypothesis was tested in pentobarbital-anesthetized, artificially ventilated, male Wistar rats. A mesenteric arterial branch was cannulated for monitoring blood pressure. Pressor responses were elicited predominantly from T8-T10 by injections (1.7 nmol/20 nl) of L-glutamate into the IML; maximum pressor responses (29.3 +/- 4 mmHg) were elicited from T9. Pressor responses were also elicited by injections of epinephrine into the IML at T9; maximum pressor effect (16.3 +/- 1.2 mmHg) was elicited by a dose of 0.05 pmol/20 nl. This effect of epinephrine at T9 was blocked by prior injections of prazosin (a selective alpha 1-adrenergic receptor blocker; 0.125 pmol/20 nl) at the same site. Stimulation of the VLPA by unilateral microinjections of glutamate elicited pressor responses (56 +/- 12 mmHg). Bilateral injections of prazosin at T8-T10, in the dose (0.125 pmol) that blocked a maximally effective dose of epinephrine, did not block the pressor responses to subsequent injections of glutamate into the VLPA. On the other hand, bilateral microinjections of AP-7 (an NMDA receptor blocker; 1 nmol/20 nl), but not DNQX (10 pmol; a non-NMDA receptor blocker), into the IML at T8-T10 blocked the pressor effects of the subsequent injections of glutamate into the VLPA.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Glands↗
PubMed1993

Complete vesiculation of Golgi membranes and inhibition of protein transport by a novel sea sponge metabolite, ilimaquinone.

We have identified a novel natural metabolite, ilimaquinone (IQ), from sea sponges that causes Golgi membranes to break down completely in vivo into small vesicular structures (called vesiculated Golgi membranes [VGMs]). Under these conditions, transport of newly synthesized proteins from endoplasmic reticulum (ER) to the cis-Golgi-derived VGMs is unaffected; however, further transport along the secretory pathway is blocked. Upon removal of the drug, VGMs reassemble rapidly into a Golgi complex, and protein transport is restored. By employing a cell-free system that reconstitutes vesicular transport between successive Golgi cisternae, we provide evidence that the inhibition of protein transport by IQ is specifically due to an inhibition of transport vesicle formation. In addition, like brefeldin A (BFA), IQ treatment prevents the association of beta-COP and ADP-ribosylation factor to the Golgi membranes; however, unlike BFA treatment, there is no retrograde transport of Golgi enzymes into ER.

Animals↗
PubMed1993

Microtubule independent vesiculation of Golgi membranes and the reassembly of vesicles into Golgi stacks.

We have recently shown that ilimaquinone (IQ) causes the breakdown of Golgi membranes into small vesicles (VGMs for vesiculated Golgi membranes) and inhibits vesicular protein transport between successive Golgi cisternae (Takizawa et al., 1993). While other intracellular organelles, intermediate filaments, and actin filaments are not affected, we have found that cytoplasmic microtubules are depolymerized by IQ treatment of NRK cells. We provide evidence that IQ breaks down Golgi membranes regardless of the state of cytoplasmic microtubules. This is evident from our findings that Golgi membranes break down with IQ treatment in the presence of taxol stabilized microtubules. Moreover, in cells where the microtubules are first depolymerized by microtubule disrupting agents which cause the Golgi stacks to separate from one another and scatter throughout the cytoplasm, treatment with IQ causes further breakdown of these Golgi stacks into VGMs. Thus, IQ breaks down Golgi membranes independently of its effect on cytoplasmic microtubules. Upon removal of IQ from NRK cells, both microtubules and Golgi membranes reassemble. The reassembly of Golgi membranes, however, takes place in two sequential steps: the first is a microtubule independent process in which the VGMs fuse together to form stacks of Golgi cisternae. This step is followed by a microtubule-dependent process by which the Golgi stacks are carried to their perinuclear location in the cell. In addition, we have found that IQ has no effect on the structural organization of Golgi membranes at 16 degrees C. However, VGMs generated by IQ are capable of fusing and assembling into stacks of Golgi cisternae at 16 degrees C. This is in contrast to the cells recovering from BFA treatment where, after removal of BFA at 16 degrees C, resident Golgi enzymes fail to exit the ER, a process presumed to require the formation of vesicles. We propose that at 16 degrees C there may be general inhibition in the process of vesicle formation, whereas the process of vesicle fusion is not affected.

Animals↗
PubMed1993

Rectal histopathology in endemic Shigella and Salmonella diarrhea.

Rectal histopathology was evaluated in 34 cases (2 months-12 yrs old) of endemic "invasive diarrhea" [> 20 WBCs per high-power field on stool microscopy with (RBC positive) or without (RBC negative) associated RBCs] where S. dysenteriae (n = 9), S. flexneri (n = 11), and nontyphoidal Salmonella were isolated as the sole identifiable enteropathogens. Persistent diarrhea (> 14 days duration) was more common with Salmonella infection whereas RBC-positive "invasive diarrhea" was more frequent with Shigella, particularly S. dysenteriae (all cases) infection. The histopathological profile was comparable to the earlier descriptions of infective colitis to a large extent and the nature of the infecting organism could not be determined on the basis of rectal histology alone. The other noteworthy features were as follows: (i) mild crypt distortion (26%) and branching (21%) in both Shigella and Salmonella infection; in Salmonella infection, dilation of the glands was significantly greater with persistent diarrhea; (ii) presence of chronic inflammatory cells either alone or in combination with neutrophils in 62%; a predominant neutrophilic response was significantly higher with S. dysenteriae infection and an acute presentation; (iii) pseudomembrane formation (six subjects; 18%) especially in S. dysenteriae (four cases); and (iv) a significant association of neutrophilic response, edema, and neutrophils within the vessels in the lamina propria and mucin depletion in the glands with RBC-positive "invasive diarrhea."

Ampicillin↗
PubMed1992

Human giardiasis: correlation of specific secretory IgA levels in duodenal fluid to the severity of disease and infestation by Giardia lamblia.

Giardia lamblia specific secretory immunoglobulin A (sIgA) levels in the duodenal fluid of adult giardiasis cases are reported for the first time. The sIgA levels in the study group were found to be significantly higher (p less than 0.01) than in the 20 age- and sex-matched controls comprising cases classified as non-ulcerative dyspepsia who did nor reveal any G. lamblia in their stools and the duodenal fluid. An inverse relationship between the clinical severity of giardiasis and the level of sIgA in the duodenal fluid was noted. Cases with a higher trophozoite load in duodenal aspirate tended to be associated with envanescent G. lamblia-specific antibodies.

Adult↗
PubMed1992

Solitary rectal ulcer syndrome.

Solitary rectal ulcer syndrome (SRUS) clinically presents with rectal bleed. Twenty three cases of SRUS are described highlighting that it is a distinct clinicopathological entity which can be diagnosed in the presence of typical clinical features, sigmoidoscopic findings and histopathological appearance of mucosal biopsy.

Adolescent↗
PubMed1991

Displacement of apolipophorin III from the surface of low density lipophorin by human apolipoprotein A-I.

A hybrid low density lipophorin particle (LDLp) was prepared by incubation with human apolipoprotein (apo) A-I in vitro. ApoA-I associated with LDLp in a concentration dependent, saturable manner which was accompanied by dissociation of apolipophorin III (apoLp-III). The apoA-I hybrid LDLp had the same lipid composition, density and morphology as native LDLp indicating that displacement of apoLp-III by apoA-I did not affect its structural properties. The molar ratio of apoLp-I:apoLp-II:apoLp-III was maximally reduced from 1:1:16 to 1:1:2 in native versus hybrid LDLp with the latter particle binding 7 molecules of apoA-I. The inability of apoA-I to displace the remaining 2 apoLp-III supports the concept that these apoLp-III molecules are not equivalent to the other fourteen. Native and hybrid LDLp particles were both metabolized to high density lipophorin in vivo. The displacement reaction represents a novel method for the production of apolipoprotein hybrids of LDLp and the results indicate that apoA-I has an inherently higher affinity for lipid surfaces than apoLp-III.

Animals↗