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Biomedical subjects

M Munir

Publications and source records attributed to M Munir.

At least 19 recordsLinked to original sources
PubMed2003

Using flowering times and leaf numbers to model the phases of photoperiod sensitivity in Antirrhinum majus L.

A model has been developed that can be used to determine the phases of sensitivity to photoperiod for seedlings subjected to reciprocal transfers at regular intervals between long (LD) and short day (SD) conditions. The novel feature of this approach is that it enables the simultaneous analysis of the time to flower and number of leaves below the inflorescence. A range of antirrhinum cultivars were grown, all of which were shown to be quantitative long-day plants. Seedlings were effectively insensitive to photoperiod when very young (juvenile). However, after the end of the juvenile phase, SD delayed flowering and increased the number of leaves below the inflorescence. Plants transferred from LD to SD showed a sudden hastening of flowering and a decrease in leaf number once sufficient LD had been received for flower commitment. Photoperiod had little effect on the rate of flower development. The analysis clearly identified major cultivar differences in the length of the juvenile phase and the photoperiod-sensitive inductive phase in both LD and SD.

Antirrhinum↗
PubMed2000

Ameloblastoma of the jaws.

Ameloblastoma is a histologically benign tumor derived from odontogenic apparatus. The tumor can infiltrate into surrounding tissues. Although it is benign, it presents symptoms of a malignant tumor, such as infiltration into the lungs, pleura, regional and distant metastases, orbit, base of skull, brain and has resulted in death. It also has a high incidence of recurrences, the existence of regional or distant metastasis, showing a microscopic pattern of ameloblastic carcinoma with cytologic features of an increasing nuclear/cytoplastic ratio, nuclear hyperchromatism, and the presence of mitosis. We report a study of 12 patients of ameloblastoma of the jaws between January 1992 and December 1996 consisting of 8 affected in the mandible and 4 in the maxilla. One patient with a tumor in the maxilla was excluded from this study, due to a different histological and clinical behaviour of the ameloblastoma.

Adult↗
PubMed2000

Diagnosis of Clostridium difficile antibiotic associated diarrhoea culture versus toxin assay.

OBJECTIVE: To compare the results of Clostridium Difficile (CD) on culture with detection of C. difficile toxin by Enzyme Immunoassay (EIA) in the stool specimens of hospitalized patients with antibiotic associated diarrhoea (AAD). PATIENTS AND METHODS: The study included 80 adult patients with AAD and 20 adult patients with non-AAD. Stool specimens of all these subjects were inoculated on cycloserine cefoxitin fructose agar and incubated anaerobically to isolate C. difficile. At the same time, all the stool specimens were tested for C. difficile toxin by EIA technique using cytoclone A and B kit manufactured by Cambridge Biotech Corporation, Worcester, Massachusette. RESULTS: Out of 80 adult patients with AAD, thirty were females and fifty males. C. difficile was isolated on culture from stool specimen of 16 patients, while twenty-three stool specimens were positive for C. difficile toxin. From 20 control subjects, C. difficile was isolated from stool specimen of only one subject. No stool specimen from the controls was positive for toxin. CONCLUSION: Diagnosis of CDAAD by culture is difficult and time consuming because of strict anaerobic nature of organism. Moreover, mere isolation of C. difficile on culture is not sufficient to establish the pathogenic role of these isolates. C. difficile toxin detection by EIA technique is a highly sensitive and specific method for diagnosis of CDAAD. Using this method, results are available in three hours time. Therefore, EIA is recommended for rapid diagnosis of CDAAD.

Adolescent↗
PubMed1998

The glutamate transporter, GLT-1, is expressed in cultured hippocampal neurons.

There are multiple subtypes of Na+-dependent glutamate transporters. Several studies suggest that EAAC1 and EAAT4 are expressed in neurons, while GLT-1 and GLAST expression is thought to be restricted to glia. In the present study, expression of GLT-1 and EAAC1 was examined in cultured rat hippocampal neurons using single cell mRNA amplification and immunocytochemistry with subtype specific antibodies. GLT-1 and EAAC1 mRNAs were observed in all neurons examined. Neuronal phenotype was confirmed in these cells by expression of neurofilament (NF-L) mRNA and absence of glial fibrillary acidic protein (GFAP) mRNA. EAAC1 immunoreactivity was observed in essentially all cells which expressed neuron specific enolase (NSE) and GLT-1 immunoreactivity was detected in the majority (approximately 90%) of NSE-positive cells. Consistent with the glial expression of GLT-1, GLT-1 immunoreactivity was also observed in NSE-negative cells. These studies provide evidence that GLT-1 expression is not intrinsically restricted to glial cells, but can occur in neurons under certain circumstances.

ATP-Binding Cassette Transporters↗
PubMed1998

Regulation of the glial Na+-dependent glutamate transporters by cyclic AMP analogs and neurons.

Sodium-dependent transport into astrocytes is critical for maintaining the extracellular concentrations of glutamate below toxic levels in the central nervous system. In this study, the expression of the glial glutamate transporters GLT-1 and GLAST was studied in primary cultures derived from cortical tissue. In primary astrocytes, GLAST protein levels were approximately one half of those observed in cortical tissue, but GLT-1 protein was present at very low levels compared with cortical tissue. Maintenance of these astrocytes in medium supplemented with dibutyryl-cAMP (dbcAMP) caused a dramatic change in cell morphology, increased GLT-1 and GLAST mRNA levels approximately 5-fold, increased GLAST protein approximately 2-fold, and increased GLT-1 protein >/=8-20-fold. These increases in protein expression were accompanied by 2-fold increases in the Vmax and Km values for Na+-dependent L-[3H]glutamate transport activity. Although GLT-1 is sensitive to inhibition by dihydrokainate in heterologous expression systems, no dihydrokainate sensitivity was observed in astrocyte cultures that expressed GLT-1. Biotinylation with a membrane-impermeant reagent, separation of the biotinylated/cell surface proteins, and subsequent Western blotting demonstrated that both GLT-1 and GLAST were present at the cell surface. Coculturing of astrocytes with neurons also induced expression of GLT-1, which colocalized with the glial specific marker, glial fibrillary acidic protein. Neurons induced a small increase in GLAST protein. Several studies were performed to examine the mechanism by which neurons regulate expression of the glial transporters. Three different protein kinase A (PKA) antagonists did not block the effect of neurons on glial expression of GLT-1 protein, but the addition of dbcAMP to mixed cultures of neurons and astrocytes did not cause GLT-1 protein to increase further. This suggests that neurons do not regulate GLT-1 by activation of PKA but that neurons and dbcAMP regulate GLT-1 protein through convergent pathways. As was observed with GLT-1, the increases in GLAST protein observed in cocultures were not blocked by PKA antagonists, but unlike GLT-1, the addition of dbcAMP to mixed cultures of neurons and astrocytes caused GLAST protein to increase approximately 2-fold. Neurons separated from astrocytes with a semipermeable membrane increased GLT-1 protein, indicating that the effect of neurons was mediated by a diffusible molecule. Treatment of cocultures with high concentrations of either N-methyl-D-aspartate or glutamate killed the neurons, caused GLT-1 protein to decrease, and caused GLAST protein to increase. These studies suggest that GLT-1 and GLAST protein are regulated independently in astrocyte cultures and that a diffusible molecule secreted by neurons induces expression of GLT-1 in astrocytes.

ATP-Binding Cassette Transporters↗
PubMed1997

Gastric adenocarcinoma and dysplasia in fundic gland polyps of a patient with attenuated adenomatous polyposis coli.

Gastric adenocarcinoma has been previously recognized as a potential complication of familial adenomatous polyposis coli (APC) and attenuated forms of APC (AAPC). This tumor has only been reported to originate from adenomatous polyps of the gastric mucosa in these clinical conditions. There have been no previous case reports of gastric adenocarcinoma arising from the more commonly found fundic gland polyps associated with AAPC or APC. We report the first definitive case of gastric adenocarcinoma arising from a hyperplastic polyp of the fundis of a patient with AAPC.

Adenocarcinoma↗
PubMed1996

Pharmacological and immunological characterization of N-methyl-D-aspartate receptors in human NT2-N neurons.

NT2 cells are a clonal line of human teratocarcinoma cells that exhibit N-methyl-D-aspartate (NMDA) receptor-mediated excitotoxicity after terminal differentiation into NT2-N neurons. In this study, we used modulation of glutamate excitotoxicity to characterize the pharmacological properties and specific antibodies to determine the individual subunits of NMDA receptors expressed by NT2-N neurons. The glycine site antagonist 7-chlorokynurenic acid completely blocked glutamate toxicity in a dose-dependent manner. Histamine and the polyamine agonists spermine and spermidine enhanced glutamate toxicity in a dose-dependent manner consistent with expression of an NR1-NR2B combination of subunits. The efficacy of polyamine agonists suggests the expression of one or more splice variants of the NR1 subunit that lack the putative surface loop encoded by exon 5. Surprisingly, the putative inverse agonists diaminodecane and diaminododecane also enhanced toxicity in a dose-dependent manner. The antagonists arcaine and ifenprodil completely blocked glutamate toxicity in NT2-N cells. The atypical antagonist ifenprodil inhibited toxicity with a uniformly high affinity characteristic of interaction with the NR1-NR2B combination of subunits. Expression of both NR1 and NR2 subunits were detected by Western blot analysis. Neither protein was detectable in undifferentiated cells. In contrast, 70-fold lower levels of the NR2A subunit were detected in both differentiated and undifferentiated cells. The pharmacological and immunological results indicate that a functional NR1-NR2B combination of subunits is expressed by NT2-N neurons. Despite the immunological detection of NR2A subunit, no functional combination of NR1 and NR2A subunits could be demonstrated.

Animals↗
PubMed1996

Evaluation of dipstrips, direct gram stain and pyuria as screening tests for the detection of bacteriuria.

Two hundred and fifty cases of clinically suspected urinary tract infection were analysed for the detection of bacteriuria. Parameters studied included direct Gram staining, pyuria on microscopic examination of uncentrifuged urine and dip strip method for the detection of blood, protein, nitrite and leucocyte esterase. Significant bacteriuria (colony count 10(5) per ml) was found in 112 cases with a positivity ranging from 65 to 83% for the presence of blood, protein, nitrite and leucocyte esterase. Highest positive predictive values were obtained with the presence of nitrite and leucocyte esterase (98%), blood, protein and nitrite (94%) as well as with blood, protein, nitrite and leucocyte esterase (98%). Both pyuria and direct Gram staining were positive in 85% cases. The combined presence of both these parameters gave 100% positive predictive value. Gram staining combined with pyuria was more effective and economical as compared to the dipstrips for the detection of bacteriuria.

Bacteriological Techniques↗
PubMed1995

Excitotoxic cell death and delayed rescue in human neurons derived from NT2 cells.

The excitotoxic response of NT2-N cells, a clonal line of human teratocarcinoma cells that are terminally differentiated into neuron-like cells, was examined using several endpoints. A 15 min exposure to glutamate produced a dose-dependent toxicity with a maximal cell loss of 80-90% in 6 week old cells. The rapidly triggered excitotoxicity induced by glutamate was blocked by NMDA selective antagonists, was calcium dependent and pH sensitive and could be mimicked by NMDA but not by non-NMDA agonists, AMPA, kainate or quisqualate. The non-NMDA agonists however caused toxicity on prolonged exposure. The NMDA receptor modulators glycine and spermidine enhanced glutamate-mediated toxicity whereas ifenprodil potently and completely inhibited toxicity suggesting that the toxic response is mediated by the NR1/NR2B combination of NMDA subunits. These cells can be rescued from death up to 1 hr after removal of glutamate by NMDA receptor blockade, removal of extracellular Ca2+ or lowering of pH. The extent of rescue is directly related to the time elapsed before intervention. Blockage of NMDA receptor activity for 1 hr immediately after removal of glutamate is both necessary and sufficient for complete rescue. Glutamate-mediated toxicity was not prevented by nitric oxide synthase inhibitors nor was nitric oxide synthase detected in NT2-N cells indicating that nitric oxide is not required for glutamate-mediated excitotoxicity. In summary, NT2-N cells exhibit a robust excitotoxic response and represent a novel model system in which to study the molecular basis of excitotoxic cell death.

2-Amino-5-phosphonovalerate↗
PubMed1993

Polyamines modulate the neurotoxic effects of NMDA in vivo.

The ability of polyamines to alter NMDA-induced neurotoxicity in neonatal rats was examined to determine whether polyamines modulate NMDA receptor activity in vivo. Unilateral injections of NMDA and/or polyamines were made into the striatum of 7-day-old rats. After 5 days, the brains were removed and 20 microns thick coronal sections were cut and stained with Cresyl violet. A computer-based image analysis system was used to densitometrically measure the cross-sectional area of intact tissue in the control and injected hemispheres. Administration of NMDA (5-40 nmol) produced a dose-dependent tissue damage that ranged from 7 to 52% of the area of the uninjected hemisphere. The polyamine agonist spermine (10-500 nmol) dose-dependently exacerbated the toxicity of a 15 nmol dose of NMDA, increasing the size of the lesion by up to 50%. Administration of spermine alone produced dose-dependent tissue damage that ranged from 9 to 52%. The damage produced by both NMDA and spermine could be completely inhibited by co-administration of the NMDA antagonist MK-801. The polyamine inverse agonist 1,10-diaminodecane (DA-10, 50-400 nmol) inhibited the damage produced by NMDA in a dose-dependent manner, with a maximal inhibition of 50%. Administration of DA-10 alone produced limited damage at doses above 100 nmol. The weak partial agonist diethylenetriamine had no effect by itself or on NMDA-induced toxicity at the doses tested. These results indicate that polyamines can modulate the activity of NMDA receptors in vivo and suggest that polyamines or related compounds may have important therapeutic potential as neuroprotective agents.

Animals↗
PubMed1992

Multiple mechanisms for inhibition of excitatory amino acid receptors coupled to phosphoinositide hydrolysis.

Excitatory amino acid (EAA) analogues activate receptors that are coupled to the increased hydrolysis of phosphoinositides (PIs). In these studies, hippocampal slices were prepared from neonatal rats (6-11 days old) to characterize the effects of EAA analogues on these receptors. The concentrations of ibotenate and trans-(+/-)-1-amino-1,3-cyclopentanedicarboxylate (trans-ACPD) required to evoke half-maximal stimulation (EC50 values) were 28 and 51 microM, respectively. Although the data for stimulation of PI hydrolysis by ibotenate and trans-ACPD were best fit to theoretical curves that had Hill slopes of 1, data for stimulation of PI hydrolysis by quisqualate were best fit to two sites. The EC50 values were 0.43 and 44 microM. The high-affinity sites were 70% of the total. A number of EAA analogues were tested for inhibition of PI metabolism. One of these, L-aspartate-beta-hydroxamate (L-A beta HA), was identified as a novel inhibitor of this response. L-A beta HA was equipotent as an inhibitor of PI metabolism stimulated by ibotenate, quisqualate, and trans-ACPD. The data for this inhibition were best fit to two sites. Between 32 and 48% of the total sites had high affinity with IC50 values in the range of 1.2-6.3 microM. The low-affinity sites had IC50 values between 610 and 2,700 microM. DL-2-Amino-3-phosphonopropionate (DL-AP3) was also equipotent as an inhibitor of PI hydrolysis stimulated by ibotenate, quisqualate, and trans-ACPD (IC50 values were 480-850 microM). In contrast to the data for L-A beta HA, the data for DL-AP3 were best fit to a single site. Both of these inhibitors reduced the maximal response caused by the agonists, consistent with noncompetitive mechanisms of action. Several experiments were designed to examine potential mechanisms for these noncompetitive effects. These studies suggest that either L-A beta HA and DL-AP3 bind to a site on the receptor and irreversibly block activation of the receptor, or that these inhibitors act via a distinct site that specifically regulates EAA receptors coupled to PI hydrolysis.

Alanine↗
PubMed1989

Evaluation of the gastric antiulcerogenic effects of Solanum nigrum, Brassica oleracea and Ocimum basilicum in rats.

Antiulcerogenic activities of three plant drugs were studied against aspirin-induced gastric ulcers in rats. In addition, their effects on output of gastric acid and pepsin and hexosamine concentrations in gastric fluid were recorded in ulcerated and non-ulcerated rats. Solanum nigrum (aerial parts) powder and its methanolic extract decreased the ulcer index significantly. The activity may be due to inhibition of acid and pepsin secretions and/or their in vitro ability to bind these. Brassica oleracea (leaf) powder did not affect the ulcer index significantly but its aqueous extract lowered the index and increased hexosamine levels, suggesting gastric mucosal protection. Ocimum basilicum (aerial parts) powder and its aqueous and methanolic extracts decreased the index. Moreover, the acid output was decreased by its methanolic extract while hexosamine secretion was enhanced. This suggests that its antiulcerogenic effect is due to decreases of acid and pepsin outputs which enhance gastric mucosal strength. The reference drug gefarnate decreased the ulcer index by increasing the hexosamine level only. Cimetidine inhibited the acid production but did not decrease the ulcer index.

Animals↗
PubMed1987

Visual perceptual disorders resembling the Charles Bonnet syndrome. A study of 434 consecutive patients referred to a psychogeriatric unit.

In a retrospective study of 434 consecutive patients referred for consultation to a psychogeriatric unit over a period of 3.5 years, the diagnostic categories of the group were recorded, and in this paper their management is briefly discussed. Eight cases of visual perceptual disorders resembling the Charles Bonnet syndrome in elderly patients are described. Three significant findings emerged for these eight patients; the preponderance of female to male patients, the presence of eye pathology with poor vision, and the high mean age of 83.8 years.

Aged↗
PubMed1985

A point survey of periurban and urban malaria in Karachi.

A point survey of malaria in Karachi revealed a concentration of malaria cases in the periurban perimeter and marginal areas where immigrating groups, including Afghan refugees and Biharis from Bangladesh are concentrated. Populations of Anopheles stephensi, Karachi's main vector, were low, and were feeding chiefly on buffaloes which are also concentrated along the periurban perimeter. Maintenance of malaria transmission in periurban zones may depend on immigration of susceptibles, bovid hosts which help maintain zoophilic vector populations, and mosquito breeding sites in water tanks or buffalo hoofprints. The vector's switch to man-biting behaviour may occur either due to a 'spillover' effect from buffalo corrals to surrounding houses, or when buffaloes become less available for biting. Four types of chromosome inversions were found in the Karachi An. stephensi; as this species is not a vector in similar habitats in Lahore and Pondicherry where such inversions are not prevalent, it is likely that its status as a vector is related to chromosomal polymorphism influencing behaviour.

Adolescent↗
PubMedDate not supplied

Substrate-induced up-regulation of Na(+)-dependent glutamate transport activity.

Sodium-dependent transporters regulate extracellular glutamate in the CNS. Recent studies suggest that the activity of several different neurotransmitter transporters can be rapidly regulated by a variety of mechanisms. In the present study, we report that pre-incubation of primary 'astrocyte-poor' neuronal cultures with glutamate (100 microM) for 30 min nearly doubled the V(max) for Na(+)-dependent accumulation of L-[(3)H]-glutamate, but had no effect on Na(+)-dependent [(3)H]-glycine transport. Pre-incubation with glutamate also increased the net uptake of non-radioactive glutamate, providing evidence that the increase in accumulation of L-[(3)H]-glutamate was not related to an increase in intracellular glutamate and a subsequent increase in exchange of intracellular non-radioactive glutamate for extracellular radioactive glutamate. The glutamate receptor agonists, alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate, quisqualate, and (1 S, 3R)-1-aminocyclopentane-1,3-dicarboxylic acid did not mimic the effect of pre-incubation with glutamate and the glutamate-induced increase was not blocked by receptor antagonists. However, compounds known to interact with the transporters, including L-aspartate, D-aspartate, L-(-)-threo-3-hydroxyaspartate (L-THA) and L-trans-pyrrolidine-2,4-dicarboxylate (L-trans-PDC), caused variable increases in transport activity and attenuated the increase induced by glutamate, suggesting that the increase is related to the interaction of glutamate with the transporters. Several studies were attempted to define the mechanism of this regulation. We found no evidence for increases in transporter synthesis or cell surface expression. Inhibitors of signaling molecules known to regulate other neurotransmitter transporters had no effect on this stimulation. Using a variety of cultures, evidence is provided to suggest that this substrate-induced up-regulation of glutamate transport is specific for the GLT-1 and GLAST subtypes and does not influence transport mediated by EAAC1. These studies suggest that the interaction of glutamate with some of the subtypes of glutamate transporters causes an increase in transport activity. Conceivably, this phenomenon provides an endogenous mechanism to increase the clearance of glutamate during periods of prolonged elevations in extracellular glutamate.

ATP-Binding Cassette Transporters↗