Lipoma in fossa of Rosenmüller.
We report the first case of a lipoma originating in the fossa of Rosenmüller. Although lipomas are a common benign tumour in the body, lipomas of the nasopharynx are rare.
Adult↗
Biomedical subjects
M Tariq
Publications and source records attributed to M Tariq.
Penetrating neck injury: case report and evaluation of management.
Greater urban violence has resulted in an increased incidence of penetrating neck trauma. Penetrating neck wounds can present difficult diagnostic and therapeutic dilemmas. The evaluation and management of such injuries, however, remains controversial. There is no universally accepted specific approach to the management of patients with penetrating neck injuries, with some surgeons advocating mandatory neck exploration whilst others believe in selective surgical intervention. We believe that an equal willingness for both conservative and surgical intervention as dictated by serial bedside evaluation with adequate radiological and endoscopic support can provide the clinician a safe and effective means of managing a potentially complex and lethal problem.
Adult↗
Pleomorphic adenoma of the retropharyngeal space: a rare location.
A case of an isolated pleomorphic adenoma of the retropharyngeal space is reported, this has not been documented previously in the literature. Attention is drawn to the wide spectrum of benign and malignant neoplasms that can potentially occur within this complex anatomical region. The importance of a systematic and logical approach to the management of such lesions is emphasized.
Adenoma, Pleomorphic↗
Effect of aluminum on neurological recovery in rats following spinal cord injury.
OBJECT: This investigation was undertaken to study the effect of aluminum on neurobehavioral, electrophysiological, structural, and biochemical changes in rats following spinal cord injury (SCI). METHODS: Adult male Sprague-Dawley rats classified into different groups were given aluminum sulfate-dosed drinking water in the concentrations of 0%, 0.25%, 0.5% and 1%, respectively. After 30 days of aluminum treatment, the animals were subjected to spinal cord trauma. Laminectomy was performed at T7-8 in anesthetized rats, followed by placement of a compression plate (2.2 x 5 mm) loaded with a 35-g weight over the exposed spinal cord for 5 minutes. Control animals underwent the same surgical procedure, but the compression injury was not induced (sham). Postoperative neurological function was assessed using the inclined-plane test and by obtaining a modified Tarlov score and vocal/sensory score daily for 10 days. Electrophysiological changes were assessed using corticomotor evoked potentials, whereas pathological changes were assessed by light microscopy. The level of vitamin E in the spinal cord was measured as an index of antioxidant defense. The behavioral, biochemical, and histological analyses were performed in a blinded fashion. CONCLUSIONS: Analysis of results obtained in the behavioral studies revealed that the compression of spinal cord produced transient paraparesis in which a maximum motor deficit occurred at Day 1 following SCI and resolved over a period of 10 days. Administration of aluminum significantly impaired the recovery following SCI. Analysis of the results of the biochemical, electrophysiological, and histopathological studies also confirmed the deleterious effects of aluminum on recovery from SCI in rats.
Aluminum↗
Identification of a novel fusion gene involving hTAFII68 and CHN from a t(9;17)(q22;q11.2) translocation in an extraskeletal myxoid chondrosarcoma.
A proportion of extraskeletal myxoid chondrosarcomas (EMC) have been shown to have a characteristic translocation t(9;22)(q22;q12) involving the EWS gene at 22q12 and the CHN orphan nuclear receptor gene at 9q22. This translocation appears to be largely specific for EMC, but has not been detected in all such tumours. We report here a case of EMC with a t(9;17)(q22;q11.2) as the sole chromosome abnormality. We have determined that the translocation results in the fusion of the entire coding region of CHN to the N-terminal transactivation domain of RBP56/hTAFII68. This is the first report of a translocation involving RBP56/hTAFII 68, a protein with sequence homology to both EWS and TLS/FUS. The involvement of RBP56/hTAFII68 may explain some unusual features of the tumour.
Amino Acid Sequence↗
Nitric oxide synthase inhibitor aminoguanidine potentiates iminodipropionitrile-induced neurotoxicity in rats.
This investigation was undertaken to study the effect of nitric oxide synthase inhibitor, aminoguanidine on iminodipropionitrile (IDPN)-induced neurobehavioral and vestibular toxicity in rats. The dyskinetic syndrome was produced in male Wistar rats by i.p. injections of IDPN (100 mg/kg) for 6 days. Aminoguanidine was administered orally in the doses of 50, 150 and 300 mg/kg, 60 min before IDPN in three different groups. Control rats received vehicle only, whereas another group was treated with 300 mg/kg of aminoguanidine alone (without IDPN). Our results showed that aminoguanidine significantly and dose dependently exacerbated the incidence and intensity of IDPN-induced dyskinetic head movements. Aminoguanidine potentiated IDPN-induced loss of air righting reflex. The histopathological examination of inner ear showed aggravation of IDPN-induced degeneration of sensory hair cells in the crista ampullaris by aminoguanidine. These results suggest the role of nitric oxide in IDPN-induced neurobehavioral and vestibular toxicity.
Administration, Oral↗
Mapping of autosomal dominant progressive external ophthalmoplegia to a 7-cM critical region on 10q24.
OBJECTIVE: To map the gene responsible for autosomal dominant progressive external opthalmoplegia. BACKGROUND: The pathogenesis of progressive external ophthalmoplegia (PEO) can be associated with multiple deletions of mitochondrial DNA (mtDNA). PEO may show autosomal dominant (adPEO) or autosomal recessive (arPEO) patterns of inheritance, indicating that the genetic defect has a Mendelian basis and most likely involves a nuclear gene encoding a protein that interacts with the mitochondrial genome. adPEO is heterogeneous genetically, and thus far disease loci have been identified on chromosomes 3 and 10. The locus on chromosome 10q23-q25 was assigned by linkage analysis in a single Finnish family. METHODS: Samples from a large Pakistani family with adPEO, in which clinical symptoms are bilateral ptosis, limitations of eye movements, and varying degrees of proximal muscle weakness, were collected. Muscle biopsy and mtDNA rearrangement analysis was used to confirm the diagnosis. Genomewide linkage analysis was set up using a set of 391 microsatellite markers. RESULTS: The muscle biopsy from an affected member showed ragged red fibers, increased succinic dehydrogenase staining, lack of cytochrome oxidase activity, and multiple deletions of mtDNA. The disease locus was mapped to 10q23.31-q25.1 by linkage analysis, and a maximum lod score of 5.72 was obtained with D10S1267. CONCLUSION: By analysis of meiotic recombinations in affected individuals, the critical region was restricted to the 7-cM interval between D10S198 and D10S1795.
Adult↗
Protection by 2-deoxy-D-glucose against beta,beta'-iminodipropionitrile-induced neurobehavioral toxicity in mice.
This investigation was undertaken to study the effect of 2-deoxy-D-glucose (2-DG) on beta, beta'-iminodipropionitrile (IDPN)-induced neurobehavioral toxicity in mice. Animals were divided into five groups of nine animals each. One of the groups served as control and received vehicle only, whereas the remaining four groups were treated with IDPN (250 mg/kg, i.p.) daily for 11 days. 2-DG was injected intraperitoneally in the doses of 0 (vehicle only), 100, 300, and 600 mg/kg daily 30 min before IDPN administration. The animals were observed for dyskinetic behavior including vertical (retrocollis) and horizontal (laterocollis) head movements and circling. Twenty-four hours after the last dose of IDPN, the animals were sacrificed by decapitation and striata were isolated from the brain for the analysis of serotonin (5-HT). Our results showed that 2-DG significantly and dose dependently attenuated the incidence and severity of IDPN-induced neurobehavioral toxicity. Administration of 2-DG also protected mice against IDPN-induced increase in striatal 5-HT levels. Further studies are warranted to investigate the neuroprotective mechanism of 2-DG against IDPN-induced neurotoxicity.
Animals↗
Effect of acrylamide on neurological recovery following spinal cord injury in rats.
Acrylamide (ACR) is a cumulative neurotoxin which causes axonal degeneration in animals and man. Industrial workers exposed to ACR have been reported to suffer from a variety of central and peripheral neuropathological symptoms including numbness of hands and feet, skin peeling and muscular weakness of legs. These reports suggest that the body burden of ACR may be a risk factor in recovery patterns following neurotrauma. The present study was designed to assess the effect of ACR on neurological recovery following spinal cord injury (SCI) in rats. Male Sprague-Dawley rats weighing 200-230 g were anaesthetised with chloral hydrate and laminectomy was performed at T 7-8 level leaving the dura intact. A compression plate (2.2 x 5.0 mm) loaded with a weight of 35 g was placed on the exposed cord for 5 minutes. Animals were divided into seven groups of eight rats each. The animals in Group 1 served as control whereas rats in Group 2 underwent laminectomy alone (sham). The rats in Group 3 to 6 were subjected to SCI as mentioned above. Animals in Groups 4, 5 and 6 also received ACR in the doses of 10 mg/kg, 20 mg/kg and 40 mg/kg, i.p., respectively in addition to SCI, whereas the rats in Group 7 received ACR alone at a dose of 40 mg/kg body weight. The first dose of ACR was given 30 minutes before SCI, followed by daily administration of drug for 7 days. Post traumatic neurological recovery was recorded daily for 10 days using a modified Tarlov score, inclined plane test and sensory and vocal score. Electrophysiological changes were assessed using somatosensory and corticomotor evoked potentials. The animals were sacrificed at different time intervals and the injured site of the spinal cord was analysed for lipid hydroperoxides (LPH), conjugated dienes (CD) and glutathione (GSH). Neuropathological changes in the spinal cord were assessed using light microscopy. The rats exposed to compression injury alone showed a maximum neurological deficit at 24 hr and then a gradual recovery was observed over a period of 10 days. The rats treated with ACR along with SCI showed poor or no recovery over a period of 10 days. Our electrophysiological and histopathological studies also confirmed that concomitant exposure to ACR produces a significant deleterious effect on the recovery from SCI. SCI induced increase in oxidative stress (increase in LPH and CD and decrease in GSH) is also exacerbated by ACR suggesting a role of free radicals. The results of this study suggest that increased body burden of ACR may retard the recovery from neurotrauma or even lead to permanent disability.
Acrylamide↗
N-acetylcysteine attenuates cyclosporin-induced nephrotoxicity in rats.
BACKGROUND: Cyclosporin (CsA) has played an important role in the improvement of solid-organ transplant patients and graft survival. However, nephrotoxicity due to CsA remains an important clinical challenge. The renal toxicity of CsA is attributed to reduced renal blood flow which leads to hypoxia reoxygenation injury accompanied by excessive generation of oxygen-derived free radicals (ODFR). N-acetyl-L-cysteine (NAC) is a highly potent antioxidant that has been shown to reduce ODFR injury. In this study an attempt was made to assess the effect of NAC on CsA-induced lipid peroxidation and nephrotoxicity. METHODS: Adult Sprague-Dawley rats were treated orally with CsA (25 and 50 mg/kg) alone and in combination with different doses of NAC (10, 20 and 40 mg/kg) for a period of 3 weeks. Twenty-four hours after the last treatment, animals were sacrificed and blood was analysed for blood urea nitrogen (BUN) and serum creatinine (SCr), and kidney samples were analysed for lipid hydroperoxides, conjugated dienes and glutathione, and histopathological changes. RESULTS: Treatment of rats with CsA produced a significant increase in BUN and SCr level and histological abnormalities. CsA-induced impairment of renal toxicity was accompanied by significant increase in renal oxidative stress. NAC treatment significantly protected animals against CsA-induced structural and functional impairment of kidney. CONCLUSIONS: CsA-induced nephrotoxicity was significantly attenuated by NAC. This study clearly suggests the role of oxidative stress in the pathogenesis of CsA-induced nephrotoxicity. Concomitant use of antioxidants such as NAC to minimize CsA-induced nephrotoxicity in humans warrant further studies.
Acetylcysteine↗
Aluminum exacerbates cyclosporin induced nephrotoxicity in rats.
Cyclosporin (CSA) has been universally used as an immunosuppressant for the management of allotransplantation and autoimmune diseases. However, nephrotoxicity of CSA limits its use to optimum level. Aluminum (Al) is an extensively distributed element in the environment and human exposure to this metal is unavoidable. Recent studies suggest that even a slight impairment of renal function may increase the Al body burden significantly, which may lead to neurotoxicity, nephrotoxicity, osteodystrophy or hypochromic anemia. In the present study, an attempt was made to study the effect of concomitant use of Al and CSA on structure and function of kidney in rats. This study was undertaken in two steps. In the first set of experiments, the effect of single dose of Al (1% Al2(SO4)3 18H2O) on the nephrotoxicity of multiple doses of CSA (12.5 mg/kg, 25 mg/kg and 50 mg/kg) was studied, where as in the second set of experiments the effect of multiple doses of Al (0.25%, 0.5% and 1%) on single dose of CSA (50 mg/kg) was undertaken. Male Sprague-Dawley rats (weighing 230 +/- 20 g) were used in this study. CSA was given once a day by gavage for seven days, where as Al was given in drinking water for the same period. Twenty four hours after the last dose of CSA, animals were sacrificed and blood and kidney were collected for biochemical and histopathological studies. The bio-chemical parameters included blood urea nitrogen (BUN), serum creatinine (SCr), CSA and Al levels. The kidney homogenates were assayed for malondialdehyde (MDA) and lipid hydroperoxides (LPH). Treatment of rats with CSA alone produced dose-dependent structural and functional changes in kidney. Although Al alone failed to produce any deleterious effect on renal function, it significantly increased the bioavailability and nephrotoxicity of CSA. Al also exacerbated CSA induced increase in oxidative stress (as evident by increased MDA and LPH). Thus, the exacerbation of CSA nephrotoxicity by Al may be attributed to increased bioavailability of CSA and excessive generation of free radicals following concomitant use of these drugs.
Alum Compounds↗
Lingual thyroid gland: clinical evaluation and comprehensive management.
Although lingual thyroid gland is the most common benign mass found at the junction of the anterior two-thirds and the posterior one-third of the tongue, it is still a rare clinical entity. This developmental anomaly is the result of an arrested descent of the gland anlage early in the course of embryogenesis. Patients may have symptoms of dysphagia due to obstruction or even hemorrhage. These symptoms can occur at any time from infancy through adulthood. The clinical findings, laboratory tests, and radiographic imaging studies employed in confirming the diagnosis and in planning appropriate treatment have been evaluated. The primary therapeutic goal is to restore thyroid function. We describe a case of lingual thyroid gland and summarize the current management principles for this condition.
Adult↗
Congenital myasthenic syndromes. Studies of the AChR and other candidate genes.
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Humans↗
Metastatic testicular teratoma of the nasal cavity: a rare cause of severe intractable epistaxis.
Malignant neoplasms of the nasal cavity and paranasal sinuses are uncommon. Choriocarcinoma is a highly malignant germ cell tumour occurring in the reproductive organs. Metastasis may be principally by the lymphatic route as in other germ cell tumours but choriocarcinoma is also known to spread haematogenously. We present a rare case of metastatic choriocarcinoma to the nasal cavity from testicular teratoma presenting with intractable epistaxis in a 32-year-old Caucasian male, who ultimately succumbed to this disease.
Adult↗
Neurological recovery in diabetic rats following spinal cord injury.
This study was designed to assess the effect of spinal cord injury on neurobehavioral, electrophysiological, structural, and biochemical changes in normal and diabetic rats. Experimental diabetes was induced in Sprague-Dawley male rats (weighing 250-280 g) with streptozotocin (50 mg/kg i.p.). Eight weeks after the treatment with streptozotocin the animals were anaesthetized with chloral hydrate and laminectomy was performed at T 7-8 level leaving the dura intact. A compression plate (2.2 x 5.0 mm) loaded with a weight of 35 g was placed on the exposed spinal cord for 5 min. Postoperative neurological function was assessed using inclined plane test, modified Tarlov score, and vocal and sensory score daily for 10 days. Electrophysiological changes were assessed using somatosensory and corticomotor evoked-potentials. The animals were sacrificed at different time intervals and injured site of the spinal cord was analyzed for changes in vitamin E and glutathione levels (as markers of oxidative stress). Pathological changes in spinal cord were also studied using light microscopy. The data on neurobehavioral study clearly indicated that the compression of spinal cord produced highly significant neurological deficit and poor recovery in diabetic rats as compared to nondiabetic rats. Our histopathological and electrophysiological results also confirmed that diabetic animals are more susceptible to compressive spinal cord injury as compared to nondiabetic animals. A higher depletion of antioxidant defense markers (vitamin E and glutathione) was observed in diabetic rats as compared to nondiabetic rats. These results point toward the role of free radicals in poor recovery in diabetic rats following neurotrauma. Further studies are warranted to assess the neuroprotective potential of antioxidants to retard the secondary pathophysiological events following neurotrauma and to enhance the recovery.
Animals↗
Effect of chronic administration of magnesium sulfate on 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced neurotoxicity in mice.
This investigation was aimed to study the effect of magnesium on 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced neurotoxicity in mice. Four groups of mice were given magnesium sulfate (MgSO4.7H2O) in drinking water at four different concentrations of 0.0 g/l (control), 2.5 g/l (low), 5.0 g/l (medium) and 10.0 g/l (high) respectively for a period of 16 weeks; these animals also received MPTP (30 mg/kg, intraperitoneally daily) during the last five days of Mg treatment. Other four groups of mice were given similar dose regimen of MgSO4 but received injections of saline instead of MPTP. Seventy-two hr after the last dose of MPTP, neurobehavioural studies including locomotor activity, pole climbing test and heart nociception test were performed and striata were collected for the analysis of dopamine. The results of this study show that treatment of mice with MgSO4 or MPTP individually has no effect on their behaviour. Concomitant administration of low dose of MgSO4 (2.5 g/l) along with MPTP produced increase in motor activity and latency to heat stimuli; whereas medium and high doses of MgSO4 in combination with MPTP produced opposite (as compared to low dose) effects resulting in a decrease in motor activity and latency to heat stimuli and increase in pole climbing time. However, MgSO4 dose-dependently exacerbated MPTP-induced depletion of striatal dopamine. The mortality was drastically increased (30-55%) in the animals receiving combined treatments of MPTP and MgSO4 as compared to the mice treated with MPTP alone (12%). This study clearly points towards the ability of MgSO4 to modify MPTP-induced neurotoxicity.
1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
Functional recovery and vitamin E level following sciatic nerve crush injury in normal and diabetic rats.
Extensive biochemical data document the involvement of oxygen derived free radicals (ODFR) in recovery following neurotrauma as well as diabetic neuropathy. Vitamin E is considered as one of the principle protective mechanism against oxidative damage in neuronal tissue. The present study was undertaken to determine the association between functional recovery and vitamin E levels following sciatic nerve crush injury in normal and diabetic rats. The sciatic nerve of normal and streptozotocin (STZ) induced diabetic rats was crushed using a haemostat. The walking track analysis and vitamin E levels were recorded on 10, 20 and 30th day. Maximum functional deficiency and depletion of vitamin E in sciatic nerve was observed on 10th day following crush injury in both normal and diabetic animals. A progressive motor recovery and repletion of vitamin E was observed on day 20 and 30 following injury in both diabetic and normal rats. The functional recovery was slower whereas vitamin E level was higher in diabetic animals as compared to normal injured rats during healing phase suggesting that vitamin E alone may not be an efficient indicator of oxidative stress during regeneration of axons following trauma in diabetic rats.
Animals↗
Effect of quinacrine, a phospholipase A2 inhibitor on stress and chemically induced gastroduodenal ulcers.
Quinacrine, a phospholipase A2 inhibitor, has been studied for its ability to inhibit gastric secretion and to protect the gastric and duodenal mucosa against chemically and stress-induced ulcers. Acid secretion studies were undertaken in pylorus-ligated rats with and without quinacrine treatment. Experimental gastric lesions were induced by water-immersion restraint stress, indomethacin and 80% ethanol in rats; whereas duodenal ulcers were produced by treatment of rats with cysteamine. The level of nonprotein sulfhydryl compounds and gastric wall mucus were also measured in the glandular stomach of the rats following ethanol-induced gastric lesions. The results of this study demonstrate that quinacrine produces a dose-dependent inhibition of gastric acid secretion in rats. Pretreatment with quinacrine significantly attenuated the formation of stress-, indomethacin- and ethanol-induced gastric lesions. Quinacrine also protected intestinal mucosa against cysteamine-induced duodenal ulcers. The antiulcer activity of quinacrine was associated with appreciable inhibition of ethanol-induced depletion of nonprotein sulfhydryls and gastric wall mucus. These findings point towards the mediation of sulfhydryls in quinacrine-induced gastrointestinal cytoprotection. In conclusion, this study demonstrates that quinacrine possesses significant antiulcer and cytoprotective activity against various experimentally induced gastroduodenal lesions. Although the mechanism of action of quinacrine requires further evaluation, the experimental observations derived from this study may have future clinical relevance and therefore deserve to be investigated thoroughly.
Animals↗