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Biomedical subjects

H S Sharma

Publications and source records attributed to H S Sharma.

At least 73 records · Page 4Linked to original sources
PubMed2000

Ear lobe crease: incidence in a healthy Malay population.

The incidence of ear lobe crease (ELC) was studied in 1576 healthy Malay subjects (566 males and 1010 females), randomly selected from the residents of Kota Bharu, Malaysia. ELC was present in 31.1% of males and in 3.6% of females; this difference in incidence between the two sexes is statistically significant (p > 0.05). In males the incidence of Type I crease was highest (10.1%) while that of Type III crease was lowest (2.3%). In females Type II crease showed the highest incidence (1.9%) and Type III the lowest. The incidence of bilateral presence of all three types of ELC showed an age-related increase in males. The ELC often starts unilaterally and later develops bilaterally and earlier in males than in females.

Adolescent↗
PubMed2000

Kimura's disease: a report of three cases with a brief review of literature.

Kimura's disease (KD) is an uncommon chronic inflammatory condition of unknown aetiology involving subcutaneous tissue, presenting as a tumor like lesion with a predilection for the head and neck region. Clinically it is often confused with parotid tumor with lymph node metastasis. It is difficult to diagnose before tissue biopsy. Fine needle aspiration cytology has only limited value. Unless the pathologists are aware of this entity, it might be misdiagnosed. Surgery, radiotherapy and steroid therapy have been tried but none is proved best and recurrence is common. Three cases of KD seen in our hospital and the problems encountered in them are presented.

Adult↗
PubMed1999

Quantitative analysis of collagens and fibronectin expression in human right ventricular hypertrophy.

One of the main features in human tetralogy of Fallot (TF) is right ventricular hypertrophy (RVH) due to pressure (sub-pulmonary stenosis) and volume overload (ventricular septal defect). Currently, primary correction at a young age is the treatment of choice. To unravel the role of extracellular matrix in RVH, we examined myocardial expression of collagens and fibronectin in TF patients with primary correction (TF1, age 0.7 +/- 0.2 yr.), secondary surgery (TF2, age 36.9 +/- 4.6 yr), and in age-matched control patients. Sirius red staining quantified by video imaging showed significantly increased interstitial staining for collagens in both TF1 and TF2 groups as compared to respective controls. Fibronectin was expressed in extracellular spaces, perivascular regions, and in some cardiomyocytes. Quantitative analysis of fibronectin revealed increased expression in only TF1 group as compared to respective control. Our results indicate an increased amount of myocardial extracellular matrix deposition as a sign of fibrosis during RVH in patients with TF.

Adult↗
PubMed1999

Orbital abscess due to acute ethmoiditis in a neonate.

Orbital complications due to ethmoiditis are not uncommon in children. However, they are very rare in infants. A case of orbital abscess due to acute ethmoiditis in a 10 days old boy is reported. Causative microorganisms isolated from the operated specimen were Staphylococcus aureus and aspergillosis. Successful outcome was achieved following antimicrobial therapy, external ethmoidectomy, and surgical drainage of the abscess. The aetiopathogenesis and management of this clinical entity is discussed, with a brief review of the literature.

Abscess↗
PubMed1999

Expression patterns of heat shock proteins in lungs of neonates with congenital diaphragmatic hernia.

BACKGROUND: Congenital diaphragmatic hernia (CDH) is associated in many cases with pulmonary hypertension. Currently, extracorporeal membrane oxygenation (ECMO) is one of the possible modalities of treatment of pulmonary hypertension and prevention of parenchymal lung injury in neonates with CDH. HYPOTHESIS: Molecular stress is present in the lungs of neonates with CDH. To test this hypothesis, we investigate the expression pattern of stress genes (heat shock proteins [HSPs] 27 and 70) in lungs of patients with CDH who have pulmonary hypertension, and evaluate the influence of ECMO on the expression levels of these genes to understand the underlying molecular mechanisms. DESIGN: Paraffin-embedded lung autopsy specimens from patients with CDH and lung hypoplasia who either did or did not receive ECMO treatment and age-matched controls were immunostained by means of monoclonal antihuman antibodies against HSP 70 and HSP 27, with the streptavidin-biotin complex method. SETTING: Level III academic children's hospital. MAIN OUTCOME MEASURES: Expression levels of both HSP 27 and HSP 70 were semiquantitatively evaluated in bronchial epithelium, as well as in medial smooth muscle cells (SMCs) and endothelium of large and small pulmonary arteries, by means of a score ranging from 0 to 4. Statistical analysis of the data was performed with the nonparametric Mann-Whitney test, with significant probability value at P < or = .05. RESULTS: For HSP 70, the most pronounced immunoreactivity was observed in the bronchial epithelium, followed by the medial SMCs of small arteries (of external diameter < 200 microm). The overall expression was significantly higher in patients with CDH than controls in bronchi as well as in pulmonary arteries. For HSP 27, intense expression was found in medial SMCs, followed by the bronchial epithelium in controls, with significantly increased expression in medial SMCs of large and small arteries in patients with CDH. Treatment with ECMO was associated with significantly reduced expression levels of HSP 70 in medial SMCs of both large and small arteries, whereas HSP 27 expression levels were decreased only in small arteries. In addition, the expression levels of both HSPs were significantly lower in endothelium of small arteries. CONCLUSIONS: Increased expression of HSPs in CDH points to a condition of pulmonary stress. This pulmonary stress appears to be partially ameliorated by ECMO treatment. This may point to one of the mechanisms by which ECMO alleviates pulmonary hypertension associated with CDH.

HSP70 Heat-Shock Proteins↗
PubMed1999

Impaired structural remodelling of pulmonary arteries in newborns with congenital diaphragmatic hernia: a histological study of 29 cases.

Congenital diaphragmatic hernia (CDH) is associated in many cases with lung hypoplasia and pulmonary hypertension (PH). The pathogenetic mechanisms underlying the pulmonary hypertension in CDH are not completely understood. In order to alleviate the pulmonary hypertension, new therapeutic modalities have been introduced including extracorporeal membrane oxygenation (ECMO). This paper reports a study of the histology of the lungs of 29 CDH autopsy cases, with special attention to the pulmonary arteries, and relating the findings to gestational age and ECMO treatment. Formalin-fixed and paraffin-embedded specimens were stained with haematoxylin and eosin (H&E) and elastic van Gieson (EvG) stains, followed by morphometric measurements of the arterial media and adventitia. As expected, there was a significant decrease in adventitial percentage and total wall thicknesses of small pulmonary arteries with an external diameter less than or equal to 150 microm in term control newborns compared with pre-term controls (p=0.0004 and 0.05). In CDH newborns, all the measured values of the arterial wall remained significantly higher. The increase of adventitial thickness also affected the supernumerary arteries in CDH neonates. CDH newborns subjected to ECMO treatment showed a significantly thinner arterial adventitia than CDH cases who did not receive ECMO (p=0.0001), the former approaching normal values. These results indicate that in CDH, there is failure of the normal arterial remodelling processes occurring in the perinatal period. The adventitial thickening, which has been reported previously in term CDH patients only, was related in the present study to differences in gestational ages. This appears to be partially reversed by ECMO treatment, thus constituting one of the mechanisms by which ECMO treatment aids in alleviating the associated PH in CDH newborns.

Actins↗
PubMed1999

Enhanced expression and localization of heme oxygenase-1 during recovery phase of porcine stunned myocardium.

Myocardial adaptation to ischemia involves up-regulated expression of a number of genes implicated in conferring cytoprotection. We have previously shown that myocardial ischemia followed by reperfusion leads to a co-ordinated expression of mRNAs encoding heme oxygenase-1 (HO-1) and ubiquitin in pigs. HO-1 participates in biological reaction leading to the formation of the antioxidant, bilirubin and the putative cellular messenger, carbon monoxide. In the present study, we examined the expression and cellular localization of HO-1 in the heart during myocardial stunning in anesthetized pigs. After thoracotomy, the LAD was occluded for 10 min and reperfused for 30 min (group I, n = 4), again occluded for 10 min and reperfused for 30 min (group II, n = 6), 90 min (group III, n = 4), 210 min (group IV, n = 5) and for 390 min (group V, n = 4). Myocardial tissue specimens were collected in 10% formalin as well as in liquid nitrogen and processed for immunohistochemistry and mRNA expression analysis, respectively. In the distribution territory of the LAD (experimental, E), systolic wall thickening was significantly decreased (39 +/- 6%) as compared to that of the area perfused by left circumflex coronary artery (LCx, control) in group I and remained depressed in all subsequent groups. Northern blot analysis revealed that the expression of a single mRNA species of 1.8 kb encoding HO-1 was significantly induced in E as compared to control in groups II and III with maximum mRNA levels in group II (1.9 +/- 0.4 fold vs. control). Immunoreactive HO-1 was localized in the cytoplasm of cardiomyocytes as well as in the perivascular regions in all groups. Semiquantitative analysis of HO-1 staining showed significantly enhanced levels of HO-1 in perivascular region in E as compared to respective controls derived from groups III and IV. These results suggest that myocardial adaptive response to ischemia involves up-regulation of HO-1 in cells of perivascular region indicating that this enzyme may participate in regulating vascular tone via CO and thereby, contributing in pathophysiologically important defense mechanism(s) in the heart.

Animals↗
PubMed1999

Malignant paraganglioma of frontoethmoidal region.

Nonchromaffin paragangliomas are unusual tumours arising from widely distributed paraganglionic tissues probably of neural crest origin. In the head and neck region they are usually seen as carotid body or jugulotympanic tumours. Other rarely reported sites in the head and neck region are the orbit, nose and larynx. This report deals with a case of sinonasal paraganglioma which was initially treated with surgery and radiotherapy. Twenty two years later the tumour recurred and showed a rapid growth due to malignant transformation which we believe is late effect of radiotherapy. The clinical features, histopathology and role of radiotherapy in sinonasal paragangliomas together with a review of the medical literature have been discussed.

Adult↗
PubMed1999

Antioxidant properties of melatonin: a pulse radiolysis study.

Various one-electron oxidants such as OH*, tert-BuO*, CCl3OO*, Br2*- and N3*, generated pulse radiolytically in aqueous solutions at pH 7, were scavenged by melatonin to form two main absorption bands with lambda(max) = 335 nm and 500 nm. The assignment of the spectra and determination of extinction coefficients of the transients have been reported. Rate constants for the formation of these species ranged from 0.6-12.5x10(9) dm3 mol(-1) s(-1). These transients decayed by second order, as observed in the case of Br2*- and N3* radical reactions. Both the NO2* and NO* radicals react with the substrate with k = 0.37x10(7) and 3x10(7) dm3 mol(-1) s(-1), respectively. At pH approximately 2.5, the protonated form of the transient is formed due to the reaction of Br2*- radical with melatonin, pKa ( MelH* <=> Mel* + H+) = 4.7+/-0.1. Reduction potential of the couple (Mel*/MelH), determined both by cyclic voltammetric and pulse-radiolytic techniques, gave a value E(1)7 = 0.95+/-0.02 V vs. NHE. Repair of guanosine radical and regeneration of melatonin radicals by ascorbate and urate ions at pH 7 have been reported. Reactions of the reducing radicals e(aq)- and H* atoms with melatonin have been shown to occur at near diffusion rates.

Antioxidants↗
PubMed1999

Management of laryngeal foreign bodies in children.

Foreign body aspiration is one of the leading causes of accidental death in children. Food items are the most common items aspirated in infants and toddlers, whereas older children are more likely to aspirate non-food items. Laryngeal impaction of a foreign body is very rare as most aspirated foreign bodies pass through the laryngeal inlet and get lodged lower down in the airway. Two rare cases of foreign body aspiration with subglottic impaction in very young children (under 2 years of age) are described. In both the cases subglottic impaction occurred consequent to attempted removal of foreign body by blind finger sweeping. The clinical presentation, investigations, and management of these rare cases are discussed.

Emergency Treatment↗
PubMed1999

Enhanced expression of vascular endothelial growth factor in lungs of newborn infants with congenital diaphragmatic hernia and pulmonary hypertension.

BACKGROUND: Pulmonary hypoplasia accompanied by pulmonary hypertension resistant to treatment is an important feature of congenital diaphragmatic hernia (CDH). The pathogenesis of the pulmonary vascular abnormalities in CDH remains to be elucidated at the molecular level. Vascular endothelial growth factor (VEGF), an endothelial cell specific mitogen, is known to play a role in pulmonary angiogenesis and vascular remodelling but there are no data on VEGF expression in patients with CDH. METHODS: Necroscopic lung specimens from 21 patients with CDH with lung hypoplasia and from seven age matched control newborn infants without lung hypoplasia were processed for immunohistochemical analysis using affinity purified anti-human VEGF antibodies. All the cases of CDH had pulmonary hypoplasia, indicated by a lung/body weight index of </=0.012, and pulmonary hypertension indicated by repeated cardiac ultrasonography. Cellular localisation of VEGF was semiquantitatively analysed using a staining score ranging from 0 (no staining) to 4 (very strong staining). RESULTS: Significantly raised levels of VEGF immunoreactivity were observed in lung specimens from cases of CDH compared with controls. VEGF was detected mainly in the bronchial epithelium and the medial smooth muscle cells of large (>200 microm) and small (<200 microm) pulmonary arteries, the most intense staining being in the medial smooth muscle cells of the small pulmonary arteries. Endothelial cells were positive for VEGF staining in patients with CDH but not in controls. CONCLUSIONS: This is the first study of VEGF expression in newborn infants with CDH. Increased levels of VEGF, especially in the small, pressure regulating pulmonary arteries, point to a potential role in vascular remodelling. This may reflect an unsuccessful attempt by the developing fetus to increase the pulmonary vascular bed in the hypoplastic lungs to alleviate the associated pulmonary hypertension.

Case-Control Studies↗
PubMed1998

Nitric oxide in the pathophysiology of hyperthermic brain injury. Influence of a new anti-oxidant compound H-290/51. A pharmacological study using immunohistochemistry in the rat.

The possibility that nitric oxide (NO) is involved in the pathophysiology of brain injury caused by heat stress (HS) was examined using neuronal nitric oxide synthase (NOS) immunohistochemistry in a rat model. In addition, to find out a role of oxidative stress in NOS upregulation and cell injury, the effect of a new antioxidant compound H-290/51 (Astra Hässle, Mölndal, Sweden) was examined in this model. Subjection of conscious young rats to 4 h HS in a biological oxygen demand (BOD) incubator at 38 degrees C resulted in a marked upregulation of NOS in many brain regions compared to control rats kept at room temperature (21 +/- 1 degree C). This NOS immunoreactivity was found mainly in distorted neurons located in the edematous regions not normally showing NOS activity. Breakdown of the blood-brain barrier (BBB) permeability, increase in brain water content and marked neuronal, glial and myelin reaction were common findings in several brain regions exhibiting upregulation of NOS activity. Pretreatment with H-290/51 significantly attenuated the upregulation of NOS in rats subjected to HS. In these animals breakdown of the BBB permeability, edema and cell changes were considerably reduced. Our results suggest that hyperthermic brain injury is associated with a marked upregulation of NOS activity in the CNS and this upregulation of NOS and concomitant cell injury can be reduced by prior treatment with an antioxidant compound H 290/51. These observations indicate that oxidative stress seems to be an important endogenous signals for NOS upregulation and cell reaction in hyperthermic brain injury.

Animals↗
PubMed1998

Spinal nerve lesion induces upregulation of neuronal nitric oxide synthase in the spinal cord. An immunohistochemical investigation in the rat.

The possibility nitric oxide (NO) is involved the neurodegenrative mechanisms in the spinal cord following a chronic peripheral nerve lesion was examined using NOS immunohistochemistry. Spinal nerve lesion at L-5 and L-6 level was produced according to the Chung model, a model of neuropathic pain and rats were allowed to survive for 8 weeks. In one group of animals L-NAME was given intraperitoneally (1-2 mg/kg, i.p. daily) for 6 weeks. Sham operated rats, in which the spinal nerve was exposed but not ligated, served as controls. Ligation of spinal nerves in rats resulted in an upregulation of NOS which was most pronounced in the ipsilateral gray matter of the spinal cord compared to the contralateral side. In these rats, ultrastructural investigations showed distorted neurons, membrane disruption and myelin vesiculation. Sham operated rats did not show either NOS upregulation or structural changes in the spinal cord. Pretreatment with L-NAME significantly reduced NOS upregulation and the structural changes in the spinal cord were less pronounced. These observations strongly indicate a putative role of NOS in the pathophysiology of chronic nerve lesion. Our results may provide a new strategy to treat chronic neuropathic pain or to minimise neurodegeneration in the patients suffering from such diseases of the nervous system.

Animals↗
PubMed1998

Brain derived neurotrophic factor and insulin like growth factor-1 attenuate upregulation of nitric oxide synthase and cell injury following trauma to the spinal cord. An immunohistochemical study in the rat.

The possibility that brain derived neurotrophic factor (BDNF) and insulin like growth factor-1 (IGF) induced neuroprotection is influenced by mechanisms involving nitric oxide was examined in a rat model of focal spinal cord injury. BDNF or IGF-I (0.1 microgram/10 microliters in phosphate buffer saline) was applied topically 30 min before injury on the exposed spinal cord followed by repeated doses of growth factors immediately before and 30 min after injury. Thereafter application of BDNF or IGF was carried out at every 1 h interval until sacrifice. Five hours after injury, the tissue pieces from the T9 segment were processed for nNOS immunostaining, edema and cell injury. Untreated injured rats showed a profound upregulation of nNOS which was most pronounced in the nerve cells of the ipsilateral side. A marked increase in the blood-spinal cord barrier (BSCB) permeability to 125I-albumin, water content and cell injury in these perifocal segments was also found. Pretreatment with BDNF and IGF significantly reduced the upregulation of nNOS in the spinal cord. This effect of the growth factors was most pronounced in the contralateral side. Rats treated with these neurotrophic factors showed much less signs of BSCB damage, edema and cell injury. These results suggest that BDNF and IGF pretreatment is neuroprotective in spinal cord injury and that these neurotrophic factors have the capacity to down regulate nNOS expression following trauma to the spinal cord. Our data provide new experimental evidences which suggest that BDNF and IGF may exert their potential neuroprotective effects probably via regulation of NOS activity.

Animals↗
PubMed1998

Spinal cord evoked potentials and edema in the pathophysiology of rat spinal cord injury. Involvement of nitric oxide.

The possibility that nitric oxide is somehow involved in the early bioelectrical disturbances following spinal cord injury in relation to the later pathophysiology of the spinal cord was examined in a rat model of spinal cord trauma. A focal trauma to the rat spinal cord was produced by an incision of the right dorsal horn of the T 10-11 segments under urethane anaesthesia. The spinal cord evoked potentials (SCEP) were recorded using epidural electrodes placed over the T9 and T12 segments of the cord following supramaximal stimulation of the right tibial and sural nerves in the hind leg. Trauma to the spinal cord significantly attenuated the SCEP amplitude (about 60%) immediately after injury which persisted up to 1 h. However, a significant increase in SCEP latency was seen at the end of 5 h after trauma. These spinal cord segments exhibited profound upregulation of neuronal nitric oxide synthase (NOS) immunoreactivity, and the development of edema and cell injury. Pretreatment with a serotonin synthesis inhibitor drug p-chlorophenylalanine (p-CPA) or an anxiolytic drug diazepam significantly attenuated the decrease in SCEP amplitude, upregulation of NOS, edema and cell injury. On the other hand, no significant reduction in SCEP amplitude, NOS immunolabelling, edema or cell changes were seen after injury in rats pretreated with L-NAME. These observations suggest that nitric oxide is somehow involved in the early disturbances of SCEP and contribute to the later pathophysiology of spinal cord injury.

Animals↗
PubMed1998

Pulmonary vascular balance in congenital diaphragmatic hernia: enhanced endothelin-1 gene expression as a possible cause of pulmonary vasoconstriction.

BACKGROUND: Pulmonary hypoplasia and persistent pulmonary hypertension (PPH) are the principal causes of the ongoing mortality in congenital diaphragmatic hernia (CDH) presenting with respiratory insufficiency within 6 hours after birth. Endothelin-1 (ET-1) is an endothelial-derived vasoconstrictor, which could play an important role in modulating pulmonary vascular tone in PPH. ET-1 exerts its role in controlling vascular tone through two different subtype receptors, endothelin-A receptor (ETA) which is responsible for vasoconstriction and endothelin-B receptor (ETB) which is responsible for vasodilatation by induction of nitric oxide synthase. METHODS: We examined the pulmonary expression of ET-1, ETA and ETB mRNAs in a rat model of CDH. CDH was induced in rats by administration of 100 mg of nitrofen dissolved in olive oil on day 10 of gestation. Fetal lungs were collected after cesarean section on gestational day 22 (term) and processed for Northern blot analysis and quantitative polymerase chain reaction (PCR). RESULTS: Significantly (P<.05) enhanced levels of ET-1 mRNA were observed in CDH rats compared with control rats. In contrast to equal levels of ETB mRNA, a two- to fourfold increase in ETA mRNA levels were observed in CDH as compared with control rats. CONCLUSIONS: The upregulated expression of ET-1 and ETA receptor mRNA before birth strongly support the reason for pulmonary vasoconstriction and altered pulmonary vascular muscularization in CDH. Consequently in the clinical setting, the use of endothelin receptor blockade for the treatment of PPH may be considered against the background of the unpredictable and variable response to inhaled nitric oxide in newborns with CDH.

Animals↗