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Biomedical subjects

S Husain

Publications and source records attributed to S Husain.

At least 55 records · Page 3Linked to original sources
PubMed1998

Hermansky-Pudlak syndrome: report of a case with histological, immunohistochemical and ultrastructural findings.

We report a 38-year-old female of Puerto Rican descent with Hermansky-Pudlak syndrome and decreased levels of von Willebrand factor. Histologic and ultrastructural findings of non-sunexposed skin showed melanocytes with short dendritic processes and decreased numbers of melanosomes. Ultrastructural examination of platelets revealed greatly reduced numbers of delta granules. Recognition of this syndrome is important because skin neoplasms, ceroid deposition and hemorrhagic manifestations can be causes of morbidity and of potential death in patients affected with this syndrome.

Adult↗
PubMed1998

Contribution of nitric oxide to reactive hyperemia: impact of endothelial dysfunction.

Our objectives were to (1) test the hypothesis that nitric oxide (NO) contributes to peak reactive hyperemia (RH) in the human peripheral vasculature, (2) examine the impact of atherosclerosis and its risk factors on RH, and (3) investigate whether L-arginine will improve RH in patients with endothelial dysfunction. The endothelium contributes to shear stress-mediated vasomotion by releasing a variety of dilating factors, including NO, but the contribution of NO to peak RH in patients with and without endothelial dysfunction is unknown. Endothelium-dependent and endothelium-independent function was assessed with intrafemoral arterial acetylcholine (ACh) and sodium nitroprusside. RH was produced by occlusion of blood flow to the leg for 3 minutes. The study was repeated after NG-monomethyl-L-arginine (L-NMMA) in 44 subjects and L-arginine in 9 patients with atherosclerosis. There were 15 normal control subjects without risk factors for atherosclerosis and 29 patients with risk factors or angiographic atherosclerosis. Microvascular vasodilation in response to ACh, but not to sodium nitroprusside, was lower in the patients with risk factors or atherosclerosis compared with normal control subjects, P=0.048, and the inhibition of ACh-induced microvascular dilation by L-NMMA was also greater in normal control subjects (P=0.045). Similarly, RH, including the peak response, was inhibited by L-NMMA in normal control subjects (P=0.0011) but not in patients with risk factors or atherosclerosis, suggesting that the contribution of NO to both ACh-induced dilation and RH was diminished in patients with risk factors or atherosclerosis. L-Arginine did not affect vasodilation in response to ACh, sodium nitroprusside, or RH. We concluded that (1) NO contributes to all phases of RH in the normal human peripheral vasculature, (2) patients with atherosclerosis or its risks have abnormal NO bioactivity in response to pharmacological and physiological stimulation, and (3) L-arginine does not improve RH in atherosclerosis. Reduced physiological vasodilation in atherosclerosis may contribute to or exacerbate hypertension and ischemia.

Acetylcholine↗
PubMed1998

Results of surgical decompression of ulnar nerve in leprosy.

Ulnar neurolysis in 279 cases of leprosy was performed with objectives of relief in neuritic pain and impending/ existing sensory motor loss of varying extent. Of the above, 193 could be followed between 3-10 years. Neuritic pain was first to disappear. 48.7% of the 193 cases showed sensory recovery. Motor power gain and/or further fall in muscle power was prevented as a result of preventive neurolysis in 173 (89.6%) cases. In this series benefits of appropriate and timely surgical intervention have been observed.

Adolescent↗
PubMed1997

Coronary vascular nitric oxide activity in hypertension and hypercholesterolemia. Comparison of acetylcholine and substance P.

BACKGROUND: Whether the abnormal responses of the human coronary circulation to acetylcholine in patients with hypertension and hypercholesterolemia extend to other, nonmuscarinic stimulators of the endothelium and whether this signifies a specific abnormality of NO is not known. METHODS AND RESULTS: We studied 26 patients with angiographically normal coronary arteries, 10 without risk factors, and 16 with either hypertension (n = 9) and/or hypercholesterolemia (n = 10). Dose-response curves were performed with acetylcholine, substance P, and sodium nitroprusside before and after NG-monomethyl-L-arginine (L-NMMA). Substance P produced predominantly epicardial coronary dilation, whereas the dilating effect of acetylcholine was mainly microvascular. There was no correlation between the responses to the two drugs. L-NMMA did not affect the response to sodium nitroprusside, but it suppressed dilation in response to both substance P and acetylcholine, suggesting that the latter promote bioavailability of NO from the coronary vascular endothelium. Compared with patients without risks, those with hypercholesterolemia and hypertension had significantly reduced vasodilation with substance P: 21% versus 12.6% (P = .004) increase in epicardial coronary diameter and 35% versus 19% (P < .05) decrease in vascular resistance. Similar differences were noted with acetylcholine but not with sodium nitroprusside or adenosine. Epicardial and microvascular dilations with substance P or acetylcholine after L-NMMA were similar in patients with and without risk factors, indicating that the reduced effect of endothelium-dependent vasodilators in those with hypertension and hypercholesterolemia is due to diminished NO activity. CONCLUSIONS: (1) Substance P- and acetylcholine-induced coronary vasodilation, like that to acetylcholine, is at least partly due to stimulation of NO activity, indicating that the dysfunction of the coronary vascular endothelial cell layer is not restricted to muscarinic receptors. (2) Hypertension and hypercholesterolemia are associated with depression of both basal and pharmacologically stimulated bioavailability of NO.

Acetylcholine↗
PubMed1997

Nitric oxide activity in the atherosclerotic human coronary circulation.

OBJECTIVES: We determined the activity of nitric oxide at rest and after acetylcholine in the atherosclerotic human coronary circulation. BACKGROUND: Although responses to acetylcholine, an endothelium-dependent vasodilator, are abnormal in patients with coronary atherosclerosis, whether this reflects abnormal nitric oxide activity in humans in vivo has not been investigated previously. METHODS: We investigated the effects of intracoronary L-NG-monomethyl arginine (L-NMMA), a specific antagonist of nitric oxide synthesis, on coronary vascular resistance and epicardial coronary artery diameter at rest and after acetylcholine in 24 patients with coronary artery disease and in 12 subjects with angiographically normal coronary arteries who were free from atherosclerotic risk factors. RESULTS: With L-NMMA, the 13 +/- 4% (mean +/- SEM) increase in coronary vascular resistance and the 4 +/- 1% lumen diameter narrowing in atherosclerotic patients were lower than the 38 +/- 9% increase in resistance and the 15 +/- 2% decrease in diameter (both p < 0.01) observed in normal control subjects, indicating reduced basal nitric oxide activity in atherosclerosis. The degree of angiographic atherosclerotic narrowing did not correlate with the magnitude of diameter reduction. Acetylcholine-induced coronary epicardial and microvascular dilation was also depressed in atherosclerotic patients (32.2 +/- 9% reduction in coronary vascular resistance with 10(-6) mol/liter acetylcholine) compared with normal control subjects (65.5 +/- 2% decrease, p < 0.01). L-NMMA inhibited acetylcholine-induced epicardial and microvascular vasodilation in both patient groups, but the inhibition was greater in normal control subjects than in atherosclerotic patients, indicating that stimulation of nitric oxide activity by acetylcholine is reduced in atherosclerotic patients compared with normal control subjects. Coronary vascular dilation with sodium nitroprusside was similar in both groups and was not suppressed by L-NMMA. Furthermore, L-arginine reversed the constrictor effects of L-NMMA, indicating that the action of L-NMMA is specifically caused by inhibition of nitric oxide production from L-arginine. CONCLUSIONS: These findings indicate that 1) there is a reduced basal activity of nitric oxide in the human atherosclerotic epicardial and microvascular coronary circulation; and 2) acetylcholine-induced coronary vascular dilation is at least partly due to stimulation of the activity of nitric oxide, and the reduced response to acetylcholine is due to attenuation in the stimulated activity of nitric oxide in patients with atherosclerosis.

Acetylcholine↗
PubMed1997

Inhibition of muscarinic-stimulated polyphosphoinositide hydrolysis and Ca2+ mobilization in cat iris sphincter smooth muscle cells by cAMP-elevating agents.

The effects of carbachol (CCh) on inositol 1,4,5-trisphosphate (IP3) production and intracellular calcium ([Ca2+]i) mobilization, and their regulation by cAMP-elevating agents were investigated in SV-40 transformed cat iris sphincter smooth muscle (SV-CISM-2) cells. CCh produced time- and dose-dependent increases in IP3 production; the t1/2 and EC50 values were 68 s and 0.5 microM, respectively. The muscarinic agonist provoked a transient increase in [Ca2+]i which reached maximum within 77 s, and increased [Ca2+]i mobilization in a concentration-dependent manner with an EC50 of 1.4 microM. Thapsigargin, a Ca(2+)-pump inhibitor, caused a rapid rise in [Ca2+]i and subsequent addition of CCh was without effect. Both CCh-induced IP3 production and CCh-induced [Ca2+]i mobilization were more potently antagonized by 4-DAMP, an M3 muscarinic receptor antagonist, than by pirenzepine, an M1 receptor antagonist, suggesting that both responses are mediated through the M3 receptor subtype. Treatment of the cells with U73122, a phospholipase C (PLC) inhibitor, resulted in a concentration-dependent decrease in both CCh-stimulated IP3 production and [Ca2+]i mobilization. These data indicate close correlation between enhanced IP3 production and [Ca2+]i mobilization in these smooth muscle cells and suggest that the CCh-stimulated increase in [Ca2+]i could be mediated through increased IP3 production. Isoproterenol (ISO) inhibited CCh-induced IP3 production (IC50 = 80 nM) and [Ca2+]i mobilization (IC50 = 0.17 microM) in a concentration-dependent manner. Microsomal fractions isolated from SV-CISM-2 cells contained phospholipase C (PLC) which was stimulated by CCh (10 microM) and GTP gamma S (0.1 microM). Pretreatment of the cells with ISO or forskolin, 5 microM each, produced membrane fractions in which CCh-stimulated PLC activity was significantly attenuated. Furthermore, when microsomal fractions isolated from SV-CISM-2 cells were phosphorylated with Protein kinase A (PKA), the CCh- and GTP gamma S-stimulated IP3 production were significantly inhibited. It can be concluded from these studies that in SV-CISM-2 cells, activation of M3 muscarinic receptors results in stimulation of PLC-mediated PIP2 hydrolysis, generating IP3 which mobilizes [Ca2+]i. Furthermore, elevation of cAMP may inhibit IP3 production and [Ca2+]i mobilization through mechanisms involving PKA-dependent phosphorylation of PLC, G-proteins, IP3 receptor and/or IP3 metabolizing enzymes.

Adrenergic beta-Agonists↗
PubMed1997

Bone mineral density in Turner's syndrome--a longitudinal study.

OBJECTIVE: Osteoporosis is a recognized problem in adult women with Turner's syndrome, the aetiology of which is unclear. The aim of this study was to examine bone mineralization longitudinally in a group of girls with Turner's syndrome and to study the effect of different treatments on bone mineral density. DESIGN: A prospective observational study. PATIENTS: Eighteen girls with Turner's syndrome aged 4-17 years attending a paediatric endocrine clinic. MEASUREMENTS: Bone mineral density of the lumbar spine was assessed using dual energy X-ray absorptiometry at several time points over a 2.5-year period. RESULTS: Only one girl had evidence of a significant reduction in bone density when comparisons were made with control data related to body weight and pubertal status. No advantage was found for any form of treatment in optimizing bone mineralization. CONCLUSIONS: As there is little evidence of reduced bone mineral density in girls with Turner's syndrome there is no justification for an early introduction of oestrogen replacement during the prepubertal years.

Adolescent↗
PubMed1997

Rifampicin and isoniazid in the treatment of leprous nerve abscesses.

Thirty nine cases of borderline tuberculoid leprosy having nerve abscesses (15 with sinuses) were treated with daily dose of rifampicin and isoniazid for six months along with standard multidrug therapy. The patients were followed up for three to five years. No recurrence of abscess or sinus was observed. Observations indicate that medical approach is required at times to supplement surgical intervention for management of these cases.

Abscess↗
PubMed1996

DNA breakage by uric acid and Cu(II): binding of uric acid to DNA and biological activity of the reaction.

Uric acid is present in human plasma in relatively high concentrations and is considered to be a natural physiological antioxidant. We have earlier shown that in the presence of Cu(II) and molecular oxygen, uric acid causes strand breakage in DNA. In this article, we show that uric acid fluorescence is quenched by addition of DNA, indicating the formation of uric acid-DNA complex. Uric acid-Cu(II)-mediated DNA strand scission is capable of bacteriophage inactivation and such inactivation is mediated through reduction of Cu(II) to Cu(I) and the generation of oxygen-derived radicals. It is indicated that the DNA breakage is repaired in E. coli and involves the repair of DNA polymerase.

Bacteriophage lambda↗
PubMed1996

Extensor indicis opposition transfer in the ulnar and median palsied thumb in leprosy.

Twenty seven opponensplasties for ulnar and median paralysis in 25 leprosy patients were performed using extensor indicis proprius. An additional transfer of the radial half of flexor pollicis longus to extensor pollicis longus was done to stabilize the metacarpophalangeal joint of the thumb. The biomechanical aspects of extensor indicis proprius tendon transfer were studied and results evaluated using various anatomical and functional parameters. Extensor indicis proprius provides adequate strength to position the thumb. However, sometimes it does not reach its new insertion. There is no significant deficit at the donor site but in a few cases the index finger may lose its capability for independent extension and sometimes a proximal interphalangeal joint contracture may develop.

Adolescent↗
PubMed1996

Immobilization and stabilization of horseradish peroxidase isoforms.

Purified anionic and cationic isoforms of horseradish peroxidase (HRP) immobilized by coupling the amino acid side-chain amino groups and/or carbohydrate moieties to Sepharose have been studied for their resistance to denaturation. The isoforms were treated with periodate followed by ethylenediamine to generate additional amino groups in the glycosyl residues. The immobilized preparations were: Preparation I (Sp-aHRP, Sp-cHRP), in which HRP was covalently immobilized via side-chain amino groups exclusively; Preparation II (Sp-NHaHRP, Sp-NHcHRP), in which periodate and ethylenediamine-treated HRP was covalently immobilized via side-chain amino groups and amino groups incorporated into glycosyl residues. HRP isoforms in preparation II lacked about 33-55% carbohydrate. Both strategies of immobilization induced significant stabilization against denaturation. Inclusion of 2 mM calcium enhanced isoenzyme stability significantly.

Calcium↗
PubMed1996

Transfer of Cl- across placenta of anesthetized rat.

The mechanisms of Cl- transfer across the rat placenta have been investigated. Clearance across the intact placenta from mother to fetus (m-->f) of 51Cr-EDTA (paracellular diffusion marker) and 36Cl- (Kmf) was 1.9 +/- 0.1 and 37.3 +/- 4.1 microliters/min, respectively (mean +/- SE, n = 10), the large difference indicating that most m-->f transfer of Cl- is transcellular. The clearance of 36Cl- across the dually perfused placenta in m-->f and fetal-to-maternal directions was symmetrical and highly sensitive to the anion-exchange inhibitor 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (0.1 mM). The Kmf of 36Cl- was not inhibited by anoxia and had a low temperature quotient (Q10 between 32 and 37 degrees C was 1.52). The m --> f transfer of Cl- seemed to be fully saturated at physiological concentrations of Cl-. 36Cl- could be displaced from the transporter on the maternal side by other anions with the following order of affinity: Cl- approximately NO3- > Br- > lactate- >> gluconate. It is concluded that most of the Cl- transfer across the rat placenta is effected by an anion exchanger.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1996

Protein kinase C isoforms in iris sphincter smooth muscle: differential effects of phorbol ester on contraction and cAMP accumulation are species specific.

Objectives were to identify PKC isoforms in iris sphincter isolated from rabbit, cat, dog and bovine irides, to determine their subcellular distribution, and to investigate the effects of the phorbol ester, PDBu, on contraction and cAMP accumulation in this tissue. Using six isoform (alpha, beta, gamma, epsilon, delta, zeta)-specific polyclonal antibodies, PKC alpha, beta, epsilon, delta, and zeta were detected in the four species, whereas PKC gamma was detected only in dog and bovine. PKC alpha and epsilon are the most abundant isoforms in this tissue. PKC alpha is mainly cytosolic in rabbit and bovine and membrane associated in cat and dog. PKC gamma is equally distributed in cytosol and membrane fractions of bovine, but mostly cytosolic in dog. PKC beta, delta and epsilon are mainly membraneous and PKC zeta is mainly cytosolic in all species. PDBu (100 nM) induced a contractile response in rabbit- and cat-, but not in dog and bovine, sphincters, and increased cAMP accumulation in rabbit, cat, dog and bovine by 111, 130, 458 and 294%, respectively. Therefore, the lack of effect of PDBu on contraction in dog and bovine, as compared to rabbit and cat, may be due: (a) to the presence of PKC gamma isoform, and (b) to the stronger stimulatory effects of the phorbol ester on cAMP production in the non-contracting species. In addition to demonstrating the presence of various PKC isoforms in the iris sphincter and the activation of adenylyl cyclase by this protein kinase, we have shown that the distribution of the PKC isoforms in this tissue is species specific. Furthermore, our data suggest that there may be specific physiological functions associated with each of the PKC isoforms and that PKC is involved in the contractile response of some but not all smooth muscles.

Animals↗