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S Hosseini

Publications and source records attributed to S Hosseini.

11 recordsLinked to original sources
PubMed2001

Solar ultraviolet-induced erythema in human skin and nuclear factor-kappa-B-dependent gene expression in keratinocytes are modulated by a French maritime pine bark extract.

The procyanidin-rich French maritime pine bark extract Pycnogenol (PBE) has been investigated for its effect in protecting human skin against solar UV-simulated light-induced erythema. Twenty-one volunteers were given an oral supplementation of Pycnogenol: 1.10 mg/kg body weight (b. wt.)/d for the first 4 weeks and 1.66 mg/kg b. wt./d for the next 4 weeks. The minimal erythema dose (MED) was measured twice before supplementation (baseline MED), once after the first 4 weeks of supplementation, and a last time at the end of the study. The UVR dose necessary to achieve 1 MED was significantly increased during PBE supplementation. Since the activation of the pro-inflammatory and redox-regulated transcription factor NF-kappaB is thought to play a major role in UVR-induced erythema, the effect of PBE was also investigated in the human keratinocyte cell line HaCaT. PBE, added to the cell culture medium, inhibited UVR-induced NF-kappaB-dependent gene expression in a concentration-dependent manner. However, NF-kappaB-DNA-binding activity was not prevented, suggesting that PBE affects the transactivation capacity of NF-kappaB. These data indicate that oral supplementation of PBE reduces erythema in the skin. Inhibition of NF-kappaB-dependent gene expression by PBE possibly contributes to the observed increase in MED.

Administration, Oral↗
PubMed2001

Novel mtDNA mutations and oxidative phosphorylation dysfunction in Russian LHON families.

Leber's hereditary optic neuropathy (LHON) is characterized by maternally transmitted, bilateral, central vision loss in young adults. It is caused by mutations in the mitochondrial DNA (mtDNA) encoded genes that contribute polypeptides to NADH dehydrogenase or complex I. Four mtDNA variants, the nucleotide pair (np) 3460A, 11778A, 14484C, and 14459A mutations, are known as "primary" LHON mutations and are found in most, but not all, of the LHON families reported to date. Here, we report the extensive genetic and biochemical analysis of five Russian families from the Novosibirsk region of Siberia manifesting maternally transmitted optic atrophy consistent with LHON. Three of the five families harbor known LHON primary mutations. Complete sequence analysis of proband mtDNA in the other two families has revealed novel complex I mutations at nps 3635A and 4640C, respectively. These mutations are homoplasmic and have not been reported in the literature. Biochemical analysis of complex I in patient lymphoblasts and transmitochondrial cybrids demonstrated a respiration defect with complex-I-linked substrates, although the specific activity of complex I was not reduced. Overall, our data suggests that the spectrum of mtDNA mutations associated with LHON in Russia is similar to that in Europe and North America and that the np 3635A and 4640C mutations may be additional mtDNA complex I mutations contributing to LHON expression.

Adolescent↗
PubMed2000

Cloning of neuronal mtDNA variants in cultured cells by synaptosome fusion with mtDNA-less cells.

Synaptosome cybrids were used to confirm the presence of heteroplasmic mtDNA sequence variants in the human brain. Synaptosomes contain one to several mitochondria, and when fused to mtDNA-deficient (rho degrees ) mouse or human cell lines result in viable cybrid cell lines. The brain origin of mouse synaptosome cybrid mtDNAs was confirmed using sequence polymorphisms in the mtDNA COIII, ND3 and tRNA(Arg)genes. The brain origin of the human synaptosome cybrids was confirmed using a rare mtDNA Mbo I polymorphism. Fusion of synaptosomes from the brain of a 35-year-old woman resulted in 71 synaptosome cybrids. Sequencing the mtDNA control region of these cybrid clones revealed differences in the number of Cs in a poly C track between nucleotide pairs (nps) 301 and 309. Three percent of the cybrid clones had mtDNAs with 10 Cs, 76% had nine, 18% had eight and 3% had seven Cs. Comparable results were obtained by PCR amplification, cloning and sequencing of mtDNA control regions directly from the patient's brain tissue, but not when the control region was amplified and cloned from a synaptosome cybrid homoplasmic for a mtDNA with nine Cs. Thus, we have clonally recovered mtDNA control region length variants from an adult human brain without recourse to PCR, and established the variant mtDNAs within living cultured cells. This confirms that some mtDNA heteroplasmy can exist in human neurons, and provides the opportunity to study its functional significance.

Adult↗
PubMed2000

Pine bark extract reduces platelet aggregation.

The effects of long-term consumption of the bioflavonoid mixture, French maritime pine bark extract (Pycnogenol(R)), were assessed on aggregation of platelets from cigarette smokers and nonsmokers. Previously we showed that a single dose of Pycnogenol(R) reduced platelet aggregation in cigarette smokers in a dose-response fashion. Cigarette smoking increased platelet reactivity aggregation when measured 2 h after smoking the first cigarette of the day. Blood was collected immediately before and 5 min after smoking three cigarettes each. Smoking increased platelet aggregation (1.17 +/- 0.04). However 200 mg Pycnogenol(R)/day, taken 3 h prior to first cigarette for the day for 2 months, significantly (p <.0023) reduced smoke-induced platelet aggregation (0.98 +/- 0.05) to the level of nonsmokers. In a group of 19 nonsmokers, platelet aggregation was measured during in vitro stimulation by platelet aggregation factor (PAF) after 4 or 8 weeks of 200 mg/day of Pycnogenol(R) consumption. Platelet aggregation was significant when induced in vitro by PAF. However, Pycnogenol(R) consumption did not change platelet aggregation, suggesting that Pycnogenol(R)'s regulation of aggregation is by another mechanism. Thromboxane A2 (TxA2) is increased in smokers by release from platelets and rapidly becomes thromboxane B2 (TxB2). Smoking increased TxB2, which was prevented by Pycnogenol(R), lowering TxB2 levels to those of nonsmokers. However, Pycnogenol(R) had no effect on the lower levels of TxB2 in nonsmokers. These observations suggest that Pycnogenol(R) supplementation reduces a risk factor for cardiovascular diseases, that is, platelet aggregation in smokers. The bioflavonoids in Pycnogenol(R) reduced platelet aggregation stimulated by tobacco smoke.

Journal Article↗
PubMed1999

Inhibition of smoking-induced platelet aggregation by aspirin and pycnogenol.

The effects of a bioflavonoid mixture, Pycnogenol, were assessed on platelet function in humans. Cigarette smoking increased heart rate and blood pressure. These increases were not influenced by oral consumption of Pycnogenol or Aspirin just before smoking. However, increased platelet reactivity yielding aggregation 2 hours after smoking was prevented by 500 mg Aspirin or 100 mg Pycnogenol in 22 German heavy smokers. In a group of 16 American smokers, blood pressure increased after smoking. It was unchanged after intake of 500 mg Aspirin or 125 mg Pycnogenol. In another group of 19 American smokers, increased platelet aggregation was more significantly reduced by 200 than either 150 mg or 100 mg Pycnogenol supplementation. This study showed that a single, high dose, 200 mg Pycnogenol, remained effective for over 6 days against smoking-induced platelet aggregation. Smoking increased platelet aggregation that was prevented after administration of 500 mg Aspirin and 125 mg Pycnogenol. Thus, smoking-induced enhanced platelet aggregation was inhibited by 500 mg Aspirin as well as by a lower range of 100-125 mg Pycnogenol. Aspirin significantly (p<0.001) increased bleeding time from 167 to 236 seconds while Pycnogenol did not. These observations suggest an advantageous risk-benefit ratio for Pycnogenol.

Adult↗
PubMed1999

Educational experiences and quality of life of gastroenterology fellows in the United States.

OBJECTIVE: The objective of this study was to investigate the education and quality of life of United States gastroenterology fellows. METHODS: A 3-page, 74-question survey incorporating a 5-point Likert scale was designed. All US gastroenterology fellowship program directors were contacted by mail and asked to distribute the survey to graduating fellows. Surveys were sent on 3/29/1998 and collected until 6/1/98. RESULTS: Fellows who would not train at the same institution again had less supervision, clinical instruction, research mentorship, and support services than those who would. Fellows who had loans had lower personal satisfaction scores than those who did not. Fellows who did not hold second jobs (moonlight) had higher job satisfaction scores. Those with vision or dental insurance had higher job and personal satisfaction scores. Regarding quality of life, only 23% of fellows agreed they were not overworked, 23% agreed they were not stressed, 25% agreed they were financially stable, 54% agreed they were happy with fellowship, and 84% agreed they were happy with their career choice. Regarding education, 56% agreed there was more emphasis on productivity than on education, 39% agreed they received adequate mentorship for research, 86% agreed there was adequate supervision, 48% of fellows agreed they had autonomy in making clinical decisions, and 41% agreed they had continuity of care in seeing patients. CONCLUSIONS: Most fellows were happy about their career choice and clinical instruction, but there were deficiencies regarding quality of life (stress, overwork, financial security), education (research support, continuity of care) and job benefits (health coverage).

Adult↗
PubMed1999

Immune dysfunction during alcohol consumption and murine AIDS: the protective role of dehydroepiandrosterone sulfate.

Acquired immune deficiency syndrome (AIDS) is a clinical disorder caused by the human immunodeficiency virus (HIV) after development of severe immunosuppressive changes. Chronic ethanol (EtOH) consumption accentuates the severity of murine AIDS (MAIDS). Because hormone production is often suppressed by chronic EtOH intake, as well as retrovirus infection, we investigated whether hormone supplementation during chronic EtOH consumption contributes to slowing immune dysfunction caused by LP-BM5 infection and/or EtOH use. Because dehydroepiandrosterone sulfate (DHEAS) was previously shown to have immune-enhancing properties during MAIDS, we determined whether DHEAS reduced cytokine dysregulation otherwise exacerbated by chronic EtOH intake during MAIDS. Adult female C57BL/6 mice were infected with LP-BM5 murine retrovirus. Some were fed 40% EtOH in drinking water and agar gel for 16 weeks postinfection. EtOH consumption further inhibited T- and B-cell proliferation beyond suppression due to retrovirus infection. Interleukin (IL)-2 release produced by concanavalin A-stimulated splenocytes was reduced by EtOH use by infected and uninfected mice. DHEAS overcame much of the effects induced by retrovirus infection and/or EtOH use. IL-4 secretion and IL-6 secretion were enhanced. Hepatic vitamin E levels were decreased by murine retrovirus infection, as well as by EtOH use in both uninfected and infected mice. In addition, DHEAS (0.01%) supplementation during MAIDS prevented the further dysregulation of cytokines and hepatic lipid peroxidation due to EtOH intake, partially restored T- and B-cell proliferation, and maintained hepatic vitamin E levels to near normal levels.

Adult↗
PubMed1998

Detecting single base substitutions, mismatches and bulges in DNA by temperature gradient gel electrophoresis and related methods.

Temperature gradient gel electrophoresis (TGGE) and related methods can separate DNA fragments that differ by a single base pair or defect. This article describes the basic features of TGGE, and reviews the theoretical model of DNA unwinding and its ability to predict DNA mobility in a temperature gradient gel. Recent applications of TGGE and related methods that were directed at detecting point mutations, and evaluating the effects of single site defects are also reported.

Animals↗
PubMed1992

Haemodynamic sequelae of pulmonary fibrosis following intratracheal bleomycin in rats.

OBJECTIVE: Intratracheal instillation of bleomycin in rats has been extensively used as an animal model of pulmonary fibrosis in humans, although it produces a patchy, airway based response. We proposed that the haemodynamic sequelae of the bleomycin model might be less severe than those associated with more diffuse lung injury. METHODS: Pulmonary and systemic haemodynamic indices were examined in adult Sprague-Dawley rats (approximately 400 g, n = 10) both at rest and during submaximal exercise on a rodent treadmill, approximately 60 days after intratracheal bleomycin (6 units.kg-1), and the results compared to a control group (n = 6). RESULTS: Compared to controls, mean pulmonary artery pressure (PPA) was increased by intratracheal bleomycin (p = 0.02) both at rest [24.5 (SEM 2.6) v 18.2(0.9) mm Hg] and during exercise [34.7(3.0) v 26.7(0.7) mm Hg]. PPA-pulse product was also increased, with a similar trend in right ventricular work index, but cardiac index was not altered. Right ventricular hypertrophy was noted on necropsy examination. Consistent with pulmonary fibrosis, lung dry weight, total protein, and hydroxyproline were also raised, and these values correlated strongly with (mean) PPA at rest (r2 = 0.86, 0.81, 0.69, respectively) and during exercise (r2 = 0.81, 0.79, 0.65, respectively). Packed cell volume was increased by intratracheal bleomycin, at 49(1) v 45(1)%, p = 0.02. CaO2 tended to decrease with exercise in the bleomycin group, although this was not statistically significant, while systemic oxygen delivery and consumption were not altered. CONCLUSIONS: Pulmonary hypertension and right ventricular hypertrophy occur in this model of lung fibrosis, and correlate with the severity of fibrosis. However, these sequelae were less severe than those previously demonstrated in association with crotalaria ingestion. We suggest that the haemodynamic sequelae of the intratracheal bleomycin model are consistent with patchy, airway based fibrosis, but reflect less well the haemodynamic sequelae of more diffuse fibrotic injury associated with systemic processes.

Animals↗
PubMed1988

Modulation of rat granulocyte traffic by a surface active agent in vitro and bleomycin injury.

Pluronic F68 (F68) is a nonionic surfactant which has been reported to inhibit the in vitro adherence and migration of polymorphonuclear leukocytes (PMN) obtained from some species. We demonstrated similar effects on PMN obtained from rats, with diminished adherence to nylon wool and diminished chemotaxis toward zymosan-activated serum. We then examined the in vivo effects of 12-hr F68 infusion on the injury induced by intratracheal bleomycin instillation (ITB) in rats. When sacrificed 24 hr following injury, rats demonstrated neutrophilia, neutrophil-prominent lung lavage cellularity, and increased lung weights. F68 decreased lavage leukocyte counts and lung weight gain in ITB-injured animals. Lung weights of ITB-injured animals correlated (r = 0.81, P less than 0.001) with logarithmic values of lavage PMN. F68 also enhanced neutrophilia and decreased spleen weight gain in injured animals. The acute effects of F68 on circulating leukocyte counts, osmolality, and total complement were also examined. The data demonstrate that F68 can affect PMN traffic both in vitro and in vivo. The data also confirm the prominence of PMN in lavage fluid early in ITB injury, and suggest that an influx of relatively few PMN is associated with lung weight gain in this model.

Animals↗