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Biomedical subjects

S Tenenbaum

Publications and source records attributed to S Tenenbaum.

8 recordsLinked to original sources
PubMed2002

An experimental comparison of Pycnogenol and methylphenidate in adults with Attention-Deficit/Hyperactivity Disorder (ADHD).

Twenty-four adults (24 to 53 years old) with Attention-Deficit/Hyperactivity Disorder (ADHD), Combined Type, were studied in a double-blind, placebo-controlled, crossover study of Pycnogenol and methylphenidate. Pycnogenol is an antioxidant derived from the bark of the French maritime pine tree. Methylphenidate is a standard pharmaceutical intervention for ADHD. Anecdotal reports suggest that Pycnogenol improves concentration in adults with ADHD without adverse side effects. Participants received Pycnogenol, methylphenidate, and placebo, each for three weeks, in a randomized and counterbalanced order. Although ADHD symptoms improved during treatment, neither methylphenidate nor Pycnogenol outperformed the placebo control, as measured by self-report rating scales, rating scales completed by the individual's significant other, and a computerized continuous performance test. The conservative dosage levels and relatively brief length of treatment may have contributed to the absence of significant differences among treatment conditions. Implications for future research are noted.

Adjuvants, Immunologic↗
PubMed1996

The interaction of a type A retroviral particle and class II human leukocyte antigen susceptibility genes in the pathogenesis of Graves' disease.

We have previously reported that over 85% of patients with Graves' disease have detectable serum antibodies against a human intracisternal type A retroviral particle (HIAP), which are not present in age- and gender-matched controls, suggesting a role for HIAP in triggering the autoimmune process leading to Graves' disease. To investigate the interaction of this viral particle with genetic factors, 35 members of 3 kindreds, selected because of a high family prevalence of Graves' disease (a total of 11 members affected), were examined for clinical signs of thyroid dysfunction, goiter, and opthalmopathy. Thyroid function tests and autoimmune serological profiles were also obtained. In addition, subjects were tested for the presence of antibodies against HIAP by means of immunoblot analysis of their sera, and their human leukocyte antigen (HLA) class II alleles were determined by DNA methodology. Molecular genetic analyses enabled the detection of postulated HLA susceptibility haplotypes in each family. These families had 8, 4, and 5 members, respectively, with such apparent susceptibility genes and 11, 5, and 9 members, respectively, with immunological evidence of retroviral exposure. In the presence of both factors (codetected in a total of 15 members of the 3 kindreds), the incidence of Graves' disease was 100%, 67%, and 80%, respectively. One additional member of family B and 3 in family C with both viral and genetic susceptibility factors were found to have serological abnormalities and/or goiter and ocular signs consistent with evolving or preclinical Graves' disease. In families A and C, tight linkage between HLA haplotypes and Graves' disease was demonstrated in a manner consistent with recessive inheritance. The association between the occurrence of both anti-HIAP-I antibody positivity and HLA susceptibility and the presence of Graves' disease was highly significant (P < 0.001). The pathogenesis of Graves' disease in these families appears to be attributable to the interaction between the immune response to an intracisternal type A retroviral particle and immunogenetic susceptibility, leading to the autoimmune processes that underlie Graves' disease, with subsequent development of the characteristic features of the illness. Data from these families suggest that both of these factors are necessary for final disease expression. These results imply that serological evidence of retroviral exposure together with genetic HLA susceptibility are the two major predisposing factors underlying the pathogenesis of Graves' disease. Further studies will establish whether prospective identification of persons at risk for Graves' disease is possible by this means.

Adult↗
PubMed1995

Evidence for a retroviral trigger in Graves' disease.

An apparently high frequency of Graves' disease encountered in New Orleans, Louisiana, prompted an investigation for a possible infectious agent that might be triggering the disease in genetically susceptible individuals. We studied 40 patients with Graves' disease, and compared them to the following groups of controls: age and gender matched healthy subjects; patients with multinodular goiter (non-autoimmune thyroid controls); patients with chronic lymphocytic thyroiditis (autoimmune thyroid disease controls) and additional organ or tissue specific autoimmune controls exclusive of thyroid autoimmunity, including patients with Type I diabetes and other endocrine autoimmune complex disorders. Serum antibodies against a prototypic strain of a human intracisternal A-type retroviral particle type 1 (HIAP-1) were detected by a sensitive and specific immunoblotting assay. In 87.5% (35/40) of the Graves' disease patients there was a positive reaction against several HIAP-1-associated proteins, predominantly 97 Kd and 80 Kd, with only 5 showing no reactivity to any. In contrast, 2% (2/105) of sera from normal controls showed positive reactivity. Furthermore, only 10% (1/10) of sera from multinodular goiter control patients and 10% (1/10) of Hashimoto's patients showed reactivity (p < 0.0005). Sera from 3 of 20 (15%) of Type I diabetic patients none of whom had Graves' disease, showed reactivity but there was no reactivity in 9 other patients with one or more of the endocrine autoimmune complex disorders, including Addison's disease, vitiligo, myasthenia gravis and pernicious anemia. In addition we studied two individuals with Graves' disease from each of two families residing outside Louisiana, all of whom were positive for these antibodies.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1984

A quantitative in vitro assay for the evaluation of phototoxic potential of topically applied materials.

A quantitative in vitro method for phototoxic evaluation of chemicals has been developed and validated. The assay uses Saccharomyces cerevisiae, seeded in an agar overlay on top of a plate count agar base. 8-Methoxy psoralen is used as a reference standard against which materials are measured. Activity is quantified by cytotoxicity measured as zones of inhibition. Several known phototoxins (heliotropine, lyral, phantolid, and bergamot oil) and photoallergens (6-methyl coumarin and musk ambrette) are used to validate the assay. An excellent correlation is observed between in vivo studies employing Hartley albino guinea pigs and the in vitro assay for several fragrance raw materials and other chemicals. The in vitro assay exhibits a greater sensitivity from 2-500 fold. For three fragrance oils, the in vitro assay detects low levels of photobiological activity while the in vivo assay is negative. Although the in vitro assay does not discriminate between phototoxins and photoallergens, it can be used for screening of raw materials so that reduction in animal usage can be achieved while maintaining the protection of the consumer.

Administration, Topical↗
PubMedDate not supplied

Prevention of duodenal ulcer formation in the rat by dietary vitamin A supplementation.

We have shown previously that supplemental vitamin A (Vit. A) increases the early inflammatory response to wounding and enhances the collagen content of the intestine of normal and injured rats. We now report the effect of dietary supplementation with Vit. A on the prevention of duodenal ulcer (DU) in rats caused by intragastric administration of cysteamine-HCl. A major way cysteamine-HCl induces DU formation is by enhancing gastric acid secretion. Adult male rats were divided into two groups: (1) rats fed a standard rat Chow (Purina) (15 IU Vit. A/g diet) containing two to three times the National Research Council recommended daily allowance for Vit. A for normal rats; (2) rats fed the same supplemented with 150 IU of Vit. A palmitate per/g Chow. One week later, all rats were given 1 ml of cysteamine-HCl (135 mg) intragastrically. The rats were maintained on their respective diets. Two days later, all rats were killed with ether, the stomach and duodenum excised, and examined for the presence of ulcers. No gastric ulcers were found in either group. There was a statistically significant decrease in the incidence of DUs in the Vit. A-supplemented group when compared to the control group (p less than 0.01) 48 hr following cysteamine-HCl administration; 32% of the Vit. A-supplemented rats developed a DU whereas 74% of rats fed standard Chow had DUs. Most rats had a single DU in the first part of the duodenum, occasionally a second ulcer was noted in the same area. Dietary supplementation with Vit. A had no effect on gastric acid production. In conclusion, our data show that Vit. A dietary supplementation is effective in preventing formation of DUs caused by cysteamine-HCl administration to rats. This effect does not appear to be due to reduction of gastric acid output.

Animals↗