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Selected AbstractsEffects of Finasteride (1 mg) on Hair TransplantDERMATOLOGIC SURGERY, Issue 10 2005Matt Leavitt DO Background. The improved scalp coverage achieved by hair transplant for men with androgenetic alopecia can be diminished by continued miniaturization and loss of preexisting, nontransplanted hairs. Objectives. To evaluate whether finasteride 1 mg, administered daily from 4 weeks before until 48 weeks after hair transplant, improves scalp hair and growth of nontransplanted hair in areas surrounding the transplant and to evaluate the safety and tolerability of finasteride for men undergoing hair transplant. Methods. In this randomized, double-blind, placebo-controlled study, 79 men with androgenetic alopecia (20,45 years of age) were assigned to treatment with finasteride 1 mg (n = 40) or placebo (n = 39) once daily from 4 weeks before until 48 weeks after hair transplant. Efficacy was evaluated by review of global photographs by an expert dermatologist and by macrophotography for scalp hair counts. Results. Treatment with finasteride resulted in significant improvements from baseline, compared with placebo, in scalp hair based on global photographic assessment (p < .01) and hair counts (p < .01) at week 48. Visible increases in superior/frontal scalp hair post-transplant were recorded for 94% and 67% of patients in the finasteride and placebo groups, respectively. Finasteride treatment was generally well tolerated. Conclusion. For men with androgenetic alopecia, therapy with finasteride 1 mg daily from 4 weeks before until 48 weeks after hair transplant improves scalp hair surrounding the hair transplant and increases hair density. [source] Post natal oestrogen administration stimulates precocious endometrial gland development in the horseEQUINE VETERINARY JOURNAL, Issue 7 2009S. WILSHER Summary Reasons for performing study: Fillies completely devoid of endometrial glands (uterine gland knockout; UGKO) would make ideal experimental models in which to study the role of endometrial histotroph in embryogenesis and early fetal development in the mare. Hypothesis: Administration of a synthetic progestagen plus oestrogen to newborn filly foals and, thereafter, at regular intervals to age 6 months, would permanently suppress endometrial gland development. Methods: Nine half-sister Thoroughbred filly foals were treated, in 3 groups, with: A) the weakly active progestagen, norgestomet, administered from birth to age 6 months, in subcutaneous implant form plus oestradiol valerate and norgestomet i.m. at fortnightly intervals; B) the strongly active oral progestagen, altrenogest, administered daily from birth to age 6 months plus fortnightly injections of oestradiol valerate and norgestomet; C) nothing (untreated controls). Endometrial biopsies were recovered from all fillies at ages 6 months and 2 years to assess the degree of endometrial gland morphogenesis and to determine immunohistochemically the presence or absence of oestrogen and progesterone receptors in the endometrial tissues. Results: Groups B and C showed no endometrial gland development, whereas Group A fillies showed a high degree of endometrial gland development, plus strong staining for both oestrogen and progesterone receptors at age 6 months. All 9 fillies showed full normal endometrial gland morphogenesis, development and function at age 2 years. Conclusions and relevance: While the administration of a strongly active progestagen over-rode the actions of the concomitantly administered oestrogen and suppressed endometrial gland development during the period of administration, treatment with oestradiol valerate together with a weakly active progestagen, stimulated precocious endometrial gland development. Neither steroid was able to create the desired UGKO experimental model and all fillies showed normal endometrial gland development and fertility after puberty. Hence, ovarian oestrogen, not progesterone, appears to be the basic stimulus for endometrial gland morphogenesis in the horse. [source] Partial and transient modulation of the CD3,T-cell receptor complex, elicited by low-dose regimens of monoclonal anti-CD3, is sufficient to induce disease remission in non-obese diabetic miceIMMUNOLOGY, Issue 1 2010Devangi S. Mehta Summary It has been established that a total of 250 ,g of monoclonal anti-mouse CD3 F(ab,)2 fragments, administered daily (50 ,g per dose), induces remission of diabetes in the non-obese diabetic (NOD) mouse model of autoimmune diabetes by preventing , cells from undergoing further autoimmune attack. We evaluated lower-dose regimens of monoclonal anti-CD3 F(ab,)2 in diabetic NOD mice for their efficacy and associated pharmacodynamic (PD) effects, including CD3,T-cell receptor (TCR) complex modulation, complete blood counts and proportions of circulating CD4+, CD8+ and CD4+ FoxP3+ T cells. Four doses of 2 ,g (total dose 8 ,g) induced 53% remission of diabetes, similarly to the 250 ,g dose regimen, whereas four doses of 1 ,g induced only 16% remission. While the 250 ,g dose regimen produced nearly complete and sustained modulation of the CD3 ,TCR complex, lower doses, spaced 3 days apart, which induced similar remission rates, elicited patterns of transient and partial modulation. In treated mice, the proportions of circulating CD4+ and CD8+ T cells decreased, whereas the proportions of CD4+ FoxP3+ T cells increased; these effects were transient. Mice with greater residual ,-cell function, estimated using blood glucose and C-peptide levels at the initiation of treatment, were more likely to enter remission than mice with more advanced disease. Thus, lower doses of monoclonal anti-CD3 that produced only partial and transient modulation of the CD3,TCR complex induced remission rates comparable to higher doses of monoclonal anti-CD3. Accordingly, in a clinical setting, lower-dose regimens may be efficacious and may also improve the safety profile of therapy with monoclonal anti-CD3, potentially including reductions in cytokine release-related syndromes and maintenance of pathogen-specific immunosurveillance during treatment. [source] Evaluation of the antithyroid, antioxidative and antihyperglycemic activity of scopoletin from Aegle marmelos leaves in hyperthyroid ratsPHYTOTHERAPY RESEARCH, Issue 12 2006Sunanda Panda Abstract Scopoletin (7-hydroxy-6-methoxy coumarin) was isolated from the leaves of Aegle marmelos and evaluated for its potential to regulate hyperthyroidism, lipid peroxidation and hyperglycemia in levo-thyroxine-induced hyperthyroid rats. Scopoletin (1.00 mg/kg, p.o.) administered daily for 7 days to levo-thyroxine-treated animals decreased the levels of serum thyroid hormones and glucose as well as hepatic glucose-6-phosphatase activity, demonstrating its potential to regulate hyperthyroidism and hyperglycemia. Scopoletin also inhibited hepatic lipid peroxidation and increased the activity of antioxidants, superoxide dismutase and catalase. Compared with the standard antithyroid drug, propylthiouracil, scopoletin exhibited a superior therapeutic activity, since unlike propylthiouracil, it also inhibited hepatic lipid peroxidation. These findings indicate that scopoletin has the potential to inhibit thyroid function and hyperglycemia without hepatotoxicity. Copyright © 2006 John Wiley & Sons, Ltd. [source] |