Lack of association between leptin G2548A gene polymorphism and Behçet''s disease

Background Behçet's disease is a chronic, multisystem, inflammatory disease characterized by the predominance of T‐helper 1 cytokines. The disease is also characterized by infiltration of lymphocytes and neutrophils into the affected tissues. Because cytokines are involved in the regulation of lymphocyte and phagocyte functions, they may play an important role in the pathogenesis of Behçet's disease. Leptin, a member of the gp 130 family of cytokines, induces a strong T‐helper 1 response and is regarded as a proinflammatory inducer. Recent studies have shown that serum leptin concentration was increased in patients with Behçet's disease and correlated with disease activity. Objectives We aimed to investigate the role of G2548A polymorphism of leptin gene in patients with Behçet's disease and compare the results with healthy controls. Patients and methods A total of 93 subjects with Behçet's disease and 125 healthy controls were included in this study. Analyses of G‐2548A polymorphism of the LEP gene were performed using the PCR‐restriction fragment length polymorphism technique. The genotypes (GG, GA, and AA of leptin G2548A) and alleles (G and A of leptin 2548) were scored and the frequency was estimated. The frequencies of the alleles and genotypes in patients and controls were compared. We analysed the correlation between leptin gene polymorphism and the clinical features of BD. Results Both genotype and allele frequencies were not significantly different between controls and Behçet's disease patients [OR = 0.67, 95% CI (0.35–1.29), P = 0.197 and OR = 0.77, 95% CI (0.52–1.15), P = 0.184]. We did not find any significant relationship between leptin gene polymorphism and the clinical features of BD (P > 0.05). Conclusion In the present case‐control study, we found no evidence of an association between the G‐2548A variant of the leptin gene and BD among Turks. Further studies are needed to investigate serum leptin level to explain the mechanisms behind the lack of association between leptin G2548A gene polymorphism and BD.     

Ranitidine 300 mg twice daily and 150 mg four-times daily are effective in healing erosive oesophagitis.

BACKGROUND: Ranitidine 150 mg q.d.s. is the currently recommended dosage in the United States for the treatment of erosive oesophagitis. To determine whether a higher dose of ranitidine administered less frequently would also be effective in healing erosive oesophagitis, we compared ranitidine 300 mg b.d. with ranitidine 150 mg q.d.s. in the treatment of erosive oesophagitis. METHODS: This multicentre, double- blind, randomized, placebo-controlled study conducted in the United States compared two dosages of ranitidine in 772 patients with endoscopically diagnosed erosive oesophagitis. Patients were treated with ranitidine 300 mg b.d., ranitidine 150 mg q.d.s. or placebo for up to 12 weeks. Endoscopies were repeated after 4, 8 and 12 weeks of treatment. RESULTS: Ranitidine 300 mg b.d. was significantly more effective than placebo in healing erosive oesophagitis at weeks 8 and 12 (51 vs. 36% and 66 vs. 52%, respectively; P < or = 0.004). Significantly higher healing rates were also achieved with ranitidine 150 mg q.d.s. compared with placebo at 4, 8 and 12 weeks (37 vs. 21%, 62 vs. 36% and 77 vs. 52%, respectively; P < 0.001). Healing rates were significantly higher with ranitidine 150 mg q.d.s. than with ranitidine 300 mg b.d. at all scheduled endoscopies (P < or = 0.041). CONCLUSIONS: Ranitidine 300 mg b.d. is effective in healing erosive oesophagitis and may be appropriate as an alternative dosage regimen to ranitidine 150 mg q.d.s. in some patients with erosive oesophagitis.     

医院也要引进市场营销的理念

介绍了市场营销的理念,讨论了市场营销观念的演变在医院经营实践中的价值、医院在市场营销中的部分操作方法与全员参与.     

Androgen Receptor Expression Along with Loss of bcl-2, ER, and PR Expression in Benign and Malignant Apocrine Lesions of the Breast: Implications for Therapy

Abstract: Apocrine lesions of the breast are not uncommon. Limited studies have suggested that apocrine cells may be under the influence of an androgenic, rather than an estrogenic, regulatory system. Furthermore, a recent study has shown that metaplastic apocrine cells of the breast lack expression of bcl-2, a B-cell leukemia/lymphoma gene protein whose expression in the breast is believed to be regulated by estrogen. This study was undertaken to immunohistochemi-cally assess the status of expression of estrogen receptor (ER), progesterone receptor (PR), bcl-2, and androgen receptor (AR), in a series of mammary apocrine lesions ranging from simple metaplasia to metastatic carcinoma, and to determine whether there is any possible interrelationship or correlation between the expression of these hormone receptors and that of bcl-2. Among 102 apocrine lesions (68 benign and 34 malignant) evaluated, 100 (98%) were ER and PR negative; only two intraductal carcinomas (IDCA, 2%) were weakly positive for ER and PR. Bcl-2 was detectable only in these two IDCA, but not in any of the other apocrine lesions. In contrast, AR positivity was evident in 15 of 16 (94%) benign apocrine lesions and 18 of 25 (72%) cancerous apocrine lesions (13 of 16 IDCA, 5 of 8 invasive carcinomas, and 0 of 1 metastatic carcinoma) evaluated; all 7 AR negative cancerous lesions (3 IDCA, 3 invasive carcinomas, and 1 metastatic carcinoma) were poorly differentiated with pronounced atypia. These results suggest that apocrine differentiation appears to be associated with retention of AR positivity and a reversal of the usual mammary hormone receptor expression profile for ER, PR, and bcl-2 oncoprotein. These findings warrant exploration of the value of androgenic hormone manipulations in management of AR-positive apocrine carcinomas.?