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BackgroundTaxol is a powerful chemotherapy agent leading to mitotic arrest and cell death; however, its clinical efficacy has been hampered due to the development of drug resistance. Taxol specifically targets the cell cycle. Progress through mitosis (M stage) is an absolute requirement for drug-induced death because cell death is markedly reduced in cells blocked at the G1-S transition. The measured doubling time for ovarian cancer cells is about 27 h. As such, during treatment with Taxol most of the cells are not in the M stage of the cell cycle. Thus, the effect of cell-cycle synchronization was investigated in regard to reversing Taxol resistance in ovarian cancer cells.MethodsGiemsa-Wright staining was used for assessing the morphology of the cells. The doubling time of the cells was calculated using formula as follows: Td = In2/slope. The resistant index and cell cycle were measured via MTT assays and flow cytometry. Thymidine was used to induce cell-cycle synchronization, and cell apoptosis rates following exposure to Taxol were measured using a flow cytometer.ResultsThe growth doubling time of two Taxol-resistant cell lines were longer than that of Taxol-sensitive cells. Apoptotic rates in Taxol-sensitive and -resistant cell lines after synchronization and exposure to Taxol were all higher compared to unsynchronized controls (p <0.05).ConclusionsSynchronization of the cell-cycle resulted in an increased effectiveness of Taxol toward ovarian cancer cell lines. We speculated that formation of drug resistance toward Taxol in ovarian cancer could be partly attributed to the longer doubling time of these cells.

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Objective: Apathetic hyperthyroidism can be misdiagnosed or diagnosed late, and older patients are often susceptible to adverse effects of treatment for thyrotoxicosis. The aim of this study was to identify factors associated with apathetic hyperthyroidism. Methods: We retrospectively examined serum calcium, phosphorus and bone-specific alkaline phosphatase (BAP) levels and thyroid-associated variables in 140 patients with apathetic hyperthyroidism, 456 patients with typical hyperthyroidism and 120 healthy subjects. Results: Significant differences were identified with respect to age, serum calcium and corrected calcium, serum phosphorus, thyroid-stimulating hormone (TSH), free triiodothyronine (FT₃), free thyroxine (FT₄), the FT₃/FT₄ ratio, alanine aminotransferase (ALT), aspartate aminotransferase (AST), creatinine, BAP and albumin among the typical and apathetic hyperthyroid and normal groups (all p < 0.001). Univariate logistic regression showed that age, serum calcium and corrected calcium, serum phosphorus, TSH, FT₄, FT₃/FT₄ ratio, ALT, AST and BAP were significantly associated with apathetic hyperthyroidism, and multivariate logistic regression showed that age, corrected calcium, TSH, FT₄, FT₃/FT₄ ratio, BAP and ALT were significantly associated with apathetic hyperthyroidism. Conclusion: Greater age, increased corrected calcium levels, decreased TSH levels, increased FT₄, a decreased FT₃/FT₄ ratio, increased BAP levels and increased ALT levels may be significant factors for differentiating apathetic from typical hyperthyroidism. Coordinated assessment of these variables may aid in the accurate diagnosis and treatment of this disorder.

Objective: Estrogen receptor-α36 (ER-α36), a newly identified variant of ER-α, is predominantly membrane-based and mainly mediates nongenomic estrogen signaling. In this study, we investigated the expression of ER-α36 in human endometrial carcinoma tissues to understand the relationship between its expression and clinicopathological characteristics. Methods: ER-α36 expression was assessed by immunostaining in 73 endometrial carcinomas, 20 normal endometrial tissues, and 9 with atypical endometrial hyperplasia. Correlations between ER-α36 protein expression and clinicopathological characteristics were investigated. Results: The expression of ER-α36 in endometrial carcinoma tissues was significantly lower than in normal endometrial tissues and atypical hyperplasia (p < 0.01). ER-α36-negative tissues were significantly more likely than ER-α36-positive tumors to have tumor involvement of the cervix (p < 0.05). The disease-free survival rate of patients with ER-α36 expression was poorer than that of those who were negative for ER-α36 expression (p < 0.01). There was no significant relationship between ER-α36 expression and patient age, surgical staging, histological differentiation, myometrial invasion, lymph node metastasis, and pathological types (p > 0.05). Conclusions: ER-α36 may be an important biomarker for diagnosis, prognostication, and treatment choice in endometrial carcinoma.