Concurrent Chemoradiotherapy Induces Body Composition Changes in Locally Advanced Head and Neck Squamous Cell Carcinoma: Comparison between Oral Cavity and Non-Oral Cavity Cancer.

Few prospective cohort trials have evaluated the difference in treatment-interval total body composition (TBC) changes assessed by dual-energy X-ray absorptiometry (DXA) between two patient subgroups with locally advanced head and neck squamous cell carcinoma (LAHNSCC) receiving concurrent chemoradiotherapy (CCRT): oral cavity cancer with adjuvant CCRT (OCC) and non-oral cavity with primary CCRT (NOCC). This study prospectively recruited patients with LAHNSCC. Clinicopathological variables, blood nutritional/inflammatory markers, CCRT-related factors, and TBC data assessed by DXA before and after treatment were collected. Multivariate linear regression analysis identified the factors associated with treatment-interval changes in body composition parameters, including lean body mass (LBM), total fat mass (TFM), and bone mineral content (BMC). A total of 127 patients (OCC (n = 69) and NOCC (n = 58)) were eligible. Body composition parameters were progressively lost during CCRT in both subgroups. Extremities lost more muscle mass than the trunk for LBM, whereas the trunk lost more fat mass than the extremities for TFM. BMC loss preferentially occurred in the trunk region. Different factors were independently correlated with the interval changes of each body composition parameter for both OCC and NOCC subgroups, particularly mean daily calorie intake for LBM and TFM loss, and total lymphocyte count for BMC loss. In conclusion, treatment-interval TBC changes and related contributing factors differ between the OCC and NOCC subgroups.

Effects of phytoestrogens on the activity and growth of primary breast cancer cells ex vivo.

AIM: To explore the ex vivo effects of phytoestrogens on primary human breast cancer cells. METHODS: Breast cancer cells were obtained from patients who underwent primary breast cancer surgery, which were treated with 10-8 M 17ß-estradiol (E2 ), one of three phytoestrogens (genistein, resveratrol and quercetin, 10-7 M), and a combination of E2 and one of the three phytoestrogens for 48 h. These cells were then extracted for viability and apoptosis assay. The proteins involved in the proliferative and apoptotic pathways were evaluated by western blot analysis. RESULTS: Human breast cancer cell viability was inhibited by all phytoestrogens but induced by E2 with or without phytoestrogen. Apoptotic cells, as well as the proteins involved in apoptotic pathway and estrogen receptor (ER) ß, were significantly increased in the cells treated with phytoestrogen alone. The use of E2 with or without a phytoestrogen revealed completely opposite results. The proteins involved in the proliferative pathway and ER α expression were all increased in the cultures with E2 with or without phytoestrogens. CONCLUSION: In the presence of E2 , these phytoestrogens lose the effects of suppressing breast cancer cells; contrastingly, induce growth stimulatory effects by inhibiting apoptosis and stimulating proliferation in primary breast cancer cells. Thus, the effects of phytoestrogens on breast cancer should be considered as E2 still present in breast cancer tissue.

Efficacy of Femarelle for the treatment of climacteric syndrome in postmenopausal women: An open label trial.

OBJECTIVE: To assess the effects of 2 months of treatment with Femarelle for climacteric syndrome in Taiwanese postmenopausal women. MATERIALS AND METHODS: A multi-center, open-label trial of 260 postmenopausal women, age ≥ 45 years with vasomotor symptoms. Women were enrolled after obtaining a detailed medical history and a thorough physical examination. They then received Femarelle (640 mg/d) twice daily for 8 weeks. The primary outcome was the changes in the frequency and severity of hot flushes from baseline to 4 weeks (1 month) and 8 weeks (2 months). Changes of general climacteric syndrome were assessed using a modified climacteric scale designed by Greene. RESULTS: The frequency and severity of hot flushes were significantly improved with Femarelle use (p < 0.001). After 8 weeks of treatment, the percentage of women with various climacteric syndromes was reduced (from 100% to 20.9% for hot flushes, from 97.7% to 87.9% for psychological symptoms, from 93.8% to 78.8% for somatic symptoms, and from 87.8% to 74.9% for sexual symptoms). General climacteric syndrome scores also significantly decreased, from 20.8 ± 0.7 at the time of enrollment to 12.9 ± 0.7 after 8 weeks of Femarelle treatment (p < 0.0001). Participants experienced improvement of various climacteric symptoms and signs after 8 weeks of treatment (75.1% for hot flushes, 68.7% for psychological symptoms, 70.6% for somatic symptoms, and 69.0% for sexual problems respectively). After 4 weeks and 8 weeks of treatment with Femarelle, patients showed statistically significant improvement in climacteric symptoms (p < 0.0001). Three women (1.2%) withdrew from the study after 4 weeks of treatment due to adverse effects. CONCLUSION: Femarelle significantly improved climacteric symptoms in Taiwanese postmenopausal women. However, further evaluation is needed regarding the safety of long-term consumption.

[Effect of Dahuangzhechong pill on the gene expression spectra of preventing arterial thrombosis].

OBJECTIVE: To investigate the effect of Dahuangzhechong pill on the gene expression spectra of preventing arterial thrombosis, and reveal its mechanism on molecule level. METHODS: Mononuclear cell and blood platelet of the arterial thrombosis patients were separated before and after treatment by Dahuangzhechong pill. Their RNA was extracted respectively and the genes expressions were detected using gene array containing 14,000 gene. RESULTS: 44 genes up-expressed and 299 genes down-expressed in blood platelet, 252 genes expression increased and 299 genes expression decreased in mononuclear cell genes after treated with Dahuangzhechong pill. The cluster analysis showed that the genes contained ion channel and transport protein, apoptosis related protein, DNA synthesis, repair and transcription factor, cell receptor, cell signal and transducin, and protein translation and synthesis, etc. CONCLUSION: Dahuangzhechong pill may prevent arterial thrombosis through genes containing ion channel and transport protein, apoptosis related protein, DNA synthesis, repair and transcription factor, cell receptor, cell signal and transducin, and protein translation and synthesis, etc.

[Effects of Tongxinluo on cell viability and tissue factor in AngII induced vascular endothelial cells].

OBJECTIVE: To determine the effects of Tongxinluo on cell viability and tissue factor (TF) in AngII induced vascular endothelial cells and to investigate its mechanism. METHODS: AngII(10(-6)mol/L) was added to human vascular endothelial cells (HUVECs) culture media alone or with various concentration of Tongxinluo drug containing plasma (5%,10%, and 20%) added 30 minutes before AngII. Cell viability was evaluated after 24-hour incubation with AngII in a dose manner. TF, AngII type 1 receptor (AT(1)) mRNA, NO synthase (NOS) and NO were observed after 24-hour incubation with AngII. In addition, NOS inhibitor nomega-nitro-larginine (L-NAME) was added 30 minutes before Tongxinluo and AngII. Cell viability, TF, AT(1)mRNA, the level of NOS and NO were evaluated after 24-hour incubation with Tongxinluo and AngII. RESULTS: Tongxinluo significantly improved AngII induced endothelial cell viability and the effect was the most obvious at 10%. Tongxinluo (10%) decreased the TF and AT(1) mRNA while increased the NOS and NO levels. L-NAME obviously inhibited the effects of Tongxinluo on cell viability, TF, AT(1) mRNA, and NOS and NO levels. CONCLUSION: Up-regulating NOS-NO signaling may be the mechanism of Tongxinluo on cell viability and TF in AngII induced vacular endothelial cells.

Effect of Feitai on bleomycin-induced pulmonary fibrosis in rats.

The current therapeutic approaches for pulmonary fibrosis, which is characterized by fibroblast proliferation and extracellular matrix remodeling, are unsatisfactory. Feitai, consisting of several herbs, is a folk formula for pulmonary tuberculosis therapy in China. To investigate the effects of Feitai on pulmonary fibrosis, Feitai was administered orally to bleomycin (BLM)-treated rats, and the lung toxicity effects were evaluated according to inflammatory cell count, protein concentration, and lactate dehydrogenase (LDH) activity in the bronchoalveolar lavage fluid (BALF), malondialdehyde level and hydroxyproline content in lung tissue 28 days post-BLM. Serial sections of the lung were stained with hematoxylin and eosin (HE) and Masson trichrome, respectively. The degree of fibrosis was assessed quantitatively using LEICA QWin image analyzer. Results showed that Feitai inhibited BLM-induced lung fibrotic lesions in a dose-dependent manner as reflected by decreased the lung hydroxyproline content and lung fibrosis fraction 28 days after BLM instillation. Treatment with Feitai also significantly ameliorated the BLM-induced lung toxicity effects detected in BALF and lung tissue. The effects in vitro on WI-38 human lung fibroblast cell line showed that Feitai significantly reduced the cell proliferation and transforming growth factor (TGF)-beta stimulated type I collagen synthesis. These results strongly demonstrate that Feitai may be useful in the treatment of pulmonary fibrosis.

Feitai attenuates bleomycin-induced pulmonary fibrosis in rats.

Pulmonary fibrosis is a common consequence of numerous pulmonary diseases. The current therapeutic approaches for this condition are unsatisfactory. Feitai, a composite formula consisting of several herbs, is used in China as a folk remedy for treating patients with pulmonary tuberculosis. In this study, we extensively investigate the effects and mechanisms of Feitai on bleomycin (BLM)-induced pulmonary fibrosis in rats. One hundred and twenty male Sprague-Dawley rats were randomly divided into four groups, referred to as the saline-water, saline-Feitai, BLM-water, and BLM-Feitai groups. Following a single instillation of BLM (5 mg/kg) or saline, rats were orally administered Feitai at a dose of 3 g/kg body weight or sterilized distilled water once daily. Rats were killed at 7, 14, or 28 d post-BLM. Inflammatory cell count, protein concentration, and lactate dehydrogenase activity in bronchoalveolar lavage fluid were measured, and myeloperoxidase activity and lipid peroxide content in lung homogenates were analyzed. Treatment with Feitai inhibited lung fibrotic progression induced by BLM, as indicated by the decrease in lung hydroproline content and lung fibrosis score at 28 d post-BLM. This was accompanied by significant amelioration of BLM-induced body weight loss, lung edema, and inflammatory response during the development of lung injury in the acute phase. The results strongly indicate the beneficial effects of Feitai in protecting against BLM-induced pulmonary fibrosis. Furthermore, the inflammatory response and lipid peroxidation were inhibited by Feitai, suggesting that the effect of this formula on BLM-induced lung injury and fibrosis is associated with antiinflammatory and antioxidant properties.

[Relationship between pathological development of phlegm-stasis and expression of actin in vascular smooth muscle cell in atherosclerosis rat model].

OBJECTIVE: To explore the dynamic change of Phlegm-stasis in the rat atherosclerotic model as the time goes on. METHODS: Adopting high fat forage fed to develop the atherosclerotic model in rats, and the changes of blood lipid, hemorrheology, blood glucose, insulin and vascular smooth muscle cell (VSMC) actin expression were detected by biochemical and immunohistochemical assay at various time points after modeling. RESULTS: The expression of VSMC actin gradually increased along with the change of model rats' Syndrome from Phlegm to stasis, i.e., the change of parameters, including blood lipid, hemorrheologic parameters, blood glucose, insulin and insulin sensitive indexes along with the aggravation of disease. CONCLUSION: The expression of VSMC actin could be the molecular mechanism for the Syndrome developing from Phlegm to stasis in atherosclerotic rats.