Climatic conditions and the onset of primary spontaneous pneumothorax: an investigation of the influence of solar terms

To study the correlation between climatic changes and the development of primary spontaneous pneumothorax [PSP]. We retrospectively studied the relationship between 337 patients with conservatively treated PSP and meteorological conditions during a 3-year period in the urban area of Xi'an, China. The comparison was made depending on solar terms and on different aspects of atmospheric pressure, outdoor temperature, relative humidity, and wind speed. Significant differences were found between PSP and non-PSP days depending on daily mean values of outdoor temperature and atmospheric pressure [p = 0.001 and p < 0.001, respectively]. However, no obvious differences of meteorological factor variations between the 'PSP day' and the 'pre-PSP day' on days with and without PSP were found. The occurrence of PSP was associated with the solar terms Spring Equinox [p < 0.05] and End of Heat [p < 0.01]. Among the factors examined in our study, daily mean outdoor temperature and atmospheric pressure showed a strong correlation with the occurrence of PSP. The solar terms Spring Equinox and End of Heat were found to be closely related with PSP development, which shed light on a new way for PSP incidence evaluation

Effect of fractioned irradiation on HIF-1alpha and MDR1 expression in esophageal cancer cells / 南方医科大学学报

<p><b>OBJECTIVE</b>To examine the effect of fractioned ionizing radiation on the expression of hypoxia inducible factor-1alpha (HIF-1alpha) and multidrug resistance (MDR1) in human esophageal cancer cells.</p><p><b>METHODS</b>The mRNA and protein levels of HIF-1alpha and MDR1 in esophageal caner EC9706 cells incubated in the presence of 150 micromol/L CoCl(2) were measured before and after the irradiation by quantitative RT-PCR and Western blotting, respectively. The chemosensitivity and radiosensitivity of the cells were analyzed by MTT assay and clone formation assay.</p><p><b>RESULTS</b>MDR1 and HIF1alpha expressions were significantly up-regulated in the cells following hypoxia or irradiation (P<0.05). The surviving cell fraction in the exclusive irradiation group was significantly lower than that irradiation+hypoxia group (P<0.05). Compared with exclusive hypoxia group, MDR1 and HIF1alpha expressions were decreased significantly in irradiation+hypoxia group (P<0.05). HIF1alpha expression showed a positive correlation to MDR1 expression (P<0.01).</p><p><b>CONCLUSION</b>Hypoxia is an important factor to induce resistance to chemo- and radiotherapy. Low-dose fractioned irradiation can lower MDR1 and HIF1alpha expressions in esophageal cancer cells, which should be considered when combining radiotherapy chemotherapy for esophageal cancer patients.</p>

nm23-H1 gene inhibits lung cancer cell invasion through down-regulation of PKC signal pathway / 中华肿瘤杂志

<p><b>OBJECTIVE</b>To study the molecular mechanisms of nm23-H1 for regulating PKC signal pathway before and after transfection with nm23-H1 gene.</p><p><b>METHODS</b>Using Western-blot, Boyden-chamber, MTT and laser scanning confocal microscopy (LSCM) techniques to detect the distribution of PKC in cytosol and plasma membrane, changes of invasion and proliferation activity, PKC translocation status and changes of intracellular Ca(2+) concentration among different human pulmonary carcinoma cells with transfected or untransfected nm23-H1 gene, and changes of the three cell lines after treatment with Calphostin C, a PKC inhibitor.</p><p><b>RESULTS</b>(1) The expression of PKCalpha, PKCbeta II on L9981 and L9981-pLXSN cell membrane, which was in activated status, was remarkably higher than those in L9981-nm23-H1 cell line (P < 0.001). The expression of PKCalpha, PKCbeta II in cytosol in L9981 and L9981-pLXSN cell lines, which was in inactivated status, was lower than those in L9981-nm23-H1 cell line (P < 0.001). It means that the PKC signal pathway was activated in L9981 and L9981-pLXSN cell lines. (2) PKCalpha and PKCbeta II mainly located in nuclei and perinuclear area in L9981 and L9981-pLXSN cells, which were in active status, and the Ca(2+) concentration in these cells was obviously higher than that in L9981-nm23-H1 cell line (P < 0.01). In L9981-nm23-H1 cell line, which was transfected with nm23-H1 gene, PKCalpha and PKCbeta II mainly located in soluble cytosolic section, in an inactive status. (3) The invasion and proliferation ability of L9981 and L9981-pLXSN lung cancer cells was higher than that of L9981-nm23-H1 cell line (P < 0.001). There was no statistically significant difference between L9981 and L9981-pLXSN cell lines (P > 0.05). (4) After treated with PKC inhibitor Calphstin C, the expression of PKC and PKCbeta II in membrane in L9981 and L9981-pLXSN cell lines was down-regulated (P < 0.001), PKCalpha and PKCbeta II were mainly located in cytosolic area, mainly in an inactive status, and the Ca(2+) concentration was found to be decreased in all the three cell lines. The invasion and proliferation ability of the three lung cancer cell lines were obviously decreasing (P < 0.001). However, the invasion and proliferation ability of L9981-nm23-H1 lung cancer cell line was still lower than that of L9981 and L9981-pLXSN lung cancer cell lines (P < 0.001). There was also no significant difference between L9981 and L9981-pLXSN cell lines (P > 0.05).</p><p><b>CONCLUSION</b>The results of this study suggest that nm23-H1 gene might inhibit the invasion and metastasis of lung cancer cells by down-regulating PKC signaling pathway. The Ca(2+) in cells might be involved in this process.</p>