Prostate cancer is one of the malignant tumors which exhibit resistance to anticancer drugs, at least in part due to enhanced antiapoptotic mechanisms. Therefore, the understanding of such mechanisms should improve the design of chemotherapy against prostate cancer. Galectin-3 (Gal-3), a multifunctional oncogenic protein involved in the regulation of tumor proliferation, angiogenesis, and apoptosis has shown antiapoptotic effects in certain cell types. Here, we show that the expression of exogenous Gal-3 in human prostate cancer LNCaP cells, which do not express Gal-3 constitutively, inhibits anticancer drug-induced apoptosis by stabilizing the mitochondria. Thus, Gal-3-negative cells showed 66.31% apoptosis after treatment with 50 Mmol/L cis-diammine-dichloroplatinum for 48 hours, whereas two clones of Gal-3-expressing cells show only 2.92% and 1.42% apoptotic cells. Similarly, Gal-3-negative cells showed 43.8% apoptosis after treatment with 300 Mmol/L etoposide for 48 hours, whereas only 15.38% and 14.51% of Gal-3-expressing LNCaP cells were apoptotic. The expression of Gal-3 stimulated the phosphorylation of Ser 112 of Bcl-2-associated death (Bad) protein and down-regulated Bad expression after treatment with cis-diammine-dichloroplatinum. Gal-3 also inhibited mitochondrial depolarization and damage after translocation from the nuclei to the cytoplasm, resulting in inhibition of cytochrome c release and caspase-3 activation. These findings indicate that Gal-3 inhibits anticancer drug-induced apoptosis through regulation of Bad protein and suppression of the mitochondrial apoptosis pathway. Therefore, targeting Gal-3 could improve the efficacy of anticancer drug chemotherapy in prostate cancer. (Cancer Res 2006; 66(6): 3114-9)
The purpose of this investigation was to determine whether the concept of the critical power could be applied to competitive swimming by using critical swimming speed (CS) as determined both in the swimming flume (CS-flume) and in the normal swimming pool (CS-pool) and whether CS could be utilized as a practical index for assessing a swimmer's endurance performance. CS defined as the swimming speed which could be theoretically maintained continuously without exhaustion was expressed as the slope of a regression line between swimming distance (D) and its duration (T) obtained at various swimming speeds. Eight highly trained swimmers were instructed to swim until onset of fatigue at four predetermined swimming speed levels in the swimming flume and at maximal effort over four different swimming distances in the swimming pool. In the results of CS-flume and CS-pool, the regression relations between D and T were expressed in the general form, D = a+b x T, with r2 being higher than 0.998 (p less than 0.01), respectively. These results both from the flume and the pool indicated extremely good linearity. Furthermore, maximal oxygen uptake (VO2max) during the incremental exercise test, swimming speed corresponding 4 mM of blood lactate concentration (V-OBLA) and mean velocity in the 400 m freestyle (V-400) were measured on each subject.(ABSTRACT TRUNCATED AT 250 WORDS)
To explore the effect of mirror box therapy based on the mirror neuron (MN) system of the primary motor cortex (M1), we examined if direct (without a mirror) and indirect (with a mirror) observation of self-movement in healthy subjects induced changes in motor evoked potential (MEP) evoked by transcranial magnetic stimulation (TMS). MEPs were elicited from the first dorsal interosseous (FDI) and the flexor carpi radialis (FCR) muscles. Somatosensory evoked potentials (SEPs) during self-movement observation were also recorded. Both observations of self-movement with and without a mirror increased MEP amplitude. In addition, increase in MEP amplitude was specific to the prime mover muscle involved in the observed movement. The SEPs increased similar to the MEPs during both observations of self-movement with and without a mirror. We conclude that although the MN system can be activated by observing self-movement in a manner similar to that achieved by observing movement of another person, there were no detectable effect on corticospinal excitability that were specific to movements observed with a mirror.
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