THE COMPARISON OF DIFFERENT ELASTIC TENSION OF KINESIO TAPING ON GASTROCNEMIUS MUSCLE ACTIVATION

The purpose of this study was to compare the effect of different elastic tension of Kinesio taping on gastrocnemius muscle activation. Thirty-seven healthy athletes was recruited and randomly divided into three groups: Elastic tension 0% (N = 13), 10% (N = 12), and 20% (N = 12). All athletes were applied Kinesio taping on gastrocnemius muscle in 3 different elastic tape tensions. The wireless electromyography was used to assess the gastrocnemius muscle activation before and after applied Kinesio taping while jogging on treadmill. The results showed that a significant interaction between different elastic tape tension and pre-post taping applied (

Distinct Tumor Microenvironment at Tumor Edge as a Result of Astrocyte Activation Is Associated With Therapeutic Resistance for Brain Tumor

Tumor vasculatures and hypoxia are critical tumor micro-environmental factors associated with tumor response to the therapy and heterogeneous in both time- and location-dependent manner. Using a murine orthotopic anaplastic astrocytoma model, ALTS1C1, this study showed that brain tumor edge had a very unique microenvironment, having higher microvascular density (MVD) and better vessel function than the tumor core, but on the other hand was also positive for hypoxia markers, such as pimonidazole (PIMO), hypoxia inducible factor-1α (HIF-1α), and carbonic anhydrase IV (CAIX). The hypoxia at tumor edge was transient, named as peripheral hypoxia, and caused by different mechanisms from the chronic hypoxia in tumor core. The correlation of CAIX staining with astrocyte activation marker, glial fibrillary acid protein (GFAP), at the tumor edge indicated the involvement of astrocyte activation on the development of peripheral hypoxia. Peripheral hypoxia was a specific trait of orthotopic brain tumors at tumor edge, regardless of tumor origin. The hypoxic cells were resistant to the therapy, regardless of their location. Surviving cells, particularly those at the hypoxic region of tumor edge, are likely the cause of tumor recurrence after the therapy. New therapeutic platform that targets cells in tumor edge is likely to achieve better treatment outcomes

Genetic polymorphisms in glutathione S-transferase (GST) superfamily and risk of arsenic-induced urothelial carcinoma in residents of southwestern Taiwan

<p>Abstract</p> <p>Background</p> <p>Arsenic exposure is an important public health issue worldwide. Dose-response relationship between arsenic exposure and risk of urothelial carcinoma (UC) is consistently observed. Inorganic arsenic is methylated to form the metabolites monomethylarsonic acid and dimethylarsinic acid while ingested. Variations in capacity of xenobiotic detoxification and arsenic methylation might explain individual variation in susceptibility to arsenic-induced cancers.</p> <p>Methods</p> <p>To estimate individual susceptibility to arsenic-induced UC, 764 DNA specimens from our long-term follow-up cohort in Southwestern Taiwan were used and the genetic polymorphisms in GSTM1, GSTT1, GSTP1 and arsenic methylation enzymes including GSTO1 and GSTO2 were genotyped.</p> <p>Results</p> <p>The GSTT1 null was marginally associated with increased urothelial carcinoma (UC) risk (HR, 1.91, 95% CI, 1.00-3.65), while the association was not observed for other GSTs. Among the subjects with cumulative arsenic exposure (CAE) ≥ 20 mg/L*year, the GSTT1 null genotype conferred a significantly increased cancer risk (RR, 3.25, 95% CI, 1.20-8.80). The gene-environment interaction between the GSTT1 and high arsenic exposure with respect to cancer risk was statistically significant (multiplicative model, <it>p </it>= 0.0151) and etiologic fraction was as high as 0.86 (95% CI, 0.51-1.22). The genetic effects of GSTO1/GSTO2 were largely confined to high arsenic level (CAE ≥ 20). Diplotype analysis showed that among subjects exposed to high levels of arsenic, the AGG/AGG variant of GSTO1 Ala140Asp, GSTO2 5'UTR (-183)A/G, and GSTO2 Asn142Asp was associated with an increased cancer risk (HRs, 4.91, 95% CI, 1.02-23.74) when compared to the all-wildtype reference, respectively.</p> <p>Conclusions</p> <p>The GSTs do not play a critical role in arsenic-induced urothelial carcinogenesis. The genetic effects of GSTT1 and GSTO1 on arsenic-induced urothelial carcinogenesis are largely confined to very high exposure level.</p