Transcranial direct current stimulation (tDCS) is a technique used to modulate neuronal excitability through non-invasive brain stimulation that can enhance exercise performance. We hypothesize that tDCS would improve submaximal running time to exhaustion (TTE) and delay the increase in the rating of perceived exertion (RPE) over time. We also hypothesize that tDCS would not lead to difference in cardiorespiratory responses. We employed a randomized, single-blinded, and counterbalanced design in which 10 trained men participated. After receiving either 20 min of 1.98 mA anodal tDCS applied over the primary motor cortex (M1) or sham-operated control on separate days, participants completed a constant-load test involving running at a speed equivalent to 80% of their own maximum oxygen consumption (VO 2 max). During this constant-load test, RPE, heart rate (HR), VO 2 , pulmonary ventilation (VE), respiratory exchange ratio (RER), and ventilatory threshold (VT) were continuously monitored. TTE was recorded at the end of the test. TTEs were significantly longer in the tDCS than in the sham conditions (21.18 ± 7.13 min; 18.44 ± 6.32 min; p = 0.011). For TTE, no significant differences were found in RPE between conditions at isotime. In addition, no significant differences in HR, VO 2 , VE, RER, and VT were found during TTE between the two stimulation conditions at any time point. These results indicate that the application of tDCS does not induce a change of the exercise performance-related index; however, it can affect the increase of the exercise duration due to the stimuli in the M1 area.

Risedronate, a nitrogen-containing bisphosphonate, is widely used in the clinical field for the treatment of osteoporosis. Risedronate is known to exert its effects through binding to hydroxyapatite in bone tissue, inhibiting osteoclastic activity, and inducing apoptosis of osteoclasts. The purpose of this study was to determine the effects of risedronate on osteoclast differentiation in vitro and on an inflammatory bone loss model in vivo. Risedronate inhibited osteoclast differentiation in co-culture of bone marrow cells (BMCs) and osteoblasts, and suppressed receptor activator of nuclear factor (NF)-k kB ligand (RANKL)-mediated osteoclast differentiation from bone marrow-derived macrophages (BMMs) in a dose-dependent manner without toxicity. Risedronate significantly inhibited expression of c-Fos and nuclear factor of activated T cells (NFAT) c1 induced by RANKL. To examine the effect of risedronate on bone loss in vivo, we used a mouse model of lipopolysaccharide (LPS)-mediated bone loss. Micro-CT analysis of the femurs showed that LPS treatment caused bone loss. However, bone loss was significantly attenuated in mice administered with risedronate. Taken together, we conclude that risedronate exerts beneficial effects on osteoporosis by inhibiting osteoclast differentiation both directly and indirectly. In infectious conditions, the inhibitory effect of risedronate on bone erosion was excellent. Thus risedronate could be a treatment option for osteoporosis caused by inflammatory and infectious conditions.

Golf, as with most complex motor skills, requires multiple different brain functions, including attention, motor planning, coordination, calculation of timing, and emotional control. In this study we assessed the correlation between swing components and brain connectivity from the cerebellum to the cerebrum. Ten female golf players and 10 age-matched female controls were recruited. In order to determine swing consistency among participants, the standard deviation (SD) of the mean swing speed time and the SD of the mean swing angle were assessed over 30 swings. Functional brain connectivity was assessed by resting state functional MRI. Pro-golfers showed greater positive left cerebellum connectivity to the occipital lobe, temporal lobe, parietal lobe and both frontal lobes compared to controls. The SD of play scores was positively correlated with the SD of the impact angle. Constant swing speed and back swing angle in professional golfers were associated with functional connectivity (FC) between the cerebellum and parietal and frontal lobes. In addition, the constant impact angle in professional golfers was associated with improved golf scores and additional FC of the thalamus.

Glycyrrhiza uralensis has a potential for preventing or ameliorating gastric mucosal ulceration. To understand the molecular mechanism about the medicinal effect of G. uralensis, we isolated four single compounds from G. uralensis and one related compound and screened for the cellular protective effect against H(2)O(2)-induced damage in gastric epithelial AGS cells. Interestingly, we found that ammonium glycyrrhizinate (AG) prepared from glycyrrhizin dramatically protects AGS cells from H(2)O(2)-induced damage as measured by the integrity of actin cytoskeleton. AG also inhibited FeSO(4)-induced reactive oxygen radicals in a dose-dependent manner, suggesting the role for AG as a free radical scavenger. To better understand the protective role of AG at the transcriptional level, we performed genome-wide expression profiling using high-density oligonucleotide microarrays, followed by validation using RT-PCR. Among the 33,096 genes that were screened in the microarray, 936 genes were found to be differentially expressed in a statistically significant manner in the presence or absence of H(2)O(2) and AG. Among the 936 genes, 51 genes were differentially expressed at least 3-fold in response to the H(2)O(2) treatment. AG blocked the expression of genes related to apoptotic cell death (GDF15, ATF3, TNFRSF10A, NALP1) or oxidative stress path-ways (HMOX1) which was elevated in response to H(2)O(2) treatment, suggesting a potential protective role for AG in oxidative stress-induced cell death. Collectively, current results demonstrate that AG is a novel antioxidant that could be effective for the treatment of gastric diseases related to the oxidative stress-induced mucosal damage.

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