Chun‐Ming Shih

BACKGROUND: Inhibitory control, or the ability to suppress planned but inappropriate prepotent actions in the current environment, plays an important role in the control of human performance. Evidence from empirical studies utilizing a sport-specific design has shown that athletes have superior inhibitory control. However, less is known about whether this superiority might (1) still be seen in a general cognitive task without a sport-related context; (2) be modulated differentially by different sporting expertise (e.g., tennis versus swimming). METHODOLOGY/PRINCIPAL FINDINGS: Here we compared inhibitory control across tennis players, swimmers and sedentary non-athletic controls using a stop-signal task without a sport-specific design. Our primary finding showed that tennis players had shorter stop-signal reaction times (SSRTs) when compared to swimmers and sedentary controls, whereas no difference was found between swimmers and sedentary controls. Importantly, this effect was further confirmed after considering potential confounding factors (e.g., BMI, training experience, estimated levels of physical activity and VO2max), indicative of better ability to inhibit unrequired responses in tennis players. CONCLUSIONS/SIGNIFICANCE: This suggests that fundamental inhibitory control in athletes can benefit from open skill training. Sport with both physical and cognitive demands may provide a potential clinical intervention for those who have difficulties in inhibitory control.

The use of microneedles for transdermal drug delivery is limited due to the risk of infection associated with formation of channels through the stratum corneum layer of the epidermis. The risk of infection associated with use of microneedles may be reduced by imparting these devices with antimicrobial properties. In this study, a photopolymerization-micromolding technique was used to fabricate microneedle arrays from a photosensitive material containing polyethylene glycol 600 diacrylate, gentamicin sulfate, and a photoinitiator. Scanning electron microscopy indicated that the photopolymerization-micromolding process produced microneedle arrays that exhibited good microneedle-to-microneedle uniformity. An agar plating assay revealed that microneedles fabricated with polyethylene glycol 600 diacrylate containing 2 mg mL(-1) gentamicin sulfate inhibited growth of Staphylococcus aureus bacteria. Scanning electron microscopy revealed no platelet aggregation on the surfaces of platelet rich plasma-exposed undoped polyethylene glycol 600 diacrylate microneedles and gentamicin-doped polyethylene glycol 600 diacrylate microneedles. These efforts will enable wider adoption of microneedles for transdermal delivery of pharmacologic agents.

BACKGROUND AND PURPOSE: Current methods used to treat critical limb ischaemia (CLI) are hampered by a lack of effective strategies, therefore, therapeutic vasculogenesis may open up a new field for the treatment of CLI. In this study we investigated the ability of the DPP-4 inhibitor, sitagliptin, originally used as a hypoglycaemic agent, to induce vasculogenesis in vivo. EXPERIMENTAL APPROACH: Sitagliptin were administered daily to C57CL/B6 mice and eGFP transgenic mouse bone marrow-transplanted ICR mice that had undergone hindlimb ischaemic surgery. Laser Doppler imaging and flow cytometry were used to evaluate the degree of neovasculogenesis and circulating levels of endothelial progenitor cells (EPCs) respectively. Cell surface markers of EPCs and endothelial NOS (eNOS) in vessels were studied. KEY RESULTS: Sitagliptin elevated plasma glucagon-like peptide-1 (GLP-1) levels in mice subjected to ischaemia, decreased plasma dipeptidyl peptidase-4 (DPP-4) concentration, and augmented ischaemia-induced increases in stromal cell-derived factor-1 (SDF-1) in a dose-dependent manner. Blood flow in the ischaemic limb was significantly improved in mice treated with sitagliptin. Circulating levels of EPCs were also increased after sitagliptin treatment. Sitagliptin also enhanced the expression of CD 34 and eNOS in ischaemic muscle. In addition, sitagliptin promoted EPC mobilization and homing to ischaemic tissue in eGFP transgenic mouse bone marrow-transplanted ICR mice. CONCLUSION AND IMPLICATIONS: Circulating EPC levels and neovasculogenesis were augmented by the DPP-4 inhibitor, sitagliptin and this effect was dependent on an eNOS-related pathway in a mouse model of hindlimb ischaemia. The results indicate that oral administration of sitagliptin has therapeutic potential as an inducer of vasculogenesis.