In this study, fibrin was added to a photo-polymerizable gelatin-based bioink mixture to fabricate cardiac cell-laden constructs seeded with human induced pluripotent stem cell-derived cardiomyocytes (iPS-CM) or CM cell lines with cardiac fibroblasts (CF). The extensive use of platelet-rich fibrin, its capacity to offer patient specificity, and the similarity in composition to surgical glue prompted us to include fibrin in the existing bioink composition. The cell-laden bioprinted constructs were cross-linked to retain a herringbone pattern via a two-step procedure including the visible light cross-linking of furfuryl-gelatin followed by the chemical cross-linking of fibrinogen via thrombin and calcium chloride. The printed constructs revealed an extremely porous, networked structure that afforded long-term in vitro stability. Cardiomyocytes printed within the sheet structure showed excellent viability, proliferation, and expression of the troponin I cardiac marker. We extended the utility of this fibrin-gelatin bioink toward coculturing and coupling of CM and cardiac fibroblasts (CF), the interaction of which is extremely important for maintenance of normal physiology of the cardiac wall in vivo. This enhanced "cardiac construct" can be used for drug cytotoxicity screening or unraveling triggers for heart diseases in vitro.Sine oculis homeobox 1 (SIX1), a key transcription factor for regulating aerobic glycolysis, participates in the occurrence of various cancer types. However, the role of SIX1 in melanoma and the upstream regulating mechanisms of SIX1 remain to be further investigated. MicroRNAs (miRNAs) have emerged as key regulators in tumorigenesis and progression. Here, we show that miR-489-3p suppresses SIX1 expression by directly targeting its 3' untranslated region (3' UTR) in melanoma cells. miR-489-3p suppressed melanoma cell proliferation, migration, and invasion through inhibition of SIX1. Mechanistically, by targeting SIX1, miR-489-3p dampens glycolysis, with decreased glucose uptake, lactate production, ATP generation, and extracellular acidification rate (ECAR), as well as an increased oxygen consumption rate (OCR). Importantly, glycolysis regulated by the miR-489-3p/SIX1 axis is critical for its regulation of melanoma growth and metastasis both in vitro and in vivo. In melanoma patients, miR-489-3p expression is negatively correlated with SIX1 expression. In addition, patients who had increased glucose uptake in tumors and with metastasis assessed by positron emission tomography (PET) scans showed decreased miR-489-3p expression and increased expression of SIX1. Collectively, our study demonstrates the importance of the miR-489-3p/SIX1 axis in melanoma, which can be a potential and a promising therapeutic target in melanoma. © 2019 The Author(s).The aim of this study was to examine the effects of overspeed or overload plyometric training on jump height and lifting velocity in resistance trained females without plyometric training experience. Fifty-six participants (age 21.2±1.7 years; body mass 65.1±8.2 kg; height 168.0±5.9 cm) were randomly allocated to either an overspeed (n=18), overload (n=18), or passive control (n=16) group. The two training groups completed 18.7±1.7 sessions consisting of three different plyometric exercises with overspeed or overload over eight weeks. Apart from the external loading, the two training modalities were identical. Following the training period, the changes in the recorded variables were not significantly different from those in the control group, nor did the training groups differ from each other. The training groups improved peak and average lifting velocity in the 40 and 60% of body mass loading conditions (9.50-33.37%, p= less then 0.001-0.038), whereas only the average lifting velocity improved in the 80% of body mass loading condition (OS 14.47%, p less then 0.001 and OL 23.13%, p less then 0.001). No significant changes occurred in the control group (9.18-13.55%, P=0.062-0.980). Overspeed and overload plyometric training may be viable methods for improving lifting velocity, but not squat jump height, in a population without plyometric training experience.The purpose of this study was to evaluate the relationship between 1) laboratory-determined cycling peak oxygen consumption (VO 2max ) and AS performance in a new underwater swim test (UWST), and 2) cycling VO 2max and ventilatory threshold (VT) in cycling and performance score during a simulated AS solo routine. Trained artistic swimmers (n=15, 15.8±0.8 yrs., height 169.1±5.4 cm, body mass 57.1±6.3 kg) completed (1) a maximal incremental cycle test to exhaustion to determine VO 2max , (2) the UWST which comprised 275 m of freestyle and underwater breaststroke, and (3) a simulated solo competition where artistic swimming elements were evaluated by five FINA judges.  https://www.selleckchem.com/products/1-azakenpaullone.html  There was a significant correlation between mean element score and (i) VO 2max (48±4 mL . kg . min -1 , r=0.44, p =0.05), and (ii) UWST (r=-0.64, p =0.005). However, there was an insignificant relationship between cycling ventilatory threshold and mean element score (r=-0.36, p =0.10). In addition, the results demonstrate a significant relationship between HR at the ventilatory threshold and peak HR of the UWST (r=-0.64, p =0.014). The results of this study demonstrate that VO 2max is an important determinant of AS performance. In addition, the UWST appears to be a useful indicator of AS performance.Volumetric muscle loss (VML) is defined as the loss of skeletal muscle tissue which exceeds the body's repair capabilities leading to sustained functional deficits over time. Some etiologies leading to VML include traumatic injuries, congenital diseases, and degenerative myopathies. Currently, the lack of standardized animal models prevents an appropriate estimation of the severity of injury capable of exceeding self-regeneration. Recent work in our laboratory has shown that a 30% VML does not create a sustained functional loss in rats after 3 months. Therefore, the purpose of this study was to evaluate the percentage threshold of muscle loss that results in permanent functional deficits. We surgically created models of 30, 40, and 50% VML injuries in the tibialis anterior (TA) of rats, and subsequently evaluated TA function and structure after a 90-day recovery period. TA muscle force production was measured in situ by stimulating the sciatic nerve to obtain a maximum tetanic force. Results revealed that the maximum force produced by rats with a 30% VML was not significantly different from the uninjured muscle, while the maximum force of the 40% and 50% VML groups was significantly lower in comparison to the uninjured muscle.