Little is known about the relationship between real and perceived water competence among youth in the context of drowning prevention or of their perceptions of their risk of drowning. This study reports the findings of an international project entitled Can You Swim? Collegiate physical education students (n = 373) were assessed in a two-part study using an initial questionnaire survey to provide self-estimates of water competency and risk perception, followed by six practical tests in the water. Correlation coefficients between perceived and real swimming (r s = 0.369) and floating (r s = 0.583) skills were significant but only moderate in strength. No significant gender differences in real or perceived water competency were found. Significantly more males than females estimated lower risk of drowning associated with a series of aquatic scenarios (p = 0.016). The implications of these findings on drowning prevention and the need for further investigation are discussed.While the role of swimming proficiency in drowning prevention may appear axiomatic, its protective capacity is not well understood. Brenner, Saluja, and Smith (2003) have argued that increased swimming competency is almost certain to be protective in a drowning situation and, if so, then differences in swimming competency may help explain why some are at greater risk of drowning than others. The relationship between swimming competency, swimming lessons, and the risk of drowning for young children has been the subject of some inquiry (Brenner, Moran, Stallman, Gilchrist, & McVan, 2006), but little is known about this relationship with respect to young adults, one of the most at-risk groups of drowning in most developed countries.A systematic, large-scale review of childhood and youth drowning noted that even though studies have shown that swimming lessons improved the ability to dive,

The purpose of this study was to examine the physiological responses and RPE during water walking using the Flowmill, which has a treadmill at the base of a water flume, in order to obtain basic data for prescribing water walking for people of middle and advanced age. Twenty healthy female volunteers with an age of 59.1 ± 5.2 years took part in this study. They belonged to the same swimming club and regularly swam and exercised in water. Walking in water took place in the Flowmill. Subjects completed four consecutive bouts of 4 min duration at progressively increasing speeds (20, 30, 40 and 50 m/min) with 1 min rest between each bout. In addition, water velocity was adjusted to the walking speed of each bout. Subjects were instructed to swing both arms in order to maintain their balance during walking in water. The water depth was to the level of the xiphoid process and the water temperature was 30.31 ± 0.08°C. Both heart rate (HR) and oxygen • uptake (VO2) increased exponentially as walking speed • increased. HR was 125 ± 15 bpm, and VO2 was 18.10 ± 2.72 ml/kg·min -1 during walking in water at 50 m/ min, which was the highest speed. The exercise intensity at this speed was equivalent to 5.2 ± 0.8 Mets. The• relationship between HR and VO2 during walking in water showed a highly significant linear relationship in each subject. There was also a highly significant linear • relationship in the mean HR and VO2 of all subjects. Blood lactate concentration (LA) measured at rest and immediately after each bout was 1.1 ± 0.4 mmol/l at rest, 1.0 ± 0.2 mmol/l at 20 m/min, 1.0 ± 0.3 mmol/l at 30 m/ min, 1.1 ± 0.2 mmol/l at 40 m/min, and 2.4 ± 0.7 mmol/ l at 50 m/min. LA at 50 m/min was significantly higher than at rest and at the other speeds. The relationship between HR and RPE during walking in water showed a highly significant linear relationship. The relationship between walking speed and energy expenditure calculated• from VO2 and the respiratory exchange ratio (R) showed a high significant exponential relationship. These results suggested that HR and RPE can be effective indices for exercise prescription during Flowmill walking as with land walking.

Alport syndrome is a hereditary glomerular disease caused by mutation in type IV collagen α3-α5 chains (α3-α5(IV)), which disrupts trimerization, leading to glomerular basement membrane degeneration. Correcting the trimerization of α3/α4/α5 chain is a feasible therapeutic approach, but is hindered by lack of information on the regulation of intracellular α(IV) chain and the absence of high-throughput screening (HTS) platforms to assess α345(IV) trimer formation. Here, we developed sets of split NanoLuc-fusion α345(IV) proteins to monitor α345(IV) trimerization of wild-type and clinically associated mutant α5(IV). The α345(IV) trimer assay, which satisfied the acceptance criteria for HTS, enabled the characterization of intracellular- and secretion-dependent defects of mutant α5(IV). Small interfering RNA-based and chemical screening targeting the ER identified several chemical chaperones that have potential to promote α345(IV) trimer formation. This split luciferase-based trimer formation assay is a functional HTS platform that realizes the feasibility of targeting α345(IV) trimers to treat Alport syndrome.

STAT3 inhibition significantly ameliorated the renal dysfunction in AS mice. Our finding identifies STAT3 as an important regulator in AS progression and provides a promising therapeutic target for AS.

Metformin is widely used for the treatment of type 2 diabetes, and increasing numbers of studies have shown that metformin also ameliorates tumor progression, inflammatory disease, and fibrosis. However, the ability of metformin to improve non-diabetic glomerular disease and chronic kidney disease (CKD) has not been explored. To investigate the effect of metformin on non-diabetic glomerular disease, we used a mouse model of Alport syndrome (Col4a5 G5X) which were treated with metformin or losartan, used as a control treatment. We also investigated the effect of metformin on adriamycin-induced glomerulosclerosis model. Pathological and biochemical analysis showed that metformin or losartan suppressed proteinuria, renal inflammation, fibrosis, and glomerular injury and extended the lifespan in Alport syndrome mice. Transcriptome analysis showed that metformin and losartan influenced molecular pathways-related to metabolism and inflammation. Metformin altered multiple genes including metabolic genes not affected by losartan. Metformin also suppressed proteinuria and glomerular injury in the adriamycin-induced glomerulosclerosis mouse model. Our results showed that metformin ameliorates the glomerular sclerosis and CKD phenotype in non-diabetic chronic glomerular diseases. Metformin may have therapeutic potential for not only diabetic nephropathy but also non-diabetic glomerular disease including Alport syndrome.