Usefulness of a novel higher brain dysfunction screening test for evaluating higher brain function in healthy persons

To accurately and rapidly screen for higher brain dysfunction, we developed a screening test named the “higher brain dysfunction screening test” (HIBRID-ST). Previous studies have reported a decrease in higher brain function with age. However, whether HIBRID-ST can detect a decrease in higher brain function in healthy persons remains unclear.We aimed to assess the usefulness of HIBRID-ST for evaluating higher brain function in healthy persons. We recruited 60 persons without physiological abnormalities and divided them into six equal groups based on their age (20s−70s). HIBRID-ST addresses orientation, short-term memory, word recall, situational awareness, visual short-term memory, and graphic replication and includes the Trail Making and Kanahiroi tests. There was a significant negative correlation between the participants’ age and their total HIBRID-ST score (ρ= −0.68, p<0.01). The total HIBRID-ST score of participants in their 70s was significantly lower than that of participants in their 20s−60s ; the total HIBRID-ST score of participants in their 60s was significantly lower than that of participants in their 20s−50s. Our findings show that HIBRID-ST accurately detects an age-related decline in higher brain function. Further studies are needed to examine the usefulness of HIBRID-ST in patients with higher brain dysfunction

Long-term prognosis and clinical characteristics of young adults (≤40 years old) who underwent percutaneous coronary intervention

AbstractBackgroundLimited data exist regarding the long-term prognosis of percutaneous coronary intervention (PCI) in young adults. The aim of this study was to retrospectively assess the long-term clinical outcomes in young patients who underwent PCI.Methods and resultsBetween 1985 and 2011, 7649 consecutive patients underwent PCI, and data from 69 young adults (age ≤40 years) and 4255 old adults (age ≧65 years) were analyzed. A Cox proportional hazards regression analysis was used to determine the independent predictors of a composite endpoint that included all-cause death and acute coronary syndrome (ACS) during the follow-up period. The mean age of the 69 young patients was 36.1±4.9 years, and 96% of them were men. Approximately 30% were current smokers, and their body mass index (BMI) was 26.7±5.0kg/m2. The prevalence of diabetes and hypertension was 33% and 48%, respectively. All patients had ≥1 conventional cardiovascular risk factor. At a median follow-up of 9.8 years, the overall death rate was 5.8%, and new-onset ACS occurred in 8.7%. Current smoking was an independent predictor of the composite endpoint (hazard ratio 4.46, confidence interval 1.08–19.1, p=0.04) for young adults.ConclusionCurrent smoking and obesity (high BMI) are the important clinical characteristics in young Japanese coronary heart disease patients who undergo PCI. The long-term prognosis in young patients is acceptable, but current smoking is a significant independent predictor of death and the recurrence of ACS in young Japanese coronary heart disease patients who are obese

Cell competition with normal epithelial cells promotes apical extrusion of transformed cells through metabolic changes

Recent studies have revealed that newly emerging transformed cells are often apically extruded from epithelial tissues. During this process, normal epithelial cells can recognize and actively eliminate transformed cells, a process called epithelial defence against cancer (EDAC). Here, we show that mitochondrial membrane potential is diminished in RasV12-transformed cells when they are surrounded by normal cells. In addition, glucose uptake is elevated, leading to higher lactate production. The mitochondrial dysfunction is driven by upregulation of pyruvate dehydrogenase kinase 4 (PDK4), which positively regulates elimination of RasV12-transformed cells. Furthermore, EDAC from the surrounding normal cells, involving filamin, drives the Warburg-effect-like metabolic alteration. Moreover, using a cell-competition mouse model, we demonstrate that PDK-mediated metabolic changes promote the elimination of RasV12-transformed cells from intestinal epithelia. These data indicate that non-cell-autonomous metabolic modulation is a crucial regulator for cell competition, shedding light on the unexplored events at the initial stage of carcinogenesis