Obesity is a known cause of metabolic syndrome which includes Type II diabetes, hypertension, and dyslipidemia. It is well documented that insulin resistance contributes to the mortality and the incidence of metabolic syndromes including central obesity, dyslipidemia, hyperglycemia and hypertension. Both obesity and diabetes are emerging topics for researchers to consider as having a possible causal association with cancer since the two factors have been viewed as risk factors for cancer. The present paper introduced the hypothesis of a possible causal relationship between obesity, insulin resistance and cancer and reviews relevant existing studies in this area. More efforts and studies are needed to clarify the mechanisms and the common risk factors which might be incorporated into interventions to prevent cancer and cardiovascular diseases as top causes of death.

Herein, we present an unconventional method for multimodal characterization of three-dimensional cardiac organoids. This method can monitor and control the mechanophysiological parameters of organoids within a single device. In this method, local pressure distributions of human-induced pluripotent stem-cell-derived cardiac organoids are visualized spatiotemporally by an active-matrix array of pressure-sensitive transistors. This array is integrated with three-dimensional electrodes formed by the high-resolution printing of liquid metal. These liquid-metal electrodes are inserted inside an organoid to form the intraorganoid interface for simultaneous electrophysiological recording and stimulation. The low mechanical modulus and low impedance of the liquid-metal electrodes are compatible with organoids’ soft biological tissue, which enables stable electric pacing at low thresholds. In contrast to conventional electrophysiological methods, this measurement of a cardiac organoid’s beating pressures enabled simultaneous treatment of electrical therapeutics using a single device without any interference between the pressure signals and electrical pulses from pacing electrodes, even in wet organoid conditions.

In Korea, subjective health inequalities arise from different socioeconomic status, but this difference is decreased by health behavioral factors. Therefore, socioeconomic inequity in self-rated health status can be corrected more effectively by promotional health behaviors.

OBJECTIVESThe aim of this study was to investigate the effect of changes in cardiovascular disease (CVD) risk factors on progression from prehypertension (PreHTN) to hypertension (HTN) using an 8-yr prospective Korean Cancer Prevention Study (KCPS) by the National Health Insurance Corporation (NHIC) in Korea.METHODSA total of 16,229 subjects, aged 30 to 54, with new onset preHTN at baseline (1994-1996) in a biennial national medical exam were selected and followed up till 2004 at 2-yr intervals. All subjects underwent a biennial health examination including biochemical measurements and behavior. The log-rank test was performed to assess the relationship between changes in CVD risk factors and progression to HTN. The Cox proportional hazard model was used to identify factors influencing progression to HTN.RESULTSWith regards the progression rate in men, ex-smokers (42.9%), abstainers (37.5%), and regular exercisers (37.6%) showed a slower progression rate than continuous smokers (49.5%) and continuous drinkers (50.9%). In women, those who participated in regular exercise (22.6%) had a lower rate of progression than continuous non-exercisers (36.1%). According to the results of the Cox proportional hazard model, improvements in smoking (hazard ratio [HR], 0.756), drinking (HR, 0.669), regular exercise (HR, 0.653), body mass index (HR, 0.715), and total cholesterol (HR, 0.788) played a protective role in progression to HTN in men, while in women, participating in regular exercise (HR, 0.534) was beneficial.CONCLUSIONImprovements in CVD-related behaviors diminished the progression rate of HTN. This study suggests that individuals with PreHTN should be targeted for specific health behavioral intervention to prevent the progression of HTN.