Although sarcopenia is known to be a risk factor for non-alcoholic fatty liver disease (NAFLD), whether NAFLD is a risk factor for the development of sarcopenia is not clear. We investigated relationships between NAFLD and low skeletal muscle mass index (LSMI) using three different datasets. Participants were classified into LSMI and normal groups. LSMI was defined as a body mass index (BMI)-adjusted appendicular skeletal muscle mass <0.789 in men and <0.512 in women or as the sex-specific lowest quintile of BMI-adjusted total skeletal muscle mass. NAFLD was determined according to NAFLD liver fat score or abdominal ultrasonography. The NAFLD groups showed a higher hazard ratios (HRs) with 95% confidence intervals (CIs) for LSMI than the normal groups (HRs = 1.21, 95% CIs = 1.05-1.40). The LSMI groups also showed a higher HRs with 95% CIs for NAFLD than normal groups (HRs = 1.56, 95% CIs = 1.38-1.78). Participants with NAFLD had consistently less skeletal muscle mass over 12 years of follow-up. In conclusion, LSMI and NAFLD showed a relationship. Maintaining muscle mass should be emphasized in the management of NAFLD.

We evaluated the expression of PDLIM2 in human kidney cancer cell lines from primary or metastatic origins and found that PDLIM2 expression was highly elevated in metastatic kidney cancers. We evaluated the effect of PDLIM2 inhibition by RNA interference method. PDLIM2 knockdown showed the decreased proliferation and metastatic character in human metastatic kidney cancer cells. By repeated round of orthotopic injection of RenCa mouse kidney cancer cell line, we obtained metastatic prone mouse kidney cancer cell lines. PDLIM2 expression was highly expressed in these metastatic prone cells comparing parental cells. In addition, we evaluated the in vivo efficacy of PDLIM2 knockout on the tumor formation and metastasis of kidney cancer cells using a PDLIM2 knockout mice. The experimental metastasis model with tail vein injection and orthotopic metastasis model injected into kidney all showed reduced lung metastasis cancer formation in PDLIM2 knockout mice comparing control Balb/c mice. Overall, our findings indicate that PDLIM2 is required for cancer formation and metastasis in metastatic kidney cancer, indicating that PDLIM2 may be a new therapeutic target for metastatic kidney cancer.

It has been recognized that alternate day calorie restriction (ADCR) or exercise has positive effects on cardio-metabolic risk factors. It is unclear whether the combined effect of ADCR and exercise (aerobic + resistance training) influences risk. We investigated effects of an 8-week ADCR and exercise program (aerobic + resistance training) on cardio-metabolic risk factors in overweight and obese adults.

Ischemic stroke and cerebral infarction triggered by the blockage of blood supply can cause damage to the brain via a complex series of pathological changes. Recently, diverse therapies have emerged as promising candidates for the treatment of stroke. These treatments exert therapeutic effects by acting on diverse target molecules and cells in different time windows from the acute to chronic phases. Here, using immunohistochemistry, we show pathophysiological changes in the brain microenvironment at the hyperacute (within 6 h), acute (1~3 days), subacute (7 days), and chronic (1 month) phases following ischemic injury. Ischemic injury in rats was induced by occluding the middle cerebral artery and was validated by magnetic resonance imaging. The progression of damage to the brain was evaluated by immunohistochemistry for NeuN+ neurons, GFAP+ astrocytes, and Iba1+ microglia, and by the emergence of the cell death-related molecules such as AIF, FAF1, and activated caspase-3. Our data regarding the spatial and temporal information on pathophysiological changes may warrant the investigation of the timing of administration of therapeutic treatments in preclinical studies with an animal model of stroke.

The research should consider the complex dynamics of social interaction to better understand smartphone dependence among adolescents. In social situations, adolescents can choose to interact with their peers or use their smartphones, and smartphone dependence can drive adolescents far away from interaction with their peers. Adolescents, conversely, may use smartphones to avoid peer interaction because they have experienced social withdrawal or negative peer relationships. Previous research has not discussed enough what precedes or follows in longitudinal relationships. This study aims to examine the reciprocal longitudinal effects between adolescents' negative peer relationships, social withdrawal, and smartphone dependence. The analysis used longitudinal panel data collected yearly between 2018 and 2020 from the Korean Children and Youth Panel Survey (KCYPS) sampled from adolescents in the Republic of Korea and employed autoregressive cross-lagged modeling on 2230 participants. The reciprocal longitudinal relationships differed depending on the sub-factors of smartphone dependence. For instance, the sub-factor of smartphone dependence, including virtual life orientation and withdrawal, had reciprocal longitudinal relationships with negative peer relationships. The other sub-factor of smartphone dependence, including daily life disturbance and tolerance, influenced negative peer relationships consistently, but the converse path did not. In addition, social withdrawal longitudinally affected negative peer relationships the following year. However, the reciprocal longitudinal relationships between social withdrawal and smartphone dependence were not significant in any path in this research. This research provides practical implications for intervention to reduce smartphone dependence among young adolescents.

The visceral adiposity index (VAI), an indirect marker of visceral adipose tissue, serves as a model associated with cardiometabolic risk, but has limitations regarding the Asian population. We sought to develop a new VAI (NVAI) for the Korean population and compare it to VAI for prediction of atherosclerotic cardiovascular disease (ASCVD) risk and development of major cardiovascular diseases (CVD) and stroke.

Colorectal cancer (CRC) survivors are known to experience various symptoms that significantly affect their quality of life (QOL); therefore, it is important to identify clinical markers related with CRC survivor QOL. Here we investigated the relationship between serum chemerin levels, a newly identified proinflammatory adipokine, and QOL in CRC survivors.

Remifentanil has been used to suppress peri-extubation cough. Palonosetron, a 5-HT3 receptor antagonist, is an effective antiemetic, and 5-HT receptors mediate the cough reflex. We assessed the impact of palonosetron on effect-site concentration (Ce) of remifentanil for preventing emergence cough in females. Forty-five female patients undergoing laparoscopic cholecystectomy randomly received 0.075 mg of palonosetron (n = 21) or normal saline (n = 24) intravenously at the end of surgery. The remifentanil Ce for 50% (EC50) and for 95% (EC95) of patients were estimated via Dixon's up-and-down method or isotonic regression. Using Dixon's method, EC50 in the control group (1.33 ± 0.38 ng/mL) was comparable to that of the palonosetron group (1.42 ± 0.75 ng/mL) (p = 0.813). Using isotonic regression, EC50 (83% CIs) and EC95 (95% CIs) did not reveal significant differences between the control and the palonosetron groups (1.17 (0.86-1.43) and 1.90 (1.45-1.96) ng/mL and 0.88 (0.78-1.23) and 2.43 (1.94-2.47) ng/mL, respectively). No difference was found in the remifentanil Ce to suppress emergence cough in the palonosetron group compared with the control group. It may indicate no effect of palonosetron on antitussive activity of remifentanil.

Obesity, especially visceral obesity, is known to be an important correlate for cardiovascular disease and increased mortality. On the other hand, high cardiorespiratory fitness is suggested to be an effective contributor for reducing this risk. This study was conducted to determine the combined impact of cardiorespiratory fitness and visceral adiposity, otherwise known as fitness and fatness, on metabolic syndrome in overweight and obese adults.

The purposes of this study were (1) to determine the association between lipoprotein subfraction profiles and metabolically healthy overweight (MHO) phenotype, as defined by visceral adiposity; and (2) to identify the strongest predictor of metabolic health among the lipoprotein measurements.

Transplantation of mesenchymal stem cells (MSCs) has been shown to enhance the recovery of brain functions following ischemic injury. Although immune modulation has been suggested to be one of the mechanisms, the molecular mechanisms underlying improved recovery has not been clearly identified. Here, we report that MSCs secrete transforming growth factor-beta (TGF-β) to suppress immune propagation in the ischemic rat brain. Ischemic stroke caused global death of resident cells in the infarcted area, elevated the monocyte chemoattractant protein-1 (MCP-1) level, and evoked massive infiltration of circulating CD68+ immune cells through the impaired blood-brain barrier. Transplantation of MSCs at day 3 post-ischemia blocked the subsequent upregulation of MCP-1 in the ischemic area and the infiltration of additional CD68+ immune cells. MSC-conditioned media decreased the migration and MCP-1 production of freshly isolated immune cells in vitro, and this effect was blocked by an inhibitor of TGF-β signaling or an anti-TGF-β neutralizing antibody. Finally, transplantation of TGF-β1-silenced MSCs failed to attenuate the infiltration of CD68+ cells into the ischemic brain, and was associated with only minor improvements in motor function. These results indicate that TGF-β is key to the ability of MSCs to beneficially attenuate immune reactions in the ischemic brain. Our findings offer insight into the interactions between allogeneic MSCs and the host immune system, reinforcing the prospective clinical value of using MSCs in the treatment of neurological disorders involving inflammation-mediated secondary damage.