Background and Aim: The presence of malnutrition in hospitalized geriatric patients is associated with an increased risk of mortality. This study aimed to examine the performance of Nutritional Risk Screening 2002 (NRS2002) and Mini Nutritional Assessment Short Form (MNA-SF) in predicting mortality for hospitalized geriatric patients in China. Methods: A prospective analysis was performed in 536 hospitalized geriatric patients aged ≥65 years. Nutrition status was assessed using the MNA-SF and NRS2002 scales within 24 hrs of admission. Anthropometric measures and biochemical parameters were carried out for each patient. Patients were follow-up for up to 2.5 years. Results: At baseline, 161 (30.04%) patients had malnutrition/nutritional risk according to NRS2002 assessment. According to MNA-SF, 284 (52.99%) patients had malnutrition/ nutritional risk. Malnutrition/nutritional risk patients had lower anthropometric and biochemical parameters (P<0.05). NRS2002 and MNA-SF had a strong correlation with classical nutritional markers (P<0.05). NRS2002 versus MNA-SF showed moderate agreement (kappa=0.493, P<0.001). During a median follow-up time of 795 days (range 10-947 days), 118 (22%) participants died. The Kaplan-Meier curve demonstrated that malnutrition/nutritional risk patients according to NRS2002 or MNA-SF assessment had a higher risk of mortality than the normal nutrition patients (χ 2 =17.67, P<0.001; χ 2 =28.999, P<0.001, respectively). From the components of the Cox regression multivariate models, only the NRS2002 score was an independent risk factor influencing the mortality. Conclusion: Both NRS2002 and MNA-SF scores could predict mortality in Chinese hospitalized geriatric patients. But only NRS2002 score was the independent predictor for mortality.

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The presence of NAFLD was significantly associated with AD, as indicated by abnormal sudomotor function. The association was independent from various conventional risk factors.

Background/Aim: Curcumin is a polyphenol that exerts a variety of pharmacological activities and plays an anti-cancer role in many cancer cells. It was recently reported that gasdermin E (GSDME) is involved in the progression of pyroptosis. Materials and Methods: HepG2 cells were treated with various concentrations of curcumin and cell viability was examined using MTT assay, apoptosis was analysed using flow cytometry, reactive oxygen species (ROS) levels using dihydroethidium, LDH release using an LDH cytotoxicity assay, and protein expression using western blot. Results: Curcumin increased the expression of the GSDME N-terminus and proteins involved in pyrolysis, promoted HspG2 cell pyrolysis and increased intracellular ROS levels. Moreover, inhibition of the production of intracellular ROS with nacetylcysteine (NAC) improved the degree of apoptosis and pyrolysis induced by curcumin. Conclusion: Curcumin induces HspG2 cell death by increasing apoptosis and pyroptosis, and ROS play a key role in this process. This study improves our understanding of the potential anti-cancer properties of curcumin in liver cancer. Curcumin[1,7-bis-(4-hydroxy-3-methoxyphenyl)-1,6heptadiene-3,5-dione (diferuloy l methane)] is a type of polyphenol extracted from the rhizomes of ginger plants, such as turmeric and zedoary (1), which has been shown to display various pharmacological activities, including antiinflammatory (2), antioxidant (3), hypolipidemic (4), antitumor (5), and immune regulatory (6). Previous studies have also demonstrated that curcumin exerts anti-cancer effects in many types of cancer cells, including stomach (7), colon (8), lung (9), liver (10) and breast (11). In addition, it has been reported that curcumin can affect the cellular redox balance, resulting in increased cellular reactive oxygen species (ROS) production (12). Excessive ROS can directly or indirectly affect the regulation of anti-or pro-apoptotic proteins by Bcl-2 family members, leading to cellular apoptosis (13). Moreover, ROS accumulation has been shown to induce cellular apoptosis, necroptosis, endoplasmic reticulum stress, and autophagy in various cancer cells (14). Therefore, curcumin may also affect cell death in liver cancer cells.Pyroptosis is a recently discovered type of programmed cell death that depends on the activation of the inflammationrelated caspases 1, 4, 5, and 11, as well as apoptosis-related caspase-3 (15). The morphology of cells undergoing pyroptosis differs from that in apoptosis or necrosis, and is characterized by cell swelling, membrane breakage, pore formation, and osmotic lysis (16). It was recently reported that gasdermin E (GSDME) is involved in the progression of pyroptosis (17). In particular, activated caspase-3 was found to cleave GSDME between the N-terminus (GSMDE-N) and C-terminus under certain apoptotic stimuli, thus relieving the self-inhibition of the C-terminus and releasing the active GSDME-N-terminus as well as the pore-forming domain (PFD). Consequently, nonselective pores are formed in the cell membra...

Oxidative stress induced by free fatty acid overload in pancreatic β-cells is a potential contributory factor to dysfunction of insulin secretion and apoptotic cell death. Perilipin 5 (Plin5) has been reported to ameliorate oxidative stress-mediated damage in non-insulin-secreting tissues. We tested the hypothesis that Plin5 plays a similar role in pancreatic β-cells, which are extremely sensitive to oxidative stress. Here, our in vitro data showed that Plin5-mediated alleviation of palmitate-triggered apoptosis involves the mitochondrial pathway. And the protective role of Plin5 on β-cells was partially dependent on its modulation in oxidative stress. Upregulation of Plin5 in INS-1 cells decreased reactive oxygen species production, enhanced cellular glutathione levels, and induced expression of antioxidant enzymes glutamate-cysteine ligase catalytic subunit and heme oxygenase-1. However, knocking out of Plin5 abolished all of these beneficial effects. Furthermore, by using the O 2− scavenger MnTMPyP, we verified that altering Plin5 expression impacted lipotoxic cell death partially via modulating oxidative stress. Mechanistic experiments revealed that Plin5 induced Nrf2-ARE system, a master regulator in the cellular adaptive response to oxidative stress, by activating PI3K/Akt and ERK signal pathways, contributing to the increase of antioxidant defense and consequently improving β-cell function and survival in the presence of lipotoxic oxidative stress. Overall, our findings indicate that Plin5 abrogates oxidative damage in INS-1 β-cells during lipotoxic stress partially through the enhancement of antioxidant defense involving the PI3K/Akt and ERK mediated Nrf2-ARE system.