Objective: The Global Leader Initiative on Malnutrition (GLIM) criteria have been recommended for malnutrition diagnosis recently, for which the first step is malnutrition risk screening with any validated tool. This study aims to investigate the incidence of nutritional risk and malnutrition in Crohn’s disease inpatients and compare the suitability of Nutritional Risk Screening 2002 (NRS-2002) and Malnutrition Universal Screening Tool (MUST) as the first-step screening tool for GLIM criteria.Methods: We retrospectively analyzed the clinical data of Crohn’s disease inpatients in our hospital from August 2016 to December 2019. NRS-2002 and MUST were used for nutritional screening at the time of admission. GLIM and Patient Generated-Subjective Global Assessment (PG-SGA) were used for malnutrition assessment, respectively. Patients without nutritional risk screened by NRS-2002 but with malnutrition risk screened by MUST were especially screened out. The appendicular skeletal muscle mass index (ASMI), fat-free mass index (FFMI), body fat percent (BFP), and body cell mass (BCM) were measured by the Biospace Inbody S10 composition analyzer.Results: A total of 146 Crohn’s disease patients were enrolled, of which 62.3 and 89.7% had nutritional or malnutrition risk according to NRS-2002 and MUST, respectively. The prevalence of malnutrition assessed by GLIM was 59.6% (87 cases) and 82.2% (120 cases) when NRS-2002 and MUST were used as the first step of GLIM respectively. Meanwhile, 99 patients (67.8%) had malnutrition when assessed by PG-SGA. There were 41 patients who were not at nutritional risk according to NRS-2002 but were at malnutrition risk determined by MUST. At last, 33 patients were GLIM-defined, and 16 patients were PG-SGA-defined malnutrition among the 41 patients.Conclusion: The nutritional risk or malnutrition is common in Crohn’s disease inpatients. It is recommended to use a variety of nutritional assessment tools for Crohn’s disease inpatients. MUST can be used as a good supplement for the patients with a score of NRS-2002 lower than 3 in order to decrease the miss rate of GLIM-defined malnutrition.

Diabetes-associated fracture risk and impaired fracture healing represents a serious health threat. It is well known that type 1 diabetes mellitus (T1DM) impairs fracture healing due to its effect on osteoblasts and their progenitor cells. Previous studies have showed that primary cilia and intraflagellar transport protein 80 (IFT80) are critical for bone formation. However, whether TIDM impairs fracture healing due to influencing ciliary gene expression and cilia formation is unknown. Here, we investigated the effect of T1DM on primary cilia in a streptozotocin induced diabetes mouse model and examined the impact of cilia on fracture healing in osteoblasts by deletion of IFT80 in osteoblast linage using osterix (OSX)-cre (OSX^cretTAIFT80^f/f). The results showed that diabetes inhibited ciliary gene expression and primary cilia formation to an extent that was similar to normoglycemic mice with IFT80 deletion. Moreover, diabetic mice and normoglycemic mice with cilia loss in osteoblasts (OSX^cretTAIFT80^f/f) both exhibited delayed fracture healing with significantly reduced bone density and mechanical strength as well as with reduced expression of osteoblast markers, decreased angiogenesis and proliferation of bone lining cells at the fracture sites. In vitro studies showed that advanced glycation end products (AGEs) downregulated IFT80 expression in osteoblast progenitors. Moreover, AGEs and IFT80 deletion significantly reduced cilia number and length which inhibited differentiation of primary osteoblast precursors. Thus, this study for the first time report that primary cilia are essential for bone regeneration during fracture healing and loss of cilia caused by diabetes in osteoblasts resulted in defective diabetic fracture healing.

Background: 17AAG has been extensively studied for its antitumor effects that protect cells from lethal stress by maintaining protein stability. The role of 17AAG in sevoflurane-induced neuronal injury has never been studied. We aim to investigate the effect of 17AAG on sevoflurane-induced neurotoxicity in vivo and in vitro. Methods: Sevoflurane-induced hippocampal neuron injury model was established in aged Sprague–Dawley rats. Pretreatment of vehicle or 17AAG was administered prior to sevoflurane inhalation. H4 neuroglioma cells were pretreated with vehicle or 17AAG and exposed to sevoflurane. Apoptosis, oxidative stress, expression of interleukin-6 (IL-6), and activation of the nuclear factor-κB (NF-κB) signaling pathway in H4 cells were examined by Hoechst assay, flow cytometry, Western blot, and immunofluorescent staining. RNA interference against HSPA1A was performed to test the function of HSP70 in neuroprotection. Results: Exogenous 17AAG reduced sevoflurane-induced apoptosis and oxidative stress in rat hippocampal neurons and in H4 cells. In H4 cells, 17AAG suppressed sevoflurane-induced upregulation of IL-6 and activation of NF-κB signaling. 17AAG enhanced sevoflurane-induced upregulation of HSP70 in rat hippocampal neurons and in H4 cells. Conversely, silencing of HSPA1A in H4 cells blocked the cytoprotective effect of 17AAG against sevoflurane-induced apoptosis and oxidative stress, and prevented upregulation of IL-6 and activation of NF-κB signaling. Conclusions: 17AAG protects against sevoflurane-induced neurotoxicity in vivo and in vitro via HSP70-dependent inhibition of apoptosis, oxidative stress, and pro-inflammatory signaling pathway.

Objective: This study was to explore the role and necessity of muscle mass [fat-free mass index (FFMI) and appendicular skeletal muscle index (ASMI) measured by bioelectrical impedance analysis (BIA)] in nutritional status evaluation of patients with locally advanced (III, IVa) nasopharyngeal carcinoma (NPC).Methods: One hundred and thirty locally advanced NPC patients were recruited. Their nutritional status was assessed by albumin (ALB), body mass index (BMI), Nutritional Risk Screening 2002 (NRS 2002), Patient generated-Subjective Global Assessment (PG-SGA), and muscle mass. Consistency test and McNemar test were used to evaluate the consistency of muscle mass with ALB, BMI, NRS 2002, and PG-SGA, and correlation analysis was performed on muscle mass and PG-SGA or BMI.Results: 61/130 (46.9%) of the patients had nutritional risks according to NRS 2002, 68/130 (53.1%) of the patients had malnutrition according to PG-SGA assessment. FFMI and ASMI could determine the loss of muscle mass that cannot be detected by albumin (30.2 and 65.6%), BMI (28.0 and 35.3%), NRS 2002 (26.1 and 25.0%), and PG-SGA (18.6 and 55.6%). McNemar test showed that the malnutrition results assessed by FFMI and BMI were inconsistent (P <0.001), but further Pearson correlation analysis showed that BMI was positively correlated with FFMI (rs = 0.300, P = 0.001).Conclusion: The commonly used nutritional assessment scale/parameters cannot identify the muscle mass loss in patients with locally advanced NPC. Analysis of human body composition is important for nutritional assessment in patients with locally advanced NPC.

Background and Aims:To investigate the relationship among maternal demographic and clinical characteristics, gestational and postpartum oral glucose tolerance test (ppOGTT) results in patients with gestational diabetes mellitus (GDM).Methods:Patients with gestational diabetes mellitus from January 1, 2016, to August 31, 2019, were enrolled. General characteristics, dietary energy intake, pre-gestational body mass index (BMI), gestational oral glucose tolerance test (gOGTT), and 42 days ppOGTT results of all participants were collected. The relationships among maternal clinical characteristics, fasting glucose of gOGTT (gOGTT-FPG), 1 h postprandial glucose of gOGTT (gOGTT-1h PG), 2 h postprandial glucose of gOGTT (gOGTT-2h PG), and maternal postpartum glucose outcomes were evaluated.Results:A total of 156 patients with GDM were included in this study. Among them, 73.7% had inadequate daily total energy intake, an insufficient ratio of carbohydrates and protein, and an excessive fat ratio. Most of the patients (81.4%) were normal in their ppOGTT examination. Less than 20% of the patients (16.7%) were in the pre-diabetic situation, and 3 patients (1.9%) had diabetes. Pre-pregnancy BMI of patients with GDM was a risk factor for increased gOGTT-FPG levels. Those who were overweight before pregnancy had a greater risk for a higher gOGTT-FPG compared to those who had normal pre-pregnancy BMI (P= 0.021, odds ratio[OR] = 4.583). Abnormal gOGTT-2hPG was a risk factor for abnormal ppOGTT (P= 0.04). Those who had an elevated gOGTT-2hPG (≧8.5 mmol/L) had a 2.426 times higher risk for abnormal ppOGTT than those who had normal gOGTT-2hPG (<8.5 mmol/L) results.Conclusion:For women who are overweight before pregnancy, it is better to control their BMI to normal before getting pregnant. Women who had abnormal gOGTT-2h PG should pay more attention to the ppOGTT results.

Resveratrol, a naturally occurring polyphenolic compound, exhibits a neuroprotective role in models of central nervous system diseases, including cerebral ischemia/reperfusion injury. Apurinic/apyrimidinic endonuclease 1 (APE1) is a multifunctional enzyme that contributes to base excision repair of oxidative DNA damage and redox activation of transcription factors, associated with neuronal survival against hypoxic‑ischemic injury. It was hypothesized that resveratrol protects HT22 cells against oxygen‑glucose deprivation and re‑oxygenation (OGD/R)‑induced injuries through upregulation of APE1. It was demonstrated that resveratrol pretreatment significantly increased the viability of HT22 cells and decreased the release of lactate dehydrogenase (LDH), accompanied by the upregulation of APE1 mRNA, and protein levels, as well as the activity of APE1 under OGD/R conditions. In addition, resveratrol reversed OGD/R‑induced oxidative DNA damage as evidenced by the decreases in the levels of 8‑hydroxy‑2'‑deoxyguanosine and APE sites. However, APE1 knockdown using short hairpin RNA sequence targeting APE1 abolished resveratrol‑elicited beneficent effects against OGD/R‑induced cytotoxicity and oxidative stress. This was indicated by decreased cell viability, superoxide dismutase activity and glutathione levels, and increased LDH release and reactive oxygen species levels. The results of the present study indicate that APE1 contributes to the protective effects of resveratrol against neonatal hypoxic‑ischemic brain injuries, and suggest that DNA repair enzymes, including APE1, may be a unique strategy for neuroprotection against this disease.