Based on data from a single hospital registry in East Asia, a shorter duration of resuscitation was demonstrated to be a predictor of immediate survival with ROSC and survival to hospital discharge.

ObjectivesTo investigate the distribution of serum calcium and the relationship between serum calcium and serum metabolic parameters in endometrial carcinoma (EC) patients.MethodsRetrospective assessment of patients diagnosed with endometrial cancer from Peking University People's Hospital from 2004 to 2009. Clinical characteristics as well as pretreatment serum calcium, albumin, fasting plasma glucose (FPG), serum triglycerides (TG), high-density lipoprotein (HDL), low-density lipoprotein (LDL), and total cholesterol (TC) value were extracted from patient records. Serum calcium was corrected for albumin. Unpaired t test and analysis of covariance were used to compare serum calcium among categorical variables. Simple correlation analyses and partial correlation analyses were used to assess the associations between serum calcium and continuous variables.ResultsTwo-hundred twenty patients were included in this study. After adjusting for confounders, postmenopausal patients had higher total serum calcium (p=0.002) and albumin-corrected serum calcium (p=0.012) than premenopausal patients, endometrioid endometrial carcinoma (EEC) patients had higher total serum calcium than non-endometrioid endometrial carcinoma (NEEC) patients (p=0.037). Significant positive correlations were found between total serum calcium and FPG (p=0.017), TG (p=0.043), HDL (p=0.042), LDL (p<0.001), and TC (p<0.001) after adjusting for multiple variables, and the corrected serum calcium showed no significant correlation with metabolic parameters.ConclusionTotal serum calcium might be a more sensitive parameter for metabolic syndrome in endometrioid endometrial cancer patients than lipids.

Background Metabolic disorder is considered a well-established risk factor for endometrial carcinoma (EC). However, the mechanism remains unclear. Insulin resistance and excessive flux of free fatty acids serve as fundamental pathogenic factors in metabolic disorders, including obesity and type 2 diabetes. The aim of this study was to test the correlation between insulin resistance and dyslipidaemia in EC and to determine the effect of insulin and saturated fatty acids on EC cells. Methods A retrospective study on the medical records of patients with EC and RNA-seq from the TCGA database analysed with edgR and Gene Ontology (GO) were used to assess the correlation of dyslipidaemia and diabetes as well as obesity. Crystal violet assays and CCK-8 assays were used to detect the proliferation of EC cells, and Annexin V-PI was used to examine apoptosis. Transient changes in mitochondrial Ca2+ and reactive oxygen species (ROS) were monitored via confocal microscopy. DNA damage was assessed by comet assays. Changes in signalling pathways were detected via phospho-kinase array. western blotting was used to assess the molecular changes in endoplasmic reticulum (ER) stress and DNA damage. Results We found that glucose metabolism disorders accompanied dyslipidaemia in patients with EC. As a key regulator of glucose metabolism disorders, insulin promoted DNA damage, ROS and Ca2+ homoeostasis imbalance in a panel of established EC cell lines. Interestingly, excessive insulin boosted saturated fatty acid-induced pro-apoptotic effects in EC cells. Furthermore, our data showed that insulin synergised with saturated fatty acids to activate the mechanistic target of rapamycin kinase/70 kDa ribosomal protein S6 kinase (mTOR/p70S6K) pathway and ER stress, resulting in Ca2+ release from ER and unfolded protein response (UPR) activation, which contributed to combined insulin and saturated fatty acid treatment-induced apoptosis and tumour progression. Conclusions Our data are the first to illustrate that impaired glucose metabolism accelerates dyslipidaemia-promoted EC progression, which is attributed to hyperinsulinaemia and saturated fatty acid-induced Ca2+ dyshomoeostasis and UPR activation in EC cells via ER stress.

ObjectiveTo date, there is no convincing evidence comparing the impact of combined chemotherapy and radiotherapy with chemotherapy alone in postoperative uterine serous carcinoma (USC), which remains an unclear issue. We conducted a meta-analysis assessing the impact of combined chemotherapy and radiotherapy compared to chemotherapy alone on overall survival in postoperative USC.MethodsA comprehensive search was performed in the databases of EMBASE, PubMed, Web of Science, and Cochrane Library from inception to March 2016. Studies comparing survival among patients who underwent combined chemotherapy and radiotherapy or chemotherapy alone after surgery for USC were included. Quality assessments were carried out by the Newcastle–Ottawa Scale. Hazard ratio (HR) for overall survival was extracted, and a random-effects model was used for pooled analysis. Publication bias was assessed using both funnel plot and the Egger regression test. Statistical analyses were performed using Stata version 13.0 software.ResultNine retrospective studies with relatively high quality containing 9354 patients were included for the final meta-analysis. The pooled results demonstrated that combined chemotherapy and radiotherapy significantly reduced the risk of death (HR, 0.72; P < 0.0001) compared to chemotherapy alone with a low heterogeneity (I2 = 21.0%, P = 0.256). Subgroup analyses indicated that calculating HR by unadjusted method may cause the heterogeneity among studies. Exploratory analyses showed that either patients with early stage disease (HR, 0.73; P = 0.011) or advanced stage disease (HR, 0.80; P < 0.0001) have survival benefits from combined chemotherapy and radiotherapy. No significant evidence of publication bias was found.ConclusionsThis is the first meta-analysis examining the role of combined chemotherapy and radiotherapy compared to chemotherapy alone in USC. Our results suggest the potential survival benefits of combined chemotherapy and radiotherapy. Further studies, preferably randomized clinical trials, are needed to confirm our results.