Considerable attention has been directed toward studying the impact of diabetes on the central nervous system. The current study investigates the biochemical changes in the brain tissue of streptozotocin (STZ)-induced diabetic rat using 31P magnetic resonance spectroscopy (31P MRS). The 31P NMR spectra of the whole brain show no significant changes of phosphomonoesters and phosphodiesters levels one week after STZ induction, suggesting no apparent structural changes in cell membranes. The results identifies the increased level of adenosine diphosphate, negligible changes of phosphocreatine ( PCr ) and adenosine triphosphate ( ATP) , but the decreased ratio of PCr/ATP, indicating that PCr plays a role of balancing the energy. Moreover, the decreased pH value indicates the changes of the intracellular environment in STZ-diabetic brains in rats. After 15 weeks of STZ injection, the metabolism of phospholipid membrane and brain energy metabolism has been obviously disturbed. Our study successfully shows that 31 P MRS can not only study phospholipid and energy metabolism non-invasively, but also measure intracellular pH and other important biochemical information. All of these spectroscopic characterizations contribute significantly to the understanding of pathogenesis and evolution of diabetes, and provide theoretical basis for early diagnosis and clinical treatment in diabetes.

The prevention and treatment of posthepatectomy liver failure (PHLF) is a difficult problem for hepatectomy. PHLF is characterized by many risk factors, limited treatment methods and high mortality. There are many factors that lead to the insufficient quantity or quality of postoperative remnant liver cells, such as the comorbid conditions of patients, underlying disease of the liver, excessive liver resection and so on, which are increase the incidence of PHLF. However, the therapeutic treatment of PHLF is limited at present, the key to reduce the morbidity and mortality of PHLF lies in the accurate evaluation and screening of high-risk patients. This paper reviewed the relevant literature on the definition, risk factors and clinical prevention and treatment of posthepatectomy liver failure.

Objective To investigate the perioperative risk factors for posthepatectomy liver failure (PHLF) in patients with hepatocellular carcinoma (HCC).Methods Data of 322 cases of liver resection for HCC were retrospectively analyzed from Sep 2013 to Sep 2018.Logistic regression was used to analyze the risk factors for PHLF.The receiver operating characteristic (ROC) curve was used to analyze the predictive power of the ALBI score and the Child-Pugh score for PHLF.Results Child-Pugh score,ALBI score,intraoperative bleeding amount,ICG R15 and liver fibrosis,peritoneal effusion were independent factors affecting PHLF of HCC patients(P ＜ 0.05).ROC analysis of Child-Pugh and ALBI scores predicting PHLF showed that area under the ROC was respectively 0.621 (95％ CI:0.531-0.712) in the Child-Pugh score and 0.729 (95％ CI:0.645-0.812)in the ALBI score.The best critical value,sensitivity and specificity of PHLF that were predicted by ALBI score were-2.74,71.7％ and 71.4％,respectively.Conclusions The prognostic power of the ALBI score was greater than that of the Child-Pugh score in predicting PHLF.

Metastasis accounts for 90% of breast cancer deaths, where the lethality could be attributed to the poor drug accumulation at the metastatic loci. The tolerance to chemotherapy induced by breast cancer stem cells (BCSCs) and their particular redox microenvironment further aggravate the therapeutic dilemma. To be specific, therapy-resistant BCSCs can differentiate into heterogeneous tumor cells constantly, and simultaneously dynamic maintenance of redox homeostasis promote tumor cells to retro-differentiate into stem-like state in response to cytotoxic chemotherapy. Herein, we develop a specifically-designed biomimic platform employing neutrophil membrane as shell to inherit a neutrophil-like tumor-targeting capability, and anchored chemotherapeutic and BCSCs-differentiating reagents with nitroimidazole (NI) to yield two hypoxia-responsive prodrugs, which could be encapsulated into a polymeric nitroimidazole core. The platform can actively target the lung metastasis sites of triple negative breast cancer (TNBC), and release the escorted drugs upon being triggered by the hypoxia microenvironment. During the responsiveness, the differentiating agent could promote transferring BCSCs into non-BCSCs, and simultaneously the nitroimidazole moieties conjugated on the polymer and prodrugs could modulate the tumor microenvironment by depleting nicotinamide adenine dinucleotide phosphate hydrogen (NADPH) and amplifying intracellular oxidative stress to prevent tumor cells retro-differentiation into BCSCs. In combination, the BCSCs differentiation and tumor microenvironment modulation synergistically could enhance the chemotherapeutic cytotoxicity, and remarkably suppress tumor growth and lung metastasis. Hopefully, this work can provide a new insight in to comprehensively treat TNBC and lung metastasis using a versatile platform.