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Major symptoms of depression are commonly observed in patients requiring total hip arthroplasty (THA), and this is associated with increased pain scores and opioid consumption. We aimed to investigate the analgesic effect of duloxetine in these high-risk patients.Among 263 patients scheduled for primary unilateral THA, 67 patients who scored at least 8 on the 17-item Hamilton Depression Scale (HAMD) were enrolled in this study. Patients were randomized to the duloxetine group (60 mg daily, from the day of surgery to postoperative day 6) or the placebo group. The postoperative visual analog scale (VAS) score during walking, the VAS score during hip flexion, and resting VAS score was measured. Postoperative morphine consumption, hip range of motion (ROM), Harris hip score (HHS), Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) function, postoperative length of stay (LOS), and adverse events were recorded.The duloxetine group had significantly lower VAS scores during walking and hip flexion from postoperative day 3 to week 3 than the placebo group. With regard to the resting VAS score, duloxetine showed a better analgesic effect from postoperative day 3 to week 2 than placebo. Patients in the duloxetine group had less consumption of morphine. The duloxetine group exhibited better hip function scores, including ROM, HHS, and WOMAC function scores than the placebo group. No significant difference was observed in LOS or adverse events between groups.Perioperative short-term duloxetine provides advantages in decreasing pain, reducing morphine consumption, and increasing hip function in THA patients who have depressive symptoms.

Depressed mice have lower numbers of microglia in the dentate gyrus (DG). Reversal of this decline by a single low dose of lipopolysaccharide (LPS) may have antidepressant effects, but there is little information on the molecular mechanisms underlying this effect. It is known that impairment of brain-derived neurotrophic factor (BDNF) signaling is involved in the development of depression. Here, we used a combination of neutralizing antibodies, mutant mice, and pharmacological approaches to test the role of BDNF-tyrosine kinase receptor B (TrkB) signaling in the DG in the effect of microglial stimulation. Our results suggest that inhibition of BDNF signaling by infusion of an anti-BDNF antibody, the BDNF receptor antagonist K252a, or knock-in of the mutant BDNF Val68Met allele abolished the antidepressant effect of LPS in chronically stressed mice. Increased BDNF synthesis in DG, mediated by extracellular signal-regulated kinase1/2 (ERK1/2) signaling but not protein kinase B (Akt)-mammalian target of rapamycin (mTOR) signaling, was essential for the antidepressant effect of microglial stimulation. These results suggest that increased BDNF synthesis through activation of ERK1/2 caused by a single LPS injection and subsequent TrkB signaling are required for the antidepressant effect of hippocampal microglial stimulation.

In this work, a composite film was prepared by combining reduced graphene oxide (RGO) and starch nanocrystals (SNC). The results show that SNC can be well dispersed on graphene after mixed with the graphene oxide solutions. SNC had a greater impact on the morphology and microstructure of the composite film. Moreover, the introduction of SNC and the efficient reduction process of graphene oxide (GO) render these composite films good mechanical properties as well as high electrical conductivity. The tensile strength of the composite film was improved after being combined with graphene. However, as the addition rate of SNC increased, the strain-to-failure of the composite film decreased. Therefore, 10% reduced graphene-starch nanocrystals (10%RGO-SNC) was used as multifunctional sensor materials. And it had strong responses to different external stimuli, such as, temperature, humidity, bending/stretching, and solutions.

Since the outer surface interaction of Q[n]s (OSIQ, including self-, anion- and aromatic-induced OSIQs) was proposed in 2014, it has become the most important research area in our group to construct various Q[n]-based supramolecular frameworks via the OSIQ strategy. Herein, we report a novel supramolecular framework constructed using cucurbit[8]uril (Q[8]) and 4-sulfocalix[6]arene (SC[6]A). This Q[8]/SC[6]A-based supramolecular framework is a product via the perfect combination of self-, anion- and aromatic-induced OSIQs. This framework has the characteristics of easy preparation and high stability with the most important feature being the sequence selective capture of specific metal cations, such as common alkali- and alkaline earth metal ions, and renewability. Thus, this framework may be used in seawater desalination, potassium ion enrichment, radioactive cesium ion pollution source treatment, Gruinard's treatment or water softening and other applications.

Chemoresistance is a major challenge for the treatment of cancer with metastasis. We investigated the mechanisms of lipid metabolites involved in drug resistance. Here, metastatic cancer cells isolated from mouse models were resistant to paclitaxel treatment in vitro and in vivo when compared with parental cancer cells. FOXM1, an oncogenic transcriptional factor, was highly expressed in metastatic cancer cells, and overexpression of FOXM1 conferred parental cancer cells resistance to paclitaxel. Lipidomic analysis showed that FOXM1 increased unsaturated triglyceride (TG) and phosphatidylcholine (PC) abundance, which are the main components of lipid droplet (LD). Inhibition of LD formation sensitized cells to paclitaxel. Mechanistically, the enzyme phospholipase D1 (PLD1) was identified as a potential effector target of FOXM1. PLD1 promoted LD accumulation, which reduced the level of reactive oxygen species (ROS) and maintained endoplasmic reticulum (ER) homeostasis in resistant cells with the treatment of paclitaxel. Moreover, inhibition of PLD1 reversed FOXM1-conferred paclitaxel resistance in vitro and in vivo. This study, for the first time, reveals the role of FOXM1-mediated PLD1 in LD accumulation and paclitaxel resistance. Targeting PLD1 or LD formation may help reverse chemoresistance in metastatic cancer cells. Generally, our results identified FOXM1 as a driver of paclitaxel resistance via activation of PLD1 to promote of LD accumulation, which contributes to the maintenace of ER homeostasis when metastatic cancer cells are confronted with ROS induced by paclitaxel.

Objective: Increasing obstetric medical litigations had great impacts in health care system resulted in lower recruitment of residents and higher medical cost of defensive medicine in Taiwan. In order to reduce medical litigation, the “Childbirth Accident Emergency Relief Act” was implemented in June 2016. This study presented five-year results of a novel childbirth accident compensation system. Materials and methods: The purpose of the Relief Act was to establish a national relief system to ensure timely relief, reduce medical disputes, promote the partnership between patient and medical personnel. The compensations included maximal 2 million NTD for maternal death, maximal 0.3 million NTD for neonatal and fetal deaths, and 3, 2, and 1.5 million NTD for maternal or neonatal profound, severe, and moderate disabilities, respectively. Puerperal hysterectomy was included with maximal 0.8 million NTD compensation. Results: Since June 30, 2016 to June 30, 2021, there were 1340 applications reviewed by Committee and 1258 were approved with total relief of 744.7 million NTD (26.6 million USD) with approve rate of 93.9%. It took an average of 109.8 days to start application from childbirth and 102.4 days to get compensation from application. 66.1% of accident victims agreed this system can restore doctor–patient relationship by immediate care and assistance from medical institutions. Conclusion: The Relief Act is the first government leading compensation system to establish a national relief system. It was enacted to reduce medical disputes, promote the partnership between patient and medical personnel, and enhance health and safety of women during childbirth. A no-fault compensation would be an efficient alternative disputes resolution to childbirth accidents.

Obesity-related hyperglycemia, with hepatic insulin resistance, has become an epidemic disease. Central neural leptin signaling was reported to improve hyperglycemia. The aim of this study was to investigate the effect of hepatic leptin signaling on controlling hyperglycemia.First, the effect of leptin signaling on gluconeogenesis was investigated in primary mouse hepatocytes and hepatoma cells. Second, glucose tolerance, insulin tolerance, blood glucose levels, and hepatic gluconeogenic gene expression were analyzed in obese mice overexpressing hepatic OBRb. Third, expression of mitogen-activated protein kinase phosphatase (MKP)-3, phosphorylation level of signal transducer and activator of transcription (STAT) 3, and extracellular regulated protein kinase (ERK) were analyzed in hepatocytes and mouse liver. Fourth, the role of MKP-3 in hepatic leptin signaling regulating gluconeogenesis was analyzed. Lastly, the role of ERK and STAT3 in the regulation of MKP-3 protein by leptin signaling was analyzed.Activation of hepatic leptin signaling suppressed gluconeogenesis in both hepatocytes and obese mouse liver, and improved hyperglycemia, insulin tolerance, and glucose tolerance in obese mice. The protein level of MKP-3, which can promote gluconeogenesis, was decreased by leptin signaling in both hepatocytes and mouse liver. Mkp-3 deficiency abolished the effect of hepatic leptin signaling on suppressing gluconeogenesis in hepatocytes. STAT3 decreased the MKP-3 protein level, while inactivation of STAT3 abolished the effect of leptin signaling on reducing the MKP-3 protein level in hepatocytes. Moreover, STAT3 could combine with MKP-3 and phospho-ERK1/2, which induced the degradation of MKP-3, and leptin signaling enhanced the combination.Hepatic leptin signaling could suppress gluconeogenesis at least partially by decreasing the MKP-3 protein level via STAT3-enhanced MKP-3 and ERK1/2 combination.

This study presents a detailed review on the ultrathin catalyst layer (UTCL) design strategy for high-performance proton exchange membrane fuel cell (PEMFC). Specifically, the motivation towards the further reduced Pt loadings by applying the UTCL electrode design is firstly introduced from both the historical and mechanism deductions. Then, the recent developments on the UTCL designs belonging to different classifications are summarized with their respective merits. In particular, the critical issues remained on these ultra-thin, low Pt-loaded electrodes are proposed with alternative solutions. Finally, the whole review is concluded with the perspectives on the possible future directions settling the remaining challenges.

The replacement of the disulfide bridge of CPI-1, a peptide inhibitor of light chain of Botulinum toxin serotype A, with the thioether-containing and biscarba-containing diaminodiacid bridge leads to a significant decrease in the degradation by trypsin and increase in the detoxification activity in vivo, the addition of hydrophobic or positive amino acid at C-terminus of modified peptides further improves the inhibitory activity.

Lithium-sulfur batteries (LiSBs) are widely deemed as the most promising energy storage devices to substitute for traditional Li-ion batteries. However, its wide application is impeded by the soluble lithium polysulfides (LiPSs), which is called the shuttle effect, and the irregular distribution of final product Li2S. Herein, based on the interfaces engineering, CoO Co4N hetero-nanocages are used as the sulfur host for LiSBs. Taking advantage of the polarity of CoO with the conductivity of Co4N, CoO Co4N nanocages not only can provide large void space for sulfur volume fluctuation, but also can adsorb polysulfides and simultaneously regulate the nucleation of solid Li2S by the ‘trapping-diffusion-conversion’ mechanism, which significantly enhances the redox kinetic of LiSBs and the utilization of active materials. Eventually, LiSBs with CoO Co4N nanocages host exhibit higher rate capacity (737 mAh·g−1 at 2 C) and cycling stability (662 mAh·g−1 at 1 C after 350 cycles). Even when the areal sulfur loading is as high as 3.0 mg cm−2, a high capacity of 713 mAh·g−1 can still be achieved after 100 cycles at 0.2 C. This host with sufficient polar-conductive interfaces expands ‘trapping-diffusion-conversion’ concept for the design of fast kinetic and high performance LSBs.