A Critical Review on Black Phosphorus-Based Photocatalytic CO2 Reduction Application.

Energy shortages and greenhouse effects are two unavoidable problems that need to be solved. Photocatalytically converting CO2 into a series of valuable chemicals is considered to be an effective means of solving the above dilemmas. Among these photocatalysts, the utilization of black phosphorus for CO2 photocatalytic reduction deserves a lightspot not only for its excellent catalytic activity through different reaction routes, but also on account of the great preponderance of this relatively cheap catalyst. Herein, this review offers a summary of the recent advances in synthesis, structure, properties, and application for CO2 photocatalytic reduction. In detail, the review starts from the basic principle of CO2 photocatalytic reduction. In the following section, the synthesis, structure, and properties, as well as CO2 photocatalytic reduction process of black phosphorus-based photocatalyst are discussed. In addition, some possible influencing factors and reaction mechanism are also summarized. Finally, a summary and the possible future perspectives of black phosphorus-based photocatalyst for CO2 reduction are established.

Bone cement implantation syndrome during hip replacement in a patient with pemphigus and Parkinson's disease: A case report.

BACKGROUND: Bone cement implantation syndrome (BCIS) is characterized by hypotension, arrhythmia, diffuse pulmonary microvascular embolism, shock, cardiac arrest, any combination of these factors, or even death following bone cement implantation. CASE SUMMARY: An 80-year-old patient with pemphigus and Parkinson's disease underwent total hip replacement under spinal subarachnoid block and developed acute pulmonary embolism after bone cement implantation. The patient received mask mechanical ventilation with a continuous intravenous infusion of adrenaline (2 µg/mL) at a rate of 30 mL/h. Subsequently, the symptoms of BCIS were markedly alleviated, and the infusion rate of adrenaline was gradually reduced until the infusion was completely stopped 45 min later. The patient was then transferred to the Department of Orthopedics, and anticoagulation therapy began at 12 h postoperatively. No other complications were observed. CONCLUSION: This is a rare case of BCIS in a high-risk patient with pemphigus and Parkinson's disease.

Immobilization of 6-O-α-maltosyl-ß-cyclodextrin on the surface of black phosphorus nanosheets for selective chiral recognition of tyrosine enantiomers.

A novel chiral sensing platform, 6-O-α-maltosyl-ß-cyclodextrin (Mal-ßCD)-based film, is proposed for selective electrochemical recognition of tyrosine (Tyr) enantiomers. Black phosphorus nanosheets (BP NSs) and Mal-ßCD modified glassy carbon electrode (Mal-ßCD/BP NSs/GCE) were prepared by a layer-to-layer drop-casting method, and the platform was easy to fabricate and facile to operate. It is proposed that the amino and hydroxyl groups of the Tyr enantiomers and the chiral hydroxyl groups of Mal-ßCD selectively form intermolecular hydrogen bonds to dominate effective chiral recognition. Two linear equations of Ip (µA) = 11.40 CL-Tyr (mM) + 0.28 (R2 = 0.99147) and Ip (µA) = 7.96 CD-Tyr (mM) + 0.22 (R2 = 0.99583) in the concentration range 0.01-1.00 mM have been obtained. The limits of detection (S/N=3) for L-Tyr and D-Tyr were 4.81 and 6.89 µM, respectively. An interesting phenomenon was that the value of IL-Tyr/ID-Tyr (1.51) in this work was slightly higher than the value of IL-Trp/ID-Trp (1.49) reported in our previous study, where tryptophan (Trp) enantiomers were electrochemically recognized by Nafion (NF)-stabilized BPNSs-G2-ß-CD composite. The two similar sensors fabricated by different methods showed different recognition ability toward either Tyr or Trp enantiomers, and the underlying mechanism was discussed in detail. More importantly, the proposed chiral sensor enables prediction of the percentages of D-Tyr in racemic Tyr mixtures. The chiral sensor may provide a novel approach for the fabrication of novel chiral platforms in the practical detection of L- or D-enantiomer in racemic Tyr mixtures.Graphical abstract.

Altered resting-state fMRI signals and network topological properties of bipolar depression patients with anxiety symptoms.

BACKGROUND: This study aims to explore the changes in functional neuroimaging in bipolar depression patients with anxiety symptoms (BDP-A). METHODS: Forty-five BDP-A patients, 22 bipolar depression patients without anxiety symptoms (BDP-NA), and 48 healthy controls (HC) were finally involved. The low-frequency oscillation characteristics, functional connectivity (FC), and network properties among the three groups of participants were analyzed. RESULTS: Compared with the BDP-NA group, BDP-A patients exhibited significantly decreased amplitude of low-frequency fluctuation (ALFF) in the left middle frontal gyrus (MFG), superior occipital gyrus, and inferior parietal, but supramarginal and angular gyri (IPL). Enhanced FC from left IPL to middle temporal gyrus, from left precentral gyrus (PreCG) to bilateral angular gyri, medial superior frontal gyrus, and left superior frontal gyrus (SFG)/MFG were also revealed. Compared with HC, the BDP-A group showed remarkably increased ALFF in the left MFG/PreCG, right superior parietal gyrus, while decreased ALFF in the left inferior frontal gyrus, opercular part, and SFG. In addition, higher regional homogeneity in the left MFG/PreCG was found. LIMITATIONS: The limitations are as follows: (1) relatively small sample size; (2) not all the patients were drug-naive; (3) lack of pure anxiety disorder patients as a controlled group; (4) mental health conditions of HC were not systemic evaluated. CONCLUSIONS: BDP-A patients showed significant differences in resting-state fMRI properties when compared with BDP-NA or HC group. These results may infer the dysfunction of the dorsal attention network, the default network, and the fronto-limbic system as well as disrupted brain network efficiency in BDP-A patients.

General anesthesia affecting on developing brain: evidence from animal to clinical research.

As the recent update of General anaesthesia compared to spinal anaesthesia (GAS) studies has been published in 2019, together with other clinical evidence, the human studies provided an overwhelming mixed evidence of an association between anaesthesia exposure in early childhood and later neurodevelopment changes in children. Pre-clinical studies in animals provided strong evidence on how anaesthetic and sedative agents (ASAs) causing neurotoxicity in developing brain and deficits in long-term cognitive functions. However pre-clinical results cannot translate to clinical practice directly. Three well designed large population-based human studies strongly indicated that a single brief exposure to general anesthesia (GAs) is not associated with any long-term neurodevelopment deficits in children's brain. Multiple exposure might cause decrease in processing speed and motor skills of children. However, the association between GAs and neurodevelopment in children is still inconclusive. More clinical studies with larger scale observations, randomized trials with longer duration exposure of GAs and follow-ups, more sensitive outcome measurements, and strict confounder controls are needed in the future to provide more conclusive and informative data. New research area has been developed to contribute in finding solutions for clinical practice as attenuating the neurotoxic effect of ASAs. Xenon and Dexmedetomidine are already used in clinical setting as neuroprotection and anaesthetic sparing-effect, but more research is still needed.

Dexmedetomidine Attenuates High Glucose-induced HK-2 Epithelial-mesenchymal Transition by Inhibiting AKT and ERK.

OBJECTIVE: To explore the protective effects of dexmedetomidine (Dex) against high glucose-induced epithelial-mesenchymal transition in HK-2 cells and relevant mechanisms. METHODS: HK-2 cells were exposed to either glucose or glucose+Dex for 6 h. The production of ROS, morphology of HK-2 cells, and cell cycle were detected. Moreover, the expression of AKT, p-AKT, ERK, p-ERK, PI3K, E-Cadherin, Claudin-1, and α-SMA were determined and compared between HK-2 cells exposed to glucose and those exposed to both glucose and Dex with or without PI3K/AKT pathway inhibitor LY294002 and ERK pathway inhibitor U0126. RESULTS: Compared with HK-2 cells exposed to high level of glucose, the HK-2 cells exposed to both high level of glucose and Dex showed: (1) lower level of ROS production; (2) cell morphology was complete; (3) more cells in G1 phase; (4) lower expression of p-AKT, p-ERK and α-SMA, higher expression of E-Cadherin and Claudin-1. PI3K/AKT inhibitor LY294002 and ERK inhibitor U0126 decreased the expression of p-AKT, p-ERK and α-SMA, and increased the expression of E-Cadherin and Claudin-1. CONCLUSION: Dex can attenuate high glucose-induced HK-2 epithelial-mesenchymal transition by inhibiting AKT and ERK.

Propofol Target-controlled Infusion in Anesthesia Induction during Painless Gastroscopy.

OBJECTIVE: To investigate the feasibility of using the eyelash reflex as an indicator to calculate the individualised optimal target concentration in anesthesia induction during painless gastroscopy. STUDY DESIGN: Experimental study. PLACE AND DURATION OF STUDY: China-Japan Union Hospital of Jilin University, China, from January to December in 2016. METHODOLOGY: A total of 180 patients, who were scheduled to receive painless fibergastroscopic examination or treatment in the last three months, were enrolled in this study. All patients were randomly divided into three groups, according to the doctor visiting order (n=60, each). During the induction of anesthesia using propofol target-controlled infusion, the effectsite concentration upon the disappearance of the eyelash reflex (C0) was recorded first. Then, one ug/kg of fentanyl was injected. At the same time, the target effect-site concentration induced by propofol was determined: the effect-site concentration in group A was 1.5 times of C0, the effect-site concentration in group B was two times of C0, and the effectsite concentration in group C was 2.5 times of C0. RESULTS: During anesthesia induction, the incidence of motor responses was higher in group A than in groups B and C (p<0.05), and the incidence of hypoxemia was significantly higher in group C than in groups A and B (p<0.01). CONCLUSION: In the anesthesia option of fentanyl combined with propofol target-controlled infusion, the effect-site concentration of propofol can be set to two times of that at the time the eyelash reflex disappears. This study provides a new pre-assessment method for the induction dose of propofol in painless gastroscopy.

Efficacy of different analgesic or sedative drug therapies in pediatric patients with congenital heart disease undergoing surgery: a network meta-analysis.

BACKGROUND: Surgery is an effective therapy for congenital heart disease (CHD) and the management after surgery poses challenges for the clinical workers. We performed this network meta-analysis to enhance the corresponding evidence with respect to the relative efficacy of different drug treatments applied after the CHD surgery. METHODS: Embase and PubMed were systematically retrieved to identify all published controlled trials investigating the effectiveness of drugs for patients up to 25 August, 2018. Mean differences (MD), odds ratios and their 95% credible intervals (CrIs) were used to evaluate multi-aspect comparisons. Surface under cumulative ranking curve (SUCRA) was used to analyze the relative ranking of different treatments in each endpoint. RESULTS: Compared to saline, all the drugs achieved better preference under the efficacy endpoints except fentanyl in JET. As for ventilator time, all drugs were more effective than saline while only the difference of dexmedetomidine was statistically obvious (MD = 6.92, 95% CrIs 1.77-12.54). Under the endpoint of ICU time, dexmedetomidine was superior to saline as well (MD = 1.26, 95% CrIs 0.11-2.45). When all the endpoints were taken into consideration and with the help of ranking probabilities and SUCRA values, fentanyl combined with dexmedetomidine was one of the recommended drugs due to its shorter time on ventilator and stay in hospital as well as lower mortality. CONCLUSIONS: Overall, based on the comprehensive consideration of all the endpoints, fentanyl combined with dexmedetomidine was considered to be the best-recommended clinical interventions among all the methods.

Ginsenoside impedes proliferation and induces apoptosis of human osteosarcoma cells by down-regulating ß-catenin.

BACKGROUND: Osteosarcoma (OS) is the most commonly occurred primary bone malignancy with high incident rates among children and adolescents. In pharmacologic treatment, the drug ginsenoside has been shown to exert anticancer effects on several malignant diseases. The purpose of this research was to investigate the effect of ginsenoside on the apoptosis and proliferation of human OS MG-63 and Saos-2 cells by regulating the expression of ß-catenin. METHODS: Human OS MG-63 and Saos-2 cells were assigned into control group, and four groups with treatment by varying concentrations (12.5 µg/mL, 25 µg/mL, 50 µg/mL and 100 µg/mL) of ginsenoside, respectively. Cell growth after treatment was observed through cell slides. The proliferation rate of MG-63 and Saos-2 cells in each group was detected by CCK-8. After cell transfection at 48 h, cell cycle and cell apoptosis were detected by FITC-Annexin V staining and flow cytometry. The protein and mRNA expressions of ß-catenin, Cyclin D1, Bcl-2, Bax and cleaved caspase-3 were detected by RT-qPCR and western blot analysis. RESULTS: With increased exposure and concentration of ginsenoside, the cell density, total cell numbers and the absorbance of MG-63 and Saos-2 cells gradually decreased. FITC-Annexin V and FITC-Annexin V/PI staining demonstrated that the cell proportion at S phase decreased, whereas the total apoptotic rate of MG-63 and Saos-2 cells was increased. Furthermore, RT-qPCR and western blot analysis highlighted a gradual decrease in protein and mRNA expressions of ß-catenin, Bcl-2 and Cyclin D1, while an elevation in those of Bax and cleaved caspase-3. CONCLUSION: The results of this study demonstrate that ginsenoside inhibits proliferation and promotes apoptosis of human OS MG-63 and Saos-2 cells by reducing the expressions of ß-catenin, Bcl-2 and Cyclin D1 and increasing the expression of Bax and cleaved caspase-3.

Long non-coding RNA LINC00968 attenuates drug resistance of breast cancer cells through inhibiting the Wnt2/ß-catenin signaling pathway by regulating WNT2.

BACKGROUND: Breast cancer is one the most common cancers, making it the second leading cause of cancer-related death among women. Long non-coding RNAs (lncRNAs), with tightly regulated expression patterns, also serve as tumor suppressor during tumorigenesis. The present study aimed to elucidate the role of LINC00968 in breast cancer via WNT2-mediated Wnt2/ß-catenin signaling pathway. METHODS: Breast cancer chip GSE26910 was utilized to identify differential expression in LINC00968 and WNT2. The possible relationship among LINC00968, transcriptional repressor HEY and WNT2 was analyzed and then verified. Effects of LINC00968 on activation of the Wnt2/ß-catenin signaling pathway was also tested. Drug resistance, colony formation, cell migration, invasion ability and cell apoptosis after transfection were also determined. Furthermore, tumor xenograft in nude mice was performed to test tumor growth and weight in vivo. RESULTS: WNT2 expression exhibited at a high level, whereas LINC00968 at a low expression in breast cancer which was also associated with poor prognosis in patients. LINC00968 targeted and negatively regulated WNT2 potentially via HEY1. Either overexpressed LINC00968 or silenced inhibited activation of the Wnt2/ß-catenin signaling pathway, thereby reducing drug resistance, decreasing colony formation ability, as well as suppressing migration and invasion abilities of breast cancer cells in addition to inducing apoptosis. Lastly, in vivo experiment suggested that LINC00968 overexpression also suppressed transplanted tumor growth in nude mice. CONCLUSION: Collectively, overexpressed LINC00968 contributes to reduced drug resistance in breast cancer cells by inhibiting the activation of the Wnt2/ß-catenin signaling pathway through silencing WNT2. This study offers a new target for the development of breast cancer treatment.

Cytosolic HMGB1 Mediates Autophagy Activation in an Emulsified Isoflurane Anesthesia Cell Model.

Inhalation anesthetic isoflurane may cause an increased risk of cognitive impairment. Previous studies have indicated that this cognitive decline is associated with neuroinflammation mediated by high mobility group box 1 (HMGB1). HMGB1 is released from cells and acts as a damage-associated molecule in neurodegenerative diseases. However, the effect of intracellular HMGB1 during emulsified isoflurane (EI) exposure is poorly understood. The purpose of this study was to investigate the effect of autophagy on neuroprotection, evaluate variation of HMGB1, and determine its role in autophagic flux after EI exposure in vitro. We observed that EI decreased cell viability in a concentration-dependent manner, accompanied by an increase in autophagic flux. EI exposure also elevates the HMGB1 level in cytoplasm. Further, cytosolic HMGB1 was necessary for autophagy by perturbing the beclin1-Bcl-2 interaction. Most importantly, autophagy induction by rapamycin alleviated EI-provoked cell injury, and HMGB1 knockdown induced autophagy inhibition, which exacerbated cell damage. Based on these findings, we propose that autophagic flux is sustained and upregulated in response to EI exposure by increased cytosolic HMGB1, and that autophagy activation serves as a protective mechanism against EI-induced cytotoxicity. Thus, the complex roles of HMGB1 make it pivotal in reducing EI-induced neuronal damage.

A novel electrochemical chiral interface based on the synergistic effect of polysaccharides for the recognition of tyrosine enantiomers.

Electrochemical chiral interface based on two polysaccharides, soluble starch (SS) and chitosan (CS), was fabricated and used for chiral recognition of tyrosine (Tyr) enantiomers via square wave voltammetry (SWV). The SS-CS composite was characterized by scanning electron microscopy (SEM) and Brunauer-Emmett-Teller (BET) method. Under the optimized experimental conditions, the oxidation peak current ratio of L-Tyr to D-Tyr (IL/ID) and the difference between the peak potential (ΔEp = ED - EL) were observed to be 1.38 and 12 mV at the SS-CS/GCE. In addition, a good linear relationship between Tyr enantiomer concentration and peak current could be observed. The SS-CS/GCE exhibited good coefficients of determination (R2D-Tyr = 0.99631 and R2L-Tyr = 0.98333) for D-Tyr and L-Tyr in the concentration range 0.01-1.00 mM. The novel SS-CS/GCE showed an ability to predict the ratios of L- and D-Tyr in a racemic mixture and exhibited the possibility of qualitative and quantitative determination of Tyr enantiomers. The proposed SS-CS/GCE-based chiral sensor exhibited high anti-interference ability in the presence of 10-fold higher concentrations of physiological substances and various metal compounds. Meanwhile, the SS-CS/GCE possessed good repeatability and excellent reproducibility.

Analgesic effects of microRNA-129-5p against bone cancer pain through the EphB1/EphrinB2 signaling pathway in mice.

The study aims to investigate the analgesic effects of microRNA-129-5p (miR-129-5p) on bone cancer pain (BCP) by targeting Eph receptor B1 (EphB1) through the EphB1/EphrinB2 signaling pathway. BCP mice models were established, and C3H/HeJ female mice were classified into the normal, blank, negative control (NC), miR-129-5p mimics, miR-129-5p inhibitors, EphB1 knockout (KO), and miR-129-5p inhibitors + EphB1 KO groups. Quantitative reverse transcription polymerase chain reaction and Western blot analysis were used to evaluate the miR-129-5p expression, and messenger RNA (mRNA) and protein expressions of EphB1, p-EphB1, EphrinB2, and p-EphrinB2. EphB1 and EphrinB2 were highly activated in the tibias of BCP mice 7 days after the operation. EphB1 is a target gene of miR-129-5p. The mechanical withdrawal threshold increased in the miR-129-5p mimics, EphB1 KO and miR-129-5p inhibitors + EphB1 KO groups, but decreased in the miR-129-5p inhibitors group. Compared with the blank and the NC groups, the expression of miR-129-5p was significantly increased in the miR-129-5p mimics group, and the mRNA and protein expressions of EphrinB2, p-EphrinB2, EphB1, and p-EphB1 were significantly decreased, while in the miR-129-5p inhibitors group, the results were opposite (all P < 0.05); the mRNA and protein expressions of EphrinB2, p-EphrinB2, EphB1, and p-EphB1 were significantly decreased in the EphB1 KO group (all P < 0.05); the expression of miR-129-5p was significantly decreased in the miR-129-5p inhibitors + EphB1 KO group ( P < 0.05), while the mRNA and protein expressions of EphrinB2 and p-EphrinB2 were not significantly different ( P > 0.05). The results indicated that upregulated miR-129-5p alleviate BCP via downregulation of the EphB1/EphrinB2 signaling pathway.

Downregulation of the long noncoding RNA MBNL1-AS1 protects sevoflurane-pretreated mice against ischemia-reperfusion injury by targeting KCNMA1.

Total knee arthroplasty (TKA) is the most common and cost-effective treatment for older adults with long-standing osteoarthritis. During TKA, muscle cells suffer from prolonged oxygen deficiency, which leads to altered cell metabolism that reduces the energy demand and maintains cell homeostasis before blood flow is restored. This study focused on the role of the lncRNA muscleblind-like 1 antisense RNA 1 (MBNL1-AS1) in protecting sevoflurane-pretreated mice against ischemia-reperfusion (I/R) injury after TKA, as well as the elucidation of the potential associated mechanism. Identification of differentially expressed lncRNAs was performed using the microarray dataset GSE21164, which was extracted from the GEO database. Target genes of the lncRNA were determined using Multi-Experiment Matrix (MEM), a dual-luciferase reporter gene assay, and KEGG enrichment analyses. The results showed that MBNL1-AS1 was overexpressed in skeletal muscle cells in mice, while KCNMA1, which was enriched in the cGMP-PKG signaling pathway, was negatively regulated by MBNL1-AS1. Furthermore, I/R mice displayed serious inflammatory reactions. Down-regulation of MBNL1-AS1 increased the expression of KCNMA1, PKGII, VASP, VEGF, Bcl-2, Cyclin D1, Cyclin D3, and Cdc 42 but decreased the expression of Bax, cleaved caspase-3, and cleaved PARP. Furthermore, upon MBNL1-AS1 upregulation, the rate of cell apoptosis increased while the rate of cell proliferation decreased. Our data suggested that down-regulated lncRNA MBNL1-AS1 might promote the proliferation and inhibit the apoptosis of skeletal muscle cells by upregulating KCNMA1 expression via activation of the cGMP-PKG signaling pathway, thus protecting sevoflurane-pretreated mice against I/R injury after TKA.

Propofol elicits autophagy via endoplasmic reticulum stress and calcium exchange in C2C12 myoblast cell line.

In this study, we investigated the relationship between propofol and autophagy and examined whether this relationship depends on ER stress, production of ROS (reactive oxygen species), and disruption of calcium (Ca2+) homeostasis. To this end, we measured C2C12 cell apoptosis in vitro, along with Ca2+ levels; ROS production; and expression of proteins and genes associated with autophagy, Ca2+ homeostasis, and ER stress, including LC3 (microtubule-associate protein 1 light chain 3), p62, AMPK (adenosine 5'-monophosphate (AMP)-activated protein kinase), phosphorylated AMPK, mTOR (the mammalian target of rapamycin), phosphorylated mTOR, CHOP (C/BEP homologous protein), and Grp78/Bip (78 kDa glucose-regulated protein). We found that propofol treatment induced autophagy, ER stress, and Ca2+ release. The ratio of phosphorylated AMPK to AMPK increased, whereas the ratio of phosphorylated mTOR to mTOR decreased. Collectively, the data suggested that propofol induced autophagy in vitro through ER stress, resulting in elevated ROS and Ca2+. Additionally, co-administration of an ER stress inhibitor blunted the effect of propofol.

LncRNA NONRATT021972 Was Associated with Neuropathic Pain Scoring in Patients with Type 2 Diabetes.

BACKGROUND: Long noncoding RNAs were involved in the processes of diabetes. Our study was aimed to explore clinical potential of LncRNA NONRATT021972 in diabetic neuropathic pain and investigate detailed mechanisms. METHODS: 154 patients with type 2 diabetes were enrolled as experimental group paired with control. Patients without diabetes but neuropathy were enrolled to explore exclusive role of LncRNA NONRATT021972 in neuropathy. Real-time PCR and ELISA were performed to examine expression of LncRNA and TNF-α in flood. Neuropathic pain scores were calculated with data from NPQ. Streptozotocin was used for SD adult male rats to establish diabetes for NONRATT021972 siRNA or saline treatment. Neuropathic pain behaviors and expression of TNF-α were assessed. RESULT: Patients with type 2 diabetes had a significantly higher concentration of LncRNA NONRATT021972 in blood and more severe symptoms of neuropathic pain. LncRNA NONRATT021972 was positively associated with neuropathic pain scores of type 2 diabetes. TNF-α level increased in patients with type 2 diabetes. Animal experiment showed that LncRNA NONRATT021972 siRNA attenuated inflammation via decreasing TNF-α and alleviated neuropathic pain. CONCLUSION: LncRNA NONRATT021972 increased in type 2 diabetes and was positively associated with neuropathic pain scoring in type 2 diabetes. LncRNA NONRATT021972 exacerbated neuropathic pain via TNF-α related pathways.