Effectiveness of Global Leadership Initiative on Malnutrition and Subjective Global Assessment for diagnosing malnutrition and predicting wound healing in patients with diabetic foot ulcers.

Malnutrition significantly hampers wound healing processes. This study aimed to compare the effectiveness of the Global Leadership Initiative on Malnutrition (GLIM) and Subjective Global Assessment (SGA) in diagnosing malnutrition and predicting wound healing in patients with diabetic foot ulcers (DFU). GLIM criteria were evaluated for sensitivity (SE), specificity (SP), positive predictive value, negative predictive value and kappa (κ) against SGA as the reference. Modified Poisson regression model and the DeLong test investigated the association between malnutrition and non-healing ulcers over 6 months. This retrospective cohort study included 398 patients with DFU, with a mean age of 66·3 ± 11·9 years. According to SGA and GLIM criteria, malnutrition rates were 50·8 % and 42·7 %, respectively. GLIM criteria showed a SE of 67·3 % (95 % CI 60·4 %, 73·7 %) and SP of 82·7 % (95 % CI 76·6 %, 87·7 %) in identifying malnutrition, with a positive predictive value of 80·0 % and a negative predictive value of 71·1 % (κ = 0·50) compared with SGA. Multivariate analysis demonstrated that malnutrition, as assessed by SGA, was an independent risk factor for non-healing (relative risk (RR) 1·84, 95 % CI 1·45, 2·34), whereas GLIM criteria were associated with poorer ulcer healing in patients with estimated glomerular filtration rate ≥ 60 ml/min/1·73m2 (RR: 1·46, 95 % CI 1·10, 1·94). SGA demonstrated a superior area under the receiver's operating characteristic curve for predicting non-healing compared with GLIM criteria (0·70 (0·65-0·75) v. 0·63 (0·58-0·65), P < 0·01). These findings suggest that both nutritional assessment tools effectively identify patients with DFU at increased risk, with SGA showing superior performance in predicting non-healing ulcers.

Quantitative proteomics reveals PPAR signaling pathway regulates the cardiomyocyte activity of neonatal mouse heart.

Cardiovascular diseases (CVDs) are among the most morbid and deadly types of diseases worldwide, while the existing therapeutic approaches all have their limitations. Mouse heart undergoes a very complex postnatal developmental process, including the 1-week window in which cardiomyocytes (CMs) maintain relatively high cell activity. The underlying mechanism provides an attractive direction for CVDs treatment. Herein, we collected ventricular tissues from mice of different ages from E18.5D to P8W and performed iTRAQ-based quantitative proteomics to characterize the atlas of cardiac development. A total of 3422 proteins were quantified at all selected time points, revealing critical proteomic changes related to cardiac developmental events such as the metabolic transition from glycolysis to beta-oxidation. A cluster of significantly dysregulated proteins containing proteins that have already been reported to be associated with cardiac regeneration (Erbb2, Agrin, and Hmgb) was identified. Meanwhile, the peroxisome proliferator-activated receptor (PPAR) signaling pathway (Cpt1α, Hmgcs2, Plin2, and Fabp4) was also found specifically enriched. We further revealed that bezafibrate, a pan-activator of PPAR signaling pathway markedly enhanced H9C2 cardiomyocyte activity via enhancing Cpt1α expression. This work provides new hint that activation of PPAR signaling pathway could potentially be a therapeutic strategy for the treatment of CVDs.

Quantitative Proteomics Reveals Down-Regulated Glycolysis/Gluconeogenesis in the Large-Duct Type Intrahepatic Cholangiocarcinoma.

Intrahepatic cholangiocarcinoma (iCCA) is a lethal hepatobiliary malignancy that arises from the epithelial cells of the intrahepatic bile ducts, accounting for approximately 10% of cholangiocarcinoma (CCA). According to the 2019 World Health Organization (WHO) classification of tumors of the digestive system, iCCA is divided into small-duct type (SD-type) and large-duct type (LD-type). However, it remains unknown which molecular events contribute to the disparity. To explore the proteomic characteristics of iCCA, we used an isobaric tag for relative and absolute quantitation (iTRAQ) based quantitative proteomics strategy to investigate stably dysregulated proteins in the SD-type and LD-type of iCCA tissues. Importantly, we found three glycolysis/gluconeogenesis-related enzymes, triosephosphate isomerize 1 (TPI1), glyceraldehyde-3-phosphate dehydrogenase (GAPDH), and phosphoglycerate kinase 1 (PGK1), were significantly down-regulated in the LD-type iCCA, which were further confirmed by immunohistochemistry using tissue microarray. Moreover, we demonstrated that the knockdown of these three candidate proteins by siRNAs notably increased the ability of proliferation in two CCA cell lines (HuH28 and RBE), suggesting that effective down-regulation of the glycolysis/gluconeogenesis pathway might be an underlying novel mechanism contributing to the LD-type iCCA.

Uniform Na Metal Plating/Stripping Design for Highly Reversible Solid-State Na Metal Batteries at Room Temperature.

Solid-state alkaline metal batteries are highly sought out for their improved energy density and security over the current lithium-ion batteries. However, their practical application is heavily hindered by the interfacial issues originating from the solid electrolyte/electrode mismatch. This work demonstrates that a CuO coating layer as an active interphase can thoroughly promote the intimate contact between a Na3 Zr2 Si2 PO12 solid electrolyte and a Na metal anode through an in situ conversion reaction. The resultant Cu/Na2 O matrix forms a mixed electron/ion conducting scaffold, which facilitates stable and homogeneous Na metal plating without dendrite formation. Moreover, the symmetric Na metal cell realizes impressively steady plating/stripping cycles for 5000 h even under a high current density of 0.3 mA cm-2 . The novelty is further manifested as a room-temperature solid-state Na metal full battery of Na3 V1.5 Al0.5 (PO4 )3 |CuO@NZSPO|Na is assembled and exhibits a highly reversible cyclability (99.85% coulombic efficiency and 99.0% capacity retention) under a charge/discharge rate of 5 C for 2250 cycles. This work effectively solves the interfacial issues at the Na metal/solid electrolyte interface and provides a convenient way toward high-performance solid-state Na metal batteries operated at room temperature.

Discrimination of enantiomers for chiral molecules using analytically designed microwave pulses.

We perform a theoretical exploration of quantum coherent control of enantio-selective state transfer (ESST) of chiral molecules with three rotational states connected by the a-type, b-type, and c-type components of the transition dipole moments. A pulse-area theorem based on a closed-loop three-level system is derived without applying the rotating-wave approximation and used to analytically design three linearly polarized microwave pulses with optimal amplitudes and phases. By utilizing two optimized microwaves to mix two excited rotational states into the maximal coherence, we find that the discrimination of enantiomers via ESST for chiral molecules can be achieved by controlling the delay time of the third optimized microwave pulse. We examine the robustness of such control schemes against the Rabi frequency and detuning errors and the environment effect through pure dephasing processes for practical applications. This work provides an alternative approach to analytically designing optimal control fields for quantum control of ESST by using complex pulse areas.

Co- or Ni-modified Sn-MnOx low-dimensional multi-oxides for high-efficient NH3-SCR De-NOx: Performance optimization and reaction mechanism.

NH3-SCR performances were explored to the relationship between structure morphology and physio-chemical properties over low-dimensional ternary Mn-based catalysts prepared by one-step synthesis method. Due to its strong oxidation performance, Sn-MnOx was prone to side reactions between NO, NH3 and O2, resulting in the generation of more NO2 and N2O, here most of N2O was driven from the non-selective oxidation of NH3, while a small part generated from the side reaction between NH3 and NO2. Co or Ni doping into Sn-MnOx as solid solution components obviously stronged the electronic interaction for actively mobilization and weakened the oxidation performance for signally reducing the selective tendency of side reactions to N2O. The optimal modification resulted in improving the surface area and enhancing the strong interaction between polyvalent cations in Co/Ni-Mn-SnO2 to provide more surface adsorbed oxygen, active sites of Mn3+ and Mn4+, high-content Sn4+ and plentiful Lewis-acidity for more active intermediates, which significantly broadened the activity window of Sn-MnOx, improved the N2 selectivity by inhibiting N2O formation, and also contributed to an acceptable resistances to water and sulfur. At low reaction temperatures, the SCR reactions over three catalysts mainly obeyed the typical Elye-rideal (E-R) routs via the reactions of adsorbed l-NHx (x = 3, 2, 1) and B-NH4+ with the gaseous NO to generate N2 but also N2O by-products. Except for the above basic E-R reactions, as increasing the reaction temperature, the main adsorbed NOx-species were bidentate nitrates that were also active in the Langmuir-Hinshelwood reactions with adsorbed l-NHx species over Co/Ni modified Mn-SnO2 catalyst.

Surface Potential Regulation Realizing Stable Sodium/Na3 Zr2 Si2 PO12 Interface for Room-Temperature Sodium Metal Batteries.

Inorganic Na3 Zr2 Si2 PO12 is prospective with a high ionic conductivity but suffers large interfacial resistance and stability issues against sodium metal, hindering its practical application in all-solid-state sodium batteries. A surface potential regulation strategy is adopted to address these issues. Na3 Zr2 Si2 PO12 (NZSP) ceramic with homogeneously-sintered surface is synthesized by a simple two-step sintering method to promote its uniform surface potential, which is favorable for mitigating the potential fluctuations at the interface against Na metal and enhancing interfacial compatibility. The Na/NZSP interface can be stabilized for over 4 months with a low interfacial resistance of 129 Ω cm2 at 25 °C. The symmetrical Na/NZSP/Na cell exhibits ultra-stable sodium platting/stripping cycling for over 1000 cycles under 0.1 mA cm-2 . Superior interfacial performance is well retained even under 0.2 mA cm-2 at room temperature. The robust interface is further signified by its excellence under higher current densities of up to 0.85 mA cm-2 at 60 °C. A 4 V all-solid-state Na3 V1.5 Cr0.5 (PO4 )3 /NZSP/Na metal battery is demonstrated at ambient conditions, which exhibits superior rate capability and delivers a high reversible capacity of 103 mA h g-1 under 100 mA g-1 for over 400 cycles with a Coulombic efficiency of over 99%.

Grain Boundary Design of Solid Electrolyte Actualizing Stable All-Solid-State Sodium Batteries.

Advanced inorganic solid electrolytes (SEs) are critical for all-solid-state alkaline metal batteries with high safety and high energy densities. A new interphase design to address the urgent interfacial stability issues against all-solid-state sodium metal batteries (ASSMBs) is proposed. The grain boundary phase of a Mg2+ -doped Na3 Zr2 Si2 PO12 conductor (denoted as NZSP-xMg) is manipulated to introduce a favorable Na3-2 δ Mgδ PO4 -dominant interphase which facilitates its intimate contact with Na metal and works as an electron barrier to suppress Na metal dendrite penetration into the electrolyte bulk. The optimal NZSP-0.2Mg electrolyte endows a low interfacial resistance of 93 Ω cm2 at room temperature, over 16 times smaller than that of Na3 Zr2 Si2 PO12 . The Na plating/stripping with small polarization is retained under 0.3 mA cm-2 for more than 290 days (7000 h), representing a record high cycling stability of SEs for ASSMBs. An all-solid-state NaCrO2 //Na battery is accordingly assembled manifesting a high capacity of 110 mA h g-1 at 1 C for 1755 cycles with almost no capacity decay. Excellent rate capability at 5 C is realized with a high Coulombic efficiency of 99.8%, signifying promising application in solid-state electrochemical energy storage systems.

Association of gonadal hormones and sex hormone binding globulin with risk of diabetes: A cohort study in middle-aged and elderly Chinese males.

AIM: Late-onset hypogonadism in men is related to the development of diabetes. The association of gonadal hormones, sex hormone binding globulin with diabetes has been studied in various studies. However, there is no cohort study on the relationship between gonadal hormone, sex hormone binding globulin and diabetes in Chinese. We aimed to provide an insight into the possible association in middle-aged and elderly Chinese males. METHODS: We included a population sample of 673 subjects aged 40 years or older. Total testosterone (TT), sex hormone binding globulin (SHBG), follicle-stimulating hormone (FSH) and luteinising hormone (LH) were detected. The homeostasis model assessment of insulin resistance (HOMA-IR) was calculated to estimate insulin sensitivity. Diabetes was diagnosed according to the 2010 American Diabetes Association criteria. RESULTS: With an average follow-up time of 3.2 ± 0.5 years, 9.8% of participants had developed diabetes. The prevalence of diabetes was decreased according to increasing SHBG quartiles (Q1:13.1%, Q2: 12.0%, Q3: 11.2%, Q4: 3.0%, P for trend < .0001) and TT (Q1:16.0%, Q2: 7.9%, Q3: 9.0%, Q4: 6.4%, P for trend < .0001). The ORs of diabetes for increasing SHBG quartiles were 4.52 (95% CI 1.40-14.57), 4.32 (95% CI 1.33-14.06), 3.89 (95% CI 1.21-12.50) and 1.00 (reference) respectively. But the odds of prevalent diabetes were not increased in different quartiles of TT, FSH and LH. In subgroup analyses, the relationship between SHBG and risk of incident diabetes was significantly increased in the population aged over 60, without insulin resistance and with eGFR < 90 mL/min per 1.73 m2 . CONCLUSIONS: Compared with gonadal hormones, a lower level of SHBG is independently associated with the risk of diabetes in middle-aged and elderly Chinese males.

Roles of the CSE1L-mediated nuclear import pathway in epigenetic silencing.

Epigenetic silencing can be mediated by various mechanisms, and many regulators remain to be identified. Here, we report a genome-wide siRNA screening to identify regulators essential for maintaining gene repression of a CMV promoter silenced by DNA methylation. We identified CSE1L (chromosome segregation 1 like) as an essential factor for the silencing of the reporter gene and many endogenous methylated genes. CSE1L depletion did not cause DNA demethylation. On the other hand, the methylated genes derepressed by CSE1L depletion largely overlapped with methylated genes that were also reactivated by treatment with histone deacetylase inhibitors (HDACi). Gene silencing defects observed upon CSE1L depletion were linked to its nuclear import function for certain protein cargos because depletion of other factors involved in the same nuclear import pathway, including KPNAs and KPNB1 proteins, displayed similar derepression profiles at the genome-wide level. Therefore, CSE1L appears to be critical for the nuclear import of certain key repressive proteins. Indeed, NOVA1, HDAC1, HDAC2, and HDAC8, genes known as silencing factors, became delocalized into cytosol upon CSE1L depletion. This study suggests that the cargo specificity of the protein nuclear import system may impact the selectivity of gene silencing.

Glycochenodeoxycholate induces cell survival and chemoresistance via phosphorylation of STAT3 at Ser727 site in HCC.

Glycochenodeoxycholate (GCDA) is closely associated with carcinogenesis and chemoresistance of hepatocellular carcinoma (HCC). Signal transducer and activator of transcription 3 (STAT3), a transcription factor, is involved in various human tumors. Whether GCDA induces chemoresistance through STAT3 and the mechanism of action remains elusive. In this study, we firstly found that the expression level of STAT3 has a positive correlation with chemoresistance of HCC cells. Moreover, GCDA can upregulate the expression of STAT3 protein. Hence, we suspect that GCDA may induce chemoresistance of HCC cells via STAT3. Mechanistically, GCDA stimulates phosphorylation of STAT3 at Ser727 site and mediates pSer727-STAT3 protein to translocate and aggregate in the nucleus, which is important for cell survival. When Ser727 of STAT3 mutated to Asp, the capacity of STAT3 to accumulate in the nucleus was attenuated, STAT3-induced cell survival was impaired and GCDA-induced chemoresistance was abolished. In addition, while activation of extracellular signal-regulated kinase 1/2 (ERK1/2) was inhibited by PD98059, phosphorylation of STAT3 at Ser727 induced by GCDA was suppressed. Taken together, these data demonstrate that GCDA-enhanced survival of liver cancer cells may occur through the activation of STAT3 by phosphorylation at Ser727 site via mitogen-activated protein kinase/ERK1/2 pathway, which may contribute to the progression of human liver cancer and chemoresistance.

Microgravity-induced hepatogenic differentiation of rBMSCs on board the SJ-10 satellite.

Bone marrow-derived mesenchymal stem cells (BMSCs) are able to differentiate into functional hepatocytelike cells, which are expected to serve as a potential cell source in regenerative medicine, tissue engineering, and clinical treatment of liver injury. Little is known about whether and how space microgravity is able to direct the hepatogenic differentiation of BMSCs in the actual space microenvironment. In this study, we examined the effects of space microgravity on BMSC hepatogenic differentiation on board the SJ-10 Recoverable Scientific Satellite. Rat BMSCs were cultured and induced in hepatogenic induction medium for 3 and 10 d in custom-made space cell culture hardware. Cell growth was monitored periodically in orbit, and the fixed cells and collected supernatants were retrieved back to the Earth for further analyses. Data indicated that space microgravity improves the differentiating capability of the cells by up-regulating hepatocyte-specific albumin and cytokeratin 18. The resulting cells tended to be maturated, with an in-orbit period of up to 10 d. In space, mechanosensitive molecules of ß1-integrin, ß-actin, α-tubulin, and Ras homolog gene family member A presented enhanced expression, whereas those of cell-surface glycoprotein CD44, intercellular adhesion molecule 1, vascular cell adhesion molecule 1, vinculin, cell division control protein 42 homolog, and Rho-associated coiled-coil kinase yielded reduced expression. Also observed in space were the depolymerization of actin filaments and the accumulation of microtubules and vimentin through the altered expression and location of focal adhesion complexes, Rho guanosine 5'-triphosphatases, as well as the enhanced exosome-mediated mRNA transfer. This work furthers the understanding of the underlying mechanisms of space microgravity in directing hepatogenic differentiation of BMSCs.-Lü, D., Sun, S., Zhang, F., Luo, C., Zheng, L., Wu, Y., Li, N., Zhang, C., Wang, C., Chen, Q., Long, M. Microgravity-induced hepatogenic differentiation of rBMSCs on board the SJ-10 satellite.

The epidemiology and clinical information about COVID-19.

In December 2019, pneumonia of unknown cause occurred in Wuhan, Hubei Province, China. On 7 January 2020, a novel coronavirus, named as severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), was identified in the throat swab sample of one patient. The World Health Organization (WHO) announced the epidemic disease caused by SARS-CoV-2 as coronavirus disease 2019 (COVID-19). Currently, COVID-19 has spread widely around the world, affecting more than seventy countries. China, with a huge burden of this disease, has taken strong measures to control the spread and improve the curative rate of COVID-19. In this review, we summarized the epidemiological characteristics, clinical features, diagnosis, treatment, and prognosis of COVID-19. A comprehensive understanding will help to control the disease.

Obesity-associated secondary hypogonadism in young and middle-aged men in Guangzhou: A single-centre cross-sectional study.

AIM: Male obesity-associated secondary hypogonadism (MOSH) is becoming a public health issue. We aimed to know MOSH among young and middle-aged men in our hospital, to analyse their sex hormones and other index, and to determine leptin as a risk factor for MOSH. METHODS: In total, 258 men (ages ranging from 20 to 60, mean 38 ± 15) were enrolled in this study, and 242 of these men had their complete data, body mass index (BMI), waist circumference and sex hormones retrospectively investigated. The leptin and lipid levels were also evaluated, and comparisons were made between young (20-39 years old) and middle-aged (40-60 years old) men. RESULTS: Among all the participants, 7 were thin, with a BMI < 18.5 kg/m2 , 95 had a normal BMI (18.5 ≤ BMI < 23.9 kg/m2 ), 87 (35.9%) were overweight (24 ≤ BMI ≤ 27.9 kg/m2 ) and 53 (21.9%) were obese (BMI ≥ 28 kg/m2 ), 173 (71.5%) had a waist sized ≥ 85 cm. Among the 242 men, 104 (43%) had hypogonadism (TT ≤ 331.412 ng/dL). Compared with the men of normal weight, the level of testosterone of the obese men decreased (P = .006), while the level of serum lipids (including total cholesterol, TG and low-density lipoprotein cholesterol, P < .05) was elevated, higher UA, FSH and leptin were also present in the obese men. There were 83 (34.2%) men with MOSH. Compared with middle-aged men with MOSH, the FSH in young men was significantly reduced (P < .05); no significant increase in estradiol was observed in the MOSH group. The leptin levels in the MOSH group were significantly higher than those in the hypogonadism only group (P < .001). CONCLUSION: Obesity increases the prevalence of hypogonadism. The decrease in testosterone levels in young men maybe due to inhibition of the hypothalamic pituitary gonadal axis. Leptin is an independent risk factor for MOSH.

Nicotine induces cell survival and chemoresistance by stimulating Mcl-1 phosphorylation and its interaction with Bak in lung cancer.

Nicotine is a major carcinogen in cigarettes, which can enhance cell proliferation and metastasis and increase the chemoresistance of cancer cells. Our previous data found that nicotine promotes cell survival in lung cancer by affecting the expression of antiapoptotic protein Mcl-1, suggesting that the Mcl-1 may be a therapeutic target for patients with lung cancer. In this study, we found that the effects of drug resistance on nicotine-induced lung cancer cell lines were shown to influence the phosphorylation of Mcl-1. Moreover, nicotine induces Mcl-1 phosphorylation exclusively at the T163 site, which results in enhancement of the antiapoptotic activity of Mcl-1 and increased cell survival. Meanwhile, nicotine can reduce the sensitivity of H1299 cells to CDDP via enhancement of the binding of Mcl-1 to Bak, which inhibits the proapoptotic effect of Bak and ultimately leads to increased survival and drug resistance of lung cancer cells. Thus, nicotine-induced cell survival and chemoresistance may occur in a mechanism by stimulating Mcl-1 phosphorylation and its interaction with Bak, which may contribute to improving the efficacy of chemotherapy in the treatment of human lung cancer.

Bile salt (glycochenodeoxycholate acid) induces cell survival and chemoresistance in hepatocellular carcinoma.

OBJECTIVE: Glycochenodeoxycholate acid (GCDA) is a toxic component in bile salts. It plays an important role in the development and progression of liver cancer. In this study, we investigated the underlying mechanism of GCDA in hepatocarcinogenesis and chemotherapy resistance. MATERIALS AND METHODS: Cell proliferation was measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and clonality by Ki-67 and colony-formation assay. Apoptosis was examined by flow cytometry. Real-time polymerase chain reaction (PCR) and western blot analysis were used to measure messenger RNA and protein levels, respectively. Short hairpin RNA was used to silence signal transducer and activator of transcription 3 (Stat3) expression. RESULTS: Bile salts (GCDA) promoted the proliferation of hepatocellular carcinoma (HCC) cells (HepG2 and QGY-7703), and GCDA treatment reduced the chemosensitivity of 5-fluorouracil (5FU) in HepG2 and QGY-7703 cells. GCDA upregulated the expression of antiapoptosis proteins Mcl-1/Survivin/Bcl-2. GCDA had no discernible effect on basal protein level or subcellular localization of phosphorylated Stat3. 5FU increased the apoptosis of HepG2 cells with silenced Stat3 expression, but GCDA-induced chemoresistance was not reversed. CONCLUSIONS: GCDA-reduced HCC cell chemosensitivity may occur by upregulating antiapoptosis proteins Mcl-1/Survivin/Bcl-2. Stat3 may be a target for enhancing the chemosensitivity of hepatocellular carcinoma cells, but GCDA-induced chemoresistance is independent of Stat3.

TREM2 Attenuates Aß1-42-Mediated Neuroinflammation in BV-2 Cells by Downregulating TLR Signaling.

The pathogenesis of late-onset Alzheimer's disease (LOAD) mainly involves abnormal accumulation of extracellular ß-amyloid (Aß) and the consequent neurotoxic effects. The triggering receptor expressed on myeloid cells 2 (TREM2) gene is associated with the pathogenesis of LOAD and plays important roles in mediating the phagocytosis of Aß by microglia and regulating inflammation in central nervous system. However, the exact mechanisms of these processes have not yet been clarified. In this study, we investigated the mechanism by which TREM2 regulates neuroinflammation and promotes Aß1-42 clearance by BV-2 cells and further elucidated the underlying molecular mechanisms. We either silenced or overexpressed TREM2 in BV-2 cells and evaluated the cell viability, Aß1-42 content, and expression of inflammatory markers (IL-1ß, IL-6, and TNF-α). TREM2 overexpression up-regulated cell activity, promoted clearance of Aß1-42 by BV-2 cells, and down-regulated expression of the inflammatory factors. In addition, TREM2 overexpression downregulation the expression of the TLR family (TLR2, TLR4 and TLR6) in BV-2 cells. Moreover, LPS, as an agonist of the TLR family, up-regulated the expression of inflammatory cytokines (IL-1ß, TNF-α, and IL-6) in BV-2 cells overexpressing TREM2. In conclusion, TREM2 promoted clearance of Aß1-42 by BV-2 cells and restored BV-2 cell viability from Aß1-42-mediated neuroinflammation by downregulating TLRs. These findings suggest that TREM2 may be a target for LOAD therapy.

Correction to: TREM2 Attenuates Aß1-42-Mediated Neuroinflammation in BV-2 Cells by Downregulating TLR Signaling.

The article titled "TREM2 Attenuates Aß1­42­Mediated Neuroinflammation in BV­2 Cells by Downregulating TLR Signaling", written by Huiping Long, Gang Zhong, Chengzhi Wang, Jian Zhang, Yueling Zhang, Jinglian Luo, Shengliang Shi, was originally published electronically on the publisher's internet portal (currently SpringerLink) on 27 May 2019 with open access.

Pollution characteristics of antibiotics and antibiotic resistance of coliform bacteria in the Yitong River, China.

In this study, the concentrations of nine typical antibiotics, including sulfadiazine (SD), sulfamerazine (SMR), sulfamethazine (SM2), sulfamethoxazole (SMZ), ofloxacin (OFX), ciprofloxacin (CIP), trimethoprim (TMP), oxytetracycline (OTC), and tetracycline hydrochloride (TC), were detected in the Yitong River by solid-phase extraction high-performance liquid chromatography. The concentrations of the antibiotics were analyzed. Additionally, an improved immobilized substrate enzyme substrate method (DST-enzyme substrate method) was developed and used to evaluate the antibiotic resistance of coliform bacteria to OFX, CIP, enrofloxacin (ENR), TC, sulfisoxazole (SOX), and TMP in the Yitong River. The results showed that the concentrations of the nine antibiotics ranged from nd (not detected) to 1.361 µg/L. The detection rate and concentration of OFX were the highest, followed by CIP, and the detection rate and concentration of SM2 and OTC were the lowest. The detection rate and concentrations of antibiotics were higher in August and November than those in May. The antibiotics were mainly distributed in the livestock sewage discharge and suburban domestic sewage discharge areas. Moreover, the drug resistance of total coliform bacteria to fluoroquinolones, sulfonamides, tetracyclines, and TMP varied with season.

Multi-genic pattern found in rare type of hypopituitarism: a whole-exome sequencing study of Han Chinese with pituitary stalk interruption syndrome.

Pituitary stalk interruption syndrome (PSIS) is a rare type of hypopituitarism manifesting various degrees of pituitary hormone deficiency. Although mutations have been identified in some familial cases, the underpinning mechanisms of sporadic patients with PSIS who are in a vast majority remain elusive, necessitating a comprehensive study using systemic approaches. We postulate that other genetic mechanisms may be responsible for the sporadic PSIS. To test this hypothesis, we conducted a study in 24 patients with PSIS of Han Chinese with no family history using whole-exome sequencing (WES) and bioinformatic analysis. We identified a group of heterozygous mutations in 92% (22 of 24) of the patients, and these genes are mostly associated with Notch, Shh, Wnt signalling pathways. Importantly, 83% (20 of 24) of the patients had more than one mutation in those pathways suggesting synergy of compound mutations underpin the pathogenesis of sporadic PSIS.