Hypothetical chloroplast reading frame 51 encodes a photosystem I assembly factor in cyanobacteria.

Hypothetical chloroplast open reading frames (ycfs) are putative genes in the plastid genomes of photosynthetic eukaryotes. Many ycfs are also conserved in the genomes of cyanobacteria, the presumptive ancestors of present-day chloroplasts. The functions of many ycfs are still unknown. Here, we generated knock-out mutants for ycf51 (sll1702) in the cyanobacterium Synechocystis sp. PCC 6803. The mutants showed reduced photoautotrophic growth due to impaired electron transport between photosystem II (PSII) and PSI. This phenotype results from greatly reduced PSI content in the ycf51 mutant. The ycf51 disruption had little effect on the transcription of genes encoding photosynthetic complex components and the stabilization of the PSI complex. In vitro and in vivo analyses demonstrated that Ycf51 cooperates with PSI assembly factor Ycf3 to mediate PSI assembly. Furthermore, Ycf51 interacts with the PSI subunit PsaC. Together with its specific localization in the thylakoid membrane and the stromal exposure of its hydrophilic region, our data suggest that Ycf51 is involved in PSI complex assembly. Ycf51 is conserved in all sequenced cyanobacteria, including the earliest branching cyanobacteria of the Gloeobacter genus, and is also present in the plastid genomes of glaucophytes. However, Ycf51 has been lost from other photosynthetic eukaryotic lineages. Thus, Ycf51 is a PSI assembly factor that has been functionally replaced during the evolution of oxygenic photosynthetic eukaryotes.

Astragaloside IV protects renal tubular epithelial cells against oxidative stress-induced injury by upregulating CPT1A-mediated HSD17B10 lysine succinylation in diabetic kidney disease.

Tubular injury and oxidative stress are involved in the pathogenesis of diabetic kidney disease (DKD). Astragaloside IV (ASIV) is a natural antioxidant. The effects and underlying molecular mechanisms of ASIV on DKD have not been elucidated. The db/db mice and high-glucose-stimulated HK2 cells were used to evaluate the beneficial effects of ASIV in vivo and in vitro. Succinylated proteomics was used to identify novel mechanisms of ASIV against DKD and experimentally further validated. ASIV alleviated renal dysfunction and proteinuria, downregulated fasting blood glucose, and upregulated insulin sensitivity in db/db mice. Meanwhile, ASIV alleviated tubular injury, oxidative stress, and mitochondrial dysfunction in vivo and in vitro. Mechanistically, ASIV reversed downregulated 17beta-hydroxysteroid dehydrogenase type 10 (HSD17B10) lysine succinylation by restoring carnitine palmitoyl-transferase1alpha (Cpt1a or CPT1A) activity in vivo and in vitro. Molecular docking and cell thermal shift assay revealed that ASIV may bind to CPT1A. Molecular dynamics simulations demonstrated K99 succinylation of HSD17B10 maintained mitochondrial RNA ribonuclease P (RNase P) stability. The K99R mutation of HSD17B10 induced oxidative stress and disrupted its binding to CPT1A or mitochondrial ribonuclease P protein 1 (MRPP1). Importantly, ASIV restored the interaction between HSD17B10 and MRPP1 in vivo and in vitro. We also demonstrated that ASIV reversed high-glucose-induced impaired RNase P activity in HK2 cells, which was suppressed upon K99R mutation of HSD17B10. These findings suggest that ASIV ameliorates oxidative stress-associated proximal tubular injury by upregulating CPT1A-mediated K99 succinylation of HSD17B10 to maintain RNase P activity.

The expression mechanism of programmed cell death 1 ligand 1 and its role in immunomodulatory ability of mesenchymal stem cells.

Programmed cell death 1 ligand 1 (PD-L1) is an important immunosuppressive molecule, which inhibits the function of T cells and other immune cells by binding to the receptor programmed cell death-1. The PD-L1 expression disorder plays an important role in the occurrence, development, and treatment of sepsis or other inflammatory diseases, and has become an important target for the treatment of these diseases. Mesenchymal stem cells (MSCs) are a kind of pluripotent stem cells with multiple differentiation potential. In recent years, MSCs have been found to have a strong immunosuppressive ability and are used to treat various inflammatory insults caused by hyperimmune diseases. Moreover, PD-L1 is deeply involved in the immunosuppressive events of MSCs and plays an important role in the treatment of various diseases. In this review, we will summarize the main regulatory mechanism of PD-L1 expression, and discuss various biological functions of PD-L1 in the immune regulation of MSCs.

Population pharmacokinetics and limited sampling strategies of polymyxin B in critically ill patients.

OBJECTIVES: To characterize the pharmacokinetics (PK) of polymyxin B in Chinese critically ill patients. The factors significantly affecting PK parameters are identified, and a limited sampling strategy for therapeutic drug monitoring of polymyxin B is explored. METHODS: Thirty patients (212 samples) were included in a population PK analysis. A limited sampling strategy was developed using Bayesian estimation, multiple linear regression and modified integral equations. Non-linear mixed-effects models were developed using Phoenix NLME software. RESULTS: A two-compartment population PK model was used to describe polymyxin B PK. Population estimates of the volumes of central compartment distribution (V) and peripheral compartment distribution (V2), central compartment clearance (CL) and intercompartmental clearance (Q) were 7.857 L, 12.668 L, 1.672 L/h and 7.009 L/h. Continuous renal replacement therapy (CRRT) significantly affected CL, and body weight significantly affected CL and Q. The AUC0-12h of polymyxin B in patients with CRRT was significantly lower than in patients without CRRT. CL and Q increased with increasing body weight. A limited sampling strategy was suggested using a two-sample scheme with plasma at 0.5h and 8h after the end of infusion (C0.5 and C8) for therapeutic drug monitoring in the clinic. CONCLUSIONS: A dosing regimen should be based on body weight and the application of CRRT. A two-sample strategy for therapeutic drug monitoring could facilitate individualized treatment with polymyxin B in critically ill patients.

Association of Intravenous Tirofiban with Functional Outcomes in Acute Ischemic Stroke Patients with Acute Basilar Artery Occlusion Receiving Endovascular Thrombectomy.

INTRODUCTION: The aim of this study was to test the hypothesis that intravenous tirofiban improves functional outcomes without promoting the risk of intracranial hemorrhage (ICH) in stroke secondary to basilar artery occlusion (BAO) receiving endovascular thrombectomy. METHODS: Patients with acute BAO stroke who were treated with endovascular thrombectomy and had tirofiban treatment information were derived from "BASILAR": a nationwide, prospective registry. All eligible patients were divided into tirofiban and no-tirofiban groups according to whether tirofiban was used intravenously. The primary endpoint was the 90-day severity of disability as assessed by the modified Rankin scale score. Safety outcomes were the frequency of ICH and mortality. RESULTS: Of 645 patients included in this cohort, 363 were in the tirofiban group and 282 were in the no-tirofiban group. Thrombectomy with intravenous tirofiban reduced the 90-day disability level over the range of the modified Rankin scale (adjusted common odds ratio, 2.08; 95% confidence interval (CI), 1.45-2.97; p < 0.001). The 90-day mortality of patients in the tirofiban group was lower than that in the no-tirofiban group (41.6% vs. 52.1%; adjusted hazard ratio, 0.60; 95% CI, 0.47-0.77; p < 0.001). The frequency of any ICH (6.7% vs. 13.7%; p = 0.004) and symptomatic ICH (4.8% vs. 10.1%; p = 0.01) in the tirofiban group was significantly lower than that in the no-tirofiban group. CONCLUSIONS: In patients with acute BAO stroke who underwent endovascular treatment, intravenous tirofiban might be associated with favorable outcome, reduced mortality, and a decreased frequency of ICH.

Source-specific probabilistic risk evaluation of potentially toxic metal(loid)s in fine dust of college campuses based on positive matrix factorization and Monte Carlo simulation.

Contamination, hazard level and source of 10 widely concerned potentially toxic metal(loid)s (PTMs) Co, As, Pb, Cr, Cu, Zn, Ni, Mn, Ba, and V in fine dust with particle size below 63 µm (FD63) were investigated to assess the environmental quality of college campuses and influencing factors. PTMs sources were qualitatively analyzed using statistical methods and quantitatively apportioned using positive matrix factorization. Probabilistic contamination degrees of PTMs were evaluated using enrichment factor and Nemerow integrated enrichment factor. Eco-health risk levels of content-oriented and source-oriented for PTMs were evaluated using Monte Carlo simulation. Mean levels of Zn (643.8 mg kg-1), Pb (146.0 mg kg-1), Cr (145.9 mg kg-1), Cu (95.5 mg kg-1), and Ba (804.2 mg kg-1) in FD63 were significantly larger than soil background values. The possible sources of the concerned PTMs in FD63 were traffic non-exhaust emissions, natural source, mixed source (auto repair waste, paints and pigments) and traffic exhaust emissions, which accounted for 45.7%, 25.4%, 14.5% and 14.4% of total PTMs contents, respectively. Comprehensive contamination levels of PTMs were very high, mainly caused by Zn pollution and non-exhaust emissions. Combined ecological risk levels of PTMs were low and moderate, chiefly caused by Pb and traffic exhaust emissions. The non-cancer risks of the PTMs in FD63 to college students fell within safety level, while the carcinogenic PTMs in FD63 had a certain cancer risks to college students. The results of source-specific health risk assessment indicated that Cr and As were the priority PTMs, and the mixed source was the priority pollution source of PTMs in FD63 from college campuses, which should be paid attention to by the local government.

Icariin Alleviates Nonalcoholic Fatty Liver Disease in Polycystic Ovary Syndrome by Improving Liver Fatty Acid Oxidation and Inhibiting Lipid Accumulation.

(1) Background: Icariin is the main component of the Chinese herb Epimedium. A number of studies have shown that it alleviates abnormal lipid metabolism. However, it is not clear whether and how icariin can ameliorate hepatic steatosis with polycystic ovary syndrome (PCOS). This study was designed to explore the anti-hepatosteatosis effect of icariin in rats with polycystic ovary syndrome. (2) Methods: Female Sprague Dawley(SD)rats were treated with a high-fat diet and letrozole for 21 days to make nonalcoholic fatty liver disease (NAFLD) in the polycystic ovary syndrome model. Then model rats were treated with icariin (by gavage, once daily) for 28 days. Serum hormones and biochemical variables were determined by ELISA or enzyme. RNA-sequence analysis was used to enrich related target pathways. Then, quantitative Real-time PCR (qRT-PCR) and Western blot were performed to verify target genes and proteins. (3) Results: Icariin treatment reduced excess serum levels of Testosterone (T), Estradiol (E2), Luteinizing hormone (LH), Follicle-stimulating hormone (FSH), LH/FSH ratio, insulin, triglycerides (TG), and aspartate aminotransferase (AST) in high-fat diet (HFD) and letrozole fed rats. Meanwhile, icariin ameliorated HFD and letrozole-induced fatty liver, as evidenced by a reduction in excess triglyceride accumulation, vacuolization, and Oil Red O staining area in the liver of model rats. Results of RNA-sequencing, western blotting, and qRT-PCR analyses indicated that icariin up-regulated fatty acid translocase (CD36), in mitochondria, and peroxisome proliferator-activated receptor α (PPARα) expression, which led to the enhancement of fatty acid oxidation molecules, such as cytochrome P450, family 4, subfamily a, polypeptide 3 (CYP4A3), carnitine palmitoyltransferase 1 α (CPT1α), acyl-CoA oxidase 1 (ACOX1), medium-chain acyl-CoA dehydrogenase (MCAD), and long-chain acyl-CoA dehydrogenase (LCAD). Besides, icariin reduced lipid synthesis, which elicited stearoyl-Coenzyme A desaturase 1 (SCD1), fatty acid synthase (FASN), and acetyl-CoA (ACC). (4) Conclusion: Icariin showed an ameliorative effect on hepatic steatosis induced by HFD and letrozole, which was associated with improved fatty acid oxidation and reduced lipid accumulation in the liver.

Hydrochloride Berberine ameliorates alcohol-induced liver injury by regulating inflammation and lipid metabolism.

AIMS: Berberine hydrochloride (BBR) is efficacious in relieving alcoholic liver injury (ALI) in animal models, but its underlying mechanisms remains largely unclear. METHODS AND RESULTS: In the study, the rats were divided into control group, model group, model with BBR group, and control with BBR group, and given corresponding treatment for 4 weeks. RNA-Seq, ELISA and RT-PCR were performed to explore the potential mechanisms of BBR in ALI. Treatment of rats with BBR (200 mg/kg/d, gavage, once daily) over 4 weeks diminished 4 g/kg/d alcohol-induced inflammation and lipid deposition. Attenuation of the increased vacuolization and Oil Red O staining area was evident on histological examination of liver in BBR-treated rats. Hepatic gene expression profile detected that BBR suppressed ethanol-stimulated overexpression of thyroid hormone responsive gene-THRSP. And overexpression of THRSP-responsive genes (fatty acid synthase-FASN, adenosine monophosphate activated protein kinase α-AMPK-α, acetyl-CoA carboxylase-ACC, ATP-citrate lyase-ACLY) responsible for fatty acid synthesis was also downregulated by BBR. Additionally, BBR downregulated expression of cluster of differentiation 36-CD36 and upregulated expression of peroxisome proliferator-activated receptor α (PPARα) and its target genes (carnitine palmitoyltransferase 1 α-CPT1α and acyl-CoA oxidase 1-ACOX1). Meanwhile, BBR treatment suppressed systemic inflammation by mediating a reduction in IL-10, TNF-α, LPS, and ET, but elevated IL-6. CONCLUSIONS: The results indicated that BBR alleviated alcoholism-induced hepatic injury by suppressing inflammation (IL-10, TNF-α, LPS, ET and IL-6), and regulating fatty acids uptake (CD36), lipid synthesis (THRSP, FASN, AMPK-α, ACC, ACLY) and lipid oxidation (PPARα, CPT1α, ACOX1), and THRSP may be its novel target.

Baicalin ameliorates alcohol-induced hepatic steatosis by suppressing SREBP1c elicited PNPLA3 competitive binding to ATGL.

Baicalin is a flavonoid compound abundant in multiple edible and medicinal plants such as Scutellaria baicalensis Georgi. In this study, we provide evidence to support the fact that baicalin ameliorates alcohol-induced hepatic steatosis via regulating SREBP1c elicited PNPLA3 competitive binding to ATGL. Results showed that baicalin significantly attenuated the development of metabolic disorders and hepatic steatosis in alcohol-induced rats after four weeks of treatment. It was evident that baicalin treatment significantly normalized the serous contents of hepatic triglyceride (TG), alanine aminotransferase (ALT), and aspartate aminotransferase (AST), and attenuated the increase of hepatic vacuolization and Oil Red O staining area caused by alcohol. Meanwhile, baicalin relieves alcohol-induced hepatic fibrosis by masson staining and RT-qPCR analysis. Mechanistically, alcohol aggravated the nuclear expression of SREBP1c, which contributed to the high expression of PNPLA3 and FASN, thereby enhancing the binding of PNPLA3 to ABHD5, and indirectly impairing the binding ability between ATGL and ABHD5, ultimately causing a decline in the hydrolysis capacity in liver lipid droplets. As expected, these alcohol-induced pathobolism were reversed by baicalin treatment both in vivo and in vitro. In conclusion, this study has demonstrated that baicalin can protect against alcohol-induced hepatic lipid accumulation by activating hepatic lipolysis via suppressing SREBP1c elicited PNPLA3 competitive binding to ATGL. Baicalin is a promising natural product for preventing alcohol-induced hepatic steatosis.

Spatial distribution, pollution level, and health risk of Pb in the finer dust of residential areas: a case study of Xi'an, northwest China.

The spatial distribution, pollution level, and exposure risk of Pb in the finer dust (particle size < 63 µm) of residential areas in Xi'an, northwest China were investigated in this study. Geographical information systems and geodetector methods were used to analyze the spatial variability of Pb content in the finer dust of Xi'an and its forming mechanism. The enrichment factor was used to assess the extent of Pb pollution, and the hazard index was used to evaluate the health risks to children and adults exposed to Pb. The results showed that the average content of Pb in the finer dust of residential areas in Xi'an was 99.9 mg kg-1. In the Xi'an urban area, a higher Pb content was mainly found in the finer dust near the Second Ring Road of Xi'an City, and the Pb content in the old town of Xi'an City was relatively lower than that near the Second Ring Road. The results of geodetector analysis indicate that the spatial variability of Pb in the finer dust of the Xi'an urban area was primarily controlled by the interaction among vehicle emissions, daily behavior of residents, and industrial emissions. Pb in the finer dust from residential areas in all districts showed moderate enrichment. The non-cancer risks of Pb in the finer dust were within the safe range for both children and adults. However, the prolonged exposure risk of Pb in the finer dust of residential areas should be considered for children.

Risk and sources of heavy metals and metalloids in dust from university campuses: A case study of Xi'an, China.

College students study and live at university for several years; however, the pollution levels, ecological health risks, and sources of heavy metals and metalloids (HMMs) in the dust found at university campuses are still unknown. In this study, dust samples from university campuses in Xi'an were collected and the Zn, Mn, As, Pb, V, Cr, Co, Cu, Ba, and Ni contents were measured using X-ray fluorescence spectrometry. The pollution levels and ecological health risks of these HMMs were evaluated using the geo-accumulation, pollution load, and potential ecological risk indices and a health risk assessment model while their sources were apportioned using positive matrix factorization. The mean HMM concentrations in the dust were higher than the corresponding background values in the topsoil of Shaanxi Province. The Mn, V, Co, As, and Ni concentrations in the dust samples analyzed were within the levels categorized as no pollution by the geo-accumulation index standard, whereas other HMMs caused pollution to different degrees. Assessment of the pollution load index indicated that the dust samples analyzed were moderate contamination with HMMs. Pb and Cu in the dust presented considerable and moderate ecological risks, respectively; the other HMMs presented low ecological risks. The combined ecological risk of the HMMs measured in the dust samples was considerable. The non-carcinogenic and carcinogenic risks to male and female college students were within the safe levels. This study found three main sources of the HMMs measured in the dust: traffic, natural, and mixed sources (the latter including automobile repair industry waste and paints and pigments), which accounted for 47.5%, 29.3%, and 23.2% of the total HMM concentration, respectively.

The correlation between cytokine levels in the aqueous humor and the prognostic value of anti-vascular endothelial growth factor therapy for treating macular edema resulting from retinal vein occlusion.

PURPOSE: To determine the correlation between aqueous humor cytokine levels and the prognostic value of anti-vascular endothelial growth factor (VEGF) therapy for treating macular edema resulting from retinal vein occlusion (RVO-ME). METHODS: This prospective study included 47 RVO-ME and 32 senile cataract cases. Aqueous humor collection was performed in patients with RVO-ME before intravitreal injection of ranibizumab and in patients before cataract surgery. VEGF, monocyte chemotactic protein 1 (MCP-1), interleukin (IL)-8, IL-6, basic fibroblast growth factor (b-FGF), and tumor necrosis factor-α (TNF-α) levels were measured in the aqueous humor. Central retinal thickness (CRT) was measured before ranibizumab treatment and during each follow-up visit. The recovery rate following ranibizumab treatment was calculated as (CRTBT-CRTAT1W)/CRTBT, in which CRTBT was the CRT measured before treatment and CRTAT1W was measured 1 week after treatment. The recurrence time of RVO-ME was recorded. RESULTS: VEGF, MCP-1, IL-8, and IL-6 levels in the aqueous humor of patients with RVO-ME were significantly higher compared with control and were positively correlated with the CRTBT. Ranibizumab significantly reduced CRT, and VEGF levels positively correlated with the recovery rate. The mean recurrence time of RVO-ME was 43.5 days. IL-6 levels negatively correlated with the recurrence time of ME. CONCLUSION: VEGF, MCP-1, IL-8, and IL-6 levels were significantly increased in patients with RVO-ME and were positively correlated with ME. Higher VEGF levels were indicative of CRT recovery, and higher IL-6 levels were indicative of ME recurrence after ranibizumab treatment.

Mere15, a novel polypeptide from Meretrix meretrix, inhibits proliferation and metastasis of human non-small cell lung cancer cells through regulating the PI3K/Akt/mTOR signaling pathway.

Mere15, an anticancer polypeptide with a molecular weight of 15 kDa, is extracted from the marine species Meretrix meretrix. A previous study in our laboratory has confirmed that Mere15 displays a potent antitumor activity. However, the underlying mechanism of Mere15 still remains unclear. The effect of Mere15 on the growth of a variety of tumor cells was measured by the CCK-8 assay. Hoechst33342/PI double staining and flow cytometry assays were used to detect the apoptosis status of cancer cells. Western blotting was used to detect the expression of apoptosis-related proteins, migration and invasion-related protein, and the changes in the PI3K/Akt/mTOR signaling pathway-related proteins. Treatment with Mere15 inhibited cancer cell growth significantly. Scratch wound-healing assay, as well as Transwell experiments, revealed that the polypeptide was able to inhibit the invasion and migration of NSCLC cells significantly. Western blotting analysis confirmed that treatment with Mere15 inhibited the phosphorylation of PI3K, Akt, and mTOR significantly. The effects of Mere15 were also evaluated in the presence of an activator or inhibitor of the PI3K/Akt/mTOR pathway. Downregulated expression of MMP-2, MMP-9, and Snail, and increased expression of E-cadherin were also found in cells treated with Mere15. In vivo study revealed that Mere15 inhibited tumor growth significantly in xenograft nude mice bearing NCI-H460 cancer cells. The study provides evidence that Mere15 has the potential to be developed as a novel antimetastatic agent for the treatment of NSCLC patients. The work also provides further evidence that targeting PI3K/Akt/mTOR pathway is an important strategy for overcoming cancer metastasis.

Analyzing environmental risk, source and spatial distribution of potentially toxic elements in dust of residential area in Xi'an urban area, China.

A comprehensive study on concentration, spatial distribution, pollution, ecological-health risk and source of potentially toxic elements (PTEs) in dust of residential area in Xi'an, China were conducted to explore the environmental quality of residential area in urban district. The results show that the concentrations of V, Ni, and Mn in the dust were less than, while the contents of Cr, Zn, Pb, Cu, and Ba in the dust were obviously larger than, the soil background values of Shaanxi. The high-value area of PTEs primarily concentrated in densely populated areas, heavily trafficked areas and the surroundings of plants. Cr, Pb and Zn posed moderate enrichment and Pb possessed moderate ecological risk in the dust. The comprehensive pollution levels of PTEs in the dust were uncontaminated to moderately contaminated and their comprehensive ecological risk were moderate. The non-carcinogenic risks of the PTEs for adults and children were in the safe level and the carcinogenic risks of Ni and Cr were under the current acceptable value. Four major sources were discriminated on basis of the multivariate statistical analysis results and the content characteristics, enrichment degrees, and the spatial distribution features of the PTEs, viz. Mn, V, and Ni primarily came from natural source; Pb, Zn, and Cu mainly originated from traffic source; and Ba and Cr were respectively from construction source and coal-fired power plant source, which respectively contributed 22.8%, 28.3%, 47.3%, and 1.6% to the total content of PTEs determined in the dust.

Suppression of long noncoding RNA MALAT1 inhibits the development of uveal melanoma via microRNA-608-mediated inhibition of HOXC4.

This study explored the effects of the metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) on the development of uveal melanoma. Moreover, the role of the MALAT1/microRNA-608 (miR-608)/homeobox C4 (HOXC4) axis was assessed by evaluating the proliferation, invasion, and migration, as well as the cell cycle distribution of uveal melanoma in vitro after knocking down MALAT1 or HOXC4 and/or overexpression of miR-608 in uveal melanoma cells (MUM-2B and C918). Moreover, the effects of the MALAT1/miR-608/HOXC4 axis in uveal melanoma in vivo were further evaluated by injecting the C918 cells into the NOD/SCID mice. HOXC4 was found to be a gene upregulated in uveal melanoma, while knockdown of its expression resulted in suppression of uveal melanoma cell migration, proliferation, and invasion, as well as cell cycle progression. In addition, the upregulation of miR-608 reduced the expression of HOXC4 in the uveal melanoma cells, which was rescued by overexpression of MALAT1. Hence, MALAT1 could upregulate the HOXC4 by binding to miR-608. The suppressed progression of uveal melanoma in vitro by miR-608 was rescued by overexpression of MALAT1. Additionally, in vivo assays demonstrated that downregulation of MALAT1 could suppress tumor growth through downregulation of HOXC4 expression via increasing miR-608 in uveal melanoma. In summary, MALAT1 downregulation functions to restrain the development of uveal melanoma via miR-608-mediated inhibition of HOXC4.

Non-conjugated polymer carbon dots for fluorometric determination of metronidazole.

Non-conjugated polymer carbon dots (PCDs) with a 9% fluorescence quantum yield were synthesized by a pyrolytic method using polyethyleneimine as the sole precursor. The PCDs have an average size about 2.1 nm and a blue fluorescence, with excitation/emission maxima at 380/457 nm, that is quenched by the drug metronidazole. The method has a linear response in the 0.06-15 µg mL-1 metronidazole concentration range and a 20 ng mL-1 detection limit. Milk samples were spiked at two levels (0.6 and 5.0 µg mL-1), and the recoveries of metronidazole are in the range of 96.7-102.2%. Graphical abstract Schematic representation of preparation of non-conjugated polymer carbon dots (PCDs) and detection of metronidazole. Metronidazole with negative charge is easy to produce electrostatic interaction with polyethyleneimine chain with positive charge, which leads to PCDs fluorescence quenching, so as to realize metronidazole detection.

[Effect of Hope on Self-efficacy and Self-management in Patients with Chronic Kidney Disease(Stages 1-3)].

Objective To describe the status of hope,self-efficacy,and self-management in patients with chronic kidney disease(CKD)(stages 1-3)and to explore the interactions between these three variables.Methods Herth Hope Index,self-efficacy scale,and CKD self-management instrument were used to evaluate the patients with CKD(stages 1-3)in PUMC Hospital(n=153). Structural equation modeling was used to establish the structural equation model of hope,self-efficacy,and self-management.Results The median score of hope was 40.0(36.0,44.5),and 85.0% of patients were in higher level of hope. The median score of self-efficacy was 8.3(7.1,9.4)and the overall score of self-management was 89.0±13.4. There were no significant differences in level of hope and self-management among patients with different age,gender,marital status,educational level,course of disease,and CKD stages(all P>0.05). Age and marriage status were significantly associated with self-efficacy. Self-efficacy was significantly higher in >65 years group than in other age groups(P<0.05)and was significantly higher in married group than in single group(P<0.05).The level of hope had direct effect on self-efficacy(ß=0.67,P<0.05)and self-management(ß=0.46,P<0.05).Conclusions The levels of hope,self-efficacy,and self-management are high in patients with CKD(stages 1-3). Hope directly affects the self-efficacy and self-management of these patients.

A reference gene set for sex pheromone biosynthesis and degradation genes from the diamondback moth, Plutella xylostella, based on genome and transcriptome digital gene expression analyses.

BACKGROUND: Female moths synthesize species-specific sex pheromone components and release them to attract male moths, which depend on precise sex pheromone chemosensory system to locate females. Two types of genes involved in the sex pheromone biosynthesis and degradation pathways play essential roles in this important moth behavior. To understand the function of genes in the sex pheromone pathway, this study investigated the genome-wide and digital gene expression of sex pheromone biosynthesis and degradation genes in various adult tissues in the diamondback moth (DBM), Plutella xylostella, which is a notorious vegetable pest worldwide. RESULTS: A massive transcriptome data (at least 39.04 Gb) was generated by sequencing 6 adult tissues including male antennae, female antennae, heads, legs, abdomen and female pheromone glands from DBM by using Illumina 4000 next-generation sequencing and mapping to a published DBM genome. Bioinformatics analysis yielded a total of 89,332 unigenes among which 87 transcripts were putatively related to seven gene families in the sex pheromone biosynthesis pathway. Among these, seven [two desaturases (DES), three fatty acyl-CoA reductases (FAR) one acetyltransferase (ACT) and one alcohol dehydrogenase (AD)] were mainly expressed in the pheromone glands with likely function in the three essential sex pheromone biosynthesis steps: desaturation, reduction, and esterification. We also identified 210 odorant-degradation related genes (including sex pheromone-degradation related genes) from seven major enzyme groups. Among these genes, 100 genes are new identified and two aldehyde oxidases (AOXs), one aldehyde dehydrogenase (ALDH), five carboxyl/cholinesterases (CCEs), five UDP-glycosyltransferases (UGTs), eight cytochrome P450 (CYP) and three glutathione S-transferases (GSTs) displayed more robust expression in the antennae, and thus are proposed to participate in the degradation of sex pheromone components and plant volatiles. CONCLUSIONS: To date, this is the most comprehensive gene data set of sex pheromone biosynthesis and degradation enzyme related genes in DBM created by genome- and transcriptome-wide identification, characterization and expression profiling. Our findings provide a basis to better understand the function of genes with tissue enriched expression. The results also provide information on the genes involved in sex pheromone biosynthesis and degradation, and may be useful to identify potential gene targets for pest control strategies by disrupting the insect-insect communication using pheromone-based behavioral antagonists.

MiR-592 functions as a tumor suppressor in glioma by targeting IGFBP2.

A growing body of evidence suggests that microRNA-592 is involved in tumor initiation and development in several types of human cancers. However, the biological functions and molecular mechanism of microRNA-592 in glioma remain unclear. In this study, we explored the potential role of microRNA-592 in glioma as well as the possible molecular mechanisms. Our results proved that microRNA-592 expression was significantly downregulated in glioma tissues and cell lines (p < 0.01). Functional assays revealed that overexpression of microRNA-592 dramatically reduced the cell proliferation, migration, and invasion and induced cell arrest at G1/G0 phase in vitro. Mechanistic investigations defined insulin-like growth factor binding protein 2 as a direct and functional downstream target of microRNA-592, which was involved in the microRNA-592-mediated tumor-suppressive effects in glioma cells. Moreover, the in vivo study showed that microRNA-592 overexpression produced the smaller tumor volume and weight in nude mice. In summary, these results elucidated the function of microRNA-592 in glioma progression and suggested a promising application of it in glioma treatment.