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Plantago lanceolata has been increasingly cultivated in recent years as a forage crop due to its high feeding quality, good adaptability and medicinal benefits. Between 2015 and 2023, Alternaria leaf spot (ALS), appearing as reddish‐brown necrotic spots with a greyish white to pale brown centre, was commonly observed in two forage germplasm nurseries of P. lanceolata of Sichuan Province, China. Initially, 139 Alternaria strains were isolated from leaf lesions, and then identified using the identity of rDNA internal transcribed spacer (ITS) sequences in the NCBI database and the similarity of morphological characteristics. By pure culture technique, six representative isolates were finally obtained for the present study. Based on both multilocus phylogeny (SSU, LSU, ITS, gapdh, rpb2, tef1, endoPG, OPA10‐2, alt a 1, KOG1058 and KOG1077) and morphology, four Alternaria species were identified: three new records of A. alternata, A. arborescens species complex and A. gossypina on this host in China, belonging to section Alternaria, and a new species of section Porri, namely, A. lanceolatae sp. nov. Pathogenicity tests by inoculation on both detached leaves and whole plants revealed that A. lanceolatae was the most important causal agent of ALS, while the other three species were nonpathogenic to P. lanceolata. This study characterized a novel pathogenic Alternaria species of section Porri from P. lanceolata in China and could contribute as useful research for possible ALS management. [ABSTRACT FROM AUTHOR]

Results MA-Induced Neurotoxicity in Mice MA-Induced Locomotor Sensitization and Depression/Anxiety-Like Behaviors in Mice Compared to saline treatment, MA injections from day 3 significantly increased the total distance traveled ( I p i < 0.01), and this was sustained throughout the development phase (Figure 1B). Determination of MA Concentration The concentration of MA in serum and fecal samples from MA group mice were determined using LC-MS/MS method. Keywords: methamphetamine; gut microbiome; serum metabolome; colonic inflammation; neurotoxicity EN methamphetamine gut microbiome serum metabolome colonic inflammation neurotoxicity 1 16 16 04/21/22 20220418 NES 220418 Introduction Methamphetamine (MA) is a highly addictive and illegal psychostimulant with serious health effects ([14]; [9]). MA Altered Serum Metabolome in Mice Effects of MA on Serum Metabolic Composition We performed UPLC-TOF/MS analyses to determine the status of serum metabolome. [Extracted from the article]

Background: The incidence of type 1 diabetes mellitus (T1DM) is increasing among youth worldwide, translating to an increased risk ofearly-onset cardiovascular disease (CVD). Mounting studies have shown that metformin may reduce maximal carotidintima-media thickness (cIMT), improve insulin resistance and metabolic control in subjects with T1DM, and thus, may extend cardioprotective benefits. This systematic review and meta-analysis was performed to assess the efficacy and safety of metformin added to insulin therapy on reducing CVD risks and improving metabolism in T1DM.Methods: PubMed, EMBASE, and the Cochrane Library were systematically searched for randomized controlled trials (RCTs) that compared metformin and insulin combination (duration ≥3 months) to insulin treatment alone in T1DM. Data were expressed as weighted/standardized mean differences (MDs/SMDs) for continuous outcomes and risk ratios (RRs) for dichotomous outcomes, along with 95% confidence intervals (CIs). The Grading of Recommendations Assessment, Development and Evaluation (GRADE) was used to evaluate the overall certainty of the evidence.Results: Nineteen RCTs (n = 1540) met the eligibility criteria. Metformin treatment significantly reduced carotid artery intima-media thickness (MD -0.06 mm [95% CI -0.88, -0.28], P < .001). Though no significant difference was found in insulin sensitivity (SMD 2.21 [95% CI -1.88, 6.29], P = .29), the total daily insulin dosage (SMD -0.81 [95% CI -1.25, -0.36], P < .001) along with traditional CVD risk factors showed improvement by better glycaemic control, partial lipid profiles, diastolic blood pressure, and limited weight gain, with neutral effect on diabetic ketoacidosis, lactic acidosis, and hypoglycaemia. However, metformin therapy increased the incidence of gastrointestinal adverse events.Conclusions: Metformin with insulin has the potential to retard the progression of atherosclerosis and provides better metabolic control in patients with T1DM, and thus, providing a potential therapeutic strategy for patients with T1DM on reducing CVD risks. [ABSTRACT FROM AUTHOR]

Background: The mechanisms of bone fragility in type 1 diabetes (T1D) are not fully understood. Whether glucagon-like peptide-1 receptor (GLP-1R) agonists could improve bone quality in T1D context also remains elusive. Aims: We aimed to explore the possible mechanisms of bone loss in T1D and clarify whether liraglutide has effects on bone quality of T1D mice using transcriptomics. Methods: Female streptozotocin-induced diabetic C57BL/6J mice were randomly divided into four groups and received the following treatments daily for 8 weeks: saline as controls, insulin, liraglutide, and liraglutide combined with insulin. These groups were also compared with non-STZ-treated normal glucose tolerance (NGT) group. Trunk blood and bone tissues were collected for analysis. Three tibia from each of the NGT, saline-treated, and liraglutide-treated groups were randomly selected for transcriptomics. Results: Compared with NGT mice, saline-treated T1D mice manifested markedly hyperglycemia and weight loss, and micro-CT revealed significantly lower bone mineral density (BMD) and deficient microarchitectures in tibias. Eight weeks of treatment with liraglutide alone or combined with insulin rescued the decreased BMD and partly corrected the compromised trabecular microarchitectures. Transcriptomics analysis showed there were 789 differentially expressed genes mainly mapped to osteoclastogenesis and inflammation pathways. The RT-qPCR verified that the gene expression of Trem2 , Nfatc1 , Trap , and Ctsk were significantly increased in the tibia of T1D compared with those in the NGT group. Liraglutide treatment alone or combined with insulin could effectively suppress osteoclastogenesis by downregulating the gene expression of Trem2 , Nfatc1 , Ctsk , and Trap. Conclusions: Taken together, increased osteoclastogenesis with upregulated expression of Trem2 played an important role in bone loss of T1D mice. Liraglutide provided protective effects on bone loss in T1D mice by suppressing osteoclastogenesis. [ABSTRACT FROM AUTHOR]

Methamphetamine (METH) is a major psychostimulant drug of abuse worldwide, and its neurotoxicity has been studied extensively. In addition to neurotoxicity, METH can also induce hepatotoxicity. The underlying mechanism of intestinal microorganisms in METH-induced hepatotoxicity remains unclear. In this study, mice have received antibiotics intragastrically or PBS once each day for 1 week, followed by METH or saline. The antibiotics attenuated METH-induced hepatotoxicity as evidenced by histopathological observation and biochemical analysis; furthermore, they alleviated METH-induced oxidative stress. The effect of antibiotics on METH-induced hepatotoxicity was investigated using RNA-sequencing (RNA-seq). The RNA-seq results demonstrated that antibiotics could regulate 580 differentially expressed genes (DEGs), of which 319 were upregulated after METH treatment and then downregulated with antibiotic pretreatment and 237 were first downregulated after METH administration and then upregulated after antibiotic pretreatment, in addition to 11 upregulated and 13 downregulated ones simultaneously in METH and antibiotic-pretreated groups. RNA-seq analyses revealed that TLR4 is one of the hub genes. Western blot analysis indicated that antibiotics inhibited the increase of TLR4, MyD88 and Traf6 induced by METH. This research suggests that antibiotics may play an important role in preventing METH-induced liver injury by regulating oxidative stress and TLR4/MyD88/Traf6 axis, though further investigation is required. [ABSTRACT FROM AUTHOR]

Background: There are many methods to diagnose diabetic autonomic neuropathy (DAN); however, often, the various methods do not provide consistent results. Even the two methods recommended by the American Diabetes Association (ADA) guidelines, Ewing's test and heart rate variability (HRV), sometimes give conflicting results. The purpose of this study was to evaluate the degree of agreement of the results of the Composite Autonomic Symptom Score 31 (COMPASS-31), skin sympathetic reaction (SSR) test, Ewing's test, and HRV in diagnosing DAN. Methods: Patients with type 2 diabetes were recruited and each received the COMPASS-31, SSR, Ewing's test, and HRV for the diagnosis of DAN. Patients were categorized as DAN(+) and DAN(–) by each of the tests. Kappa consistency tests were used to evaluate the agreement of diagnosing DAN between any two methods. Spearman's correlation test was used to evaluate the correlations of the severity of DAN between any two methods. Receiver operating characteristic (ROC) analyses were used to evaluate the diagnostic value and the cutoff value of each method. Results: A total of 126 type 2 diabetic patients were included in the study. The percentages of DAN(+) results by HRV, Ewing's test, COMPASS-31, and SSR were 61, 40, 35, and 33%, respectively. COMPASS-31 and Ewing's test had the best agreement for diagnosing DAN (κ = 0.512, p < 0.001). COMPASS-31 and Ewing's test also had the best correlation with respect to the severity of DAN (r = 0.587, p < 0.001). Ewing's test and COMPASS-31 had relatively good diagnostic values (AUC = 0.703 and 0.630, respectively) in the ROC analyses. Conclusions: COMPASS-31 and Ewing's test exhibit good diagnostic consistency and severity correlation for the diagnosis of DAN. Either test is suitable for the diagnosis of DAN and treatment follow-up. [ABSTRACT FROM AUTHOR]

The function of M‐Phase Phosphoprotein 9 (MPHOSPH9) has not been investigated in gastric cancer yet. In the present study, the public cancer databases Oncomine and TCGA were analyzed, and MPHOSPH9 was found upregulated in gastric cancer tumor tissues. Immunohistochemistry (IHC) was also carried out to further confirm the results, and IHC analysis showed MPHOSPH9 was elevated in tumor tissues compared with the paracancerous tissues. QRT‐PCR analysis also revealed that MPHOSPH9 mRNA was upregulated in gastric cancer cell lines. In addition, Kaplan–Meier estimates showed gastric cancer patients with high MPHOSPH9 level predicted a poor prognosis. Then, Western blot and CCK‐8 assay showed overexpressed MPHOSPH9 enhanced gastric cancer cell proliferation, but MPHOSPH9 knockdown suppressed gastric cancer cell proliferation. Additionally, Western blot showed that MPHOSPH9 regulated the activation of mTOR, and overexpressed MPHOSPH9 reduced the inhibitory effects of mTOR inhibitors on cell survival in gastric cancer cells. Taken together, our results suggested that MPHOSPH9.could be an oncogene in gastric cancer by regulating mTOR signaling. [ABSTRACT FROM AUTHOR]

Differences, arising from differences in gross primary production (GPP) model structures and driving forces, have fuelled arguments concerning interannual changes of GPP in China since 2000. To better investigate the interannual variability of GPP and its covariance with climate factors in China, this study adopted a multi‐model analysis based on three GPP models (i.e., Terrestrial Ecosystem Carbon flux model [TEC], Breathing Earth System Simulator model [BESS], and MOD17 GPP model). The results show that annual GPP in China increased by 0.021–0.057 Pg C year−1 from 2000 to 2015 attributable to atmospheric‐CO2 fertilization effects and favourable climate change, that is, increasing precipitation (Pr) and temperature (Ta). However, northern China and southern China had a large difference in the amplitude of these GPP changes; annual GPP increased by 0.017–0.039 Pg C year−1 in northern China but only 0.001–0.018 Pg C year−1 in southern China. Northern China and southern China occupy contrasting climate zones and this contrast produced different interannual variability of GPP through different mechanisms. Northern China has a dry climate with GPP changes sensitive to Pr. As a result, more Pr along with higher Ta in northern China produced the strong uptrend of GPP from 2000 to 2015. In contrast, southern China has a wet climate with its GPP sensitive to solar radiation and Ta. For the interval of 2000–2015, decreasing radiation plus drought exerted a negative influence on GPP in southern China. This study highlights the diverse mechanisms in which climate change affects GPP in dry and wet climate zones. A robust multi‐model analysis is preferred to reduce uncertainties arising from a single GPP model and its driving data. [ABSTRACT FROM AUTHOR]

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Abstract: Granulocyte colony‐stimulating factor (G‐CSF) has been widely used in the field of allogeneic haematopoietic stem cell transplantation (allo‐HSCT) for priming donor stem cells from the bone marrow (BM) to peripheral blood (PB) to collect stem cells more conveniently. Donor‐derived natural killer (NK) cells have important antitumour functions and immune regulatory roles post‐allo‐HSCT. The aim of this study was to evaluate the effect of G‐CSF on donors' NK cells in BM and PB. The percentage of NK cells among nuclear cells and lymphocyte was significantly decreased and led to increased ratio of T and NK cells in BM and PB post‐G‐CSF in vivo application. Relative expansion of CD56bri NK cells led to a decreased ratio of CD56dim and CD56bri NK subsets in BM and PB post‐G‐CSF in vivo application. The expression of CD62L, CD54, CD94, NKP30 and CXCR4 on NK cells was significantly increased in PB after G‐CSF treatment. G‐CSF treatment decreased the IFN‐γ‐secreting NK population (NK1) dramatically in BM and PB, but increased the IL‐13‐secreting NK (NK2), TGF‐β‐secreting NK (NK3) and IL‐10‐secreting NK (NKr) populations significantly in BM. Clinical data demonstrated that higher doses of NK1 infused into the allograft correlated with an increased incidence of chronic graft‐vs‐host disease post‐transplantation. Taken together, our results show that the in vivo application of G‐CSF can modulate NK subpopulations, leading to an increased ratio of T and NK cells and decreased ratio of CD56dim and CD56bri NK cells as well as decreased NK1 populations in both PB and BM. [ABSTRACT FROM AUTHOR]

In recent decades, extensive studies have indicated that IL-17A plays an important role in tumor progression and metastasis, but the underlying mechanisms are not immediately clear. In this review, we examined the literature from the recent years concerning the study of IL-17A in four kinds of tumor transfer paths, including hematogenous metastasis, lymphatic metastasis, local invasion and transcoelomic metastasis, to summarize the roles and underlying mechanisms of IL-17A on tumor metastasis. [ABSTRACT FROM PUBLISHER]

Colorectal cancer (CRC) is a common human gastrointestinal cancer, and recent studies indicate that circular RNA (circRNA) may regulate cancer development. In this study, we assess the role of circRNA specifically in colorectal cancer. Our quantitative PCR assays demonstrate an upregulation of the circRNA has_circ_0020397 and a downregulation of miR-138 in CRC cells, as well as a negative correlation between these two. Using a dual-luciferase reporter assay, we show evidence of miR-138-binding sites on hsa_circ_0020397, and that overexpression of hsa_circ_0020397 could inhibit the downregulation of luciferase activity by miR-138. Although hsa_circ_0020397 did not influence miR-138 expression per se, has_circ_0020397 did inhibit miR-138 activity, as examined via the expression of miR-138 targets telomerase reverse transcriptase (TERT) and programmed death-ligand 1 (PD-L1). Control treatments with plasmids overexpressing linear hsa_circ_0020397 did not have these effects. Hsa_circ_0020397 promoted cell viability and invasion of CRC cells and inhibited their apoptosis, whereas miR-138 had the opposite effect. Nevertheless, hsa_circ_0020397 antagonized miR-138 suppression of cell growth. When TERT or PD-L1 expression was suppressed with siRNAs, the above functions of hsa_circ_0020397 were attenuated, suggesting that hsa_circ_0020397 can regulate CRC cell viability, apoptosis and invasion by promoting the expression of miR-138 target genes. These findings support the role of circRNA in CRC pathogenesis. [ABSTRACT FROM AUTHOR]

Although Polychlorinated biphenyl (PCB) levels are decreased in the environment, the adverse effects of gestational exposure on the mother and offspring cannot be ignored due to the vulnerability of the fetus. In the present study, pregnant Balb/c mice were administered PCB52 (1 mg/kg BW/day) or corn oil vehicle by gavage until parturition. In the dams, PCB52 caused histopathological changes in the liver, higher serum levels of aminotransferase and alanine aminotransferase, and activated apoptosis and autophagy, suggesting hepatotoxicity. Overexpressed indicators of TLR4 pathway were observed in the liver of PCB52-exposed dams, indicated hepatic inflammation. Moreover, PCB52 exposure weakened the intestinal barrier and triggered inflammatory response, which might contribute to the hepatic inflammation by gut-liver axis. In the pups, prenatal PCB52 exposure affected the sex ratio at birth and reduced birth length and weights. Similar to the dams, prenatal PCB52 exposure induced hepatotoxicity in the pups without gender difference. Consistent with the alteration of gut microbiota, intestinal inflammation was confirmed, accompanying the disruption in the intestinal barrier and the activation of apoptosis and autophagy in the PCB52-exposed pups. Intestinal injury might be responsible for hepatotoxicity at least in part. Taken together, these findings suggested that gestational PCB52 exposure induced hepatic and intestinal injury in both maternal and offspring mice by arousing inflammation. [Display omitted] • Gestational PCB52 exposure induced hepatic inflammation and toxicity in the dams. • PCB52 exposure weakened the intestinal barrier in the dams. • Prenatal PCB52 exposure affected the sex ratio at birth and decreased the birth length and weight. • Prenatal PCB52 exposure caused intestinal dyshomeostasis and inflammation without sex bias. • Disruption of intestinal homeostasis might contribute to hepatotoxicity in both dams and pups. [ABSTRACT FROM AUTHOR]

Objective. The RNAFH study (effect of rosuvastatin on nonalcoholic fatty liver disease in metabolic syndrome patients without overt diabetes evaluated by 1H-MRS) is a prospective randomized, single-center, open-label trail designed to assess the effect of rosuvastatin on the intrahepatocellular lipid (IHCL) level of nonalcoholic fatty liver disease (NAFLD). Methods. 40 NAFLD patients meeting inclusion and exclusion criteria with metabolic syndrome (MS) but without overt diabetes mellitus will be included. Patients will be randomized to 52-week treatment with either rosuvastatin (10 mg/d) or blank control. The primary end point is IHCL evaluated by 1H-MRS, which was considered to be the most accurate noninvasive method for the evaluation of NAFLD. Secondary end points include homeostasis model assessment of insulin resistance (HOMA-IR) index on behalf of insulin resistance level and lipid parameters. Safety indicators will be monitored such as liver function, renal function, muscle stability, and glucose metabolism. The aims of the present study are noteworthy in respect that (1) IHCL is a quantitative indicator for evaluating the degree of fatty liver disease and 1H-MRS is a noninvasive technique to provide this specific index precisely, (2) meanwhile the HOMA-IR index and lipid parameters will be monitored, and (3) the safety of rosuvastatin treatment for 52 weeks will be evaluated including glucose metabolism, muscle stability, liver function, and renal function. [ABSTRACT FROM AUTHOR]

A method allowing the fabrication of quantum-dot or photonic crystal loaded bead-shaped hybrid microfiber arrays in a Rayleigh instability driven drop-sliding manner is demonstrated. [ABSTRACT FROM AUTHOR]

Methamphetamine (METH) is a psychostimulant abused worldwide. Its abuse induces intestinal toxicity. Moreover, the gut microbiota is altered by drugs, which induces intestinal injury. Whether gut microbiota mediates METH-induced intestinal toxicity remains to be validated. In the present study, wild-type and TLR4−/− mice were treated with METH. Gut microbiota was determined using 16S rRNA gene sequencing. Transcriptomics of the intestinal mucosa was performed by RNA-Sequencing. Blood levels of pro-inflammatory cytokines and lipopolysaccharide (LPS), the intestinal barrier, and inflammation were also assessed. METH treatment weakened the intestinal barrier and increased pro-inflammatory cytokines and LPS levels in the blood. Moreover, METH treatment significantly decreased the diversity of probiotics but increased the abundance of pathogenic gut microbiota, contributing to the over-production of LPS and disruption of intestinal barrier. Inflammatory pathways were enriched in the intestinal mucosa of METH-treated mice by KEGG analysis. Consistently, activation of the TLR4 pathway was determined in METH-treated mice, which confirmed intestinal inflammation. However, pretreatment with antibiotics or Tlr4 silencing significantly alleviated METH-induced gut microbiota dysbiosis, LPS over-production, intestinal inflammation, and disruption of the intestinal barrier. These findings suggested that the gut microbiota and LPS-mediated inflammation took an important role in METH-induced intestinal injury. Taken together, these findings suggest that METH-induced intestinal injury is mediated by gut microbiota dysbiosis and LPS-associated inflammation. • METH treatment induced intestinal injury. • METH treatment altered gut microbiota and resulted in the over-production of LPS. • Inflammatory pathways were enriched in intestinal mucosa of METH groups by RNA-Seq. • TLR4 pathway was activated by METH treatment in intestinal mucosa. • Antibiotics or Tlr4 silencing alleviated intestinal injury. [ABSTRACT FROM AUTHOR]

The exploration of methods allowing chemical reactions to be carried out at ultrasmall scales is of great scientific and technological interest. We report herein a microfluidic spinning technique for the fabrication of softened-polymer microarrays for use as multidimensional microreactors and the application of these microreactors in the synthesis of fluorescent nanocrystals. Highly aligned microarrays and controlled-angle grids were readily constructed from microfluidically spun polyvinylpyrrolidone (PVP) microfibers. One-zero dimensional (1D-0D), one-one dimensional (1D-1D), and one-two dimensional (1D-2D) microreactors were then produced by the intersections between microfibers and droplets, crossed microfibers, and microfibers and a PVP film, respectively; each component can be doped with different reagents. Specific examples show that these multidimensional microreactors enable the in situ generation of fluorescent nanocrystals without ligands within minutes. [ABSTRACT FROM AUTHOR]

A new pentacarboxylate ligand, 5,5′-(6-(4-carboxyphenylamino)-1,3,5-triazine-2,4-diyldiimino) diisophthalic acid (H5L), was designed and used for the assembly of metal organic materials using Mn2+, Co2+, Cd2+ and Cu2+ as nodes. Four compounds, (Me2NH2)[Mn2L(H2O)]·3DMF·3H2O (1), (Me2NH2)[Co2L(H2O)]·3DMF·3H2O (2), (Me2NH2)[Cd2L(H2O)]·3DMF·3H2O (3) and [Cu4L(μ3-OH)2(NO3)(μ2-NMP)]·4.5NMP·2H2O (4) (DMF = dimethylformamide, NMP = N-methyl-2-pyrrolidone) have been synthesized and structurally characterized. Single crystal X-ray diffraction analyses show that 1 and 3 are isostructural, both based on {M2(CO2)5} molecular building blocks (MBBs) and L ligands. The topology of the 5-connected anionic framework may be described as (44)(66) (Schläfli symbol). Preliminary structural analysis indicates 2 may have the same structure as that of 1 and 3. 4 features a 5-connected 3D neutral framework based on “butterfly” {Cu4(μ3-OH)2(COO)5} MBBs and L ligands. The corresponding Schläfli symbol is (46)(64). N2 sorption isotherms of 2 shows typical type I behavior with BET surface area of 1251 m2 g−1 and a micropore volume of 0.491 cm3 g−1. Luminescent analysis indicates 3 exhibits linker-localized emission. Magnetic investigation of 4 reveals overall antiferromagnetic interactions. The compounds were further characterized by infrared (IR) and thermogravimetric analyses (TGA). [ABSTRACT FROM AUTHOR]

The roles of Th17 cells and IL-21 in the pathogenesis of chronic graft-versus-host disease (c GVHD) in patients who undergo allogeneic transplantation are still unknown. Here, we examined this question by monitoring eight patients with new-onset c GVHD for the presence of Th17 cells, Th1 cells, and IL-21. Allografts from an additional 41 patients were also analyzed for Th17 and Th1 cells. Out of these 41 patients, the last 32 enrolled patients were further analyzed for Th17 cells, Th1 cells, and plasma IL-21 levels at day 30 post-transplantation regarding c GVHD. Th17 cells and IL-21 plasma levels were significantly increased at c GVHD onset and drastically decreased after complete remission. Patients who received a higher number of Th17 cells in their allograft had a higher incidence of c GVHD compared with patients who received a lower number of Th17 cells. Meanwhile, positive plasma IL-21 levels at day 30 post-transplantation predicted c GVHD occurrence. These results suggest that Th17 cells and IL-21 may contribute to the development of c GVHD. [ABSTRACT FROM AUTHOR]

Abstract: The in vitro effects of abscisic acid (ABA) and nitric oxide (NO) on the nematode-trapping fungus Drechslerella stenobrocha AS6.1 were examined. The average number of traps (constricting rings) per colony and the percentage of nematodes (Caenorhabditis elegans) trapped were greatly increased by addition of ABA but greatly suppressed by addition of sodium nitroprusside (SNP, an NO donor) to corn meal agar. The suppressive effect of SNP was not negated by addition of an NO synthase competitive inhibitor (l-naphthylacetic acid, L-NNA) or an NO-specific scavenger [2-(4-carboxyphenyl)-4,4, 5,5-tetramethylimidazoline-1-oxyl-3-oxide, cPTIO]. When added without SNP, however, L-NNA and cPTIO caused moderate increases in trap number and trapping. The results indicate that the trap formation and nematode-trapping ability of D. stenobrocha were enhanced by ABA but decreased by exogenous NO. [Copyright &y& Elsevier]

Abstract: To study the relationship between cultivated ramie (Boehmeria nivea) and its wild relatives and the origin of B. nivea, the karyomorphology of interphase nuclei and chromosome numbers were investigated in 19 species and 5 varieties of ramie and sequences of the internal transcribed spacers (ITS) of nuclear ribosomal DNA and the chloroplast trnL-F were analyzed in 18 species and 9 varieties of ramie. On the basis of cytological observation of interphase karyomorphology, the interphase nuclei of sections Tilocnide and Boehmeria were prochromosome type and those of sections Zollingeriana, Phyllostachys, and Duretia were prochromosome or diffuse type. The cytogenetic examination of B. nivea and its 23 wild relatives showed that 19, 3, 1, and 1 taxa were diploid (2n = 28), triploid (2n = 42), tetraploid (2n = 56), and pentaploid (2n = 70), respectively, of which triploid taxa were all from section Duretia. From the phylogenetic trees based on ITS and trnL-F sequences, Boehmeria taxa were grouped into 3 clades and several subclades. Different individuals or clones of B. clidemioides var. diffusa fell into different clades, indicating the possible hybridization and reticulate evolution among species in Boehmeria, and the introgression between B. nivea and B. clidemioides var. diffusa. The core species of wild ramie resources should not only involve B. nivea and its 3 varieties but also B. malabarica var. leioclada and B. clidemioides var. diffusa. It was inferred that 2 evolution routes existed in Boehmeria: prochromosome evolution line and diffuse evolution line. In the former route, section Tilocnide originated from section Boehmeria. In the latter route, the evolution direction was section Boehmeria → Zollingeriana → Phyllostachys → Duretia. Both routes probably originated from the same ancestor. Based on the morphological traits of interphase nucleus and molecular experiment, close relationships were found among sections Zollongerie, Phyllostachys, and Duretia. However, their systematic relationships based on morphological traits were not supported by the cytological evidence and phylogenetic trees of ITS and trnL-F sequences. [Copyright &y& Elsevier]

Objective: To identify the genetic defects of the the adiponectin (APM1) gene that contribute to the development of type 2 diabetes (T2DM) and determine the functional single nucleotide polymorphisms (SNPs) in the APM1 gene associated with T2DM in Han nationality. Methods: The APM1 gene 5''-UTR was screened by direct sequencing to identify common polymorphisms. Identified SNPs were genotyped in 585 nondiabetic controls, 278 subjects with impaired glucose intolerance (IGT) and 212 patients with T2DM. The functions of SNPs in the regulatory region were assessed by reporter gene assay. Possible association between SNPs and plasma APM1 levels or metabolic parameters was statistically assessed. Results: Three SNPs were identified in the APM1 gene 5''-UTR. A case-control study revealed that SNP −11377 G/C had significant differences in allele frequencies between T2DM patients and nondiabetic controls (G 0.314/C 0.686 vs. G 0.265/C 0.735, P=0.03). Haplotype analysis of three SNPs in the APM1 gene showed that no significant association of haplotypes with T2DM. IGT was detected in the present study. Reporter gene assay showed that SNP did not influence the transcription efficiency in the 3T3-L1 cell line. Conclusion: SNP −11377 G/C in the proximal promoter region of the APM1 gene contributes to the development of T2DM in Han nationality but may not be a functional SNP in the APM1 gene. [Copyright &y& Elsevier]

Objective: To investigate the association of ghrelin gene polymorphisms with metabolic syndrome in Han Nationality Chinese. Methods: A total of 240 patients with metabolic syndrome and 427 adults aged above forty years were recruited. Genotypes were determined by polymerase chain reaction and restriction fragment length polymorphism analysis. Results: The allelic frequency of the Leu72Met polymorphism was 17.3% in the patient group and 11.9% in the control group (χ2=7.36, P=0.007). Metabolic syndrome was more prevalent among carriers of the Met72 variant (43.8 vs 33.1%, age- and sex-adjusted odds ratio=1.57, P=0.01). No Arg51Gln variants were found in our study subjects. Conclusion: Rather than being associated with its individual components, Leu72Met polymorphism is associated with metabolic syndrome in the Han Nationality Chinese. Arg51Gln polymorphism is rare in the Han Nationality Chinese. [Copyright &y& Elsevier]

Misuse of the psychostimulant methamphetamine (METH) could induce serious hepatotoxicity. Our previous study revealed the effects of luteolin on alleviating METH-induced hepatotoxicity, however, the detailed mechanisms have not been elucidated. In this study, rats were orally pretreated with 100 mg/kg luteolin or sodium dodecyl sulfate water, and then METH (15 mg/kg, intraperitoneal [i.p.]) or saline was administered. Histopathological and biochemical analyses were used to determine the alleviative effects of luteolin. Based on the RNA-sequencing data, METH induced 1859 differentially expressed genes (DEGs) in comparison with the control group, which were enriched into 11 signaling pathways. Among these DEGs, 497 DEGs could be regulated through luteolin treatment and enriched into 16 pathways. The p53 signaling pathway was enriched in both METH administered and luteolin pretreated rats. Meanwhile, luteolin significantly suppressed METH-induced elevation of p53, caspase9, caspase3, cleaved caspase3, the ratio of Bax/Beclin-2, as well as autophagy-related Beclin-1, Atg5, and LC3-II. Luteolin also relieved METH-induced hepatotoxicity by decreasing inflammation factors, including TNF-α, IL-1β, and IL-18. Moreover, the levels of PI3K, p -Akt, and the normalized ratio of p -Akt/Akt declined after METH administration, whereas luteolin pretreatment failed to reverse these effects. Our results suggest that luteolin alleviates METH-induced hepatic apoptosis, autophagy, and inflammation through repressing the p53 pathway. It further illustrates the protective mechanisms of luteolin on METH-induced hepatotoxicity and provides a research basis for clinical treatment. [ABSTRACT FROM AUTHOR]

New Delhi metallo-β-lactamase (NDM) is a series of enzyme conferring resistance to β-lactam antibiotics including the carbapenems. The bla NDM gene has been reported in a variety of Gram-negative bacilli, especially in the Entero bacteriaceae and Acinetobacter spp., which is deeply disconcerting for public health worldwide. In this study, recombinase polymerase amplification assays using a basic detection (Basic-RPA) and a real-time fluorescent detection (Exo-RPA) were established for detecting bla NDM gene. The RPA reactions were performed at 39 °C and finished within 20 min. Using different copy numbers of pMD18T-NDM plasmid DNA as templates, we identified the detection limit of Basic-RPA assay (1.85 × 103 copies/μL), conventional PCR assay (1.85 × 104 copies/μL), Exo-RPA assay (1.85 × 102 copies/μL) and real-time PCR assay (1.85 × 102 copies/μL). Both Basic-RPA and Exo-RPA assays were highly specific for detecting bla NDM , as there were no cross-reactions with the strains without bla NDM gene. Examination of 62 clinical samples by RPA assays and PCR assays showed the same results, suggesting that RPA assays are reliable in clinical diagnosis. The amplification time of RPA is much shorter than that of other molecular techniques, it is easy to implement and has the potential for clinical application. Note: Recombinase polymerase amplification assays using a basic detection (Basic-RPA) and a real-time fluorescent detection (Exo-RPA) were established for bla NDM gene. The RPA reaction was performed at 39 °C, and the results were obtained within 20 min. The analytical sensitivity of the RPA assay was tested, using a 10-fold serial dilution of plasmid pMD18T-NDM DNA. The results showed that RPA had high sensitivity. Both Basic-RPA and Exo-RPA assays were highly specific for the detection of bla NDM. Unlabelled Image • Exo-RPA and Basic-RPA assays were developed and evaluated for rapid detection of bla NDM gene. • The Exo-RPA assay was highly specific and sensitive. • The Exo-RPA and Basic-RPA assays were as sensitive as conventional PCR and real-time PCR on clinical sample detection. [ABSTRACT FROM AUTHOR]

Fabrication and electrical characteristics of individual ZnO submicro-wire field-effect transistors (FETs) are investigated by a simple micro-grid template method. The fabricated back-gate ZnO submicro-wire FET is characterized at room temperature in air. The gate voltage Vgs curves reveal gating effect characteristic of n-type conductivity. The field effect mobility of the ZnO submicro-wire is determined to be 7.9 cm2/ V·s at Vds = 2 V, the capacitance and transconductance are estimated to be about 3.9 fF and 15.5 nS, respectively. UV sensitive property is measured using a 325-nm laser as the excitation source. Compared to the result carried in darkness, the ZnO submicro-wire FET is sensitive to UV irradiation, which indicates its potential application on UV detectors. Experimental results show that the approach introduced here allows the possibility of fabricating low-cost, reliable and flexible microelectronic devices. [ABSTRACT FROM AUTHOR]

Objectives: This study aimed to investigate serum chemerin concentrations in obese children and adolescents and to investigate the associations of chemerin with body mass index (BMI), lipid levels, and insulin sensitivity. Methods: Forty-eight obese and 40 nonobese Chinese children and adolescents were included in the study. BMI and levels of chemerin, lipids, glucose, and insulin were measured following an overnight fast. The Homeostatic Model Assessment of Insulin Resistance (HOMA-IR) and BMI standard deviation score (BMI-SDS) were determined for all participants. Results: Serum chemerin levels were found to be significantly higher in obese children and adolescents than in control group members (94.83 ± 5.99 ng/mL vs 56.43 ± 4.16 ng/mL, P <.001). There were significant correlations between chemerin and age, BMI, BMI-SDS, total triglyceride (TG) levels, insulin levels, and HOMA-IR. After controlling for age, we found that chemerin levels were also significantly correlated with BMI-SDS (r =+ 0.284, P =.008) and HOMA-IR (r =+ 0.241, P =.034). In a stepwise multiple regression analysis, we observed only BMI-SDS to be an important determinant of chemerin level. Conclusions: In our sample of Chinese children and adolescents, chemerin levels were significantly higher in the obese group than in the control group. Chemerin levels were positively correlated with BMI-SDS and HOMA-IR and negatively correlated with age. We thus believe that further study is necessary to investigate the risk of metabolic abnormalities in young obese children and adolescents. [ABSTRACT FROM AUTHOR]