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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]

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]

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]

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]

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]

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]

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]