Evaluation of the Growth, Sporulation, Fungicide Efficacy, and Host Range of Ramularia sphaeroidea.

Ramularia sphaeroidea was primarily identified based on the characteristics of its conidia and several sequences. The fungus causes severe leaf spot disease on hairy vetch (Vicia villosa var. glabrescens) in Yunnan Province in China. The growth, sporulation, fungicide efficacy, and host range of the pathogen were evaluated to aid in disease management. Different types of culture media and carbon and nitrogen sources were used to evaluate the growth of R. sphaeroidea. Oatmeal, maltose, and potassium nitrate agar had a higher amount of sporulation. Difenoconazole (10%) was the most effective fungicide against the leaf disease caused by R. sphaeroidea. In addition, foliar inoculation sprays were used to assess the host range of R. sphaeroidea in six different plant species, including alfalfa (Medicago sativa L.), sainfoin (Onobrychis viciifolia Scop.), erect milkvetch (Astragalus adsurgens Pall.), common vetch (Vicia sativa L.), red clover (Trifolium pratense L.), and white clover (Trifolium repens L.). R. sphaeroidea successfully infected these plants, indicating that it has a wider host range than hairy vetches.

Comparative transcriptome analysis provides insights into the resistance regulation mechanism and inhibitory effect of fungicide phenamacril in Fusarium asiaticum.

Fusarium asiaticum is a destructive phytopathogenic fungus that causes Fusarium head blight of wheat (FHB), leading to serious yield and economic losses to cereal crops worldwide. Our previous studies indicated that target-site mutations (K216R/E, S217P/L, or E420K/G/D) of Type I myosin FaMyo5 conferred high resistance to phenamacril. Here, we first constructed one sensitive strain H1S and three point mutation resistant strains HA, HC and H1R. Then we conducted comparative transcriptome analysis of these F. asiaticum strains after 1 and 10 µg·mL-1 phenamacril treatment. Results indicated that 2135 genes were differentially expressed (DEGs) among the sensitive and resistant strains. The DEGs encoding ammonium transporter MEP1/MEP2, nitrate reductase, copper amine oxidase 1, 4-aminobutyrate aminotransferase, amino-acid permease inda1, succinate-semialdehyde dehydrogenase, 2, 3-dihydroxybenzoic acid decarboxylase, etc., were significantly up-regulated in all the phenamacril-resistant strains. Compared to the control group, a total of 1778 and 2097 DEGs were identified in these strains after 1 and 10 µg·mL-1 phenamacril treatment, respectively. These DEGs involved in 4-aminobutyrate aminotransferase, chitin synthase 1, multiprotein-bridging factor 1, transcriptional regulatory protein pro-1, amino-acid permease inda1, ATP-dependent RNA helicase DED1, acetyl-coenzyme A synthetase, sarcoplasmic/endoplasmic reticulum calcium ATPase 2, etc., showed significantly down-regulated expression in phenamacril-sensitive strain but not in resistant strains after phenamacril treatment. In addition, cyanide hydratase, mating-type protein MAT-1, putative purine nucleoside permease, plasma membrane protein yro2, etc., showed significantly co-down-regulated expression in all the strains after phenamacril treatment. Taken together, This study provides deep insights into the resistance regulation mechanism and the inhibitory effect of fungicide phenamacril and these new annotated proteins or enzymes are worth for the discovery of new fungicide targets.

Association of lipid-modifying therapy with risk of obstructive sleep apnea: A drug-target mendelian randomization study.

BACKGROUND: Obstructive sleep apnea (OSA) is considered to be an important contributor of dyslipidemia. However, there lacks observational studies focusing on the potential effect of lipid management on OSA risk. Thus, we aimed to investigate the genetic association of lipid-modifying therapy with risk of OSA. METHODS: A drug-target mendelian randomization (MR) study using both cis-variants and cis-expression quantitative trait loci (eQTLs) of lipid-modifying drug targets was performed. The MR analyses used summary-level data of genome wide association studies (GWAS). Primary MR analysis was conducted using inverse-variance-weighted (IVW) method. Sensitivity analysis was performed using weighted median (WM) and MR-pleiotropy residual sum and outlier (MR-PRESSO) methods. RESULTS: Genetically proxied low-density lipoprotein cholesterol (LDL-C)-lowering effect of cholesteryl ester transfer protein (CETP) was associated with reduced risk of OSA (odds ratio [OR] =0.75, 95% confidence interval [CI]: 0.60-0.94, false discovery rate [FDR] q value = 0.046). A significant MR association with risk of OSA was observed for CETP expression in subcutaneous adipose tissue (OR = 0.94, 95%CI: 0.89-1.00, FDR q value = 0.049), lung (OR = 0.94, 95%CI: 0.89-1.00, FDR q value = 0.049) and small intestine (OR = 0.96, 95%CI: 0.93-1.00, FDR q value = 0.049). No significant effects of high-density lipoprotein cholesterol (HDL-C)-raising effect of CETP inhibition, LDL-C-lowering and triglycerides-lowering effect of other drug targets on OSA risk were observed. CONCLUSIONS: The present study presented genetic evidence supporting the association of LDL-C-lowering therapy by CETP inhibition with reduced risk of OSA. These findings provided novel insights into the role of lipid management in patients with OSA and encouraged further clinical validations and mechanistic investigations.

Multiomics Reveals Mechanisms of Alternaria oxytropis Inhibiting Pathogenic Fungi in Oxytropis ochrocephala.

Endophytic fungi can benefit the host plant and increase the plant resistance. Now, there is no in-depth study of how Alternaria oxytropis (A. oxytropis) is enhancing the ability of inhibiting pathogenic fungi in Oxytropis ochrocephala (O. ochrocephala). In this study, the fungal community and metabolites associated with endophyte-infected (EI) and endophyte-free (EF) O. ochrocephala were compared by multiomics. The fungal community indicated that there was more A. oxytropis, less phylum Ascomycota, and less genera Leptosphaeria, Colletotrichum, and Comoclathris in the EI group. As metabolic biomarkers, the levels of swainsonine and apigenin-7-O-glucoside-4-O-rutinoside were significantly increased in the EI group. Through in vitro validation experiments, swainsonine and apigenin-7-O-glucoside-4-O-rutinoside can dramatically suppress the growth of pathogenic fungi Leptosphaeria sclerotioides and Colletotrichum americae-borealis by increasing the level of oxidative stress. This work suggested that O. ochrocephala containing A. oxytropis could increase the resistance to fungal diseases by markedly enhancing the content of metabolites inhibiting pathogenic fungi.

Reliability and accuracy of a semi-automatic segmentation protocol of the nasal cavity using cone beam computed tomography in patients with sleep apnea.

OBJECTIVES: The objectives of this study included using the cone beam computed tomography (CBCT) technology to assess: (1) intra- and inter-observer reliability of the volume measurement of the nasal cavity; (2) the accuracy of the segmentation protocol for evaluation of the nasal cavity. MATERIALS AND METHODS: This study used test-retest reliability and accuracy methods within two different population sample groups, from Eastern Asia and North America. Thirty obstructive sleep apnea (OSA) patients were randomly selected from administrative and research oral health data archived at two dental faculties in China and Canada. To assess the reliability of the protocol, two observers performed nasal cavity volume measurement twice with a 10-day interval, using Amira software (v4.1, Visage Imaging Inc., Carlsbad, CA). The accuracy study used a computerized tomography (CT) scan of an OSA patient, who was not included in the study sample, to fabricate an anthropomorphic phantom of the nasal cavity volume with known dimensions (18.9 ml, gold standard). This phantom was scanned using one NewTom 5G (QR systems, Verona, Italy) CBCT scanner. The nasal cavity was segmented based on CBCT images and converted into standard tessellation language (STL) models. The volume of the nasal cavity was measured on the acquired STL models (18.99 ± 0.066 ml). RESULTS: The intra-observer and inter-observer intraclass correlation coefficients for the volume measurement of the nasal cavity were 0.980-0.997 and 0.948-0.992 consecutively. The nasal cavity volume measurement was overestimated by 1.1%-3.1%, compared to the gold standard. CONCLUSIONS: The semi-automatic segmentation protocol of the nasal cavity in patients with sleep apnea and by using cone beam computed tomography is reliable and accurate. CLINICAL RELEVANCE: This study provides a reliable and accurate protocol for segmentation of nasal cavity, which will facilitate the clinician to analyze the images within nasoethmoidal region.

Silver-Mediated Intermolecular [2 + 2 + 1] Cyclization of Terminal Alkynones with Elemental Selenium: Regioselective Synthesis of 2,4- or 3,4-Dicarbonylselenophenes.

An efficient and atom-economical silver-mediated [2 + 2 + 1] cyclization protocol for the selective synthesis of 2,4- or 3,4-dicarbonylselenophenes has been developed. Readily accessible substrates, commercially available elemental selenium, and good functional group tolerance make this procedure attractive for the selective synthesis of dicarbonylselenophenes. Preliminary mechanistic investigations indicated that silver acetylene species are possible intermediates for the formation of 3,4-dicarbonylselenophenes.

Silver-Mediated [2 + 2 + 1] Cyclization of ortho-Propioloylbenzonitriles with Elemental Selenium: Synthesis of 4H-indeno[1,2-c][1,2]selenazol-4-ones.

An efficient silver-mediated [2 + 2 + 1] cyclization protocol of ortho-propioloylbenzonitriles with elemental selenium for the synthesis of 4H-indeno[1,2-c][1,2]selenazol-4-ones has been developed. One C-Se bond, one N-Se bond, and one C-C bond were rapidly constructed in one step. The reaction might proceed via the formation of a highly reactive selenoketene intermediate, followed by intramolecular cyclization.

Microglial repopulation reverses cognitive and synaptic deficits in an Alzheimer's disease model by restoring BDNF signaling.

Over the past decade, compelling genetic evidence has highlighted the crucial role of microglial dysregulation in the development of Alzheimer's disease (AD). As resident immune cells in the brain, microglia undergo dystrophy and senescence during the chronic progression of AD. To explore the potential therapeutic benefits of replenishing the brain with new microglia in AD, we utilized the CSF1R inhibitor PLX3397 to deplete existing microglia and induce repopulation after inhibitor withdrawal in 5xFAD transgenic mice. Our findings revealed the remarkable benefits of microglial repopulation in ameliorating AD-associated cognitive deficits, accompanied by a notable elevation in synaptic proteins and an enhancement of hippocampal long-term potentiation (LTP). Additionally, we observed the profound restoration of microglial morphology and synaptic engulfment following their self-renewal. The impact of microglial repopulation on amyloid pathology is dependent on the duration of repopulation. Transcriptome analysis revealed a high resemblance between the gene expression profiles of repopulated microglia from 5xFAD mice and those of microglia from WT mice. Importantly, the dysregulated neurotrophic signaling pathway and hippocampal neurogenesis in the AD brain are restored following microglial replenishment. Lastly, we demonstrated that the repopulation restores the expression of brain-derived neurotrophic factor (BDNF) in microglia, thereby contributing to synaptic plasticity. In conclusion, our findings provide compelling evidence to support the notion that microglial self-renewal confers substantial benefits to the AD brain by restoring the BDNF neurotrophic signaling pathway. Thus, targeted microglial repopulation emerges as a highly promising and novel therapeutic strategy for alleviating cognitive impairment in AD.

Associations of systemic inflammation markers with myocardial enzymes in pediatric adenotonsillar hypertrophy: A cross-sectional study.

Objective: The present study aimed to investigate the relationship between systemic inflammation markers and myocardial enzymes in children with adenotonsillar hypertrophy (ATH). Methods: The levels of myocardial enzymes were detected and the systemic inflammatory biomarkers including neutrophil-lymphocyte ratio (NLR), platelet-lymphocyte ratio (PLR) and systemic immune inflammation index (SII) were calculated. Regression analyses were performed and a prediction model for screening myocardial injury was established by receiver operating characteristic (ROC) curve. Results: Finally, a total of 804 children with ATH were included. After adjusting for age, BMI, fasting blood glucose and lipid profiles, both NLR and SII were significantly associated with CK-MB (p = 0.041 and 0.034, respectively) and LDH (p = 0.002 and 0.001, respectively), and PLR was associated with CK-MB (p = 0.008). In addition, NLR, SII were independently associated with hyper-LDH [OR = 1.447, 95%CI (1.063, 1.968); OR = 1.001, 95%CI (1.000, 1.002), respectively] and the associations were more significant in girls. A prediction model for hyper-LDH based on SII was developed with the area under the ROC curve of 0.715 (0.682, 0.746). Conclusion: Systemic inflammation markers were only independently associated with serum hyper-LDH in children with ATH, especially in girls. Further investigation was needed to determine the relationship between systemic inflammation with myocardial enzymes in ATH children.

TREM2 receptor protects against complement-mediated synaptic loss by binding to complement C1q during neurodegeneration.

Triggering receptor expressed on myeloid cells 2 (TREM2) is strongly linked to Alzheimer's disease (AD) risk, but its functions are not fully understood. Here, we found that TREM2 specifically attenuated the activation of classical complement cascade via high-affinity binding to its initiator C1q. In the human AD brains, the formation of TREM2-C1q complexes was detected, and the increased density of the complexes was associated with lower deposition of C3 but higher amounts of synaptic proteins. In mice expressing mutant human tau, Trem2 haploinsufficiency increased complement-mediated microglial engulfment of synapses and accelerated synaptic loss. Administration of a 41-amino-acid TREM2 peptide, which we identified to be responsible for TREM2 binding to C1q, rescued synaptic impairments in AD mouse models. We thus demonstrate a critical role for microglial TREM2 in restricting complement-mediated synaptic elimination during neurodegeneration, providing mechanistic insights into the protective roles of TREM2 against AD pathogenesis.

Alternaria gansuense, a Plant Systematic Fungal Pathogen Producing Swainsonine in Vivo and in Vitro.

Astragalus adsurgens (A. adsurgens), which is considered a forage in China, grows widely in Eurasia and North America. However, Alternaria gansuense (A. gansuense) (synonym: Embellisia astragali) systematically infects A. adsurgens, producing swainsonine (SW), which poisons domesticated animals. In this study, we hypothesized that the A. gansuense SW-producing fungus is morphologically and molecularly related to the locoweed endophyte, Alternaria oxytropis (A. oxytropis), which systematically grows in host plants. Therefore, pure cultures of the fungi from diseased plants or endophytic interactions were collected from fields and assayed for SW via high-performance liquid chromatography linked to mass spectroscopy (HPLC-MS). The production of SW was also detected in A. adsurgens, A. oxytropis and diseased plants by assaying for the presence of the ß-ketoacyl synthase (KS) gene, which is required for SW synthesis. Diseased A. adsurgens and pure cultures of A. gansuense have SW and the healthy-looking A. adsurgens plants also contained SW, probably because they were infected with A. gansuense. Therefore, A. adsurgens-infected A. gansuense are not safe for livestock consumption.

Four-Component Ring-Opening Reaction of Pyrroles via C-N Bond Cleavage under Multiple Functions of Elemental Sulfur.

We report a four-component ring-opening reaction of pyrroles via C-N bond cleavage. In this process, elemental sulfur is used as the sulfur source of thiazole and thioamide and the reductant of olefin. A series of benzothiazoles functionalized with thiopropionamides at the C2 position were synthesized using this method. A plausible reaction mechanism is proposed based on the concise control experiments.

miR-96-5p is involved in alcohol-induced apoptosis in PC12 cells via negatively regulating TAp73.

OBJECTIVE: The present study opted for the adrenal phaeochromocytoma (PC12) cell line to frame a neuronal injury model induced by alcohol exposure in vitro, aiming to probe whether TAp73 and miR-96-5p are involved in the neuronal injury process induced by alcohol and elucidate the regulatory relationship between miR-96-5p and TAp73. METHODS: Immunofluorescence staining was used to observe the structural features of PC12 cells after culturing in medium with nerve growth factor (NGF). After different doses and different durations of alcohol treatment, CCK-8 assay was performed to detect the viability of PC12 cells, flow cytometry assay was carried out to detect the apoptosis rate of PC12 cells, dual-luciferase reporter assay was used to definitude the regulatory relationship between miR-96-5p and Tp73, and western blot was used to detect the protein expression of TAp73. RESULTS: The result of immunofluorescence staining demonstrated that PC12 cells abundantly expressed Map2, CCK-8 assay illustrated alcohol exposure significantly downregulated the cell viability of PC12 cells, Treatment with miR-96-5p inhibitor induced apoptosis and upregulated the expression of TAp73 in PC12 cells. Contrastingly, miR-96-5p mimic reversed the above effects and downregulation of TAp73 inhibited the apoptosis of PC12 cells. CONCLUSION: The present study demonstrated that miR-96-5p participates in alcohol-induced apoptosis in PC12 cells via negatively regulating TAp73.

Comparison of the upper airway morphology between Dutch and Chinese adults with obstructive sleep apnea.

PURPOSE: The pathogenesis of obstructive sleep apnea (OSA) is complex and may vary between different races. It has been suggested that the anatomical balance between skeletal tissues and soft tissues around the upper airway is a key pathophysiologic factor of OSA. Therefore, the aim of this study was to compare the anatomical balance of the upper airway between Dutch and Chinese patients with OSA based on cone beam computed tomography (CBCT) images. METHODS: This was a cross-sectional study performed in two centers and included Dutch and Chinese adults with OSA. CBCT scans in the supine position were obtained for both Dutch and Chinese OSA groups. The primary outcome variable was the anatomical balance of the upper airway, defined as the ratio of the tongue area and the maxillomandibular enclosure area. RESULTS: A total of 28 Dutch adults (mean age ± SD of 46.6 ± 14.1 years, body mass index [BMI] of 26.8 ± 3.5 kg/m2, and apnea-hypopnea index [AHI] of 15.7 ± 7.1 events/h) and 24 Chinese adults (age 41.0 ± 12.4 years, BMI 26.5 ± 3.3 kg/m2, and AHI 16.5 ± 7.8 events/h). There were no significant differences in AHI, age, BMI, and sex between the two groups (P = 0.14-0.76). The Dutch group had a significantly larger tongue area and tongue length compared to the Chinese group (P = 0.01 and P < 0.01). On the other hand, the Chinese group had a smaller maxilla length compared to the Dutch group (P < 0.01). However, the anatomical balance of the upper airway of both groups was not significantly different (P = 0.16). CONCLUSION: Within the limitations of this study, no significant difference was found in the anatomical balance of the upper airway between Dutch and Chinese patients with mild to moderate OSA. TRIAL REGISTRATION: The present study was registered at the ClinicalTrials.gov identifier NCT03463785.

Long noncoding RNA HOXA-AS2 ameliorates chronic intermittent hypoxia-induced lung inflammation by regulating miR-17-5p/tipe2 axis.

PURPOSE: The purpose is to confirm whether long noncoding RNA HOXA-AS2 relieves chronic intermittent hypoxia (CIH)-induced lung inflammation. METHODS: Male Sprague Dawley rats were used to establisha CIH rat model. Hematoxylin and Eosin staining was used on the lung tissue injury to determine the successful construction of CIH animal model. Arterial partial pressure of oxygen (PaO2) and carbon dioxide (PaCO2) were measured. HOXA-AS2 was overexpressed to evaluate its role in the progression and development of CIH. T cell differentiation and cytokine production were determined using flow cytometry. Cell apoptosis was determined using terminal deoxynucleotidyl transferase dUTP nick end labelling assay kit. The target of HOXA-AS2 and miR-17-5p was predicted by the Encyclopedia of RNA Interactomes (ENCORI) and confirmed using luciferase assay. RESULTS: HOXA-AS2 was downregulated in CIH rat models. Lung tissue injury was observed in CIH rats, and the injury was attenuated by the overexpression of HOXA-AS2. PaO2 was reduced and PaCO2 was induced in CIH rats, which was reversed by the overexpression of HOXA-AS2. The overexpression of HOXA-AS2 inhibited CIH-induced cell apoptosis. It also reversed alterations in the levels of interferon gamma (IFNγ), interleukin (IL)-2, IL-6, IL-1ß, tumor necrosis factor alpha (TNF-α), and transforming growth factor beta1 (TGF-ß1) in rats caused by CIH. The overexpression of HOXA-AS2 prevented the induction in CD4+ IFN-γ+ T cells and reduction in CD4+TGF-ß1+ T cells. The overexpression of HOXA-AS2 upregulated tumor necrosis factor-alpha-induced protein 8-like 2 (tipe2) key regulator through directly targeting miR-17-5p. Further experiments proved that tipe2 was the direct target of miR-17-5p. CONCLUSION: This study manifested that HOXA-AS2 acted as an anti-inflammatory regulator and protected lung tissue injury from CIH in the rat model; this was mediated by upregulation of tipe2 through directly targeting miR-17-5p. HOXA-AS2 upregulated the expression of tipe2, providing new understanding and therapeutic target for CIH.

Long noncoding RNA HOXA-AS2 ameliorates chronic intermittent hypoxia-induced lung inflammation by regulating miR-17-5p/tipe2 axis

Purpose: The purpose is to confirm whether long noncoding RNA HOXA-AS2 relieves chronic intermittent hypoxia (CIH)-induced lung inflammation. Methods: Male Sprague Dawley rats were used to establisha CIH rat model. Hematoxylin and Eosin staining was used on the lung tissue injury to determine the successful construction of CIH animal model. Arterial partial pressure of oxygen (PaO2) and carbon dioxide (PaCO2) were measured. HOXA-AS2 was overexpressed to evaluate its role in the progression and development of CIH. T cell differentiation and cytokine production were determined using flow cytometry. Cell apoptosis was determined using terminal deoxynucleotidyl transferase dUTP nick end labelling assay kit. The target of HOXA-AS2 and miR-17-5p was predicted by the Encyclopedia of RNA Interactomes (ENCORI) and confirmed using luciferase assay. Results: HOXA-AS2 was downregulated in CIH rat models. Lung tissue injury was observed in CIH rats, and the injury was attenuated by the overexpression of HOXA-AS2. PaO2 was reduced and PaCO2 was induced in CIH rats, which was reversed by the overexpression of HOXA-AS2. The overexpression of HOXA-AS2 inhibited CIH-induced cell apoptosis. It also reversed alterations in the levels of interferon gamma (IFNγ), interleukin (IL)-2, IL-6, IL-1β, tumor necrosis factor alpha (TNF-α), and transforming growth factor beta1 (TGF-β1) in rats caused by CIH. The overexpression of HOXA-AS2 prevented the induction in CD4+ IFN-γ+ T cells and reduction in CD4+TGF-β1+ T cells. The overexpression of HOXA-AS2 upregulated tumor necrosis factor-alpha-induced protein 8-like 2 (tipe2) key regulator through directly targeting miR-17-5p. Further experiments proved that tipe2 was the direct target of miR-17-5p (AU)

Effect of Epichloë gansuensis Endophyte on Seed-Borne Microbes and Seed Metabolites in Achnatherum inebrians.

The seed-borne microbiota and seed metabolites of the grass Achnatherum inebrians, either host to Epichloë gansuensis (endophyte infected [EI]) or endophyte free (EF), were investigated. This study determined the microbial communities both within the seed (endophytic) and on the seed surface (epiphytic) and of the protective glumes by using Illumina sequencing technology. Epichloë gansuensis decreased the richness of the seed-borne microbiota except for the epiphytic fungi of glumes and also decreased the diversity of seed-borne microbiota. In addition, metabolites of seeds and glumes were detected using liquid chromatography-mass spectrometry (LC-MS). Unlike with the seeds of EF plants, the presence of E. gansuensis resulted in significant changes in the content of 108 seed and 31 glume metabolites. A total of 319 significant correlations occurred between seed-borne microbiota and seed metabolites; these correlations comprised 163 (147 bacterial and 16 fungal) positive correlations and 156 (136 bacterial and 20 fungal) negative correlations. Meanwhile, there were 42 significant correlations between glume microbiota and metabolites; these correlations comprised 28 positive (10 bacterial and 18 fungal) and 14 negative (9 bacterial and 5 fungal) correlations. The presence of E. gansuensis endophyte altered the communities and diversities of seed-borne microbes and altered the composition and content of seed metabolites, and there were many close and complex relationships between microbes and metabolites. IMPORTANCE The present study was to investigate seed-borne microbiota and seed metabolites in Achnatherum inebrians using high-throughput sequencing and LC-MS technology. Epichloë gansuensis decreased the richness of the seed-borne microbiota except for the epiphytic fungi of glumes and also decreased the diversity of seed-borne microbiota. Compared with endophyte-free plants, the content of 108 seed and 31 glume metabolites of endophyte-infected plants was significantly changed. There were 319 significant correlations between seed-borne microbiota and seed metabolites and 42 significant correlations between glume microbiota and metabolites.

Colletotrichum truncatum-A New Etiological Anthracnose Agent of Sword Bean (Canavalia gladiata) in Southwestern China.

Anthracnose is a disease caused by Colletotrichum species. They are well known as major plant pathogens, and a black stem disease, specifically caused by Colletotrichum truncatum and primarily infecting sword bean (Canavalia gladiata), was observed in the Yunnan province, China. To aid disease management and to determine pathogenic characteristics, the species causing the leaf spot disease of hairy vetch was verified as C. truncatum. A sequence analysis of the ITS, ACT, GAPDH, and HIS3 genes was conducted, as well as morphological and cultural characteristics, to identify this Colletotrichum species, which has curved conidia. C. truncatum isolates from sword bean formed a distinctive group among Colletotrichum species, including those that infect other forage and field crops. Artificially inoculated sword bean seedlings showed typical symptoms of anthracnose, which were similar to field observations. To the best of our knowledge, this is the first report of C. truncatum causing black stem disease on sword beans in China.

Time-domain stepwise encoding based on a stepped photon emission material.

We demonstrate tunable lifetimes (sub-milliseconds and seconds) at the same emission wavelength of a material, along with an abrupt intensity change between the two emission states. Based on this stepped photon emission material, a time-domain stepwise encoding method is developed and applied to point-of-care testing with an ultra-large quantitative detection range.

High-frequency repetitive transcranial magnetic stimulation alleviates the cognitive side effects of electroconvulsive therapy in major depression.

Objective: The retrospective study aimed to explore the difference in mood outcomes and cognitive function between high-frequency repetitive transcranial magnetic stimulation (HF-rTMS) over dorsolateral prefrontal cortex (DLPFC) and electroconvulsive therapy in major depression disorder (MDD) patients and to examine the improvement of HF-rTMS on cognitive impairment evoked by electroconvulsive therapy (ECT). Materials and methods: A total of 116 participants with MDD, who completed a 4-week follow-up assessment, were enrolled. The cohort consisted of 26 cases classed as control, 46 participants administrated with HF-rTMS (HF-rTMS group), 22 patients treated with ECT (ECT group), and 23 cases treated with HF-rTMS and ECT at the course of hospitalization (HF-rTMS + ECT group). Medication was kept constant as well in all participants. The 17-item Hamilton Depression Rating Scale for Depression (HAMD-17) and 14-item Hamilton Anxiety Rating Scale (HAMA-14) were used to assess depression and anxiety, respectively. Montreal Cognitive Assessment (MoCA) was to elevate cognitive function. Results: No statistical significance was found for baseline in sociodemographic, characteristics of depression, anxiety and cognition, and psychopharmaceutic dosages among control, HF-rTMS, ECT, and HF-rTMS + ECT groups (p > 0.05). Compared with baseline level, total scores of HAMD-17 and HAMA-14 significantly decreased at the end of 4 weeks after treatment (p < 0.001). Furthermore, the decline in scores of HAMD-17 and its sleep disorder and retardation factors from baseline to post-treatment was greater in HF-rTMS, ECT, and HF-rTMS + ECT group than in control (p < 0.05), and there was a significant difference between control and HF-rTMS group in the decline of psychological factor of HAMA-14 (p < 0.01). ECT treatment evoked total score of MoCA to decrease significantly at the end of 4-week after intervention (p < 0.001), and the decline in scores of MoCA and its delayed recall and language performances from baseline to post-treatment was greater in ECT than control, HF-rTMS, and HF-rTMS + ECT (p < 0.05). Conclusion: High-frequency repetitive transcranial magnetic stimulation improved psychological anxiety and ameliorated the cognition impairment evoked by ECT though it had the same anti-depressant efficacy as ECT.