Search

Magnaporthe oryzae is a filamentous fungus that causes rice blast. Rice blast seriously threatens the safety of food production. The normal synthesis and metabolism of fatty acids are extremely important for eukaryotes, and acyl-CoA is involved in fatty acid metabolism. Acyl-CoA binding (ACB) proteins specifically bind both medium-chain and long-chain acyl-CoA esters. However, the role of the Acb protein in plant-pathogenic fungi has not yet been investigated. Here, we identified MoAcb1, a homolog of the Acb protein in Saccharomyces cerevisiae. Disruption of MoACB1 causes delayed hyphal growth, significant reduction in conidial production and delayed appressorium development, glycogen availability, and reduced pathogenicity. Using immunoblotting and chemical drug sensitivity analysis, MoAcb1 was found to be involved in endoplasmic reticulum autophagy (ER-phagy). In conclusion, our results suggested that MoAcb1 is involved in conidia germination, appressorium development, pathogenicity and autophagy processes in M. oryzae.

ObjectiveThis study aimed to examine age and cohort trends in disability among Chinese older adults and explore the disablement process factors that may explain the cohort trends in disability.MethodsThis study used data from five waves of the Chinese Longitudinal Healthy Longevity Survey (CLHLS). A hierarchical logistic growth model was used to analyze the A–P–C effects and the contributors of cohort trends.ResultsADL, IADL, and FL among Chinese older adults showed increasing age and cohort trends. FL was more likely to result in IADL disability than ADL disability. Among the disablement process factors, gender, residence, education, health behavior, disease, and family income contributed to most of the cohort trends in disability.ConclusionsAs older adults face increasing disability trends, it is necessary to distinguish age and cohort trends and develop more effective interventions according to relative contributors to prevent disability among them.

The association between socioeconomic status (SES) and dietary diversity score (DDS) has been widely discussed, but little is known about the age and cohort effects on DDS and how the SES effect on DDS varies with age and across successive cohorts among urban and rural older adults in China. Thus, this study aimed to examine the temporal change in DDS among Chinese older adults and SES heterogeneities in such change from the perspective of urban–rural differentiation. Data from the Chinese Longitudinal Healthy Longevity Survey (CLHLS) between 2002 and 2018 were used, and a total of 13,728 participants aged between 65 and 105 years were included in this study. A total of eight food groups were used to assess DDS, while education, family income, and perceived income status were used to assess SES. A linear mixed model was used to estimate the age and cohort effects on DDS and their urban–rural and SES disparities. The results show that higher SES, including more education, family income, and perceived income status, was associated with higher DDS (for urban older adults, β = 0.1645, p = 0.0003, β = 0.2638, p < 0.0001, β = 0.2917, p < 0.0001, respectively; for rural older adults, β = 0.0932, p = 0.0080, β = 0.4063, p < 0.0001, β = 0.2921, p < 0.0001, respectively). The DDS of older adults increased with age and across successive cohorts in both urban and rural China. Moreover, we found the three-way interaction effect of SES, age, and cohort was statistically significant in both urban and rural China. Thus, living in an urban area and having higher SES are associated with higher DDS, but these associations change with age and across successive cohorts. The dietary health of earlier cohorts and rural oldest-old in China deserves more attention.

In order to encourage residents to go to primary care facilities, China has set up differentiated basic medical insurance reimbursement ratios. The study aims to use the dynamic point of view of longitudinal data to examine the changes in the impact of basic medical insurance on primary care. The data for this study comes from the Chinese Family Panel Study (CFPS) in 2010, 2012, 2014, 2016, and 2018. We adopted Hierarchal Age-period-cohort-Cross-Classified Random Effects Models (HAPC-CCREM) to examine the changes in the impact of basic medical insurance on primary care. Compared with non-insured groups, participants of the New Rural Cooperative Medical System (coefficient = 0.730) have a relatively high incidence of primary care seeks, while Urban Residents' Basic Medical Insurance (coefficient = −0.482) and Urban Employees' Basic Medical Insurance (coefficient = −0.663) are lower, respectively. Age, period over time and cohort have a more obvious moderating effect on primary care seeks. The study of primary care behavior is an important direction for the construction of a hierarchical medical system. As basic medical insurance is the source of power for the hierarchical medical system, we can provide certain direction for policy formulation on the changes of basic medical insurance in primary care behavior.

Cardiac fibrosis is a common pathological manifestation accompanied by various heart diseases, and antifibrotic therapy is an effective strategy to prevent diverse pathological processes of the cardiovascular system. We currently report the pharmacological evaluation of a novel anthraquinone compound (1,8-dihydroxy-6-methyl-9,10-anthraquinone-3-oxy ethyl succinate) named Kanglexin (KLX), as a potent cardioprotective agent with antifibrosis activity. Our results demonstrated that the administration of KLX by intragastric gavage alleviated cardiac dysfunction, hypertrophy, and fibrosis induced by transverse aortic constriction (TAC) surgical operation. Meanwhile, KLX administration relieved endothelial to mesenchymal transition of TAC mice. In TGF β1-treated primary cultured adult mouse cardiac fibroblasts (CFs) and human umbilical vein endothelial cells (HUVECs), KLX inhibited cell proliferation and collagen secretion. Also, KLX suppressed the transformation of fibroblasts to myofibroblasts in CFs. Further studies revealed that KLX-mediated cardiac protection was due to the inhibitory role of TGF-β1/ERK1/2 noncanonical pathway. In summary, our study indicates that KLX attenuated cardiac fibrosis and dysfunction of TAC mice, providing a potentially effective therapeutic strategy for heart pathological remodeling.

Background: Although Epicutaneo cava catheters (ECCs) are being routinely used for intravenous access for long-term parenteral nutrition and prolonged medication administration in neonates, ECC use can be associated with rare but acute life-threatening events such as pleural effusion (PE). It is important to identify and maintain the ECC tip in a central location for preventing complications. Recently, intracavitary electrocardiogram (IC-ECG) has been developed for the real-time monitoring and verification of ECC tip position.Objective: To investigate the causes and preventive measures of ECC-related PE in neonates.Methods: This prospective cohort study was conducted between January 2013 and December 2017. We observed and analyzed the clinical characteristics and causes of ECC-related PE. From January to December 2017, all ECCs were guided by IC-ECG. The incidence of ECC-related PE and first-attempt success rates were analyzed before and after the introduction of IC-ECG. Additionally, the sensitivity and specificity of IC-ECG were evaluated.Results: ECC-related PE was identified in 14 infants. Catheters were malpositioned in three cases; in the other 11 cases, catheters were located centrally on insertion but had migrated to non-central locations at the time of PE. After the introduction of IC-ECG, the incidence of PE was zero (P < 0.05). The incidence of ECC-related PE was lower when veins of the lower extremities were selected as the insertion site (P < 0.05). The first-attempt success rate was significantly higher in the group with IC-ECG-guided ECC placement than in the group without (P < 0.05). The sensitivity and specificity of IC-ECG were 97.9 and 84.6%, respectively.Conclusion: ECC-related PE can be associated with either primary malposition or migration of the catheter tip. IC-ECG can help detect malposition and migration of catheter tips and improve the first-attempt success rate. Choosing a lower extremity insertion site may help decrease the rate of ECC-related PE. In neonates, IC-ECG is a reliable positioning method for ECCs with superior sensitivity and specificity.

Background: The dorsolateral prefrontal cortex (DLPFC) in both hemispheres have a central integrative function for motor control and behavior. Understanding the hemispheric difference between DLPFC and ipsilateral motor cortex connection in the resting-state will provide fundamental knowledge to explain the different roles DLPFC plays in motor behavior.Purpose: The current study tested the interactions between the ipsilateral DLPFC and the primary motor cortex (M1) in each hemisphere at rest. We hypothesized that left DLPFC has a greater inhibitory effect on the ipsilateral M1 compared to the right DLPFC.Methods: Fourteen right-handed subjects were tested in a dual-coil paired-pulse paradigm using transcranial magnetic stimulation. The conditioning stimulus (CS) was applied to the DLPFC and the test stimulus (TS) was applied to M1. Interstimulus intervals (ISIs) between CS and TS were 2, 4, 6, 8, 10, 15, 20, 25, and 30 ms. The result was expressed as a percentage of the mean peak-to-peak amplitude of the unconditioned test pulse.Results: There was stronger inhibitory effect for the left compared to the right hemisphere at ISIs of 2 (p = 0.045), 10 (p = 0.006), 15 (p = 0.029) and 20 (p = 0.024) ms. There was no significant inhibition or facilitation at any ISI in the right hemisphere.Conclusions: The two hemispheres have distinct DLPFC and M1 cortico-cortical connectivity at rest. Left hemisphere DLPFC is dominant in inhibiting ipsilateral M1.

Hypertension is a major risk factor for stroke and cardiovascular events in clinic, which is accompanied by the abnormality of vascular tone and endothelial dysfunction of small artery. Here we report that Kang Le Xin (KLX), a novel anthraquinones compound, could reduce blood pressure and the underlying mechanisms involves that KLX induces endothelium-dependent vasodilation. KLX significantly decreases the arterial blood pressure of spontaneous hypertensive rats (SHR), decreases the contractile reactivity of superior mesenteric artery to phenylephrine and increases the vasodilatory reactivity of superior mesenteric artery to carbachol in a dose-dependent manner. Besides, KLX reduces vascular tension of endothelium-intact mesenteric artery pre-constricted with phenylephrine in a dose-dependent manner, while this effect is inhibited by depriving vascular endothelium or pretreating vascular rings with L-NAME (endothelial nitric oxide synthase inhibitor) or compound C (AMP-activated protein kinase inhibitor). Moreover, KLX increases nitric oxide (NO) generation, endothelial nitric oxide synthase (eNOS), AKT and AMP-activated protein kinase (AMPK) phosphorylation in cultured human umbilical vein endothelial cells (HUVECs), while these effects are inhibited by pretreating cells with compound C. In conclusion, KLX is a new compound with the pharmacological action of reducing arterial blood pressure. The underlying mechanism involves KLX induces endothelium-dependent vasodilation through activating AMPK-AKT-eNOS signaling pathway.

Human adenovirus type 55 (HAdV-B55) is a recently identified acute respiratory disease (ARD) pathogen in HAdV species B with a recombinant genome between renal HAdV-B11 and respiratory HAdV-B14. Since HAdV-B55 first appeared in China school in 2006, no more ARD cases associated with it had been reported until 2011, when there was an outbreak of adult severe community-acquired pneumonia (CAP) in Beijing, China. Reported here is the bioinformatics analysis of the re-emergent HAdV-B55 responsible for this outbreak. Recombination and protein sequence analysis re-confirmed that this isolate (BJ01) was a recombinant virus with the capsid hexon gene from HAdV-B11. The selection pressures for the three capsid proteins, i.e., hexon, penton base, and fiber genes, were all negative, along with very low non-synonymous (dN) and synonymous (dS) substitutions/site (

With the significant increase in the global prevalence of diabetes mellitus (DM), the occurrence of diabetic peripheral neuropathy (DPN) has become increasingly common complication associated with DM. It is particularly in the peripheral nerves of the hands, legs, and feet. DPN can lead to various adverse consequences that greatly affect the quality of life for individuals with DM. Despite the profound impact of DPN, the specific mechanisms underlying its development and progression are still not well understood. Advancements in magnetic resonance imaging (MRI) technology have provided valuable tools for investigating the central mechanisms involved in DPN. Structural and functional MRI techniques have emerged as important methods for studying the brain structures and functions associated with DPN. Voxel-based morphometry allows researchers to assess changes in the volume and density of different brain regions, providing insights into potential structural alterations related to DPN. Functional MRI investigates brain activity patterns, helping elucidate the neural networks engaged during sensory processing and pain perception in DPN patients. Lastly, magnetic resonance spectroscopy provides information about the neurochemical composition of specific brain regions, shedding light on potential metabolic changes associated with DPN. By synthesizing available literature employing these MRI techniques, this study aims to enhance our understanding of the neural mechanisms underlying DPN and contribute to the improvement of clinical diagnosis. [ABSTRACT FROM AUTHOR]

Background: Amnestic mild cognitive impairment (aMCI) is an early stage of Alzheimer's disease (AD). Regional homogeneity (ReHo) and amplitude of lowfrequency fluctuation (ALFF) are employed to explore spontaneous brain function in patients with aMCI. This study applied ALFF and ReHo indicators to analyze the neural mechanism of aMCI by resting-state functional magnetic resonance imaging (rs-fMRI). Methods: Twenty-six patients with aMCI were included and assigned to the aMCI group. The other 26 healthy subjects were included as a healthy control (HC) group. Rs-fMRI was performed for all participants in both groups. Between-group comparisons of demographic data and neuropsychological scores were analyzed using SPSS 25.0. Functional imaging data were analyzed using DPARSF and SPM12 software based on MATLAB 2017a. Gender, age, and years of education were used as covariates to obtain ALFF and ReHo indices. Results: Compared with HC group, ALFF decreased in the left fusiform gyrus, left superior temporal gyrus, and increased in the left cerebellum 8, left inferior temporal gyrus, left superior frontal gyrus (BA11), and right inferior temporal gyrus (BA20) in the aMCI group (p < 0.05, FWE correction). In addition, ReHo decreased in the right middle temporal gyrus and right anterior cuneiform lobe, while it increased in the left middle temporal gyrus, left inferior temporal gyrus, cerebellar vermis, right parahippocampal gyrus, left caudate nucleus, right thalamus, and left superior frontal gyrus (BA6) (p < 0.05, FWE correction). In the aMCI group, the ALFF of the left superior frontal gyrus was negatively correlated with Montreal Cognitive Assessment (MoCA) score (r = 0.437, p = 0.026), and the ALFF of the left superior temporal gyrus was positively correlated with the MoCA score (r = 0.550, p = 0.004). The ReHo of the right hippocampus was negatively correlated with the Mini-Mental State Examination (MMSE) score (r = 0.434, p = 0.027), and the ReHo of the right middle temporal gyrus was positively correlated with MMSE score (r = 0.392, p = 0.048). Conclusion: Functional changes in multiple brain regions rather than in a single brain region have been observed in patients with aMCI. The abnormal activity of multiple specific brain regions may be a manifestation of impaired central function in patients with aMCI. [ABSTRACT FROM AUTHOR]

Background: Alzheimer's disease (AD) is a common, progressive, irreversible, and fatal neurodegenerative disorder with rapidly increasing worldwide incidence. Although much research on magnetic resonance imaging (MRI) of the white matter (WM) in AD has been published, no bibliometric analysis study has investigated this issue. Thus, this study aimed to provide an overview of the current status, hotspots, and trends in MRI of WM in AD. Methods: We searched for records related to MRI studies of WM in AD from 1990 to 2022 in the Web of Science Core Collection (WOSCC) database. CiteSpace (version 5.1.R8) and VOSviewer (version 1.6.19) software were used for bibliometric analyses. Results: A total of 2,199 articles were obtained from this study. From 1990 to 2022, the number of published articles showed exponential growth of y = 4.1374e0.1294x, with an average of 17.9 articles per year. The top country and institutions were the United States and the University of California Davis, accounting for 44.52 and 5.32% of the total studies, respectively. The most productive journal was Neurology, and the most co-cited journal was Lancet Neurology. Decarli C was the most productive author. The current research frontier trend focuses on the association between small vessel disease and AD, the clinical application and exploration of diffusion MRI, and related markers. Conclusion: This study provides an in-depth overview of publications on MRI of WM in AD, identifying the current research status, hotspots, and frontier trends in the field. [ABSTRACT FROM AUTHOR]

BackgroundA positive professional identity is key for nursing students in determining career direction and predicting future engagement in the profession. Despite its complexity and susceptibility to various influences, the factors shaping nursing students' professional identity remain poorly understood.ObjectivesThis study aims to investigate how perceived stress can directly and indirectly influence professional identity among nursing students, with self-control and self-directed learning ability as mediators.Materials and methodsA cross-sectional survey was conducted from October to December 2023, collecting data from 675 nursing students across five tertiary hospitals in Xi'an, Shaanxi Province, China. The survey captured detailed data on sociodemographic characteristics, perceived stress, self-control, self-directed learning ability, and professional identity among the participants. Descriptive analysis and correlation matrices were used to analyze participant characteristics and assess bivariate correlations. The mediation model was analyzed using the PROCESS macro for SPSS.ResultsPerceived stress showed a direct and negative influence on professional identity among nursing students; self-control was shown to play a mediating role between perceived stress and professional identity; self-directed learning ability was shown to play a mediating role between perceived stress and professional identity; and self-control and self-directed learning ability were shown to play a chain mediating role between perceived stress and professional identity.ConclusionSelf-control and self-directed learning ability have a chain mediating role in between perceived stress and professional identity among nursing students. It suggests that nursing managers and educators can improve the self-control and self-directed learning ability of nursing students to mitigate the negative impact of perceived stress on professional identity.

Maintenance of telomere length is essential to delay replicative cellular senescence. It is controversial on whether growth differentiation factor 11 (GDF11) can reverse cellular senescence, and this work aims to establish the causality between GDF11 and the telomere maintenance unequivocally. Using CRISPR/Cas9 technique and a long-term in vitro culture model of cellular senescence, we show here that in vitro genetic deletion of GDF11 causes shortening of telomere length, downregulation of telomeric reverse transcriptase (TERT) and telomeric RNA component (TERC), the key enzyme and the RNA component for extension of the telomere, and reduction of telomerase activity. In contrast, both recombinant and overexpressed GDF11 restore the transcription of TERT in GDF11KO cells to the wild-type level. Furthermore, loss of GDF11-induced telomere shortening is likely caused by enhancing the nuclear entry of SMAD2 which inhibits the transcription of TERT and TERC. Our results provide the first proof-of-cause-and-effect evidence that endogenous GDF11 plays a causal role for proliferative cells to maintain telomere length, paving the way for potential rejuvenation of the proliferative cells, tissues, and organs.

Intracellular Ca2+ overload, prolongation of the action potential duration (APD), and downregulation of inward rectifier potassium (IK1) channel are hallmarks of electrical remodeling in cardiac hypertrophy and heart failure (HF). We hypothesized that enhancement of IK1 currents is a compensation for IK1 deficit and a novel modulation for cardiac Ca2+ homeostasis and pathological remodeling. In adult Sprague-Dawley (SD) rats in vivo, cardiac hypertrophy was induced by isoproterenol (Iso) injection (i.p., 3 mg/kg/d) for 3, 10, and 30 days. Neonatal rat ventricular myocytes (NRVMs) were isolated from 1 to 3 days SD rat pups and treated with 1 μmol/L Iso for 24 h in vitro. The effects of zacopride, a selective IK1/Kir2.1 channel agonist, on cardiac remodeling/hypertrophy were observed in the settings of 15 μg/kg in vivo and 1 μmol/L in vitro. After exposing to Iso for 3 days and 10 days, rat hearts showed distinct concentric hypertrophy and fibrosis and enhanced pumping function (P < 0.01 or P < 0.05), then progressed to dilatation and dysfunction post 30 days. Compared with the age-matched control, cardiomyocytes exhibited higher cytosolic Ca2+ (P < 0.01 or P < 0.05) and lower SR Ca2+ content (P < 0.01 or P < 0.05) all through 3, 10, and 30 days of Iso infusion. The expressions of Kir2.1 and SERCA2 were downregulated, while p-CaMKII, p-RyR2, and cleaved caspase-3 were upregulated. Iso-induced electrophysiological abnormalities were also manifested with resting potential (RP) depolarization (P < 0.01), APD prolongation (P < 0.01) in adult cardiomyocytes, and calcium overload in cultured NRVMs (P < 0.01). Zacopride treatment effectively retarded myocardial hypertrophy and fibrosis, preserved the expression of Kir2.1 and some key players in Ca2+ homeostasis, normalized the RP (P < 0.05), and abbreviated APD (P < 0.01), thus lowered cytosolic [Ca2 +]i (P < 0.01 or P < 0.05). IK1channel blocker BaCl2 or chloroquine largely reversed the cardioprotection of zacopride. We conclude that cardiac electrical remodeling is concurrent with structural remodeling. By enhancing cardiac IK1, zacopride prevents Iso-induced electrical remodeling around intracellular Ca2+ overload, thereby attenuates cardiac structural disorder and dysfunction. Early electrical interventions may provide protection on cardiac remodeling.