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The delivery of ecosystem services (ESs), particularly in urban agglomerations, faces substantial threats from impending future climate change and human activity. Assessing ES bundles (ESBs) is critical to understanding the spatial allocation and interactions between multiple ESs. However, dynamic projections of ESBs under various future scenarios are still lacking, and their underlying driving mechanisms have received insufficient attention. This study examined the Beijing-Tianjin-Hebei urban agglomeration and proposed a framework that integrates patch-generating land use simulation into three shared socioeconomic pathway (SSP) scenarios and clustering analysis to assess spatiotemporal variations in seven ESs and ESBs from 1990 to 2050. The spatial trajectories of ESBs were analyzed to identify fluctuating regions susceptible to SSP scenarios. The results indicated that (1) different scenarios exhibited different loss rates of regulating and supporting services, where the mitigation of degradation was most significant under SSP126. The comprehensive ES value was highest under SSP245. (2) Bundles 1 and 2 (dominated by regulating and supporting services) had the largest total proportion under SSP126 (51.92 %). The largest total proportion of Bundles 4 and 5 occurred under SSP585 (48.96 %), with the highest provisioning services. The SSP126 scenario was projected to have the least ESB fluctuation at the grid scale, while the most occurred under SSP585. (3) Notably, synergies between regulating/supporting services were weaker under SSP126 than under either SSP245 or SSP585, while trade-offs between water yield and non-provisioning services were strongest. (4) Forestland and grassland proportions significantly affected carbon sequestration and habitat quality. Climatic factors (precipitation and temperature) acted as the dominant drivers of provisioning services, particularly water yield. Our findings advocate spatial strategies for future regional ES management to address upcoming risks.
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Reactive oxygen species (ROS) are important for plant defense against fungal attack. As a necrotrophic fungus, Botrytis cinerea can exploit ROS that originated from both sides of the host and pathogen during interaction to facilitate its infestation. Meanwhile, B. cinerea needs to exert an efficient oxidative stress responsive system to balance the intracellular redox state when encountering deleterious ROS levels. However, the machinery applied by B. cinerea to cope with ROS remains obscure. Herein, we investigated the role of the transcription factor BcMsn2 in regulating B. cinerea redox homeostasis. Disruption of the BcMsn2 gene severely impaired vegetative growth, sclerotium formation, conidial yield, and fungal virulence. The intracellular oxidative homeostasis of the ∆bcmsn2 mutant was disrupted, leading to significantly elevated levels of ROS and reduced activities of enzymes closely associated with oxygen stress, such as catalase (CAT) and superoxide dismutase (SOD). RNA-Seq and qRT-PCR analyses showed remarkable downregulation of the expression of several genes encoding ROS scavenging factors involved in maintaining the redox homeostasis in ∆bcmsn2, suggesting that BcMsn2 functions as a transcriptional regulator of these genes. Our findings indicated that BcMsn2 plays an indispensable role in maintaining the equilibrium of the redox state in B. cinerea, and intracellular ROS serve as signaling molecules that regulate the growth, asexual reproduction, and virulence of this pathogen.
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The aims of this study were to investigate the effect of hepatic sympathetic nerve removal on glucose and lipid metabolism in rats with cognitive impairment and to evaluate the relationship between these effects and liver Glut2 expression. Hippocampal injection of Aß1-42 was used to induce cognitive impairment. Impaired rats were divided into experimental, sham, and control groups. The experimental group was injected with 6-hydroxydopamine to remove the sympathetic nerve. At 4 weeks post injection, body weight, food and water intake, blood sugar, and blood lipids were measured, and periodic acid-Schiff (PAS) staining was used to assess the liver glycogen content. Liver Glut2 mRNA and protein were also detected. The experimental group showed reduced body weight, food intake, and blood glucose levels and elevated insulin levels compared with the control group. PAS staining showed higher glycogen contents in the experimental group than in controls. The expression levels of Glut2 mRNA and protein in the experimental group were significantly lower than in the controls. Metabolism was significantly impacted in rats with cognitive impairment following removal of the hepatic sympathetic nerve. Disruption to Glut2 liver expression via sympathetic nerve disruption represents a possible underlying mechanism.
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Blended learning, is a teaching approach that integrates online self-learning and classroom teaching. When designed well, blended learning courses in medicine can facilitate students to improve themselves in self-learning, understanding, and problem solving, ultimately enhancing their learning efficiency. However, blended teaching methods are usually used in only a single course, so it is unclear whether these methods can work well in a variety of basic medical courses. The goal of this study is to explore students' perceptions of whether blended laboratory courses are helpful for them in overcoming the difficulties they experience. Blended laboratory courses were taken by medical students at Guilin Medical University. Approximately 71.1% of the students agreed that online lecture courses improved their understanding of threshold concepts and the underlying theories. The majority of the students (63.01%) held the opinion that the blended laboratory courses were more effective than other types of courses in achieving the knowledge goals. The majority of the teachers believed that students' interest in experimentation operations, hands-on abilities, confidence, and other factors were greatly improved compared with those of students taught using the traditional teaching model (face to face). In addition, the average scores for the quizzes of laboratory courses were significantly improved in the blended learning method compared with the traditional learning method. Blended laboratory courses are successful and welcomed by both students and teachers in undergraduate laboratory courses.
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Instrucción por Computador/métodos , Educación a Distancia/métodos , Educación de Pregrado en Medicina/métodos , Aprendizaje , Aprendizaje Basado en Problemas/métodos , Estudiantes de Medicina/psicología , Autoevaluación Diagnóstica , Evaluación Educacional/métodos , Humanos , Aprendizaje/fisiología , Solución de Problemas/fisiologíaRESUMEN
BACKGROUND: Interleukin 10 (IL10) refers to a pleiotropic cytokine exerted immunoregulation. Aflatoxin B1 (AFB1) is a strong carcinogen, marked by causing immunosuppression. We determined the possible association between cord blood IL10 and AFB1-exposed patients with gestational diabetes (GD). METHODS: Cord blood samples from non-GD adults (nâ¯=â¯3) and GD patients (nâ¯=â¯3) were harvested for determining representative serological parameters by use of biochemical assays and enzyme linked immunosorbent assay (ELISA) tests. RESULTS: As results, GD patients showed no statistical comparable clinical data (hepatic function, lipids metabolism, immune cell count) to those in controls or references. Interestingly, cord blood contents of AFB1 in GD patients were significantly increased when compared to those in non-GD controls, characterized with visibly increased cord blood IL10. CONCLUSIONS: Preliminary clinical data reveal that IL10 may function as a biomarker for immunoregulation in AFB1-exposed GD patients.
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Aflatoxina B1/farmacología , Diabetes Gestacional/sangre , Sangre Fetal/química , Interleucina-10/sangre , Adulto , Biomarcadores/sangre , Diabetes Gestacional/inmunología , Ensayo de Inmunoadsorción Enzimática , Femenino , Humanos , Interleucina-10/inmunología , EmbarazoRESUMEN
BACKGROUND/AIMS: To investigate the effect of cognitive impairment and X-linked inhibitor of apoptosis protein (XIAP) on glucolipid metabolism. MATERIALS AND METHODS: ß-amyloid (Aß 1-42) was injected into the hippocampus of rats to establish a cognitive impairment model. Trans-activator of transcription (TAT)-XIAP fusion protein (the TAT-XIAP group), PBS (the model group), or XIAP antisense oligonucleotides (the ASODN group) was injected into the lateral ventricles of the rats to increase and decrease the activity of XIAP in the hippocampus. To determine the level of blood glucose and lipids, adenosine monophosphate-activated protein kinase (AMPK) expression of liver and hipppocamual neuronal apoptosis. RESULTS: The levels of FPG, TG, TC and LDL were significantly higher in the TAT-XIAP group, the model group and the ASODN group than in the blank group (P < 0.05); however, the HDL level showed no significant change in all groups of rats. The apoptosis indexes of the rat hippocampal CA1 neuron were 68.44 ± 4.31%, 13.21 ± 2.30%, 56.68 ± 4.771%, and 87.51 ± 6.63% in the model group, the blank group, the TAT-XIAP group and the ASODN group, respectively. Gastrointestinal motility was less frequent (per time unit) in the model group, the ASODN group and the TAT-XIAP group than in the blank group. Compared with the model group, gastrointestinal motility was significantly less frequent in the ASODN group and was significantly more frequent in the TAT-XIAP group. Compared with the blank group, the model group had a significantly lower gastric emptying rate and intestinal propulsive rate. Compared with the model group, the gastric emptying rate and intestinal propulsive rate were significantly lower in the ASODN group and were significantly higher in the TAT-XIAP group. Compared with the blank group, the expressions of AMPK mRNA, and AMPK protein were significantly reduced in the model group, the TAT-XIAP group, and the ASODN group. AMPK expression was significantly increased in the TAT-XIAP group and was significantly decreased in the ASODN group than in the model group. CONCLUSION: Cognitive impairment and hippocampal neuron apoptosis can cause glucose and lipids metabolic abnormalities, possibly by regulating gastrointestinal motility and AMPK expression in the liver. The changes in the function of XIAP, which is an anti-apoptotic protein in the hippocampus, may affect the metabolism of glucose and lipids.