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Abstract Background Tuina is an effective treatment for the decrease of skeletal muscle atrophy after peripheral nerve injury. However, the underlying mechanism of action remains unclear. This study aimed to explore the underlying mechanisms of tuina in rats with sciatic nerve injury (SNI). Methods We established an SNI rat model. After Tuina intervention, curative effects were evaluated by behavioral assessment, nerve function index, and muscle atrophy index (MAI). Pathological changes were observed by transmission electron microscopy and immunofluorescence. Insulin-like growth factor 1 (IGF-1), forkhead box O (FoxO) and p-FoxO levels were detected using enzyme-linked immunosorbent assay. Western blotting was performed to detect the expression of proteins involved in the PI3K/AKT signaling pathway. Result Behavioral assessment, nerve function index, and MAI revealed that the tuina had significantly improved muscle atrophy after SNI compared with the SNI model group. Transmission electron microscopy showed that tuina improved muscle ultramicrostructure. CD31 immunofluorescence revealed that tuina improved microcirculation. Furthermore, we observed that tuina differentially regulated the levels of IGF-1, FoxO and p-FoxO, and the protein expression of p-Phosphoinositide 3-kinase (p-PI3K), p-AKT, and vascular endothelial growth factor in the anterior tibial muscle and soleus muscles. Conclusion Tuina could effectively inhibit skeletal muscle atrophy via the microcirculation pathway in a rat model of SNI by regulating the expression of IGF-1 and FoxO. The underlying mechanism of action may involve the PI3K/Akt signaling pathway.

ObjectiveThis study aimed to analyse the research hotspots and frontiers in the field of paediatric fever between 2013 and 2023.MethodsThe included articles were visually analysed using CiteSpace 6.1.R6 software.ResultsA total of 2,662 Chinese-language articles and 1,456 English-language articles were included in the study. Based on the Chinese literature, research groups were identified represented by Xinmin Li, Jinling Hong and Hongshuang Luo. Based on the English literature, research groups were formed represented by Henriette Moll, Santiago Mintegi and Elizabeth Alpern. Tianjin University of Traditional Chinese Medicine was the institution with the largest number of publications in the Chinese literature, and the Centers For Disease Control And Prevention was the institution with the largest number of publications in the English literature. The research on paediatric fever mainly focused on mechanism exploration, green treatment and clinical management.ConclusionSeveral relatively stable research groups have been formed. Future studies on the differential diagnosis, rational drug use, standardised management and clinical practice guidelines for paediatric fever are needed.

Global warming has evolved into a global environmental concern. Despite the significant impact of rivers on greenhouse gas (GHG) emissions, there remains a lack of wide quantification of emissions at high temporal resolution. This research investigated the characteristics of the CO2 exchange flux (FCO2) and CH4 exchange flux (FCH4) at the interface of water and gas, as well as the primary determinants that impact these fluxes, at both the seasonal and 24-h scales, in the Inner Mongolia section of the Yellow River (IMYR). FCO2 was 52.52 ± 78.26 mmol·m−2·d−1 in summer, which was higher than autumn (30.81 ± 51.24 mmol·m−2·d−1) and spring (-96.09 ± 264.31 mmol·m−2·d−1). FCH4 peaked in summer (928.45 ± 513.31 μmol·m−2·d−1) and declined in the fall (326.76 ± 576.31 μmol·m−2·d−1). The lowest FCH4 was recorded in spring (61.75 ± 190.26 μmol·m−2·d−1). Wind speed (WS) and organic carbon mineralisation were the primary determinants of FCO2 at the seasonal scale, whereas temperature and dissolved oxygen (DO) were the primary determinants of FCH4. Monitoring FCO2 and FCH4 at night revealed higher average levels than during the day. FCO2 was regulated by levels of dissolved inorganic carbon (DIC) and total phosphorus (TP) levels over a 24-h period, whereas FCH4 was regulated by levels of dissolved oxygen (DO) and total nitrogen (TN). Throughout the majority of the time period, the IMYR river segment emits carbon dioxide (CO2) and methane (CH4) to the atmosphere. Due to the fact that emission patterns and driving mechanisms of riverine CO2 and CH4 differ across time scales, it is necessary to conduct more precise observations with high spatial and temporal resolution in order to acquire the most reliable data and comprehend more targeted approaches to carbon emission reduction.

Teaching is a demanding profession and maintaining teacher wellbeing is significant in ensuring educational quality. However, teacher wellbeing is easily affected by educational reforms, and systematic research on this topic is still relatively rare. In China, with the enactment of the Double Reduction Policy in 2021, the job characteristics of primary and secondary school teachers have undergone various changes. Thus, the current study examined the new job characteristics that China’s Double Reduction Policy imposed on the wellbeing of school teachers and their relationships with teachers’ inner world (i.e., emotional regulation and mindset). A cross-sectional study was carried out from June to October 2022 across China, employing self-reporting questionnaires for data collection and analysis. With a random sample of 902 teachers, we investigated the associations between teacher wellbeing, job characteristics, emotional regulation strategies, and mindset. The results indicated that teachers showed a lower level of wellbeing after the educational reform. Higher job resources contributed positively to predicting teacher wellbeing, while higher job demands contributed negatively. Genuinely expressing had positive impacts on teacher wellbeing while surface acting had negative impacts and deep acting none. Mindset was found to affect emotional regulation strategies and teacher wellbeing simultaneously. These findings shed light on how teachers can appropriately regulate emotions and maintain wellbeing in the wake of educational reforms.

Background: Tuina is an effective treatment for the decrease of skeletal muscle atrophy after peripheral nerve injury. However, the underlying mechanism of action remains unclear. This study aimed to explore the underlying mechanisms of tuina in rats with sciatic nerve injury (SNI). Methods: We established an SNI rat model. After Tuina intervention, curative effects were evaluated by behavioral assessment, nerve function index, and muscle atrophy index (MAI). Pathological changes were observed by transmission electron microscopy and immunofluorescence. Insulin-like growth factor 1 (IGF-1), forkhead box O (FoxO) and p-FoxO levels were detected using enzyme-linked immunosorbent assay. Western blotting was performed to detect the expression of proteins involved in the PI3K/AKT signaling pathway. Result: Behavioral assessment, nerve function index, and MAI revealed that the tuina had significantly improved muscle atrophy after SNI compared with the SNI model group. Transmission electron microscopy showed that tuina improved muscle ultramicrostructure. CD31 immunofluorescence revealed that tuina improved microcirculation. Furthermore, we observed that tuina differentially regulated the levels of IGF-1, FoxO and p-FoxO, and the protein expression of p-Phosphoinositide 3-kinase (p-PI3K), p-AKT, and vascular endothelial growth factor in the anterior tibial muscle and soleus muscles. Conclusion: Tuina could effectively inhibit skeletal muscle atrophy via the microcirculation pathway in a rat model of SNI by regulating the expression of IGF-1 and FoxO. The underlying mechanism of action may involve the PI3K/Akt signaling pathway. [ABSTRACT FROM AUTHOR]

We previously showed that microglial keratan sulfate (KS) was induced in amyotrophic lateral sclerosis. However, the functional roles of the glycan and its synthetic enzyme in neurodegenerative diseases, such as Alzheimer's disease (AD), a progressive disorder, are unclear. In our study, KS modified with sialic acids having a molecular mass of 125-220 kDa and the carbohydrate sulfotransferase GlcNAc6ST1 were up-regulated in the brains of two transgenic mouse models (J20 and Tg2576) and the brains of patients with AD. GlcNAc6ST1-deficient J20 (J20/GlcNAc6ST1-/-) mice demonstrated a complete absence of the microglial sialylated KS. J20/GlcNAc6ST1-/- primary microglia showed an increased level of amyloid-β phagocytosis and were hyperresponsive to interleukin 4, a potent antiinflammatory cytokine. Moreover, J20/GlcNAc6ST1-/- mice manifested reduced cerebral amyloid-β deposition. GlcNAc6ST1- synthesizing sialylated KS thus modulates AD pathology. Inhibition of KS synthesis by targeting GlcNAc6ST1 may therefore be beneficial for controlling AD pathogenesis. [ABSTRACT FROM AUTHOR]