Objective To explore the effect of modified Buzhong Yiqi decoction(MBZYQ)on thyroid function in rats with Hashimoto's thyroiditis(HT)by regulating the Toll-like receptor 2(TLR2)/myeloid differentiation factor 88(MyD88)/nuclear factor-κB(NF-κB)signaling pathway.Methods The HT rat model was constructed.The successfully modeled rats were divided into the HT group,L-MBZYQ,M-MBZYQ,H-MBZYQ(intragastric administration of 11.35,22.70,and 45.40 g/kg MBZYQ granules,respectively),and the MBZYQ+Pam3CSK4 group(intragastric administration of 45.40 g/kg MBZYQ granules+intraperitoneal injection of 20 μg TLR2 agonist Pam3CSK4),with 10 rats in each group.Another 10 normally raised rats were selected as the control group.The pathological changes of thyroid tissues and the apoptosis of thyroid tissue cells in each group were observed by HE staining and TUNEL staining respectively.The expressions of serum thyroglobulin antibody(TGAb),thyroid peroxidase antibody(TPOAb),free triiodothyronine(FT3),free thyroxine(FT4),thyroid stimulating hormone(TSH),interleukin-17(IL-17),and interleukin-10(IL-10)were detected by enzyme-linked immunosorbent assay(ELISA).Western blot was used to detect the protein expression of TLR2,MyD88 and NF-κB in thyroid tissues.Results The pathological damage of thyroid tissues in the L-MBZYQ,M-MBZYQ and H-MBZYQ groups was alleviated.The apoptosis rate of cells,the expressions of TGAb,TPOAb,TSH,IL-17,TLR2,MyD88 and NF-κB were lower than those in the HT group,while the expressions of FT3,FT4 and IL-10 were higher than those in the HT group.Moreover,the degree of decrease or increase in the M-MBZYQ and H-MBZYQ groups was greater than that in the L-MBZYQ group,and the changes in the H-MBZYQ group were greater than those in the M-MBZYQ group(P<0.05).The pathological damage of thyroid tissue in the MBZYQ+Pam3CSK4 group was further aggravated.The apoptosis rate of cells,the expressions of TGAb,TPOAb,TSH,IL-17,TLR2,MyD88 and NF-κB were higher than those in the H-MBZYQ group,while the expressions of FT3,FT4 and IL-10 were lower than those in the H-MBZYQ group(P<0.05).Conclusion MBZYQ can protect the thyroid function of HT rats,and its mechanism of action may be achieved by inhibiting the TLR2/MyD88/NF-κB signaling pathway.

With the rapid development of generative artificial intelligence(GAI)technologies,their widespread application in academic research and writing is continuously expanding the boundaries of sci-entific inquiry.However,this trend has also raised a series of ethical and regulatory challenges,inclu-ding issues related to authorship,content authenticity,citation accuracy,and accountability.In light of the growing involvement of AI in generating academic content,establishing an open,controllable,and trustworthy ethical governance framework has become a key task for safeguarding research integrity and maintaining trust within the academic community.This expert consensus outlines ethical requirements across key stages of AI-assisted academic writing-including topic selection,data management,citation practices,and authorship attribution.It aims to clarify the boundaries and ethical obligations surrounding AI use in academic writing,ensuring that technological tools enhance efficiency without compromising in-tegrity.The goal is to provide guidance and institutional support for building a responsible and sustainable research ecosystem.

Objective To explore the effect of modified Buzhong Yiqi decoction(MBZYQ)on thyroid function in rats with Hashimoto's thyroiditis(HT)by regulating the Toll-like receptor 2(TLR2)/myeloid differentiation factor 88(MyD88)/nuclear factor-κB(NF-κB)signaling pathway.Methods The HT rat model was constructed.The successfully modeled rats were divided into the HT group,L-MBZYQ,M-MBZYQ,H-MBZYQ(intragastric administration of 11.35,22.70,and 45.40 g/kg MBZYQ granules,respectively),and the MBZYQ+Pam3CSK4 group(intragastric administration of 45.40 g/kg MBZYQ granules+intraperitoneal injection of 20 μg TLR2 agonist Pam3CSK4),with 10 rats in each group.Another 10 normally raised rats were selected as the control group.The pathological changes of thyroid tissues and the apoptosis of thyroid tissue cells in each group were observed by HE staining and TUNEL staining respectively.The expressions of serum thyroglobulin antibody(TGAb),thyroid peroxidase antibody(TPOAb),free triiodothyronine(FT3),free thyroxine(FT4),thyroid stimulating hormone(TSH),interleukin-17(IL-17),and interleukin-10(IL-10)were detected by enzyme-linked immunosorbent assay(ELISA).Western blot was used to detect the protein expression of TLR2,MyD88 and NF-κB in thyroid tissues.Results The pathological damage of thyroid tissues in the L-MBZYQ,M-MBZYQ and H-MBZYQ groups was alleviated.The apoptosis rate of cells,the expressions of TGAb,TPOAb,TSH,IL-17,TLR2,MyD88 and NF-κB were lower than those in the HT group,while the expressions of FT3,FT4 and IL-10 were higher than those in the HT group.Moreover,the degree of decrease or increase in the M-MBZYQ and H-MBZYQ groups was greater than that in the L-MBZYQ group,and the changes in the H-MBZYQ group were greater than those in the M-MBZYQ group(P<0.05).The pathological damage of thyroid tissue in the MBZYQ+Pam3CSK4 group was further aggravated.The apoptosis rate of cells,the expressions of TGAb,TPOAb,TSH,IL-17,TLR2,MyD88 and NF-κB were higher than those in the H-MBZYQ group,while the expressions of FT3,FT4 and IL-10 were lower than those in the H-MBZYQ group(P<0.05).Conclusion MBZYQ can protect the thyroid function of HT rats,and its mechanism of action may be achieved by inhibiting the TLR2/MyD88/NF-κB signaling pathway.

Aberrant expression of Colgalt1 is closely associated with tumorigenesis and tumor progres-sion;however,the mechanism by which it regulates macrophages to influence tumor development remains poorly understood.This study aimed to establish a macrophage-specific Colgalt1 gene knockout mouse model to delve into the mechanisms through which Colgalt1 modulates macrophage function and subse-quently affects the occurrence and progression of tumor-related diseases.Initially,Colgalt1flox+mice were generated using gene editing techniques,followed by crossing with Lyz2-Cre+mice,which exhibit tissue-specific expression in the myeloid lineage(including monocytes and mature macrophages).Through this strategy,mice with the genotype Colgalt1-/-Lyz2-Cre+were successfully obtained,achieving conditional knockout of the Colgalt1 gene in macrophages.Colgalt1flox/flox Lyz2-Cre-mice were used as control.PCR and agarose gel electrophoresis were employed to identify the Flox and Cre genotypes of the knockout mice.RT-qPCR and Western Blot techniques were utilized to detect the expression levels of Colgalt1 in BMDMs from knockout mice at both the mRNA and protein levels,respectively.Western Blot results re-vealed a significant downregulation of Colgaltl expression in BMDMs from knockout mice compared to controls(P＜0.01).RT-qPCR results demonstrated a significant reduction in Colgalt1 mRNA levels in BMDMs from knockout mice compared to contro1s(P＜0.001),while no significant differences in Col-galt1 mRNA expression were observed in liver,lung,or spleen tissues between the two groups.Addition-ally,immunohistochemistry was employed to detect Colgalt1 expression in liver-specific macrophages,re-vealing an absence of Colgalt l-positive staining in liver macrophages from knockout mice.HE staining was used to observe cellular morphology in liver tissues from both groups of mice,showing no significant differences in cellular morphology or obvious pathological changes in tissues and organs.Moreover,the o-verall survival of the mice was not affected.Finally,RT-qPCR was used to assess the expression of mac-rophage-related inflammatory factors in BMDMs from both groups of mice.The results indicated that com-pared to controls,knockout mice exhibited downregulated expression of TNF-α(P＜0.05)and signifi-cantly upregulated expression of IL-10(P＜0.01),Arginase1(P＜0.001),and CD206(P＜0.001)in BMDMs,suggesting an anti-inflammatory trend and M2 polarization of macrophages following Colgalt 1 knockout.In summary,this study successfully established a macrophage-specific Colgalt1 gene knockout mouse model,providing a more reliable experimental animal model for in-depth exploration of the specific roles of Colgalt1 in macrophage functional regulation and the pathogenesis of tumor-related diseases.This model holds promise for identifying novel therapeutic targets and strategies for tumors and other diseases.

BACKGROUND: The protective effect of mesenchymal stem cells (MSCs) on cardiac ischemia-reperfusion (I/R) injury has been widely reported. Dental pulp-derived mesenchymal stem cells (DP-MSCs) have therapeutic effects on various diseases, including diabetes and cirrhosis. This study aimed to determine the therapeutic effects of DP-MSCs on I/R injury and elucidate the underlying mechanism. METHODS: Myocardial I/R injury model mice were treated with DP-MSCs or a miR-19a-3p mimic. The infarct volume, fibrotic area, pyroptosis, inflammation level, and cardiac function were measured. Cardiomyocytes exposed to hypoxia-reoxygenation were transfected with the miR-19a-3p mimic, miR-19a-3p inhibitor, or negative control. Pyroptosis and protein expression in the interferon regulatory factor 8/mitogen-activated protein kinase (IRF-8/MAPK) pathway were measured. RESULTS: DP-MSCs protected cardiac function in cardiac I/R-injured mice and inhibited cardiomyocyte pyroptosis. The upregulation of miR-19a-3p protected cardiac function, inhibited cardiomyocyte pyroptosis, and inhibited IRF-8/MAPK signaling in cardiac I/R-injured mice. DP-MSCs inhibited cardiomyocyte pyroptosis and the IRF-8/MAPK signaling by upregulating the miR-19a-3p levels in cardiomyocytes injured by I/R. CONCLUSION DP-MSCs protected cardiac function by inhibiting cardiomyocyte pyroptosis through miR-19a-3p under I/R conditions.
Animals ; MicroRNAs/metabolism* ; Pyroptosis/genetics* ; Mesenchymal Stem Cells/metabolism* ; Myocytes, Cardiac/cytology* ; Mice ; Male ; Mice, Inbred C57BL ; Dental Pulp/cytology* ; Myocardial Reperfusion Injury/therapy* ; MAP Kinase Signaling System/physiology*

By employing the analytic hierarchy process(AHP), the CRITIC method(a weight determination method based on indicator correlations), and the AHP-CRITIC hybrid weighting method, the weight coefficients of evaluation indicators were determined, followed by a comprehensive score comparison. The grey correlation analysis was then performed to analyze the results calculated using the hybrid weighting method. Subsequently, a backpropagation-artificial neural network(BP-ANN) model was constructed to predict the extraction process parameters and optimize the extraction process for Shenxiong Huanglian Jiedu Granules(SHJG). In the extraction process, an L_9(3~4) orthogonal experiment was designed to optimize three factors at three levels, including extraction frequency, water addition amount, and extraction time. The evaluation indicators included geniposide, berberine, ginsenoside Rg_1 + Re, ginsenoside Rb_1, ferulic acid, and extract yield. Finally, the optimal extraction results obtained by the orthogonal experiment, grey correlation analysis, and BP-ANN method were compared, and validation experiments were conducted. The results showed that the optimal extraction process involved two rounds of aqueous extraction, each lasting one hour; the first extraction used ten times the amount of added water, while the second extraction used eight times the amount. In the validation experiments, the average content of each indicator component was higher than the average content obtained in the orthogonal experiment, with a higher comprehensive score. The optimized extraction process parameters were reliable and stable, making them suitable for subsequent preparation process research.
Drugs, Chinese Herbal/analysis* ; Neural Networks, Computer

Aberrant expression of Colgalt1 is closely associated with tumorigenesis and tumor progres-sion;however,the mechanism by which it regulates macrophages to influence tumor development remains poorly understood.This study aimed to establish a macrophage-specific Colgalt1 gene knockout mouse model to delve into the mechanisms through which Colgalt1 modulates macrophage function and subse-quently affects the occurrence and progression of tumor-related diseases.Initially,Colgalt1flox+mice were generated using gene editing techniques,followed by crossing with Lyz2-Cre+mice,which exhibit tissue-specific expression in the myeloid lineage(including monocytes and mature macrophages).Through this strategy,mice with the genotype Colgalt1-/-Lyz2-Cre+were successfully obtained,achieving conditional knockout of the Colgalt1 gene in macrophages.Colgalt1flox/flox Lyz2-Cre-mice were used as control.PCR and agarose gel electrophoresis were employed to identify the Flox and Cre genotypes of the knockout mice.RT-qPCR and Western Blot techniques were utilized to detect the expression levels of Colgalt1 in BMDMs from knockout mice at both the mRNA and protein levels,respectively.Western Blot results re-vealed a significant downregulation of Colgaltl expression in BMDMs from knockout mice compared to controls(P＜0.01).RT-qPCR results demonstrated a significant reduction in Colgalt1 mRNA levels in BMDMs from knockout mice compared to contro1s(P＜0.001),while no significant differences in Col-galt1 mRNA expression were observed in liver,lung,or spleen tissues between the two groups.Addition-ally,immunohistochemistry was employed to detect Colgalt1 expression in liver-specific macrophages,re-vealing an absence of Colgalt l-positive staining in liver macrophages from knockout mice.HE staining was used to observe cellular morphology in liver tissues from both groups of mice,showing no significant differences in cellular morphology or obvious pathological changes in tissues and organs.Moreover,the o-verall survival of the mice was not affected.Finally,RT-qPCR was used to assess the expression of mac-rophage-related inflammatory factors in BMDMs from both groups of mice.The results indicated that com-pared to controls,knockout mice exhibited downregulated expression of TNF-α(P＜0.05)and signifi-cantly upregulated expression of IL-10(P＜0.01),Arginase1(P＜0.001),and CD206(P＜0.001)in BMDMs,suggesting an anti-inflammatory trend and M2 polarization of macrophages following Colgalt 1 knockout.In summary,this study successfully established a macrophage-specific Colgalt1 gene knockout mouse model,providing a more reliable experimental animal model for in-depth exploration of the specific roles of Colgalt1 in macrophage functional regulation and the pathogenesis of tumor-related diseases.This model holds promise for identifying novel therapeutic targets and strategies for tumors and other diseases.

Paraplegia caused by spinal cord injury is a serious neurological complication, for which surgery is currently the main treatment method. Due to different surgical approaches, patients are usually expected to maintain a passive prone position for a long time or switch between the supine and prone positions. Affected by multiple factors such as neurogenic sensory disorders, pathological changes in muscle tone and operative duration, the risk of intraoperative acquired pressure injury (IAPI) is significantly increased. Current clinical prevention strategies for IAPI in these patients predominantly focus on localized pressure relief during positioning, lacking systematic, standardized comprehensive prevention protocols or evidence-based guidelines. To address it, Department of Nursing, Orthopedics Branch, China International Exchange and Promotive Association for Medical and Health Care, Spinal Trauma Professional Committee, Orthopedics Branch, Chinese Medical Doctor Association, Nursing Group of Spine and Spinal Cord Professional Committee of Chinese Association of Rehabilitation Medicine organized experts in relevant fields to formulate Guideline for the prevention of intraoperative acquired pressure injury in paraplegic patients with spinal cord injury ( version 2025), based on evidence-based medical evidence and latest research results and clinical practice at home and abroad. Eleven recommendations were put forward from the aspects of preoperative risk assessment, intraoperative prevention strategies, postoperative handover and monitoring, and supportive mechanisms for IAPI prevention, aiming to standardize the prevention measures and management strategies of IAPI in paraplegic patients with spinal cord injury and accelerate the recovery of patients and improve the therapeutic effect.