ObjectiveTo explore the possible mechanism of Bimin Formula （鼻敏方） in treating lung-spleen qi deficiency syndrome of allergic rhinitis （AR） with high mucin secretion. MethodsThirty-four SD rats were randomly divided into a blank group （8 rats）， a model group （8 rats）， a low-dose Bimin Formula group （8 rats）， and a high-dose Bimin Formula group （10 rats）. Except for the blank group， the other groups were subjected to AR lung-spleen qi deficiency rat models induced by smoking， gavage of Ginkgo biloba leaf extract， and ovalbumin. After modeling， rats in the low- and high-dose Bimin Formula groups were given Bimin Formula concentrate （concentration of 2.16 g/ml） by gavage at doses of 1.08 g/100 g and 2.16 g/100 g， respectively， while rats in the model group were given 0.5 ml/100 g of normal saline by gavage， once daily for 28 days； the blank group was not intervened. Behavioral assessments were performed after intervention. ELISA was used to detect the levels of peripheral blood total immunoglobulin E （IgE）. HE staining was used to observe the pathological changes of nasal mucosa epithelium in rats， while immunohistochemistry was used to detect the expression of transmembrane protein 16A （TMEM16A） and mucin 5AC （MUC5AC） protein in nasal mucosa. Western Blot was used to detect the expression of nuclear factor kappa B （NF-κB） protein， and RT-PCR was used to detect the expression of TMEM16A， MUC5AC， and NF-κB mRNA in nasal mucosa. ResultsHE staining showed that the nasal mucosa epithelial cell structure in the blank group was intact without shedding， swelling， or necrosis； the nasal mucosa epithelial tissue of rats in the model group was thickened and partially shed， with infiltration of eosinophils and lymphocytes visible； the pathological changes in nasal mucosa tissue of rats in the high- and low-dose Bimin Formulagroups were improved， and more improvement was showen in the high-dose group. Compared with those in the blank group， the behavioral scores and peripheral blood total IgE levels of rats in the model group significantly increased， as well as the expression of TMEM16A， MUC5AC， and NF-κB proteins and mRNA in nasal mucosa （P＜0.05 or P＜0.01）. Compared with those in the model group， the behavioral scores and peripheral blood total IgE levels of rats in the high-dose Bimin Formula group decreased， and the expression of TMEM16A， MUC5AC， and NF-κB proteins and mRNA in nasal mucosaalso decreased （P＜0.05 or P＜0.01）； the behavioral scores and peripheral blood total IgE levels of rats in the low-dose Bimin Formula group were reduced， and the expression of TMEM16A and MUC5AC proteins and mRNA in nasal mucosa， as well as the expression of NF-κB protein decreased （P＜0.05 or P＜0.01）， but the difference in NF-κB mRNA expression was not statistically significant （P＞0.05）. Compared with the low-dose Bimin Formula group， the expression of NF-κB protein in the high-dose group decreased （P＜0.01）. ConclusionBimin Formula may improve the symptoms and high mucus secretion of AR lung-spleen qi deficiency by regulating the TMEM16A/NF-κB/MUC5AC signaling pathway in nasalmucosa.

Ankylosing spondylitis (AS) combined with lower cervical fracture is often categorized into unstable fracture, with a high incidence of neurological injury and a high rate of disability and morbidity. As factors such as shoulder occlusion may affect the accuracy of X-ray imaging diagnosis, it is often easily misdiagnosed at the primary diagnosis. Non-operative treatment has complications such as bone nonunion and the possibility of secondary neurological damage, while the timing, access and choice of surgical treatment are still controversial. Currently, there are no clinical practice guidelines for the treatment of AS combined with lower cervical fracture with or without dislocation. To this end, the Spinal Trauma Group of Orthopedics Branch of Chinese Medical Doctor Association organized experts to formulate Clinical guidelines for the treatment of ankylosing spondylitis combined with lower cervical fracture in adults ( version 2024) in accordance with the principles of evidence-based medicine, scientificity and practicality, in which 11 recommendations were put forward in terms of the diagnosis, imaging evaluation, typing and treatment, etc, to provide guidance for the diagnosis and treatment of AS combined with lower cervical fracture.

Cardiac-resident macrophages (CRMs) play important roles in homeostasis, cardiac function, and remodeling. Although CRMs play critical roles in cardiac regeneration of neonatal mice, their roles are yet to be fully elucidated. Therefore, this study aimed to investigate the dynamic changes of CRMs during cardiac ontogeny and analyze the phenotypic and functional properties of CRMs in the promotion of cardiac regeneration. During mouse cardiac ontogeny, four CRM subsets exist successively: CX₃CR1⁺CCR2^-Ly6C^-MHCII^- (MP1), CX₃CR1^lowCCR2^lowLy6C^-MHCII^- (MP2), CX₃CR1^-CCR2⁺Ly6C⁺MHCII^- (MP3), and CX₃CR1⁺CCR2^-Ly6C^-MHCII⁺ (MP4). MP1 cluster has different derivations (yolk sac, fetal liver, and bone marrow) and multiple functions population. Embryonic and neonatal-derived-MP1 directly promoted cardiomyocyte proliferation through Jagged-1-Notch1 axis and significantly ameliorated cardiac injury following myocardial infarction. MP2/3 subsets could survive throughout adulthood. MP4, the main population in adult mouse hearts, contributed to inflammation. During ontogeny, MP1 can convert into MP4 triggered by changes in the cellular redox state. These findings delineate the evolutionary dynamics of CRMs under physiological conditions and found direct evidence that embryonic and neonatal-derived CRMs regulate cardiomyocyte proliferation. Our findings also shed light on cardiac repair following injury.

Objective:To establish a method for automatic determination of iodine level in salt by arsenic-cerium catalytic spectrophotometry using an iodine element detector (hereinafter referred to as this method), and to provide reference for in-depth study of salt iodine detection technology.Methods:This method was used to determine the iodine level in salt, and the linear range, detection limit, precision, and accuracy (determination of salt iodine standard substance GBW10006y and GBW10007y, and addition recovery experiment) of this method were determined. The iodine level of 35 salt samples was determined by this method and redox titration method recommended by the national standard, and the results were compared.Results:This method had a good linear relationship within the range of 50 - 600 μg/L standard curve, the absolute value of the correlation coefficients was > 0.999 0, and the detection limit was 5.0 mg/kg. The relative standard deviation of iodine concentration in salt samples with low, medium and high iodine concentrations were all < 6.0%. The determination results of salt iodine standard substance GBW10006y and GBW10007y were within the given value ranges; three iodine concentrations (6.0, 10.0 and 30.0 mg/kg) were added to the salt samples, with an average recovery rate of 96.7% to 105.0%, and a total average recovery rate of 100.9%. The method comparison experiment showed that there was no statistically significant difference between the salt iodine determination results of this method and the redox titration method ( t = - 1.54, P = 0.132). Conclusion:This method has the advantages of high accuracy, good precision and wide linear range in determining salt iodine, and is suitable for the detection of large quantities of samples in salt iodine monitoring.

Ankylosing spondylitis (AS) combined with spinal fractures with thoracic and lumbar fracture as the most common type shows characteristics of unstable fracture, high incidence of nerve injury, high mortality and high disability rate. The diagnosis may be missed because it is mostly caused by low-energy injury, when spinal rigidity and osteoporosis have a great impact on the accuracy of imaging examination. At the same time, the treatment choices are controversial, with no relevant specifications. Non-operative treatments can easily lead to bone nonunion, pseudoarthrosis and delayed nerve injury, while surgeries may be failed due to internal fixation failure. At present, there are no evidence-based guidelines for the diagnosis and treatment of AS combined with thoracic and lumbar fracture. In this context, the Spinal Trauma Academic Group of Orthopedics Branch of Chinese Medical Doctor Association organized experts to formulate the Clinical guideline for the diagnosis and treatment of adult ankylosing spondylitis combined with thoracolumbar fracture ( version 2023) by following the principles of evidence-based medicine and systematically review related literatures. Ten recommendations on the diagnosis, imaging evaluation, classification and treatment of AS combined with thoracic and lumbar fracture were put forward, aiming to standardize the clinical diagnosis and treatment of such disorder.

The acute combination fractures of the atlas and axis in adults have a higher rate of neurological injury and early death compared with atlas or axial fractures alone. Currently, the diagnosis and treatment choices of acute combination fractures of the atlas and axis in adults are controversial because of the lack of standards for implementation. Non-operative treatments have a high incidence of bone nonunion and complications, while surgeries may easily lead to the injury of the vertebral artery, spinal cord and nerve root. At present, there are no evidence-based Chinese guidelines for the diagnosis and treatment of acute combination fractures of the atlas and axis in adults. To provide orthopedic surgeons with the most up-to-date and effective information in treating acute combination fractures of the atlas and axis in adults, the Spinal Trauma Group of Orthopedic Branch of Chinese Medical Doctor Association organized experts in the field of spinal trauma to develop the Evidence-based guideline for clinical diagnosis and treatment of acute combination fractures of the atlas and axis in adults ( version 2023) by referring to the "Management of acute combination fractures of the atlas and axis in adults" published by American Association of Neurological Surgeons (AANS)/Congress of Neurological Surgeons (CNS) in 2013 and the relevant Chinese and English literatures. Ten recommendations were made concerning the radiological diagnosis, stability judgment, treatment rules, treatment options and complications based on medical evidence, aiming to provide a reference for the diagnosis and treatment of acute combination fractures of the atlas and axis in adults.

Up-frameshift 1 (UPF1), as the most critical factor in nonsense-mediated messenger RNA (mRNA) decay (NMD), regulates tumor-associated molecular pathways in many cancers. However, the role of UPF1 in lung adenocarcinoma (LUAD) amino acid metabolism remains largely unknown. In this study, we found that UPF1 was significantly correlated with a portion of amino acid metabolic pathways in LUAD by integrating bioinformatics and metabolomics. We further confirmed that UPF1 knockdown inhibited activating transcription factor 4 (ATF4) and Ser51 phosphorylation of eukaryotic translation initiation factor 2α (eIF2α), the core proteins in amino acid metabolism reprogramming. In addition, UPF1 promotes cell proliferation by increasing the amino-acid levels of LUAD cells, which depends on the function of ATF4. Clinically, UPF1 mRNA expression is abnormal in LUAD tissues, and higher expression of UPF1 and ATF4 was significantly correlated with poor overall survival (OS) in LUAD patients. Our findings reveal that UPF1 is a potential regulator of tumor-associated amino acid metabolism and may be a therapeutic target for LUAD.
Activating Transcription Factor 4/genetics* ; Adenocarcinoma of Lung ; Amino Acids ; Cell Proliferation ; Eukaryotic Initiation Factor-2 ; Humans ; Lung Neoplasms ; RNA Helicases/metabolism* ; RNA, Messenger/metabolism* ; Trans-Activators/metabolism*

Objective:To explore the mechanism of B10 cell involved in cardiomyocyte hypertrophy following myocarditis, and to develop potential therapeutic strategies.Methods:BALB/c mice infected with Coxsackie virus B3 induced viral myocarditis model. The expression of angiotensin (ANG)Ⅱ and its receptor in myocarditis mice was detected. The changes of B10 cells in the hearts of control mice and myocarditis mice were analyzed by flow cytometry. After losartan was administered to myocarditis mice, the degree of myocardial inflammation was detected by HE staining, the expression of inflammatory factors was detected by ELISA, the myocardial hypertrophy was detected by wheat germ agglutinin (WGA) staining, and the changes of B10 cells in the heart were analyzed by flow cytometry. The levels of cardiac troponin T (C-TNT) and high mobility group box 1 (HMGB1) protein in neonatal mouse cardiomyocytes treated with ANGⅡ and ANGⅡ+ IL-10 were detected. Cardiomyocytes were treated with ANGⅡ, ANGⅡ+ B10 cells, ANGⅡ+ B10 cells + IL-10 receptor antibody and ANGⅡ+ B cells to detect C-TNT protein levels, and Annexin-V/PI was used to detect the apoptosis of cardiomyocytes. Cardiomyocytes were treated with oxidized HMGB1, reduced HMGB1 and disulfide HMGB1, and C-TNT expression was detected.Results:Coxsackievirus B3 infection caused cardiac hypertrophy, high expression of ANGⅡ and its receptor, and transient increase of B10 cells in mice. Losartan treatment blocked the angiotensin receptor, reduced expansion of B10 cells. B10 cells alleviated apoptosis of cardiomyocytes and inhibited the production of HMGB1 induced by ANGⅡ patch by producing IL-10, thus alleviating viral myocarditis and cardiac hypertrophy.Conclusions:B10 cells may play an important role in myocardial protection in myocarditis.

According to the pathological characteristics of symptomatic chronic thoracic and lumbar osteoporotic vertebral fracture (SCOVF), the different clinical treatment methods are selected, including vertebral augmentation, anterior-posterior fixation and fusion, posterior decompression fixation and fusion, and posterior correction osteotomy. However, there is still a lack of a unified understanding on how to choose appropriate treatment method for SCOVF. In order to reflect the new treatment concept and the evidence-based medicine progress of SCOVF in a timely manner and standardize its treatment, the clinical guideline for surgical treatment of SCOVF is formulated in compliance with the principle of scientificity, practicability and advancement and based on the level of evidence-based medicine.

Objective To investigate the expression of transcription factor forkhead/winged helix transcription factor 3 (Foxp3),immune factor transforming growth factor-beta 1 (TGF-β1),and T-lymphocyte activation related factor interleukin-2 (IL-2) in peripheral blood of patients with coal-burning arsenic poisoning,and to analyze the effects of arsenic exposure on immune function.Methods A case-control study was conducted to investigate 149 cases [94 males and 55 females,(50.69 ± 6.14) years old] of arsenic poisoning in Yuzhang coalburning arsenic poisoning area,southwestern Guizhou Province,and the cases were diagnosed based on the "Diagnosis of Endemic Arsenicosis" (WS/T 211-2015) and confirmed by clinical review.According to skin damage,the patients were divided into mild arsenic poisoning group (39 cases),moderate arsenic poisoning group (54 cases) and severe arsenic poisoning group (56 cases);and 41 cases [12 males and 29 females,(45.76 ± 7.88) years old] of non-arsenic exposed residents from 12 km of Yuzhang coal-burning area were selected as control group.Morning urine and peripheral blood samples were collected with informed consent.Urine arsenic content was measured by inductively coupled plasma mass spectrometry (ICP-MS).Urine arsenic was corrected by creatinine (Cr).Detection of regulatory T cell (Treg)-specific transcription factor Foxp3 gene expression in human peripheral blood was done by real-time fluorescence quantitative PCR,and the levels of Treg-related immune factor TGF-β1 and IL-2 in serum were detected by enzyme linked immunosorbent assay (ELISA).Results The urinary arsenic contents [median (quartile):29.13 (19.75-54.50),31.81 (17.52-53.31),30.51 (18.35-45.76) μg/g Cr] in each arsenic poisoning group were higher than that in the control group [21.62 (17.65-28.44) μg/g Cr,P ＜ 0.05].The expression levels of Foxp3 mRNA in peripheral blood of each arsenic poisoning group [median (quartile):0.58 (0.17-1.27),0.32 (0.17-0.61),0.33 (0.13-0.62)] were significantly lower than that in the control group [0.87 (0.64-1.50),P ＜ 0.05];compared with mild arsenic poisoning group,the expression of Foxp3 mRNA in peripheral blood of moderate and severe arsenic poisoning groups decreased (P ＜ 0.05).The contents of serum TGF-β1 [(13.14 ± 5.19),(12.85 ± 5.51),(12.78 ± 4.95) μg/L] in each arsenic poisoning group were significantly higher than that in the control group [(3.90 ± 1.53) μg/L,P ＜ 0.05].The levels of IL-2 in serum of each arsenic poisoning group [(9.85 ± 5.38),(11.64 ± 6.40),(12.27 ± 6.19) ng/L] were lower than that in the control group [(34.30 ± 4.84) ng/L,P ＜ 0.05];the serum level of IL-2 in severe arsenic poisoning group was higher than that in mild arsenic poisoning group (P ＜ 0.05).Conclusions Arsenic exposure can cause abnormal changes of Treg-specific transcription factor Foxp3 and related immune factors TGF-β1 and IL-2 in peripheral blood of patients.It is suggested that Treg dysfunction may be related to arsenic poisoning.