ObjectiveTo explore the improving effect of Huangqi Chifengtang（HCT） on atherosclerosis（AS）， and elucidate its mechanism in relation to adenosine monophosphate-activated protein kinase（AMPK）/peroxisome proliferator-activated receptor α（PPARα） signaling pathway and nucleotide-binding oligomerization domain（NOD）-like receptor thermal protein domain associated protein 3（NLRP3） inflammasome. MethodsEight C57BL/6J mice were set as the normal group， and 32 ApoE^-/- mice were randomly divided into the model group， the positive drug group（atorvastatin， 5 mg·kg^-1·d^-1）， HCT low- and high-dose groups（1.95， 3.90 g·kg^-1·d^-1）. ApoE^-/- mice were fed with high-fat and high-cholesterol feed to establish an AS mouse model. After modeling， they were orally administered corresponding dose of drugs for 28 days， while the normal and model groups received an equal volume of physiological saline via oral gavage. Hematoxylin-eosin（HE） staining was used to observe the pathological status of the aorta and liver in mice， Biochemical testing and enzyme-linked immunosorbent assay（ELISA） were used to detect the levels of total cholesterol（TC）， triglycerides（TG）， low-density lipoprotein cholesterol（LDL-C）， alanine aminotransferase（ALT）， aspartate aminotransferase（AST）， C-reactive protein（CRP）， interleukin（IL）-1β， IL-18 in the serum， as well as superoxide dismutase（SOD）， malondialdehyde（MDA）， and reduced glutathione（GSH） in the liver. Real-time fluorescence quantitative polymerase chain reaction（Real-time PCR） was used to measure the mRNA expression levels of NLRP3， apoptosis-associated speck-like protein（ASC）， cysteinyl aspartate specific proteinase-1（Caspase-1）， Toll-like receptor 4（TLR4） in the aorta， and fatty acid synthase（FAS）， stearoyl-CoA desaturase 1（SCD1）， PPARα， and carnitine palmitoyltransferase 1A（CPT1A） in the liver. Immunohistochemistry was used to determine the protein expressions of NLRP3， Caspase-1， and ASC in the aorta， and Western blot was used to measure the protein expressions of AMPK， p-AMPK， sterol regulatory element binding protein-1c（SREBP-1c）， CPT1A， and FAS in the liver. ResultsCompared with the normal group， the model group showed a significant increase in lipid plaque deposition in the aorta and lipid accumulation in the liver， the levels of TC， TG， LDL-C， AST， ALT， IL-1β， IL-18 and CRP in the serum were significantly increased（P<0.01）， and the mRNA and protein expressions of aortic TLR4， NLRP3， Caspase-1 and ASC were significantly upregulated（P<0.01）. The levels of SOD and GSH in the liver were significantly reduced， while the level of MDA was significantly increased（P<0.01）. The mRNA expressions of FAS and SCD1 in the liver were significantly downregulated， while the mRNA expressions of PPARα and CPT1A were significantly upregulated. The protein expressions of p-AMPK/AMPK and CPT1A in the liver were significantly reduced， while the expressions of SREBP-1c and FAS proteins were significantly increased（P<0.01）. Compared with the model group， the low- and high-dose HCT groups showed significant improvements in aortic plaques and hepatic lipid deposition. The levels of TC， LDL-C， AST， IL-1β and IL-18 in the serum of the low-dose HCT group， as well as TC， TG， LDL-C， AST， ALT， IL-1β， IL-18 and CRP in the serum of the high-dose HCT group， were significantly reduced（P<0.01）. The mRNA expressions of TLR4， NLRP3 and Caspase-1 in the aorta of the low-dose HCT group， as well as TLR4， NLRP3， Caspase-1 and ASC in the aorta of the high-dose HCT group， were significantly downregulated（P<0.01）. The protein expressions of Caspase-1 and ASC in the aorta of the low-dose HCT group， as well as NLRP3， Caspase-1 and ASC in the high-dose HCT group， were significantly downregulated（P<0.01）. The levels of SOD and GSH in the liver of the low- and high-dose HCT groups were significantly increased， while the level of MDA in the high-dose HCT group was significantly decreased（P<0.05， P<0.01）. In the HCT-treated group， the mRNA expressions of FAS and SCD1 in the liver were significantly upregulated， while the mRNA expressions of PPARα and CPT1A were significantly downregulated， the protein expressions of p-AMPK/AMPK and CPT1A in the liver were significantly increased， while the protein expressions of SREBP-1c and FAS were significantly decreased（P<0.05， P<0.01）. ConclusionHCT can improve lipid metabolism by activating the AMPK/PPARα pathway and inhibit NLRP3 inflammasome-mediated inflammatory responses， thereby reducing hepatic lipid deposition and AS plaque formation.

To investigate the efficacy and safety of glucocorticoids combined with cyclophosphamide (CTX) and rituximab (RTX) in elderly patients with anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis with renal involvement.

ObjectiveThis study aims to investigate the effect of Dictamni Cortex on intestinal barrier damage in rats and its mechanism by untargeted metabolomics and targeted metabolomics for short-chain fatty acids （SCFAs）. MethodsRats were randomly divided into a control group， a high-dose group of Dictamni Cortex （8.1 g·kg^-1）， a medium-dose group （2.7 g·kg^-1）， and a low-dose group （0.9 g·kg^-1）. Except for the control group， the other groups were administered different doses of Dictamni Cortex by gavage for eight consecutive weeks. Hematoxylin-eosin （HE） staining was used to observe the pathological changes in the ileal tissue. Enzyme-linked immunosorbent assay （ELISA） was employed to detect the level of cytokines， including tumor necrosis factor-α （TNF-α）， interleukin-6 （IL-6）， and interleukin-1β （IL-1β）， in the ileal tissue of rats. Quantitative real-time fluorescence polymerase chain reaction （Real-time PCR） technology was used to detect the expression level of tight junction proteins， including zonula occludens-1 （ZO-1）， Occludin， and Claudin-1 mRNAs， in the ileal tissue of rats to preliminarily explore the effects of Dictamni Cortex on intestinal damage. The dose with the most significant toxic phenotype was selected to further reveal the effects of Dictamni Cortex on the metabolic profile of ileal tissue in rats by non-targeted metabolomics combined with targeted metabolomics for SCFAs. ResultsCompared with the control group， all doses of Dictamni Cortex induced varying degrees of pathological damage in the ileum， increased TNF-α （P<0.01）， IL-6 （P<0.01）， and IL-1β （P<0.01） levels in the ileal tissue， and decreased the expression level of ZO-1 （P<0.05， P<0.01）， Occludin （P<0.01）， and Claudin-1 （P<0.05） in the ileal tissue， with the high-dose group showing the most significant toxic phenotypes. The damage mechanisms of the high-dose group of Dictamni Cortex on the ileal tissue were further explored by integrating non-targeted metabolomics and targeted metabolomics for SCFAs. The non-targeted metabolomics results showed that 21 differential metabolites were identified in the control group and the high-dose group. Compared with that in the control group， after Dictamni Cortex intervention， the level of 14 metabolites was significantly increased （P<0.05， P<0.01）， and the level of seven metabolites was significantly decreased （P<0.05， P<0.01） in the ileal contents. These metabolites collectively acted on 10 related metabolic pathways， including glycerophospholipids and primary bile acid biosynthesis. The quantitative data of targeted metabolomics for SCFAs showed that Dictamni Cortex intervention disrupted the level of propionic acid， butyric acid， acetic acid， caproic acid， isobutyric acid， isovaleric acid， valeric acid， and isocaproic acid in the ileal contents of rats. Compared with those in the control group， the level of isobutyric acid， isovaleric acid， and valeric acid were significantly increased， while the level of propionic acid， butyric acid， and acetic acid were significantly decreased in the ileal contents of rats after Dictamni Cortex intervention （P<0.05， P<0.01）. ConclusionDictamni Cortex can induce intestinal damage by regulating glycerophospholipid metabolism， primary bile acid biosynthesis， and metabolic pathways for SCFAs.

ObjectiveTo explore the mechanism of action of Wuwei Shenqintang in improving pulmonary fibrosis by using ultra-performance liquid chromatography-quadrupole-time-of-flight mass spectrometry （UPLC-Q-TOF-MS） for metabolomic analysis of lung tissue and feces. MethodsA rat model with pulmonary fibrosis was established by intratracheal injection of 5 mg·kg^-1 bleomycin. The successfully modeled rats were randomly divided into a blank group， a model group， a prednisone （3.15 mg·kg^-1） group， and low-dose， medium-dose， and high-dose groups of Wuwei Shenqintang （4.586， 9.172， 18.344 g·kg^-1）. The rats were given intragastric administration once a day for 28 consecutive days. Hematoxylin-eosin （HE） staining was used to measure the pathological changes in lung and colon tissue， and Masson staining was used to detect the degree of pulmonary fibrosis. Enzyme-linked immunosorbent assay （ELISA） was used to detect the expression of interleukin-1β （IL-1β）， IL-6， IL-8， tumor necrosis factor-α （TNF-α）， and secretory immunoglobulin A （SIgA） in bronchoalveolar lavage fluid and intestinal mucus. Immunohistochemistry and reverse transcription quantitative polymerase chain reaction （Real-time PCR） were used to detect the expression of type Ⅰ collagen （Col-Ⅰ）， fibronectin （FN）， and alpha smooth muscle actin （α-SMA） in lung tissue. UPLC-Q-TOF-MS was used to study the changes in the metabolic network of lung tissue and feces in rats with pulmonary fibrosis treated with Wuwei Shenqintang， screen potential biomarkers for the treatment of pulmonary fibrosis by Wuwei Shenqintang， and perform pathway enrichment analysis. ResultsCompared with the blank group， the model group showed extensive inflammatory cell infiltration and continuous fibrotic lesions in lung tissue， colonic mucosal damage， and connective tissue hyperplasia. The expression of IL-6， IL-8， IL-1β， TNF-α， and SIgA in bronchoalveolar lavage fluid and intestinal mucus was significantly increased （P<0.01）. The expression of Col-Ⅰ， FN， and α-SMA proteins and mRNAs in lung tissue was significantly upregulated （P<0.01）. Compared with the model group， the groups of Wuwei Shenqintang exhibited significantly reduced inflammatory infiltration and blue collagen deposition in lung tissue， alleviated colonic damage， decreased expression of IL-6， IL-8， IL-1β， TNF-α， and SIgA in bronchoalveolar lavage fluid and intestinal mucus （P<0.01）， and reduced average absorbance values and mRNA expression of Col-Ⅰ， FN， and α-SMA in lung tissue （P<0.05， P<0.01）， with the prednisone group and the medium-dose and high-dose groups of Wuwei Shenqintang showing the most significant effects. The metabolomics results for lung tissue showed that compared with the blank group， the model group had 19 significantly different compounds （P<0.05， P<0.01）. Wuwei Shenqintang could normalize 17 of these compounds compared with the model group （P<0.05， P<0.01）. Fecal metabolomics results showed that compared with those in the blank group， there were 42 compounds with significant differences in the model group （P<0.05， P<0.01）. Compared with the model control group， Wuwei Shenqintang could normalize 41 of these compounds （P<0.05， P<0.01）. The combined analysis results indicated that Wuwei Shenqintang might inhibit pulmonary fibrosis by regulating the biosynthesis of phenylalanine， tyrosine， and tryptophan as well as the retinol metabolism pathway. ConclusionWuwei Shenqintang can ameliorate pulmonary fibrosis， which may be related to the regulation of the "lung-intestine axis".

ObjectiveTo explore the mechanism of action of Wuwei Shenqintang in improving pulmonary fibrosis by using ultra-performance liquid chromatography-quadrupole-time-of-flight mass spectrometry （UPLC-Q-TOF-MS） for metabolomic analysis of lung tissue and feces. MethodsA rat model with pulmonary fibrosis was established by intratracheal injection of 5 mg·kg^-1 bleomycin. The successfully modeled rats were randomly divided into a blank group， a model group， a prednisone （3.15 mg·kg^-1） group， and low-dose， medium-dose， and high-dose groups of Wuwei Shenqintang （4.586， 9.172， 18.344 g·kg^-1）. The rats were given intragastric administration once a day for 28 consecutive days. Hematoxylin-eosin （HE） staining was used to measure the pathological changes in lung and colon tissue， and Masson staining was used to detect the degree of pulmonary fibrosis. Enzyme-linked immunosorbent assay （ELISA） was used to detect the expression of interleukin-1β （IL-1β）， IL-6， IL-8， tumor necrosis factor-α （TNF-α）， and secretory immunoglobulin A （SIgA） in bronchoalveolar lavage fluid and intestinal mucus. Immunohistochemistry and reverse transcription quantitative polymerase chain reaction （Real-time PCR） were used to detect the expression of type Ⅰ collagen （Col-Ⅰ）， fibronectin （FN）， and alpha smooth muscle actin （α-SMA） in lung tissue. UPLC-Q-TOF-MS was used to study the changes in the metabolic network of lung tissue and feces in rats with pulmonary fibrosis treated with Wuwei Shenqintang， screen potential biomarkers for the treatment of pulmonary fibrosis by Wuwei Shenqintang， and perform pathway enrichment analysis. ResultsCompared with the blank group， the model group showed extensive inflammatory cell infiltration and continuous fibrotic lesions in lung tissue， colonic mucosal damage， and connective tissue hyperplasia. The expression of IL-6， IL-8， IL-1β， TNF-α， and SIgA in bronchoalveolar lavage fluid and intestinal mucus was significantly increased （P<0.01）. The expression of Col-Ⅰ， FN， and α-SMA proteins and mRNAs in lung tissue was significantly upregulated （P<0.01）. Compared with the model group， the groups of Wuwei Shenqintang exhibited significantly reduced inflammatory infiltration and blue collagen deposition in lung tissue， alleviated colonic damage， decreased expression of IL-6， IL-8， IL-1β， TNF-α， and SIgA in bronchoalveolar lavage fluid and intestinal mucus （P<0.01）， and reduced average absorbance values and mRNA expression of Col-Ⅰ， FN， and α-SMA in lung tissue （P<0.05， P<0.01）， with the prednisone group and the medium-dose and high-dose groups of Wuwei Shenqintang showing the most significant effects. The metabolomics results for lung tissue showed that compared with the blank group， the model group had 19 significantly different compounds （P<0.05， P<0.01）. Wuwei Shenqintang could normalize 17 of these compounds compared with the model group （P<0.05， P<0.01）. Fecal metabolomics results showed that compared with those in the blank group， there were 42 compounds with significant differences in the model group （P<0.05， P<0.01）. Compared with the model control group， Wuwei Shenqintang could normalize 41 of these compounds （P<0.05， P<0.01）. The combined analysis results indicated that Wuwei Shenqintang might inhibit pulmonary fibrosis by regulating the biosynthesis of phenylalanine， tyrosine， and tryptophan as well as the retinol metabolism pathway. ConclusionWuwei Shenqintang can ameliorate pulmonary fibrosis， which may be related to the regulation of the "lung-intestine axis".

OBJECTIVE: To observe the effect of acupuncture at Jiaji (EX-B2) points on upper limb motor dysfunction in patients after stroke. METHODS: A total of 62 patients with upper limb motor dysfunction after stroke were randomly assigned to an observation group (n=31, 3 cases dropped out) and a control group (n=31, 2 cases dropped out). Both groups received routine medical treatment and rehabilitation training. The control group was treated with conventional acupuncture at the affected side's Jianyu (LI15), Quchi (LI11), Shousanli (LI10), Huantiao (GB30), Yanglingquan (GB34), and Zusanli (ST36) etc. On this basis, the observation group received additional acupuncture at the affected side's Jiaji points from C₄ to T₅. Treatment was administered once daily, five times a week, for four weeks. Motor evoked potential (MEP) latency and amplitude of the abductor pollicis brevis and abductor digiti minimi, Fugl-Meyer assessment for upper extremity (FMA-UE), and Wolf motor function test (WMFT) scores were compared before and after treatment in the two groups. RESULTS: After treatment, both groups showed increased MEP amplitudes and decreased latencies of the abductor pollicis brevis and abductor digiti minimi (P<0.05), as well as increased FMA-UE and WMFT scores (P<0.05); the observation group had greater MEP amplitudes, shorter latencies, and higher FMA-UE and WMFT scores compared to the control group (P<0.05). CONCLUSION Acupuncture at Jiaji (EX-B2) points could enhance the excitability of upper limb motor neural pathways in upper limb motor dysfunction after stroke patients, thereby promoting motor function recovery of the upper limb.
Humans ; Acupuncture Therapy ; Male ; Female ; Middle Aged ; Acupuncture Points ; Stroke/complications* ; Upper Extremity/physiopathology* ; Aged ; Adult ; Stroke Rehabilitation ; Treatment Outcome

Objective To explore and identify the nutritional/inflammatory indicator with the highest predictive potential for overall survival(OS)in postoperative tumor patients so as to provide guidance for postoperative rehabilitation of tumor patients.Methods Data from 3 191 surgical patients were collected,including 15 nutritional/inflammatory indicators.The maximum selection rank statistic method was used to calculate the optimal cut-off values for continuous indicators.The Kaplan-Meier method was used to assess OS,and Cox proportional hazards models were used to analyze the association between the aforementioned 15 indicators and survival.The predictive value of these 15 indicators was evaluated with receiver operating characteristic(ROC)curves and C-index.Results Multivariate analysis showed that all 15 indicators were significantly associated with poorer OS in surgical patients(P＜0.05 for all).Time-dependent area under the curve(AUC)and C-index analysis indicated that 3 indicators with the highest predictive potential in OS in postoperative tumor patients were the nutritional risk index(NRI)(C-index:0.597),C-reactive protein-to-albumin ratio(CAR)(C-index:0.587),and C-reactive protein-to-lymphocyte ratio(CLR)(C-index:0.587).The optimal cut-off value for NRI was determined to be 104.31(i.e.,NRI＜104.31 suggests malnutrition)with the maximum selection rank statistic method,the optimal cut-off value for CAR to be 0.05(i.e.,CAR≥0.05 suggests a strong inflammatory response,often accompanied by malnutrition),and the optimal cut-off value for CLR to be 1.18(i.e.,CLR≥1.18 suggests a strong inflammatory response).Subgroup analysis indicated that NRI,CAR,and CLR had good correlation with tumor staging,and there were significant differences between tumor node metastasis(TNM)Ⅲ/Ⅳ stage patients and TNM Ⅰ/Ⅱ stage patients when there was a strong inflammatory response or malnutrition.Conclusion In postoperative tumor patients,NRI,CLR,and CAR have high prognostic value.Combining these with the patient's clinical stage,it enables more precise guidance for clinical diagnosis and treatment strategies.

Objective To analyze the influencing factors of plastic bronchitis in children with Mycoplasma pneumoniae infection and put forward targeted prevention suggestions. Methods The clinical data of children with Mycoplasma pneumoniae infection who were admitted to Chengdu Third People's Hospital from September 2022 to February 2024 were retrospectively analyzed . According to whether plastic bronchitis occurred, they were divided into plastic group (n=118) and non-plastic group (n=184), and the differences between the two groups were compared and analyzed. Univariate and multivariate logistics regression analysis equations were used to analyze the independent influencing factors of plastic bronchitis in children with mycoplasma pneumoniae infection. Results Among the 302 children with Mycoplasma pneumoniae infection , 118 cases were diagnosed with plastic bronchitis. Analysis showed that the children’s age, duration of fever, hospital stay, pleural effusion rate, number of bronchoscopic lavage, allergy history, endoscopic mucosal erosion rate, WBC, NE%, LY%, CRP, LDH, PCT and D-D were the single factors influencing the occurrence of plastic bronchitis in children with mycoplasma pneumoniae infection. Binary logistics regression analysis revealed that age (OR=2.137, P=0.033, 95% CI: 1.132-16.603), allergy history （OR=3.028, P=0.014, 95% CI: 1.261-864), NE% (OR=2.395, P=0.031, 95% CI: 1.087-5.274), CRP (OR=3.864, P=0.004, 95% CI: 1.563-3.864), PCT (OR=4.125, P=0.001, 95% CI: 1.793-3.864), and D-D (OR=3.920, P=0.002, 95% CI: 1.632-3.864) were independent risk factors for plastic bronchitis in children with mycoplasma pneumoniae infection (P<0.05). Conclusion Age, allergy history, NE%, CRP, PCT and D-D are independent risk factors for plastic bronchitis in children with mycoplasma pneumoniae infection . It is necessary to take clinical intervention measures to reduce the occurrence risk.

Cemental tear is a rare and indetectable condition unless obvious clinical signs present with the involvement of surrounding periodontal and periapical tissues. Due to its clinical manifestations similar to common dental issues, such as vertical root fracture, primary endodontic diseases, and periodontal diseases, as well as the low awareness of cemental tear for clinicians, misdiagnosis often occurs. The critical principle for cemental tear treatment is to remove torn fragments, and overlooking fragments leads to futile therapy, which could deteriorate the conditions of the affected teeth. Therefore, accurate diagnosis and subsequent appropriate interventions are vital for managing cemental tear. Novel diagnostic tools, including cone-beam computed tomography (CBCT), microscopes, and enamel matrix derivatives, have improved early detection and management, enhancing tooth retention. The implementation of standardized diagnostic criteria and treatment protocols, combined with improved clinical awareness among dental professionals, serves to mitigate risks of diagnostic errors and suboptimal therapeutic interventions. This expert consensus reviewed the epidemiology, pathogenesis, potential predisposing factors, clinical manifestations, diagnosis, differential diagnosis, treatment, and prognosis of cemental tear, aiming to provide a clinical guideline and facilitate clinicians to have a better understanding of cemental tear.
Humans ; Dental Cementum/injuries* ; Consensus ; Diagnosis, Differential ; Cone-Beam Computed Tomography ; Tooth Fractures/therapy*

To develop a novel polyamino acid-based nanohydrogel drug delivery system for dexamethasone to enhance its delivery efficiency to the inner ear.