ObjectiveTo observe the effect and therapeutic effect of Kaixuan Jiedu core prescription （KXJD） on skin homing of Th17 cells in the mouse model of imiquimod （IMQ） combined with restraint stress-induced psoriasis-like skin damage， and to explore its potential mechanism from the perspective of neuro-immune axis. MethodsThirty male C57BL/6J mice were randomly allocated into five groups （n=6）： Control， model （IMQ）， restraint stress model （IMQ+RS）， KXJD， and methotrexate （MTX）. The mouse model of psoriasis-like skin damage was established by 5% IMQ combined with restraint stress. At the same time of modeling， each treatment group was treated with corresponding doses of drugs， and the control， IMQ， and IMQ+RS groups were treated with the same amount of normal saline by gavage once a day for 5 days. Hematoxylin-eosin （HE） staining was used to observe the pathological changes in the skin tissue and Baker scoring was performed. Serum levels of interleukin-1β （IL-1β） and angiopoietin-2 （Ang-2） were measured by enzyme-linked immunosorbent assay （ELISA）. The levels of matrix metalloproteinase-9 （MMP-9）， tissue inhibitor of metalloproteinase-1 （TIMP-1）， C-C motif chemokine ligand 20 （CCL20）， and C-C motif chemokine receptor 6 （CCR6） in the skin tissue were determined. Immunohistochemistry （IHC） was employed to determine the protein expression of cutaneous lymphocyte-associated antigen （CLA）， integrin α_E （CD103）， cytokeratin 10 （CK10）， and nuclear factor-kappa B （NF-κB） in the skin. Immunofluorescence double staining （DIF） was adopted to detect the expression and co-localization of vascular endothelial cadherin （VE-cadherin） and platelet-endothelial cell adhesion molecule （CD31）， CCR6， CD103， substance P （SP）， calcitonin gene-related peptide （CGRP）， and protein gene product 9.5 （PGP9.5） in the skin tissue. Real-time PCR was employed to quantify the mRNA levels of IL-10， IL-17A， and IL-23. ResultsCompared with the control group， the IMQ group and IMQ+RS group showed significant inflammatory cell infiltration， abnormal proliferation of epidermal cells， keratinization and other pathological changes in the skin tissue， and a significant increase in Baker score， elevated levels of IL-1β and Ang-2 in the serum and MMP-9， CCL20 and CCR6 in the skin lesions， upregulated expression of CLA， CD103， CK10， NF-κB， IL-17A mRNA， and IL-23 mRNA in the skin lesions， and downregulated expression of TIMP-1 and IL-10 mRNA. In addition， the fluorescence intensities of VE-cadherin and CD31 co-localization， CCR6 and CD103 co-localization， SP and PGP9.5 co-localization， and CGRP and PGP9.5 co-localization were increased （P<0.05）. Compared with the IMQ group， the above indicators in the IMQ+RS group were further aggravated. Compared with the IMQ group， the above indicators in the IMQ+RS group were further aggravated. Compared with the IMQ+RS group， KXJD and MTX significantly alleviated the pathological damage of skin lesions， significantly decreased the Baker score， lowered the levels of IL-1β and Ang-2 in the serum and MMP-9， CCL20 and CCR6 in skin lesions， downregulated the expression of CLA， CD103， CK10， NF-κB， IL-17A mRNA and IL-23 mRNA in skin lesions， and upregulated the expression of TIMP-1 and IL-10 mRNA. Furthermore， KXJD and MTX reduced the fluorescence intensities of VE-cadherin and CD31 co-localization， CCR6 and CD103 co-localization， CGRP and PGP9.5 co-localization， and SP and PGP9.5 co-localization （P<0.05）. ConclusionKXJD can significantly ameliorate the psoriasis-like skin damage induced by IMQ combined with restraint stress in mice by regulating the neural-immune axis and inhibiting the skin homing of Th17 cells.

ObjectiveTo investigate the ameliorative effect and potential mechanisms of Kaixuan Jiedu core prescription （KXJD） on imiquimod （IMQ）-combined restraint stress-induced psoriasis-like skin lesions in mice. MethodsA total of 36 C57BL/6J mice were randomly assigned to six groups （n=6 per group）： Normal group， restraint stress blank group， model group， restraint stress model group， KXJD group （30.42 g·kg^-1）， and methotrexate group （0.001 g·kg^-1）. Psoriasis-like lesions were induced by topical IMQ application combined with restraint stress. After 5 days of intervention， the severity of skin lesions was evaluated using the Psoriasis Area and Severity Index （PASI）. The following parameters were assessed： Hypothalamic-pituitary-adrenal （HPA） axis-related hormones， including adrenocorticotropic hormone （ACTH）， corticotropin-releasing hormone （CRH）， and corticosterone （CORT）， central neuronal markers， including neuronal nuclei antigen （NeuN）， microtubule-associated protein 2 （MAP2）， and beta Ⅲ-tubulin （β-Ⅲ tubulin）， microglial activation markers， including ionized calcium-binding adapter molecule-1 （Iba-1） and cluster of differentiation 11b （CD11b）， and skin nerve fiber markers， including protein gene product 9.5 （PGP9.5） and serotonin （5-HT）， as well as the expression levels of inflammatory cytokines tumor necrosis factor-alpha （TNF-α）， interleukin-6 （IL-6）， and interleukin-1 beta （IL-1β）. ResultsCompared with the normal group， both the model group and the restraint stress model group exhibited more severe psoriasis-like skin lesions， with significantly elevated serum levels of ACTH， CRH， and CORT （P<0.01）. The expression of glucocorticoid receptor （GR） and corticotropin-releasing hormone receptor 1 （CRHR1） in the skin was significantly downregulated. The expression of NeuN， MAP2， β-Ⅲ tubulin， Iba-1， and CD11b in the hypothalamus and hippocampus was significantly upregulated， suggesting abnormal changes in neuronal number or structure and aberrant activation of glial cells （P<0.05， P<0.01）. In addition， the expression of PGP9.5 and 5-HT in the skin， as well as the mRNA levels of TNF-α， IL-6， and IL-1β were all markedly elevated （P<0.05， P<0.01）. Compared with the model group， the restraint stress model group showed further exacerbation in most parameters. Compared with the restraint stress model group， the KXJD group exhibited significantly reduced PASI scores （P<0.01）， significantly decreased serum CRH， ACTH， and CORT levels （P<0.05， P<0.01）， upregulated skin GR and CRHR1 expression， inhibited abnormal neuronal changes and microglial activation in the hypothalamus and hippocampus， attenuated skin nerve fiber hyperplasia and amine signaling molecule release， and significantly reduced pro-inflammatory cytokine mRNA expression （P<0.05， P<0.01）. ConclusionKaixuan Jiedu Core prescription can effectively ameliorate IMQ combined with restraint stress-induced psoriasis-like skin lesions in mice by modulating HPA axis function， inhibiting central neuropathological changes， and attenuating skin nerve fiber hyperplasia， amine signaling molecule （5‑HT） release and local inflammatory responses.

ObjectiveTo investigate the ameliorative effects of Kaixuan Jiedu core prescription （KXJD） on skin lesions in psoriasis-like mouse models under cold environment exposure， and to analyze its influences on transient receptor potential （TRP） channels and related neuroimmune regulatory factors. MethodsThirty-six C57BL/6J mice were randomized into 6 groups， with 6 mice in each group. Two feeding conditions were set： Normal temperature and cold ［simulating a cold environment at （10±0.5） ℃， for 6 h daily］. Mice were induced to develop psoriasis-like lesions by applying imiquimod externally. The model mice were allocated into model groups and KXJD （30.42 g·kg^-1， continuous gavage for 5 days） groups. Normal mice were used as the control group. Specifically， mice were allocated into normal temperature， normal temperature model， normal temperature+KXJD， cold exposure control， cold exposure model， and cold exposure+KXJD groups. The pathological changes in skin lesions were observed by hematoxylin-eosin （HE） staining. The expression of cluster of differentiation （CD） 3⁺ T lymphocytes， CD11c⁺ dendritic cells （DCs）， phosphorylated extracellular signal-regulated kinase （p-ERK）， and substance P （SP） were detected by immunofluorescence assay. The protein level of transient receptor potential cation channel subfamily M member 8 （TRPM8） in the skin tissue was determined by Western blot. The expression of TRPM8， transient receptor potential cation channel subfamily V member 1 （TRPV1）， transient receptor potential cation channel subfamily A member 1 （TRPA1）， and transient receptor potential cation channel subfamily V member 2 （TRPV2） at the protein and mRNA levels was determined by immunohistochemistry and Real-time PCR， respectively. The levels of calcitonin gene-related peptide （CGRP） and neuropeptide Y （NPY） in the serum were analyzed by enzyme-linked immunosorbent assay （ELISA）. The enrichment analysis of differentially expressed genes （DEGs） and TRP pathway network construction were conducted based on the GEO database. The co-expression of TRPM8 and CGRP in the skin lesions was verified by immunofluorescence double labeling. ResultsBoth the normal temperature and cold exposure model groups showed typical psoriasis-like skin lesions. Compared with the normal temperature and cold exposure control groups， the model groups had excessive epidermal keratinization， thickened spinous layer， and inflammatory infiltration in the dermis， with increased pathological scores （P<0.05）， increased infiltration of CD3⁺ and CD11c⁺ cells and expression of p-ERK and SP， upregulated mRNA levels of TRPM8， TRPA1， and TRPV2， downregulated mRNA level of TRPV1 （P<0.05）， and reduced content of CGRP and increased content of NPY in the serum. Compared with the normal temperature and cold exposure model groups， KXJD reduced the pathological manifestations and pathological scores of psoriasis-like skin lesions （P<0.05）， and inhibited the infiltration of CD3⁺ and CD11c⁺ cells and the expression of p-ERK and SP. Gene enrichment analysis suggested that the DEGs of psoriasis were significantly enriched in the interleukin （IL）-17 signaling pathway and TRP channel inflammatory regulation. Compared with the normal temperature and cold exposure model groups， KXJD reversed the abnormal mRNA levels of genes related to the TRP channel subfamilies （P<0.05）， increased the CGRP level， and decreased the NPY level. Immunofluorescence double labeling further confirmed that compared with the model groups， KXJD down-regulated the co-expression of TRPM8 and CGRP in the skin lesions. ConclusionKXJD may ameliorate psoriasis-like skin lesions by downregulating the overexpressed cold-sensitive receptor TRPM8 in skin lesions and correcting the disorder of neuropeptide （such as SP and CGRP） release mediated by it， thereby inhibiting the IL-23/helper T cell 17 （Th17） core inflammatory pathway， suppressing the infiltration of inflammatory cells and the activation of the ERK signaling pathway， and regulating the Xuanfu （sweat pore）-TRPM8-neuroimmune response axis.

ObjectiveTo observe the influence and therapeutic effect of quercetin on cuproptosis in rheumatoid arthritis rats and to explore its possible mechanism based on the solute carrier family 31 member 1 （SLC31A1）/ferredoxin 1 （FDX1） pathway. MethodsSixty male SD rats were divided into six groups： A control group， a model group， high- and low-dose quercetin groups （150 and 50 mg·kg^-1）， a cuproptosis inhibitor （tetrathiomolybdate， TTM） group （10 mg·kg^-1）， and a methotrexate group （2 mg·kg^-1）， 10 rats in each group. Except for the control group， the model of rheumatoid arthritis （CIA） rats was established by type Ⅱ collagen induction method. After successful modeling， each drug group was intervened according to the corresponding dose of drugs， and the control group and the model group were given the same amount of normal saline by gavage， once a day， which lasted for 4 weeks. The swelling degree of rats' feet was observed， and the clinical arthritis scores were determined. The levels of serum rheumatoid factor （RF）， matrix metalloproteinase-3 （MMP-3）， tumor necrosis factor-α （TNF-α）， interleukin-1β （IL-1β）， interleukin-10 （IL-10）， and ceruloplasmin （Cp） were detected by enzyme-linked immunosorbent assay （ELISA）. The content of copper ion （Cu）， malondialdehyde （MDA）， superoxide dismutase （SOD）， and glutathione （GSH） in joint tissue was detected. Hematoxylin-eosin （HE） staining was used to observe the pathological changes of joint tissue. The levels of reactive oxygen species （ROS） and dihydrolipoic acid transacetylase （DLAT） were detected by immunofluorescence （IF）. The protein and mRNA expression of SLC31A1， FDX1， lipoic acid synthase （LIAS）， heat shock protein 70 （HSP70）， pyruvate dehydrogenase E1 subunit β （PDHB）， and copper transporting P-type ATPase β （ATP7B） was detected by immunohistochemistry （IHC） and real-time fluorescence quantitative polymerase chain reaction （Real-time PCR）. ResultsCompared to the control group， the model group exhibited joint swelling and deformity， significantly increased clinical arthritis scores， obvious bone destruction， synovial hyperplasia， and inflammatory cell infiltration in joint tissue. In addition， the serum levels of RF， MMP-3， TNF-α， IL-1β， and Cp showed significant elevation， while the level of IL-10 was significantly reduced. The levels of Cu， MDA， ROS， and DLAT in joint tissue were markedly increased， whereas SOD and GSH content was significantly decreased. The protein and mRNA expression of SLC31A1 and HSP70 was significantly up-regulated， while the protein and mRNA expression of FDX1， LIAS， PDHB， and ATP7B was significantly down-regulated （P<0.01）. Compared to the model group， each treatment group exhibited varying degrees of improvement in joint swelling and deformation as well as clinical arthritis scores in rats. Additionally， there was a reduction in joint bone destruction， inflammatory cell infiltration， and synovial hyperplasia in rats. Furthermore， the serum levels of RF， MMP-3， TNF-α， IL-1β， and Cp significantly decreased， while the level of IL-10 increased significantly. In joint tissue， the levels of Cu， MDA， ROS， and DLAT showed significant decreases， while SOD and GSH content exhibited significant increases. The protein and mRNA expression of SLC31A1 and HSP70 was down-regulated， while the protein and mRNA expression of FDX1， LIAS， PDHB， and ATP7B was up-regulated （P<0.05）. ConclusionQuercetin effectively reduces synovial hyperplasia and inflammatory infiltration in rats with rheumatoid arthritis， thereby alleviating pathological damage to joint tissue. This effect may be attributed to the blockade of the SLC31A1/FDX1 signaling pathway activation and inhibition of excessive cuproptosis.

ObjectiveTo investigate the effect and therapeutic role of quercetin on ferroptosis in lipopolysaccharide （LPS）-induced acute kidney injury （AKI） rats based on the Kelch-like epichlorohydrin-related protein-1 （Keap1）/nuclear factor erythroid-2-related factor 2 （Nrf2）/antioxidant response element （ARE） pathway. MethodsSixty male SD rats were randomly divided into normal group， model group， quercetin high-dose （100 mg·kg^-1） and low-dose （10 mg·kg^-1） groups， ferroptosis inhibitor Ferrostatin 1 （FER1） group （5 mg·kg^-1）， and quercetin high-dose + Nrf2 inhibitor group （ML385， 30 mg·kg^-1）. Except for the normal group， the AKI rat model was established in each group by intraperitoneal injection of LPS （10 mg·kg^-1）. Following successful modeling， each treatment group received the corresponding dose of drug intervention， while the normal and model groups were administered an equal volume of normal saline. The intervention lasted for 3 weeks. Serum creatinine （SCr） and blood urea nitrogen （BUN） levels were measured biochemically to assess renal function. Serum tumor necrosis factor-α （TNF-α） and interleukin （IL）-1β and IL-6 levels were detected by enzyme-linked immunosorbent assay （ELISA）. The levels of Fe²⁺， malondialdehyde （MDA）， superoxide dismutase （SOD）， and glutathione （GSH） in renal tissue were detected. Hematoxylin-eosin （HE）， Masson， and periodic acid-Schiff （PAS） staining were employed to observe pathological morphological changes in renal tissue. Mitochondrial morphological changes were observed using transmission electron microscopy. Reactive oxygen species （ROS） levels in renal tissue were detected by immunofluorescence （IF）. The protein and mRNA expression levels of Keap1， Nrf2， heme oxygenase-1 （HO-1）， glutathione peroxidase 4 （GPX4）， transferrin receptor （TFR1）， and kidney injury molecule-1 （KIM-1） were assessed by immunohistochemistry （IHC） and real-time fluorescence quantitative polymerase chain reaction （Real-time PCR）. ResultsCompared with the normal group， the model group exhibited significantly elevated serum levels of SCr， BUN， TNF-α， IL-1β， IL-6， Fe²⁺ and MDA in renal tissue， and significantly reduced SOD and GSH levels （P<0.01）. Pathological injury in renal tissue was severe， with evident mitochondrial damage characteristic of ferroptosis and a reduced mitochondrial count. ROS levels in renal tissue were significantly increased. The protein and mRNA expression levels of Keap1， TFR1， and KIM-1 in renal tissue were significantly elevated， while those of Nrf2， HO-1， and GPX4 were significantly decreased （P<0.01）. Compared with the model group， serum levels of SCr， BUN， TNF-α， IL-1β， IL-6， Fe²⁺ and MDA in renal tissue in the quercetin dosage groups and FER1 group showed varying degrees of reduction， while SOD and GSH levels were significantly increased （P<0.05）. Pathological injury in renal tissue was markedly alleviated， mitochondrial damage improved， and mitochondrial counts increased. ROS levels in renal tissue were significantly reduced. The protein and mRNA levels of Keap1， TFR1， and KIM-1 in renal tissue were significantly decreased， while those of Nrf2， HO-1， and GPX4 were significantly increased， with the most notable improvement in the high-dose quercetin group （P<0.05）. In comparison to the high-dose quercetin group， the ML385 group significantly weakened the protective effect of quercetin on AKI rats （P<0.05）. ConclusionQuercetin effectively inhibits ferroptosis， improves renal tissue injury， and repairs renal function in AKI rats， and its mechanism may be related to the activation of the Keap1/Nrf2/ARE pathway.

ObjectiveTo use bioinformatics technology to screen the molecular patterns and diagnostic biomarkers of ferroptosis closely related to psoriasis， observe the therapeutic effect of Kaixuan Jiedu core prescription on psoriasis and explore its potential mechanism through animal experiments. MethodsPsoriasis microarray data from GEO were analyzed to identify differentially expressed genes （DEGs）. Intersection with a ferroptosis gene set yielded psoriasis ferroptosis-related genes （FRGs）， which underwent correlation， consensus clustering， enrichment， and immune infiltration analyses. Core diagnostic FRGs （Hub-FRGs） were identified using random forest （RF）， support vector machine （SVM）， LASSO regression， Nomogram， and ROC analyses. In vivo， imiquimod （5% cream） induced psoriasis in mice （except controls）. Drug treatment groups received respective doses， while control and model groups received saline via daily gavage for 7 days. Back skin changes were recorded and PASI scored. Hematoxylin-eosin （HE） staining assessed histopathology. The levels of ferrous ion （Fe²⁺）， malondialdehyde （MDA）， 4-hydroxynonenal （4-HNE） and free fatty acid （FFA） in skin tissue were detected. The level of reactive oxygen species （ROS） in skin tissue was detected by immunofluorescence. Immunohistochemistry was used to detect the expression of ChaC glutathione-specific γ-glutamyl transferase 1 （CHAC1）， arachidonic acid 12-lipoxygenase β （ALOX12B）， trimotif protein 21 （TRIM21）， proliferation marker （Ki67） and nuclear transcription factor-κB （NF-κB） protein. ResultsAnalysis of GSE30999 identified 2 100 DEGs and 24 FRGs. Gene Ontology （GO） and Kyoto Encyclopedia of Genes and Genomes （KEGG） enrichment revealed 1 000 biological functions and 75 pathways. After cluster analysis， combined with three machine learning algorithms， Nomogram and ROC curve analysis， the core Hub-FRGs （CHAC1， ALOX12 B， TRIM21） were obtained. Immunoinfiltration showed inactive memory CD4⁺T cells and activated dendritic cells abundance significantly correlated with Hub-FRGs. In vivo， model group vs. control showed significantly increased PASI/Baker scores （P<0.05）， epidermal hyperkeratosis， inflammatory infiltration， and elevated levels of Fe²⁺， MDA， 4-HNE， FFA， ROS， CHAC1， ALOX12B， TRIM21， Ki67， and NF-κB （P<0.05）. Drug groups vs. model group exhibited significantly reduced scores （P<0.05）， alleviated skin lesions， and decreased levels of Fe²⁺， MDA， 4-HNE， FFA， ROS， Hub-FRGs， Ki67， and NF-κB （P<0.05）. ConclusionKaixuan Jiedu core prescription can significantly improve the skin pathological injury of psoriasis mice， showing good therapeutic and repair effects， and its mechanism may be related to regulating the expression of ferroptosis genes CHAC1， ALOX12B and TRIM21， which are closely related to the pathogenesis of psoriasis.

ObjectiveTo use bioinformatics technology to screen the molecular patterns and diagnostic biomarkers of ferroptosis closely related to psoriasis， observe the therapeutic effect of Kaixuan Jiedu core prescription on psoriasis and explore its potential mechanism through animal experiments. MethodsPsoriasis microarray data from GEO were analyzed to identify differentially expressed genes （DEGs）. Intersection with a ferroptosis gene set yielded psoriasis ferroptosis-related genes （FRGs）， which underwent correlation， consensus clustering， enrichment， and immune infiltration analyses. Core diagnostic FRGs （Hub-FRGs） were identified using random forest （RF）， support vector machine （SVM）， LASSO regression， Nomogram， and ROC analyses. In vivo， imiquimod （5% cream） induced psoriasis in mice （except controls）. Drug treatment groups received respective doses， while control and model groups received saline via daily gavage for 7 days. Back skin changes were recorded and PASI scored. Hematoxylin-eosin （HE） staining assessed histopathology. The levels of ferrous ion （Fe²⁺）， malondialdehyde （MDA）， 4-hydroxynonenal （4-HNE） and free fatty acid （FFA） in skin tissue were detected. The level of reactive oxygen species （ROS） in skin tissue was detected by immunofluorescence. Immunohistochemistry was used to detect the expression of ChaC glutathione-specific γ-glutamyl transferase 1 （CHAC1）， arachidonic acid 12-lipoxygenase β （ALOX12B）， trimotif protein 21 （TRIM21）， proliferation marker （Ki67） and nuclear transcription factor-κB （NF-κB） protein. ResultsAnalysis of GSE30999 identified 2 100 DEGs and 24 FRGs. Gene Ontology （GO） and Kyoto Encyclopedia of Genes and Genomes （KEGG） enrichment revealed 1 000 biological functions and 75 pathways. After cluster analysis， combined with three machine learning algorithms， Nomogram and ROC curve analysis， the core Hub-FRGs （CHAC1， ALOX12 B， TRIM21） were obtained. Immunoinfiltration showed inactive memory CD4⁺T cells and activated dendritic cells abundance significantly correlated with Hub-FRGs. In vivo， model group vs. control showed significantly increased PASI/Baker scores （P<0.05）， epidermal hyperkeratosis， inflammatory infiltration， and elevated levels of Fe²⁺， MDA， 4-HNE， FFA， ROS， CHAC1， ALOX12B， TRIM21， Ki67， and NF-κB （P<0.05）. Drug groups vs. model group exhibited significantly reduced scores （P<0.05）， alleviated skin lesions， and decreased levels of Fe²⁺， MDA， 4-HNE， FFA， ROS， Hub-FRGs， Ki67， and NF-κB （P<0.05）. ConclusionKaixuan Jiedu core prescription can significantly improve the skin pathological injury of psoriasis mice， showing good therapeutic and repair effects， and its mechanism may be related to regulating the expression of ferroptosis genes CHAC1， ALOX12B and TRIM21， which are closely related to the pathogenesis of psoriasis.

Objective:To explore the risk factors for different severities of epiphyseal injury caused by distal tibial fractures in adolescents.Methods:A retrospective analysis was conducted on 195 children with distal tibial fractures accompanied by epiphyseal injuries who were admitted to the Honghui Hospital Affiliated to Xi'an Jiaotong University from January 2018 to December 2023. Among them, there were 132 males and 63 females; the age was 11.7±2.1 years (range, 5-15 years). Among them, 91 cases were on the left side and 104 cases were on the right side. Salter-Harris classification of epiphyseal injuries: there were 42 cases of type I, 90 cases of type II, 34 cases of type III, 26 cases of type IV, and 3 cases of type V. Causes of injury: 37 cases were sports injuries, 29 cases were traffic accident injuries, 120 cases were fall injuries, and 9 cases were fall from height injuries. Dias-Tachdjian classification of injury mechanisms: there were 65 cases of supination-adduction type, 59 cases of supination-plantar flexion type, 35 cases of supination-external rotation type, and 36 cases of pronation-abduction-external rotation type. Among them, 72 cases were complicated with fibular fractures, and 56 cases were accompanied by periosteum incarceration. The age, gender, side of injury, body mass index, cause of injury, presence or absence of fibular fracture, and injury mechanism of children with each type of Salter-Harris injury were compared. The indicators with statistically significant differences were included in the multiple logistic regression analysis to determine the independent risk factors for each type of Salter-Harris injury.Results:The ages of patients with type I-IV were 10.70±2.77, 12.18±1.70, 11.32±2.08, 12.35±1.19, and 11.67±2.08 years old respectively, and the difference was statistically significant ( F=4.794, P=0.001). The body mass indexes were 11.90±3.84, 21.30±4.48, 21.41±4.08, 22.42±3.74, and 24.32±4.82 kg/m 2 respectively, and the difference was statistically significant ( F=1.914, P=0.009). The numbers of cases of sports injuries/traffic accident injuries/fall injuries/fall-from-height injuries were 6/7/23/6, 17/12/59/2, 6/5/22/1, 7/4/15/0, and 1/1/1/0 respectively, and the difference was statistically significant ( P=0.032). The numbers of cases of supination-adduction/pronation-abduction-external rotation/supination-plantar flexion/supination-external rotation were 21/6/9/6, 21/16/37/16, 19/6/8/1, 4/7/4/11, and 0/1/1/1 respectively, and the difference was statistically significant ( P=0.001). The numbers of cases of periosteum incarceration (none/yes) were 32/10, 54/36, 27/7, 25/1, and 1/2 respectively, and the difference was statistically significant (χ 2=17.156, P=0.002). There was no statistically significant difference in gender, side of injury, and presence or absence of fibular fracture among patients with each type of epiphyseal injury ( P>0.05). Age, body mass index, cause of injury, injury mechanism, and periosteum incarceration were included in the multiple logistic regression analysis. The results showed that age [ OR=1.337, 95% CI (1.097, 1.628), P=0.004], the supination varus type of the injury mechanism [ OR=0.257, 95% CI (0.075, 1.013), P=0.015] in the Salter-Harris type II, and the supination plantar flexion type of the injury mechanism [ OR=0.154, 95% CI (0.027, 0.872), P=0.034] in the Salter-Harris type IV were independent risk factors for the severity of epiphyseal injury caused by distal tibial fractures in adolescents. Conclusion:The severity of distal tibial fractures accompanied by epiphyseal injuries in adolescents is related to multiple factors such as age, body mass index, cause of injury, injury mechanism, and periosteum incarceration. For every one-year increase in age, the risk of epiphyseal injury in children with Salter-Harris type II is 1.337 times higher than that in those with type I. The type I epiphyseal injury caused by supination varus injury is 3.891 times that of type II injury, and the type I epiphyseal injury caused by supination plantar flexion injury is 6.493 times that of type IV injury.

Objective:To explore the risk factors for different severities of epiphyseal injury caused by distal tibial fractures in adolescents.Methods:A retrospective analysis was conducted on 195 children with distal tibial fractures accompanied by epiphyseal injuries who were admitted to the Honghui Hospital Affiliated to Xi'an Jiaotong University from January 2018 to December 2023. Among them, there were 132 males and 63 females; the age was 11.7±2.1 years (range, 5-15 years). Among them, 91 cases were on the left side and 104 cases were on the right side. Salter-Harris classification of epiphyseal injuries: there were 42 cases of type I, 90 cases of type II, 34 cases of type III, 26 cases of type IV, and 3 cases of type V. Causes of injury: 37 cases were sports injuries, 29 cases were traffic accident injuries, 120 cases were fall injuries, and 9 cases were fall from height injuries. Dias-Tachdjian classification of injury mechanisms: there were 65 cases of supination-adduction type, 59 cases of supination-plantar flexion type, 35 cases of supination-external rotation type, and 36 cases of pronation-abduction-external rotation type. Among them, 72 cases were complicated with fibular fractures, and 56 cases were accompanied by periosteum incarceration. The age, gender, side of injury, body mass index, cause of injury, presence or absence of fibular fracture, and injury mechanism of children with each type of Salter-Harris injury were compared. The indicators with statistically significant differences were included in the multiple logistic regression analysis to determine the independent risk factors for each type of Salter-Harris injury.Results:The ages of patients with type I-IV were 10.70±2.77, 12.18±1.70, 11.32±2.08, 12.35±1.19, and 11.67±2.08 years old respectively, and the difference was statistically significant ( F=4.794, P=0.001). The body mass indexes were 11.90±3.84, 21.30±4.48, 21.41±4.08, 22.42±3.74, and 24.32±4.82 kg/m 2 respectively, and the difference was statistically significant ( F=1.914, P=0.009). The numbers of cases of sports injuries/traffic accident injuries/fall injuries/fall-from-height injuries were 6/7/23/6, 17/12/59/2, 6/5/22/1, 7/4/15/0, and 1/1/1/0 respectively, and the difference was statistically significant ( P=0.032). The numbers of cases of supination-adduction/pronation-abduction-external rotation/supination-plantar flexion/supination-external rotation were 21/6/9/6, 21/16/37/16, 19/6/8/1, 4/7/4/11, and 0/1/1/1 respectively, and the difference was statistically significant ( P=0.001). The numbers of cases of periosteum incarceration (none/yes) were 32/10, 54/36, 27/7, 25/1, and 1/2 respectively, and the difference was statistically significant (χ 2=17.156, P=0.002). There was no statistically significant difference in gender, side of injury, and presence or absence of fibular fracture among patients with each type of epiphyseal injury ( P>0.05). Age, body mass index, cause of injury, injury mechanism, and periosteum incarceration were included in the multiple logistic regression analysis. The results showed that age [ OR=1.337, 95% CI (1.097, 1.628), P=0.004], the supination varus type of the injury mechanism [ OR=0.257, 95% CI (0.075, 1.013), P=0.015] in the Salter-Harris type II, and the supination plantar flexion type of the injury mechanism [ OR=0.154, 95% CI (0.027, 0.872), P=0.034] in the Salter-Harris type IV were independent risk factors for the severity of epiphyseal injury caused by distal tibial fractures in adolescents. Conclusion:The severity of distal tibial fractures accompanied by epiphyseal injuries in adolescents is related to multiple factors such as age, body mass index, cause of injury, injury mechanism, and periosteum incarceration. For every one-year increase in age, the risk of epiphyseal injury in children with Salter-Harris type II is 1.337 times higher than that in those with type I. The type I epiphyseal injury caused by supination varus injury is 3.891 times that of type II injury, and the type I epiphyseal injury caused by supination plantar flexion injury is 6.493 times that of type IV injury.

[Objective]To study and summarize the experience of traditional Chinese medicine Master ZHOU Zhongying in treating systemic sclerosis from the pathogenesis of phlegm-stasis-heat junction,providing references for clinical practice.[Methods]Through the clinical learning,collation and analysis of Professor ZHOU's medical cases in the treatment of systemic sclerosis,the paper elaborated his clinical thinking and experience in the treatment of systemic sclerosis,which included etiology,pathogenesis,therapy and characteristic clinical medication,and verified it with medical records.[Results]Professor ZHOU thinks the key pathogenesis is phlegm-stasis-heat junction,pathological factors of systemic sclerosis mainly include phlegm,blood stasis and heat,which can depend on each other mutually throughout the course of disease.According to the progression of the disease and the evolution of pathological factors,treatment is primarily focused on phlegm-stasis-heat junction.Phlegm and blood stasis are interrelated,obstructing the circulation of Qi-blood so as to lead to pain and swelling,the treatment should be resolving phlegm,removing blood stasis and activating meridians;phlegm and heat are lingered each other,exacerbating the progression of the condition,it is appropriate to clear away phlegm and heat so that symptoms of skin redness and swelling can be relieved;blood and heat are interweaved together,which invade the skin and joints seriously,it is advisable to expel pathogenic factors by clearing away heat and resolving blood stagnation;Yin is damaged and Qi is consumed terribly,subsequently deficiency-heat is gradually emerging,the way to solve it is to supplement Qi,nourish Yin and strengthen the body resistance to eliminate pathogenic factors.The case was diagnosed as accumulation of phlegm stasis heat,blockage of wind-dampness and deficiency of Qi and Yin by Professor ZHOU,and treated with dissipating phlegm and removing blood stasis,clearing heat and unblocking collaterals,supplementing Qi and nourishing Yin,and the recipe Baiwei Decoction combined with Qinjiao Biejia Powder modified was used.[Conclusion]ZHOU Zhongying,the traditional Chinese medicine Master,who advocates attaching importance to the pathogenesis firstly in the process of syndrome differentiation,treating systemic sclerosis from the pathogenesis of phlegm-stasis-heat junction,which plays a unique role in relief of clinical symptoms,and his experiences are worthy of inheritance and promotion.