ObjectiveTo identify potential influencing factors of urate crystal deposition at ankle/foot in patients with hyperuricemia （HUA）， and to analyze the predictive value of inflammatory indicators for urate crystal deposition in patients with different traditional Chinese medicine （TCM） syndromes， so as to provide potential reference for clinical risk assessment and individualized TCM intervention. MethodsA retrospective study was carried out with the enrollment of 231 HUA patients from The Third Affiliated People's Hospital of Fujian University of Traditional Chinese Medicine between January 2021 and December 2024. The enrolled patients were further divided into a crystal deposition-positive group （143 cases） and a crystal deposition-negative group （88 cases） according to the results of dual-energy computed tomography （CT）. Sociodemographic data， living habits， serum uric acid levels， and inflammatory indicators of the enrolled patients were collcted， and TCM syndrome differentiation was performed. Furthermore， univariate analysis was used to compare inter-group differences in clinical characteristics. MMultivariate Logistic regression was applied to identify the influencing factors of urate crystal deposition. In addition， the receiver operating characteristic （ROC） curves were plotted to evaluate the predictive efficacy of inflammatory indicators for crystal deposition across different TCM syndromes. ResultsThere were statistically significant inter-group differences in the proportion of males， age， body mass index， proportion of mental labor， rate of low water intake， and rate of high-sugar beverage consumption （P<0.05），whereas no significant difference in low exercise intensity was found between the two groups. Furthermore， compared with the negative group， the positive group had higher serum uric acid level， neutrophil-to-lymphocyte ratio （NLR）， and platelet-to-lymphocyte ratio （PLR）， but lower systemic immune-inflammation index （SIRI） （P<0.05）. Regarding the distribution of TCM syndromes， the positive group was dominated by the dampness-heat accumulation syndrome （55/143，38.46%）， while the negative group was mainly characterized by the phlegm-turbidity obstruction syndrome （44/88，50.00%）. Multivariate Logistic regression analysis revealed that high-sugar beverage consumption， elevated NLR， and elevated PLR were risk factors for urate crystal deposition ［odd ratio （OR） = 8.002， 5.377， 1.034， respectively； 95% CI 1.572-40.732， 2.179-13.270， 1.013-1.054，all P<0.05］， while SIRI was a protective factor （OR = 0.869， 95% CI 0.778-0.971， P<0.05）. In the positive group， patients with the dampness-heat accumulation syndrome exhibited the highest NLR， while the lowest PLR and SIRI， showing statistically significant differences with those of other syndromes （all P<0.05）. In addition， ROC curve analysis indicated that for the dampness-heat accumulation syndrome， the combined "NLR + PLR" model had an area under the curve （AUC） of 0.901 （95% CI 0.850-0.951， P<0.01）， with a sensitivity of 89.1% and a specificity of 79.5%； for the blood stasis-heat obstruction syndrome， the combined "NLR + PLR" model had an AUC of 0.880 （95% CI 0.825-0.934， P<0.01）， with a sensitivity of 100.0% and a specificity of 67.3%； for the liver-kidney Yin-deficiency syndrome， the single PLR model had an AUC of 0.842 （95% CI 0.731-0.952， P<0.01）， with a sensitivity of 83.3% and a specificity of 84.0%. ConclusionUrate crystal deposition in HUA patients exhibits intimate associations with high-sugar beverage consumption as well as elevated NLR and PLR levels. Meanwhile， TCM syndrome differentiation has potential correlation with inflammatory characteristics. The inflammatory indicator-based prediction model constructed based on TCM syndromes exhibits good predictive value.

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 establish the mouse models of psoriasis-like lesions induced by continuous cold exposure or intermittent cold exposure combined with imiquimod （IMQ）， and to evaluate the interventional effects of Kaixuan Jiedu core prescription （KXJD） on the two models. MethodsMale C57BL/6J mice were selected and classified into two experimental batches. The first batch of 36 mice was randomized into a room temperature group， a continuous cold exposure （10 ℃/24 h） group， and an intermittent cold exposure （10 ℃/6 h） group. Each group was further divided into a normal subgroup and a model subgroup （topical application of IMQ to induce skin lesions）， with 6 mice in each subgroup， for modeling and evaluation. The second batch of 54 mice， with 6 in each group， were subjected to the same temperature grouping with an additional KXJD （30.42 g·kg^-1， continuous gavage for 5 days） group. Comprehensive evaluation of model characteristics and KXJD efficacy was conducted through Psoriasis Area and Severity Index （PASI） scoring， skin temperature measurement by infrared thermography， histopathological observation by hematoxylin-eosin （HE） staining， detection of vascular endothelial growth factor （VEGF） and platelet endothelial cell adhesion molecule 1 （CD31） by immunohistochemistry， detection of Claudin-1 and Occludin by immunofluorescence assay， determination of serum levels of tumor necrosis factor-α （TNF-α） and interleukin （IL）-10 by enzyme-linked immunosorbent assay （ELISA）， and quantification of mRNA levels of IL-17A， IL-23， IL-6， and chemokine ligand 20 （CCL20） in skin lesions by quantitative Real-time polymerase chain reaction （Real-time PCR）. ResultsModel mice in all temperature groups exhibited typical psoriasis-like skin lesions. Compared with the normal groups， the model groups showed increased PASI scores， decreased skin temperatures （P<0.05）， obvious epidermal thickening， parakeratosis， and dermal inflammatory cell infiltration， as well as elevated mRNA levels of IL-17A， IL-23， IL-6， and CCL20 （P<0.05）. Cold exposure further aggravated psoriasis. The total PASI score of the intermittent cold exposure model group was higher than that of the room temperature model group （P<0.05）. The serum IL-10 did not show a compensatory elevation， and the blood vessels presented a characteristic of elevated CD31 expression （P<0.05） without a synchronous increase in VEGF. The continuous cold exposure model group exhibited more significant dermal capillary tortuosity and dilation， with the highest mRNA levels of IL-17A， IL-23， IL-6， and CCL20 among all groups. Compared with the respective model groups， KXJD intervention alleviated skin lesions， reduced epidermal thickness and inflammatory cell infiltration， and increased skin temperature， with the temperature increase being particularly significant in the intermittent cold exposure+KXJD group （P<0.05）. Furthermore， KXJD down-regulated the expression of VEGF and CD31， restored the expression of Claudin-1 and Occludin， decreased the mRNA levels of IL-17A and IL-23 （P<0.05）， and reduced the serum TNF-α level. ConclusionThis study successfully established compound psoriasis-like mouse models induced by cold exposure combined with IMQ. It confirms that cold aggravates the severity of psoriasis by exacerbating the closure of Xuanfu （sweat pores）， microcirculation disorders， and immune imbalance. Moreover， different cold exposure patterns have distinct mechanism differences. Continuous cold exposure focuses on enhancing the inflammatory response via the IL-23/IL-17 axis and angiogenesis， simulating chronic aggravation under a long-term cold environment. Intermittent cold exposure tends to impair immune regulation and induce microvascular endothelial stress， corresponding to acute exacerbations caused by sudden temperature drops. KXJD can effectively alleviate psoriasis-like skin lesions under cold conditions by unblocking Xuanfu， regulating vasomotor function， and correcting abnormal immune-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 investigate the ameliorative effects and mechanisms of Kaixuan Jiedu core prescription （KXJD） on neuroimmunological inflammation in imiquimod （IMQ）-induced psoriasis-like mice. MethodsA total of 24 C57BL/6J mice were randomly divided into four groups （n=6）： Normal， model， KXJD， and tropomyosin receptor kinase A （TrkA） inhibitor GW441756 groups. The mice in the model， KXJD， and GW441756 groups were topically treated with 5% IMQ cream （62.5 mg·d^-1） on the back to induce psoriasis-like inflammation. The KXJD group received KXJD by gavage （30.42 g·kg^-1）， the GW441756 group received intraperitoneal injection of GW441756 （10 mg·kg^-1）， and the normal and model groups received an equal volume of normal saline by gavage， with continuous intervention for 5 days. The severity of skin lesions was evaluated using the psoriasis area and severity index （PASI）. Hematoxylin-eosin （HE） staining was used to measure epidermal thickness and observe pathological changes in the lesioned skin. Immunohistochemistry was employed to detect the expression of proliferating cell nuclear antigen （Ki67） and interleukin-17A （IL-17A） in the lesioned skin. Enzyme-linked immunosorbent assay （ELISA） was used to quantify the levels of interleukin-23 （IL-23） and calcitonin gene-related peptide （CGRP） in the lesioned tissues. Western blot was used to detect the expression of TrkA and phosphorylated TrkA （p-TrkA）. Immunofluorescence assay was performed to detect the expression of TrkA receptor， protein gene product 9.5 （PGP9.5）， cluster of differentiation 11c （CD11c）， and CGRP in the lesions. Flow cytometry was used to detect the activation of splenic dendritic cells （DCs）. ResultsCompared with the normal group， the model group exhibited typical psoriasis-like inflammation， characterized by erythema， infiltration and scaling， with histopathological findings of epidermal hyperkeratosis and acanthosis. The model group showed significantly increased expression of Ki67， IL-17A， IL-23 and p-TrkA （P<0.05， P<0.01）， increased fluorescence intensity of CD11c， and significantly decreased CGRP expression （P<0.05）. The splenic DC activation was significantly enhanced， as indicated by the increased mean fluorescence intensity （MFI） of CD86 （P<0.05）. Compared with the model group， both the KXJD and GW441756 groups showed amelioration of the psoriasis-like skin inflammation， with significantly down-regulated expression of IL-17A， IL-23 and p-TrkA （P<0.05， P<0.01）， significantly up-regulated expression of CGRP （P<0.01）， reduced CD11c⁺ DC infiltration， and restored splenic DC activation balance （down-regulated CD86 MFI and up-regulated CD80 and CD40 MFI）. Furthermore， the inhibitory effect of KXJD on Ki67 was significantly superior to that of the GW441756 group （P<0.01）. ConclusionKXJD may alleviate IMQ-induced psoriasis-like inflammation in mice by targeting and inhibiting TrkA receptor phosphorylation， regulating CGRP expression in the lesions， and ameliorating aberrant activation of dendritic cells， while also significantly inhibiting keratinocyte proliferation.

ObjectiveTo investigate the effects and molecular mechanisms of Kaixuan Jiedu core prescription （KXJD） on neuroinflammation and immuno-inflammation in the mouse model of imiquimod （IMQ）-induced psoriasis-like skin lesions by regulating the nerve growth factor （NGF）-tropomyosin receptor kinase A （TrkA）/transient receptor potential vanilloid 1 （TRPV1）-protease-activated receptor-2 （PAR-2） signaling pathway. MethodsA psoriasis-like skin lesion model was established in male C57BL/6J mice with IMQ. A total of 24 mice were randomized into four groups （n=6 per group）： Blank control， model， methotrexate （MTX， 1 mg·kg^-1）， and KXJD （30.42 g·kg^-1）. Immunohistochemistry was employed to detect the expression of cluster of differentiation 3 （CD3）， EGF-like module-containing mucin-like hormone receptor-like 1 （F4/80）， lymphocyte antigen 6 complex locus G （Ly-6G）， substance P （SP）， calcitonin gene-related peptide （CGRP）， NGF， phosphorylated TrkA （p-TrkA）， phosphorylated TRPV1 （p-TRPV1）， and PAR-2 in skin lesions. Serum levels of interleukin-17A （IL-17A） and interleukin-23 （IL-23） were measured by enzyme-linked immunosorbent assay （ELISA）. Immunofluorescence assay and Western blot were employed to determine the expression of phosphorylated p38 mitogen-activated protein kinase （p-p38 MAPK） and phosphorylated nuclear factor-κB p65 （p-NF-κB p65）. Reverse transcription quantitative polymerase chain reaction （Real-time PCR） was used to measure the mRNA levels of interleukin-1β （IL-1β）， tumor necrosis factor （TNF）， interleukin-6 （IL-6）， and C-X-C motif chemokine ligand 1 （CXCL1） in skin lesions. Correlation analysis was performed. ResultsCompared with the blank control group， the model group showed increased positive areas of CD3⁺， F4/80⁺， and Ly-6G⁺ in skin lesions （P<0.05）， elevated serum levels of IL-17A and IL-23 （P<0.05）， increased positive areas of SP and CGRP in skin lesions （P<0.05）， increased positive areas of NGF， p-TrkA， p-TRPV1， and PAR-2 （P<0.05）， elevated ratios of p-p38 MAPK/p38 MAPK and p-NF-κB p65/NF-κB p65 （P<0.05）， and upregulated mRNA levels of IL-1β， TNF， IL-6， and CXCL1 （P<0.05）. Compared with those in the model group， all the above indicators were reversed in the KXJD group （P<0.05）. MTX only downregulated the expression of p-TRPV1 and PAR-2 （P<0.05）， with no significant effects on the expression of NGF， p-TrkA， or CGRP. ConclusionKXJD inhibits the NGF-TrkA/TRPV1-PAR-2 signaling pathway to reduce neuropeptide release and simultaneously downregulates the p38 MAPK/NF-κB signaling pathway and the expression of downstream pro-inflammatory factors to ameliorate psoriasis-like neuroinflammation and immuno-inflammation. The therapeutic effect of KXJD on psoriasis-like inflammation is closely associated with the inhibition of the NGF-TrkA/TRPV1-PAR-2 signaling pathway. This study provides experimental evidence for the modern interpretation of the Xuanfu theory.

Objective To investigate the therapeutic effect and underlying mechanism of piceatannol against hepatic ischemia-reperfusion injury (HIRI) in fatty liver. Methods A mouse model of fatty liver combined with HIRI was established, and experimental animals were assigned into four groups: sham operation group, fatty liver HIRI group, fatty liver HIRI + piceatannol group, and fatty liver HIRI + piceatannol + ML385 group (n=5). Serum levels of alanine transaminase (ALT), aspartate transaminase (AST) and lactate dehydrogenase (LDH) were detected in each group. Hepatic tissue injury was evaluated by hematoxylin-eosin staining. Biochemical assays were performed to measure the contents of malondialdehyde (MDA), glutathione (GSH) and superoxide dismutase (SOD). Reactive oxygen species (ROS) were quantified using the DHE fluorescent probe method, while the expression of 4-hydroxynonenal (4-HNE) was determined via immunohistochemical staining. Western blot was adopted to detect the protein expression of glutathione peroxidase 4 (GPX4), acyl-CoA synthetase long-chain family member 4 (ACSL4), heme oxygenase-1 (HO-1) and nuclear factor E2-related factor 2 (Nrf2). Primary mouse hepatocytes were isolated and cultured in vitro. After treatment with palmitic acid, an hypoxia/reoxygenation (H/R) model was established. Cellular experiments were divided into control group, steatosis H/R group, steatosis H/R + piceatannol group, and steatosis H/R + piceatannol + ML385 group. Calcein-AM/PI dual staining was used to observe cell viability, C11 BODIPY staining was used to determin lipid peroxidation levels, and DCFH-DA fluorescent probe was utilized to test intracellular ROS levels. Western blot was used to detect the protein abundances of GPX4, ACSL4, HO-1 and Nrf2, and real-time fluorescence quantitative polymerase chain reaction was applied to quantify their corresponding messenger RNA (mRNA) expression levels. Results Compared with the sham operation group, the levels of ALT, AST and LDH, liver injury score, DHE positive rate, MDA level and 4-HNE level increased, the levels of GSH and SOD decreased, the relative expression level of ACSL4 protein increased, and the relative expression levels of GPX4, Nrf2 and HO-1 proteins decreased in the fatty liver HIRI group; compared with the fatty liver HIRI group, the levels of ALT, AST and LDH, liver injury score, DHE positive rate, MDA level and 4-HNE level decreased, the levels of GSH and SOD increased, the relative expression level of ACSL4 protein decreased, and the relative expression levels of GPX4, Nrf2 and HO-1 proteins increased in the fatty liver HIRI + piceatannol group; compared with the fatty liver HIRI + piceatannol group, the levels of ALT, AST and LDH, liver injury score, DHE positive rate, MDA level and 4-HNE level increased, the levels of GSH and SOD decreased, the relative expression level of ACSL4 protein increased, and the relative expression levels of Nrf2 and HO-1 proteins decreased in the fatty liver HIRI + piceatannol + ML385 group (all P<0.05). Compared with the control group, the mean fluorescence intensity of DCFH-DA and MDA level increased, the levels of GSH and SOD decreased, the proportion of oxidized lipids increased, the protein and mRNA expression levels of ACSL4 increased, and the protein and mRNA expression levels of GPX4, HO-1 and Nrf2 decreased in the steatosis H/R group; compared with the steatosis H/R group, the mean fluorescence intensity of DCFH-DA and MDA level decreased, the levels of GSH and SOD increased, the proportion of oxidized lipids decreased, the relative protein and mRNA expression levels of ACSL4 decreased, and the relative protein and mRNA expression levels of GPX4, HO-1 and Nrf2 increased in the steatosis H/R + piceatannol group; compared with the steatosis H/R + piceatannol group, the mean fluorescence intensity of DCFH-DA and MDA level increased, the levels of GSH and SOD decreased, the proportion of oxidized lipids increased, the relative protein and mRNA expression levels of ACSL4 increased, and the relative protein and mRNA expression levels of GPX4, HO-1 and Nrf2 decreased in the steatosis H/R + piceatannol + ML385 group (all P<0.05). Conclusions Piceatannol relieves HIRI in fatty liver by activating the Nrf2/HO-1 signaling pathway to suppress ferroptosis in hepatocytes.

The growth and development of children is an important stage for health, and its monitoringand intervention are related to the long-term development of individuals. The construction of a standardized and multi-dimensional database of pediatric growth and development-related diseases is an important basis for realizing precise diagnosis and treatment and health management. Based on the needs of clinical practice, this study proposes to establish a specialized database of pediatric growth and development-related diseases that integrates facial phenotypes and clinical diagnosis and treatment information. This study elaborates on the construction process, including data sources, data collection content, and the operation and management of the database; and proposes key points for quality control, including the establishment of quality control nodes, database construction standards, and a full-process quality control framework. The above ensure the integrity, logic and effectiveness of the data, so that the database can provide an objective basis for the screening and diagnosis of pediatric growth and development-related diseases. On the basis of scientific data management and strict quality control, the database will help reveal the patterns of children's growth and development, and promote the level of children's health management.

Objective To evaluate the interpersonal communication competence of doctors in 10 dimensions of standardized training for specialized doctors and their communication differences with various groups,and to analyze the existing problems and solutions.Methods The 10-item short-form version of the Interpersonal Communication Competence Scale(ICCS-SF)was used to assess the communication abilities of 395 physicians undergoing training at six specialized physician training bases in Shanghai.Descriptive statistics,chi-square tests,non-parametric tests,and multiple linear regression of methods were employed to analyze the communication status and training status of specialist physicians.Results The maximum score for interpersonal communication competence is 50 points,and the average score for the specialist physicians in this study was 38.0(35.0～41.0)points.The impact of the training on the scores is reflected in the total score and the two sub-dimensions of social relaxation and self-affirmation,with statistically significant differences(P＜0.05).Compared to patients and colleagues,specialized training physicians reported the greatest difficulty in communicating with interdisciplinary teams.Physicians who recognized the importance of communication and those whose training included a greater variety of skills achieved higher ICCS-SF scores(P＜0.001).Conclusion It is necessary to further strengthen the coverage and standardization of training,and pay attention to the cultivation of communication competence between interdisciplinary teams on the basis of attaching importance to the communication competence between doctors and patients.

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.