To summarize the clinical experience of Professor LIU Shangyi in treating pruritus vulvae. It is believed that women have the physiological characteristics of liver and kidney as the root， and their pubic area is easily attacked by wind-dampness pathogenic qi， so the core mechanism of pruritus vulvae is proposed as wind-dampness accumulation and deficiency of liver and kidney. The core treatment method is to dispel wind-dampness and nourish the liver and kidneys， and modify the Danggui Decoction （当归饮子） to form a self-prescribed Yinyang Formula （阴痒方） as the basic prescription to treat pruritus vulvaen.

Nonalcoholic steatohepatitis （NASH） is a chronic metabolic disease characterized by hepatocyte fatty degeneration and ballooning degeneration， and it plays an important role in the progression of hepatic steatosis. Recent studies have shown that immune homeostasis imbalance between T helper 17 （Th17） and regulatory T （Treg） cells are closely associated with the pathological process of NASH. Transforming growth factor-β1 （TGF-β1） is a key cytokine for regulating the differentiation and proliferation of Th17/Treg cells， and TGF-β1 binds to its receptor and activates the Smad signaling pathway， thereby regulating the immune balance of Th17/Treg cells and the expression of inflammatory factors and participating in the repair of liver inflammation. This article systematically reviews the molecular mechanism of the TGF-β1/Smad signaling pathway in affecting NASH by regulating the immune balance of Th17/Treg cells， in order to provide a theoretical basis for the research on the pathogenesis of NASH and related treatment strategies.

TGF-β1 is considered a key mediator in the formation of hepatic fibrosis and mainly acts by activating the downstream Smad signaling pathway.Smad2 and Smad3 are two major downstream regulators that promote TGF-β1-mediated tissue fibrosis,while Smad7 is a negative-feedback regulator of the TGF-β1/Smad pathway and inhibits TGF-β1-mediated hepatic fibrosis.A growing number of studies are showing that natural products can delay the progression of hepatic fibrosis by regulating the TGF-β1/Smad pathway,inhibiting HSC activation,and reducing ECM deposition.This article reviews the molecular mechanism of the TGF-β1/Smad signaling pathway in hepatic fibrosis,and summarizes the natural products that target the regulation of this pathway,providing a reference for research into the treatment of hepatic fibrosis.

Objective:To explore the correlation between cardiometabolic index(CMI) and the severity of coronary artery stenosis and long-term prognosis in patients with acute myocardial infarction(AMI).Methods:A total of 712 patients with AMI who were admitted to the Xinjiang Uygur Autonomous Region People′s Hospital from January 2018 to December 2019 were included as the subjects. According to the tertile of CMI, the subjects were divided into high, medium, and low value groups. Gensini score was used to quantitatively assess the degree of coronary artery stenosis. The endpoint event was defined as the occurrence of major cardiovascular adverse events(MACEs). Spearman correlation analysis was conduceted to explore the correlation between CMI and Gensini score. Multivariate Cox regression was utilized to analyze the independent influencing factors of MACEs. A restricted cubic spline plot was employed to analyze the nonlinear relationship between CMI and the risk of MACEs. Kaplan- Meier curve was used to analyze survival differences between groups. Subgroup analysis was performed to evaluate the consistency of the predictive value of CMI for MACEs. Results:Spearman correlation analysis showed that CMI was positively correlated with Gensini score( r=0.13, P<0.001). After adjusting for confounding, multivariate Cox regression analysis showed that CMI was an independent risk factor for MACEs( HR=1.709, 95% CI 1.052-2.778, P=0.031). The restricted cubic spline analysis revealed an L-shaped nonlinear effect relationship between CMI and MACEs risk( P=0.024). Kaplan- Meier survival curve analysis demonstrated that the cumulative incidence of MACEs in AMI patients increased significantly with the increase of CMI( P<0.05). Subgroup analysis indicated that CMI independently predicted the occurrence of MACEs across different subgroups, and had higher predictive value in patients with normal lipids and normal body weight. Conclusion:CMI is closely associated with the severity of coronary stenosis in AMI patients, and is an independent predictor of the risk of long-term MACEs.

Objective:To explore the role and mechanism of Vγ4 T cell depletion in epidermal tissue repair after ultraviolet damage to mouse skin.Methods:The study was an experimental study. Fifty-four female C57BL/6J wild-type mice aged 6 to 8 weeks were divided into Vγ4 T cell depletion group and control group (27 mice in each group) according to the random number table, and the Armenian hamster anti-mouse Vγ4 T cell receptor (TCR) monoclonal antibody of 200 μg and an equal amount of homologous control IgG antibody were intraperitoneally injected, respectively. At one week after injection (the same time point to harvest mice below), dermal cells and lymph node cells were respectively extracted from the back skin tissue, armpit and inguinal lymph nodes of 3 mice in each group (mice in following study were all taken from these 2 groups), and the proportions of Vγ4 T cells in dermal cells and lymph node cells were detected by flow cytometry. Five mice from each group were harvested for observation of skin on the back and skin tissue structure was observed and the epidermal tissue thickness was measured after hematoxylin-eosin (HE) staining. Five mice from each group were harvested for detection of proportion of dendritic epidermal T cells (DETCs) in epidermal cells by flow cytometry after extracted. Three mice were taken from each group and recruited in Vγ4 T cell depletion+5 times ultraviolet irradiation (UVR) group and control+5 times UVR group, respectively, then UVR was administered once per day for 5 times, and the condition of skin on the back was observed immediately after daily irradiation. Five mice were taken from each group and divided into Vγ4 T cell depletion+1 UVR group and control+1 UVR group, respectively. Immediately after one UVR treatment, the epidermal tissue thickness was measured after HE staining. Three mice from each group were selected and recruited in Vγ4 T cell depletion alone group and control alone group, then 3 mice from each group rwere recruited in Vγ4 T cell depletion+1 time UVR group and control+1 time UVR group, respectively, and were treated as before. The mRNA expressions of insulin-like growth factor-Ⅰ (IGF-Ⅰ), keratinocyte growth factor (KGF), Vγ5 TCR, interleukin-15 (IL-15), IL-1β, IL-23, natural killer group 2 member D (NKG2D), histocompatibility antigen 60 (H60), mouse UL16-binding protein-like transcript 1 (Mult1), and retinoic acid early inducible protein 1 (Rae1) in the epidermal tissue were detected by real-time fluorescent quantitative reverse transcription polymerase chain reaction.Results:At one week after injection, the proportions of Vγ4 T cells in dermal cells and lymph node cells of mice in Vγ4 T cell depletion group were significantly lower than those in control group (with t values of 27.99 and 13.12, respectively, P<0.05); there were no statistically significant differences in the skin general condition and tissue structure of mice between Vγ4 T cell depletion group and control group; the epidermal tissue thickness of mice between Vγ4 T cell depletion group and control group was similar ( P>0.05); the proportion of DETCs in epidermal cells of mice in Vγ4 T cell depletion group was (3.9±0.8)%, which was significantly higher than (1.6±0.5)% in control group ( t=4.84, P<0.05). Compared with that in control+5 times UVR group, the skin scale increased after one UVR treatment, scaly scab appeared after 2 times of irradiation, and scaly scab increased significantly after 3 to 5 times of irradiation in Vγ4 T cell depletion+5 times UVR group. Immediately after UVR treatment, the epidermal tissue thickness of mice in Vγ4 T cell depletion+1 time UVR group was significantly increased compared with that in control+1 time UVR group ( t=11.50, P<0.05). Compared with those in control alone group, the mRNA expression of Vγ5 TCR in the epidermal tissue of mice in Vγ4 T cell depletion alone group was up-regulated ( t=41.16, P<0.05), while the mRNA expression of IL-23 was down-regulated ( t=6.52, P<0.05); compared with those in control alone group, the mRNA expressions of Vγ5 TCR and KGF in the epidermal tissue of mice in control+1 time UVR group were significantly up-regulated (with t values of 15.22 and 13.22, respectively, P<0.05), while the mRNA expressions of IGF-Ⅰ and IL-23 were significantly down-regulated (with t values of 3.71 and 4.95, respectively, P<0.05); compared with those in Vγ4 T cell depletion alone group, the mRNA expressions of IGF-Ⅰ and KGF in the epidermal tissue of mice in Vγ4 T cell depletion+1 time UVR group were significantly up-regulated (with t values of 11.40 and 18.88, respectively, P<0.05), while the mRNA expression of IL-1β was significantly down-regulated ( t=4.42, P<0.05); compared with those in control+1 time UVR group, the mRNA expressions of Vγ5 TCR, IGF-Ⅰ, and KGF in the epidermal tissue of mice in Vγ4 T cell depletion+1 time UVR group were significantly up-regulated (with t values of 4.52, 15.24, and 9.43, respectively, P<0.05); the mRNA expression of IL-15 in the epidermal tissue of mice in these 4 groups was generally similar ( P>0.05). Compared with those in control alone group, the mRNA expressions of NKG2D and Rae1 in the epidermal tissue of mice in Vγ4 T cell depletion alone group were significantly up-regulated (with t values of 3.67 and 47.40, respectively, P<0.05), the mRNA expressions of NKG2D, Mult1, and Rae1 in the epidermal tissue of mice in control+1 time UVR group were significantly up-regulated (with t values of 5.30, 6.50, and 9.16, respectively, P<0.05); compared with those in Vγ4 T cell depletion alone group, the mRNA expressions of NKG2D, H60, Mult1, and Rae1 in the epidermal tissue of mice in Vγ4 T cell depletion+1 time UVR group were significantly down-regulated (with t values of 4.57, 4.13, 4.67, and 27.36, respectively, P<0.05); compared with those in control group+1 time UVR group, the mRNA expressions of NKG2D, H60, Mult1, and Rae1 in the epidermal tissue of mice in Vγ4 T cell depletion+1 time UVR group were significantly down-regulated (with t values of 5.77, 8.18, 12.90, and 8.08, respectively, P<0.05). Conclusions:The clearance of Vγ4 T cells is conducive to the proliferation and down-regulation of cytotoxicity of DETCs, and may promote the repair of mouse epidermal damage after UVR.

Objective To explore the predictive value of novel anthropometric indicators for the long-term prognosis in patients with acute myocardial infarction(AMI).Methods A total of 712 patients diagnosed with AMI in the People's Hospital of Xinjiang Uygur Autonomous Region from January 2018 to December 2019 were selected as research subjects,and divided into an event group and a non-event group according to whether major cardiovascular adverse events(MACEs)occurred during the period of follow-up.Gensini score was used to quanti-tatively assess the degree of coronary artery stenosis.Spearman correlation analysis was used to explore the correla-tion between the new anthropometric indicators and Gensini score.Receiver operating characteristic(ROC)curve was used to evaluate the ability of new anthropometric indicators to predict MACEs,and the patients were grouped according to the optimal cut-off value.Kaplan-Meier curve was used to analyze the survival difference between the groups.Multivariate Cox regression was used to analyze the independent risk factors of MACEs.Results During a median follow-up of 27(20,39)months,a total of 125 patients developed MACEs.As compared with those in the non-event group,the patients in the event group had a higher proportion of hypertension,diabetes and abdominal obesity,higher HbA1c and FBG levels,and longer body weight and waist circumference.The LAP index,CMI index,BRI index and Gensini score were significantly increased,and the differences were statistically significant(P＜0.05).Spearman correlation analysis showed that LAP index,CMI index and BRI index were positively corre-lated with Gensini score(r=0.233,0.126,0.272,P<0.001).ROC curve analysis showed that the AUC of LAP index,CMI index,VAI index,BRI index and ABSI index were 0.745,0.640,0.490,0.874 and 0.506 respec-tively;Kaplan-Meier curve analysis showed that the cumulative incidence of MACEs in LAP index,CMI index and BRI index was significantly increased in the high-value group(Log-rank test,P＜0.05).The results of multivariate Cox regression analysis after adjusting confounding showed that CMI index(HR=1.430,95%CI:1.049～1.952,P=0.024)and BRI index(HR=1.332,95%CI:1.234～1.439,P＜0.001)were independent risk factors for MACEs.Conclusions CMI index and BRI index of new anthropometric indicators are independent risk factors for long-term prognosis in patients with AMI.

Non-alcoholic fatty liver disease(NAFLD)is one of the common chronic liver diseases in the world.The molecular mechanism of NAFLD is complex,involving many signal molecules,and the vitamin D(VD)/VDBP/vitamin D receptor(VDR)axis is also involved.VD is a lipid-soluble steroid,which can participate in the regula-tion of lipid metabolism,insulin secretion,immune function,inflammatory response and other biological processes.Stud-ies have shown that VD deficiency is closely related to liver lipid accumulation,inflammation,insulin resistance,oxida-tive stress,intestinal flora imbalance,autophagy,apoptosis,pyroptosis and fibrosis,and plays an important role in the oc-currence and development of NAFLD.This paper reviews the research progress on Vitamin D in recent years in the field of NAFLD,including the physiological characteristics of VD and its role in the NAFLD mechanism,so as to provide referenc-es for the prevention and treatment of NAFLD.

Pathological mechanism of ulcerative colitis(UC)is not fully clear,which may be the result of Th17/Treg immune imbalance and the interaction of multiple complex factors.Numerous studies have found that classical TCM prescriptions,experienced formulas and TCM active components could regulate Th17/Treg balance by intervening in cytokines,transcription factors,and signaling pathways,restore intestinal mucosal immune function,suppress intestinal mucosal inflammatory response,and repair intestinal mucosal barrier damage.Based on the research status of UC,Th17/Treg balance and TCM treatment,this article reviewed the relationship between Th17/Treg balance and UC,and explained the key role of Th17/Treg balance in the occurrence and development of UC.At the same time,the Chinese materia medica targeting to regulate the balance of Th17/Treg in the treatment of UC in recent years was summarized,in order to provide reference for the treatment of UC.

Objective:To explore the clinical value of a trinity strategy for the treatment of multiple orthopedic trauma.Methods:A retrospective case series study was conducted to analyze the clinical data of 1 267 patients with multiple orthopedic trauma admitted to Xinhua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine and the First Affiliated Hospital of Navy Medical University from June 2013 to May 2023, including 862 males and 405 females, aged 18-93 years [(55.2±19.8)years]. Associated injuries included hemorrhagic shock in 632 patients, traumatic wet lung in 274, cranial injuries in 135, abdominal and pelvic bleeding in 116, pneumothorax in 89, urinary injury in 13, and vesical rupture in 8. All the patients were treated with the trinity strategy and the treatment process was divided into the phases of first aid, remodeling, and rehabilitation. The first aid phase focused on stabilizing symptoms and saving lives; the remodeling phase centered on restoring the anatomical structure and alignment; the rehabilitation phase aimed for functional recovery through the integration of both Western and traditional Chinese medicine. The all-cause mortality within 30 days after surgery and fracture healing time were calculated; the excellent and good rates of Constant-Murley shoulder score, Mayo elbow score, Gartland-Werley wrist score, Harris hip score, Hospital for Special Surgery (HSS) knee score and the American Orthopedic Foot & Ankle Society (AOFAS) ankle-hindfoot score at the last follow-up and the overall excellent and good rate of all joint function scores were measured. The short form health survey (SF-36) scores were collected preoperatively and at 6 months postoperatively, including 8 aspects such as physical functioning, physical role, bodily pain, general health, vitality, social functioning, emotional role, and mental health. The incidence of postoperative complications was recorded.Results:All the patients were followed up for 6-18 months [(10.2±4.2)months]. The mortality rate during the acute phase (within 30 days after surgery) was 2.37% with 12 deaths due to hemorrhagic shock, 10 due to traumatic brain injury, 6 due to multiple organ dysfunction syndrome (MODS), and 2 due to pulmonary infection. The average fracture healing time averaged 3.8-18 months [(11.5±4.2)months], with 89.49% of the patients having bone union within 12 months after surgery, 8.93% having bone union within 18 months after surgery, and 1.58% undergoing reoperation. For the patients with internal fixation failure and nonunion, the average healing time was extended to (10.2±2.2)months and (13.7±3.3)months respectively. At the last follow-up, the excellent and good rates of Constant-Murley shoulder score, Mayo elbow score, Gartland-Werley wrist score, Harris hip score, HSS knee score, and AOFAS ankle-hindfoot score were 83.93%, 90.24%, 94.12%, 85.57%, 88.46%, and 92.31% respectively, with an overall excellent and good rate of 89.11%. At 6 months after surgery, the SF-36 scores of all the patients in the eight dimensions,including the physical functioning, physical role, bodily pain, general health, vitality, social functioning, emotional role, and mental health were (74.4±8.6)points, (44.7±14.4)points, (77.4±10.9)points, (68.4±18.2)points, (72.5±16.0)points, (76.8±8.7)points, (49.9±17.6)points, and (72.8±17.9)points, significantly improved compared with those before operation [(63.4±12.7)points, (30.9±17.4)points, (56.4±18.0)points, (55.4±24.7)points, (53.5±21.0)points, (55.8±24.3)points, (36.9±24.0)points, (58.8±21.6)points] ( P<0.01). Complications of different degrees occurred in 214 patients (16.89%), including lung infections in 118 patients (9.31%), lower extremity deep vein thrombosis in 50(3.95%), pressure injuries in 26(2.05%), internal fixation failure in 12(0.95%), and nonunion in 8(0.63%). Conclusions:The trinity strategy provides whole-process management, personalized treatment, and overall rehabilitation for multiple orthopedic trauma. It can decrease mortality, shorten fracture healing time, improve joint function and quality of life, and reduce the incidence of complications.

Objective To explore the effects of Jianpi Yichang Powder on the expressions of interleukin(IL)-1β and IL-18 of NLRP3 signaling pathway in ulcerative colitis(UC)model rats.Methods Ten rats were randomly selected from 40 SD rats as the normal group,and the other rats freely drank 5%dextran sulfate solution for 7 days to replicate UC rats model.The model rats were randomly divided into model group,sulfasalazine group and Jianpi Yichang Powder group,with 10 rats in each group.Jianpi Yichang Powder group and sulfasalazine group were given corresponding liquid medicine for gavage,and the normal and model groups were given equivalent volume distilled water for gavage for consecutive 14 d.The general status was observed,and the disease activity index(DAI)was scored,the contents of NLRP3,apoptosis-associated spotted proteins(ASC),and Caspase-1 in serum were detected by ELISA,the expressions of IL-1β and IL-18 protein and mRNA in colon tissue were detected by immunohistochemistry,Western blot and RT-PCR respectively.Results Compared with the normal group,the general status of the rats in model group was relatively worse,and DAI score significantly increased(P<0.01),the contents of NLRP3,ASC and Caspase-l in serum were significantly increased(P<0.01),the expressions of IL-1β and IL-18 protein and mRNA in colon tissue were significantly increased(P<0.01).Compared with the model group,the general status of the rats in Jianpi Yichang Powder group and sulfasalazine group were significantly improved,DAI score significantly decreased(P<0.01),the contents of NLRP3,ASC and Caspase-l in serum significantly reduced(P<0.05,P<0.01),and the expressions of IL-1β and IL-18 protein and mRNA in colon tissue significantly decreased(P<0.05,P<0.01).Conclusion Jianpi Yichang Powder can inhibit IL-1β and IL-18 expression of NLRP3 signaling pathway to reduce colon immune inflammatory damage,thus play a role in treating UC.