Objective: To construct a model for clinical identification of spotted fever (SF) and severe fever with thrombocytopenia syndrome (SFTS), so as to provide insights into early identification of SF and SFTS. Methods: The clinical data of laboratory-confirmed SF and SFTS patients in secondary and tertiary hospitals in Lu'an City, Anhui Province from May 2017 to May 2021 were retrieved from Chinese Disease Prevention and Control Information System. Factors affecting SF were identified using a logistic regression model, and the model for early identification of SF and SFTS was created. The model fitting effect was evaluated using Hosmer-Lemeshow test, and the value of the model for identification of SF and SFTS was evaluated using the area under the receiver operating characteristic curve (AUC). Results: Data of 62 SF cases and 115 SFTS cases were included. Multivariable logistic regression analysis showed that rash (β=5.994), C-reactive protein (β=4.409), white blood cell (β=-3.176) and platelet (β=-3.234) were included in the model, which were scored 6, 4, -3 and -3, with a total score ranging from -5 to 10. Hosmer-Lemeshow test revealed a high model fitting effect (χ2=3.245, P=0.662). The AUC of the model was 0.992, and the sensitivity and specificity were 0.935 and 0.991 if the cutoff was 1. Conclusion A model for early identification of SF and SFTS that includes four variables of rash, C-reactive protein, white blood cell and platelet has been created, which has a high accuracy.

Objective To investigate the role and mechanism of the small-molecule inhibitor CIL56 in the death of esophageal squamous cell carcinoma cells. Methods SRB method and plate-cloning method were used to detect the effect of CIL56 on the proliferation of esophageal squamous cell carcinoma. The effect of CIL56 on the migration of esophageal squamous cell carcinoma cells was investigated by scratch-healing test. The effect of CIL56 on the concentration of iron ions in esophageal squamous cell carcinoma was detected with an iron-detection kit. A total glutathione test kit was used to examine the effect of CIL56 on glutathione concentration in esophageal squamous cell carcinoma. Western blot was used to investigate the effect of CIL56 on the expression of xCT and GPX4 proteins related to iron death, as well as YAP1 protein, in esophageal squamous cell carcinoma. Results CIL56 could significantly inhibit the proliferation (P < 0.05) and migration (P < 0.001) of esophageal squamous cell carcinoma. With the increased CIL56 concentration, the iron concentration in esophageal squamous cell carcinoma increased (P < 0.05). CIL56 could reduce the glutathione content in esophageal squamous cell carcinoma (P < 0.01). CIL56 could reduce the expression of xCT and GPX4 proteins related to iron death and decrease the level of YAP1 protein in esophageal squamous cell carcinoma (both P < 0.001). Conclusion The small-molecule inhibitor CIL56 can significantly inhibit the proliferation and migration of esophageal squamous cell carcinoma cells and reduce the expression of the iron-death-related proteins xCT and GPX4, as well as YAP1 protein.

AIM: To investigate the effects of phorbol ester (TPA) on the anti-tumor effect and renal toxicity of cisplatin (CP). METHODS: MTT assay was used to examine the effect of TPA on the proliferation inhibition of CP in A549 and SPC-A-1 lung cancer cells. Also the effect of TPA on acute toxicity of CP was observed by once injection of high dose CP through caudal vein; The tumor-bearing mice model was explored to investigate the effect of TPA on tumor inhibition ratio and renal toxicity of CP in vivo. And the effect of TPA on renal oxidative stress induced by CP was detected. RESULTS: 1 ng/mL TPA could significantly enhance the inhibitory effect of CP on cell proliferation. In acute toxicity test, TPA could significantly reduce the toxicity of CP and prolong the survival time of animals. And the tumor weight (P<0.05), serum creatinine (P<0.05) and urea nitrogen levels (P<0.01) in TPA combined with CP group were significantly lower than those in CP group. Meanwhile, the results of HE staining showed that the renal tissue damage was significantly reduced in the combined group compared with CP group. The contents of MDA in renal tissue were decreased (P<0.01). However, the contents of GSH and the activity of SOD were increased (P<0.05) in TPA and CP combined group. CONCLUSION: TPA can enhance the inhibitory effect of CP on cell proliferation and inhibit tumor growth in tumor-bearing mice. At the same time, TPA can reduce the renal toxicity of CP, which may be related to the inhibition of renal oxidative stress induced by CP.

Diabetic foot ulcer is a serious and destructive complication of diabetes， with the rates of disability and mortality increasing year by year， which poses a serious threat to human physical and mental health. In the treatment of diabetic foot ulcer with traditional Chinese medicine （TCM）， the combination of syndrome differentiation and overall concept can not only alleviate TCM syndrome but also accelerate wound healing， reduce wound recurrence， delay the further deterioration of diabetic foot ulcer， and decrease the rates of disability and mortality. Modern studies have demonstrated that the difficult healing of diabetic foot ulcer is closely associated with the abnormal distribution of cytokines such as inflammatory cytokines， growth factors， and chemokines. With the deepening of modern medical research on TCM， the treatment of diabetic foot ulcer via regulation of cytokines by Chinese medicinal monomers and prescriptions has become a research focus. This paper summarizes the current research status at home and abroad and draws the following conclusions. ① Sesamol， geniposide， Danggui Buxuetang， and Zizhu ointment can regulate tumor necrosis factor-α （TNF-α）， interleukin （IL）-1， IL-6， IL-10 and other inflammatory cytokines to inhibit wound inflammation. ② Angelicae Dahuricae Radix， salvianolic acid B， Sixiao powder， Badu Shengji ointment （Zhuang medicine）， etc.， regulate vascular endothelial growth factor （VEGF）， platelet-derived growth factor （PDGF）， transforming growth factor （TGF）， epidermal growth factor （EGF） and other growth factors to promote collagen deposition and angiogenesis on wound surface. ③ Paeoniflorin， cryptanshinone， bee venom， and Huiyang Shengji decoction regulate CXC chemokine ligand （CXCL） 1， CXCL2， C-C chemokine ligand （CCL） 2， CCL3， stromal cell-derived factor-1α （SDF-1α）， monocyte chemoattract protein-1 （MCP-1） and other chemokines to reduce inflammatory response and promote neovascularization and wound granulation tissue formation. ④ In the treatment of diabetic foot ulcer， Chinese medicinal monomers and prescriptions have different and complicated mechanisms. The multi-target treatment manner determines that Chinese medicines can act on a variety of cytokines to participate in various stages of wound healing and thus play a therapeutic role. The conclusion above aims to provide ideas for the experimental research and clinical treatment of diabetic foot ulcer with TCM in the future.