Diabetes mellitus(DM)is a disease syndrome characterized by chronic hyperglycaemia.A long-term high-glucose environment leads to reactive oxygen species(ROS)production and nuclear DNA damage.Human umbilical cord mesenchymal stem cell(HUcMSC)infusion induces significant antidiabetic effects in type 2 diabetes mellitus(T2DM)rats.Insulin-like growth factor 1(IGF1)receptor(IGF1R)is important in promoting glucose metabolism in diabetes;however,the mechanism by which HUcMSC can treat diabetes through IGF1R and DNA damage repair remains unclear.In this study,a DM rat model was induced with high-fat diet feeding and streptozotocin(STZ)administration and rats were infused four times with HUcMSC.Blood glucose,interleukin-6(IL-6),IL-10,glomerular basement membrane,and renal function were examined.Proteins that interacted with IGF1R were determined through coimmunoprecipitation assays.The expression of IGF1R,phosphorylated checkpoint kinase 2(p-CHK2),and phosphorylated protein 53(p-p53)was examined using immunohistochemistry(IHC)and western blot analysis.Enzyme-linked immunosorbent assay(ELISA)was used to determine the serum levels of 8-hydroxydeoxyguanosine(8-OHdG).Flow cytometry experiments were used to detect the surface markers of HUcMSC.The identification of the morphology and phenotype of HUcMSC was performed by way of oil red"O"staining and Alizarin red staining.DM rats exhibited abnormal blood glucose and IL-6/10 levels and renal function changes in the glomerular basement membrane,increased the expression of IGF1 and IGF1R.IGF1R interacted with CHK2,and the expression of p-CHK2 was significantly decreased in IGF1R-knockdown cells.When cisplatin was used to induce DNA damage,the expression of p-CHK2 was higher than that in the IGF1R-knockdown group without cisplatin treatment.HUcMSC infusion ameliorated abnormalities and preserved kidney structure and function in DM rats.The expression of IGF1,IGF1R,p-CHK2,and p-p53,and the level of 8-OHdG in the DM group increased significantly compared with those in the control group,and decreased after HUcMSC treatment.Our results suggested that IGF1R could interact with CHK2 and mediate DNA damage.HUcMSC infusion protected against kidney injury in DM rats.The underlying mechanisms may include HUcMSC-mediated enhancement of diabetes treatment via the IGF1R-CHK2-p53 signalling pathway.

Objective:To investigate the relationship between microRNA (miR)-1, miR-133b and hepatic fibrosis in patients with hepatic alveolar echinococcosis.Methods:From October 2020 to April 2021, patients who were definitely diagnosed as hepatic alveolar echinococcosis (9 cases), cirrhosis (9 cases) and hepatocellular carcinoma (5 cases) in the First Affiliated Hospital of Xinjiang Medical University were selected as the research subjects, and healthy volunteers in the same period were taken as the control (10 cases). Peripheral blood samples of all subjects were collected to prepare plasma, and the expression levels of miR-1 and miR-133b in peripheral blood were detected by quantitative real-time PCR. At the same time, tissue samples around the liver lesion (proximal), and the corresponding tissues about 5 cm from the lesion (distal) were collected from 5 patients with hepatic alveolar echinococcosis, and immunohistochemical staining was used to detect the cell activation related indicators [cyclinD1, cyclin dependent kinase 1 (CDK1), α-smooth muscle actin (α-SMA)], fibrosis indicators (Collagen Ⅰ, Collagen Ⅲ), transforming growth factor-β1 (TGF-β1) signal pathway related genes [TGF-β1, TGF-β1 receptor type Ⅰ/Ⅱ (TGF-β1RⅠ, TGF-β1RⅡ)] and its downstream related proteins (SMAD2, SMAD3).Results:The quantitative real-time PCR results showed that there were significant differences in the expression levels of miR-1 and miR-133b in the peripheral blood of patients with hepatic alveolar echinococcosis, cirrhosis, hepatocellular carcinoma and the control group ( H = 16.54, 28.40, P < 0.001); the expression levels of miR-1 and miR-133b in hepatic alveolar echinococcosis group were higher than those in control group, cirrhosis group ( P < 0.05). The expression levels of CDK1 (0.46 ± 0.02, 0.42 ± 0.01), α-SMA (0.54 ± 0.09, 0.51 ± 0.07), TGF-β1 (0.55 ± 0.15, 0.51 ± 0.13), TGF-β1RⅠ (0.58 ± 0.09, 0.57 ± 0.08), and TGF-β1RⅡ(0.40 ± 0.05, 0.39 ± 0.05) between the proximal and distal tissue of liver lesion in hepatic alveolar echinococcosis patients were statistically significantly different ( t = 5.56, 3.17, 3.18, 4.27, 5.65, P = 0.005, 0.034, 0.034, 0.024, 0.011). There was no statistically significant difference in the expression levels of CyclinD1, Collagen Ⅰ, Collagen Ⅲ, SMAD2 and SMAD3 between the proximal and distal tissue of liver lesion in hepatic alveolar echinococcosis patients ( t = 3.06, 3.06, 2.86, 1.43, 1.50, P = 0.055, 0.055, 0.064, 0.247, 0.230). Pearson correlation analysis showed that miR-1 in the patients' peripheral blood was positively correlated with TGF-β1RⅠ in the proximal tissue of the liver lesion ( P = 0.001); there was no correlation between miR-1, miR-133b and CDK1, α-SMA, TGF-β1, TGF-β1RⅡ( P > 0.05). Conclusions:The expression of TGF-β1 signaling pathway related factors in the proximal tissue of liver lesion in patients with hepatic alveolar echinococcosis is up-regulated. The expression of miR-1 and miR-133b in peripheral blood is upregulated, and miR-1 is positively correlated with TGF-β1RⅠ level in proximal tissue of liver lesion, suggesting that miR-1 may promote the occurrence of liver fibrosis in hepatic alveolar echinococcosis.

Objective:To investigate the immune cell infiltration width on lesion microenvironment (LME) based on different hepatic alveolar echinococcosis lesion features to underlie referential sampling range for experimental and control tissues aiming at avoiding false negativity in basic researches.Methods:Using prospective research methods, from January 2017 to December 2019, patients with hepatic alveolar echinococcosis who were diagnosed and treated surgically at the First Affiliated Hospital of Xinjiang Medical University and met the multi-site sampling method (MSS method) were investigated. A total of 26 cases were included, aged 34 (15, 65) years old, with a gender ratio of 12/14. Lesions were classified into six groups based on heterogenic scales of calcification and liquefaction: A. non-calcified and non-liquefied; B. obvious calcified and non-liquefied; C. partial calcified and partial liquefied; D. obvious calcified and partial liquefied; E. partial calcified and subtotal liquefied; F. obvious calcified and subtotal liquefied. Liver specimens were acquired with 5 mm interval off the lesion shore in LME area using MSS method. Performed immunohistochemical staining of CD3, CD19, CD68, and Masson staining of fibrous tissue, and after pathological evaluation, the layer with a sharp decrease in immune cell infiltration abundance was determined as the maximum infiltration range (width, W value). The experimental group conservatively estimated the maximum sampling range for the integer value of Q1 of W value. The control group conservatively estimated the minimum sampling range for the integer value after Q3 rounding plus 5 mm of W value. Results were analyzed using Kruskal-Wallis H and Mann-Whitney U tests, referential ranges were concluded. Results:Median W values (interquartile) for each group were 20.0 (12.5, 22.5), 15.0 (10.0, 15.0), 10.0 (10.0, 15.0), 5.0 (5.0, 10.0), 12.5 (6.3, 15.0), and 5.0 (5.0, 10.0) mm, among which A > D, A > F, C > D, and C > F ( P≤0.05); from the perspective of calcification, A > C + E, A > B + D + F ( P < 0.05), while A + B > C + D, A + B > E + F ( P < 0.05) from the perspective of liquefaction. In these groups, the experimental group conservatively estimated the maximum distance for sampling to be 12.0, 10.0, 10.0, 5.0, 6.0, and 5.0 mm, while the control group conservatively estimated the minimum distance for sampling to be 28.0, 20.0, 20.0, 15.0, 20.0, and 15.0 mm. Conclusions:Less calcification and liquefaction implicates wider immune cell infiltration range in those lesions. Tissue sampling should be individualized based on different lesion features in basic research to avoid false negativity.

Aim To explore the effect of cuminaldehyde in cumin fruit on gastric ulcer and the protective mechanism via establishing the gastric ulcer model of rats was by ethanol injury. Methods Thirty-six male R. norregicus were divided into six groups: control group, model group, omeprazole positive control group and cuminaldehyde low, medium and high dosage groups. After seven days of continuous intragastric administration, the acute gastric ulcer of R. norregicus was tested by absolute alcohol. Gastric ulcer area, inhibition rate, gastric tissue antioxidant activity, serum inflammatory factors and gastric mucosal protective factors were detected in different groups. Results The results showed that cuminaldehyde significantly reduced the area of gastric ulcer and increased the inhibition rate of gastric ulcer. The inhibition rate of cuminaldehyde at high dose group was up to 74.65%, the activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH) in gastric tissue significantly increased, and the contents of serum prolandin E

Objective:To investigate characteristics of the 18F-flurodeoxyglucose ( 18F-FDG) uptake intensity and ranges in distinct hepatic alveolar echinococcosis lesions. Methods:The clinical data of 39 patients with position emission tomography during Jan 2017 to Dec 2019 in the First Affiliated Hospital of Xinjiang Medical University were enrolled. Among them, there were 17 males and 22 females, aging from 15 to 65 years (median 34 years). Lesions were classified into six groups based on heterogenic scales of calcification and liquefaction: A. non-calcified and non-liquefied ( n=7); B. obvious calcified and non-liquefied ( n=7); C. partial calcified and partial liquefied( n=10); D. obvious calcified and partial liquefied ( n=5); E. partial calcified and subtotal liquefied ( n=5); F. obvious calcified and subtotal liquefied ( n=5). Tumor to background ratio (TBR) and width (W) of lesion infiltrative boundary were measured and calculated. Statistical comparison using Mann-Whitney U test as well as correlation analysis was performed. Results:TBR values [ M( Q1, Q3)] for each group were 4.40(3.66, 7.03), 2.55(1.69, 3.60), 3.73(3.37, 5.21), 2.90(2.75, 3.60), 3.80(3.49, 6.36), 2.49(2.21, 3.97), among which A>B, A>D, A>F, C>B, E>B ( U=3.0, 4.0, 4.5, 11.0, 5.0, all P<0.05); From the perspective of the calcification in each group, it was found that the lighter the calcification was, the greater the TBR value was. W values [ M( Q1, Q3)] for each group were [12.5(10.0, 19.5), 11.2(10.5, 12.5), 12.2(10.9, 13.2), 7.8(7.3, 9.3), 10.0(7.3, 13.4), 7.3(6.8, 7.6)] mm, among which A>D, A>F, B>D, B>F, C>D, C>F (all U=0, all P<0.05); According to the degree of calcification and liquefaction of lesions in each group, the lighter the calcification was, the greater the W value was; The heavier the liquefaction was, the smaller the W value was. A mild strength linear correlation has been observed between the TBR value and W value ( r=0.4136, P<0.05). Conclusions:Less calcification and liquefaction implicated higher 18F-FDG uptake intensity and wider range. Radical resection margins and tissue sampling should be individualized based on different lesion features in surgical treatment.

Gelatin microspheres were discussed as a scaffold material for bone tissue engineering, with the advantages of its porosity, biodegradability, biocompatibility, and biosafety highlighted. This review discusses how bone regeneration is aided by the three fundamental components of bone tissue engineering-seed cells, bioactive substances, and scaffold materials-and how gelatin microspheres can be employed for in vitro seed cell cultivation to ensure efficient expansion. This review also points out that gelatin microspheres are advantageous as drug delivery systems because of their multifunctional nature, which slows drug release and improves overall effectiveness. Although gelatin microspheres are useful for bone tissue creation, the scaffolds that take into account their porous structure and mechanical characteristics might be difficult to be created. This review then discusses typical techniques for creating gelatin microspheres, their recent application in bone tissue engineering, as well as possible future research directions.
Tissue Engineering/methods* ; Tissue Scaffolds/chemistry* ; Gelatin/chemistry* ; Microspheres ; Bone and Bones ; Porosity

【Objective】 To investigate the risk factors and clinical significance of incidental prostate cancer (IPCa) in patients undergoing radical cystoprostatectomy (PCR). 【Methods】 The clinicopathological data of 260 patients undergoing RCP in our hospital during Jan. 2010 and Jan. 2022 were retrospectively analyzed, including 39 cases of IPCa detected with postoperative pathology, and 221 non-IPCa cases. 【Results】 The detection rate of IPCa was 15%. Univariate logistic regression analysis showed age (P<0.001), smoking (P<0.05), T stage (P<0.05), number of tumors (P<0.05), involvement of trigone (P<0.05), prostate volume (P<0.05), and preoperative total prostate-specific antigen (tPSA) (P<0.05) were influencing factors of prostate cancer. Multivariate logistic regression analysis showed that age (OR=1.061, 95%CI: 1.021-1.107, P=0.004), smoking (OR=2.852, 95%CI: 1.296-6.677, P=0.012), involvement of trigone(OR=2.967, 95%CI: 2.365-3.657, P=0.019) and preoperative tPSA (OR=1.109, 95%CI: 1.011-1.223, P=0.030) were independent risk factors of IPCa. 【Conclusion】 Advanced age, smoking, bladder tumor in trigone and preoperative PSA abnormality are risk factors for incidental prostate cancer in bladder cancer patients.

The new type coronavirus disease 2019 (COVID-19) is a contagious disease of severe lung inflammation induced by 2019 novel coronavirus (2019-nCoV). The World Health Organization (WHO) nomenclature of the newly discovered coronavirus was 2019-nCoV and the disease caused by 2019-nCoV was named COVID-19 on January 12, 2020. After 2019-nCoV invasion into a human body, it can stimulate the human immune system and engender a large number of cytokines, triggering a cytokine storm, resulting in severe infection, acute lung injury, multiple organ dysfunction, etc. Therefore, theoretically, the removal of over-production of cytokines can avoid the occurrence of cytokine storm and reduce the incidence of severe critical COVID-19 and serious poor prognosis. In this review, the authors systematically reviewed the past published reports related to the occurrence of cytokine storm in sepsis resulting in deterioration of disease situation, and recently they analyzed the therapeutic effects of patients with severe critical COVID-19 using endotoxin adsorption membrane for treatment in the disease course, further providing the effective clinical evidence of applying endotoxin adsorption membrane for treatment of COVID-19.

Sepsis 3.0 is defined as a life-threatening organ dysfunction caused by the host' uncontrol response to infection, with poor prognosis, high morbidity and fatality. Sepsis is one of the main causes of death in severe patients. As lack of comprehensive recognition of its pathogenesis, there were not specific treatment on it. It is reported that the T-cell immunoglobulin and mucin-domain-containing molecule (Tim) of Tim-1 play critical role in sepsis inflammation, immune tolerance and apoptosis, which is relative specific factor in assessment of sepsis prognostic and treatment efficiency, indicating that it could be a novel target in sepsis as well as provide a novel direction. This article mainly stated the discovery, structure, distribution and immune effect of Tim-1 as well as the possible role of TIM-1in immunosuppression, lymphocyte proliferation and apoptosis, in order to provide reference for further research the treatment of sepsis.

Sepsis-induced myocardial dysfunction (SIMD) has a high morbidity and mortality, and seriously threatens human health. However, the pathogenesis of the SIMD is still unclear. The previous studies have showed that the SIMD can adversely affect cardiac function through a variety of direct or indirect mechanism, such as autonomic nervous system function damage, pro-inflammatory mediators and activated immune cells induced cardiomyopathy. There is no uniform diagnostic criteria and treatment options. A stable and reliable animal model plays important role in the study that determine the pathogenesis, pathophysiological processes and treatment of SIMD. At present, there are many animal models of cardiac dysfunction caused by sepsis, unfortunately there is no stable, reliable and specific animal model at present. Therefore, it is important to construct a stable and reliable model for studying SIMD. The unified standard of cardiac dysfunction is conducive to the integration and further research. This review focused on pathogenesis of SIMD, routine ways of animal model of SIMD, observation index and basic research to provide references for the researcher to choose the proper animal model.