Diabetic microvascular complications （DMC） are major chronic complications of diabetes，primarily including diabetic kidney disease （DKD），diabetic retinopathy （DR），diabetic cardiomyopathy （DCM），and diabetic peripheral neuropathy （DPN）. These complications significantly impact patients' quality of life and prognosis. Modern medicine primarily focuses on symptomatic control in the treatment of DMC，with limited ability to reverse the disease progression. Endoplasmic reticulum stress （ERS），as a central event under hyperglycemic toxicity，is not only a key cause of pancreatic β-cell dysfunction （reduced insulin synthesis and secretion） but also a core driver of damage in various target organs of DMC. It activates three signaling pathways of the unfolded protein response （UPR）-inositol-requiring enzyme 1 （IRE1），activating transcription factor 6 （ATF6），and protein kinase R-like endoplasmic reticulum kinase （PERK），intertwining processes such as autophagy，apoptosis，oxidative stress，and calcium homeostasis imbalance. Traditional Chinese medicine （TCM） offers multi-target and multi-pathway therapeutic advantages and can curb the pathological progression of DMC by regulating ERS. This article systematically reviews the relationships of ERS with pancreatic β-cell function，insulin synthesis，and insulin secretion，and elucidates the core signaling pathways through which ERS mediates DMC. Furthermore，it categorizes and summarizes experimental evidence and mechanisms of single medicinal herbs and their extracts，TCM compound formulas，and modern TCM preparations in regulating ERS for the treatment of various DMC subtypes. Finally，this article proposes ERS as a molecular bridge for integrating traditional Chinese and Western medicine in DMC treatment. Future research should leverage emerging technologies such as network pharmacology，multi-omics analysis，and nano-formulations to establish a synergistic network combining modern hypoglycemic drugs and TCM regulation of ERS. This approach is expected to achieve dual efficacy，enhance drug targeting and bioavailability，deepen the understanding of scientific connotation of TCM，and pave new avenues for the prevention and treatment of DMC.

Diabetic microvascular complications （DMC） are major chronic complications of diabetes，primarily including diabetic kidney disease （DKD），diabetic retinopathy （DR），diabetic cardiomyopathy （DCM），and diabetic peripheral neuropathy （DPN）. These complications significantly impact patients' quality of life and prognosis. Modern medicine primarily focuses on symptomatic control in the treatment of DMC，with limited ability to reverse the disease progression. Endoplasmic reticulum stress （ERS），as a central event under hyperglycemic toxicity，is not only a key cause of pancreatic β-cell dysfunction （reduced insulin synthesis and secretion） but also a core driver of damage in various target organs of DMC. It activates three signaling pathways of the unfolded protein response （UPR）-inositol-requiring enzyme 1 （IRE1），activating transcription factor 6 （ATF6），and protein kinase R-like endoplasmic reticulum kinase （PERK），intertwining processes such as autophagy，apoptosis，oxidative stress，and calcium homeostasis imbalance. Traditional Chinese medicine （TCM） offers multi-target and multi-pathway therapeutic advantages and can curb the pathological progression of DMC by regulating ERS. This article systematically reviews the relationships of ERS with pancreatic β-cell function，insulin synthesis，and insulin secretion，and elucidates the core signaling pathways through which ERS mediates DMC. Furthermore，it categorizes and summarizes experimental evidence and mechanisms of single medicinal herbs and their extracts，TCM compound formulas，and modern TCM preparations in regulating ERS for the treatment of various DMC subtypes. Finally，this article proposes ERS as a molecular bridge for integrating traditional Chinese and Western medicine in DMC treatment. Future research should leverage emerging technologies such as network pharmacology，multi-omics analysis，and nano-formulations to establish a synergistic network combining modern hypoglycemic drugs and TCM regulation of ERS. This approach is expected to achieve dual efficacy，enhance drug targeting and bioavailability，deepen the understanding of scientific connotation of TCM，and pave new avenues for the prevention and treatment of DMC.

Objective:Glioblastoma (GBM) is a primary malignant tumor in the central nervous system, whose tissue heterogeneity and invasive growth characteristics lead to a very poor prognosis for patients. Hub genes in GBM are screened by bioinformatics analysis; expressions of Hub genes in human GBM tissue, and their effects on GBM biological behaviors and Notch signaling pathway proteins are explored, and their regulatory roles in GBM proliferation in xenograft tumor model mice are evaluated.Methods:(1) The gene expression profiles of GBM tissue and normal brain tissue from the Gene Expression Omnibus (GEO) database were obtained; differentially expressed genes (DEGs) were screened, and gene ontology (GO) and Kyoto encyclopedia of genes and genomes (KEGG) analyses were conducted on DEGs. A co-expression network was constructed using weighted gene co-expression network analysis (WGCNA) to identify modules significantly related to GBM. Gene set enrichment analysis (GSEA) on the related module genes was performed; STRING database (version 12.0) was used to construct protein-protein interaction (PPI) network and screen the hub genes. (2) Normal brain tissue samples from 8 patients with epilepsy and GBM tissue samples from 10 patients with GBM who underwent surgical resection in Department of Neurosurgery, He'nan Provincial People's Hospital from January 1, 2022 to December 1, 2023 were collected; expressions of synaptosomal-associated protein 25 (SNAP25) and vesicle-associated membrane protein 2 (VAMP2) were detected by immunohistochemical staining and Western blotting. (3) LN229 and U87 cells were routinely cultured in vitro and divided into shRNA-SNAP25/shRNA-VAMP2 group and empty vector group, and then, cells in each group were transfected with shRNA-SNAP25/shRNA-VAMP2 lentivirus or empty vector lentivirus, respectively; 24 hours after transfection, SNAP25 and VAMP2 mRNA and protein expressions in the 2 groups were detected by real-time fluorescence quantitative reverse transcription-polymerase chain reaction (RT-qPCR) and Western blotting. LN229 and U87 cells were routinely cultured in vitro and divided into shRNA-SNAP25 group, shRNA-VAMP2 group and empty vector group; cells in each group were transfected with shRNA-SNAP25 lentivirus, shRNA-VAMP2 lentivirus or empty vector lentivirus, respectively; 48 hours after transfection, proliferation was detected by clone formation assay, proliferating cell nuclear antigen Ki-67 expression was detected by immunofluorescent staining, invasion was detected by Transwell invasion assay, and Notch1, HEY1 and HES1 protein expressions in Notch signaling pathway of LN229 cells were detected by Western blotting. (4) LN229 cells transfected with shRNA-SNAP25 lentivirus, shRNA-VAMP2 lentivirus or empty vector lentivirus for 48 hours were subcutaneously injected into the right axilla of 4-week-old BALB/c nude mice, respectively, as shRNA-SNAP25 transplantation group, shRNA-VAMP2 transplantation group and empty vector transplantation group (5 mice in each group); on 28 th day of injection, immunohistochemical staining was used to detect the Ki-67 expression in the LN229 cell-transplanted tumor tissues. Results:(1) A total of 1,473 DEGs were screened, of which 880 were upregulated and 593 were downregulated. WGCNA indicated that DEGs were divided into 5 modules (greenish-blue, blue, black, brown and gray ones), among which the greenish-blue module was significantly negatively correlated with GBM ( r=-0.700, P<0.001); GSEA analysis showed that the greenish-blue module mainly involved Notch signaling pathway, and PPI network analysis identified SNAP25 and VAMP2 as hub genes. (2) Immunohistochemical staining results showed that expressions of SNAP25 and VAMP2 in GBM tissue were significantly lower than those in normal brain tissue ( P<0.05). (3) Compared with those in the empty vector group, the SNAP25 mRNA and protein expressions in LN229 and U87 cells of the shRNA-SNAP25 group were statistically decreased ( P<0.05). Compared with those in the empty vector group, the VAMP2 mRNA and protein expressions in LN229 and U87 cells of the shRNA-VAMP2 group were significantly decreased ( P<0.05). Compared with the empty vector group, the LN229 and U87 cells in the shRNA-SNAP25 group and shRNA-VAMP2 group had significantly increased colony formation number, Ki-67 expression and invasive cell number ( P<0.05). Compared with the empty vector group, LN229 cells in the shRNA-SNAP25 group and shRNA-VAMP2 group had statistically increased Notch1, HEY1, and HES1 protein expressions ( P<0.05). Immunohistochemical staining results showed that compared with that in the empty vector group (1.00±0.00), the Ki-67 expression in LN229 cell-transplanted tumor tissues of the shRNA-SNAP25 group and shRNA-VAMP2 group was statistically increased (1.41±0.05, 1.40±0.09, P<0.05). Conclusion:Hub genes SNAP25 and VAMP2 may negatively regulate the malignant biological behavior of GBM through Notch pathway, which might be the new candidate targets for GBM precise treatment.

Objective:Glioblastoma (GBM) is a primary malignant tumor in the central nervous system, whose tissue heterogeneity and invasive growth characteristics lead to a very poor prognosis for patients. Hub genes in GBM are screened by bioinformatics analysis; expressions of Hub genes in human GBM tissue, and their effects on GBM biological behaviors and Notch signaling pathway proteins are explored, and their regulatory roles in GBM proliferation in xenograft tumor model mice are evaluated.Methods:(1) The gene expression profiles of GBM tissue and normal brain tissue from the Gene Expression Omnibus (GEO) database were obtained; differentially expressed genes (DEGs) were screened, and gene ontology (GO) and Kyoto encyclopedia of genes and genomes (KEGG) analyses were conducted on DEGs. A co-expression network was constructed using weighted gene co-expression network analysis (WGCNA) to identify modules significantly related to GBM. Gene set enrichment analysis (GSEA) on the related module genes was performed; STRING database (version 12.0) was used to construct protein-protein interaction (PPI) network and screen the hub genes. (2) Normal brain tissue samples from 8 patients with epilepsy and GBM tissue samples from 10 patients with GBM who underwent surgical resection in Department of Neurosurgery, He'nan Provincial People's Hospital from January 1, 2022 to December 1, 2023 were collected; expressions of synaptosomal-associated protein 25 (SNAP25) and vesicle-associated membrane protein 2 (VAMP2) were detected by immunohistochemical staining and Western blotting. (3) LN229 and U87 cells were routinely cultured in vitro and divided into shRNA-SNAP25/shRNA-VAMP2 group and empty vector group, and then, cells in each group were transfected with shRNA-SNAP25/shRNA-VAMP2 lentivirus or empty vector lentivirus, respectively; 24 hours after transfection, SNAP25 and VAMP2 mRNA and protein expressions in the 2 groups were detected by real-time fluorescence quantitative reverse transcription-polymerase chain reaction (RT-qPCR) and Western blotting. LN229 and U87 cells were routinely cultured in vitro and divided into shRNA-SNAP25 group, shRNA-VAMP2 group and empty vector group; cells in each group were transfected with shRNA-SNAP25 lentivirus, shRNA-VAMP2 lentivirus or empty vector lentivirus, respectively; 48 hours after transfection, proliferation was detected by clone formation assay, proliferating cell nuclear antigen Ki-67 expression was detected by immunofluorescent staining, invasion was detected by Transwell invasion assay, and Notch1, HEY1 and HES1 protein expressions in Notch signaling pathway of LN229 cells were detected by Western blotting. (4) LN229 cells transfected with shRNA-SNAP25 lentivirus, shRNA-VAMP2 lentivirus or empty vector lentivirus for 48 hours were subcutaneously injected into the right axilla of 4-week-old BALB/c nude mice, respectively, as shRNA-SNAP25 transplantation group, shRNA-VAMP2 transplantation group and empty vector transplantation group (5 mice in each group); on 28 th day of injection, immunohistochemical staining was used to detect the Ki-67 expression in the LN229 cell-transplanted tumor tissues. Results:(1) A total of 1,473 DEGs were screened, of which 880 were upregulated and 593 were downregulated. WGCNA indicated that DEGs were divided into 5 modules (greenish-blue, blue, black, brown and gray ones), among which the greenish-blue module was significantly negatively correlated with GBM ( r=-0.700, P<0.001); GSEA analysis showed that the greenish-blue module mainly involved Notch signaling pathway, and PPI network analysis identified SNAP25 and VAMP2 as hub genes. (2) Immunohistochemical staining results showed that expressions of SNAP25 and VAMP2 in GBM tissue were significantly lower than those in normal brain tissue ( P<0.05). (3) Compared with those in the empty vector group, the SNAP25 mRNA and protein expressions in LN229 and U87 cells of the shRNA-SNAP25 group were statistically decreased ( P<0.05). Compared with those in the empty vector group, the VAMP2 mRNA and protein expressions in LN229 and U87 cells of the shRNA-VAMP2 group were significantly decreased ( P<0.05). Compared with the empty vector group, the LN229 and U87 cells in the shRNA-SNAP25 group and shRNA-VAMP2 group had significantly increased colony formation number, Ki-67 expression and invasive cell number ( P<0.05). Compared with the empty vector group, LN229 cells in the shRNA-SNAP25 group and shRNA-VAMP2 group had statistically increased Notch1, HEY1, and HES1 protein expressions ( P<0.05). Immunohistochemical staining results showed that compared with that in the empty vector group (1.00±0.00), the Ki-67 expression in LN229 cell-transplanted tumor tissues of the shRNA-SNAP25 group and shRNA-VAMP2 group was statistically increased (1.41±0.05, 1.40±0.09, P<0.05). Conclusion:Hub genes SNAP25 and VAMP2 may negatively regulate the malignant biological behavior of GBM through Notch pathway, which might be the new candidate targets for GBM precise treatment.

Objective To explore the effect of exercise combined with dieting on chronic inflamma-tion based on fatty acids and peripheral blood mononuclear cell(PBMC)immunophenotypes.Methods Thirty-one obese volunteers(age:30.1±5.5 years,height:170.1±8.1 cm,weight:101.13±21.40 kg,BMI:34.66±5.01 kg/m2)were recruited and given a 5-week program of exercise combined with diet-ing.The exercise regimen consisted of daily 3-hour training at 60%-75%HRmax intensity,while the di-eting regimen was a moderate to high energy restriction model,with a daily reduction of 250 kcal in the 1st week and 600 kcal from the 2nd to 5th weeks.Before and after the intervention,all volunteers were measured morphological indicators(body weight,BMI,fat-free mass,body fat percentage,waist-to-hip ratio and visceral fat index),blood lipids(total cholesterol,triglycerides,high-density lipopro-tein cholesterol and low-density lipoprotein cholesterol),high-sensitivity C-reactive protein(hs-CRP),tumor necrosis factor-α(TNF-α),visfatin(VF),and the content of fatty acids in the blood.Moreover,the expression of cell surface receptors CD36,TLR4,and nuclear factor-κB(NF-κB)on PBMC sub-sets was tested before and after intervention.Results After intervention,a significant decrease was ob-served in the body composition indices,as well as in the four major blood lipid parameters.Levels of chronic inflammatory markers,including hs-CRP,VF and TNF-α,decreased significantly(P<0.01).Except for C6:0,C11:0,C12:0,C23:0,and C24:0,the levels of other fatty acids also decreased sig-nificantly(P<0.05,P<0.01).Among the measured fatty acids,13,31,and 15 were found to be signif-icantly and positively correlated with hs-CRP,VF,and TNF-α,respectively(P<0.05,P<0.01).More-over,the expression of monocyte cluster of differentiation 36(CD36),Toll-like receptor 4(TLR4),and nuclear factor-κB(NF-κB)in PBMC subsets decreased significantly after the intervention(P<0.05).In lymphocytes,CD36 and TLR4 expression lowered significantly after intervention(P<0.05 and P<0.01),while in granulocytes,CD36 and NF-κB expression decreased significantly(P<0.01 and P<0.05).Conclusion Exercise combined with dietary intervention can better body composition and physi-cal function in obese individuals,alleviating their chronic inflammation.The reduction in chronic in-flammation is closely related to the decrease in circulating fatty acid levels,which results in the re-duced expression of CD36 and TLR4 receptors on the surface of PBMC and the inhibition of the NF-κB signaling pathway.

Objective To investigate the effects of monocyte chemotactic protein-4(MCP-4)on pyroptosis and p38 mitogen-activated protein kinase(p38 MAPK)activation in human nasal epithelial cells(HNEpCs).Methods Forty patients diagnosed with chronic rhinosinusitis(CRS)were selected as the case group,and another 40 healthy individuals were selected as the normal group.Enzyme-linked immunosorbent assay(ELISA)was used to detect the levels of MCP-4 in serum samples from both groups.Receiver operator characteristic(ROC)curve analysis was performed to assess the diagnostic efficacy of serum MCP-4 levels for CRS.HNEpCs were divided into six groups:control group,5 mg/L lipopolysaccharide(LPS)model group,LPS+siRNA negative control(si-Con)group,LPS+siRNA MCP-4(si-MCP-4)group,LPS+pcDNA3.1-vector group,and LPS+pcDNA3.1-MCP-4 group.Cell viability was assessed using the cell counting kit-8(CCK-8),and cell proliferation activity was detected by 5-Ethynyl-2'-deoxyuridine(EdU)staining.Western blot was used to detect the expression levels of phosphorylated p38 MAPK(p-p38 MAPK),Gasdermin D(GSDMD),NOD-like receptor family,pyrin domain containing 3(NLRP3),apoptosis-associated speck-like protein(ASC),and caspase-1.ELISA was performed to measure the levels of tumor necrosis factor-α(TNF-α),interleukin-18(IL-18),and IL-1β in cell supernatants.The Transwell chamber was utilized to assess the effects of MCP-4 on the migratory capacity of HNEpCs.HNEpCs were divided into four groups:control group,10 ng/ml MCP-4 group,and 20 ng/ml MCP-4 group.Results Compared with the normal group,the level of MCP-4 in the serum of patients in the case group was significantly upregulated.ROC curve analysis showed that the area under the curve(AUC)for serum MCP-4 levels in the diagnosis of CRS was 0.921.In vitro experiments demonstrated that LPS stimulation reduced the survival rate and proliferation ability of HNEpCs,increased the expression of pyroptosis proteins,and upregulated p-p38 MAPK levels,and increased the release of TNF-α,IL-1β,and IL-18(P<0.01).Compared with the LPS model group,the LPS+si-MCP-4 group showed increased survival rate and proliferation ability of HNEpCs,decreased expression levels of p-p38 MAPK,pyroptosis proteins and reduced levels of TNF-α,IL-1β,and IL-18(P<0.01).In contrast,compared with the LPS model group,the LPS+pcDNA3.1-MCP-4 group exhibited further decreased survival rate and proliferation ability of HNEpCs,increased expression levels of p-p38 MAPK,pyroptosis proteins,and elevated levels of inflammatory cytokines TNF-α,IL-1β,and IL-18(P<0.01).Compared with the control group,there was no significant increase in the migration ability of HNEpCs in the 10 ng/mL MCP-4 and 20 ng/ml MCP-4 groups.Conclusion Inhibiting the expression of MCP-4 can block the activation of p38 MAPK,reducing pyroptosis and the release of inflammatory cytokines in HNEpCs.

Objective To investigate the effects of monocyte chemotactic protein-4(MCP-4)on pyroptosis and p38 mitogen-activated protein kinase(p38 MAPK)activation in human nasal epithelial cells(HNEpCs).Methods Forty patients diagnosed with chronic rhinosinusitis(CRS)were selected as the case group,and another 40 healthy individuals were selected as the normal group.Enzyme-linked immunosorbent assay(ELISA)was used to detect the levels of MCP-4 in serum samples from both groups.Receiver operator characteristic(ROC)curve analysis was performed to assess the diagnostic efficacy of serum MCP-4 levels for CRS.HNEpCs were divided into six groups:control group,5 mg/L lipopolysaccharide(LPS)model group,LPS+siRNA negative control(si-Con)group,LPS+siRNA MCP-4(si-MCP-4)group,LPS+pcDNA3.1-vector group,and LPS+pcDNA3.1-MCP-4 group.Cell viability was assessed using the cell counting kit-8(CCK-8),and cell proliferation activity was detected by 5-Ethynyl-2'-deoxyuridine(EdU)staining.Western blot was used to detect the expression levels of phosphorylated p38 MAPK(p-p38 MAPK),Gasdermin D(GSDMD),NOD-like receptor family,pyrin domain containing 3(NLRP3),apoptosis-associated speck-like protein(ASC),and caspase-1.ELISA was performed to measure the levels of tumor necrosis factor-α(TNF-α),interleukin-18(IL-18),and IL-1β in cell supernatants.The Transwell chamber was utilized to assess the effects of MCP-4 on the migratory capacity of HNEpCs.HNEpCs were divided into four groups:control group,10 ng/ml MCP-4 group,and 20 ng/ml MCP-4 group.Results Compared with the normal group,the level of MCP-4 in the serum of patients in the case group was significantly upregulated.ROC curve analysis showed that the area under the curve(AUC)for serum MCP-4 levels in the diagnosis of CRS was 0.921.In vitro experiments demonstrated that LPS stimulation reduced the survival rate and proliferation ability of HNEpCs,increased the expression of pyroptosis proteins,and upregulated p-p38 MAPK levels,and increased the release of TNF-α,IL-1β,and IL-18(P<0.01).Compared with the LPS model group,the LPS+si-MCP-4 group showed increased survival rate and proliferation ability of HNEpCs,decreased expression levels of p-p38 MAPK,pyroptosis proteins and reduced levels of TNF-α,IL-1β,and IL-18(P<0.01).In contrast,compared with the LPS model group,the LPS+pcDNA3.1-MCP-4 group exhibited further decreased survival rate and proliferation ability of HNEpCs,increased expression levels of p-p38 MAPK,pyroptosis proteins,and elevated levels of inflammatory cytokines TNF-α,IL-1β,and IL-18(P<0.01).Compared with the control group,there was no significant increase in the migration ability of HNEpCs in the 10 ng/mL MCP-4 and 20 ng/ml MCP-4 groups.Conclusion Inhibiting the expression of MCP-4 can block the activation of p38 MAPK,reducing pyroptosis and the release of inflammatory cytokines in HNEpCs.

Pheochromocytoma/paraganglioma is an adrenal tumor that secrets catecholamines and is extremely rare in pregnant women. Its clinical presentation is lack of specificity, and the combination of low prevalence and nonspecific clinical presentation makes diagnosis and treatment difficult. In this study, the clinical data and prognosis of 5 pregnant patients with pheochromocytoma/paraganglioma were analyzed. It was found that hypertension first occurred in 4 patients during pregnancy, and the clinical manifestations of each case were different. Surgical treatment is the first choice in the treatment, patients who cannot operate can choose radionuclide therapy, chemotherapy and targeted therapy. Through follow-up, they all showed recurrence and metastasis at different times. Among them, the patients who continued to be pregnant to the middle and late stages of surgical treatment progressed rapidly, and there were multiple bone metastases throughout the body in a short period of time, and two cases died in a short period of time. Therefore, effective diagnosis, individualized treatment and lifelong follow-up are particularly important.

ObjectiveTo investigate the association between thromboelastography (TEG) parameters and bleeding in patients with liver cirrhosis and whether TEG can be used to predict the risk of spontaneous bleeding in patients with liver cirrhosis, and to provide a basis for its preventive treatment. MethodsA retrospective analysis was performed for the clinical data of 174 patients with liver cirrhosis who attended Huadu People’s Hospital from May 2018 to April 2020 and did not receive invasive procedure, and according to the condition of bleeding, they were divided into non-bleeding group(n=64), gastrointestinal bleeding group(n=61), and mucocutaneous/oronasal bleeding group(n=49). The medical record system and laboratory information system were used to collect related information and laboratory test results for statistical analysis. The t-test was used for comparison of normally distributed continuous data between two groups; an analysis of variance was used for comparison between multiple groups, and the least significant difference t-test was used for further comparison between two groups. The Mann-Whitney U test was used for comparison of non-normally distributed continuous data between two groups, and the Kruskal-Wallis H test was used for comparison between multiple groups. MedCalc software was used for receiver operating characteristic (ROC) curve analysis, and the area under the ROC curve (AUC) was calculated for commonly used coagulation markers and TEG parameters in predicting the risk of bleeding in patients with liver cirrhosis. Cut-off value, sensitivity, specificity, positive predictive value, and negative predictive value were determined, and the Z test was used for comparison of indices in predicting mucocutaneous/oronasal bleeding. ResultsOf all 174 patients, 110 (63.2%) experienced spontaneous bleeding, among whom 61 (55.5%) had gastrointestinal bleeding and 49 (44.5%) had mucocutaneous/oronasal bleeding. There were significant differences in maximum amplitude (MA) and K between the bleeding group and the non-bleeding group (t=2.241 and -2.605, both P＜0.05). There were significant differences between the mucocutaneous/oronasal bleeding group and the non-bleeding/gastrointestinal bleeding groups in platelet count (PLT) and the TEG parameters of clot formation time, a-angle, MA, and coagulation index (CI) (F=3.947, H=12.867, F=4.007, F=8.498, F=5.420, all P＜0.05). Among the TEG parameters, reaction time and Lys30 were generally within the normal range, while there was a prolonged kinetics (K) time and reductions in a-angle, MA, and CI. PLT ≤40×109/L, MA ≤357 mm, K time ＞4.2 minutes, a-angle ≤51.6, and CI ≤-5.9 could be used to predict spontaneous mucocutaneous/oronasal bleeding in patients with liver cirrhosis (all AUC ＞0.7), with positive predictive values of 82.4, 88.9, 81.0, 72.7, and 73.7, respectively, and negative predictive values of 68.3, 72.5, 73.0, 69.4, and 66.7, respectively. ConclusionPLT and the TEG parameters of K time, a-angle, MA, and CI can predict spontaneous bleeding caused by abnormal coagulation in liver cirrhosis, while conventional coagulation parameters prothrombin time and activated partial thromboplastin time cannot predict such bleeding, which provides a basis for the treatment of coagulation disorder and transfusion of blood components for patients with liver cirrhosis.

Objective:To observe and compare the efficacy and safety of glucosamine sulfate (GS) and chondroitin sulfate (CS) in the treatment of adult Kashin-Beck disease (KBD), so as to provide effective medical evidence for the standardized treatment of adult KBD.Methods:A clinical randomized controlled trial was conducted in Fuyu County and Shangzhi City, KBD historical seriously ill areas in Heilongjiang Province. A total of 247 patients were selected according to the standard of "Diagnosis of Kashin-Beck Disease" (WS/T 207-2010). According to gender, age and KBD condition, they were randomly divided into GS and CS groups, 124 and 123 respectively. Follow up once a month to investigate the medication and clinical symptoms of patients, and distribute drugs for the next stage. Fasting blood and urine samples were collected before, during and at the end of treatment (0, 90 and 180 d). Serum interleukin (IL)-1β content and urine pyridine (PYD) level were measured by enzyme-linked immunosorbent assay (ELISA). The visual analogue scale (VAS) score, affected joints, self-evaluation of curative effect and side effects were evaluated through the questionnaire, joint dysfunction and drug efficacy were evaluated according to the criteria of "Evaluation of Therapeutic Effect of Kashin-Beck Disease" (WS/T 79-2011).Results:Expression of cytokines related to cartilage metabolism: at 180 d of treatment, serum IL-1β contents and urinary PYD levels in GS and CS groups were lower than those at 0 d of treatment ( Z = - 2.461, - 2.160, - 5.075, - 5.471, P < 0.05). VAS score: at 90 and 180 d of treatment, the scores of knee pain, stiffness and function in GS and CS groups were lower than those at 0 d of treatment ( P < 0.05); and at 180 d of treatment, the scores of knee stiffness and function in GS group were lower than those in CS group ( P < 0.05). Evaluation of affected joints: at 90 and 180 d of treatment, the scores of joint pain, swelling and stiffness in GS and CS groups were lower than those at 0 d of treatment ( P < 0.05). Self-evaluation of curative effect: at 180 d of treatment, the self-evaluation of curative of CS group were better than that at 90 d of treatment (χ 2 = 9.376, P < 0.05). Evaluation of side effects: at 90 and 180 d of treatment, the side effects in GS and CS groups were mainly gastrointestinal symptoms. Joint dysfunction score: at 90 d of treatment, the sum of effective rate and markedly effective rate in GS group was higher than that in CS group (χ 2 = 4.042, P < 0.05), but there was no significant difference between the two groups at 180 d of treatment (χ 2 = 0.869, P > 0.05). Conclusion:GS and CS have certain therapeutic effects on adult KBD, which can improve symptoms and reduce serum IL-1β content and urinary PYD level, but GS takes effects quickly, and its effect on improving joint stiffness and function are better than CS.