Objective:To observe the protective effect of deproteinized extract of calf blood (DECB) on the kidney injury of the diabetic rats, and to discuss its mechanism preliminarily.Methods:The male Wistar rats were intraperitoneally injected with STZ (65 mg·kg-1) to establish the diabetes models, then the model rats were randomly divided into model (M)group, and metformin (MMet, 105 mg·kg-1) group , low dose of combined administration (ML,105 mg·k-1 metformin+94.5 mg·kg-1 ,DECB) group, medium dose of combined administration(MM, 105 mg·kg-1 metformin+ 189 mg·kg-1 DECB) group, high dose of combined administration(MH, 105 mg·kg-1 metformin +378 mg·kg-1,DECB) group, another ten Wistar rats were selected as normal control(NC)group.The rats were intragastrically administed with metformin and intraperitoneally injected with DECB, once a day, total of 8 weeks.The rats in NC group and M group were given normal saline solution.The weights and blood glucose levels of the rats in various groups were determined;the levels of serum high density lipoprotein-cholesterol (HDL-C), low density lipoprotein-cholesterol (LDL-C), blood urea nitrogen (BUN), urinary albumin (UAlb), urine creatinine (UCR), serum creatinine (SCr), total cholesterol (TC), triglyceride (TG), uric acid (UA), glutathione (GSH), and malondialdehyde (MDA) were detected;the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were determined.The pathological changes of kidney tissue of the rats in various groups were detected by HE staining.Results:Compared with NC group, the weight of the rats in M group was reduced(P<0.05),and the levels of blood glucose,UAlb,UCr,SCr,UA,BUN,LDL-C,TC,TG,and MDA were increased(P<0.05);the levels of HDL-C and GSH were obviously reduced(P<0.05),and the activities of SOD adn GSH-Px were obviously reduced(P<0.05).Compared with M group,the weights of the rats in MM and MH groups were increased (P<0.05), and the levels of blood glucose,UAlb,UCr,SCr,UA,BUN,LDL-C,TC,TG, and MDA were decreased (P< 0.05);the levels of HDL-C and GSH were increased (P<0.05),and the activities of SOD and GSH-Px were increased (P<0.05).The pathological observation of kidney tissue showed that the rats in M group had obvios kidney tissue lesions with glomerular congestion and renal tubular edema compared with NC group;compared with M group,the pathological changes of the kidney tissue of the rats in drug administration groups were significantly improved, the renal tubular vacuoles were reduced, and the interstitial hyperplasia was not obvious.Conclusion:DECB combined with metformin can reduce the blood glucose level, regulate blood lipid, improve the pathological changes of kidney tissue in the diabetic rats, reduce the renal damage, and enhance the antioxidant capacity of the body.

Science is the power of improving the academic discipline in hospitals.Evaluation of research has always be the key issue for research management.Using stratification method to establish the evaluation system was constructed directly by high level research output and based on the process of scientific,which can conduct quantitative assessment for individual level.The contents included three parts:process indicators,basic achievement indicators and high level achievements indicators.The implementation effect was satisfied during last year.The evaluation system stimulates high level research output.

Objective:To observe the protective effect of deproteinized extract of calf blood (DECB)on the ethanol-induced liver injury of the mice,and to preliminaryly discuss its mechanism. Methods:Sixty healthy ICR mice were divided into control group,model group,positive drug group,low,medium and high doses of DECB groups (n=10).By intragastric administration,the mice in control group were given 20 mL·kg-1 saline solution, the mice in low,medium and high doses of DECB groups were administrated with 0.125,0.250,0.500 g·kg -1 DECB,and the mice in positive drug group were administrated with 0.63 g·kg -1 Hugan Tablets;once a day for 30 d. 1 h after the last administration,except control group,the mice in other groups were administrated with one-time grant of 50% ethanol 14 mL·kg -1 ,and fasted for 16 h to establish the models of acute alcohol liver injury.The endurance alcohol time and drunk time of the mice were determined,the activities of aspartate aminotransferase (ALT)and alanine transaminase (AST)activity in serum of the mice were detected,the levels of triglyceride (TG),glutathione (GSH)and malonic dialdehyde (MDA)in liver tissue were determined,and the pathological changes of liver tissue were detected.Results:Compared with model group,the drunk symptoms of the mice in different doses of DECB groups were obviously reduced,the endurance time of the mice in high dose of DECB group and positive drug group was prolonged (P <0.05),and the drinking time was shortened (P <0.05);the ALT and AST activities in serum in mediun and high doses of DECB groups were significantly lower than those in model group (P <0.05).Compared with model group,the MDA and TG levels in liver tissue of the mice in medium and high doses of DECB groups and positive drug group were obviously reduced,and the GSH levels were increased (P <0.05);compared with model group,the pathological damages of liver tissue of the mice in high dose of DECB group caused by ethanol were significantly reduced.Conclusion:DECB can improve ethanol-induced liver injury which may be related to the inhibition of hepatic oxidative stress response.

OBJECTIVETo evaluate the clinical effects of bone graft from the mandible in repairing orbital floor defects.

METHODSBone grafts from the mandible were used to treat 11 cases of orbital floor defects and followed up for 6-12 months.

RESULTSThe surgical incisions healed primarily in all 11 patients. The orbital floor structure was restored. No vision loss, limited eye movement, implant infection, or resorption were observed postoperatively, and no complications occurred in the supply area.

CONCLUSIONSBone grafts from the mandible were an ideal material to repair orbital floor defects.

Objective:To screen the characteristic gut microbiota and fecal metabolites related to the efficacy of oxaliplatin-based neoadjuvant chemotherapy in patients with colorectal cancer liver metastasis, to analyze the relationship between gut microbiota and fecal metabolites, and to evaluate the predictive value of relevant markers for the efficacy of neoadjuvant chemotherapy in patients with colorectal cancer liver metastasis.Methods:This is a case-control study, 34 patients with colorectal cancer liver metastasis who were treated in Qilu Hospital of Shandong University from October 2021 to July 2022 were selected as the research objects, and were divided into chemotherapy effective group (20 cases) and chemotherapy ineffective group (14 cases) according to the efficacy evaluation criteria. Logistic regression was used to construct a prediction model to screen the microbiota and metabolic markers capable of predicting the effect of chemotherapy, and the receiver operating characteristic (ROC) curve and survival analysis curve were plotted to evaluate the predictive effect of related microbiota and metabolites on the efficacy of neoadjuvant chemotherapy.Results:There was no significant difference in the α and β diversity of gut microbiota between the patients in the chemotherapy effective group and in the ineffective group (all P>0.05). In terms of species, the relative abundance of 5 species was up-regulated and 10 species were down-regulated in the chemotherapy-effective group compared with the chemotherapy-ineffective group, and the difference was statistically significant (all P<0.05), among which Prevotella salivae could effectively predict the chemotherapy effect (AUC=0.750, P=0.007), with a sensitivity of 80.0% and a specificity of 71.4%. The overall survival of patients with high abundance (17 cases) was lower than that of patients with low abundance (17 cases) ( χ 2=5.239, P=0.022). In terms of metabolites, 20 metabolites were up-regulated and 4 metabolites were down-regulated in the chemotherapy-effective group compared with the chemotherapy-ineffective group, and the difference was statistically significant (all P<0.05), among which threonine and prostaglandin F2α-1-ethanolamide could distinguish between patients who responded to chemotherapy and those who did not respond to chemotherapy (AUC=0.743, 0.707, all P<0.05), and the overall survival of patients with high levels of relative abundance (17 cases) was higher than that of patients with low levels (17 cases) ( χ 2=4.748, 5.407, all P<0.05). The Logistic regression model of Prevotella salivae and prostaglandin F2α-1-ethanolamide was obtained through screening analysis, and the ROC curve results showed that the model had a good predictive value (AUC=0.836, sensitivity: 90.0%, specificity: 78.6%), and the overall survival of patients with high predict probability (17 cases) predicted by the model was higher than that of patients with low predict probability (17 cases) ( χ 2=9.260, P=0.002). Conclusion:Prevotella salivae and prostaglandin F2α-1-ethanolamide can be used as predictive biomarkers of neoadjuvant chemotherapy for colorectal cancer liver metastasis, and the model has good clinical reference value for prognosis assessment of patients in this cohort.

Objective: To explore the relationship between MSX1 gene detection and tooth loss in a Van der Woude syndrome (VWS) family Methods : DNA was extracted from the venous blood of 2 patients with dental hy⁃podontia in the 9th family of Van der Woude syndrome (VWS) families and 62 controls with complete dentition. Primers were designed for the MSXl gene. The coding regions of exons 1 and 2 of the MSX1 gene were amplified by PCR. The purified products of exons 1 and 2 of the MSX1 gene were sequenced and analyzed by sequence alignment Results: The ivs2+68 C>T polymorphism in the MSX1 gene was found in the VWS9 members with tooth loss, and the VWS pa⁃tients with IRF6 gene mutations had increased tooth loss Conclusion Congenital tooth loss in the patients with con⁃genital missing teeth in VWS family 9 may be related to the ivs2 + 68 C> T polymorphism of the MSX1 gene.