Objective To investigate the sedative effects and the adverse reactions in the elderly patients received different speed of dexmedetomidine (Dex) intravenous infusion. Methods Eighty elderly cases were randomly divided into four groups. Group D0 was the control group, while the group D1, D2 and D3 were the trial groups. The heart rates, blood pressure, SpO2, Ramsay sedation score and Narcotrend value were recorded. Results The sedation onset time of the D2, D3 group was faster than those in the D0 and D1 groups (P <0.05, respectively), and the duration of sedation in groups D2 and D3 were significantly longer than that in the D0 and D1 groups (P < 0.05). Among the four groups, no significant differences in the incidence of hypotension or bradycardia needed vasopressors or atropine to treat and oxygen saturation were shown (P > 0.05). Conclusion Intravenous infusion of Dex by doses of 0.75 ~ 1.0 μg/(kg·h) during hip surgery in the elderly patients under spinal anesthesia could lead to a safe and effective sedation.

Objective To explore the relationship between plasma homocysteine levels and diabetic peripheral neuropathy (DPNP). Methods A crossectional analysis was conducted on 227 patients with type 2 diabetes. Peripheral neuropathy was confirmed using electromyography (EMG). The risk factors possibly associated with diabetic neuropathy or plasma homocysteine levels were analyzed in relation to likelihood of occurrence of DPNP. Results Eighty patients with neuropathy and 147 patients without neuropathy were included. Plasma homocysteine levels were significantly higher in patients with diabetic neuropathy [( 12. 6 ± 3.6 ) μmol/ L] than without diabetic neuropathy [( 8. 2 ± 0. 9 ) μmol/L] ( P ＜0. 001 ), and the relationship remained significant after adjusting for duration of diabetes, glycosylated hemoglobin A1c (HbA1c), age, renal status, serum folate acid and vitamin B12, and metformin [OR 1.15( 1.02-1.28 ) ,P ＜ 0. 05]. In addition, per increase of 4. 0 μmol/L plasma homocysteine was closely related to the occurrence of neuropathy after controlling for per unit increase of other confounding factors [OR 1.17(0. 94-1.33), P ＜ 0. 05]. Conclusions Hyperhomocysteinemia was an independent risk factor for the occourence of diabetic peripheral neuropathy.

Objective:To explore indicators related to visceral fat index by constructing a random forest model.Methods:In this cross-sectional study, the laboratory measures and body composition analysis records of 617 hospital employees (in-service and retired) who underwent physical examination in Heilongjiang Provincial Hospital Health Management Center from March to September 2021 were selected. The subjects were divided into a training set ( n=411) and a test set ( n=206) with the ratio of 2∶1. A total of 110 predictors were included in the model. The model was constructed with the training set and was evaluated with the test set. The optimal number of nodes and decision trees were selected to evaluate the prediction performance of the optimal model. And the top 10 relatively important factors were selected for further investigation. The 617 participants were further divided in to groups according to the visceral fat index: the normal or high visceral fat index group, and the differences of the top 10 relatively important factors were further compared between the two groups. Results:The optimal number of nodes of the final random forest model was 39 and the number of decision trees was 300. The accuracy, precision, sensitivity and specificity of the model was 83.3%, 73.9%, 89.4% and 78.7%, respectively. The area under the receiver operating characteristic curve and 95% confidence interval of the model was 0.881 (0.832-0.931). The top 10 relatively important factors in the model were body mass index, gender, age, serum uric acid, red blood cell count, monocyte cell count, C-peptide, carcinoembryonic antigen, glycosylated hemoglobin and glutamyl transpeptidase. There were significant differences in the up-mentioned 10 indicators between the subjects with normal and high visceral fat index (all P<0.05). Conclusions:The random forest model built in this study has good performance in predicting visceral fat index, and visceral fat is related with changes in liver function, pancreas function and immune function.

Objective:To investigate the role of microRNA-187-5p (miR-187-5p) on osteoporosis (OP) as well as the related molecular mechanism.Methods:The level of miR-187-5p and tartrate-resistant acid phosphatase (TRAP, the osteoclast marker) was quantitatively detected in TRANKL-induced OP group and control (con) group by reverse transcription-quantitative PCR (RT-qPCR) ; Cell counting kit 8 (CCK8) was used to measure the viability of murine macrophage cell line (RAW264.7) ; Western blot was used to detect the expression of p65 and TNFα. Moreover, the dual luciferase reporter assays was applied to detect the interaction between miR-187-5p and p65.Results:The osteoclast proliferation determined by CCK8 and the mRNA level of TRAP detected by RT-qPCR demonstrated that the growth of osteoclast was inhibited in OP group compared with that in con group ( P=0.008; P=0.017) , which reversed by miR-187-5p mimic stimulation ( P=0.023; P=0.037) . The miR-187-5p was lowly expressed in OP group compared with that in con group ( P=0.031) ,which was increased by miR-187-5p mimic treatment compared with miR-187-5p NC treatment ( P=0.041) . Moreover, western blot indicated that the protein level of p65 and TNFα in OP group were up-regulated compared with that in con group ( P=0.034; P=0.024) , which restored by the miR-187-5p mimic co-incubation ( P=0.028; P=0.036) . Moreover, the RT-qPCR indicated that the mRNA level of p65 in OP group was also increased compared with that in con group ( P=0.039) , and the miR-187-5p mimic co-incubation decreased the mRNA level of p65, compared with miR-187-5p NC group ( P=0.025) . The dual luciferase reporter assays indicated that there was an interaction between miR-187-5p and p65. Conclusion:miR-187-5p alleviates OP through inhibiting the activity of osteoclast via RANKL/NFκB signaling

Objective To observe the changes of proliferation and apoptosis of colon cancer cell line treated with oxaliplatin after the downregulation of ERRα and to investigate the mechanism.Methods Colon cancer cell lines Colo-205,HCT-116,SW620 and HT-29 were cultured by adherent cells and in accordance with the given intervention,they were divided into group XCT790-OHP-HCT-116(after oxaliplatin treatment,ERR αinhibitor XCT790 was administered),group siERRα-OHP-HCT-116(after oxaliplatin treatment,siERR α was transfected into HCT-116 cells and downregulated ERR αexpression),oxaliplatin intervention group(group OHP-HCT-116)and the control group(NC group)which was given no intervention.The experiment was divided into siERR αgroup with siERR α transfected with HCT-116 cells,downregulated ERR αexpression and the negative control group(siNC group)transfected with siNegative Control.Using Western blot method and real-time quantitative(qRT)-PCR for the detection of colorectal cancer cell ERRαprotein and mRNA expression,the expression of ERR αwas downregulated by ERR αinhibitors XCT790 and siERR,and apoptosis and proliferation of colon cancer cells were detected by flow cytometry and MTT.Western blot and qRT-PCR were used to detect apoptosis and proliferation-related gene proteins and mRNA expression.Results ERR αand mRNA protein in HCT-116 were higher than those of Colo-205,SW620 and HT-29 cell lines(P<0.05); in the XCT790-OHP-HCT-116 group,the early apoptosis rate was higher than those of the NC group and OHP-HCT-116 group(P<0.05),the survival rate of cell culture in 72 and 96 h in the XCT790-OHP-HCT-116 group was lower than those in the NC group and OHP-HCT-116 group(P<0.05).The siERR α HCT-116 cells transfected with down-regulation of ERR expression,siERR α -OHP-HCT-116 group early apoptosis rate was lower than those of NC group and OHP-HCT-116 group(P<0.05),siERR -OHP-HCT-116 group cells cultured for 72 and 96 h after the survival rate was lower than the NC group and OHP-HCT-116 group(P<0.05);After the downregulation of ERRαby siERR alpha transfected with HCT-116 cells,the early apoptotic rate in the group siERRα-OHP-HCT-116 was lower than that in the group NC and group OHP-HCT-116(P<0.05),the survival rate of the group siERRα-OHP-HCT-116 after 72 and 96 h were lower than those in the group NC and group OHP-HCT-116(P<0.05),siERR α was transfected into HCT-116 cells,compared with the siNC group,YAP1,p73,p63,MDM2, Capase 8,Capase 9 protein in the siERR group decreased(P<0.01),there was no significant difference in the level of mRNA(P>0.05).Conclusion The downregulation the expression of ERRαcan promote colon cancer cell apoptosis,inhibit proliferation,and enhance the killing effect of oxaliplatin on colon cancer cells.

Objective : To investigate the characteristic genes of Programmed cell death protein 1 ( PD-1) immuno- therapy sensitivity in Hepatocellular carcinoma ( HCC) ． Methods : The common differential genes in GSE202069 and ERP117672 data sets were investigated by Weighted Gene Co-expression Network Analysis ( WGCNA) and Difference analysis，and the characteristic genes of PD-1 immunotherapy sensitivity were screened through Lasso regression．The expression levels of characteristic genes in HCC were predicted by GEPIA and Ualcan databases， and their expression was verified by real-time quantitative reverse transcription polymerase chain reaction ( RT- qPCR) ，Western blot (WB) and Immunohistochemistry (IHC) ．3-hydroxybutyrate dehydrogenase 1 (BDH1) over- expressed cell line was constructed，followed by cell counting kit-8 ( CCK-8) ，EdU，cell scratches and Transwell experiment to investigate the effects of BDH1 on the proliferation，migration and invasion of HCC cells. Results: Total of 118 common differentially expressed genes were identified in two datasets by WGCNA and differential anal- ysis．The characteristic genes associated with PD-1 immunotherapy sensitivity screened through Lasso regression in- cluding Flavin containing dimethylaniline monoxygenase 3 ( FMO3 ) ，Peroxisomal trans-2-enoyl-CoA reductase (PECR) ，BDH1 ，Solute carrier family 7 member 1 ( SLC7A1 ) ，Cytochrome b5 type A ( CYB5A) and Phos- phoenolpyruvate carboxykinase 1 (PCK1) ． Survival analysis showed that BDH1 was most associated with HCC ( Overall survival : P＜0. 001，Recurrence : P = 0. 007) ．GEPIA and Ualcan databases showed low expression of BDH1 in HCC tissues，while RT-qPCR , WB，and IHC further confirmed this．CCK-8，plate cloning assay，EdU staining，cell scratch，and Transwell experiments showed that compared with the Hep3B pCDH group，overexpres- sion of BDH1 resulted in a decrease in the absorbance of HCC cells (t = 4. 766，P＜0. 01) ，a decrease in the num- ber of clone formation (t = 16. 02，P＜0. 000 1) ，a decrease in the proportion of proliferating cells (t = 23. 13，P ＜0. 000 1) ，a decrease in cell migration rate (t = 25. 28，P＜0. 000 1) ，and a decrease in the number of small compartments (t = 10. 78，P = 0. 004) ． Conclusion BDH1 is a characteristic gene for observing the sensitivity of PD-1 immunotherapy in HCC patients． BDH1 could inhibit the proliferation ，migration ，and invasion ability of HCC cells in vitro.