Objective To investigate the mechanistic role of LncRNA MITA1 in the progression of hepatocellular carcinoma (HCC). Methods qRT-PCR was employed to assess the expression levels of MITA1 mRNA in HCC tissues and cells. The pcDNA3.1 recombinant plasmid vector was utilized to overexpress MITA1. After treatment, SMMC7721 cells were categorized into three groups, the normal group, the OE-MITA1-NC (negative control) group, and the OE-MITA1 (overexpression) group. Cell proliferation was evaluated using a colony formation assay, while cell invasion was assessed via the Transwell assay. Cell viability was determined using the Cell Counting Kit-8 (CCK-8) assay. Protein expression levels of Vimentin, MMP-2, and N-Cadherin were measured by western blotting. Additionally, the dual-luciferase reporter assay was conducted to verify the targeting relationship between MITA1 and miR-30b-3p. Results Compared with adjacent normal liver tissues, HCC tissues and cells exhibited significantly higher expression levels of MITA1 mRNA and lower expression levels of miR-30b-3p mRNA (P<0.05). Under MITA1 overexpression conditions, the OE-MITA1 group demonstrated elevated MITA1 mRNA expression levels (P<0.05). Compared with the normal and OE-MITA1-NC groups, the OE-MITA1 group exhibited increased cell proliferation, invasion capacity, and enhanced cell viability (P<0.05). Furthermore, protein expression levels of Vimentin, MMP-2, and N-Cadherin were significantly higher in the OE-MITA1 group compared with the other two groups (P<0.05). The dual-luciferase reporter assay confirmed a targeting relationship between MITA1 and miR-30b-3p, with MITA1 expression negatively regulating miR-30b-3p expression. Conclusion LncRNA MITA1 can promotes the proliferation, invasion and cell activity of liver cancer by binding miR-30b-3p, MITA1 may serve as a potential therapeutic target for the diagnosis and treatment of HCC.

Objective To investigate the effect of LncRNA CUDR knock-down on invasion, proliferation and apoptosis of hepatocellular carcinoma cells. Methods CUDR shRNA lentivirus plasmid was used to transfect SMMC-7721 hepatoma cell line. The CUDR knockdown group, control group and empty plasmid group were set up respectively. The transfection efficiency of CUDR shRNA was detected by RT-PCR method, the invasive ability of the three groups was detected by Transwell, the ability of cell aggregation and proliferation was detected by tumor ball formation test, and the apoptosis rate of hepatocellular carcinoma cells was detected by flow cytometry. Results The results of RT-PCR detection showed that the expression of CUDR mRNA in the knockdown group was significantly lower than that in the control group and empty plasmid group after CUDR shRNA transfection（P<0.001）. The results of Transwell, tumor ball formation test and apoptosis assay showed that the invasion and aggregation abilities of hepatoma cells in the CUDR knockdown group were significantly lower than those in the control group and the empty plasmid group, and the apoptosis rate was increased in CUDR knockdown group(P<0.001). Conclusion Knocking down the expression of LncRNA CUDR can inhibit the invasion and proliferation of HCC and promote the apoptosis of hepatocellular carcinoma cells, LncRNA CUDR may be a potential therapeutic target for HCC.

Objective: To investigate the changes and significance of plasma fibrinogen (FIB) and D-dimer level in patients with different types small vessel disease (CSVD). Methods: The plasma FIB and D-dimer level of 134 CSVD patients and 75 controls were detected and the risk factors of CSVD were analyzed. Results: The ratio of hypertension, plasma FIB level and plasma D-dimer level of CSVD and its subtypes (lacunar infarction/LI, white matter lesions/WML, LI combined WML) patients were all obviously higher than controls (P<0.05). Logistic regression analysis showed that D-dimer was risk factor for CSVD, LI, WML and LI combined WML (P<0.05); FIB was risk factor for CSVD, LI and LI combined WML (P<0.05). Conclusions: As risk factors for CSVD, FIB and D-dimer involve in the development of CSVD, but the risk factors for subtypes of CSVD are different.

Objective: To explore the correlations between serum lipid level and severity of white matter lesions (WML). Methods: The clinical data of 214 WML patients were retrospectively analyzed, and 61 healthy examined people at the same term were taken as control. The blood lipid correlation indexes of all the subjects were detected; and Logistic regression was used to analyze the risk factors of WML. Results: The difference of total cholesterol (TC) and low-density lipoprotein cholesterin between control group and WML group with different severity was statistically significant (P<0.05), which was related to the severity of WML. Logistic regression showed that age, hypertension and TC are risk factors of WML. Conclusions: Clinicians can prevent the occurrence of WML or delay the course of WML by controlling the risk factors of WML, such as hypertension and high TC level.

Objective: To observe the relationships between serum matrix metalloproteinase-9 (MMP-9) level and cognitive dysfunction after cerebral infarction of patients with acute cerebral infarction.Methods: Initial cerebral infarction patients were divided into cognitive dysfunction group (≤26) and non cognitive dysfunction group (<26) according to MoCA score. Healthy checkup at the same term were taken as healthy control group. ELISA was used to detect the serum MMP-9 level of 124 subjects. Results: The serum MMP-9 level of patients in cognitive dysfunction group was obviously higher than non cognitive dysfunction group and healthy control group (P<0.05). Logistic regression showed that MMP-9 and age were independent risk factors for cognitive dysfunction after cerebral infarction. Conclusions: Increasing of serum MMP-9 level in patients with acute cerebral infarction maybe related to cognitive dysfunction after cerebral infarction.