Objective:To analyze the application of sensory stimulation based on the whole process accompanying of relatives in regain of consciousness in coma patients after aneurysm embolization.Methods:Comatose patients after aneurysm embolization in Department of Cerebrovascular Disease, Suining Central Hospital of Sichuan Province were selected as the research objects. 59 patients from June to December in 2019 were included in the control group and received routine sensory stimulation. 60 patients from January to August 2020 were included in the study group, and the sensory stimulation based on the whole process accompanying of relatives was implemented. Glasgow Coma Scale (GCS) , Chinese version of Coma Recovery Scale-Revised (CRS-R) and Mini-Mental State Examination (MMSE) were applied to compare the coma status, recovery status and cognitive function of the two groups before and after the intervention. The complications of the two groups were compared as well.Results:After 3 months of intervention, the scores of GCS, CRS-R and MMSE of the study group were all higher than those of the control group, with statistically significant differences ( P<0.05) . Within 3 months after operation, the total incidence of complications in the study group was lower than that in the control group, and the difference was statistically significant ( P<0.05) . Conclusions:Sensory stimulation based on the whole process accompanying of relatives is helpful to reduce the degree of coma, promote the recovery of patients, and reduce the incidence of complications.

Objective:To analyze and evaluate the expressions and clinical value of tuftelin (TUFT1) and Krüppel-like factor 5 (KLF5) in hepatitis B virus (HBV)-related hepatocellular carcinoma (HCC) tissues.Method:KLF5 mRNA and TUFT1 mRNA transcriptional status in cancer and non-cancer groups were compared according to the Cancer Genome Atlas (TCGA) database. The differences and prognostic value between the groups were analyzed. Postoperative liver cancer and its paired pericancerous tissues, with the approval of the ethics committee, were collected to build tissue chips. The expression of KLF5 and TUFT1 and their intracellular localization were verified by immunohistochemistry. Tissue expression and clinicopathological characteristics were analyzed by immunoblotting. SPSS software was used to analyze the relationship between SPSS and patient prognosis.Results:The transcription level of TUFT1 or KLF5 mRNA was significantly higher in the HCC group than the non-cancer group ( P ?

The monitoring of malignant transformation of hepatocytes or early diagnosis of primary hepatocellular carcinoma (PHC) remains a challenge in the medical world. Routine examinations including serum alpha-fetoprotein level and ultrasound examination have a limited value in the diagnosis of small hepatocellular carcinoma; however, the effective treatment of PHC depends on its early diagnosis. In recent years, molecular markers including important signaling molecules in PHC-related pathways, carcinoembryonic proteins, and non-coding RNA help with the monitoring of malignant transformation of hepatocytes or early diagnosis of liver cancer. This article reviews the valuable molecular markers in the monitoring of malignant transformation of hepatocytes or early diagnosis of liver cancer.

Objective The experiment project was designed to explore the variation of NaI (Tl) gamma spectrometer channels with environmental temperature. ⁶⁰Co and ¹⁵²Eu were used to verify the reliability of the correction methods. Methods Two correction methods were applicated, which were curve fitting correction method and known measurement peak correction method. Results The experimental results showed that temperature changes had an effect on NaI (Tl) measured spectra peak. The relative peak will shift to the right at 5℃ by 9.6%, and to the left at 60℃ by 16%, with the reference temperature set at 25℃. The two methods are based on the channel change due to temperature changes, and they could effectively correct the temperature peak-drift. Conclusion In order to make the measured spectrum information accurate and reliable in field monitoring, it is suggested to monitor the environmental temperature so as to correct the measured data.

Objective: To investigate the dynamic expression of hepatic carnitine palmitoyltransferase-II (CPT-II) in the mitochondrial inner membrane during hepatocyte malignant transformation induced by lipid accumulation. Methods: Male Sprague-Dawley rats were divided randomly into control, fatty liver, and induced cancer groups, which were fed with normal, high-fat (HF), and HF containing 2-fluorenylacetamide (0.05%, 2-FAA) diets, respectively, for 14 weeks. One rat from each group was sacrificed every two weeks and the blood and liver samples were collected. Liver morphological changes were evaluated with hematoxylin and eosin staining, and the liver tissue samples were divided into control, fatty liver, degeneration, precancerous, and cancerous groups accordingly. Hepatic lipids were dyed by the oil red O method. The CPT-II expression was measured by immunohistochemistry and compared with the specific CPT-II concentration (ng/mg liver protein, ng/mg P) among different groups. Serum levels of circulating total cholesterol (Tch), triglyceride (TG), alanine aminotransferase (ALT), and aspartate aminotransferase (AST) were quantitatively analyzed. Results: Massive lipid accumulation hepatocytes was seen in rats on HF and HF containing 2-FAA diets. The lipid levels in the control group were significantly lower than those in the fatty liver (t = -11.556, P < 0.001), degeneration (t = -4.847, P = 0.04), precancerous (t = -13.652, P = 0.005), and cancerous groups (t = -10.896, P = 0.008). The serum TG and Tch levels in the degeneration, precancerous, and cancerous groups were 2-3 times higher than those in the control group (P < 0.05). After 2-FAA treatment, the morphological changes of rat hepatocytes showed the progression from degeneration and precancerosis to cancerosis, with hepatocyte injury. The serum AST and ALT levels in the degeneration, precancerous, and cancerous groups were significantly higher (4-8 times) than those in the control group (P < 0.05). The specific concentration of liver CPT-II expression was significantly reduced during hepatocyte malignant transformation, as confirmed by immunohistochemistry, with the CPT-II levels significantly lower in the cancerous group than in any of other groups (P < 0.05). Conclusion Low hepatic CPT-II expression might lead to abnormal lipid accumulation in hepatocytes, which should promote the malignant transformation of hepatocytes.

Objective: To quantitatively detect CD44 expression in patients with nonalcoholic fatty liver disease (NAFLD) for comparative analysis. Methods: Patients with chronic liver diseases accompanied with or without NAFLD, including chronic hepatitis B, cirrhosis and hepatocellular carcinoma after chronic hepatitis B, and healthy blood donors as normal controls who admitted to the Affiliated Hospital of Nantong University from May to October 2018 were selected. The proportion of CD44 positive cells was analyzed by flow cytometry. CD44 level was quantified by an enzyme-linked immunosorbent assay, and the biochemical indicators such as serum aspartate aminotransferase, alanine aminotransferase activity, total cholesterol and triglyceride were routinely analyzed. The cancerous and adjacent cancerous tissues of patients accompanied with or without NAFLD were collected by self-matching method and analyzed by immunoblotting and histochemistry and compared by CD44 integrated optical density. Image-Pro Plus version 6.0, Image J, GraphPad Prism 5.0, Photoshop, Microsoft Excel and IBM SPSS statistics 23 were used to analyze and draw pictures. An independent sample t-test was used to compare the differences between groups. Results: Patients accompanied with NAFLD had hepatocyte injury and dyslipidemia. NAFLD and chronic liver disease patients had significantly elevated serum CD44 levels than normal control group (P < 0.01). CD44 positive lymphocyte ratio was 78.19 % ± 16.33 % in NAFLD patients and 68.47% ± 20.91% in chronic hepatitis B group, which was higher than the control group (46.51% ± 20.52%). Chronic hepatitis B group with steatosis had significantly higher CD44 concentration (181.42 ± 49.36) ng/ml than chronic hepatitis B group (142.52 ± 53.87) ng/ml and normal control group (99.47 ± 15.23) ng/ml. CD44/GAPDH ratio in the liver cancer group (1.306 ± 0.614) was significantly higher than paracancerous group (0.477 ± 0.291) and the difference between the two groups was statistically significant (t = 3.451, P = 0.004). The integrated optical density of CD44 in the NAFLD-related liver cancer and paracancerous group were 25.721 ± 5.881 and 14.155 ± 4.001 and the difference between the groups was statistically significant (t = 14.544, P < 0.001). The pathological features of high expression of CD44 in patients with hepatocellular carcinoma were significantly correlated with HBV infection, tumor size, single/multi-center, and lymph node metastasis, degree of differentiation, TNM grade, Child-Pugh score, portal vein tumor thrombus and extrahepatic metastasis. HCC patients with NAFLD had significantly higher serum CD44 (234.62 ± 69.40) ng/ml than patients without NAFLD (186.49 ± 58.89) ng/ml (t = -3.191, P = 0.002), but there was no statistically significant difference in the clinicopathological characteristics between the high/low CD44 groups of HCC patients with NAFLD. Conclusion The results suggest that CD44 is abnormally activated and its mechanism may play an important role in the progression of NAFLD.