[Use of indocyanine green fluorescence navigation in laparoscopic anatomical hepatectomy].

Objective: To examine the clinical value of fluorescence-guided indocyanine green (ICG) laparoscopic anatomical hepatectomy in the treatment of primary hepatocellular carcinoma. Methods: Data from patients diagnosed with hepatocellular carcinoma and who underwent laparoscopic hepatectomy with ICG fluorescence navigation in the Department of Liver Surgery and Liver Transplantation Center of West China Hospital between September 2020 and May 2022 were retrospectively collected. There were 53 males and 19 females, with an age of (55.5±12.9)years(range:42.6 to 68.4 years). Among them, 13 of the cases underwent laparoscopic anatomical liver resection(LALR) guided by tans-arterial ICG,43 of the cases received LAIR guided by portal vein negative ICG, and 16 of the cases received LALR positive by portal vein. Comparison among the three groups was performed by one-way ANOVA; and the rank sum test was used for comparison between groups. The counting data was expressed as percentage,and the χ2 test or Fisher's exact probability method was used for comparison between groups. Results: (1) Postoperative pathology: Resection R0 was achieved in all operations. The maximum tumor diameter of the patients in the arterial staining group, the reverse staining group, and the positive staining group(M (IQR)) was 2.5 (2.4) cm, 3.0 (2.5) cm and 3.0(2.4) cm,respectively. There were no statistically significant differences in the maximum tumor diameter between the three groups (P=0.364). The minimum tumor margin was 1.1 (1.1) cm, 1.0 (1.0) cm, 1.1 (1.6) cm in the the arterial staining group, reverse staining group and the positive staining group, respectively. There was no significant difference in the margin among the three groups (P=0.878). (2) Operation conditions: the operation time of the arterial staining group, the negative staining group, and the positive portal staining group was (348±93)minutes,(277±112)minutes,and (295±116)minutes,respectively. There were no significant differences in operation time among the three groups (P=0.134). The intraoperative blood loss of the three groups was 80(150)ml,200(350)ml,and 100(150)ml,respectively. There was no statistically significant difference in intraoperative bleeding volume between the three groups(P=0.743). All cases were not transfused during the operation and were not converted to laparotomy. ALT in the arterial staining group was higher than in the negative staining group in the first two days after the operation ((559±398)IU/L307(257) IU/L, q=235.5,P=0.004;(611±389)IU/L(331±242) IU/L, q=265.2, P=0.002). There was only one case of a grade III complication (Clavien-Dindo grading system) postoperative complication in the negative and positive staining group of the portal vein, respectively. Tumor markers in all patients decreased to the normal range after 2 months of operation. Conclusion: Laparoscopic anatomical hepatectomy guided by ICG fluorescence through arterial staining and portal vein staining is safe and feasible for primary hepatocellular carcinoma treatment.

[A study on the correlation between occupational radiation exposure and risk of chronic metoblis disease].

Objective: To study the correlation between occupational radiation exposure and chronic metabolic diseases. Methods: The status of chronic metabolic diseases of medical workers were compared in 5 hospitals in Hangzhou. As representatives of chronic metabolic diseases, diabetes and metabolic syndrome (MS) were compared in association with duration of radiation exposure. Results: Long-term ionizing radiation (IR) exposure was led to increased blood pressure, fasting blood glucose (FBG) , dyslipidemia, gallbladder disease, and MS. The years of radiation exposure was associated with lens opacity, gallstone and MS in men and gallbladder polyps in women. Radiation working more than 10 years is one of the independent risk factors for increased FBG and MS. Moreover, the risk of FBG increase in the group of radiation working more than 10 years was 3.052 times of that the non-exposed group, and the risk of MS occurrence was 4.132 times that of the non-exposed group. Conclusion: Long-term exposure to IR increases the risk of chronic metabolic diseases.

Screening of genes related with intervertebral disc disease by dynamic differential interaction network analysis.

AIM: Gene expression profiles for intervertebral disc (IVD) cells treated with different osmolarities were compared to identify key genes associated with intervertebral disc diseases. MATERIALS AND METHODS: Microarray data was downloaded from Gene Expression Omnibus (GEO) database and pre-processed using package of R. Gene co-expression was determined with Pearson correlation coefficient. Interaction networks were established with the protein-protein interaction (PPI) information obtained from Human Protein Reference Database (HPRD database) for the two conditions: isosmoticity and hyperosmosis, and then a comparative analysis was done to identify disease-related genes. The functional annotation was performed for these genes using network ontology analysis (NOA), which also confirmed the effectiveness of this method. RESULTS: A total of 45 feature genes were obtained through comparing 7 samples treated under isosmotic conditions and 9 high osmotic conditions. Biological processes and molecular functions were then revealed by NOA. CONCLUSIONS: A range of disease-related genes were obtained, which might serve as the potential biomarkers or drug targets. More works are needed to further elucidate their roles in the development of intervertebral disc diseases like intervertebral disc herniation.

STRAP reduces endoplasmic reticulum stress and apoptosis in cardiomyocytes and attenuates myocardial ischemia-reperfusion injury by activating PI3K/PDK1/Akt signaling pathway.

OBJECTIVE: Myocardial ischemia-reperfusion injury (MIRI) is a common problem in heart-related diseases. The aim of this study was to explore the protective effects of STRAP on cardiomyocytes in the MIRI process and its mechanisms. MATERIALS AND METHODS: We used SD rats to construct a MIRI model and increased the expression of STRAP in myocardial tissue by Entranster to detect the effect of STRAP on rat myocardial tissue. In addition, we cultured rat cardiomyocyte cell line H9c2 cells and constructed a hypoxia-reoxygenation model to detect the protective effect of STRAP on H9c2 cells. LY294002, an inhibitor of the PI3K/PDK1/Akt signaling pathway, was used to validate the mechanism by which STRAP protects cardiomyocytes. RESULTS: Overexpression of STRAP significantly reduced the activity of MDA in myocardial tissue and increased the activity of SOD. STRAP also substantially lowered CK and LDH levels in rat serum and increased Na+-K+-ATPase and Ca2+-Mg2+-ATPase activity. In addition, overexpression of STRAP considerably reduced endoplasmic reticulum stress (ERS) and apoptosis levels in H9c2 cells. However, LY294002 attenuated the protective effect of STRAP on cardiomyocytes. CONCLUSIONS: STRAP reduces ERS and apoptosis in cardiomyocytes by activating the PI3K/PDK1/Akt signaling pathway, thereby reducing myocardial MIRI.

IL-6 knockout ameliorates myocardial remodeling after myocardial infarction by regulating activation of M2 macrophages and fibroblast cells.

OBJECTIVE: To investigate the effects of interleukin-6 (IL-6) gene knockout on myocardial remodeling after myocardial infarction (MI) in mice and the potential mechanism, to provide certain references for the prevention and treatment of MI in clinic. MATERIALS AND METHODS: A total of 40 male C57 mice were divided into two groups, namely Sham group (n=20) and MI group (n=20), using a random number table. Another 20 mice with IL-6 gene knockout were enrolled into the MI + IL-6 KO group. The MI model was established by means of ligating the left anterior descending coronary artery of the mice. 28 d later, the survival status of the three groups of mice was recorded. In addition, the cardiac functions of each group of mice, including two-dimensional echocardiography, ejection fraction (EF%) and fractional shortening (FS%), were measured. The cross-sectional area and pathological change of the myocardial cells in cardiac tissues of each group of mice were detected via hematoxylin and eosin (H&E) staining. Immunohistochemistry was applied to determine the expression of tumor necrosis factor-alpha (TNF-α) in each group of mouse cardiac tissues. Moreover, immunofluorescent staining was utilized to measure the content of M2 macrophages in each group of mouse cardiac tissues. RESULTS: The 28-d survival rate of the mice with IL-6 gene knockout was remarkably higher than that of the wild-type mice (p<0.05). Furthermore, the cardiac functions of the mice in the MI + IL-6 KO group were superior to those in the MI group, with markedly improved FS% and EF% (p<0.05). According to the H&E staining results, the cross-sectional areas of the heart and myocardial cells were decreased notably in MI + IL-6 KO group compared with those in the MI group (p<0.05). The immunohistochemical staining results showed that IL-6 knockout could lower the MI-induced high expression of TNF-α (p<0.05), and Masson's trichrome staining indicated that IL-6 knockout could also repress the degree of cardiac fibrosis. Moreover, it was discovered through immunofluorescent staining that the mice in the MI + IL-6 KO group had markedly elevated content of M2 macrophages in cardiac tissues than those in the MI group (p<0.05). CONCLUSIONS: Inhibiting IL-6 gene expression can prominently ameliorate the MI-induced myocardial remodeling, whose mechanism is possibly associated with the activation of M2 macrophages and reduced collagen production in fibroblast cells.

Valproic acid attenuates the suppression of acetyl histone H3 and CREB activity in an inducible cell model of Machado-Joseph disease.

Machado-Joseph disease (MJD) is caused by a (CAG)n trinucleotide repeat expansion that is translated into an abnormally long polyglutamine tract. This disease is considered the most common form of spinocerebellar ataxia (SCA). In the present study, we developed stable inducible cell lines (PC12Tet-On-Ataxin-3-Q28/84) expressing ataxin-3 with either normal or abnormal CAG repeats under doxycycline control. The expression of acetyl histone H3 and the induction of c-Fos in response to cAMP were strongly suppressed in cells expressing the protein with the expanded polyglutamine tract. Treatment with valproic acid, a histone deacetylase inhibitor (HDACi), attenuated mutant ataxin-3-induced cell toxicity and suppression of acetyl histone H3, phosphorylated cAMP-responsive element binding protein (p-CREB) as well as c-Fos expression. These results indicate that VPA can stimulate the up-regulation of gene transcription through hyperacetylation. Thus, VPA might have a therapeutic effect on MJD.

[Effect of curcumin on the proliferation of murine CFU-GM and WEHI-3B cells].

OBJECTIVE: To evaluate the effect of curcumin on the proliferation of hematopoietic progenitor cells or leukemic stem cells. METHODS: Mouse bone marrow cells (colony forming unit-granulocyte and macrophage, CFU-GM) and WEHI-3B cells were observed using the colony assays. RESULTS: The curcumin significantly inhibited the proliferation of both CFU-GM and WEHI-3B cells in a dose-dependent manner ranging from 10(-8) to 10(-4) mol.L-1; their IC50S were 1.036 x 10(-5) mol.L-1 and 1.220 x 10(-6) mol.L-1 of curcumin respectively. CONCLUSION: The proliferation of murine CFU-GM and WEHI-3B cells can be suppressed by curcumin. The inhibitory effect of curcumin on the proliferation of WEHI-3B cells is stronger than that of CFU-GM.

[Study on the optimum experimental conditions for the steady growth of human K-562 cell line].

The results of the assays of growth state, semisolid colony culture, cytomorphological and chromosome analysis for K-562 cell line showed that the cells had the similar biological characteristics with the cells which were originally established. It suggests that the growth state of K-562 cells under the experimental conditions in our laboratory are steady.

Developmental differences in the expression of the cholera toxin sensitive subunit (Gs alpha) of adenylate cyclase in the rat small intestine.

BACKGROUND: The stimulatory guanosine triphosphate (GTP) binding protein alpha subunit (Gs alpha) of adenylate cyclase is the target protein for cholera toxin. AIMS/METHODS: The expression of this signal transducer was analysed in the small intestine of developing rats by RNA transfer (northern blot) analysis by immunoblotting, and by ADP-ribosylation of membrane proteins. RESULTS: Intestinal Gs alpha mRNA (about 1.9 kb) was increased in the neonate compared with the adult rat. Two isoforms of Gs alpha proteins, a 45,000 and a 52,000 form, were expressed in the small intestinal epithelial cell and both were ADP-ribosylated by cholera toxin. A significant increase in the larger isoform (52,000) and in its ribosylation was noted in the 2 week old suckling compared with post-weaned older animals. The protein content or ribosylation of the smaller form (45,000) did not significantly change with age. CONCLUSION: These data show that a developmental decline of intestinal Gs alpha expression seems to be, in part, regulated at the mRNA level. An increased Gs alpha expression in the immature intestine may help to explain a previously reported, dose dependent increased adenylate cyclase response and an increase in fluid secretion to cholera toxin in neonates compared with adults.