The correlation analysis of primary liver cancer with Type 2 diabetes.

OBJECTIVE: To explore the relationship between Type 2 diabetes and primary liver cancer. MATERIALS AND METHODS: In the period from December 2008 to December 2014, all blood sugar data of patients in our hospital was collected, and the total number is 18213. Except for repeatedly hospitalized diabetic person, newborn stress status, or venous transfusion blood glucose, gestational diabetes, etc., By retrieving the medical record information of patients in the hospital, and using telephone or letter follow-up the patients, we collected 127 people with type 1 diabetes and found no liver cancer patients; Type 2 diabetes, 10,794 cases of patient information, 59 with primary liver cancer. For data analysis, Stata11.0 ratio was used as the main analysis indicators, using Chi‑square test and statistical analysis. RESULTS: About 10,794 Type 2 diabetes cases with 59 primary liver cancer, the incidence is 54.66/10,000, men liver cancer incidence (92.78/10,000) than women (27.13/10,000), with significant difference (χ2 = 26.621, P < 0.001). As the growth of the age, the possibility of liver cancer in patients with diabetes increased significantly (χ2 = 19.961, P = 0.001). The rate was highest for 50–60‑year‑old men, and the women at age 70, and older incidence is highest. Irrespective of men or women with diabetes as the growth of the age, the possibility of liver cancer had significantly increased (P = 0.001, P = 0.002). Hepatitis B or hepatitis C incidence was 2.94%, but diabetes incidence of hepatitis men (3.98%) and women (2.01%) did not find significant differences (χ2 = 0.3361, P = 0.562). Three hundred and seventeen cases of Type 2 diabetes with hepatitis, the incidence of primary liver cancer was 11.67%, the liver cancer incidence of diabetes patients with hepatitis men (17.78%) than women (3.97%), with significant difference (χ2 = 37.429, P < 0.001). With the growth of age, the overall risk of getting liver cancer (χ2=15.023, P = 0.01) of diabetes and hepatitis patients is significantly increased, and with the growth of age, the risk of getting liver cancer of male patients showed significant (P < 0.05), but not the female patients. Without merge hepatitis, the morbility of primary liver cancer in 10477 cases of type2 diabetes incidence is 0.21%, the liver cancer incidence men (0.34%) than women (0.11%), with significant difference (χ2 = 6.471, P = 0.011).As the growth of age, the overall risk of getting liver cancer of diabetes patients without hepatits is significantly increased (χ2 =15.612, P = 0.008) ,and the risk of getting liver cancer of male patients showed significant (P < 0.05) as the growth of the age, but not the female patients. Diabetic persons according to the illness time can be divided into 0–5 years, 5–10 years, 10–20 years, and over 20 years of four stages, including 5–10 years and 10–20 years is liver cancer patients with diabetes incidence peak, male diabetic hepatitis in patients with liver cancer incidence than women, with significant difference (χ2 = 22.757, P < 0.001). The possibility of liver cancer in patients with diabetes increased significantly (χ2 = 15.023, P = 0.01) for longer duration of illness, but only the male patients with liver cancer incidence showed significant difference with longer duration of illness, women showed no significance. CONCLUSION: Diabetes was associated with the primary liver cancer, most likely is one of the causes of primary liver cancer.

Isolation of choline monooxygenase (CMO) gene from Salicornia europaea and enhanced salt tolerance of transgenic tobacco with CMO genes.

Glycinebetaine (GB) is an osmoprotectant accumulated by certain plants in response to high salinity, drought, and cold stress. Plants synthesize GB via the pathway choline → betaine aldehyde → glycinebetaine, and the first step is catalyzed by choline monooxygenase (CMO). In the present study, by using RT-PCR and RLM-RACE, a full-length CMO cDNA (1844 bp) was cloned from a halophyte Salicornia europaea, which showed high homology to other known sequences. In order to identify its function, the ORF of CMO cDNA was inserted into binary vector PBI121 to construct the chimeric plant expression vector PBI121-CMO. Using Agrobacterium (LBA4404) mediation, the recombinant plasmid was transferred into tobacco (Nicotiana tabacum). The PCR, Southern blot and RT-PCR analysis indicated the CMO gene was integrated into the tobacco genome, as well as expressed on the level of transcription. The transgenic tobacco plants were able to survive on MS medium containing 300 mmol/L NaCl and more vigorous than those of wild type with the same concentration salt treatment. In salt-stress conditions, transgenic plants had distinctly higher chlorophyll content and betaine accumulation than that of the control, while relative electrical conductivity of transgenic plants was generally lower. The results suggested the CMO gene transformation could effectively contribute to improving tobacco salt-resistance.

Growth inhibitory effect and Chk1-dependent signaling involved in G2/M arrest on human gastric cancer cells induced by diallyl disulfide

Diallyl disulfide (DADS) inhibits growth and induces cell cycle G2/M arrest in human gastric cancer MGC803 cells. In this study, 15 mg/L DADS exerted similar effects on growth and cell cycle arrest in human gastric cancer BGC823 cells. Due to the importance of cell cycle redistribution in DADS-mediated anti-carcinogenic effects, we investigated the role of checkpoint kinases (Chk1 and Chk2) during DADS-induced cell cycle arrest. We hypothesized that DADS could mediate G2/M phase arrest through either Chk1 or Chk2 signal transduction pathways. We demonstrated that DADS induced the accumulation of phosphorylated Chk1, but not of Chk2, and that DADS down-regulated Cdc25C and cyclin B1. The expression of mRNA and total protein for Chkl and Chk2 was unchanged. Chk1 is specifically phosphorylated by ATR (ATM-RAD3-related gene). Western blot analysis showed that phospho-ATR was activated by DADS. Taken together, these data suggest that cell cycle G2/M arrest, which was associated with accumulation of the phosphorylated forms of Chk1, but not of Chk2, was involved in the growth inhibition induced by DADS in the human gastric cancer cell line BGC823. Furthermore, the DADS-induced G2/M checkpoint response is mediated by Chk1 signaling through ATR/Chk1/Cdc25C/cyclin B1, and is independent of Chk2.