Liansuo Zhou

BACKGROUND AND AIM: The aim of this study was to investigate whether the platelet-to-lymphocyte ratio (PLR) is an independent predictor of all-cause mortality and cardiovascular (CV) events in patients with acute coronary syndrome (ACS). METHODS: PubMed, Embase, and the Cochrane Library were searched for relevant cohort studies regarding the association between PLR and outcomes of patients with ACS. Either a random- or a fixed-effect model was used for pooling data. RESULTS: Eight studies involving 6627 patients with ACS were included. The cut-off PLR value for defining risk groups was 150, and patients were assigned to the low (≤ 150) or high (> 150) PLR groups. The pooled relative risk (RR) values of in-hospital and long-term mortality were 2.15 (95% CI [confidence interval] 1.73-2.67; p < 0.00001) and 2.27 (95% CI 1.35-3.80; p = 0.002), respectively, comparing the high and the low PLR groups. Compared with the low PLR group, the high PLR group had a significantly increased risk of in-hospital (RR 1.95; 95% CI 1.30-2.91; p = 0.001) and long-term (RR 1.50; 95% CI 1.08-2.09; p = 0.01) major adverse CV events. CONCLUSIONS: Elevated PLR was found to be a predictor of all-cause mortality and CV events.

BACKGROUND: Some reports have confirmed that occurrence and development of tumor are related with lots of oncogene, anti-oncogene and cytokine. This study was to detect the expression of TNFmRNA, tumor necrosis factor (TNF) and TNF receptor (TNFR) in the gallbladder mucosa which developed from hyperplasia, dysplasia to carcinoma, and to further discuss the pathogenecity of gallbladder carcinoma. METHODS: The expression of TNFmRNA, TNF and TNFR was detected by in situ hybridization and immunohistochemistry on the surgical specimens of hyperplasia, dysplasia and carcinoma of the gallbladder. RESULTS: The percentage of positive cells expressed TNFmRNA in the gallbladder mucosa was 0%, 20%, and 90%, respectively in hyperplasia, dysplasia and carcinoma (P<0.05). The percentage of positive mononuclear cells (MNCs) expressed TNFmRNA in hyperplasia, dysplasia and carcinoma of gallbladder tissues was 15%, 85%, and 90%, respectively (P<0.05). The number of positive MNC high-power field (Hpf) was 4.85+/-1.50, 6.00+/-2.71, and 9.33+/-3.07, respectively (P<0.05). The number of carcinoma cells and MNCs expressed by TNFmRNA per high-power field was increased with the increase of tumor stage. The number of carcinoma cells/Hpf in stages I-III and IV-V was 9.13+/-4.39 and 7.13+/-2.53 (P<0.05), and that of MNC/Hpf was 14.80+/-4.02 and 11.10+/-2.23 (P<0.01). The number of carcinoma cells and MNCs expressed by TNFmRNA per Hpf was increased with the increase of tumor size. In tumors of more than 2 cm or less than 2 cm in diameter, the number of positive carcinoma cells/Hpf was 14.00+/-4.20 and 8.83+/-4.96, respectively (P<0.05), but that of MNC/Hpf was 10.50+/-2.54 and 7.00+/-2.83 (P<0.05). The pattern of TNF protein expression was similar to that of TNFmRNA, whereas TNF protein expression was more frequent and extensive than TNFmRNA expression. TNFR was expressed in endothelial cells and MNCs of carcinoma, and was negative in mucosal epithelial cells and tumor cells. A positive linear correlation in TNFmRNA expression was observed between tumor cells and MNCs (r=0.687, P<0.01), a correlation in TNFmRNA and TNF protein expression of tumor cells (r=0.847, P<0.001), and a correlation in TNFmRNA and TNF protein expression of MNC in tumor tissue (r=0.643, P<0.01). CONCLUSIONS: TNFmRNA and TNF protein expression is increased during the development of gallbladder mucosa from hyperplasia, dysplasia to carcinoma, and is increased with tumor stage. This finding suggests that TNF is involved in the pathogenesis of gallbladder carcinoma induced by gallstones and the TNF expression in cancer cells may serve as a marker for tumor stage.

Gastrectomy is the primary therapeutic option for gastric cancer. Postoperative treatment also plays a crucial role. The strategy to improve the postoperative prognosis of gastric cancer requires a combined system that includes a more efficient synergistic treatment and real-time monitoring after surgery. In this study, photothermal-chemotherapy combined nanoparticles (PCC NPs) were prepared via π-π stacking to perform chemo-photothermal synergistic therapy and continuous imaging of gastric cancer. PCC NPs had a spherical morphology and good monodispersity under aqueous conditions. The hydrodynamic diameter of PCC NPs was 59.4 ± 3.6 nm. PCC NPs possessed strong encapsulation ability, and the maximum drug loading rate was approximately 37%. The NPs exhibited extraordinary stability and pH-response release profiles. The NPs were rapidly heated under irradiation. The maximum temperature was close to 58°C. PCC NPs showed good biocompatibility both in vitro and in vivo . Moreover, the NPs could effectively be used for in vivo continuous monitoring of gastric cancer. After one injection, the fluorescent signal remained in tumor tissues for nearly a week. The inhibitory effect of PCC NPs was evaluated in a gastric cancer cell line and xenograft mouse model. Both in vitro and in vivo evaluations demonstrated that PCC NPs could be used for chemo-photothermal synergistic therapy. The suppression effect of PCC NPs was significantly better than that of single chemotherapy or photothermal treatment. This study lays the foundation for the development of novel postoperative treatments for gastric cancer.

The role of FEN1 genetic variants on gallstone and gallbladder cancer susceptibility is unknown. FEN1 SNPs were genotyped using the polymerase chain reaction-restriction fragment length polymorphism method in blood samples from 341 gallbladder cancer patients and 339 healthy controls. The distribution of FEN1-69G > A genotypes among controls (AA, 20.6%; GA, 47.2% and GG 32.2%) was significantly different from that among gallbladder cancer cases (AA, 11.1%; GA, 48.1% and GG, 40.8%), significantly increased association with gallbladder cancer was observed for subjects with both the FEN1-69G > A GA (OR = 1.73, 95% CI = 1.01-2.63) and the FEN1-69G > A GG (OR = 2.29, 95% CI = 1.31-3.9). The distribution of FEN1 -4150T genotypes among controls (TT, 21.8%;GT, 49.3% and GG 28.9%) was significantly different from that among gallbladder cancer cases (TT, 12.9%; GT, 48.4% and GG 38.7%), significantly increased association with gallbladder cancer was observed for subjects with both the FEN1-4150T GT(OR = 1.93, 95% CI = 1.04-2.91) and the FEN1-4150T GG(OR = 2.56, 95% CI = 1.37-5.39). A significant trend towards increased association with gallbladder cancer was observed with potentially higher-risk FEN1-69G > A genotypes (P < 0.001, χ2 trend test) and FEN14150G > T (P < 0.001, χ2 trend test) in gallstone presence but not in gallstone absence (P = 0.81, P = 0.89, respectively). In conclusion, this study revealed firstly that FEN1 polymorphisms and haplotypes are associated with gallbladder cancer risk.