Red and Processed Meat Intake Is Associated with Higher Gastric Cancer Risk: A Meta-Analysis of Epidemiological Observational Studies

Background

Red and processed meat was concluded as a limited-suggestive risk factor of gastric cancer by the World Cancer Research Fund. However, recent epidemiological studies have yielded inconclusive results.

Methods

We searched Medline, EMBASE, and the Cochrane Library from their inception to April 2013 for both cohort and case-control studies which assessed the association between red and/or processed meat intake and gastric cancer risk. Study-specific relative risk estimates were polled by random-effect or fixed-effect models.

Results

Twelve cohort and thirty case-control studies were included in the meta-analysis. Significant associations were found between both red (RR: 1.45, 95% CI: 1.22–1.73) and processed (RR: 1.45, 95% CI: 1.26–1.65) meat intake and gastric cancer risk generally. Positive findings were also existed in the items of beef (RR: 1.28, 95% CI: 1.04–1.57), bacon (RR: 1.37, 95% CI: 1.17–1.61), ham (RR: 1.44, 95% CI: 1.00–2.06), and sausage (RR: 1.33, 95% CI: 1.16–1.52). When conducted by study design, the association was significant in case-control studies (RR: 1.63, 95% CI: 1.33–1.99) but not in cohort studies (RR: 1.02, 95% CI: 0.90–1.17) for red meat. Increased relative risks were seen in high-quality, adenocarcinoma, cardia and European-population studies for red meat. And most subgroup analysis confirmed the significant association between processed meat intake and gastric cancer risk.

Conclusions

Our findings indicate that consumption of red and/or processed meat contributes to increased gastric cancer risk. However, further investigation is needed to confirm the association, especially for red meat.     

Phenotypic characterization of GPR120-expressing cells in the interstitial tissue of pancreas

GPR120 functions as a plasma membrane receptor for unsaturated long-chain free fatty acids and involves in GLP-1 secretion, adipogenesis and the control of energy balance. Pancreas is the key organ in fuel and energy metabolism. Here GPR120 expression in human and rat pancreas was observed by RT-PCR, and the distribution and phenotypes of GPR120-positive cells in human and rat pancreas were shown by immunohistochemical staining. GPR120 mRNA expression was found in human and rat pancreas. GPR120-positive cells were scattered mainly in the interstitial tissues of human and rat pancreas, and they were not co-localized with nestin, vimentin, alpha-SMA and glucagon, respectively. However, GPR120 was distributed on the cells positively stained by CD68, the specific marker of macrophages, and on the cells positive stained by CD34 and CD117, the markers of interstitial cells. In conclusion, this study demonstrates the expression of GPR120 in pancreas and shows the distribution of GPR120 in human and rat pancreas.     

Estrogen inhibits the early development of mouse follicles through regulating the expression of Kit ligand

Estrogen inhibits cyst breakdown and primordial follicle assembling of germ cells, but little is known about the underlying mechanisms. We aimed to analyze the effects of estrogen on the early development of mouse follicles using an in vitro ovary culture system and in vivo injection. Newborn mouse ovarian tissues were cultured in vitro for 2 or 4 days with estrogen of 0 M, 10⁻⁸ M and 10⁻⁴ M, respectively, and neonatal mice were injected with 5 mg/kg/day estrogen. We found that the percentages of different-stage follicles significantly varied between the control and estrogen-treated groups. In vitro experiments showed that the unassembled follicles accounted for 70.5 ± 2.7% and the primordial follicles accounted for 29.5 ± 2.7% in the treatment group, but in the control group, ovaries had 61.7 ± 8.4% unassembled follicles. In vivo experiments showed that the percentages of unassembled follicles and primordial follicles were 37.1 ± 5.2% and 51.6 ± 2.4% in the control group, while they were 72.6 ± 5.2% and 25.1 ± 5.5% in the treatment group. Moreover, we analyzed the expression of Kit ligand in mouse ovaries treated by estrogen with real-time PCR and western blot technology, and found that compared with the control group, both mRNA and protein expression levels were decreased in the treatment group (P < 0.05). These results indicate that estrogen inhibits the development of mouse ovarian follicles by regulating the expression of Kit ligand.     

Purification and neuroprotective effects of polysaccharides from Opuntia Milpa Alta in cultured cortical neurons

Opuntia is a traditional plant from China with medicinal applications. In this experiment, polysaccharides from Opuntia Milpa Alta (MAPs) were analyzed using gas chromatograph-mass spectrometer (GC-MS) method and result showed that MAPs contained mannose (6.37%), rhamnose (14.94%), xylose (1.99%), arabinose (24.07%), galactose (38.25%), ribose (2.63%) and glucose (11.48%). The neuroprotective effects of MAPs were evaluated at the mechanistic level in vitro models of cerebral ischemic injury. In vitro oxygen/glucose deprivation (OGD) model, MAPs (0.5 μg/ml, 5 μg/ml, 50 μg/ml) effectively increased cell viability by methyl thiazolyl tetrazolium (MTT) assay, inhibited cell cytotoxicity by lactate dehydrogenase (LDH) assay, reduced neuronal cell death, suppressed the production of intracellular reactive oxygen species (ROS), decreased of intracellular free Ca²⁺ concentrations ([Ca²⁺]_i), and reduced extracellular glutamate level. Therefore, MAPs might prevent intracellular calcium overload and decreased glutamate excitotoxicity, both of which can cause neuronal injury and death in vitro models of cerebral ischemic injury.     

Treatment with NaHSO3 greatly enhances photobiological H2 production in the green alga Chlamydomonas reinhardtii

Treatment with NaHSO₃ induces a 10-fold increase in H₂ photoproduction in the filamentous N₂-fixing cyanobacterium Anabaena sp. strain PCC 7120. However, it is unclear whether this treatment also increases H₂ photoproduction in green alga. In this study, treatment with 13 mM NaHSO₃ resulted in about a 200-fold increase in H₂ production in Chlamydomonas reinhardtii, and this increase was most probably the result of reduced O₂ content and enhanced hydrogenase activity. Compared to the conventional strategy of sulfur deprivation, NaHSO₃ treatment results in a higher maximum rate of H₂ photoproduction, greater efficiency of conversion of light energy into H₂, shorter half-time to produce the maximum accumulated H₂ levels, and reduced costs because no centrifugation is involved. We therefore conclude that NaHSO₃ treatment is an efficient, rapid, and economic strategy for improving photobiological H₂ production in the green alga C. reinhardtii.     

Theoretical studies on 2-diazo-4,6-dinitrophenol derivatives aimed at finding superior propellants

In an attempt to find superior propellants, 2-diazo-4,6-dinitrophenol (DDNP) and its –NO₂, –NH₂, –CN, –NC, –ONO₂, and –NF₂ derivatives were studied at the B3LYP/6-311++G^** level of density functional theory (DFT). Sensitivity was evaluated using bond dissociation enthalpies (BDEs) and molecular surface electrostatic potentials. The C–NO₂ bond appears to be the trigger bond during the thermolysis process for these compounds, except for the –ONO₂ and –NF₂ derivatives. Electrostatic potential results show that electron-withdrawing substituents make the charge imbalance more anomalous, which may change the strength of the bond, especially the weakest trigger bond. Most of the DDNP derivatives have the impact sensitivities that are higher than that of DDNP, making them favorable for use as solid propellants in micro-rockets. The theoretical densities (ρ), heats of formation (HOFs), detonation energies (Q), detonation pressures (P), and detonation velocities (D) of the compounds were estimated. The effects of various substituent groups on ρ, HOF, Q, D, and P were investigated. Some derivatives exhibit perfect detonation properties. The calculated relative specific impulses (I _r,sp) of all compounds except for –NH₂ derivatives were higher than that of DDNP, and also meet the requirements of propellants.     

CD40 on APCs is needed for optimal programming, maintenance, and recall of CD8+ T cell memory even in the absence of CD4+ T cell help

CD40 stimulation is one of the many signals that can activate APCs and we have recently shown it to have a unique function in generating maximum primary CD8(+) T cell responses. However, whether CD40 signaling plays a role in memory CD8(+) T cell responses is still not completely understood. In this study, we show that in the absence of CD40 on all APCs or specifically on dendritic cells, memory CD8(+) T cells are generated but at significantly reduced levels. This reduction is due to a contribution of CD40 at several different steps in the generation of CD8(+) memory. In the initial T cell response, CD40 contributes to maximizing not only the number of effector cells that are generated but also the programming of ones that will differentiate into memory. Subsequently, CD40 is needed to maintain maximal numbers of the committed memory cells in a manner that is independent of the immunizing Ag. Finally, when memory CD8(+) T cells are reactivated there is a variable requirement for CD40 depending on whether CD40 or CD4(+) Th cells were present during the primary response. Therefore, CD40 signaling on APCs plays an important role in all phases of a memory CD8(+) T cell response.     

p16 Mutation Spectrum in the Premalignant Condition Barrett's Esophagus

Background

Mutation, promoter hypermethylation and loss of heterozygosity involving the tumor suppressor gene p16 (CDKN2a/INK4a) have been detected in a wide variety of human cancers, but much less is known concerning the frequency and spectrum of p16 mutations in premalignant conditions.

Methods and Findings

We have determined the p16 mutation spectrum for a cohort of 304 patients with Barrett''s esophagus, a premalignant condition that predisposes to the development of esophageal adenocarcinoma. Forty seven mutations were detected by sequencing of p16 exon 2 in 44 BE patients (14.5%) with a mutation spectrum consistent with that caused by oxidative damage and chronic inflammation. The percentage of patients with p16 mutations increased with increasing histologic grade. In addition, samples from 3 out of 19 patients (15.8%) who underwent esophagectomy were found to have mutations.

Conclusions

The results of this study suggest the environment of the esophagus in BE patients can both generate and select for clones with p16 mutations.