Prevalence and risk factors of Helicobacter pylori infection in military personnel: a systematic review and meta-analysis

Background and Aims: Helicobacter pylori infection is prevalent and recognized as a major cause of gastrointestinal diseases in the world. Previous studies on the prevalence of H. pylori infection in military personnel have shown some conflicting results. This study aimed to estimate the pooled prevalence of H. pylori infection and evaluate its risk factors in military personnel. Methods: The PubMed, EMBASE, and Cochrane Library databases were searched. We pooled the prevalence of H. pylori infection in military personnel using a random-effect model. Metaregression analysis was used to explore the sources of heterogeneity. Pooled proportion of H. pylori infection with 95% confidence interval (CI) was calculated. Results: Sixteen studies were included. Meta-analysis showed that the overall prevalence of H. pylori infection was 32% (95% CI = 31–33) in military personnel. There was a significant heterogeneity. Metaregression analysis showed that study region (P = 0.0004) and publication year (P = 0.023) were the potential sources of heterogeneity. In the subgroup analysis by study region, the highest prevalence was found in Asia (50.2%; 95% CI = 49–51.4). In the subgroup analysis by diagnostic methods for H. pylori, the highest prevalence was found when urea breath test was employed (47.9%; 95% CI = 46.5–49.3). The most common risk factor for H. pylori infection was familial aggregation, followed by living environment and age. Conclusion: H. pylori infection is common in military personnel. In future, we may require appropriate population screening for H. pylori infection by multiple diagnostic tests and increase the knowledge and awareness of the bacterial transmission among military personnel.

Hernia Umbilical Asintomática en la Cirrosis Hepática / ASYMPTOMATIC UMBILICAL HERNIA IN LIVER CIRRHOSIS

La hernia umbilical es una complicación que puede constituirse en una amenaza para la vida en la cirrosis hepática. Aquí, demostramos dos interesantes casos de cirrosis hepática que se presentaron con hernia umbilical asintomática, pero que no fueron sometidos a ningún tipo de cirugía

Umbilical hernia is a life-threatening complication of liver cirrhosis. Herein, we demonstrated two interesting cases with liver cirrhosis that presented with asymptomatic umbilical hernia, but did not undergo any surgery.

Role of Sphk1 in the malignant transformation of breast epithelial cells and breast cancer progression.

BACKGROUND: The ojective of the following study is to investigate the role of sphingosine kinase 1 (Sphk1) in the malignant transformation of breast epithelial cells and breast cancer progression and its mechanism. MATERIALS AND METHODS: Immunohistochemistry was performed to detect Sphk1 and E‑cadherin (E‑cad) in resected breast samples. Sphk1 was transfected in normal human breast epithelial cell line (MCF‑10A) by Lentivirus and silenced in breast cancer cell line (MCF‑7) using small interfering ribonucleic acid. The effect of tumor necrosis factor alpha (TNF‑α) and/or N, N‑dimethylsphingosine (DMS) on the Sphk1 and E‑cad expression, MCF‑10A cell proliferation and invasion was investigated. Real time‑polymerase chain reaction and western‑blot was used to detect messenger ribonucleic acid and protein. Cell counting kit‑8 and transwell were used to measure cell proliferation and invasion. RESULTS: Sphk1 was positive expression in 114 breast tumors (75.50%) but negative in fibroadenomas. The expression of E‑cad and Sphk1 were negatively correlated and E‑cad (−)/Sphk1 (+) carriers showed higher ratio of axillary lymph node metastasis than E‑cad (+)/Sphk1 (−) carriers. Overexpression of Sphk1 in MCF‑10A reduced E‑cad expression and improved cell proliferation and invasion, but knockdown of Sphk1 in MCF‑7 decreased cell proliferation and invasion. TNF‑α increased Sphk1 expression, enhanced the ability of Sphk1 in decreasing E‑cad expression, which could be blocked by DMS. TNF‑α promoted MCF‑10A cell proliferation and invasion.CONCLUSION: Sphk1 plays an important role in the malignant transformation of breast epithelial cells and modulates breast cancer metastasis through the regulation of E‑cad expression. TNF‑α can up‑regulate Sphk1 expression and reduce E‑cad expression through Sphk1, which can be blocked by DMS. TNF‑α/Sphk1/E‑cad pathway may be a newly discovered pathway and plays an important role in tumorigenesis and metastasis.

Mutations in the HFE gene and sporadic amyotrophic lateral sclerosis risk: a meta-analysis of observational studies

Iron homeostasis dysregulation has been regarded as an important mechanism in neurodegenerative diseases. The H63D and C282Y polymorphisms in the HFE gene may be involved in the development of sporadic amyotrophic lateral sclerosis (ALS) through the disruption of iron homeostasis. However, studies investigating the relationship between ALS and these two polymorphisms have yielded contradictory outcomes. We performed a meta-analysis to assess the roles of the H63D and C282Y polymorphisms of HFE in ALS susceptibility. PubMed, MEDLINE, EMBASE, and Cochrane Library databases were systematically searched to identify relevant studies. Strict selection criteria and exclusion criteria were applied. Odds ratios (ORs) with 95% confidence intervals (CIs) were used to assess the strength of associations. A fixed- or random-effect model was selected, depending on the results of the heterogeneity test. Fourteen studies were included in the meta-analysis (six studies with 1692 cases and 8359 controls for C282Y; 14 studies with 5849 cases and 13,710 controls for H63D). For the C282Y polymorphism, significant associations were observed in the allele model (Y vs C: OR=0.76, 95%CI=0.62-0.92, P=0.005) and the dominant model (YY+CY vs CC: OR=0.75, 95%CI=0.61-0.92, P=0.006). No associations were found for any genetic model for the H63D polymorphism. The C282Y polymorphism in HFE could be a potential protective factor for ALS in Caucasians. However, the H63D polymorphism does not appear to be associated with ALS.

Ischemia preconditioning is neuroprotective in a rat cerebral ischemic injury model through autophagy activation and apoptosis inhibition

Sublethal ischemic preconditioning (IPC) is a powerful inducer of ischemic brain tolerance. However, its underlying mechanisms are still not well understood. In this study, we chose four different IPC paradigms, namely 5 min (5 min duration), 5×5 min (5 min duration, 2 episodes, 15-min interval), 5×5×5 min (5 min duration, 3 episodes, 15-min intervals), and 15 min (15 min duration), and demonstrated that three episodes of 5 min IPC activated autophagy to the greatest extent 24 h after IPC, as evidenced by Beclin expression and LC3-I/II conversion. Autophagic activation was mediated by the tuberous sclerosis type 1 (TSC1)-mTor signal pathway as IPC increased TSC1 but decreased mTor phosphorylation. Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) and hematoxylin and eosin staining confirmed that IPC protected against cerebral ischemic/reperfusion (I/R) injury. Critically, 3-methyladenine, an inhibitor of autophagy, abolished the neuroprotection of IPC and, by contrast, rapamycin, an autophagy inducer, potentiated it. Cleaved caspase-3 expression, neurological scores, and infarct volume in different groups further confirmed the protection of IPC against I/R injury. Taken together, our data indicate that autophagy activation might underlie the protection of IPC against ischemic injury by inhibiting apoptosis.

Expression of Rap1GAP in human myeloid disease following microarray selection

To find the underlying causes of primary myelodysplastic syndrome (MDS), the gene expression profiling of both CD34+ cells and bone marrow mononuclear cells from MDS patients was performed using oligonucleotide microarray and cDNA microarrays, respectively. Several candidate genes which were differentially expressed in MDS patients versus normal controls were selected and confirmed in expanding samples by quantitative real-time reverse transcription-polymerase chain reaction after clustering and bioinformatics analysis. one of these genes, RAP1GAP, was found to be expressed at a significantly higher level in patients with MDS in comparison with those suffering from other hematopoietic diseases including leukemia (P < 0.01). We propose that over-expression of RAP1GAP gene may play a role in the pathogenesis of MDS.