Helicobacter pylori infects approximately 50% of the world’s population and is considered the major etiological agent of severe gastric diseases, such as peptic ulcers and gastric carcinoma. Increasing resistance to standard antibiotics has now led to an ever-decreasing efficacy of eradication therapies and the development of novel and improved regimens for treatment is urgently required. Substantial progress has been made over the past few years in the identification of molecular mechanisms which are conducive to resistant phenotypes as well as for efficient strategies to counteract strain resistance and to avoid the use of ineffective antibiotics. These involve molecular testing methods, improved salvage therapies, and the discovery of novel and potent antimicrobial compounds. High rates of prevalence and gastric cancer are currently observed in Asian countries, including Japan, China, Korea, and Taiwan, where concomitantly intensive research efforts were initiated to explore advanced eradication regimens aimed at reducing the risk of gastric cancer. In this review, we present an overview of the known molecular mechanisms of antibiotic resistance and discuss recent intervention strategies for H. pylori diseases, with a view of the research progress in Asian countries.
In the literature, there was inconsistency in the risk of malaria between individuals with Rhesus blood group positive (Rh+) and negative (Rh−). The systematic review aimed to investigate the risk of malaria among participants with different Rh blood types. All observational studies that reported the occurrence of Plasmodium infection and investigation of the Rh blood group were searched in five databases (Scopus, EMBASE, MEDLINE, PubMed, and Ovid). Strengthening the Reporting of Observational Studies in Epidemiology was used to assess the reporting quality in the included studies. A random-effects model was used to calculate the pooled log odds ratio and 95% confidence intervals (CIs). Database searches yielded a total of 879 articles, of which 36 were eligible for inclusion in the systematic review. The majority of the included studies (44.4%) revealed that Rh+ individuals had a lower proportion of malaria than Rh− individuals; however, the remaining studies revealed a higher or no difference in the proportion of malaria between Rh+ and Rh− individuals. Overall, with moderate heterogeneity, the pooled results showed no difference in malaria risk between patients with Rh+ and Rh− (p = 0.85, pooled log odds-ratio: 0.02, 95% CI: −0.20–0.25, I2: 65.1%, 32 studies). The current study found no link between the Rh blood group and malaria, even though there was a moderate amount of heterogeneity. Further studies using prospective designs and a definitive method for Plasmodium identification are needed to investigate the risk of Plasmodium infection in Rh+ individuals and increase the reliability and quality of these studies.
Anemia is a major complication in over 50% of chronic kidney disease (CKD) patients. One of the main causes of anemia in CKD is the reduction of erythropoietin (EPO) synthesis from renal tubular cells. Therefore, first-line treatment of CKD is EPO administration; however, EPO unresponsiveness in several patients is frequently found. More undefined causes of anemia in CKD are under interest, especially uremic toxins, which are a group of solutes accumulated in CKD patients. The highly detectable protein-bound uremic toxin, indoxyl sulfate (IS) was investigated for its effects on in vitro erythropoiesis in this study. CD34+ hematopoietic stem cells were isolated from human umbilical cord blood and differentiated toward erythrocyte lineage for 14 days in various concentrations of IS (12.5, 25, 50, and 100 µg/mL). The effects of IS on cell proliferation, differentiation, apoptosis, and senescence were determined. Cell proliferation was investigated by manual cell counting. Cell surface marker expression was analyzed by flow cytometry. Wright’s staining was performed to evaluate cell differentiation capacity. Apoptosis and senescence marker expression was measured using reverse transcription polymerase chain reaction (RT-PCR). TUNEL assay was performed to detect apoptotic DNA fragmentation. Our results demonstrated that IS reduced cell proliferation and impaired erythrocyte differentiation capacity. In addition, this study confirmed the effects of IS on cell apoptosis and senescence during erythropoietic differentiation. Therefore, the promotion of apoptosis and senescence might be one of the possible mechanisms caused by uremic toxin accumulation leading to anemia in CKD patients.
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