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Abstract Background The results of observational studies indicate a potential link between Helicobacter pylori infection and Sjogren’s syndrome (SS), but the causal relationship between them remains unknown. This study applied Mendelian randomization (MR) to evaluate this relationship. Method Genome-wide association study (GWAS) summary statistics on H. pylori infection [sample size=8735 (EBI, https://gwas.mrcieu.ac.uk/ )] and SS [sample size=368,028 (cases=2495, controls=365533) (FinnGen, https://r9.finngen.fi/ )] were analyzed. We used bidirectional MR to evaluate the association between H. pylori infection and SS and identify causation. The major MR analysis method was inverse-variance weighted (IVW) MR, supplemented by MR‒Egger and weighted median approaches. In addition, the stability and reliability of the results were tested using the retention method, heterogeneity test, and horizontal gene pleiotropy test. Results Evidence of the impact of H. pylori infection on SS risk was found in the IVW results [odds ratio (OR)=1.6705; 95% confidence interval (CI)=1.0966 to 2.5446; P=0.0168]. Evidence of the impact of SS on H. pylori infection risk was also found (OR=1.0158; 95% CI=1.0033 to 1.0285; P=0.0128). Conclusion The results of MR analysis support a causal association between H. pylori infection and SS and indicate that SS can lead to a greater risk of H. pylori infection. Our research will support the development of novel approaches for continued H. pylori and SS-related research and therapy that consider the genetic relationship between H. pylori infection and SS.

Objective To summarize the clinical features, serological features, blood transfusion protocols and treatment of 3 cases of passenger lymphocyte syndrome(PLS) after ABO-incompatibility liver and renal transplantation in our hospital, in order to provide guidance for comprehensive clinical understanding and recognition of this disease, especially early recognition and treatment. Methods By collecting the basic information of the patients and the time of cross-matching incompatibility of homologous blood after transplantation, observing the skin yellow staining, detecting hemoglobin value and other hemolysis indexes, and blood group serological detection results before and after transfusion, the diagnosis and analysis were performed. The diagnosis and treatment effect of PLS were analyzed by collecting the clinical outcome information after immunization and blood transfusion. Results Three cases of ABO-incompatible liver transplantation showed decreased hemoglobin and hemolysis, incompatible cross-matching of homologous blood, and anti-A and anti-B IgG antibodies were confirmed by serological test. After treatment such as immunosuppression and plasma exchange, blood transfusion was effective, hemolysis was improved, and antibodies gradually disappeared. Conclusion ABO blood group antibody screening, unexpected antibody screening and direct antiglobulin test(DAT)should be performed regularly for ABO-incompatible liver and renal transplantation cases, in order to detect the PLS early. A series of laboratory tests related to PLS should be performed in time to diagnose and adjust the treatment plan, including transfusion strategy, when homologous cross-matching is incompatible.

Abstract Background There is still a lack of sufficient evidence-based medical data on the effect of resveratrol (Res) on primary osteoporosis (OP). This meta-analysis aimed to comprehensively evaluate the role of Res in animal models of primary OP. Methods The PubMed, Cochrane Library, Web of Science and Embase databases were searched up to August 2023. The risk of bias was assessed by the SYRCLE RoB tool. Random- or fixed-effects models were used to determine the 90% confidence interval (CI) or standardized mean difference (SMD). Statistical analysis was performed with RevMan 5.4 and Stata 14.0. Results A total of 24 studies containing 714 individuals were included. Compared with those in the control group, the bone mineral density (BMD) (P

Nuclear factor of activated T-cells 5 (NFAT5), an osmo-sensitive transcription factor, can be activated by isotonic stimuli, such as infection. It remains unclear, however, whether NFAT5 is required for damage-associated molecular pattern--triggered (DAMP-triggered) inflammation and immunity. Here, we found that several DAMPs increased NFAT5 expression in macrophages. In particular, serum amyloid A (SAA), primarily generated by the liver, substantially upregulated NFAT5 expression and activity through TLR2/4-JNK signalling pathway. Moreover, the SAA-TLR2/4-NFAT5 axis promoted migration and chemotaxis of macrophages in an IL-6--and chemokine ligand 2--dependent (CCL2-dependent) manner in vitro. Intraarticular injection of SAA markedly accelerated macrophage infiltration and arthritis progression in mice. By contrast, genetic ablation of NFAT5 or TLR2/4 rescued the pathology induced by SAA, confirming the SAA-TLR2/4-NFAT5 axis in vivo. Myeloid-specific depletion of NFAT5 also attenuated SAA-accelerated arthritis. Of note, inflammatory arthritis in mice strikingly induced SAA overexpression in the liver. Conversely, forced overexpression of the SAA gene in the liver accelerated joint damage, indicating that the liver contributes to bolstering chronic inflammation at remote sites by secreting SAA. Collectively, this study underscores the importance of the SAA-TLR2/4-NFAT5 axis in innate immunity, suggesting that acute phase reactant SAA mediates mutual interactions between liver and joints and ultimately aggravates chronic arthritis by enhancing macrophage activation. [ABSTRACT FROM AUTHOR]