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Bipolar disorder (BD) is a common psychiatric illness with high prevalence and disease burden. Accumulating susceptibility genes for BD have been identified in recent years. However, the exact functions of these genes remain largely unknown. Despite its high heritability, gene and environment interaction is commonly accepted as the major contributing factor to BD pathogenesis. Intestine microbiota is increasingly recognized as a critical environmental factor for human health and diseases via the microbiota‐gut‐brain axis. BD individuals showed altered diversity and compositions in the commensal microbiota. In addition to pro‐inflammatory factors, such as interleukin‐6 and tumour necrosis factor‐α, type 1 interferon signalling pathway is also modulated by specific intestinal bacterial strains. Disruption of the microbiota‐gut‐brain axis contributes to peripheral and central nervous system inflammation, which accounts for the BD aetiology. Administration of type 1 interferon can induce the expression of TRANK1, which is associated with elevated circulating biomarkers of the impaired blood‐brain barrier in BD patients. In this review, we focus on the influence of intestine microbiota on the expression of bipolar gene TRANK1 and propose that intestine microbiota‐dependent type 1 interferon signalling is sufficient to induce the over‐expression of TRANK1, consequently causing the compromise of BBB integrity and facilitating the entrance of inflammatory mediators into the brain. Activated neuroinflammation eventually contributes to the occurrence and development of BD. This review provides a new perspective on how gut microbiota participate in the pathogenesis of BD. Future studies are needed to validate these assumptions and develop new treatment targets for BD.

Objectives To investigate the diagnostic value of serum D-dimer in patients with periprosthetic joint infection (PJI). Moreover, to provide evidence for the treatment of PJI by investigating distribution of pathogenic bacteria and antibiotic resistance situation among the patients. Methods A retrospective study of the medical records of all patients undergoing arthroplasty from the Second Xiangya Hospital of Central South University from 2014 to 2018, 40 patients with periprosthetic joint infection, 37 patients with aseptic loosening and 59 patients with extra-articular infection were selected. The results of serum D-dimer, C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) were collected. As well as the bacterial types and antimicrobial susceptibility test results from tissue or joint fluid samples around the prosthetic joint of the patients were collected. All the relevant data were analyzed. Results The serum D-dimer, CRP and ESR level were significantly higher in the patients with PJI. The mean D-dimer level was 2.0795 μg/mL in PJI group compared with 0.6854 μg/mL in aseptic loosening group (p = 0.000) and 0.4556 μg/mL in extra-articular infection group (p = 0.000). For diagnosing PJI, the serum D-dimer test demonstrated better sensitivity (87.50%), and better specificity (89.19%); while the serum CRP and ESR had a sensitivity of 80.00% and 82.50% and a specificity of 78.38% and 64.86%, respectively. Moreover, the sensitivity and specificity of ESR and CRP combined was 75.00% and 83.78%, respectively. In addition, 29 strains of pathogens around the prosthesis after arthroplasty were detected, including 22 strains of Gram-positive bacteria, 3 strains of Gram-negative bacteria, and 4 strains of fungi. The staphylococcus was the major pathogen showing high resistance to Cefoxitin and ampicillin. Conclusion Patients with PJI have high levels of serum D-dimer, which is a promising marker for the diagnosis of PJI. The Gram-positive bacteria are major pathogen in PJI after arthroplasty, and Staphylococcus aureus is the most common organism. Clinical efficacy is significantly improved by reasonable choice of antibiotics and effective medicine education.

To explore the changes of serum interleukin-6 (IL-6) levels in healthy pregnant women and establish reference intervals (RIs).According to the requirements for the RIs study model and the reference population screening criteria in C28-A3 document, Serum IL-6 levels were measured by electrochemiluminescence immunoassay in 480 healthy Chinese women, including 120 pregnant women in each of the first, second and third trimester and 120 non-pregnant women as the negative control. The establishment of RIs for IL-6 were defined using nonparametric percentile.The RIs for serum IL-6 levels in healthy pregnant women is 4.19 pg/ml, the RIs for serum IL-6 levels in healthy pregnant women who are in the first trimester is 3.52 pg/ml, and the RIs for serum IL-6 levels in healthy pregnant women who are in the second and third trimester is 4.40 pg/ml.Serum IL-6 level in healthy pregnant women is higher than the healthy non-pregnant women, and the level of IL-6 who are in the second and third trimester is higher than those in the first. This paper successfully established RIs for serum IL-6 levels in pregnant women, providing a reference for clinical medical staff and laboratory workers.

Bipolar disorder (BD) is a severe affective disorder, mainly characterized by alternative depressive and manic or hypomanic episodes, yet the pathogenesis of BD has not been fully elucidated. Recent researches have implicated the altered kynurenine (KYN) metabolism involved in the neurobiology of BD. Excessive activation of the immune system also occurs in patients with BD, which further accelerates the KYN pathway for tryptophan metabolism. Changes of the KYN metabolites have effects on neuronal receptors and are involved in neuroendocrine transmissions. Interactions between KYN metabolism and the immune system may contribute to the neuropathogenesis of BD. Various studies have shown that alterations of the KYN metabolites were associated with mood, psychotic symptoms, and cognitive functions in patients with BD. In this review, we briefly introduce the KYN pathway and describe the immune dysregulation in BD as well as their interactions. We then focus on the research advances on the KYN metabolism in BD, which hold promise for identifying novel treatment targets in patients stricken with this disorder.

Butyrate is one of the most abundant short-chain fatty acids produced by intestinal bacteria. In the present study, the action of butyrate on chronic gastric mucosa lesions was investigated, as well as its underlying mechanism in mice. Male mice from the Institute of Cancer Research were randomly divided into three groups: Sham, model and butyrate groups. Butyrate was administered intragastrically for 7 days to butyrate group mice following the establishment of a gastric ulcer model. Hematoxylin and eosin staining, immunohistochemical analysis, enzyme-linked immunosorbent assay and quantitative polymerase chain reaction were used to determine the therapeutic effects and molecular mechanism of butyrate treatment. The findings demonstrated that butyrate induced a marked shift in superoxide dismutase and catalase activities, along with a decrease in malondialdehyde levels, thereby attenuating oxidative stress. Furthermore, butyrate decreased the levels of pro-inflammatory cytokines interleukin-1β, tumour necrosis factor-α and leukotriene B4, which helped combat inflammatory responses. Moreover, butyrate treatment exerted remarkable positive influences that mediate an increase in 6-keto-PGF-1α (a degradation product of prostacyclin), trefoil factor 2, MUC5AC and fibroblast growth factor-7 levels to promote gastric mucosal repair. The expression of specific receptor GPR109A for butyrate was upregulated, with no significant difference noted in the expression of GPR43 or GPR41. Overall, the present findings revealed that butyrate exerted therapeutic effects by upregulating mucosal repair factors and stimulating protective responses against oxidation and inflammation. GPR109A may be the key receptor for butyrate therapy.

The growing multidrug-resistant Neisseria gonorrhoeae is a serious global threat to gonococcal therapy. During 2017–2018, we identified a rare multidrug-resistant (ceftriaxone and azithromycin) strain (GC250) and four strains (GC185, GC195, GC196 and GC249) with both resistance to ceftriaxone and decreased susceptibility to azithromycin. All strains belonged to NG-STAR ST1143, including the mosaic penA-60.001, which is closely related to ceftriaxone resistance. The characterization of antimicrobial resistance (AMR) determinants and phylogenetic analysis showed these five strains were closely related to internationally spreading ceftriaxone-resistant N. gonorrhoeae FC428, but with higher azithromycin MIC. Findings here demonstrated that this clone not only initiated clonal expansion in China, but acquired azithromycin resistance.