BACKGROUND: The role of inflammation in the development of gestational diabetes mellitus (GDM) has recently become a focus of research. The systemic immune-inflammation index (SII) and systemic inflammation response index (SIRI), novel indices, reflect the body's chronic immune-inflammatory state. This study aimed to investigate the associations between the SII or SIRI and GDM. METHODS: A prospective birth cohort study was conducted at Beijing Obstetrics and Gynecology Hospital from February 2018 to December 2020, recruiting participants in their first trimester of pregnancy. Baseline SII and SIRI values were derived from routine clinical blood results, calculated as follows: SII = neutrophil (Neut) count × platelet (PLT) count/lymphocyte (Lymph) count, SIRI = Neut count × monocyte (Mono) count/Lymph count, with participants being grouped by quartiles of their SII or SIRI values. Participants were followed up for GDM with a 75-g, 2-h oral glucose tolerance test (OGTT) at 24-28 weeks of gestation using the glucose thresholds of the International Association of Diabetes and Pregnancy Study Groups (IADPSG). Logistic regression was used to analyze the odds ratios (ORs) (95% confidence intervals [CIs]) for the the associations between SII, SIRI, and the risk of GDM. RESULTS: Among the 28,124 women included in the study, the average age was 31.8 ± 3.8 years, and 15.76% (4432/28,124) developed GDM. Higher SII and SIRI quartiles were correlated with increased GDM rates, with rates ranging from 12.26% (862/7031) in the lowest quartile to 20.10% (1413/7031) in the highest quartile for the SII ( Ptrend <0.001) and 11.92-19.31% for the SIRI ( Ptrend <0.001). The ORs (95% CIs) of the second, third, and fourth SII quartiles were 1.09 (0.98-1.21), 1.21 (1.09-1.34), and 1.39 (1.26-1.54), respectively. The SIRI findings paralleled the SII outcomes. For the second through fourth quartiles, the ORs (95% CIs) were 1.24 (1.12-1.38), 1.41 (1.27-1.57), and 1.64 (1.48-1.82), respectively. These associations were maintained in subgroup and sensitivity analyses. CONCLUSION The SII and SIRI are potential independent risk factors contributing to the onset of GDM.
Humans ; Female ; Pregnancy ; Diabetes, Gestational/immunology* ; Prospective Studies ; Adult ; Inflammation/immunology* ; Glucose Tolerance Test ; Birth Cohort

With rapid progress and dangerous prognosis, traumatic brain injury (TBI) brings great difficulties in the clinical treatment, which becomes a prominent problem for the modern emergency and critical care medicine. In addition to the necessary surgical intervention under special circumstances, there are new understandings about the clinical management measures, noninvasive and invasive monitoring mode of TBI in recent years. This review provides a summary of the monitoring and treatment on the TBI, with our deep understanding of regulatory mechanism underlying TBI, precise modulation might be of clinical significance in preventing secondary damage of tissues and organs, which would be associated with decreases in the disability and mortality of critically ill patients.

Sepsis is caused by various pathogens and toxic factors, which can lead to multiple organ dysfunction. The underlying mechanism of sepsis appears to be complex, involving epigenetic reprogramming, metabolic failure, immune dysfunction, neuroendocrine system disorders, coagulation abnormalities, tissue or organ failure, and many other scientific issues. With our deep understanding of the host reaction and development of sepsis, it is of great significance to explore predicative markers and therapeutic targets according to the atypical characteristics of sepsis, thereby contributing to the reduction of morbidity and mortality of sepsis.

The mechanisms of burn/trauma related infection are complicated, involving uncontrolled inflammation, immune disorder, coagulation abnormality, and pathophysiological changes of multiple systems or organs. Although active management of primary diseases, application of antibiotics, and organ support treatment are the basis for the management of burn/trauma related infection, immune modulation opens up a new direction for the intervention of burn/trauma related infection and the relevant complications. In-depth understanding of inflammation-immune response and its regulatory mechanisms, and exploring new early warning biomarkers and immune interventional strategies are of great significance for improving the level of treatment of clinical burn/trauma related infections and improving the prognosis of patients.

Sepsis induced by major burns,trauma,and hemorrhage,remains a major cause of death of patients in intensive care units,and it may result in both the widespread activation and dysfunction of the innate as well as adaptive responses in host immune system.A large amount of information concerning subsets of innate and adaptive immune cells in sepsis has implicated that these cells,including neutrophils,macrophages,dendritic cells,T lymphocytes,regulatory T lymphocytes,and natural killer cells,have profound effects on immunoreactivity during acute insults or sepsis through modulating multiple receptor expressions or cytokine secretion,in turn contributing to the development and outcome of sepsis.It is of great significance that precision monitoring of immune function and the related indicators might help to assess the risk of secondary infection,the prognosis of septic patients,and guide the treatment of septic complications.

Sepsis is a severe complication which is usually caused by microbial infection,severe burns or trauma and major operations.Patients with sepsis were usually complicated with systemic inflammatory response and multi-organ dysfunction syndrome,which is the leading cause of death in the intensive care units.However,the main immunoregulatory mechanisms underlying severe sepsis remain unclear,and effective methods for monitoring immune status and immunomodulatory strategies need to be investigated.In recent years,the understanding of the mechanism of sepsis has been developed.Clinicians have learned that immune dysfunction took part in the pathophysiological process of sepsis.Therefore,rational monitoring of immune status in patients with severe sepsis after burns or major operation,seeking effective ways for diagnosis,treatment and intervention are of great significance in decreasing the mortality and improving the life quality.

Objective To observe the expression of tumor necrosis factor-α induced protein 8 like-2 (TIPE2) in CD4 + CD25 + regulatory T cells ( CD4 + CD25 + Tregs) and analyze its potential effect on immunosuppressive activity of CD4 + CD25 + Tregs. Methods CD4 + CD25 + Tregs were purified from spleen of the BALB/c mice by using magnetic cell sorting system.The expressions of TIPE2 mRNA and protein in CD4 + CD25 + Tregs were detected by using RT-PCR and Western blot.CD4 + CD25 +Tregs were further infected with the recombinant lentiviruses that carried small interference RNA(siRNA)to knock down the TIPE2 expression.Based on the expressions of cell surface molecules including cytotoxic T-lymphocyte-associated antigen (CTLA)-4 and forkhead/winged helix transcription factor p3 (Foxp3) detected by flow cytometry and the levels of cytokines including interleukin (IL)-10 and transforming growth factor (TGF)-3 examined by ELISA in CD4 + CD25 + Tregs,the functional role of TIPE2 in controlling suppressive activity of CD4 + CD25 + Tregs was analyzed.In the meantime,the proliferation activities of T effector cells were assayed by MTT test. Results A 147 bp TTPE2 gene band and a clear TIPE2 band with a molecular mass of approximately 21 000 in CD4 + CD25 + Tregs were detected by using Westem blot.Cell surface molecule as well as cytokine expressions were significantly down-regulated when the CD4 + CD25 + Treg stimulated and activated by anti-CD3/CD28 was cultured for 24 hours after the siRNA silenced CD4 + CD25 + Treg cells ( P ＜ 0.01 ).Meanwhile,the suppression role of CD4 +CD25 + Tregs on the proliferation activity of T effector cells was weakened obviously ( P ＜ 0.05 ). Conclusions As an important immunoregulatory molecule,TIPE2 not only expresses in the CD4 + CD25 +Tregs,but also affects the immunosuppressive function of CD4 + CD25 + Tregs.