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Background Thrombocytopenia is a common manifestation of antiphospholipid syndrome (APS). This study assesses the possible relationship between severe thrombocytopenia and adverse pregnancy outcomes (APOs) in obstetric APS (OAPS) patients. Methods An observational, cohort study was conducted at Peking University People’s Hospital, Beijing, China. The demographic, clinical, immunologic, and pregnancy outcomes of the OAPS patients were collected. Univariate and multivariate logistic regression analyses were applied to assess the association between APOs and severe thrombocytopenia (< 30 × 10 9 /L). The threshold effect was explored using two piecewise linear regression models by the smoothing plot. Results A total of 176 OAPS participants were included in the analysis, with 49 thrombocytopenia (< 100 × 10 9 /L) and 9 severe thrombocytopenia (< 30 × 10 9 /L). In the context of univariate logistic regression, severe thrombocytopenia demonstrated a significant association with increased APOs, encompassing preterm delivery before 34 weeks (OR, 8.74; 95%CI, 2.10–36.32, P  = 0.0028), uteroplacental insufficiency (OR, 16.28; 95%CI, 1.99–133.53, P  = 0.0093), preterm labor before 37 weeks (OR, 15.98; 95%CI, 3.16–80.80, P  = 0.0008), and SGA (OR, 7.45; 95%CI, 1.87–29.73, P  = 0.0045). A nonlinear relationship between the number of platelets and APOs was observed. The risk of APOs rose as platelet count decreased to a turning point (50 × 10 9 /L) ( P  < 0.05). Beyond a platelet count of 50 × 10 9 /L, no significant association was observed between platelet count and APO risk in OAPS patients. Conclusion The risk of adverse pregnancy outcomes in patients with OAPS is contingent upon the severity of thrombocytopenia. Maintaining platelet counts above 50 × 10 9 /L is pivotal in mitigating this risk. The effective OAPS treatments may improve pregnancy outcomes.

Kupffer cells (KCs) are the liver-resident macrophages and play a leading role in the regulation of liver homeostasis in physiological conditions and in pathology. The study aims to investigate the anti-echinococcosis effect of KCs and the effects of hepatic stellate cells (HSCs) activation in the progression of liver fibrosis in hepatic alveolar echinococcosis (hepatic AE). Hematoxylin-eosin (H&E) and Masson staining were used to assess the pathological inflammatory changes and collagen deposition, respectively. Immunohistochemistry and qRT-PCR were used to detect the number of aggregates of KCs, the expression of cytokines and activation of HSCs. In the close group, H&E staining showed that the normal lobular structure was destroyed and inflammatory infiltration around the lesion could be observed, and Masson staining showed that blue collagen fibers were clearly deposited near the portal area. IHC showed that KCs surface markers CD68 and CD163, cytokine iNOS and Arg-1 were positively expressed in the vicinity of inflammatory lesions. qRT-PCR indicated that TNF-α, IL-10, and TGF-β1 secreted by KCs were significantly higher than those in the distance group ( < 0.01). It is worth noticing that the expression levels of anti-inflammatory cytokines were slightly higher than that of pro-inflammatory cytokines. Both IHC and qRT-PCR results showed that HSCs activation markers, the expression of α-SMA and Desmin significantly increased. Our research indicates that KCs have immune-protective effect of anti-echinococcosis and promote liver fiber repair, and it also suggests that they have potential therapeutic value for patients with hepatic AE.

Background Alveolar echinococcosis is a potentially lethal zoonosis caused by the cestode Echinococcus multilocularis. This study is to investigate the dynamic changes of monocytes, macrophages, and related cytokines in animal models of persistent infection of E. multilocularis. Methods An infection model was established by intraperitoneal injection of a protoscolex suspension. The pathological changes of liver were observed by HE staining. The percentage of Ly6Chi and Ly6Clo Monocytes in peripheral blood was detected by flow cytometry. The distribution and expression of CX3CL1, CX3CR1, iNOS, CD163, and CD11b in the liver were detected by immunohistochemistry. The mRNA expression of tumor necrosis factor‐α (TNF‐α) and Arg1 in the liver was detected by quantitative reverse transcription polymerase chain reaction. The expression of INF‐γ, interleukin‐17 (IL‐17), IL‐4, and IL‐10 in peripheral blood was detected by enzyme‐linked immunosorbent assay. Results Hematoxylin‐eosin(HE) staining showed that significant lesions appeared in the later stages of infection in the liver. The proportion of Ly6Chi monocytes in the peripheral blood of the experimental group mice decreased after a brief rise, Ly6Clo monocytes decreased first and then increased. The expression of CX3CL1, CX3CR1, CD11b, CD163, and iNOS in the mice liver of the experimental group was increased. The expression level of TNF‐α and Arg1 mRNA in the liver of the experimental group mice increased. The expression level of IFN‐γ, IL‐17, IL‐4, and IL‐10 increased with the duration of infection. Conclusions Monocytes as a supplement to hepatic macrophage, monocytes and kupffer cells may both participate in Th1 and Th2 immune responses by differentiating into M1 or M2 at different stages of E. multilocularis infection. Monocytes and kupffer cells may both participate in Th1 and Th2 immune responses by differentiating into M1 or M2 at different stages of Echinococcus multilocularis infection.

Palatine tonsils are the only air-contacted lymphoid organs that constantly engage in crosstalk with commensal microorganisms and serve as the first handling sites against microbial antigens. While tonsil inflammations have been implicated in various autoimmune diseases, including rheumatoid arthritis (RA), the precise role of tonsillar microbiota in autoimmune pathogenesis remains inadequately characterized. In this study, we profiled the tonsillar microbiota and identified a notable dysbiosis in patients with RA, particularly within the Streptococcus genus. Specifically, patients with RA exhibited an enrichment of pathogenic Streptococcus species, including S. pyogenes, S. dysgalactiae, and S. agalactiae. Colonization with these bacteria significantly exacerbated arthritis severity and increased autoimmune responses in collagen-induced arthritis (CIA). Furthermore, immunization with peptides derived from these pathogenic Streptococcus species directly induced experimental arthritis. Conversely, patients with RA demonstrated a marked deficiency in commensal Streptococcus members, notably S. salivarius. Treatment of CIA mice with S. salivarius attenuated the progression of arthritis and downregulated autoimmune responses. These findings highlight a pathogenic link of tonsillar microbiota with RA, shedding light on their contribution to autoimmunity.

Rheumatoid arthritis (RA) is widespread globally, with the emergence of metabolites derived from both the host and microbes playing a pivotal role in its pathogenesis. This study aims to elucidate the relationships between serum metabolites and the immunological and clinical features of RA. Serum samples were collected from 35 RA patients and 37 healthy controls (HC). Metabolite profiling was performed using gas chromatography-mass spectrometry (GC/MS). Principal component analysis revealed a significant distinction between the RA and HC cohorts. Employing univariate statistical analysis, we identified 36 differential metabolites. Among these, 9 metabolites, including galactose and glucose, were found to be enriched, while the remaining metabolites, such as citric acid, fumaric acid, and inosine, were depleted in RA. These diverse metabolites encompassed various metabolic processes, including the biosynthesis of fatty acids, amino acids, and glucose. The enrichment of glucose and galactose in RA exhibited a substantial correlation with elevated IgG levels, as determined through correlation analysis. Conversely, the depletion of citric acid was correlated with elevated levels of C3 and CRP. Methionine, which also declined in RA patients, displayed a negative correlation with ESR. Furthermore, galactose and glucose exhibited significant positive correlations with naïve B cells, while the decreased eicosanoic acid level in RA was significantly associated with an increase in natural killer cells. Our findings suggest that the altered serum metabolite profile in RA is closely linked to disease severity and the dysregulated immune responses observed in RA patients. Key Points• Identified nine metabolites with upregulated expression and twenty-seven metabolites with downregulated expression.• Established a correlation between alterations in serum metabolite levels and inflammatory markers in RA patients.• Discovered a significant association between changes in serum metabolites and immune cell profiles in RA patients.

Objectives Pericardial effusion is a rare clinical manifestation in idiopathic inflammatory myopathies (IIMs). It has been described in a small number of literature studies worldwide. We describe the clinical and laboratory characteristics of 19 IIM patients combined with pericardial effusion, and compare them with previously reported cases. The single-center observational-study-inspired collected of 156 IIM patients with complete data from January 1, 2016 to January 1, 2021 in the First Affiliated Hospital of Xinjiang Medical University, of which 19 patients had pericardial effusion. Methods The clinical characteristics of 19 IIM patients complicated with pericardial effusion were investigated by descriptive analysis and compared with previously reported cases. Results 19 cases of IIM patients had pericardial effusion (12.2%), patients without a large amount of pericardial effusion or pericardial tamponade. There was a predominance of women in the patients with 78.9% pericardial effusion . In the clinical examination, 10 cases showed chest tightness (52.6%), pulmonary fibrosis (47.4%), and the frequency of muscle nuclear magnetic, which suggested that muscle lymphocyte infiltration rate was 63.2%. Anti-Ro-52 antibody and anti-Jo-1 antibody were positive (26.3%, 42.1%). IIM patients with pericardial effusion were accompanied by decreased serum albumin levels and elevated ESR. In the literature review, the most common clinical characteristics of IIM patients with pericardial effusion were female, pulmonary fibrosis, shortness of breath, positive anti-Ro-52 pulmonary fibrosis, and anti-Jo-1 antibody. Conclusion In the study, 19 patients of IIMs with pericardial effusion present with chest tightness, and are accompanied by pulmonary fibrosis, positive anti-Jo-1 antibody, and anti-Ro-52 antibody. It is suggested that pericardial effusion in IIM patients may be related to anti-synthetase antibody.

Background The association between social isolation, loneliness and risk of cardiovascular diseases (CVD) is not fully understood. This meta-analysis aims to explore social isolation and loneliness whether increases the risk of CVD. Methods Data sources was PubMed and Embase from inception to 10 February 2025. The risk of bias was assessed using the Newcastle-Ottawa Quality Assessment Scale (NOS). Hazard ratios (HR) with 95% confidence intervals (CI) were pooled using a random-effect model, and publication bias was assessed with funnel plots and Egger’s test. Results This meta-analysis included six cohort studies with a total of 5,253,128 participants, spanning a follow-up period of 4 to 11.3 years from publications between 1996 and 2022. All studies were of high quality (NOS score ≥ 7). The pooled analysis revealed a heightened risk of CVD among individuals experiencing social isolation or loneliness (HR = 1.17, 95% CI 1.10–1.25, I 2  = 85.1%, P  < 0.001). Subgroup analysis indicated that patients with a history of social isolation had a slightly higher risk of CVD compared to those with loneliness [HR = 1.39, 95% CI 1.15–1.68, I 2  = 90.2%, P  = 0.001]. Additionally, the risk of CVD was slightly elevated during the 4–7 year follow-up compared to 7–9 years and 10–11 years [HR = 1.87, 95% CI 1.67–2.10, I 2  = 0%, P  < 0.001]. Those with a history of social isolation or loneliness had the highest risk of stroke [HR = 1.23, 95% CI 1.07–1.43, I 2  = 74.5%, P  = 0.004]. Furthermore, Asian populations exhibited a slightly higher risk of CVD compared to North American and European populations [HR = 1.46, 95% CI 1.12–1.91, I 2  = 0%, P  = 0.005]. Conclusions The increased risk of CVD among social isolation or loneliness individuals underscore the importance of prioritizing their care in clinical practice and nursing. However, the high heterogeneity in meta-analysis suggests the need for further studies to validate and explore this association thoroughly.

Atopic dermatitis (AD) is a common recurrent chronic inflammatory skin disease, and there is increasing evidence of a possible association between AD and autoimmune diseases. This study aimed to summarize existing epidemiological studies on the association between AD and autoimmune diseases and to perform a meta-analysis of combinable results. We conducted a thorough search for cohort studies, case-control studies and cross-sectional studies across the PubMed, Cochrane Library, and Embase databases, from their inception to May 24, 2024, using medical subject headings and relevant keywords. All data were meticulously analyzed using Stata statistical software version 17.0. The protocol was registered on PROSPERO (CRD42024547282). A total of 26 cohort studies, comprising 1,629,723 patients with atopic dermatitis and 15,106,889 control subjects, were included in this meta-analysis. These studies were published between 2014 and 2024 and included 19 cohort studies, 2 case-control studies, and 5 cross-sectional studies. The current study demonstrated a significant association of atopic dermatitis with autoimmune diseases[HR 1.49, 95% CI (1.31-1.70); 0.001], including celiac disease, systemic lupus erythematosus, Sjogren's syndrome, ankylosing spondylitis, alopecia areata, rheumatoid arthritis, vitiligo, thyroid dysfunction, ulcerative colitis. The results of our study indicate a clear association between atopic dermatitis and autoimmune diseases, both in adults and children. Additionally, women were more likely to have autoimmune disease complications than men. However, due to the limited number of participants in our study, further research is needed to thoroughly investigate the relationship. https://www.crd.york.ac.uk/PROSPERO/, identifier CRD42024547282.

Acute renal artery embolism (ARAE) is a rare vascular event that precipitates renal infarction (RI) caused by abrupt disruption of renal artery blood flow. RI is frequently misdiagnosed or diagnosed late because of its rarity and frequently ambiguous clinical presentation, potentially leading to irreversible harm to the renal parenchyma or an increased risk of other embolic events affecting other organs. Risk factors for ARAEs include atrial fibrillation, valvular or ischemic heart disease, renal artery embolism/dissection, and coagulopathy, and complete unilateral renal artery embolism is rare. We present the case of one patient with unilateral ARAE caused by atrial fibrillation. We performed percutaneous endovascular therapy (PET) for the renal artery embolism, including catheter-directed thrombolysis (CDT) and aspiration thrombectomy with systemic anticoagulant therapy. At the one-year follow-up, severe atrophy of the affected kidney and compensatory enlargement of the contralateral kidney were observed. We found that procedurally successful revascularization does not necessarily translate to functional recovery of the renal parenchyma. To accurately assess long-term renal functional restoration, we propose incorporating post-thrombectomy anatomical evaluations (e.g., via renal artery angiography or CT angiography [CTA]) combined with functional renal scintigraphy into standardized clinical protocols. This multimodal approach would not only validate the angiographic outcomes but also provide critical insights into the viability of the parenchyma, thereby guiding the development of patient-specific therapeutic strategies. Recommendations for optimal treatment for renal artery embolism are needed. Therefore, we share this case with the aim of providing valuable information for the treatment of renal infarction.

The inherent limitations of conventional polyolefin separators, particularly their poor thermal stability and insufficient mechanical strength, pose significant safety risks for lithium-ion batteries (LIBs) by increasing susceptibility to thermal runaway. In this study, we developed a novel multilayer separator through sequential coating of a commercial polyethylene (PE) substrate with aluminum oxide (Al2O3), para-aramid (PA), and polyethylene wax microspheres (PEWMs) using a scalable micro-gravure process, denoted as SAPEAS, signifying a PE-based asymmetric structure separator with enhanced thermal shutdown and dimensional stability. The SAPEAS separator exhibits an early thermal shutdown capability at 105 °C, maintains structural integrity with negligible shrinkage at 180 °C, and demonstrates comprehensive performance enhancements, including enhanced mechanical strength (tensile strength: 212.3 MPa; puncture strength: 0.64 kgf), excellent electrolyte wettability (contact angle: 12.8°), a high Li+ transference number (0.71), superior ionic conductivity (0.462 mS cm−1), outperforming that of commercial PE separators. In practical LFP|Gr pouch cells with ampere-hour (Ah) level capacity, the SAPEAS separator enables exceptional cycling stability with 97.9% energy retention after 1000 cycles, while significantly improving overcharge tolerance compared to PE. This work provides an effective strategy for simultaneously improving the safety and electrochemical performance of LIBs.