Systemic lupus erythematosus (SLE) is a systemic autoimmune disease with manifestations ranging from mild skin symptoms to severe organ and neurological involvement. Thrombosis is a major complication and leading cause of mortality, though its mechanisms remain unclear. Emerging evidence highlights platelets, beyond their hemostatic role, as central players in SLE pathogenesis. This narrative review summarizes platelet-driven pathways in SLE, emphasizing their roles in thrombosis and immune regulation. Platelets interact with immune complexes, complement, and infectious agents, triggering activation and the release of mediators and microparticles. These processes increase circulating autoantigens and promote both thrombosis and autoimmune responses. Understanding these non-hemostatic platelet functions offers new insight into SLE mechanisms and may guide future platelet-targeted therapies.

The aim of this study is to investigate the role of hydroxycarboxylic acid receptor 1 (HCAR1) in glutamate-induced excitotoxic neuronal injury. The effective and safe concentrations of an endogenous HCAR1 agonist (L-lactic acid) and an exogenous HCAR1 agonist (3,5-dihydroxybenzoic acid, 3,5-DHBA) were determined using a CCK-8 assay. An excitotoxic injury model was established by stimulating mouse hippocampal neuronal cells (HT22 cells) with 20 mM glutamate, followed by intervention with safe concentrations of L-lactic acid and 3,5-DHBA. Neuronal survival and apoptosis were assessed by NeuN immunofluorescence staining and a TUNEL assay. The effects of HCAR1 agonists on glutamate transport were evaluated using vesicular glutamate transporter 1 (VGLUT1) immunofluorescence staining and qRT‒PCR. Additionally, qRT‒PCR was performed to quantify the expression of a neuronal excitability marker gene ( c-fos ), inflammatory factors and hcar1 . The results showed that HCAR1 agonists (L-lactic acid and 3,5-DHBA) significantly improved neuronal survival, reduced glutamate-induced apoptosis and decreased neuronal excitability ( p < 0.05). The activation of HCAR1 inhibited the transport of the excitatory neurotransmitter glutamate ( p < 0.05). The upregulation of HCAR1 expression led to the significant downregulation of the expression of inflammatory factors ( il-1β , il-6 and tnf-α ) ( p < 0.05). In conclusion, HCAR1 activation effectively suppresses glutamate-induced neuronal apoptosis, reduces the uptake of excitatory neurotransmitters, and downregulates proinflammatory factor expression, thereby exerting neuroprotective effects.

Aim: This study aimed to evaluate the association of FC with gastrointestinal involvement in SSc, focusing on factors such as small intestine wall thickness, esophageal dilation, and skin involvement. Background: Fecal calprotectin (FC) has emerged as a promising biomarker for intestinal inflammation, and its role in systemic sclerosis (SSc) remains under investigation. Gastrointestinal involvement in SSc is common and can significantly impact quality of life, making it crucial to identify reliable biomarkers for early detection. Objective: GI disorders significantly impact the quality of life of systemic sclerosis (SSc) patients. Materials and methods: We gathered information from the 39 patients by filling out a UCLA SCTS 2.0 questionnaire regarding their GI symptoms. Additionally, we examined their skin and determined their skin score. Blood samples were taken to assess malnutrition, and stool samples were collected to measure the calprotectin level. We also conducted a non-aggressive Barium Swallow and CT Enterography to check for GI disorders. Results: Increased levels of FC didn’t have any correlation with age ( p Value = .79), disease type ( p Value = .59), slight intestine wall thickening ( p Value = .10), esophageal dilatation ( p Value = .18), skin score ( p Value = .25), final GI score ( p Value = .30) and none of the serum tests. In our study, just 5 cases had evidence of wall thickening in CT Enterography, and all 5 cases had increased calprotectin levels. Also, as most of our patients take vitamin and mineral supplements, we couldn’t find any signs of micronutrient deficiencies or correlation with FC level. Conclusion: Our study found no significant link between fecal calprotectin and gastrointestinal involvement in systemic sclerosis. Due to sample size and design limitations, fecal calprotectin may not be a reliable biomarker. Larger studies are needed to confirm these findings.

Objective: Deep neck space abscess (DNSA) is a serious infection associated with immune response. Magnesium has fundamental multifunctions in the body. Its insufficiency is involved in immüne weakness and susceptibility to infectious diseases. The present study addressed serum magnesium status in patients with DNSA. Herein, we hypothesized that patients with DNSA may have decreased serum magnesium concentration. Materials and Methods: In the study, 23 patients with DNSA and 23 matched healthy individuals were included. The atomic absorption spectrometry was used to measure serum magnesium concentration. The groups were compared statistically for demographics and serum magnesium concentration. Results: Patients with DNSA and healthy controls were statistically similar in age ( p = .625), gender ( p = 1.0), and smoking status ( p = 1.0). However, patients with DNSA had significantly decreased serum magnesium concentration (µg/dL) than healthy controls [25.23 ± 4.98 (19.9-42.2) versus 31.98 ± 5.36 (26.8-40.8)], ( p < .001). Conclusion: This study demonstrated that decreased serum magnesium concentration is associated with DNSA. It is the first report on the research topic, and may inspire future studies.

Background: The relationship with the treating gastroenterologist has been shown to significantly influence the quality of life of patients with IBD (Inflammatory Bowel Disease). Still, the expectations of patients have not been studied in detail. This study aimed to explore the messages and recommendations of IBD patients towards their gastroenterologists who treat them. Methods: This qualitative study was conducted using the DIPEx method developed by the Health Experiences Research Group at Oxford University. Semi-structured interviews with 36 participants (19 with Crohn’s disease and 17 with ulcerative colitis) were analysed using thematic analysis. Results: Three main areas emerged as relevant for patients: doctors’ expertise, patient-physician relationships, and the organisation of the healthcare system. Participants underscored the importance of comprehensive information, symptom recognition, exceptional care, and addressing outcome disparities by their treating physicians. Patient-centeredness, including dignified treatment, collaborative management of embarrassment, and trust, was mentioned as crucial for a good patient-physician relationship. The patients stressed the importance of sufficient time for care and the incorporation of mental health interventions. They emphasised professionalism, expertise, and friendly rapport as crucial for building trust in treating the unpredictable nature of IBD. The study also highlights the systemic impact of these interactions on healthcare systems. Conclusions: Patients actively engaged in their treatment bring novel perspectives, underscoring the value of a collaborative, respectful, and patient-physician dynamic. The implementation of this approach requires systemic healthcare shifts. This qualitative study on patient expectations underscores factors for a robust patient-physician bond, including gastroenterologists’ expertise, personalised care, and adequate time provision.

Background: Therapeutics of urticaria in Chinese outpatients remain to be illustrated. Objectives: To investigate clinical treatment of outpatients with urticaria, and provide real-world evidence for selection of medication regimens. Methods: In this hospital-based multicenter study, urticaria outpatients filled in a questionnaire at initial visit and were followed-up (once per week, for 4 weeks). Results: We recruited 1715 urticaria outpatients and 647 completed 4 week’s follow-up. Their total UAS7 was reduced (27.44 at baseline, 16.87 in 1 week, 12.39 in 2 weeks, 7.21 in 3 weeks, 4.2 in 4 weeks). 71.8% patients recovered from urticaria (therapy was highly effective in 11%, whereas effective in 14.2%). The second-generation H1 antihistamines (sgAHs) (at conventional dose) were the most commonly prescribed drugs, with ebastine, levocetirizine and olopatadine being the leading ones (41.1%, 36.2%, and 16%, respectively). Combinations of several antihistamines (649 cases, 37.8%) at conventional dose were far more common than a single drug at escalated dose (59 cases, 3.4%). The combination of ebastine with levocetirizine was the most frequent options (18.25%, 313 cases), followed by combination of ebastine with compound glycyrrhizin (18.2%, 312 cases). The usage rates of tripterygium glycoside (19.6%), hydroxychloroquine (17.2%) and system application glucocorticoids (5.5%) in angioedema were much higher than in symptomatic dermographism and chronic spontaneous urticaria. Conclusions: This study identifies curative therapy for Chinese outpatients with urticaria. The sgAHs, especially ebastine, are the most commonly prescribed drugs. Olopatadine has fast-acting and curative effects. Compound glycyrrhizin holds potential as a versatile collaborator. Combinations of several antihistamines at conventional dose is common.

Objective: To conduct a systematic review and meta-analysis of all available published data related to rats about spermatogenesis to provide a comprehensive overview of the effects of cigarette smoke exposure on the parameters of spermatogenesis.Methods: A comprehensive search of electronic databases including PubMed, EBSCO, ProQuest, Science Direct, Taylor & Francis, Springer Link, GARUDA, and Google Scholar, spanning from their inception until January 29th, 2021, was conducted to retrieve relevant studies and full-text articles evaluating the effect of cigarette smoke exposure on the parameters of spermatogenesis in rats. Data were taken from eligible studies. We use SYRCLE’s Risk of Bias tool for this animal studies. The overall size effect was measured, and forest plots and funnel plots were generated using the statistical software JASP.Results: The present study comprised 23 studies involving 527 rats. The findings of this meta-analysis revealed that parameters of spermatogenesis, such as sperm count, morphology, and viability, were substantially impaired in response to conventional cigarette smoke exposure, exhibiting and aggregate correlation coefficient of 0,70 (95% CI:0.61-0.79, p < .001).Conclusion: Exposure to conventional cigarette smoke has a significant negative effect on spermatogenic parameters in rats, particularly in terms of sperm count, morphology, and viability.

Systemic lupus erythematosus (SLE) manifests itself in the form of damage to various organs as a result of an autoimmune reaction to the organism's own molecules. Understanding the processes leading to the activation of the autoimmune response, as well as identifying potential autoantigens and their role in the pathogenesis of SIE, is an important task for understanding the mechanisms underlying the pathogenesis of SLE. Here we describe a model of SLE pathogenesis in which the induction of an autoimmune response is based on mitochondrial antigens. In addition to options for initiating an autoimmune response involving mitochondrial components, the model describes the role of pathways and immune cells of these pathways of adaptive immunity in SLE, as well as factors leading to the development of chronic inflammation in SLE. The creation of such models is important for a better understanding of the pathogenesis of SLE, as well as the identification of new therapeutic targets for this disease.

Objectives: Epithelial-mesenchymal transition (EMT) of renal tubular epithelial cells (RTECs) is a pathogenic factor for renal interstitial fibrosis (RIF). Interleukin-33 (IL-33) is related to the occurrence and development of RIF, but the underlying mechanism remains unclear. Here, we investigated whether IL-33 mediates the EMT of RTECs by activating the NF-κB/Twist1 signalling pathway. Methods: In vivo, the RIF animal model induced by unilateral ureteral obstruction (UUO) was established. The effects of exogenous IL-33 and anti-IL-33 antibodies were evaluated. In vitro, the EMT of RTECs was induced by IL-33. The inhibition of the nuclear factor kappa-B (NF-κB) by the pyrrolidine dithiocarbamate (PDTC) and the knockdown of the suppression of tumorigenicity 2 (ST2) by small interference RNA were used to observe whether IL-33 mediates the EMT of RTECs through the NF-κB/Twist1 signaling pathway. Results: In vivo, exogenous IL-33 significantly aggravated UUO-induced pathological damage and collagen deposition, down-regulated E-cadherin expression, and up-regulated α-smooth muscle actin and Vimentin expressions. Moreover, exogenous IL-33 increased the levels of phospho-IκB-α (p-IκB-α) and phospho-NF-κB p65 (p-NF-κB p65), NF-κB p65 nuclear translocation, and Twist1 nuclear expression. However, these effects were reversed by the anti-IL-33 antibody. In vitro , the increases in the levels of p-IκB-α, p-NF-κB p65, NF-κB p65 nuclear translocation, and Twist1 nuclear expression induced by IL-33 were inhibited by the knockdown of PDTC or ST2. IL-33-mediated EMT of RTECs was also significantly reversed. However, NF-κB inhibitor PDTC had no significant effect on ST2 expression. Conclusions: The IL-33/ST2 axis may up-regulate the expression of Twist1 through the NF-κB signalling pathway, thereby inducing the EMT of RTECs and leading to RIF.