Ying Chen

Cirrhosis is a severe liver disease characterized by inflammation, fibrosis, and immune dysregulation. This study exploits publicly available single-cell s

Background: Breastfeeding promotion is a public health priority in China, yet the exclusive breastfeeding rate remains below national targets. Nursing students, as future key promoters, often report insufficient knowledge, but their attitudes are less clear. Objective: This study aimed to assess breastfeeding attitudes and identify their associated factors among Chinese nursing undergraduates, thereby providing an evidence base for the design of effective educational interventions. Design, Setting and Participants: A cross-sectional study was conducted from October 2024 to January 2025 at a medical university in Anhui Province, China, with 753 nursing students participating. Methods: The participants completed the General Information Questionnaire, the Chinese version of the Comprehensive Breastfeeding Knowledge Scale (CBKS), and the Iowa Infant Feeding Attitude Scale (IIFAS). We analyzed the data via Spearman correlation, univariate analysis, and multiple linear regression. Results: The overall IIFAS score for nursing students was 54 (51, 59), with attitude scores showing a significant positive correlation with knowledge (r = 0.462, p < 0.001). Multiple linear regression revealed that breastfeeding attitudes were significantly predicted by CBKS score (β = 2.975), grade (β = 2.887), major (β = 3.235), and breastfeeding intention (β = 8.089, all p < 0.001), as well as by feeding type before six months (β = −1.591, p = 0.020). The overall model accounted for 32.7% of the variance (R² = 0.327, F = 51.666, p < 0.001). Conclusions: This study demonstrates that Chinese nursing undergraduates hold predominantly neutral attitudes toward breastfeeding. These attitudes show significant associations with their knowledge level and personal feeding intention, which underscores the necessity of integrating attitude-focused education into nursing curricula.

Objective(s): The combination of TNF-alpha inhibitors and vitamin D in colitis remains to be elucidated. In the present study, we revealed the benefit of infliximab (IFX) and vitamin D in a mouse model of Ulcerative colitis (UC). Materials and Methods: A dextran sulfate sodium-induced colitis model was used. The therapeutic effect of the combination was evaluated by symptom and histopathology analysis. The synergistic mechanism was explored by detecting the regulatory effect of the combined therapy on Regulatory T cell (Treg) differentiation. Results: IFX and 1,25-dihydroxyvitamin D3 (VitD3) synergistically prevented the development of colitis by improving clinical signs, pathological and hematological manifestation, and inhibiting intestinal inflammation (decreasing TNF-alpha, IL-1 beta, and IL-6). Co-administration of IFX (2.5 mg/kg) with VitD3 or IFX (5.0 mg/kg) with VitD3 was more effective than administration of IFX (2.5 mg/kg, 5.0 mg/kg). There was no difference in therapeutic effect between IFX (5.0 mg/kg) and VitD3+ IFX (2.5 mg/kg) groups or between the VitD3+IFX (5.0 mg/kg) and VitD3+ Azathioprine (AZA) groups. VitD3 or combination therapy showed more powerful regulation of splenetic Treg differentiation and IL-10 production than IFX alone. Moreover, VitD3 alone or in combination induced higher levels of Foxp3 and IL-10 than IFX in colon tissue. In ulcerative colitis patients, serum VitD3 levels positively correlated with Treg levels. Conclusion: VitD3 and IFX synergistically inhibit colitis based on their powerful regulation of Treg differentiation. VitD3 combined with IFX is an alternative therapy for patients who are intolerant to standard doses of IFX or combination of IFX and AZA.

Macrophage therapy for liver fibrosis is on the cusp of meaningful clinical utility. Due to the heterogeneities of macrophages, it is urgent to develop safer macrophages with a more stable and defined phenotype for the treatment of liver fibrosis. Herein, a new macrophage‐based immunotherapy using macrophages stably expressing a pivotal cytokine from Toxoplasma gondii , a parasite that infects ≈ 2 billion people is developed. It is found that Toxoplasma gondii macrophage migration inhibitory factor‐transgenic macrophage (Mφ ^tgmif ) shows stable fibrinolysis and strong chemotactic capacity. Mφ ^tgmif effectively ameliorates liver fibrosis and deactivates aHSCs by recruiting Ly6C ^hi macrophages via paracrine CCL2 and polarizing them into the restorative Ly6C ^lo macrophage through the secretion of CX3CL1. Remarkably, Mφ ^tgmif exhibits even higher chemotactic potential, lower grade of inflammation, and better therapeutic effects than LPS/IFN‐γ‐treated macrophages, making macrophage‐based immune therapy more efficient and safer. Mechanistically, Tg MIF promotes CCL2 expression by activating the ERK/HMGB1/NF‐κB pathway, and this event is associated with recruiting endogenous macrophages into the fibrosis liver. The findings do not merely identify viable immunotherapy for liver fibrosis but also suggest a therapeutic strategy based on the evolutionarily designed immunomodulator to treat human diseases by modifying the immune microenvironment.

Zhang L, et al. J Korean Acad Nurs. 2024 Nov;54(4):509-518. https://doi.org/10.4040/jkan.24044

Background and Purpose: Necroptosis plays an essential role in acute kidney injury and is mediated by receptor‐interacting protein kinase 1 (RIPK1), receptor‐interacting protein kinase 3 (RIPK3), and mixed lineage kinase domain‐like pseudokinase (MLKL). A novel RIPK3 inhibitor, compound 42 (Cpd‐42) alleviates the systemic inflammatory response. The current study was designed to investigate whether Cpd‐42 exhibits protective effects on acute kidney injury and reveal the underlying mechanisms.Experimental Approach: The effects of Cpd‐42 were determined in vivo through cisplatin‐ and ischaemia/reperfusion (I/R)‐induced acute kidney injury and in vitro through cisplatin‐ and hypoxia/re‐oxygenation (H/R)‐induced cell damage. Transmission electron microscopy and periodic acid–Schiff staining were used to identify renal pathology. Cellular thermal shift assay and RIPK3‐knockout mouse renal tubule epithelial cells were used to explore the relationship between Cpd‐42 and RIPK3. Molecular docking and site‐directed mutagenesis were used to determine the binding site of RIPK3 with Cpd‐42.Key Results: Cpd‐42 reduced human proximal tubule epithelial cell line (HK‐2) cell damage, necroptosis and inflammatory responses in vitro. Furthermore, in vivo, cisplatin‐ and I/R‐induced acute kidney injury was alleviated by Cpd‐42 treatment. Cpd‐42 inhibited necroptosis by interacting with two key hydrogen bonds of RIPK3 at Thr94 and Ser146, which further blocked the phosphorylation of RIPK3 and mitigated acute kidney injury.Conclusion and Implications: Acting as a novel RIPK3 inhibitor, Cpd‐42 reduced kidney damage, inflammatory response and necroptosis in acute kidney injury by binding to sites Thr94 and Ser146 on RIPK3. Cpd‐42 could be a promising treatment for acute kidney injury.

Toxoplasma gondii dense granule protein GRA3 has been shown to promote Toxoplasma gondii transmission and proliferation by interacting with the host cell endoplasmic reticulum (ER) through calcium-regulated cyclophilin ligands (CAMLG). Although many studies have focused on the interaction between the host cell endoplasmic reticulum and GRA3, no polyclonal antibodies (PcAbs) against GRA3 have been reported to date. According to the antigenicity prediction and exposure site analysis, three antigen peptide sequences were selected to prepare polyclonal antibodies targeting GRA3. Peptide scans revealed that the major antigenic epitope sequences were ¹²⁵ELYDRTDRPGLK¹³⁶, ²⁰²FFRRRPKDGGAG²¹³, and ⁶⁸NEAGESYSSATSG⁸⁰, respectively. The GRA3 PcAb specifically recognized the GRA3 of T. gondii type Ⅱ ME49. The development of PcAbs against GRA3 is expected to elucidate the molecular mechanisms by which GRA3 regulates host cell function and contribute to the development of diagnostic and therapeutic strategies for toxoplasmosis.

Toxoplasmosis, a common parasitic disease, is caused byToxoplasma gondii, which infects approximately 30% of the world’s population. This obligate intracellular protozoan causes significant economic losses and poses serious public health challenges worldwide. However, the development of an effective toxoplasmosis vaccine in humans remains a challenge to date. In this study, we observed that the knockout of calcium-dependent protein kinase 3 (CDPK3) in the type II ME49 strain greatly attenuated virulence in mice and significantly reduced cyst formation. Hence, we evaluated the protective immunity of ME49Δcdpk3as a live attenuated vaccine against toxoplasmosis. Our results showed that ME49Δcdpk3vaccination triggered a strong immune response marked by significantly elevated proinflammatory cytokine levels, such as IFN-γ, IL-12, and TNF-α, and increased the percentage of CD4⁺ and CD8⁺ T-lymphocytes. The high level ofToxoplasma-specific IgG was maintained, with mixed IgG1/IgG2a levels. Mice vaccinated with ME49Δcdpk3were efficiently protected against the tachyzoites of a variety of wild-type strains, including type I RH, type II ME49, Chinese 1 WH3 and Chinese 1 WH6, as well as the cysts of wild-type strains ME49 and WH6. These data demonstrated that ME49Δcdpk3inoculation induced effective cellular and humoral immune responses against acute and chronicToxoplasmainfections with various strains and was a potential candidate to develop a vaccine against toxoplasmosis.

Sepsis is defined as a life-threatening organ dysfunction caused by the dysregulated host response to infection, and is one of the main causes of death in intensive care unit (ICU) patients. Coagulation dysfunction runs through the pathophysiological progress of sepsis whose severity should be closely related to the prognosis of sepsis. Neutrophil extracellular traps (NETs) is a three-dimensional network structure with DNA as the skeleton and inlaid with various protein components. The excessive production of NETs can lead to sepsis-induced coagulopathy (SIC) by activating the coagulation system, inhibiting the anticoagulation system, resisting fibrinolysis, damaging vascular endothelial cells and the interaction of platelets. At present, the treatment of SIC is mainly symptomatic treatment, and there is no recognized effective anticoagulation strategy. Interventions for NETs and their components, and drugs for antiplatelets are expected to become new directions for disease treatment.