Iron,a vital trace element and redox-active metal in the human body,is pivotal in cellular processes and en-gages in a multitude of biological reactions.Ferroptosis,an emerging form of regulated cell death,is predominantly instiga-ted by the excessive free iron that catalyzes reactive oxygen species(ROS)production via the Fenton reaction.This process results in the peroxidation of polyunsaturated fatty acids within the cellular lipid membrane,compromising the membrane's integrity and thereby inducing ferroptosis.In the context of diabetic retinopathy(DR),ferroptosis plays a sig-nificant role.The disruption of iron metabolism,the excessive accumulation of ROS,and the imbalance of the antioxidant system are key mechanisms contributing to ferroptosis in retinal tissues and the exacerbation of DR's pathological progres-sion.This review provides a systematic summary and in-depth discussion of the advancements in understanding the role of ferroptosis in DR pathogenesis,intending to offer valuable insights for future research endeavors in this field.

Innate immune system serves as the primary defense mechanism against pathogen infections,recognition of structural components of pathogens is referred to as pathogen-associated molecular patterns(PAMPs).Toll-like receptors(TLRs)are a family of transmembrane receptors that can identify PAMPs,which interact with myeloid differentiation factor 88(MyD88)and activate NF-κB dimerization,leading to the release of downstream inflammatory factors and ultimately triggering the adaptive immune system.Conse-quently,TLRs are regarded as adapters that regulate the transition from innate immunity to adaptive immunity.TLR/MyD88/NF-κB signaling pathway plays a crucial role in inflammatory diseases,infectious diseases and tumor immunity.This review article aims to explore the regulatory function of TLR/MyD88/NF-κB signaling pathway in host responses to viral,bacterial,and other microbial in-fections,providing novel insights into the immune response during the process of infection control.

Innate immune system serves as the primary defense mechanism against pathogen infections,recognition of structural components of pathogens is referred to as pathogen-associated molecular patterns(PAMPs).Toll-like receptors(TLRs)are a family of transmembrane receptors that can identify PAMPs,which interact with myeloid differentiation factor 88(MyD88)and activate NF-κB dimerization,leading to the release of downstream inflammatory factors and ultimately triggering the adaptive immune system.Conse-quently,TLRs are regarded as adapters that regulate the transition from innate immunity to adaptive immunity.TLR/MyD88/NF-κB signaling pathway plays a crucial role in inflammatory diseases,infectious diseases and tumor immunity.This review article aims to explore the regulatory function of TLR/MyD88/NF-κB signaling pathway in host responses to viral,bacterial,and other microbial in-fections,providing novel insights into the immune response during the process of infection control.

Iron,a vital trace element and redox-active metal in the human body,is pivotal in cellular processes and en-gages in a multitude of biological reactions.Ferroptosis,an emerging form of regulated cell death,is predominantly instiga-ted by the excessive free iron that catalyzes reactive oxygen species(ROS)production via the Fenton reaction.This process results in the peroxidation of polyunsaturated fatty acids within the cellular lipid membrane,compromising the membrane's integrity and thereby inducing ferroptosis.In the context of diabetic retinopathy(DR),ferroptosis plays a sig-nificant role.The disruption of iron metabolism,the excessive accumulation of ROS,and the imbalance of the antioxidant system are key mechanisms contributing to ferroptosis in retinal tissues and the exacerbation of DR's pathological progres-sion.This review provides a systematic summary and in-depth discussion of the advancements in understanding the role of ferroptosis in DR pathogenesis,intending to offer valuable insights for future research endeavors in this field.

Objective:Bacterial liver abscess is one of the common infectious diseases of the digestive system.Invasive Klebsiella pneumoniae liver abscess syndrome(IKLAS)refers to cases where,in addition to liver abscess,there are migratory infections foci or other invasive manifestations.The clinical characteristics and risk factors of IKLAS are not fully elucidated,and there is a lack of research on the effectiveness and cost-effectiveness of different treatment methods.This study aims to compare the clinical characteristics of patients with IKLAS and non-IKLAS,and explore effective and economical treatment methods. Methods:This retrospective study collected medical records of patients with Klebsiella pneumoniae liver abscess treated at Xiangya Hospital of Central South University from January 2010 to December 2023.A total of 201 patients were included,dividing into an IKLAS group(n=37)and a non-IKLAS group(n=164).Differences in demographics,symptoms and signs,laboratory indicators,imaging characteristics,comorbidities,treatment methods,treatment outcomes,and direct treatment costs between 2 groups were analyzed.The study also compared the effectiveness and costs of different treatment methods. Results:Compared with the non-IKLAS group,the proportion of patients with diabetes,Quick Sequential Organ Failure Assessment(qSOFA)≥2,immune deficiency,anemia,and thrombocytopenia in the IKLAS group was higher,and the level of procalcitonin at the onset in the IKLAS group was also higher(all P<0.05).In terms of symptoms and signs,the IKLAS group had a higher proportion of visual abnormalities and a lower proportion of complaints of abdominal pain(both P<0.05).In terms of complications,the incidence of combined pleural effusion,pulmonary infection,acute renal failure,respiratory failure,and multiple organ failure was higher in the IKLAS group(all P<0.05).The IKLAS group had a higher proportion of patients treated with antibiotics alone(24.32%vs 11.59%),while the non-IKLAS group had a higher proportion of patients treated with antibiotics combined with puncture and drainage(86.59%vs 64.86%,both P<0.05).The overall effective rate of the IKLAS group(83.78%)was lower than that of the non-IKLAS group(95.73%),and the treatment and drug costs were higher(all P<0.05).The treatment method of antibiotics combined with surgical resection of infectious foci showed a 100%improvement rate,antibiotics combined with abscess puncture and drainage had an 84.9%improvement rate,and in antibiotics alone had an 82.1%improvement rate,with statistical differences among the 3 treatment methods(P<0.05).In terms of treatment costs,antibiotics alone were the most expensive(P<0.05). Conclusion:Patients with IKLAS have poorer prognosis and higher direct medical costs.The combination of abscess puncture and drainage or surgery has a higher improvement rate and lower hospitalization costs compared to antibiotics alone,suggesting that surgical intervention may reduce antibiotic costs and save medical expenses.

Encephalomyocarditis virus (EMCV) is a non-enveloped, positive-sense, single-stranded RNA virus that belongs to the family Picornaviridae and the genus Cardiovirus. EMCV has the ability to infect various mammals, such as mice, pigs, and cattle. In addition, humans are susceptible to EMCV infection, and the seropositivity rate of relevant antibodies in healthy populations is steadily increasing, which poses a potential risk of epidemics. The initial step of viral infection in cells involves recognition and attachment to cell surface receptors, followed by endocytosis into the cells. Subsequently, viral proteins interact with host proteins within the cells to promote their own replication. With the progress made in protein-protein interaction studies and the development of high-throughput sequencing technologies, multiple host proteins that interact with EMCV have been identified. This article summarizes the host proteins that interact with EMCV during infection, explores the mechanisms by which these proteins facilitate or inhibit viral invasion, discusses the latest progress in EMCV-induced endocytosis and intracellular signaling, hoping to provide reference for better elucidating EMCV receptor proteins, understanding viral infection and replication mechanisms, studying virus-host interactions and tissue tropism, and developing novel targeted antiviral drugs and prevention strategies.

AIM: To explore retinal microvascular changes in migraine patients using meta-analysis.METHODS: The National Library of Medicine PubMed, Embase, and Cochrane Library were searched to find relevant studies, and the search period was from the creation of database to June 2023. Two investigators independently screened the literatures, extracted data, and evaluated the quality of included studies using the NOS scale. STATA15.0 was used for Meta-analysis and publication bias evaluation, sensitivity analysis was performed for results with large heterogeneity, and the funnel plot and Egger were used to assess the publication bias of the literature.RESULTS:A total of 12 studies, including 217 patients(252 eyes)with migraine with aura(MA), 283 patients(388 eyes)with migraine without aura(MO), and 374 healthy individuals(479 eyes), were included in this Meta-analysis. Several optical coherence tomography angiography(OCTA)indicators, including foveal avascular zone(FAZ)macular or optic disc perfusion density were compared and analyzed. The Meta-analysis results showed that compared with healthy controls, patients with MA had a significant increase in FAZ area and perimeter, a significant decrease in perfusion density of the macular deep capillary plexus(mDCP)except for the fovea, and a significant decrease in perfusion density of the radial peripapillary capillaries(RPC)around the optic disc; the FAZ parameters were significantly increased in MO, while the differences in perfusion density of the macular superficial capillary plexus(mSCP), mDCP and RPC were not statistically significant, except for the perfusion density in the parafovea mDCP.CONCLUSIONS: Both MA and MO patients had an enlarged FAZ area, patients with MA had a significant decrease in mDCP perfusion density, and migraine patients had some degree of retinal ischemia.

BACKGROUND: Previous study demonstrated that hypoxia preconditioning promoted mesenchymal stem cells survival and their therapeutic efficacy, and this effect was mediated by hypoxia induced factor-1α (HIF-1α). However, specific downstream mechanism remained unclear. OBJECTIVE: To observe the influence of hypoxia preconditioning on the survival and vascularization potential of bone marrow mesenchymal stem cells in vitro and explore the regulatory mechanism of HIF-1α/MALAT1/VEGFA pathway. METHODS: Bone marrow mesenchymal stem cells were obtained and cultured in vitro. Cells were divided into hypoxia (1% O2) and normoxia control groups (20% O2), and cultured for 24 hours. Cells proliferation, apoptosis and vascularization were evaluated. The expression of HIF-1α, MALAT1, and VEGFA was detected. HIF-1α and MALAT1 were inhibited by their siRNAs separately. HIF-1α siRNA scramble and MALAT1 siRNA scramble were used as negative controls before hypoxia preconditioning. Alterations of the molecules were examined and compared in different groups. RESULTS AND CONCLUSION: (1) Compared with the normoxia control group, cell viability was significantly enhanced; and cell apoptosis percentage was significantly declined in the hypoxia group; vascular lumen like structure was also increased significantly in the hypoxia group (P < 0.01); expression of HIF-1α, MALAT1, and VEGFA was significantly increased in the hypoxia group (P < 0.01). (2) After the inhibition of HIF-1α and hypoxia preconditioning, both MALAT1 and VEGFA expression levels were significantly reduced (P < 0.01). The expression of VEGFA was also significantly suppressed after the blockage of MALAT1 (P < 0.01). (3) This study suggested that hypoxia preconditioning effectively promoted bone marrow mesenchymal stem cell survival and vascularization through the activation of HIF-1α/MALAT1/VEGFA pathway.

Objective: To investigate effects of personal innovation behaviors, self-efficacy and colleague solidarity of nurses on career success, and to provide the basis for career planning and management of clinical nurses. Methods: A total of 441 registered nurses from eight grade three and first-class hospitals in Tianjin were measured with personal innovation behaviors scale, self-efficacy scale, colleague solidarity of nurses' scale and career success scale. Results: The total score of personal innovation behavior was (21.58±4.81). The total score of self-efficacy was (27.68±6.53). The total score of colleague solidarity of nurses was (95.12±9.42). The total score of career success was (35.75±9.27). The personal innovation behaviors, self-efficacy, colleague solidarity of nurses career success and each dimension showed positive correlation(r=0.115-0.915, P<0.05). Multiple linear regression analysis showed that innovation behaviors, self-efficacy and academic solidarity entered career success regression equation(β=0.090-0.554, P<0.05), and explained 49.7% of the total variation.Path analysis model showed innovative behavior, self-efficacy and colleague solidarity of nurses were positively predictive of career success, and the path coefficients were 0.62, 0.18 and 0.12.Hierarchical regression analysis showed both self-efficacy and colleague solidarity of nurses played mediating roles between innovative behavior and career success(β=0.207-0.104, P<0.05). Conclusion Hospital managers should take measures to improve nurses' innovative behavior, self-efficacy and colleague solidarity of nurses to promote their career success.

AIM:To analyze the alterations of angiotensin Ⅱ (Ang Ⅱ), connexin 43 (Cx43), angiotenisinⅡreceptor type 1 (AT1) and signaling molecules in the TGF-β1/Smad pathway in different regions of the left ventricular heart tissue for exploring whether Ang Ⅱregulates Cx43 expression via the TGF-β1/Smad signaling pathway in myocardial infarction ( MI) rats.METHODS:MI was induced in 20 male Sprague-Dawley rats by the left anterior descending coronary artery ligation.The rats were then randomized into 2 groups.In the losartan group, 20 mg· kg-1· d-1 of losartan were ad-ministered for 2 weeks.Heart functions were assessed after surgery and 2 weeks later again following the above treatments . All the rats were sacrificed and relevant molecules , including Ang Ⅱ, AT1, and Cx43 were determined thereafter in diffe-rent areas of the left ventricle .TGF-β1 and its downstream signaling molecules , including Smad 2, Smad 3 and Smad 7, were also detected .RESULTS:In losartan group , both left ventricular internal dimension diastole ( LVIDd) and left ven-tricular internal dimension systole (LVIDs) were smaller, with diminished interventricular septal thickness (IVSd) and left ventricular posterior wall depth ( LVPWd ) and distinct improvement of left ventricular ejection fraction ( LVEF ) ( P<0.05 ) .Losartan therapy exhibited a reduction of Ang Ⅱin the infarct zone and the border zone in the cardiac tissues .AT1 was obviously attenuated in the infarct zone with an enhanced expression of Cx 43, which was also elevated in the border zone and none infarct zone .TGF-β1, Smad 2 and Smad 3 were decreased in different zones of the left ventricle , while Smad 7, in contrary to the above factors , presented a converse alteration .CONCLUSION:The activation of Ang Ⅱpro-vokes downregulation of Cx 43 through TGF-β1/Smad signaling pathway in MI rats .