Objective To understand the epidemiological characteristics of newly reported occupational diseases and provide a basis for the formulation of occupational disease prevention and control plans in Nanjing. Methods A descriptive analysis was conducted on newly reported occupational disease cases in Nanjing from 2014 to 2024. Results A total of 325 new cases of occupational diseases were reported in Nanjing, primarily concentrated in occupational otorhinolaryngological and oral diseases, as well as pneumoconiosis. Male cases outnumbered female cases across all types of occupational diseases. The median age at diagnosis was 53 (44, 65) years, and the median length of employment was 13 (6, 24) years. The distribution of occupational diseases varied significantly by gender and age at diagnosis (P<0.01). The distribution of occupational diseases also showed significant differences based on the length of exposure to hazards (χ²=120.63, P<0.01). Large enterprises, state-owned enterprises, and manufacturing industries accounted for the majority of cases (120 cases, 36.92%; 154 cases, 47.38%; 232 cases, 71.38%). The distribution of newly reported occupational diseases across different age groups at diagnosis was statistically significant (H=97.66, P<0.01; H=84.06, P<0.01; H=34.64, P<0.01; H=20.05, P<0.01; H=21.70, P<0.01). Except for occupational diseases caused by physical factors, the distribution of other newly reported occupational diseases across different employment length groups was also statistically significant (H=105.45, P<0.01; H=97.05, P<0.01; H=34.14, P<0.01; H=42.69, P<0.01). Conclusion The prevention and control of newly reported occupational diseases in Nanjing remain challenging. Attention should be paid to key occupational otorhinolaryngological and oral diseases, as well as pneumoconiosis. It is necessary to strengthen supervision and management of medium and large state-owned enterprises and manufacturing industries.

OBJECTIVE To establish a high-risk medication list and preventive and therapeutic measures for drug-induced hypofibrinogenemia， and to provide a reference for the prevention and treatment of this condition. METHODS By integrating domestic and international case reports， retrospective case-control studies， and spontaneous adverse drug reaction reporting databases， 19 domestically marketed high-risk drugs for drug-induced hypofibrinogenemia were identified. Based on the clinical characteristics and mechanisms of these drugs， relevant risk factors were systematically reviewed， and existing treatment options were summarized， leading to the preliminary development of recommended preventive and therapeutic measures. A two-round Delphi consultation was conducted to evaluate， revise， and ultimately reach consensus on the preliminary findings， using a mean importance score of ≥3.5 points for indicators and a coefficient of variation ＜0.3 as screening criteria. RESULTS The coefficient of expert authority for both rounds of expert consultation was 0.904. In the first round， the Kendall coordination coefficients （Kendall’s W ） for the high-risk medication list and the proposed preventive and therapeutic measures were 0.390 and 0.223 （ P ＜0.05）， respectively. In the second round， the Kendall’s W were 0.227 and 0.200 （ P ＜0.05）， respectively. After two rounds of expert consultation and discussion， 11 high-risk drugs for drug-induced hypofibrinogenemia， represented by hemocoagulase and certain anti-infective agents， were ultimately identified， along with 5 preventive and therapeutic measures spanning the entire process of “pre-medication assessment， intra-medication monitoring， and bleeding event management”. CONCLUSIONS This study has established a scientific and reliable high-risk medication list， and corresponding preventive and therapeutic measures for drug-induced hypofibrinogenemia， providing a theoretical basis and practical support for the early identification， stratified management， and precise intervention of this condition.

The Type III Secretion System (T3SS) serves as a pivotal virulence apparatus for numerous Gram-negative bacterial pathogens, enabling them to infect both animal and plant hosts. Functioning as a molecular syringe, the T3SS directly translocates bacterial effector proteins from the bacterial cytoplasm into the interior of eukaryotic host cells. These effectors are central weapons that precisely manipulate a wide spectrum of host cellular physiological processes, ranging from cytoskeletal dynamics to immune signaling, to establish a favorable niche for bacterial survival and proliferation. Among the diverse arsenal of T3SS effectors, the YopJ family constitutes a critical group of virulence factors. Members of this family are characterized by a conserved catalytic triad structure—a hallmark of the CE clan of cysteine proteases that has been evolutionarily repurposed to confer acetyltransferase activity. A defining and intriguing feature of these enzymes is their stringent dependence on a host-derived eukaryotic cofactor, inositol hexakisphosphate (IP₆), for allosteric activation. This requirement acts as a sophisticated molecular safeguard, ensuring enzymatic activity only within the appropriate host environment, thereby preventing detrimental effects on the bacterium itself. While seminal studies on individual members such as Yersinia’s YopJ and Salmonella’s AvrA have provided deep mechanistic insights, a systematic and integrative understanding of the structure-function relationships across the entire family remains fragmented. Key questions persist regarding how a conserved catalytic core has diverged to recognize distinct host substrates in different kingdoms of life. To address this gap, this article provides a systematic review of the YopJ family, focusing on three interconnected aspects: their structural features, their catalytic mechanism, and their divergent immunosuppressive strategies in animal versus plant hosts. By conducting a comparative analysis of the sequences and resolved three-dimensional structures of three representative members (e.g., HopZ1a, PopP2, AvrA), we elucidate regions of significant variation embedded within the conserved core catalytic architecture. These variable regions, often involving surface loops and substrate-binding interfaces, are crucial determinants of target specificity and functional specialization. The functional divergence of this effector family is most apparent when comparing their modes of action in different hosts. In animal hosts, YopJ-family effectors primarily sabotage innate immune signaling pathways. They achieve this by acetylating key serine and threonine residues within the activation loops of critical kinases in the MAPK and NF‑κB pathways. This post-translational modification blocks the phosphorylation and subsequent activation of these kinases, leading to potent suppression of inflammatory cytokine production. Conversely, in plant hosts, the strategy broadens to dismantle the two-tiered plant immune system. YopJ homologs target a more diverse set of substrates, including immune-associated receptor-like cytoplasmic kinases (RLCKs), microtubule networks via tubulin acetylation (which disrupts cellular trafficking and signaling), and transcription factors central to defense gene regulation. This multi-target approach effectively suppresses both Pattern-Triggered Immunity (PTI) and Effector-Triggered Immunity (ETI). In conclusion, this synthesis aims to deepen the mechanistic understanding of YopJ family-mediated pathogenesis by integrating structural biology with cellular function across host kingdoms. Elucidating the precise molecular basis for substrate selection—how conserved platforms achieve target diversity—is a major frontier. Furthermore, this knowledge provides a vital theoretical foundation for developing novel anti-virulence strategies. Targeting the conserved IP₆-binding pocket or the catalytic acetyltransferase activity itself represents a promising avenue for designing broad-spectrum inhibitors that could disarm this critical family of bacterial effectors, potentially offering new therapeutic approaches against a range of pathogenic bacteria.

Objective To investigate the clinical safety and efficacy of predictive extracorporeal membrane oxygenation (ECMO) support during liver transplantation in high-risk recipients. Methods A single-center retrospective study was conducted. A total of 35 liver transplant recipients who underwent predictive ECMO assistance during surgery at the Second Affiliated Hospital of Guangxi Medical University from January 2021 to April 2025 were included. Baseline characteristics, ECMO application, ECMO operating parameters and hemodynamic conditions during ECMO operation were analyzed. The cumulative survival rate was calculated using the Kaplan-Meier method and survival curves were plotted. Results Veno-arterial ECMO in 35 recipients was established after induction of general anesthesia. The median ECMO operation time was 8.5 h, and the success rate of weaning from ECMO was 97%. The cardiac index (CI) during the non-liver period and the new liver period was higher than that before cannulation, and CI increased during the non-liver period and before weaning (all P<0.001). The mean invasive arterial pressure and central venous pressure remained stable. No ECMO-related complications occurred in the recipients. The average survival time was (25 ± 3) months. The main causes of death were severe pulmonary infection and multiple organ failure. Conclusions For liver transplant recipients with severe cardiopulmonary dysfunction, hemodynamic disorders, or multiple organ failure risk factors, implementing predictive ECMO support during liver transplantation through active risk prediction is a safe and effective circulatory guarantee strategy.

Collagen is a major structural protein in the matrix of animal cells and the most widely distributed and abundant functional protein in mammals. Collagen’s good biocompatibility, biodegradability and biological activity make it a very valuable biomaterial. According to the source of collagen, it can be broadly categorized into two types: one is animal collagen; the other is recombinant collagen. Animal collagen is mainly extracted and purified from animal connective tissues by chemical methods, such as acid, alkali and enzyme methods, etc. Recombinant collagen refers to collagen produced by gene splicing technology, where the amino acid sequence is first designed and improved according to one’s own needs, and the gene sequence of improved recombinant collagen is highly consistent with that of human beings, and then the designed gene sequence is cloned into the appropriate vector, and then transferred to the appropriate expression vector. The designed gene sequence is cloned into a suitable vector, and then transferred to a suitable expression system for full expression, and finally the target protein is obtained by extraction and purification technology. Recombinant collagen has excellent histocompatibility and water solubility, can be directly absorbed by the human body and participate in the construction of collagen, remodeling of the extracellular matrix, cell growth, wound healing and site filling, etc., which has demonstrated significant effects, and has become the focus of the development of modern biomedical materials. This paper firstly elaborates the structure, type, and tissue distribution of human collagen, as well as the associated genetic diseases of different types of collagen, then introduces the specific process of producing animal source collagen and recombinant collagen, explains the advantages of recombinant collagen production method, and then introduces the various systems of expressing recombinant collagen, as well as their advantages and disadvantages, and finally briefly introduces the application of animal collagen, focusing on the use of animal collagen in the development of biopharmaceutical materials. In terms of application, it focuses on the use of animal disease models exploring the application effects of recombinant collagen in wound hemostasis, wound repair, corneal therapy, female pelvic floor dysfunction (FPFD), vaginal atrophy (VA) and vaginal dryness, thin endometritis (TE), chronic endometritis (CE), bone tissue regeneration in vivo, cardiovascular diseases, breast cancer (BC) and anti-aging. The mechanism of action of recombinant collagen in the treatment of FPFD and CE was introduced, and the clinical application and curative effect of recombinant collagen in skin burn, skin wound, dermatitis, acne and menopausal urogenital syndrome (GSM) were summarized. From the exploratory studies and clinical applications, it is evident that recombinant collagen has demonstrated surprising effects in the treatment of all types of diseases, such as reducing inflammation, promoting cell proliferation, migration and adhesion, increasing collagen deposition, and remodeling the extracellular matrix. At the end of the review, the challenges faced by recombinant collagen are summarized: to develop new recombinant collagen types and dosage forms, to explore the mechanism of action of recombinant collagen, and to provide an outlook for the future development and application of recombinant collagen.

Objective To explore the relationship between PANoptosis and hepatic ischemia-reperfusion injury (HIRI), and to screen the key genes of PANoptosis in HIRI. Methods PANoptosis-related differentially expressed genes (PDG) were obtained through the Gene Expression Omnibus database and GeneCards database. Gene ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and Gene Set Enrichment Analysis (GSEA) were used to explore the biological pathways related to PDG. A protein-protein interaction network was constructed. Key genes were selected, and their diagnostic value was assessed and validated in the HIRI mice. Immune cell infiltration analysis was performed based on the cell-type identification by estimating relative subsets of RNA transcripts. Results A total of 16 PDG were identified. GO analysis showed that PDG were closely related to cellular metabolism. KEGG analysis indicated that PDG were mainly enriched in cellular death pathways such as apoptosis and immune-related signaling pathways such as the tumor necrosis factor signaling pathway. GSEA results showed that key genes were mainly enriched in immune-related signaling pathways such as the mitogen-activated protein kinase (MAPK) signaling pathway. Two key genes, DFFB and TNFSF10, were identified with high accuracy in diagnosing HIRI, with areas under the curve of 0.964 and 1.000, respectively. Immune infiltration analysis showed that the control group had more infiltration of resting natural killer cells, M2 macrophages, etc., while the HIRI group had more infiltration of M0 macrophages, neutrophils, and naive B cells. Real-time quantitative polymerase chain reaction results showed that compared with the Sham group, the relative expression of DFFB messenger RNA in liver tissue of HIRI group mice increased, and the relative expression of TNFSF10 messenger RNA decreased. Cibersort analysis showed that the infiltration abundance of naive B cells was positively correlated with DFFB expression (r=0.70, P=0.035), and the infiltration abundance of M2 macrophages was positively correlated with TNFSF10 expression (r=0.68, P=0.045). Conclusions PANoptosis-related genes DFFB and TNFSF10 may be potential biomarkers and therapeutic targets for HIRI.

The accumulation of uremic toxins such as urea nitrogen, blood creatinine, and uric acid of patients with renal failure in vivo would lead to aggravated kidney damage. In this study, coated aldehyde oxy-starch (CAO) was used as an adsorbent to investigate its in vitro adsorption performance on renal failure indexes for urea, indoxyl sulfate (INS), monomethylamine (MMA), dimethylamine (DMA), uric acid (UA), and creatinine (Cr). The effects of variables such as pH, temperature, concentration, dosage, and time on the adsorption capacity of CAO were systematically investigated, employing analytical techniques of high-performance liquid chromatography (HPLC) and gas chromatography (GC). The results revealed that CAO exhibited a strong adsorption capacity for urea, INS, and MMA, alongside a moderate adsorption capacity for DMA, UA, and Cr. The adsorption kinetics and thermodynamic studies indicated that the adsorption of urea and UA by CAO were fitted in pseudo-first-order kinetics, and the adsorption isotherm aligned with the Freundlich adsorption model. The enthalpy change ΔH of urea in adsorption was in the range of 40 to 60 kJ·mol^-1, which demonstrated the presence of strong adsorption force due to the interactions of coordinating groups. The ΔH of UA was greater than 80 kJ·mol^-1, indicating the generation of chemical bonds during the adsorption. Both of them, Gibbs free energy ΔG was less than 0, within the range of -20 to 0 kJ·mol^-1, suggested that the adsorption of urea and UA by CAO occurred spontaneously as physical adsorption process. The adsorption entropy ΔS of urea and UA was > 0, which indicated an increase in entropy throughout the adsorption. The infrared spectroscopygram showed the formation of a chemical bond, specifically the imine bond, following the adsorption of urea by CAO, thereby indicating a chemical reaction during the adsorption. This study elucidates the adsorption mechanism of CAO on various indexes of renal failure, providing a scientific basis for its clinical usage.

Objective: To compare and analyze the antibacterial effects of platelets against five common clinical pathogenic bacteria including MRSA, SE, SA, E. coli, and CRKP, and to preliminarily explore the role of DCD sensitivity in the observed variations of antibacterial effects. Methods: The same number of platelets were used to establish co-culture systems of platelets and platelet lysates with the five pathogenic bacteria. The antibacterial effects of platelets and platelet lysates on the five pathogenic bacteria were evaluated by observing the turbidity of the bacterial solution, measuring the OD value of the bacterial solution and counting the colonies. The supernatant protein of platelets co-cultured with MRSA was collected for quantitative proteomics analysis to explore the important antibacterial proteins of platelets. The content of DCD in the supernatant after co-culture of platelets and platelet lysates with the five pathogenic bacteria was detected by ELISA to preliminarily analyze the reasons for the different antibacterial effects of platelets on the five pathogenic bacteria. Results: Compared with the control group of MRSA, SA, and SE, the turbidity of the bacterial solution decreased after co-culture of platelets and platelet lysates with MRSA, SA, and SE for 12 h, and the OD value and colony count were significantly reduced (P<0.05). The turbidity of the bacterial solution did not change significantly after co-culture of platelets and platelet lysates with E. coli for 24 h, but the OD value decreased (P<0.05), and the colony count decreased to 10 CFU/mL but the difference was not statistically significant (P>0.05). Compared with the control group of CRKP, the turbidity, OD value, and colony count of the bacterial solution did not change significantly after co-culture of platelets and platelet lysates with CRKP (P>0.05). Proteomics results showed that after co-culture with MRSA, important proteins related to platelet activation, including collagen, fibrinogen, von Willebrand factor, integrin αIIbβ3, platelet glycoprotein V and IV were significantly up-regulated. ELISA results showed that after co-culture with the five pathogenic bacteria, platelets could secrete a large amount of DCD, with the content around 3 μg/mL. Conclusion: The antibacterial effect of platelets on Gram-positive bacteria MRSA, SA, and SE is better than that on Gram-negative bacteria E. coli and CRKP, and platelets have the best antibacterial effect on MRSA. The differences in antibacterial effects of platelets on the five pathogenic bacteria may be related to the sensitivity of DCD antibacterial peptides to the five pathogenic bacteria.

Objective To examine the toxicity and sublethal effects of calcium cyanamide against susceptible isolates of Aedes albopictus, so as to provide insights into rational use of calcium cyanamide for integrated management of Ae. albopictus. Methods The sublethal concentrations [30% lethal concentration (LC₃₀) and median lethal concentration (LC₅₀)] of calcium cyana mide against susceptible strains of Ae. albopictus were determined using the larval immersion test. With 100 mL of dechlorinated water as the control group, after the larvae of susceptible strains of Ae. albopictus were immersed in calcium cyanamide for 24 hours, the pupation rate, pupation duration, emergence rate, number of eggs laid, percentage of eggs hatched, and lifespan of Ae. albopictus were calculated and compared post-treatment with calcium cyanamide at different sublethal concentrations. The midgut tissues of larvae of susceptible strains of Ae. albopictus treated with 100 mg/L calcium cyanamide were sampled for pathological sectioning to observe midgut tissue damages. To evaluate the residual activity, 100 larvae of susceptible strains of Ae. albopictus were treated with 200 mg/L and 500 mg/L calcium cyanamide, and the mortality of larvae was calculated every 24 hour, with dead larvae replaced until no larval death. Results The regression equation for the toxicity of calcium cyanamide against larvae of susceptible strains of Ae. albopictus was y = -9.441 + 4.657x, with an LC₅₀ of 106.42 mg/L [95% confidence interval (CI): (94.64, 118.36) mg/L] and an LC₃₀ of 82.17 mg/L [95% CI: (94.64, 118.36) mg/L], respectively. After larvae of susceptible strains of Ae. albopictus were treated with sublethal concentrations (LC₃₀ and LC₅₀) of calcium cyanamide for 24 hours, there were reduced pupation and emergence rates of larvae (all P values < 0.000 1), prolonged pupal stage (both P values < 0.000 1), reduced numbers of eggs laid by survival female Ae. albopictus (both P values < 0.000 1), reduced percentages of eggs hatched by Ae. albopictus eggs (both P values < 0.000 1), and reduced median survival period of survival female Ae. albopictus (χ² = 9.36 and 20.33, both P values < 0.01) in the LC₃₀ and LC₅₀ groups relative to the control group. There was a numerical decline in the median survival period of survival female Ae. albopictus in the LC₃₀ groups relative to the control group (χ² = 2.42, P > 0.05), and there was a significant decline in the median survival period of survival female Ae. albopictus in the LC₅₀ group relative to the control group (χ² = 11.42, P < 0.01). Histopathological examinations showed severe damages to the midgut tissues of larvae of susceptible strains of Ae. albopictus, and residual activity assay revealed that the mortality of larvae of susceptible strains of Ae. albopictus was both 0 on day 32 post-treatment with calcium cyanamide at a concentration of 200 mg/L and on day 70 post-treatment with calcium cyanamide at a concentration of 500 mg/L, showing complete loss of the larvicidal activity of calcium cyanamide. Conclusions Calcium cyanamide is highly toxic against susceptible strains of Ae. albopictus, and calcium cyanamide at sublethal concentrations (LC₃₀ and LC₅₀) may inhibit growth, development, and reproductive capability of susceptible strains of Ae. albopictus, and shorten the lifespan of adult mosquitoes.

The receptors of Newcastle disease virus(NDV)are sialic acid receptors that mainly in-clude neu5ac-α-2,3gal-β-1,4Glc(SAα2,3Gal)and neu5ac-2-s-α-2,6Gal10Me(SAα2,6Gal).The distribution and abundance of the two receptors in host cells have important effects on virus sus-ceptibility and intracellular proliferation.In order to further explore the effects of sialic acid recep-tors on susceptibility and proliferation characteristics of NDV different strains,the expression lev-els of SAα2,3Gal and SAα2,6Gal receptors on BHK-21 cell membrane were adjusted by overex-pression and RNAi assays,and the TCID50 values were determined after different BHK-21 cells were inoculated with NDV strains Ⅰ and LaSota.The results suggested that NDV strain LaSota preferentially binds to SAα2,6Gal and strain Ⅰ selectively binds to SAα2,3Gal receptor.Further-more,the viral titers of NDV strains LaSota and Ⅰ in cell culture were positively correlated with the expression levels of SAα2,6Gal and SAα2,3Gal receptors on host cell membrane respectively.In conclusion,our studies provide an understanding of the relationship between infectivity of NDV different strains and receptor types of host cell,and provide a method to increase viral titer of NDV for cell-based vaccine production.