In recent years, with the development of corneal cross-linking technology, corneal cross-linking therapy combined with adopting riboflavin and ultraviolet has been widely used in several corneal disorders, not only for keratoconus, but also for other corneal diseases, including infectious keratitis,chemical corneal injury, bullous keratopathy, and refractive surgery. Corneal cross-linking is a non-invasive procedure with the virtue of minor damage, rapid rehabilitation, convenient operation, and high safety. This review aims to investigate the mechanism of corneal cross-linking therapy, emphasizing the new progress of its efficacy and safety in the application of treating non-expanding corneal diseases, including infectious keratitis, chemical burns, bullous keratopathy and marginal degeneration. Corneal cross-linking therapy may be potentially helpful in the treatment of non-expanding corneal diseases.

Schistosomiasis is prevalent in 78 countries and territories worldwide, while the eastern and western parts of sub-Sahara Africa bear the highest disease burden due to schistosomiasis. Recently, climate change, international trade and travel, urbanization and war have increased the risk of cross-boundary importation and transmission of schistosomiasis, and schistosomiasis has increasingly become a public health concern in non-endemic countries and territories. Biomphalaria straminea, the intermediate host of Schistosoma mansoni, has colonized in southern China and its habitats continue to move northward. In addition, cross-boundary imported cases of schistosomiasis have been reported occasionally in China. However, the real number of cases may be underestimated greatly due to insufficient diagnostic capacity and weak awareness of case reporting for overseas imported schistosomiasis in healthcare facilities. It is necessary to establish a multi-party collaborative mechanism, improve corresponding systems and technical specifications, reinforce surveillance and early warning, and border management, enhance technical reserves and capability building, and improve the awareness of schistosomiasis prevention and healthcare-seeking among entry-exit personnel, in order to effectively address the threat of cross-boundary imported schistosomiasis.

Objective To analyze the structural and phylogenetic characteristics of the mitochondrial genome from Bulinus globosus, so as to provide a theoretical basis for classification and identification of species within the Bulinus genus, and to provide insights into understanding of Bulinus-schistosomes interactions and the mechanisms of parasite transmission. Methods B. globosus samples were collected from the Ruya River basin in Zimbabwe. Mitochondrial DNA was extracted from B. globosus samples and the corresponding libraries were constructed for high-throughput sequencing on the Illumina NovaSeq 6000 platform. After raw sequencing data were subjected to quality control using the fastp software, genome assembly was performed using the A5-miseq and SPAdes tools, and genome annotation was conducted using the MITOS online server. Circular maps and sequence plots of the mitochondrial genome were generated using the CGView and OGDRAW software, and the protein conservation motifs and structures were analyzed using the TBtools software. Base composition and codon usage bias were analyzed and visualized using the software MEGA X and the ggplot2 package in the R software. In addition, a phylogenetic tree was created in the software MEGA X after sequence alignment with the software MAFFT 7, and visualized using the software iTOL. Results The mitochondrial genome of B. globosus was a 13 730 bp double-stranded circular molecule, containing 2 ribosomal RNA (rRNA) genes, 22 transfer RNA (tRNA) genes, and 13 protein-coding genes, with a marked AT preference. The mitochondrial genome composition of B. globosus was similar to that of other species within the Bulinus genus. Phylogenetic analysis revealed that the complete mitochondrial genome sequence of B. globosus was clustered with B. truncatus, B. nasutus, and B. ugandae into the same evolutionary clade, and gene superfamily analysis showed that the metabolism-related proteins of B. globosus were highly conserved, notably the cytochrome c oxidase family, which showed a significant consistency. Conclusions This is the first whole mitochondrial genome sequencing to decode the compositional features of the mitochondrial genome of B. globosus from Zimbabwe and its evolutionary relationship within the Bulinus genus, which provides important insights for further understanding of the phylogeny and mitochondrial genome characteristics of the Bulinus genus.

Objective: Adolescent depression is a highly prevalent and disabling mental disorder with unclear pathophysiology and unfavorable treatment outcomes. Recent efforts have been focusing on searching for biomarkers as specific indicators of adolescent depression. We performed a systematic literature review and meta-analysis, specifically including studies with healthy control groups as an inclusion criterion. This approach helps to avoid confounding factors and provides more accurate results regarding the inflammatory and immune biomarkers associated with adolescent depression. Methods: Three electronic databases were searched for studies comparing the means and changes in the biomarkers between depressed adolescent patients and healthy controls published in English until February 2024. Two authors independently performed the screening, quality assessment, and data extraction of the studies. A meta-analysis was conducted on outcomes reported by two or more studies using a random-effects model and presented Forrest plots and test statistics (I2) for heterogeneity analysis. Results: Nine studies were included in the review, including seven case-control studies and two cross-sectional studies. These studies included 24 target biomarkers, 13 of which were quantified in 2 or more studies. Compared to the healthy controls, the depressed adolescents had significantly higher values in ten indicators. Additionally, the depressed adolescents had lower procalcitonin levels than the healthy controls. The two groups showed no significant differences in the remaining 13 biomarkers. Conclusion Our findings offer fresh insights into the pathophysiology of inflammatory and immune aspects of adolescent depression and provide helpful guidance in developing targeted and effective intervention and prevention strategies to address adolescent depression.

Objective: Adolescent depression is a highly prevalent and disabling mental disorder with unclear pathophysiology and unfavorable treatment outcomes. Recent efforts have been focusing on searching for biomarkers as specific indicators of adolescent depression. We performed a systematic literature review and meta-analysis, specifically including studies with healthy control groups as an inclusion criterion. This approach helps to avoid confounding factors and provides more accurate results regarding the inflammatory and immune biomarkers associated with adolescent depression. Methods: Three electronic databases were searched for studies comparing the means and changes in the biomarkers between depressed adolescent patients and healthy controls published in English until February 2024. Two authors independently performed the screening, quality assessment, and data extraction of the studies. A meta-analysis was conducted on outcomes reported by two or more studies using a random-effects model and presented Forrest plots and test statistics (I2) for heterogeneity analysis. Results: Nine studies were included in the review, including seven case-control studies and two cross-sectional studies. These studies included 24 target biomarkers, 13 of which were quantified in 2 or more studies. Compared to the healthy controls, the depressed adolescents had significantly higher values in ten indicators. Additionally, the depressed adolescents had lower procalcitonin levels than the healthy controls. The two groups showed no significant differences in the remaining 13 biomarkers. Conclusion Our findings offer fresh insights into the pathophysiology of inflammatory and immune aspects of adolescent depression and provide helpful guidance in developing targeted and effective intervention and prevention strategies to address adolescent depression.

Objective: To investigate the abnormal fluctuation of coagulation function indicators in pediatric Burkitt lymphoma patients, and to analyze its correlation with disease progression and prognosis. Methods: The data of 172 children with Burkitt lymphoma in Children's Medical Center, Shanghai Jiao Tong University School of Medicine from January 2020 to December 2023 were retrospectively analyzed, and 120 healthy children were used as control group. Plasma prothrombin time (PT), activated partial thromboplastin time (APTT), thrombin time (TT), fibrinogen (Fib), International standardized ratio (INR), D-dimer (D-D), fibrinogen degradation products (FDP), and antithrombin (AT) were measured. Appropriate statistical methods were used to compare the data between two groups, and the Cox regression model was employed to analyze the influencing factors. A P-value <0.05 was considered statistically significant. Results: Levels of D-D, FDP, INR, and PT were significantly higher in children with Burkitt lymphoma than in the healthy controls [median (P25, P75) for the case group: 0.35 (0.13, 1.22), 3.10 (1.30, 10.20), 1.16 (1.06, 1.24), 12.60 (11.43, 13.50); median (P25, P75) for the healthy control group: 0.10 (0.07, 0.15), 0.60 (0.20, 1.08), 1.06 (1.02, 1.13), 11.50 (11.00, 12.30)](P<0.05). Levels of D-D, FDP, INR, PT, and TT were significantly elevated in children with recurrence compared to those without recurrence [median (P25, P75) for the recurrent group: 0.44 (0.16, 1.42), 3.85 (1.50, 12.25), 1.17 (1.08, 1.24), 12.70 (11.73, 13.50), 16.20 (14.80, 17.80); median (P25, P75) for the non-recurrent group: 0.21 (0.11, 0.69), 2.00 (1.00, 6.85), 1.11 (1.03, 1.24), 11.90 (11.10, 13.43), 15.20 (14.50, 16.40)](P<0.05). Levels of D-D, FDP in children with metastasis were significantly higher than those without metastasis [median (P25, P75) for the metastatic group: 0.51 (0.17, 1.84), 4.38 (1.70, 13.45); median (P25, P75) for the non-metastatic group: 0.20 (0.11, 0.39), 1.50 (1.00, 3.10)] (P<0.05). Levels of D-D and FDP were significantly higher in children with advanced stage than in those with early stage [median (P25, P75) for the high-stage group: 0.33 (0.14, 1.20), 3.10 (1.40, 10.23); median (P25, P75) for the low-stage group: 0.12 (0.08, 0.24), 0.90 (0.50, 2.50)] (P<0.05). Levels of D-D and FDP in high-risk children were significantly higher than those of low-risk [median (P25, P75) for the high-risk group: 0.28 (0.13, 1.01), 2.90 (1.15, 9.65); median (P25, P75) for the low-risk group: 0.12 (0.08, 0.17), 0.80 (0.43, 1.98)] (P<0.05). Levels of D-D, FDP, INR, and PT were significantly higher in children with poor prognosis than in those with favorable prognosis [median (P25, P75) for the poor prognosis group: 1.76 (0.80, 2.72), 13.45 (7.20, 25.30), 1.19 (1.12, 1.32), 12.85 (12.10, 14.35); median (P25, P75) for the favorable prognosis group: 0.23 (0.12, 0.52), 2.00 (1.00, 4.80), 1.14 (1.05, 1.23), 12.30 (11.40, 13.40)] (P<0.05). INR levels significantly increased with accumulating chemotherapy cycles [median (P25, P75) for one session: 1.09 (1.02, 1.20); two sessions: 1.31 (1.23, 1.38); three sessions: 1.79 (1.52, 2.41)] (P<0.05). Age, APTT, D-D, FDP, INR, PT, recurrence and metastasis had a significant effect on the survival of children with Burkitt lymphoma (P<0.05). Conclusion: Patients with Burkitt lymphoma exhibit coagulation disorders, which are influenced by recurrence, metastasis, clinical stage, risk stratification, and prognosis. In clinical practice, it is crucial to prioritize the monitoring of coagulation indicators to facilitate timely detection of coagulation dysfunction.

Objective: To explore the laboratory testing methods and clinical management strategies for immune hemolytic anemia induced by Ceftizoxime sodium drug-dependent antibodies. Methods: Patient blood samples were subjected to blood typing, direct antiglobulin test, and unexpected antibody identification. Ceftizoxime sodium drug-dependent antibodies were detected using the immune complex method and drug-sensitized red cell method. The properties and titers of the drug antibodies were further assessed. Flow cytometry was used to assess the complement activation capacity of the drug antibodies in vitro. Results: Direct antiglobulin tests (IgG and C3d) were positive. Ceftizoxime sodium drug-dependent antibodies were identified using both the immune complex method and the sensitized red cell method, their titers significantly increased following the addition of the drug. Flow cytometry confirmed the complement activation capability of these antibodies and identified 30 minutes as the optimal time for activation in vitro. The patient's condition improved rapidly after drug withdrawal and supportive transfusion, resulting in a favorable outcome. Conclusion: Ceftizoxime sodium can cause drug-induced immune hemolytic anemia via complement activation mediated by drug-dependent antibodies. Serological testing is essential for diagnosing drug-induced hemolytic anemia. Clinicians should be vigilant for this adverse reaction. The offending drug must be promptly discontinued, and supportive care should be initiated upon the onset of symptoms.

ObjectiveTo evaluate the antipyretic effect of the Qingwen Baiduling prescription in a dry yeast-induced rat fever model and to investigate its antipyretic mechanism， providing a theoretical basis for its clinical application. MethodsSPF-grade male SD rats were randomly assigned to six groups （n=6 per group）： control， model， aspirin （20 mg·kg^-1）， and high-， medium-， and low-dose Qingwen Baiduling prescription groups （14.40， 7.20， 3.60 g·kg^-1）. The fever model was established by subcutaneous injection of dry yeast suspension on the back. After model induction， body temperature was recorded every 1 hour. Drugs were administered at 6 hours after modeling， and body temperature was continuously recorded hourly for 12 hours. Record the body temperature of rats to observe the trend of changes in body temperature. Serum interleukin-6 （IL-6）， interleukin-1β （IL-1β）， and tumor necrosis factor-α （TNF-α） levels， as well as hypothalamic prostaglandin E₂ （PGE₂） and cyclic adenosine monophosphate （cAMP）， were measured using enzyme-linked immunosorbent assay （ELISA）. Hypothalamic tissue morphology was examined by hematoxylin and eosin （HE） staining. Western blot was used to detect hypothalamic expression of Toll-like receptor 4 （TLR4）， myeloid differentiation factor 88 （MyD88）， nuclear factor-κB p65 （NF-κB p65）， inhibitor κBα （IκBα）， phosphorylated IκBα （p-IκBα）， IκB kinase α （IKKα）， IKKβ， phosphorylated IKKα/β （p-IKKα/β）， and cyclooxygenase-2 （COX2）. ResultsCompared with the control group， the model group showed a significant increase in body temperature 6 hours after modeling （P0.01）， confirming successful fever induction. Serum IL-6， IL-1β， TNF-α， and hypothalamic cAMP and PGE₂ levels were significantly elevated （P0.01）. Hypothalamic neurons exhibited irregular morphology and disordered distribution， accompanied by inflammatory cell infiltration and microglial aggregation. Expression levels of TLR4/NF-κB pathway-related proteins and phosphorylated proteins were significantly increased （P0.05， P0.01）. Compared with the model group， 2-3 hours after administration， all Qingwen Baiduling prescription dose groups significantly reduced body temperature （P0.01）. All dose groups significantly decreased serum IL-6， IL-1β， TNF-α， and hypothalamic cAMP and PGE₂ levels （P0.05， P0.01）. Neuronal morphology was markedly improved in the high- and medium-dose groups， with narrowed intercellular spaces and reduced inflammatory infiltration. The prescription effectively inhibited hypothalamic expression of TLR4， MyD88， NF-κB p65， p-IκBα， p-IKKα/β， and COX2 proteins （P0.05， P0.01）. ConclusionQingwen Baiduling prescription effectively reduces body temperature in rats by mitigating the further effects of inflammatory cytokines on the hypothalamic thermoregulatory center through the blood-brain barrier. Its antipyretic mechanism may be related to inhibition of NF-κB pathway activation.