Tropical diseases, the transmission of which is affected by multiple natural and social factors, pose a great challenge to global public health, notably in African countries. During the past several decades, China and African countries have continuously collaborated for the control of neglected tropical diseases and malaria, which has become an important part of global South-to-South cooperation and global health governance. This article reviews the history of China-Africa cooperation for tropical diseases control, summarizes the experiences and achievements over the past decade, analyzes the current challenges in the coopera tion, and proposes future recommendations. The China-Africa cooperation has achieved significant progress in the control of tropical diseases, such as malaria, schistosomiasis, and filariasis, and established a China-Africa cooperation network for tropical diseases control. Through the "Three-Step" strategy of China-Africa cooperation, the effectiveness of China's integrated control strategies has been validated in Africa, and the application of China's tropical disease control technologies has been promoted in African disease-epidemic countries. Currently, China-Africa collaboration, however, still experiences multiple realistic challenges, such as insufficient resources, difficulty in technology transfer, and weak primary healthcare systems. In the future, both sides are recommended to further strengthen policy coordination, deepen technological cooperation, innovate cooperation models, aiming to continuously promote the high-quality development of China-Africa cooperation for tropical diseases control.

ObjectiveMultiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the central nervous system (CNS); however, its underlying neurological pathogenic mechanisms remain incompletely understood. Endogenous formaldehyde (FA), a metabolic byproduct of methylation-demethylation cycles, has recently been implicated in neurotoxicity, oxidative damage, and cognitive impairment. This study aimed to investigate whether excessive FA contributes to myelin sheath demyelination in mice and to evaluate the protective effects and mechanisms of two FA-elimination strategies: sodium bisulfite (NaHSO₃), a classical FA scavenger, and polyethylene glycol-modified astaxanthin nanoparticles (PEG-ATX@NPs), a brain-targeted nano-antioxidant formulation. MethodsA chronic demyelination model was established by feeding female C57BL/6J mice a diet containing 0.2% cuprizone (CPZ) for four weeks, followed by a two-week intervention period. Eighty mice were randomly assigned to four groups: NS (normal saline), CPZ+NS, CPZ+NaHSO₃, and CPZ+PEG-ATX@NPs. Behavioral tests, including open-field, Y-maze, and pole-climbing assays, were conducted to assess locomotor activity, motor coordination, and working memory. FA levels in serum, corpus callosum, and spinal cord were measured using an Na-FA fluorescent probe and quantified via in vivo and ex vivo fluorescence imaging. Neuroinflammatory responses were evaluated by measuring TNF-α, IL-1β, and IL-6 levels using ELISA, while oxidative stress was assessed by reactive oxygen species (ROS) fluorescence intensity. Demyelination was examined via Luxol fast blue staining, and microglial activation was analyzed by Iba1 immunofluorescence. Correlation analyses were performed to explore relationships among FA levels, inflammatory cytokines, ROS intensity, and behavioral parameters. ResultsCompared with the NS group, mice in the CPZ+NS group exhibited significant weight loss, impaired motor coordination and memory, and markedly reduced myelin regeneration (P<0.05). FA levels and pro-inflammatory cytokines were significantly elevated in serum, corpus callosum, and spinal cord (P<0.05). FA-associated fluorescence in brain and spinal tissues, as well as ROS intensity across all tissues examined, also increased substantially (P<0.05). CPZ treatment induced pronounced microglial activation and severe demyelination in the corpus callosum (P<0.01). Both NaHSO₃ and PEG-ATX@NPs effectively reduced FA accumulation in the brain and spinal cord, attenuated demyelination, suppressed microglial activation, decreased inflammatory cytokine levels, and improved motor and cognitive performance. These results confirm that CPZ induced severe demyelination accompanied by oxidative stress, neuroinflammation, and abnormal FA accumulation. Following intervention with either NaHSO₃ or PEG-ATX@NPs, endogenous FA levels in the CNS were substantially reduced. Both treatments alleviated demyelination and significantly decreased the number of activated microglia. Levels of TNF-α, IL-1β, and IL-6 in serum, corpus callosum, and spinal cord were downregulated. Behavioral performance improved significantly, as evidenced by enhanced locomotor activity, better coordination, and improved memory function. These findings indicate that both FA-scavenging agents mitigate CPZ-induced biochemical and behavioral abnormalities. ConclusionThis study demonstrates that excessive endogenous FA is closely associated with cognitive impairment, inflammatory dysregulation, and demyelination in a CPZ-induced chronic demyelination mouse model. Clearing abnormally elevated FA effectively reduces neuroinflammation, suppresses microglial overactivation, decreases oxidative stress, and alleviates demyelination, ultimately improving motor and cognitive outcomes in mice. These results suggest that targeting endogenous FA represents a promising therapeutic strategy for MS and other demyelinating disorders. Further investigations are warranted to explore the long-term safety, dosage optimization, and molecular pathways involved in FA-mediated neurotoxicity.

ObjectiveMultiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the central nervous system (CNS); however, its underlying neurological pathogenic mechanisms remain incompletely understood. Endogenous formaldehyde (FA), a metabolic byproduct of methylation-demethylation cycles, has recently been implicated in neurotoxicity, oxidative damage, and cognitive impairment. This study aimed to investigate whether excessive FA contributes to myelin sheath demyelination in mice and to evaluate the protective effects and mechanisms of two FA-elimination strategies: sodium bisulfite (NaHSO₃), a classical FA scavenger, and polyethylene glycol-modified astaxanthin nanoparticles (PEG-ATX@NPs), a brain-targeted nano-antioxidant formulation. MethodsA chronic demyelination model was established by feeding female C57BL/6J mice a diet containing 0.2% cuprizone (CPZ) for four weeks, followed by a two-week intervention period. Eighty mice were randomly assigned to four groups: NS (normal saline), CPZ+NS, CPZ+NaHSO₃, and CPZ+PEG-ATX@NPs. Behavioral tests, including open-field, Y-maze, and pole-climbing assays, were conducted to assess locomotor activity, motor coordination, and working memory. FA levels in serum, corpus callosum, and spinal cord were measured using an Na-FA fluorescent probe and quantified via in vivo and ex vivo fluorescence imaging. Neuroinflammatory responses were evaluated by measuring TNF-α, IL-1β, and IL-6 levels using ELISA, while oxidative stress was assessed by reactive oxygen species (ROS) fluorescence intensity. Demyelination was examined via Luxol fast blue staining, and microglial activation was analyzed by Iba1 immunofluorescence. Correlation analyses were performed to explore relationships among FA levels, inflammatory cytokines, ROS intensity, and behavioral parameters. ResultsCompared with the NS group, mice in the CPZ+NS group exhibited significant weight loss, impaired motor coordination and memory, and markedly reduced myelin regeneration (P<0.05). FA levels and pro-inflammatory cytokines were significantly elevated in serum, corpus callosum, and spinal cord (P<0.05). FA-associated fluorescence in brain and spinal tissues, as well as ROS intensity across all tissues examined, also increased substantially (P<0.05). CPZ treatment induced pronounced microglial activation and severe demyelination in the corpus callosum (P<0.01). Both NaHSO₃ and PEG-ATX@NPs effectively reduced FA accumulation in the brain and spinal cord, attenuated demyelination, suppressed microglial activation, decreased inflammatory cytokine levels, and improved motor and cognitive performance. These results confirm that CPZ induced severe demyelination accompanied by oxidative stress, neuroinflammation, and abnormal FA accumulation. Following intervention with either NaHSO₃ or PEG-ATX@NPs, endogenous FA levels in the CNS were substantially reduced. Both treatments alleviated demyelination and significantly decreased the number of activated microglia. Levels of TNF-α, IL-1β, and IL-6 in serum, corpus callosum, and spinal cord were downregulated. Behavioral performance improved significantly, as evidenced by enhanced locomotor activity, better coordination, and improved memory function. These findings indicate that both FA-scavenging agents mitigate CPZ-induced biochemical and behavioral abnormalities. ConclusionThis study demonstrates that excessive endogenous FA is closely associated with cognitive impairment, inflammatory dysregulation, and demyelination in a CPZ-induced chronic demyelination mouse model. Clearing abnormally elevated FA effectively reduces neuroinflammation, suppresses microglial overactivation, decreases oxidative stress, and alleviates demyelination, ultimately improving motor and cognitive outcomes in mice. These results suggest that targeting endogenous FA represents a promising therapeutic strategy for MS and other demyelinating disorders. Further investigations are warranted to explore the long-term safety, dosage optimization, and molecular pathways involved in FA-mediated neurotoxicity.

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.

Recently, there has been an increasing risk of importation of tropical diseases into China and the resultant re-transmission in the country with the in-depth implementation of the “Belt and Road” Initiative, which poses a serious threat to the national public health security. To effectively respond to the cross-border transmission risk of tropical diseases and facilitate the process towards tropical disease control and elimination in China and the countries along the “Belt and Road” Initiative, this article analyzes the current status and governance risks of major imported tropical diseases, cross-border joint prevention and control polices implemented for tropical diseases and challenges in the establishment of the joint prevention and control system for tropical diseases in China, and discusses the establishment and implementation path of the joint prevention and control system for tropical diseases in countries along the “Belt and Road” Initiative. This path covers the establishment of cross-border cooperation mechanisms, research and development and pilot production of Chinese public health products, and implementation of key cross-border tropical disease prevention and control projects. The establishment of this system will further improve Chinese prevention and control capabilities for key cross-border tropical diseases, build a demonstrative prevention and control model for tropical diseases, and promote international technical exchanges and cooperation of tropical diseases.

Blue light inactivation technology, particularly at the 405 nm wavelength, has demonstrated distinct and multifaceted mechanisms of action against both Gram-positive and Gram-negative bacteria, offering a promising alternative to conventional antibiotic therapies. For Gram-positive pathogens such as Bacillus cereus, Listeria monocytogenes, and methicillin-resistant Staphylococcus aureus (MRSA), the bactericidal effects are primarily mediated by endogenous porphyrins (e.g., protoporphyrin III, coproporphyrin III, and uroporphyrin III), which exhibit strong absorption peaks between 400-430 nm. Upon irradiation, these porphyrins are photoexcited to generate cytotoxic reactive oxygen species (ROS), including singlet oxygen, hydroxyl radicals, and superoxide anions, which collectively induce oxidative damage to cellular components. Early studies by Endarko et al. revealed that (405±5) nm blue light at 185 J/cm² effectively inactivated L. monocytogenes without exogenous photosensitizers, supporting the hypothesis of intrinsic photosensitizer involvement. Subsequent work by Masson-Meyers et al. demonstrated that 405 nm light at 121 J/cm² suppressed MRSA growth by activating endogenous porphyrins, leading to ROS accumulation. Kim et al. further elucidated that ROS generated under 405 nm irradiation directly interact with unsaturated fatty acids in bacterial membranes, initiating lipid peroxidation. This process disrupts membrane fluidity, compromises structural integrity, and impairs membrane-bound proteins, ultimately causing cell death. In contrast, Gram-negative bacteria such as Salmonella, Escherichia coli, Helicobacter pylori, Pseudomonas aeruginosa, and Acinetobacter baumannii exhibit more complex inactivation pathways. While endogenous porphyrins remain central to ROS generation, studies reveal additional photodynamic contributors, including flavins (e.g., riboflavin) and bacterial pigments. For instance, H. pylori naturally accumulates protoporphyrin and coproporphyrin mixtures, enabling efficient 405 nm light-mediated inactivation without antibiotic resistance concerns. Kim et al. demonstrated that 405 nm light at 288 J/cm² inactivates Salmonella by inducing genomic DNA oxidation (e.g., 8-hydroxy-deoxyguanosine formation) and disrupting membrane functions, particularly efflux pumps and glucose uptake systems. Huang et al. highlighted the enhanced efficacy of pulsed 405 nm light over continuous irradiation for E. coli, attributing this to increased membrane damage and optimized ROS generation through frequency-dependent photodynamic effects. Environmental factors such as temperature, pH, and osmotic stress further modulate susceptibility, sublethal stress conditions (e.g., high salinity or acidic environments) weaken bacterial membranes, rendering cells more vulnerable to subsequent ROS-mediated damage. The 405 nm blue light inactivates drug-resistant Pseudomonas aeruginosa through endogenous porphyrins, pyocyanin, and pyoverdine, with the inactivation efficacy influenced by bacterial growth phase and culture medium composition. Intriguingly, repeated 405 nm exposure (20 cycles) failed to induce resistance in A. baumannii, with transient tolerance linked to transient overexpression of antioxidant enzymes (e.g., superoxide dismutase) or stress-response genes (e.g., oxyR). For Gram-positive bacteria, porphyrin abundance dictates sensitivity, whereas in Gram-negative species, membrane architecture and accessory pigments modulate outcomes. Critically, ROS-mediated damage is nonspecific, targeting DNA, proteins, and lipids simultaneously, thereby minimizing resistance evolution. The 405 nm blue light technology, as a non-chemical sterilization method, shows promise in medical and food industries. It enhances infection control through photodynamic therapy and disinfection, synergizing with red light for anti-inflammatory treatments (e.g., acne). In food processing, it effectively inactivates pathogens (e.g., E. coli, S. aureus) without altering food quality. Despite efficacy against multidrug-resistant A. baumannii, challenges include device standardization, limited penetration in complex materials, and optimization of photosensitizers/light parameters. Interdisciplinary research is needed to address these limitations and scale applications in healthcare, food safety, and environmental decontamination.

Purpose To investigate the expression of POLR2M in colorectal cancer(CRC)and its effects on cell growth,apoptosis and invasion.Methods GEPIA2.0,TCGA and Kaplan-Meier Plotter databases were used to ana-lyze the differential expression of POLR2M in CRC tissues and normal adjacent tissues,and to evaluate its prognostic significance using the Log-rank test.Quantitative real-time PCR(qRT-PCR)was used to detect the expression of POLR2M in human colorectal cancer cell lines SW480,HCT-8,RKO,LOVO,DLD-1,HCT-116,SW620 and human normal colorectal cell line FHC.DLD-1 and RKO cells were stably transfected with lentivirus,and the POLR2M groups were up-regulated into the control group(LV-NC)and experimental group(LV-POLR2M),and the transient transfec-tion of SW620 and SW480 cells with interfering fragments of SiRNA was used to down-regulate the POLR2M groups into the control group(Si-NC)and experimental group(Si-POLR2M),and the transfection efficiency of each group was verified.CCK-8,plate cloning,Transwell and scratch healing assays were used to detect cell proliferation,invasion and migration.Flow cytometry was used to detect the effects of POLR2M on cell cycle and apoptosis.Results GE-PIA2.0,TCGA and Kaplan-Meier Plotter database analysis showed that the expression of POLR2M in colorectal cancer was significantly higher than in normal adjacent tissues(P＜0.05),and the expression of POLR2M was closely associ-ated with the histological type of colorectal cancer and lymph node metastasis(P＜0.05),but not with the age,gen-der,tumor grade and vascular invasion of patients(P＞0.05).The prognosis of patients with POLR2M overexpression was poor(P＜0.05).The results of qRT-PCR showed that compared with FHC cells,the mRNA expression of POLR2M in SW480,HCT-8,RKO,LOVO,DLD-1,HCT-116 and SW620 cell lines was increased(F=97.7,P＜0.05),and POLR2M stable overexpression and interference cell lines were successfully constructed.Compared with the LV-NC group,the viability,colony number,number of cells passing through the chamber and cell mobility of DLD-1 and RKO cells in the LV-POLR2M group were significantly increased(P＜0.05).Compared with the Si-NC group,the viability,colony number,number of cells passing through the chamber,and cell mobility of SW620 and SW480 cells in the Si-POLR2M group were significantly decreased(P＜0.05).Downregulation of POLR2M induced cell cycle arrest in G1 phase and promotes apoptosis(P＜0.05).Conclusion POLR2M may play a role as a pro-tumor gene in CRC,and its high expression can significantly promote the proliferation and invasion of CRC cells.

Objective To explore the mechanism by which the sanguis draconis flavones(SDF)regulates the reactive oxygen species(ROS)/thioredoxin-interacting protein(TXNIP)pathway to mediate cell pyroptosis and improve cerebral ischemia-reperfusion injury(CIRI)in rats.Methods The experimental rats were randomly divided into the control group(Ctrl),the CIRI group,the low-dose SDF group(SDF-L),the high-dose SDF group(SDF-H),and the SDF-H+ROS/TXNIP pathway activator,trimethylamine oxide(TMAO)group(SDF-H+TMAO).Among them,except for the control group,the remaining rats all needed to establish the CIRI rat model by the modified suture method.Zea Longa scoring was performed on rats from each group.ELISA was used to detect the levels of serum inflammatory factors interleukin(IL)-1β,IL-18 and oxidative stress-related factors superoxide dismutase(SOD),malondialdehyde(MDA),glutathione peroxidase(GSH-Px).Flow cytometry was used to measure the ROS levels.Cerebral edema was detected.Cerebral infarction was detected by 2,3,5-triphenyl tetrazolium chloride(TTC)staining.HE staining was used to detect the pathological changes of brain tissue.Immunohistochemistry was used to detect the expression of pyrolytic effector protein dermolin D(GSDMD).Western blotting was used to detect the expression of proteins related to the ROS/TXNIP pathway.Results Compared with the control group,a large area of cerebral infarctions were observed in the brain tissue of the CIRI group,accompanied by mild hemorrhage and obvious infiltration of inflammatory cells.Neuronal cells underwent degeneration and necrosis,with sparse and disordered arrangement.The phenomena of nuclear condensation and nucleolus lysis were obvious.The Zea Longa score,cerebral infarction volume,brain tissue water content,levels of IL-1β,IL-18,ROS,MDA,and the expressions of GSDMD,TXNIP,nucleotide-binding oligomerization domain-like receptor protein 3(NLRP3),apoptosis-related punctate protein(ASC),and Caspase-1 increased,while the activities of SOD and GSH-Px decreased(P＜0.05).Compared with the CIRI group,the pathological damage of brain tissues in the SDF-L group and the SDF-H group was significantly improved.The Zea Longa score,cerebral infarction volume,brain tissue water content,levels of IL-1β,IL-18,ROS,MDA,and the expressions of GSDMD,TXNIP,NLRP3,ASC,and Caspase-1 decreased.The activities of SOD and GSH-Px increased(P＜0.05);TMAO treatment partially reversed the improvement effect of SDF on CIRI in rats.Conclusion SDF ameliorates cerebral CIRI in rats by inhibiting ROS/TXNIP pathway-mediated pyroptosis.

Owing to their high genetic and physiological similarities to humans,non-human primates(NHPs)have become pivotal animal models in life sciences research and biomedical development.NHP laboratory animals are not only an ideal platform for exploring the mechanisms of neurological diseases and infectious diseases,but they are also widely used in preclinical safety evaluations of macromolecular drugs,which are considered the"gold standard".Nevertheless,this biological similarity increases the risk of zoonotic disease transmission to personnel working with NHP laboratory animals,their tissues,and body fluids.In light of recent domestic and international outbreaks of zoonotic diseases as well as the implementation of the Biosafety Law,this study examines the occupational risk factors encountered by personnel working with NHPs.This includes biological,chemical,and physical factors.This paper also covers common zoonoses,classification of the corresponding pathogens,transmission routes,risk severity levels,and protocols for post-exposure management.A multidimensional prevention and control framework is proposed,which includes the following components.(1)Risk Assessment and Emergency Response:Regularly identify hazards through an Occupational Health and Safety Committee(OHSC)and develop post-exposure emergency protocols.(2)Optimization of Management Systems:Improve facility design,optimize the allocation of personal protective equipment,and enhance health surveillance and vaccination programs.(3)Technical Training and Standardized Operations:Provide specialized training in NHP laboratory animal ethology and biosafety practices.Additionally,implement intelligent monitoring technologies to reduce the occurrence of aggressive incidents.This paper outlines measures designed to enhance health and safety awareness among personnel working with NHP laboratory animals.It emphasizes the need for strengthened guidance on the use of personal protective equipment(PPE)and the standardization of professional operational practices.The goal is to safeguard personnel health and safety,reduce occupational exposure rates,and effectively prevent occupational diseases related to laboratory animals.

Purpose To investigate the expression of POLR2M in colorectal cancer(CRC)and its effects on cell growth,apoptosis and invasion.Methods GEPIA2.0,TCGA and Kaplan-Meier Plotter databases were used to ana-lyze the differential expression of POLR2M in CRC tissues and normal adjacent tissues,and to evaluate its prognostic significance using the Log-rank test.Quantitative real-time PCR(qRT-PCR)was used to detect the expression of POLR2M in human colorectal cancer cell lines SW480,HCT-8,RKO,LOVO,DLD-1,HCT-116,SW620 and human normal colorectal cell line FHC.DLD-1 and RKO cells were stably transfected with lentivirus,and the POLR2M groups were up-regulated into the control group(LV-NC)and experimental group(LV-POLR2M),and the transient transfec-tion of SW620 and SW480 cells with interfering fragments of SiRNA was used to down-regulate the POLR2M groups into the control group(Si-NC)and experimental group(Si-POLR2M),and the transfection efficiency of each group was verified.CCK-8,plate cloning,Transwell and scratch healing assays were used to detect cell proliferation,invasion and migration.Flow cytometry was used to detect the effects of POLR2M on cell cycle and apoptosis.Results GE-PIA2.0,TCGA and Kaplan-Meier Plotter database analysis showed that the expression of POLR2M in colorectal cancer was significantly higher than in normal adjacent tissues(P＜0.05),and the expression of POLR2M was closely associ-ated with the histological type of colorectal cancer and lymph node metastasis(P＜0.05),but not with the age,gen-der,tumor grade and vascular invasion of patients(P＞0.05).The prognosis of patients with POLR2M overexpression was poor(P＜0.05).The results of qRT-PCR showed that compared with FHC cells,the mRNA expression of POLR2M in SW480,HCT-8,RKO,LOVO,DLD-1,HCT-116 and SW620 cell lines was increased(F=97.7,P＜0.05),and POLR2M stable overexpression and interference cell lines were successfully constructed.Compared with the LV-NC group,the viability,colony number,number of cells passing through the chamber and cell mobility of DLD-1 and RKO cells in the LV-POLR2M group were significantly increased(P＜0.05).Compared with the Si-NC group,the viability,colony number,number of cells passing through the chamber,and cell mobility of SW620 and SW480 cells in the Si-POLR2M group were significantly decreased(P＜0.05).Downregulation of POLR2M induced cell cycle arrest in G1 phase and promotes apoptosis(P＜0.05).Conclusion POLR2M may play a role as a pro-tumor gene in CRC,and its high expression can significantly promote the proliferation and invasion of CRC cells.