ObjectiveTo explore the effect of Bushen Zhuyun Formula（补肾助孕方， BZF） on macrophage pola-rization in mouse uterine tissue with embryo implantation failure based on the janus kinase 2 （JAK2）/ signal transducer and activator of transcription 3 （STAT3） signaling pathway. MethodsFifty female and 25 male C57BL/6 mice were randomly divided into five groups including blank group， model group， low- and high-dose BZF groups， and dydrogesterone group， with 10 female and 5 male mice in each group. Except for the blank group， female mice in the estrous phase were subjected to superovulation induction. At 18：00 on the same day， female mice were co-housed with male mice at a ratio of 2∶1. The presence of sperm in vaginal exfoliated cells was examined on the following day， which was designated as gestational day 1 （GD1）. On GD4， an oil-based mifepristone solution was subcutaneously injected into the neck region of female mice to establish an embryo implantation dysfunction model. Beginning on GD1， mice in the low- and high-dose BZF groups were given 11.18 and 22.36 g/kg of the BZF solution by gavage， respectively. The dydrogesterone group was given 2.6 mg/kg of dydrogesterone solution by gavage. The blank group and the model group were given 10 g/kg of normal saline by gavage once daily. Interventions were administered once a day until GD4. On GD5， uterine tissues were collected， and HE staining was performed to evaluate endometrial morphology， endometrial thickness， and glandular number in female mice. The proportions of M1 and M2 macrophages in uterine tissues were detected by flow cytometry， and the levels of transforming growth factor-β1 （TGF-β1） and interleukin-10 （IL-10） in uterine tissue were measured by ELISA. The protein expression levels of Janus kinase 2 （JAK2）， phosphorylated JAK2 （p-JAK2）， signal transducer and activator of transcription 3 （STAT3）， and phosphorylated STAT3 （p-STAT3） in uterine tissue were detected by western blotting， and the mRNA expressions of JAK2， STAT3， IL-10， and TGF-β1 in uterine tissue was detected by real-time quantitative PCR. ResultsCompared to the blank group， the model group exhibited smaller and straighter endometrial glands， denser stroma， and fewer blood vessels， with reduced endometrial thickness and decreased glandular numbers. The proportion of M1 macrophages in uterine tissue increased， while the proportion of M2 macrophages and the levels of IL-10 and TGF-β1 decreased. The protein expression levels of JAK2， p-JAK2， STAT3， and p-STAT3， as well as the p-JAK2/JAK2 and p-STAT3/STAT3 ratios， were reduced. The mRNA expressions of JAK2， STAT3， IL-10， and TGF-β1 also decreased （P＜0.05）. Compared to the model group， the above indicators were improved in the low- and high-dose BZF groups， while some indicators were improved in the dydrogesterone group （P＜0.05）. Compared to the dydrogesterone group and the low-dose BZF group， the high-dose BZF group showed superior effects in improving endometrial morphology， endometrial thickness， glandular number， the proportion of M1 macrophages in uterine tissues， TGF-β1 levels， JAK2， p-JAK2， and p-STAT3 protein expression levels， the p-STAT3/STAT3 and p-JAK2/JAK2 ratios， as well as JAK2， IL-10， and TGF-β1 mRNA expressions （P＜0.05）. ConclusionBZF can improve the morphology of the endometrium during implantation in mice with embryo implantation failure， which may be related to specific regulation of the JAK2/STAT3 signaling pathway， modulation of macrophage polarization， and promotion of anti-inflammatory cytokine expression.

Objective: To assess the status of sexual behaviors, HIV/AIDS knowledge awareness, and novel synthetic drug use among school attending young students in Guangdong Province, so as to provide evidence base for formulating targeted intervention strategies. Methods: From September to December 2024, a convenience sampling method was employed to conduct an anonymous online survey among 41 119 students from 20 higher education institutions and vocational colleges in Guangdong Province. Chi square test was utilized for rate comparisons and univariate analysis, and a multivariate Logistic regression model was applied to analyze factors associated with novel synthetic drug use. Results: The self reported rate of sexual behavior was 5.2%. Among sexually active students, the rates of unprotected sexual intercourse, having temporary sexual partners, and having commercial sexual partners were 32.4%, 34.5%, and 26.3%, respectively. The awareness rate of HIV related knowledge was 75.7%. The overall use rate of novel psychoactive substances(NPS) was 1.0%, and among sexually active students it was 6.5%. Multivariate Logistic regression analysis showed that students with sexual experience ( OR =4.15) and those with HIV testing history ( OR =9.38) had higher risks of NPS use; among sexually active students, those with unprotected sexual intercourse ( OR =6.83) and those with commercial sexual partners ( OR = 4.68 ) had higher risks of NPS use (all P <0.05). Conclusions The HIV/AIDS knowledge level among surveyed students needs further improvement, and high risk sexual behaviors are cross linked with novel synthetic drug use. It is recommended to carry out integrated health education for all students and implement comprehensive targeted interventions for sexually active students.

OBJECTIVE To optimize the extraction process of polysaccharides from Abelmoschus manihot flowers， and to investigate the antioxidant， moisturizing and hygroscopicity activities of the polysaccharides.METHODS The optimal ratio of composite enzymes was determined by orthogonal experiments， and the extraction process of polysaccharides was optimized by single-factor experiments and Box-Behnken response surface methodology， and validated. The scavenging rates of 2，2′-azino-bis （3-ethylbenzothiazoline-6-sulfonic acid） （ABTS） free radicals， hydroxyl free radicals， and superoxide anion free radicals， as well as the total reducing ability of the polysaccharides were investigated by the ABTS method， Fenton-salicylic acid colorimetric method， pyrogallol autoxidation method， and potassium ferricyanide reduction method， respectively. The moisturizing and hygroscopicity activities of the polysaccharides were evaluated by the weighing method.RESULTS The optimal ratio of composite enzymes was 136 000 U of papain， 125 000 U of pectinase，and 5 000 U of cellulase. The optimal extraction process was as follows： enzymatic hydrolysis time of 2.8 h， enzymatic hydrolysis temperature of 57.50 ℃， pH of the sodium dihydrogen phosphate-disodium hydrogen phosphate buffer was 5.5， and solid-to-liquid ratio of 1∶40. The results of three experiments showed that the average polysaccharides extraction rate of 23.595%， with an RSD of 0.90%. The scavenging rates of ABTS free radicals， hydroxyl free radicals， superoxide anion free radicals， and total reducing ability were 81.759%， 87.110%， 54.244%， and 1.129 （the mass concentrations of polysaccharides were 10、 5、 10， and 10 mg/mL， respectively）， respectively. At relative humidity of 43% for 12 h， the moisturizing rate and hygroscopicity rate of polysaccharides were 99.387% and 100.478%， respectively； at relative humidity of 83% for 12 h， they were 99.764% and 100.455%， respectively.CONCLUSIONS The optimal extraction process of polysaccharides from A.manihot flowers based on the composite enzymes is stable and feasible； the polysaccharides obtained under this process have good antioxidant， moisturizing， and hygroscopicity activities.

ObjectiveTo investigate whether the inhibitory effect of Panax quinquefolium saponins （PQS） on non-small cell lung cancer （NSCLC） is enhanced under graphene-mediated far-infrared therapy （GFIR）， and to analyze its relationships with mitochondrial dysfunction， mitochondrial DNA （mtDNA） leakage， and the activation of cyclic GMP-AMP synthase （cGAS）/stimulator of interferon genes （STING） signaling pathways. MethodsIn the cell experiments， the cell-counting kit 8 （CCK-8） was employed to assess the inhibitory effects of PQS alone or in combination with GFIR （PQS+GFIR） on A549 cell viability. The scratch assay and the colony formation assay were adopted to evaluate cell migration and colony formation capabilities， respectively. Flow cytometry was employed to assess apoptosis， mitochondrial membrane potential， and reactive oxygen species （ROS） levels. Immunofluorescence （IF） assay was performed to assess mitochondrial localization. Real-time polymerase China reaction（PCR） was used to detect mitochondrial DNA （mtDNA） leakage. A STING knockdown cell model was established by transfecting cells with small interfering RNA （siRNA）， and the knockdown efficiency was assessed by Real-time PCR and Western blot. The cell viability and apoptosis following gene knockdown were assessed through the CCK-8 assay and flow cytometry. In the animal experiments， an allogeneic xenograft mouse model was established with Lewis lung cancer cells. Mice were randomized into a control group， a model group， a cisplatin group， a low-dose PQS （PQS-Low， 90 mg·kg^-1） group， a high-dose PQS （PQS-High， 180 mg·kg^-1） group， a low-dose PQS combined with GFIR （PQS-Low+GFIR， 90 mg·kg^-1） group， and a high-dose PQS combined with GFIR （PQS-High+GFIR， 180 mg·kg^-1） group. Treatment lasted for 14 days， and the fluorescence intensity was monitored at the tumor site by small-animal in vivo imaging during the treatment period. Flow cytometry was utilized to determine the proportions of T-lymphocyte subsets， B-lymphocyte levels， and peripheral blood NK cell levels in the spleens of mice. Immunohistochemical （IHC） staining was performed to assess the infiltration of CD3⁺， CD4⁺， and CD8⁺ T-lymphocytes in the tumor tissue. Enzyme-linked immunosorbent assay （ELISA） was conducted to measure the levels of interferon-α （IFN-α）， interferon-β （IFN-β）， tumor necrosis factor-α （TNF-α）， and interleukin-6 （IL-6） in mouse tumors. The mRNA levels of cGAS， STING， TANK-binding kinase 1 （TBK1）， interferon regulatory factor 3 （IRF3）， interferon beta 1 （IFNB1）， and nuclear factor κB p65 （NF-κB p65） were determined by Real-time PCR. The protein levels of cGAS， STING， p-STING， TBK1， p-TBK1， IRF3， p-IRF3， NF-κB p65， and p-NF-κB p65 were quantified via Western blot. ResultsThe cell experiment results showed that compared with the control group， PQS inhibited the viability and migration of A549 cells， promoted apoptosis， affected mitochondrial localization， reduced mitochondrial membrane potential， increased the ROS level， and promoted mtDNA leakage. Following STING knockdown， the reductions in cell viability and the apoptosis-inducing effects caused by PQS were partially reversed （P<0.05， P<0.01）. Compared with the PQS group， the PQS+GFIR group showed inhibited A549 cell migration and colony formation， exacerbated apoptosis， downregulated mitochondrial membrane potential， elevated ROS levels， and promoted mtDNA leakage. After STING knockdown， the reduced A549 cell viability and abnormal apoptosis phenotype were further reversed （P<0.05， P<0.01）. The animal experiment results showed that compared with the control group， the model group mice exhibited reduced proportions of T-lymphocyte subsets， CD19⁺ B-lymphocyte levels， and peripheral blood NK1.1⁺ cell levels in the spleen （P<0.01）. Compared with the model group， the PQS group showed increased immune cell parameters in mice （P<0.05， P<0.01）. Compared with the PQS group， the PQS+GFIR group exhibited enhanced levels of the aforementioned indicators （P<0.01）. Compared with the model group， the PQS group showed significantly reduced fluorescence intensity in transplanted tumors， significantly upregulated expression of CD3 and CD4 in the tumor tissue， elevated levels of IFN-α and IL-6 in tumors， and upregulated mRNA levels of cGAS， STING， TBK1， IRF3， IFNB1， and NF-κB p65 as well as upregulated protein level of cGAS and phosphorylation level of STING in tumors （P<0.05， P<0.01）. Compared with the PQS group， the PQS+GFIR group demonstrated further reduced tumor fluorescence intensity， elevated levels of CD3， CD4， and CD8 as well as cytokine levels in tumor tissue， and upregulated mRNA levels of genes related to the cGAS/STING pathway as well as upregulated protein level of cGAS and phosphorylation levels of STING， TBK1， IRF3， and NF-κB p65 （P<0.05， P<0.01） ConclusionGFIR enhances the inhibitory effect of PQS on NSCLC， potentially through mitochondrial dysfunction， mtDNA leakage， and activation of the cGAS/STING signaling pathway.

ObjectiveTo investigate whether the inhibitory effect of Panax quinquefolium saponins （PQS） on non-small cell lung cancer （NSCLC） is enhanced under graphene-mediated far-infrared therapy （GFIR）， and to analyze its relationships with mitochondrial dysfunction， mitochondrial DNA （mtDNA） leakage， and the activation of cyclic GMP-AMP synthase （cGAS）/stimulator of interferon genes （STING） signaling pathways. MethodsIn the cell experiments， the cell-counting kit 8 （CCK-8） was employed to assess the inhibitory effects of PQS alone or in combination with GFIR （PQS+GFIR） on A549 cell viability. The scratch assay and the colony formation assay were adopted to evaluate cell migration and colony formation capabilities， respectively. Flow cytometry was employed to assess apoptosis， mitochondrial membrane potential， and reactive oxygen species （ROS） levels. Immunofluorescence （IF） assay was performed to assess mitochondrial localization. Real-time polymerase China reaction（PCR） was used to detect mitochondrial DNA （mtDNA） leakage. A STING knockdown cell model was established by transfecting cells with small interfering RNA （siRNA）， and the knockdown efficiency was assessed by Real-time PCR and Western blot. The cell viability and apoptosis following gene knockdown were assessed through the CCK-8 assay and flow cytometry. In the animal experiments， an allogeneic xenograft mouse model was established with Lewis lung cancer cells. Mice were randomized into a control group， a model group， a cisplatin group， a low-dose PQS （PQS-Low， 90 mg·kg^-1） group， a high-dose PQS （PQS-High， 180 mg·kg^-1） group， a low-dose PQS combined with GFIR （PQS-Low+GFIR， 90 mg·kg^-1） group， and a high-dose PQS combined with GFIR （PQS-High+GFIR， 180 mg·kg^-1） group. Treatment lasted for 14 days， and the fluorescence intensity was monitored at the tumor site by small-animal in vivo imaging during the treatment period. Flow cytometry was utilized to determine the proportions of T-lymphocyte subsets， B-lymphocyte levels， and peripheral blood NK cell levels in the spleens of mice. Immunohistochemical （IHC） staining was performed to assess the infiltration of CD3⁺， CD4⁺， and CD8⁺ T-lymphocytes in the tumor tissue. Enzyme-linked immunosorbent assay （ELISA） was conducted to measure the levels of interferon-α （IFN-α）， interferon-β （IFN-β）， tumor necrosis factor-α （TNF-α）， and interleukin-6 （IL-6） in mouse tumors. The mRNA levels of cGAS， STING， TANK-binding kinase 1 （TBK1）， interferon regulatory factor 3 （IRF3）， interferon beta 1 （IFNB1）， and nuclear factor κB p65 （NF-κB p65） were determined by Real-time PCR. The protein levels of cGAS， STING， p-STING， TBK1， p-TBK1， IRF3， p-IRF3， NF-κB p65， and p-NF-κB p65 were quantified via Western blot. ResultsThe cell experiment results showed that compared with the control group， PQS inhibited the viability and migration of A549 cells， promoted apoptosis， affected mitochondrial localization， reduced mitochondrial membrane potential， increased the ROS level， and promoted mtDNA leakage. Following STING knockdown， the reductions in cell viability and the apoptosis-inducing effects caused by PQS were partially reversed （P<0.05， P<0.01）. Compared with the PQS group， the PQS+GFIR group showed inhibited A549 cell migration and colony formation， exacerbated apoptosis， downregulated mitochondrial membrane potential， elevated ROS levels， and promoted mtDNA leakage. After STING knockdown， the reduced A549 cell viability and abnormal apoptosis phenotype were further reversed （P<0.05， P<0.01）. The animal experiment results showed that compared with the control group， the model group mice exhibited reduced proportions of T-lymphocyte subsets， CD19⁺ B-lymphocyte levels， and peripheral blood NK1.1⁺ cell levels in the spleen （P<0.01）. Compared with the model group， the PQS group showed increased immune cell parameters in mice （P<0.05， P<0.01）. Compared with the PQS group， the PQS+GFIR group exhibited enhanced levels of the aforementioned indicators （P<0.01）. Compared with the model group， the PQS group showed significantly reduced fluorescence intensity in transplanted tumors， significantly upregulated expression of CD3 and CD4 in the tumor tissue， elevated levels of IFN-α and IL-6 in tumors， and upregulated mRNA levels of cGAS， STING， TBK1， IRF3， IFNB1， and NF-κB p65 as well as upregulated protein level of cGAS and phosphorylation level of STING in tumors （P<0.05， P<0.01）. Compared with the PQS group， the PQS+GFIR group demonstrated further reduced tumor fluorescence intensity， elevated levels of CD3， CD4， and CD8 as well as cytokine levels in tumor tissue， and upregulated mRNA levels of genes related to the cGAS/STING pathway as well as upregulated protein level of cGAS and phosphorylation levels of STING， TBK1， IRF3， and NF-κB p65 （P<0.05， P<0.01） ConclusionGFIR enhances the inhibitory effect of PQS on NSCLC， potentially through mitochondrial dysfunction， mtDNA leakage， and activation of the cGAS/STING signaling pathway.

[Objective] To study the molecular biological mechanism for a case of ABO blood group B subtype, and perform three-dimensional modeling of the mutant enzyme. [Methods] The ABO phenotype was identified by the tube method and microcolumn gel method; the ABO gene of the proband was detected by sequence-specific primer polymerase chain reaction (PCR-SSP), and the exon 6 and 7 of the ABO gene were sequenced and analyzed. Homologous modeling of Bw.03 glycosyltransferase (GT) was carried out by Modeller and analyzed by PyMOL2.5.0 software. [Results] The weakening B antigen was detected in the proband sample by forward typing, and anti-B antibody was detected by reverse typing. PCR-SSP detection showed B, O gene, and the sequencing results showed c.721 C>T mutation in exon 7 of the B gene, resulting in p. Arg 241 Trp. Compared with the wild type, the structure of Bw.03GT was partially changed, and the intermolecular force analysis showed that the original three hydrogen bonds at 241 position disappeared. [Conclusion] Blood group molecular biology examination is helpful for the accurate identification of ambiguous blood group. Homologous modeling more intuitively shows the key site for the weakening of Bw.03 GT activity. The intermolecular force analysis can explain the root cause of enzyme activity weakening.

Objective: To explore the impacts of coal mine dust on lung function in rats, so as to provide the basis for the early prevention and treatment of coal worker's pneumoconiosis. Methods: Seventy-two SPF-grade 8-week-old male Sprague-Dawley rats were randomly divided into the coal dust group, the coal-silica dust group, the silica dust group and the control group. The rats in the first three groups of rats were administered 1 mL corresponding dust suspension into the lungs using non-exposure tracheal instillation, while the rats in the control group were administered 1 mL normal saline. Respiratory rate (f), forced vital capacity (FVC), peak expiratory flow (PEF) and dynamic pulmonary compliance (Cdyn) were measured at 1, 3 and 6 months after dust exposure. Lung tissues were collected to measure reactive oxygen species (ROS) and adenosine triphosphate (ATP) levels using corresponding ELISA kits and ATP assay kits, respectively. The relative mRNA expressions of peroxisome proliferators-activated receptor gamma coactivator 1-alpha (PGC-1α) and mitochondrial transcription factor A (TFAM) were detected using real-time fluorescent quantitative polymerase chain reaction assay. The relative protein expressions of PGC-1α and TFAM were detected using Western blotting. Results: There was no interaction between dust type and exposure duration on f (P>0.05), but there were interactions on FVC, PEF and Cdyn (all P<0.05). Compared with the control group at 6 months after dust exposure, the f of the rats in the silica dust group were increased, while the FVC and PEF of the rats in the coal-silica dust and silica dust groups were decreased, and Cdyn of the rats in the coal dust, coal-silica dust and silica dust groups were decreased (all P<0.05). There were interactions between dust type and exposure duration on ROS and ATP levels, the relative mRNA and protein expressions of PGC-1α and TFAM (all P<0.05). Compared with the control group at 3 and 6 months after dust exposure, the ROS levels in the rats in the coal dust, coal-silica dust and silica dust groups were increased, while the ATP levels, the relative mRNA and protein expressions of PGC-1α and TFAM were decreased (all P<0.05). Conclusion The lung function impairment in rats caused by different types of coal mine dust is related to PGC-1α-mediated mitochondrial biogenesis dysfunction, which leads to increased ROS levels, decreased ATP and TFAM levels.

Background Mitochondrial biogenesis is pivotal in coal workers' pneumoconiosis fibrosis, yet the role of the peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α)-nuclear respiratory factor 1 (NRF1)-mitochondrial transcription factor A (TFAM) pathway inmitochondrial biogenesis remains elusive, warranting further investigation. Objective To elucidate the role of the PGC-1α-NRF1-TFAM pathway in mitochondrial biogenesis in a rat coal workers' pneumoconiosis model through in vivo and in vitro experiments. Methods (1)n vivo: twelve SPF male SD rats (200-220 g) were randomized into a control group and a coal dust group (n=6 per group). After acclimatization, the coal dust group received 1 mL 50 mg·mL⁻¹ coal dust suspension via intratracheal instillation; the controls received saline. Lung tissues were harvested after two months for histopathology [HE, Masson, and transmission electron microscopy (TEM) ], protein and mRNA analysis, and mitochondrial DNA (mtDNA) quantification by quantitative real-time polymerase chain reaction (qPCR). (2) In vitro: rat lung type II epithelial cells (RLE-6TN) cells were exposed to coal dust (50, 100, 200, and 400 mg·L⁻¹, 24 h). CCK-8 assay determined optimal doses. Ultrastructural changes were analyzed by TEM. Cells were transfected with OE-PGC-1α (PGC-1α overexpression) or shRNA-PGC-1α plasmids (PGC-1α knockdown), and the transfection efficiency was determined by reverse transcription quantitative real-time polymerase chain reaction (RT-qPCR). The expression levels of alpah-smooth muscle actin (α-SMA), citrate synthase (CS), PGC-1α, NRF1, TFAM, and fibronectin (Fn) proteins and their corresponding mRNA were detected using Western blot and RT-qPCR, respectively. The relative content of mtDNA was determined by qPCR. Results In vivo: the control group lung samples exhibited soft, pink parenchyma, while the coal dust-exposed lungs showed blackened surfaces with soft texture. The histopathological evaluation revealed intact alveolar walls in the controls versus structural destruction, micro-nodules, and fibrotic areas in the coal dust group. After Masson staining, coal dust deposits were found surrounded by blue collagen fibers in the exposed lungs, but absent in the controls. The coal dust group displayed significant upregulation of fibrotic marker α-SMA and downregulation of mitochondrial biogenesis markers (CS, PGC-1α, NRF1, TFAM) and mtDNA compared to the controls (P<0.05). In vitro: coal dust exposure reduced cell density and induced morphological alterations. TEM revealed evenly distributed normal mitochondria in controls versus mitochondrial swelling, disrupted cristae, and reduced numbers in exposed cells. The mitochondrial biogenesis markers were elevated in the coal dust + OE-PGC-1α group compared to the coal dust + OE-NC group (P<0.05); in contrast, they were decreased in the coal dust + shRNA-PGC-1α group compared to the coal dust + shRNA-NC group (P<0.05). Compared to the control group, the expression levels of the fibrosis marker α-SMA mRNA and protein were increased in the coal dust group (P<0.05). Overexpression of PGC-1α reduced α-SMA expression, while downregulation of PGC-1α increased its expression (P<0.05). Conclusion Coal dust exposure induces mitochondrial dysfunction and pulmonary fibrosis in vivo and in vitro via the PGC-1α-NRF1-TFAM pathway dysregulation. Targeting this pathway may mitigate coal dust-induced fibrosis by restoring mitochondrial biogenesis.

China emerges as a major country in nuclear energy development and the application of nuclear and radiologic technology. The diagnosis and treatment of acute radiation syndrom (ARS) caused by external irradiation represent a core function in the country′s medical rescue of nuclear and radiological emergencies. Clinically, ARS manifests hematopoietic, gastrointestinal, cutaneous, and central nervous system syndromes, with specific clinical manifestations, signs, severity, and prognosis strongly correlated with radiation dose. China has established a number of national and provincial centers for treating radiation-induced damage. Nevertheless, most medical staff have limited experience in ARS treatment. This consensus presents a summary of recent experience in treating ARS of China. In combination with recommendations from international organizations such as the World Health Organization (WHO), this consensus proposes key evidence of critical clinical issues of ARS, covering all links in the rescue of external irradiation-induced ARS. Initially, clinical diagnosis, syndromes, and severe degrees should be determined based on clinical symptoms and dose estimates. It is necessary to normalize clinical treatment measures for hematopoietic recovery, gastrointestinal injury treatment, infection control, symptomatic treatment, and multi-organ function preservation. To this end, this consensus offers cautions. This consensus provides principles of treatment with traditional Chinese medicine, psychological intervention, and follow-up. Additionally, it highlights multidisciplinary collaboration. It is recommended that this consensus be applied in relevant treatment centers.

Objective To explore the influencing factors of olfactory dysfunction in patients with Parkinson's disease(PD)and conduct a systematic review and Meta-analysis.Methods Articles on factors influencing olfactory dysfunction in PD were retrieved from databases including SinoMed,VIP,China National Knowledge Infrastructure,Wanfang Data Knowledge Service Platform,Web of Science,PubMed,Cochrane,Embase,and MEDLINE.The search period spanned from the inception of each database to November 30,2024.Results A total of 13 articles(with a total sample size of 2465)were included,with a total of 18 influencing factors summarized as two themes:core features and progression factors of PD,and individual background and environmental interaction factors.Meta-analysis showed that age(MD=1.01,95％CI:-0.46-2.49,P=0.18),smoking(OR=0.88,95％CI:0.57-1.37,P=0.57),and constipation(OR=1.22,95％CI:0.38-3.93,P=0.74)were not factors affecting olfactory dysfunction in PD patients.Conclusion Factors influencing olfactory dysfunction in PD are predominantly associated with non-motor symptoms.Intervention strategies targeting non-motor symptoms(such as improving sleep quality,vitamin D supplementation,and early cognitive training)may provide novel approaches for delaying the progression of olfactory dysfunction.