Microbial infections are a prevalent challenge in the prevention and treatment of oral diseases. Antibiotic therapy faces clinical limitations due to its single-target mechanism and tendency to induce resistance with repeated use, necessitating novel antibacterial strategies. Stimuli-responsive antibacterial materials, whose antimicrobial activity can be modulated by external stimuli, offer advantages such as remote controllability, potential for localized precision treatment, and a reduced risk of inducing resistance. Among these materials, mechanical force-triggered piezoelectric materials exhibit significant antibacterial activity in the biomedical field owing to their unique piezoelectric effect, excellent stability, and good biocompatibility. Research has shown that piezoelectric materials can convert mechanical energy into electrical energy in response to external forces, which enables antibacterial effects without requiring an external power source. The underlying mechanisms primarily include direct electric field effects, generation of reactive oxygen species, and immune modulation. Preliminary applications in treating oral infections (e.g., dental caries, periodontitis, and peri-implantitis) have confirmed their stability and biocompatibility, establishing a foundation for clinical translation. However, long-term efficacy and biosafety in the complex oral microenvironment require further validation. Future research should focus on optimizing material preparation protocols to enhance antibacterial efficacy and stability, further investigating the underlying antimicrobial mechanisms, and systematically evaluating their therapeutic outcomes and safety profiles across various types of oral infections. This review summarizes the antibacterial effects, mechanisms, stability, safety, and research progress of piezoelectric materials in the stomatologic field, aiming to provide new insights for further research and application in this area.

ObjectiveTo explore the potential mechanism of Xianglian Huazhuo prescription （XLHZ） in treating chronic atrophic gastritis （CAG） by regulating cell cycle and inhibiting proliferation， using bioinformatics technology and animal experiments. MethodsDifferential expressed genes （DEGs） related to CAG were screened using GEO database and GEO2R tool. Weighted gene co-expression network analysis （WGCNA） was employed to search for hub genes of CAG. These hub genes were intersected with cell cycle proliferation based on GeneCards database. Eenrichment analysis of the intersecting genes was performed to obtain signaling pathways and biological processes related to CAG. Protein protein interaction （PPI） analysis of genes was conducted using the Protein Interaction Platform （STRING） database to search the super hub gene （hub 2.0）， and animal experiments were conducted for further validation. Fourteen of 70 male Wistar rats were randomly selected as the normal group， and the remaining 56 rats were prepared by the combined modeling method of "starvation disorder+N-methyl-N-nitro-N-nitrosoguanidine （MNNG） + sodium salicylate". The successfully modeled rats were randomly divided into the model group， XLHZ-H， XLHZ-M， and XLHZ-L groups （36， 18， 9 g·kg^-1， respectively）， and Morodan group （1.4 g·kg^-1）. Each group was given corresponding intervention for 60 days. Hematoxylin-eosin （HE） staining was used to observe the histopathological changes of gastric mucosa in rats. The ultrastructure of gastric mucosal tissue cells was observed by transmission electron microscopy. The relative expression levels of TGF-β₁， Smad2 and Smad3 proteins， S/G₂/M phase marker geminin and proliferation marker MCM2 were detected by Western blot in gastric mucosal tissue， and Spearman correlation analysis was performed. ResultsA total of 15 hub 2.0 genes were identified， including TGF-β₁， suggesting the involvement of the TGF-β₁ signaling pathway in the CAG pathogenesis. Compared with the normal group， the expressions of TGF-β₁， Smad2， geminin and MCM2 proteins in the gastric mucosa tissue of the model group were increased （P<0.05）， and the expression of Smad3 protein was decreased （P<0.05）. Compared with the model group， the expressions of TGF-β₁ and geminin in the gastric mucosa were decreased in the drug groups （P<0.05）. The XLHZ-M group， XLHZ-H group and Morodan group had significantly decreased protein expression of Smad2 and MCM2 （P<0.05）. The protein expression of Smad3 was significantly increased in XLHZ-M， XLHZ-H， and Morodan groups （P<0.05）. Spearman correlation analysis showed that Smad3 was negatively correlated with other indicators， and positively correlated with other indicators （P<0.01）. ConclusionXLHZ may inhibit TGF-β₁/Smads signaling pathway， regulate cell cycle， and inhibit proliferation in the treatment of CAG.

AIM: To evaluate the safety and efficacy of low-dose transscleral cyclophotocoagulation(TSCP)in the management of persistent ocular hypertension after an acute attack of angle-closure glaucoma(AACG).METHODS:This retrospective study enrolled patients diagnosed with persistent ocular hypertension after an acute AACG attack at the No.988 Hospital of the Joint Logistics Support Force of the Chinese PLA between September 2023 and September 2024. All patients underwent low-dose TSCP using a semiconductor diode laser. Subsequent cataract surgery combined with goniosynechialysis was performed once intraocular pressure(IOP)was stabilized. Changes in anterior chamber depth(ACD), best-corrected visual acuity(VA), and IOP were compared before and after TSCP, as well as before and after phacoemulsification. Post-TSCP complications were also documented.RESULTS: A total of 21 patients(21 eyes)were enrolled, including 8 males and 13 females, with a mean age of 67.95±7.25 y. Compared with pre-cyclophotocoagulation values, ACD increased significantly at 3 d post-TSCP(1.49±0.18 vs 1.22±0.21 mm; P<0.001). BCVA and IOP decreased significantly at 1 d post-TSCP, pre-phacoemulsification, 1 wk post-phacoemulsification, and 1 mo post-phacoemulsification compared with pre-TSCP IOP(all P<0.01). Regarding postoperative complications, 2 eyes experienced pain on the day of the procedure, 5 eyes developed mild corneal endothelial folds, 2 eyes exhibited moderate anterior chamber inflammatory reaction, and 12 eyes showed shallow ciliary body detachment. No serious complications occurred during the 1-month follow-up period.CONCLUSION:Low-dose TSCP appears to be an effective bridging therapy for patients with persistent ocular hypertension following an AACG attack. It facilitates rapid IOP reduction, alleviates symptoms, and helps preserve visual function with a favorable safety profile, thereby reducing the risks associated with subsequent intraocular surgery.

ObjectiveTo explore the potential mechanism of Xianglian Huazhuo prescription （XLHZ） in treating chronic atrophic gastritis （CAG） by regulating cell cycle and inhibiting proliferation， using bioinformatics technology and animal experiments. MethodsDifferential expressed genes （DEGs） related to CAG were screened using GEO database and GEO2R tool. Weighted gene co-expression network analysis （WGCNA） was employed to search for hub genes of CAG. These hub genes were intersected with cell cycle proliferation based on GeneCards database. Eenrichment analysis of the intersecting genes was performed to obtain signaling pathways and biological processes related to CAG. Protein protein interaction （PPI） analysis of genes was conducted using the Protein Interaction Platform （STRING） database to search the super hub gene （hub 2.0）， and animal experiments were conducted for further validation. Fourteen of 70 male Wistar rats were randomly selected as the normal group， and the remaining 56 rats were prepared by the combined modeling method of "starvation disorder+N-methyl-N-nitro-N-nitrosoguanidine （MNNG） + sodium salicylate". The successfully modeled rats were randomly divided into the model group， XLHZ-H， XLHZ-M， and XLHZ-L groups （36， 18， 9 g·kg^-1， respectively）， and Morodan group （1.4 g·kg^-1）. Each group was given corresponding intervention for 60 days. Hematoxylin-eosin （HE） staining was used to observe the histopathological changes of gastric mucosa in rats. The ultrastructure of gastric mucosal tissue cells was observed by transmission electron microscopy. The relative expression levels of TGF-β₁， Smad2 and Smad3 proteins， S/G₂/M phase marker geminin and proliferation marker MCM2 were detected by Western blot in gastric mucosal tissue， and Spearman correlation analysis was performed. ResultsA total of 15 hub 2.0 genes were identified， including TGF-β₁， suggesting the involvement of the TGF-β₁ signaling pathway in the CAG pathogenesis. Compared with the normal group， the expressions of TGF-β₁， Smad2， geminin and MCM2 proteins in the gastric mucosa tissue of the model group were increased （P<0.05）， and the expression of Smad3 protein was decreased （P<0.05）. Compared with the model group， the expressions of TGF-β₁ and geminin in the gastric mucosa were decreased in the drug groups （P<0.05）. The XLHZ-M group， XLHZ-H group and Morodan group had significantly decreased protein expression of Smad2 and MCM2 （P<0.05）. The protein expression of Smad3 was significantly increased in XLHZ-M， XLHZ-H， and Morodan groups （P<0.05）. Spearman correlation analysis showed that Smad3 was negatively correlated with other indicators， and positively correlated with other indicators （P<0.01）. ConclusionXLHZ may inhibit TGF-β₁/Smads signaling pathway， regulate cell cycle， and inhibit proliferation in the treatment of CAG.

The multimorbidity of rheumatoid arthritis （RA） and periodontitis （PD） has drawn increasing attention， as both conditions are characterized by chronic inflammation， immune dysregulation， and progressive bone destruction. Modern research confirms that PD is a significant risk factor for RA development， and their coexistence mutually exacerbates disease progression. However， traditional Chinese medicine （TCM） currently lacks a systematic theoretical explanation for this complex multimorbid relationship. This study， based on the TCM theory of abnormal collateral， thoroughly examines the intrinsic connection between RA and PD multimorbidity， proposing "abnormal collateral as the pivot， with accumulated toxins eroding bone" as the core TCM pathogenesis. The research elucidates PD as the "origin of abnormal collateral"， where its pathogens act as toxic factors that invade the joints through collaterals， triggering RA via mechanisms such as molecular mimicry. The dynamic pathological progression of RA-PD multimorbidity can be described as follows： the displacement of Ying and Wei at the microscopic level manifests as immune hyperactivation， leading to collateral malnutrition； heat-toxins traversing collaterals induce collateral hyperactivity， resulting in pathological angiogenesis； ultimately， toxin accumulation at the pivotal abnormal collateral site erodes bone， activating the receptor activator of nuclear factor kappa-B ligand （RANKL）-receptor activator of nuclear factor kappa-B （RANK） signaling pathway-driven osteoclast differentiation. This theoretical framework innovatively integrates modern findings in oral microbiology， immune-inflammation， and bone metabolism， offering a holistic and dynamic perspective to understand the complexity of multimorbidity. Given the limited efficacy of current periodontal treatments for RA and the scarcity of reported TCM compound interventions for multimorbidity， the abnormal collateral theory proposes a systematic intervention strategy centered on "governing diseases through collaterals and regulating collaterals with herbs"， along with TCM therapeutic principles such as "unblocking， clearing， and nourishing collaterals". Potential herbal treatments for multimorbidity are also highlighted. Future research should focus on refining TCM syndrome patterns in multimorbid patients and leveraging omics technologies for deeper exploration， thereby providing a theoretical foundation and research direction for TCM in addressing complex multimorbid conditions.

The multimorbidity of rheumatoid arthritis （RA） and periodontitis （PD） has drawn increasing attention， as both conditions are characterized by chronic inflammation， immune dysregulation， and progressive bone destruction. Modern research confirms that PD is a significant risk factor for RA development， and their coexistence mutually exacerbates disease progression. However， traditional Chinese medicine （TCM） currently lacks a systematic theoretical explanation for this complex multimorbid relationship. This study， based on the TCM theory of abnormal collateral， thoroughly examines the intrinsic connection between RA and PD multimorbidity， proposing "abnormal collateral as the pivot， with accumulated toxins eroding bone" as the core TCM pathogenesis. The research elucidates PD as the "origin of abnormal collateral"， where its pathogens act as toxic factors that invade the joints through collaterals， triggering RA via mechanisms such as molecular mimicry. The dynamic pathological progression of RA-PD multimorbidity can be described as follows： the displacement of Ying and Wei at the microscopic level manifests as immune hyperactivation， leading to collateral malnutrition； heat-toxins traversing collaterals induce collateral hyperactivity， resulting in pathological angiogenesis； ultimately， toxin accumulation at the pivotal abnormal collateral site erodes bone， activating the receptor activator of nuclear factor kappa-B ligand （RANKL）-receptor activator of nuclear factor kappa-B （RANK） signaling pathway-driven osteoclast differentiation. This theoretical framework innovatively integrates modern findings in oral microbiology， immune-inflammation， and bone metabolism， offering a holistic and dynamic perspective to understand the complexity of multimorbidity. Given the limited efficacy of current periodontal treatments for RA and the scarcity of reported TCM compound interventions for multimorbidity， the abnormal collateral theory proposes a systematic intervention strategy centered on "governing diseases through collaterals and regulating collaterals with herbs"， along with TCM therapeutic principles such as "unblocking， clearing， and nourishing collaterals". Potential herbal treatments for multimorbidity are also highlighted. Future research should focus on refining TCM syndrome patterns in multimorbid patients and leveraging omics technologies for deeper exploration， thereby providing a theoretical foundation and research direction for TCM in addressing complex multimorbid conditions.

ObjectiveTo investigate the mechanism by which Xiebai San regulates respiratory tract and intestinal mucosal immunity in rats with allergic asthma. MethodsForty male SD rats were randomly divided into four groups based on body weight: control group, model group, positive control group, and Xiebai San group. The model group, positive control group, and Xiebai San group were sensitized with ovalbumin to establish a rat model of allergic asthma. From day 21 (the aerosol challenge phase), each group received daily gavage interventions simultaneously: the positive control group was administered dexamethasone (0.068 mg/kg), the Xiebai San group received Xiebai San solution (2 g/mL, 11.3 mL/kg), while the control and model groups were given an equal volume of normal saline, once daily for 14 consecutive days. After euthanasia, lung and intestinal tissues were collected. Hematoxylin and eosin staining was used to observe histopathological changes. Transmission electron microscopy was employed to examine tissue ultrastructure. Immunohistochemistry was applied to detect the positive reaction areas of phosphatidyl-inositol 3-kinase (PI3K) and protein kinase B (Akt) proteins. Total protein and total RNA were extracted from lung and intestinal tissues, then the protein and mRNA expression levels of PI3K and Akt genes were detected by Western blotting and real-time quantitative PCR, respectively. ResultsHistopathological results showed alveolar emphysema accompanied by inflammatory cell infiltration, and intestinal mucosal injury with inflammatory cell infiltration in the model group as compared with the control group; the cellular structure of lung tissues was disrupted in the model group, with reduced organelles, while the ultrastructural lesions in the intestine were relatively mild. Compared with the model group, Xiebai San group exhibited milder pathological changes in lung tissues, with occasional alveolar wall damage and a small amount of inflammatory cell infiltration; the intestinal mucosal structure was improved, glands were arranged regularly, and pathological changes such as tissue loosening and inflammatory infiltration were alleviated; the cellular structure of lung tissues was relatively intact with reduced severity of lesions, and no ultrastructural pathological changes were observed in intestinal tissues. Immunohistochemistry and Western blotting results showed that compared with the control group, the specific positive reaction areas of PI3K and Akt in lung and intestinal tissues were significantly increased in the model group (all P<0.001); meanwhile, the protein expression levels of PI3K and Akt were significantly upregulated (all P<0.05). Compared with the model group, the positive area of Akt protein in lung tissue was significantly reduced in the Xiebai San group (P<0.001), and the positive area of PI3K in intestinal tissue was also significantly decreased (P<0.000 1). Additionally, the protein expression levels of PI3K and Akt in lung and intestinal tissues were significantly downregulated (all P<0.01). Real-time quantitative PCR results showed that compared with the control group, the mRNA expression levels of PI3K and Akt genes in lung and intestinal tissues were significantly elevated in the model group (all P<0.05). Compared with the model group, the mRNA expression levels of PI3K and Akt genes in lung and intestinal tissues were significantly reduced in the Xiebai San group (all P<0.05). ConclusionXiebai San exerts protective effects on rats with allergic asthma by inhibiting the expression of key nucleic acids and proteins in the PI3K-Akt signaling pathway in lung and intestinal tissues, improving the morphological structure of lung tissue, and maintaining intestinal mucosal integrity, and regulating intestinal mucosal immune function.

Background A diverse cohort of patients and susceptible individuals congregate in healthcare facilities, where exposure to pathogenic microorganisms associated with respiratory infectious diseases constitutes a significant risk factor for cross-infection. Central air-conditioning ventilation systems improve some indoor environment indicators while exacerbating the risk of transmission of respiratory infectious diseases. Objective To investigate the distribution characteristics of microbial communities in the central air-conditioning ventilation systems of hospitals, providing a scientific basis for the selection of microbial indicators in hygiene standards for hospital central air-conditioning ventilation systems and for hospital risk early warning systems. Methods In October 2023, two central air-conditioning ventilation systems were selected from a Grade 3A hospital in Shanghai: one was an all-air air-conditioning system serving the waiting area on the ground floor, and the other was a fan coil plus fresh air system serving the outpatient area on the third floor. Samples from four different components of the ventilation systems—air outlets, filters, surface coolers, and condensate trays—were collected for high-throughput sequencing of the 16S rRNA gene to analyze bacterial communities. Alpha-diversity and beta-diversity analyses were performed to investigate the microbial community composition and diversity characteristics of the hospital central air-conditioning ventilation systems. Functional analysis was conducted to determine the relative abundance of bacterial functions in these systems.Results A total of 528 operational taxonomic units (OTUs) were identified, encompassing 20 bacterial phyla, 37 classes, 79 orders, 123 families, and 240 genera. The analysis revealed that the bacterial community was predominantly composed of Proteobacteria, Gemmatimonadates, Bacteroidetes, and Actinobacteria. The diversity analysis indicated that bacterial community richness and diversity were highest in the condensate trays, while no statistically significant differences (P > 0.05) were observed in the bacterial community composition among the air outlets, filters, and surface coolers. The functional analysis showed that the bacterial communities in the central air-conditioning ventilation systems primarily exhibited chemoheterotrophic, oxidative energy-dependent heterotrophic, and ureolytic functional characteristics. Conclusion The dominance of Proteobacteria suggests that this phylum exhibits strong adaptability in the central air-conditioning ventilation systems, possibly related to its ability to survive and reproduce under varying environmental conditions. The diversity analysis indicates that the condensate tray is a critical area for bacterial proliferation in the central air-conditioning ventilation systems. The similarity in environmental conditions among the air outlets, filters, and surface coolers result in similar bacterial community structures. The functional analysis reveals that the bacterial communities possess robust energy conversion and metabolic capabilities, potentially contributing to processes such as organic matter decomposition and nitrogen cycling within the central air-conditioning ventilation systems.

Objective: To explore the potential application of PAK4-PROTAC targeted degradation drug (PpD) in renal cancer immunotherapy. Methods: TIMER 2.0 and TISIDB databases were used to analyze the relationship among PAK4 expression, tumor purity and abundance of immune cell infiltration in renal tumor microenvironment (TEM).Renal cancer cell lines OS-RC-2, 786-O and ACHN were treated with 0, 125 and 250 nmol/L PpD, and the effects of Jurkat cell co-culture on the results were investigated.The cell apoptosis was detected with flow cytometry, and the expression of programmed cell death 1 ligand 1 (PD-L1) in renal cancer cells was detected with immunoblotting. Results: The high expression of PAK4 was positively related to immune purity, and inhibited the abundance of immune killer cells in TEM, such as CD8 T cells, CD4 T cells, natural killer cells and dendritic cells.With 250 nmol/L PpD treatment, there were 21.02% apoptotic cells in OS-RC-2, 29.67% apoptotic cells in 786-O, and 15.39% apoptotic cells in ACHN, respectively.However, with the same concentration of 250 nmol/L PpD treatment, cell apoptotic rate was sharply increased to 70.13% in OS-RC-2/Jurkat, 70.68% in 780-O/Jurkat, and 60.27% in ACHN/Jurkat co-culture models, respectively. Conclusion: PpD can promote apoptosis of renal cancer cells by reducing the expression of PAK4 protein, and enhance the killing effects of immune cells on tumor cells.

ObjectiveTo investigate the effect of the herb pair Cuscutae Semen-Lycii Fructus on oxidative stress-induced blood-testis barrier dysfunction and spermatogenesis in the rat model of oligoasthenozoospermia （OAS） and decipher the mechanism based on the silent information regulator 1 （SIRT1）/nuclear factor erythroid 2-related factor 2 （Nrf2） signaling pathway. MethodsThirty-five male SD rats were randomized into a blank group （n=7） and a modeling group （n=28）. The OAS model was established by gavage of hydrocortisone aqueous solution combined with single factor electrical stimulation. The modeled rats were randomly assigned into the following groups： model， Cuscutae Semen-Lycii Fructus granules （3.2 g·kg^-1）， Cuscutae Semen-Lycii Fructus total flavonoids （0.34 g·kg^-1）， and L-carnitine （0.38 g·kg^-1）， and treated for 4 weeks. The sperm quality of rats was assessed by an automatic sperm analyzer. The levels of superoxide dismutase （SOD）， malondialdehyde （MAD）， and glutathione peroxidase （GSH-Px） in the testicular tissue were determined by enzyme-linked immunosorbent assay. Hematoxylin-eosin staining was employed to reveal the pathological changes in the testicular tissue and score the spermatogenic function. Transmission electron microscopy was employed to observe the ultrastructural changes of Sertoli cells. Western blot and Real-time PCR were employed to determine the protein and mRNA levels， respectively， of SIRT1， Nrf2， Occludin， zonula occludens-1 （ZO-1）， connexin 43 （CX43）， and β-catenin. ResultsCompared with the blank group， the model group showed decreased total sperm count and motility （P<0.05， P<0.01）， obvious damage in the testicular tissue and blood-testis barrier structure， reduced score of spermatogenic function （P<0.01）， declined levels of GSH-Px and SOD in the testicular tissue （P<0.05）， elevated level of MDA， and down-regulated protein levels of SIRT1， Nrf2， ZO-1， CX43， β-catenin， and occludin （P<0.05， P<0.01） and mRNA levels of SIRT1， Nrf2， ZO-1， CX43， and β-catenin in the testicular tissue （P<0.05， P<0.01）. After treatment， the testicular tissue， blood-testis barrier structure， and score of spermatogenic function （P<0.01） were improved in the Cuscutae Semen-Lycii Fructus granules group， Cuscutae Semen-Lycii Fructus total flavonoids group， and L-carnitine group. Compared with the model group， the treatment groups presented lowered levels of GSH-Px and SOD （P<0.05， P<0.01）， and the Cuscutae Semen-Lycii Fructus granule group showed a decline in MDA level. The protein and mRNA levels of SIRT1， Nrf2， ZO-1， CX43， β-catenin， and occludin were up-regulated in the Cuscutae Semen-Lycii Fructus granules group and total flavonoids group （P<0.05， P<0.01）. ConclusionThe herb pair Cuscutae Semen-Lycii Fructus can regulate the SIRT1/Nrf2 pathway to inhibit oxidative stress and alleviate the blood-testis barrier damage， thereby improving the spermatogenic function in the rat model of OAS. Total flavonoids may be the material basis for the therapeutic effect of Cuscutae Semen-Lycii Fructus.