BACKGROUND:Studies have shown that there is a close relationship between pyroptosis,inflammatory factors and osteoporosis.OBJECTIVE:To review the effects of pyroptosis and inflammatory factors on the pathogenesis of osteoporosis from the perspectives of osteogenic differentiation and osteoclastic differentiation,based on an overview of pyroptosis in relation to the interaction of relevant inflammatory factors.METHODS:The first author used the computer to search the literature published by each database until 2024,and searched CNKI,WanFang,VIP and PubMed databases with the search terms of"pyroptosis,inflammatory factors,osteoporosis,osteoblast,osteoclast,bone metabolism,signaling pathway,review"in Chinese and English.A total of 79 papers were finally included according to the inclusion criteria.RESULTS AND CONCLUSION:The progression of osteoporosis is closely related to inflammation,in which pyroptosis plays a key role.Immune cells induce pyroptosis through apoptosis pathway,promote the secretion of inflammatory factors such as interleukin-18,interleukin-1β and NLRP3,build an inflammatory immune microenvironment,and regulate bone metabolism through complex signaling pathways,resulting in enhanced bone absorption and reduced bone formation,thereby leading to osteoporosis.Previous studies have shown that inhibiting pyroptosis is anti-inflammatory and slows the progression of osteoporosis,and it has been shown to improve inflammatory bone loss in vitro and in animal models.At present,research on pyroptosis and osteoporosis is limited.On the one hand,the exact mechanism of osteoporosis and the pathogenesis of pyroptosis are unknown,and the specific pathways and regulatory mechanisms remain to be understood.On the other hand,therapeutic strategies targeting pyroptosis are still theoretical,not clinically proven,and drug side effects are unknown.In the future,the research focus is to further explore the pathogenesis,especially the mechanism of pyroptosis,identify potential therapeutic targets,further study the pyroptosis signaling pathway and Gasdermin protein,and develop new drugs to improve the therapeutic effect in patients with osteoporosis.

Objective To explore the clinical efficacy of robot-assisted coronary artery bypass grafting through a small incision in the left intercostal space in the treatment of multivessel coronary disease. Methods A retrospective analysis was conducted on the clinical data of patients who underwent coronary artery bypass grafting through a small incision in the left intercostal space at Central China Fuwai Hospital of Zhengzhou University from January 1, 2023 to October 15, 2024. Patients were divided into a robotic group and a minimally invasive group based on whether the surgery was assisted by the Da Vinci robot. Results A total of 81 patients were included, with 57 in the minimally invasive group, including 41 males and 16 females, with a median age of 65.0 (57.5, 69.5) years; and 24 in the robotic group, including 17 males and 7 females, with a median age of 61.0 (56.0, 69.0) years. There was no statistically significant difference in baseline data between the two groups (P>0.05). The robotic group had less intraoperative bleeding [300 (200, 438) mL vs. 500 (375, 600) mL, P=0.006], shorter postoperative mechanical ventilation time [15.0 (13.3, 23.5) h vs. 22.0 (15.5, 39.5) h, P=0.037], and lower incidence of postoperative pain [8 (33.3%) vs. 33 (57.9%), P=0.043]. The hospitalization cost in the robotic group was higher than that in the minimally invasive group [130491 (123298, 135691) yuan vs. 123892 (115543, 133449) yuan, P=0.023]. There was no statistical difference in postoperative laboratory indicators between the two groups (P>0.05). There was also no statistical difference in the duration of surgery, postoperative 24 h drainage volume, ICU stay time, postoperative hospital stay or incidences of perioperative compications including pleural effusion, transfusion, new-onset atrial fibrillation, acute kidney injury, non-union of incision, major cardiovascular and cerebrovascular adverse events, and reoperation between the two groups (P>0.05). Conclusion Compared with the minimally invasive group, the robotic group shows satisfactory efficacy and can effectively reduce postoperative pain and intraoperative bleeding, and shorten postoperative mechanical ventilation time.

Background Previous studies have found that exposure to benzo[a]pyrene (BaP) can lead to functional impairment of the human pancreas. Pancreatic and duodenal homeobox factor 1 (PDX-1) may play a role in regulating mitochondrial function. It is hypothesized that BaP exposure may interfere with PDX-1 expression in human pancreatic ductal epithelial cells (H6C7), thereby affecting mitochondrial transcription factor A (TFAM). This process could induce mitochondrial DNA (mtDNA) damage, disrupt pancreatic development and function, and elevate the risk of diabetes onset. Objective To investigate the mechanism of BaP-induced mtDNA damage through disruption of the PDX-1/TFAM pathway in a H6C7 cell model. Methods A H6C7 cell injury model was established using different concentrations of BaP. Cell viability was determined using cell counting kit-8 (CCK-8). After 24 h of BaP exposure (5,10, and 20 μmol·L⁻¹), cell morphological and mitochondrial membrane potential (MMP) changes were observed via confocalmicroscopy, and PDX-1/TFAM protein expression levels were assessed. Bioinformatics analysis combined with dual-luciferase reporter assays was used to confirm PDX-1 directly targeting the TFAM promoter. Following PDX-1 overexpression or silencing in BaP treated cells, flow cytometry was used to evaluate viability and apoptosis, while Western blot and quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR) measured PDX-1/TFAM expression and mitochondrial DNA copy number (mtDNA-cn). Results The cell injury model demonstrated that, compared with the control group, BaP exposure reduced cell viability, disrupted membrane integrity, induced nuclear fragmentation, and decreased MMP. Protein expression levels of PDX-1 and TFAM were significantly downregulated in the 10 and 20 μmol·L⁻¹ groups (P<0.05). Dual-luciferase reporter assays confirmed that PDX-1 overexpression upregulated TFAM levels. Flow cytometry revealed that PDX-1 overexpression significantly reduced apoptosis rate (P<0.001), whereas PDX-1 silencing increased apoptosis rate (P<0.001). Compared with the BaP-only group, BaP+PDX-1 overexpression elevated TFAM protein and mRNA expression as well as mtDNA-cn (P<0.01), while BaP+siRNA-PDX-1 suppressed these parameters (P<0.001). Conclusion BaP exposure promotes apoptosis in human pancreatic cells. PDX-1, a key gene in pancreatic development, regulates the expression of TFAM, a core regulator of mitochondrial function. This interaction triggers changes in MMP and mtDNA-cn, activates the PDX-1/TFAM/mtDNA axis, and ultimately leads to pancreatic cell injury.

Background Previous studies have found that exposure to benzo[a]pyrene (BaP) can lead to functional impairment of the human pancreas. Pancreatic and duodenal homeobox factor 1 (PDX-1) may play a role in regulating mitochondrial function. It is hypothesized that BaP exposure may interfere with PDX-1 expression in human pancreatic ductal epithelial cells (H6C7), thereby affecting mitochondrial transcription factor A (TFAM). This process could induce mitochondrial DNA (mtDNA) damage, disrupt pancreatic development and function, and elevate the risk of diabetes onset. Objective To investigate the mechanism of BaP-induced mtDNA damage through disruption of the PDX-1/TFAM pathway in a H6C7 cell model. Methods A H6C7 cell injury model was established using different concentrations of BaP. Cell viability was determined using cell counting kit-8 (CCK-8). After 24 h of BaP exposure (5,10, and 20 μmol·L⁻¹), cell morphological and mitochondrial membrane potential (MMP) changes were observed via confocalmicroscopy, and PDX-1/TFAM protein expression levels were assessed. Bioinformatics analysis combined with dual-luciferase reporter assays was used to confirm PDX-1 directly targeting the TFAM promoter. Following PDX-1 overexpression or silencing in BaP treated cells, flow cytometry was used to evaluate viability and apoptosis, while Western blot and quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR) measured PDX-1/TFAM expression and mitochondrial DNA copy number (mtDNA-cn). Results The cell injury model demonstrated that, compared with the control group, BaP exposure reduced cell viability, disrupted membrane integrity, induced nuclear fragmentation, and decreased MMP. Protein expression levels of PDX-1 and TFAM were significantly downregulated in the 10 and 20 μmol·L⁻¹ groups (P<0.05). Dual-luciferase reporter assays confirmed that PDX-1 overexpression upregulated TFAM levels. Flow cytometry revealed that PDX-1 overexpression significantly reduced apoptosis rate (P<0.001), whereas PDX-1 silencing increased apoptosis rate (P<0.001). Compared with the BaP-only group, BaP+PDX-1 overexpression elevated TFAM protein and mRNA expression as well as mtDNA-cn (P<0.01), while BaP+siRNA-PDX-1 suppressed these parameters (P<0.001). Conclusion BaP exposure promotes apoptosis in human pancreatic cells. PDX-1, a key gene in pancreatic development, regulates the expression of TFAM, a core regulator of mitochondrial function. This interaction triggers changes in MMP and mtDNA-cn, activates the PDX-1/TFAM/mtDNA axis, and ultimately leads to pancreatic cell injury.

Objective: To investigate the correlation between color parameters (L^*, a^*, b^*, Eab^*) and the contents of reducing sugars, total polysaccharides, total oligosaccharides, as well as four saccharides (fructose, glucose, sucrose, and kestose) during the nine cycles of steaming and sun-drying processing of Polygonatum kingianum, and to preliminarily explore the optimal processing duration.
Methods: The color changes were objectively evaluated using a colorimeter. The anthrone-sulfuric acid method was employed to determine total polysaccharides and oligosaccharides. The 3,5-dinitrosalicylic acid (DNS) colorimetric method was used to measure total reducing sugar content. High-performance liquid chromatography coupled with charged aerosol detection (HPLC-CAD) was applied for quantitative analysis of fructose, glucose, sucrose, and kestose. Multivariate statistical analysis was conducted to assess samples from different processing stages.
Results: Significant variations in color and component contents were observed across processing stages. The herbal pieces progressively darkened with increased processing cycles: brightness (L^*) and total color difference (Eab^*) initially decreased then stabilized, while a^* (red-green) and b^* (yellow-blue) values first increased then declined. Total polysaccharides and oligosaccharides showed overall decreasing trends, whereas reducing sugars initially increased before stabilizing. Fructose and glucose levels rose continuously, while sucrose and kestose decreased progressively, becoming undetectable after five cycles.
Conclusion: The chromatic alteration and saccharide composition of P. kingianum showed significant correlation with processing duration. Both total color difference (Eab^*) and reducing sugar content stabilized after four processing cycles (12 hours), suggesting that four cycles of steaming and sun-drying may represent the optimal processing duration.

BACKGROUND:Studies have shown that there is a close relationship between pyroptosis,inflammatory factors and osteoporosis.OBJECTIVE:To review the effects of pyroptosis and inflammatory factors on the pathogenesis of osteoporosis from the perspectives of osteogenic differentiation and osteoclastic differentiation,based on an overview of pyroptosis in relation to the interaction of relevant inflammatory factors.METHODS:The first author used the computer to search the literature published by each database until 2024,and searched CNKI,WanFang,VIP and PubMed databases with the search terms of"pyroptosis,inflammatory factors,osteoporosis,osteoblast,osteoclast,bone metabolism,signaling pathway,review"in Chinese and English.A total of 79 papers were finally included according to the inclusion criteria.RESULTS AND CONCLUSION:The progression of osteoporosis is closely related to inflammation,in which pyroptosis plays a key role.Immune cells induce pyroptosis through apoptosis pathway,promote the secretion of inflammatory factors such as interleukin-18,interleukin-1β and NLRP3,build an inflammatory immune microenvironment,and regulate bone metabolism through complex signaling pathways,resulting in enhanced bone absorption and reduced bone formation,thereby leading to osteoporosis.Previous studies have shown that inhibiting pyroptosis is anti-inflammatory and slows the progression of osteoporosis,and it has been shown to improve inflammatory bone loss in vitro and in animal models.At present,research on pyroptosis and osteoporosis is limited.On the one hand,the exact mechanism of osteoporosis and the pathogenesis of pyroptosis are unknown,and the specific pathways and regulatory mechanisms remain to be understood.On the other hand,therapeutic strategies targeting pyroptosis are still theoretical,not clinically proven,and drug side effects are unknown.In the future,the research focus is to further explore the pathogenesis,especially the mechanism of pyroptosis,identify potential therapeutic targets,further study the pyroptosis signaling pathway and Gasdermin protein,and develop new drugs to improve the therapeutic effect in patients with osteoporosis.

BACKGROUND:One of the advantages of clear aligner treatment is molar distalization.However,tooth tilting movement and loss of anterior anchorage may occur during treatment.There are few studies on whether these problems can be improved by selecting clear aligners with different thicknesses and edges to improve the clinical treatment effect.OBJECTIVE:To analyze the control ability of clear aligners with different thickness and edges on the central incisor,lateral incisor,and second molar when pushing the maxillary second molar distally by three-dimensional finite element analysis.METHODS:Three-dimensional finite element analysis models of bilateral maxillary second molar distalization with clear aligner,maxillary dentition,periodontal ligament,and alveolar bone with different thicknesses and margins were established by Mimics,Geomagic Wrap,3-matic and SolidWorks software,respectively.There were 16 combinations of four thicknesses(0.4,0.5,0.625,and 0.75 mm)and four margins(scallop,straight,straight extension 2 mm and straight extension 4 mm).The data were imported into Ansys Workbench software for design and solution.The mean value,peak value and distribution of the periodontal ligament equivalent stress of the second molar,the equivalent stress and the maximum initial displacement of the second molar,and the control ability of each appliance on the second molar,central incisor,and lateral incisor were analyzed.RESULTS AND CONCLUSION:(1)The mean equivalent stress of periodontal ligament of the second molar,the equivalent stress of the second molar and the maximum initial displacement of the second molar increased with the extension of the appliance edge and the increase of the thickness of the appliance in the 16 groups of models.(2)When the thickness of appliances was the same,the maximum equivalent stress of the second molar in the linear appliance group was the highest,and the maximum equivalent stress of the second molar in the linear extended appliance group was greater than that in the scallop appliance group.When the edge of the appliance was the same,the periodontal ligament equivalent stress peak of the second molar increased with the increase of the thickness of the appliance.The equivalent stress distribution in the periodontal ligament of the second molar in the linear extendable appliance group was more uniform than that in the scallop appliance group and the linear appliance group.(3)When the thickness of the appliance was the same,the scallop-shaped appliance had the worst control on the second molar.When the edge of the appliance was the same,with the increase of the thickness of the appliance,the control of the second molar by the linear extender appliance was gradually stronger than that by the linear appliance.The control of the central incisor was stronger and more stable with the linear extended 2 mm appliance,while the control of the lateral incisor was stronger and more stable with the linear appliance.(4)The results showed that when using clear aligners to push molars distally,extending the edge of the appliance could improve the control of the molars and reduce the tilting movement of the teeth.The design of a straight extension margin of 2 mm for the central incisor and a straight edge for the lateral incisor can enhance the control of the anchorage incisor and reduce the labial inclination of the anterior teeth.

Objective: To explore the correlation between Candida albicans and the development of oral leukoplakia (OLK), and to provide a basis for improving the pathogenic mechanism of the malignant transformation of OLK. Methods: Oral microbiome data were obtained from public databases (NCBI BioProject, PRJNA788378; GEO, GSE227919), and bioinformatic methods were employed to evaluate the correlation between Candida albicans infection and OLK. Approval was obtained from the institutional Medical Ethics Committee. A tissue microarray was constructed using samples collected from an OLK clinical cohort. Hematoxylin and eosin (H&E) staining and periodic acid-Schiff (PAS) staining were performed to analyze the relationship between the Candida albicans detection rate and clinicopathological features. Approval was obtained from the institutional Animal Ethics Committee. A mouse model was established by combining 4-nitroquinoline-1-oxide (4NQO) in drinking water with oral inoculation of Candida albicans (4NQO + Candida albicans group), while mice treated with 4NQO in drinking water and PBS served as the control group (4NQO + PBS group). The degree of epithelial dysplasia was compared between the two groups to assess the impact of Candida albicans infection on lesion progression (defined in this study as the progression from mild/moderate epithelial dysplasia to severe dysplasia/carcinoma in situ or invasive squamous cell carcinoma). Results: Bioinformatic analysis revealed that the detection rate of Candida albicans in OPMDs and OLK tissues was significantly higher than that in the healthy control group. Staining results of clinical samples demonstrated that Candida albicans colonized OLK lesions; compared with Candida albicans-negative patients, positive patients exhibited a state of high-grade progression. Animal experiments indicated that, compared with the 4NQO + PBS group, the degree of oral epithelial dysplasia in the 4NQO + Candida albicans group was significantly exacerbated, and the malignant transformation rate was higher, suggesting that Candida albicans promotes the high-grade progression of OLK. Conclusion Candida albicans exhibits a increasing trend during the malignant progression of the OLK. It aggravates the degree of epithelial dysplasia in OLK and promotes its transformation into high-grade lesions, suggesting that Candida albicans plays a crucial promoting role in the high-grade progression of OLK.

ObjectiveTo explore the molecular mechanisms by which serum containing Gegen Qinlian Tang （GQT） inhibits glycolysis and enhances chemotherapy sensitivity in 5-fluorouracil （5-FU）-resistant colorectal cancer （CRC） cells based on the cyclin-dependent kinase 16 （CDK16）/MYC proto-oncogene （MYC） pathway. MethodsHCT-116/5-FU cells were treated with different concentrations （5%， 10%， 20%， 30%） of GQT-containing serum. Cell viability and 5-FU sensitivity were assessed using the cell counting kit-8 （CCK-8） assay， and the experimental concentrations of 5-FU and GQT for subsequent experiments were determined. Cell proliferation and apoptosis under individual 5-FU， GQT， and combined 5-FU + GQT treatments were evaluated using 5-ethynyl-2′-deoxyuridine （EDU） staining and annexin V-FITC/PI double staining， respectively. Glucose consumption， adenosine triphosphate （ATP） production， and lactate levels were measured by colorimetric assays. Expression levels of glycolysis-related proteins， CDK16， MYC， and phosphorylated MYC were detected by Western blot. Co-immunoprecipitation （CoIP） was used to examine the protein interaction between CDK16 and MYC， and cycloheximide （CHX） treatment was applied to assess the effect of CDK16 overexpression on MYC protein stability. ResultsCCK-8 assays showed that 2.5 mg·L^-1 5-FU significantly inhibited HCT-116 cell viability in a dose-dependent manner. In HCT-116/5-FU cells， significant inhibition was observed only at 5 mg·L^-1 5-FU （P<0.05）， which was used for model establishment. Compared with 5-FU alone， addition of 5% GQT-containing serum significantly suppressed HCT-116/5-FU cell viability （P<0.05）， with stronger inhibition at higher serum concentrations. Thus， 5% GQT-containing serum was used in subsequent experiments. Compared with the control group， 5-FU， GQT， and 5-FU + GQT treatments all significantly reduced cell proliferation （P<0.05） and increased apoptosis （P<0.01）. The 5-FU + GQT combination showed superior inhibition of proliferation compared with 5-FU or GQT alone （P<0.01）， accompanied by more pronounced reductions in glucose consumption， ATP production， and lactate generation （P<0.01）. Additionally， compared with control， 5-FU， and GQT groups， the 5-FU + GQT group exhibited stronger suppression of MYC and its phosphorylated forms （P<0.01） and greater inhibition of glycolytic enzymes， including hexokinase 2 （HK2）， 3-phosphoinositide-dependent protein kinase 1 （PDK1）， lactate dehydrogenase A （LDHA）， and pyruvate kinase M2 （PKM2） （P<0.01）. CDK16， MYC， and MYC phosphorylation expression levels were significantly downregulated in the 5-FU + GQT group compared with the 5-FU group （all P<0.01）. MYC protein stability decreased in a time-dependent manner in the 5-FU + GQT group （P<0.05）， which was rescued by CDK16 overexpression （P<0.05）. ConclusionGQT significantly enhances the sensitivity of HCT-116/5-FU cells to 5-FU， potentially by inhibiting CDK16 and thereby reducing MYC-mediated glycolysis.

LIU Wansu， as the foremost of the four great masters of the Jin-Yuan period， established the "theory of fire-heat'' and extended the fire-heat pathogenesis framework to the field of stroke， thereby forming the theory of ''fire-heat inducing stroke''. This achieved a paradigmatic shift in stroke etiology from ''exogenous wind inducing stroke'' to ''fire-heat inducing stroke''. This paper systematically reviews the developmental trajectory of LIU Wansu's ''fire-heat inducing stroke'' theory and explores the social background， academic origins， and core connotations of its theoretical construction. The study found that， based on the ''Nineteen Pathomechanisms'' in the Huangdi's Internal Classic （Huang Di Nei Jing） and combined with clinical practice， LIU Wansu proposed that fire-heat is the fundamental cause of stroke， and that the Six Climatic Factors and the Five Zhi-Emotions can all transform into fire. He further constructed a stratified syndrome differentiation and therapeutic system centered on clearing heat and purging fire， emphasizing differentiated treatment of exterior and interior syndromes， Six Meridians syndrome differentiation， and seasonally adjusted medication. This theory not only resolved the diagnostic and therapeutic dilemmas of febrile epidemic diseases during the Jin-Yuan period， but also exerted a profound influence on later physicians such as ZHANG Zihe and ZHU Danxi， thereby promoting the pluralistic development of stroke theory in traditional Chinese medicine （TCM）. Modern pharmacological research provides solid scientific evidence， confirming that the ''fire-heat'' pathological state is highly associated with key mechanisms such as excessive inflammatory responses， oxidative stress， and excitatory amino acid toxicity following cerebral ischemia. Heat-clearing and fire-purging prescriptions and agents， such as Huanglian Jiedu Tang and baicalin， can exert multi-target neuroprotective effects by regulating inflammatory signaling， enhancing antioxidant enzyme activity， and balancing neurotransmitters. This not only verifies the scientific basis of the ''fire-heat inducing stroke'' theory from a modern biological perspective but also provides conclusive evidence for the clinical application of heat-clearing and fire-purging therapy. LIU Wansu's ''fire-heat inducing stroke'' theory represents a major milestone in the historical understanding of stroke pathogenesis， and its academically transitional insights continue to hold core guiding value for the pattern identification and treatment of ischemic stroke today.