Nifedipine-induced gingival overgrowth (NIGO) refers to gingival hyperplasia caused by long-term use of the hypertensive drug nifedipine (NIF), and it is a drug adverse reaction. NIGO is characterized by a high incidence rate and a large patient base, and it is one of the most common types of gingival hyperplasia in clinical practice. Previous studies on the etiology of NIGO mainly focused on the pharmacological effects of NIF, while in recent years, it has been proposed that inflammation may also be a major risk factor for NIGO. Plaque is the initiating factor of periodontal inflammation. However, the role and mechanism of bacteria in the pathogenesis of NIGO remain unclear at present. Therefore, this article reviews relevant research and finds that bacteria may be involved in the pathogenesis of NIGO through the following pathways: ① Hypertensive drugs represented by NIF can cause dysbiosis of the oral flora, increasing the relative abundance of periodontal pathogenic bacteria. The inflammatory chemokines released by fibroblasts in the immune response to bacteria can work in synergy with NIF to promote excessive collagen production or recruit immune cells to participate in tissue fibrosis. ② Transforming growth factor-β (TGF-β) plays a significant role in fibrotic diseases. Bacterial infections can significantly increase the level of TGF-β, promoting epithelial-mesenchymal transition or allowing TGF-β and its downstream substances to directly participate in gingival fibrosis. ③ Bacteria can also cause massive proliferation of gingival fibroblasts, increased collagen synthesis and reduced degradation by activating the Wnt/β-catenin pathway, interfering with integrin α2β1 expression, and inhibiting miR-200 to alter the cell cycle, ultimately exacerbating NIGO. In conclusion, bacteria may be an important factor in aggravating NIGO, and oral health management for patients with hypertension should be given due attention. Future research can focus on the interaction between the oral microbiota and immune cells in NIGO patients, providing new strategies for their prevention and treatment.

ObjectiveTo observe the effect of M1 bone marrow-derived macrophages （M1-BMDM） with Wnt5a knockdown on liver fibrosis and regeneration in a rat model of liver cirrhosis， and to investigate its gain-of-function effect compared with unmodified M1-BMDM. MethodsPrimary bone marrow-derived macrophages were isolated from rats and were polarized to M1 phenotype to construct M1-BMDM^Wnt5a-KD cells. A rat model of liver cirrhosis induced by CCl₄/2-AAF was established， and at the end of week 8， rats were randomly divided into model group， M1-BMDM group， M1-BMDM Wnt5a-knockdown empty vector group （M1-BMDM^KD-EV group）， and M1-BMDM Wnt5a-knockdown group （M1-BMDM^Wnt5a-KD group）， with 6 rats in each group. On the first day of week 9， the rats in each group were given a single injection of the corresponding cells via the caudal vein， along with an intraperitoneal injection of a CCR2 inhibitor. Six rats without any treatment were used as normal control group. Samples were collected at the end of week 12 to assess liver histopathology， serum liver function parameters， hepatic stellate cell activation， and the expression levels of mature hepatocyte markers. A one-way analysis of variance was used for comparison of continuous data between multiple groups， and the least significant difference t-test was used for further comparison between two groups. ResultsCompared with the model group， all cell treatment groups had significant alleviation of liver inflammatory response and significant reductions in the activities of alanine aminotransferase and aspartate aminotransferase （AST） in serum （all P<0.01）， and the M1-BMDM^Wnt5a-KD group had a significantly lower serum level of AST than the M1-BMDM group （P<0.05）. The semi-quantitative analysis based on immunohistochemical staining showed that compared with the model group， all cell treatment groups had a significant reduction in the percentage of CD68-positive area （all P<0.05）， and compared with the M1-BMDM^KD-EV group， the M1-BMDM^Wnt5a-KD group had a significant reduction in the percentage of CD68-positive area and a significant increase in the percentage of CD163-positive area （both P<0.05）. Compared with the model group， all cell treatment groups had significant reductions in the mRNA expression levels of CD68 and tumor necrosis factor-α （all P<0.05） and the protein expression level of CD68 （all P<0.01）； compared with the M1-BMDM^KD-EV group， the M1-BMDM^Wnt5a-KD group had significant increases in the protein and mRNA expression levels of CD163 （both P<0.05）， significant reductions in the protein and mRNA expression levels of CD68 （both P<0.05）， and a significant reduction in the protein expression level of tumor necrosis factor-α （P<0.01）. Sirius Red collagen staining and alpha-smooth muscle actin （α-SMA） immunohistochemical staining showed that compared with the model group， all cell treatment groups had significant alleviation of liver collagen deposition and α-SMA-positive area， with the most significant changes in the M1-BMDM^Wnt5a-KD group， and compared with the M1-BMDM^KD-EV group， the M1-BMDM^Wnt5a-KD group had significantly smaller Sirius Red-positive area and α-SMA-positive area and a significantly lower content of hydroxyproline in liver tissue （all P<0.05）. Compared with the M1-BMDM^KD-EV group， the M1-BMDM^Wnt5a-KD group had significant reductions in the protein and mRNA expression levels of α-SMA and the mRNA expression level of COL-I and TGF-β （all P<0.05）. Compared with the model group， all cell treatment groups had a significant increase in the protein expression level of HNF-4α in liver tissue （all P<0.05）， and the M1-BMDM^Wnt5a-KD group had significantly higher protein and mRNA expression levels of HNF-4α and hepatocyte specific antigen than the M1-BMDM^KD-EV group （both P<0.05）. The M1-BMDM^Wnt5a-KD group had a significantly higher serum level of albumin than the M1-BMDM^KD-EV group （P<0.01）. Immunofluorescence co-staining showed that compared with the model group， all cell treatment groups had a significant increase in the number of cells stained positive for HNF and HNF-4α and Ki67 （all P<0.01）， and the M1-BMDM^Wnt5a-KD group had a significantly higher number of such cells than the M1-BMDM^KD-EV group （P<0.05）. ConclusionInhibition of Wnt5a expression enhances the therapeutic effect of M1-BMDM on rats with liver cirrhosis induced by CCl₄/2-AAF， which provides new ideas for enhancing the anti-cirrhotic effect of M1-BMDM through genetic modification.

Congenital blood group chimerism refers to the coexistence of two or more distinct blood types within an individual, resulting from the presence of hematopoietic cell populations with different genotypes. Consequently, red blood cells in such individuals may express different blood group antigens. Based on the timing and mechanism of formation, blood group chimerism can be classified as either congenital or acquired. Although congenital blood group chimerism is rare and involves complex mechanisms, it holds significant implications in transfusion medicine, transplantation, and obstetrics. This article reviews the formation mechanisms, detection methods, and clinical significance of congenital blood group chimerism in transfusion medicine. Particular emphasis is placed on the principles, advantages, and limitations of various detection techniques. Furthermore, the potential applications of these technologies in clinical diagnosis are discussed, providing a technical foundation for the development of precise transfusion strategies.

Background/Aims: Acetyl coenzyme A (acetyl-CoA) is one of the most essential metabolites in cell metabolism but its function and concentration in hepatocellular carcinoma (HCC) remain elusive and controversial. Methods: A comprehensive analysis of acetyl-CoA levels and acetyl-CoA synthetase 2 (ACSS2) expression across a range of samples, including patient specimens from both hepatitis B virus (HBV) positive and HBV negative HCC individuals, HBV-transgenic mouse HCC models, and multiple cell lines. Furthermore, to evaluate the functional significance of ACSS2 in HBV-related HCC, we implemented both genetic and pharmacological inhibition strategies targeting ACSS2. Molecular mechanism and mitophagy assessment were revealed by cleavage under target and tagmentation sequencing, RNA sequencing, bioinformatic analyses, transmission electron microscopy and JC-1 staining. Results: Our study revealed a distinct metabolic signature of HBV-related HCC, marked by elevated acetyl-CoA, which was driven by ACSS2. ACSS2 was upregulated by the carbohydrate response element-binding protein in HBV-related HCC. Furthermore, ACSS2 improved tumor cell proliferation, an effect that was dependent on its enzymatic activity. Mechanistically, ACSS2-induced acetyl-CoA accumulation activated voltage-dependent anion channels 1 transcription through increased H3K27ac occupancy, which subsequently promoted mitophagy and HBV-related HCC tumorigenesis. Notably, targeting ACSS2 by depletion or inhibition with a catalytic inhibitor significantly suppressed tumor growth. Conclusions These findings not only illustrate the interplay between metabolic reprogramming, epigenetic modification, and tumorigenesis in the context of HBV infection, but also highlight ACSS2 as a novel metabolic vulnerability in HBV-related HCC. Therefore, targeting ACSS2 could be a novel strategy against HBV-related HCC.

ObjectiveTo develop and validate a diagnostic prediction model for differentiating pulmonary tuberculosis from community-acquired pneumonia based on routine blood parameters. MethodsA total of 642 patients with pulmonary tuberculosis and 503 patients with community-acquired pneumonia were retrospectively enrolled from the Seventh Hospital of Tangshan. They were randomly divided into a training set and an internal validation set at a 7∶3 ratio. Additionally， 218 patients from the 981st Hospital were independently included as an external validation set. The Boruta algorithm and recursive feature elimination were employed to select predictors from 82 blood parameters， sex， and age. A multivariate Logistic regression model was established and evaluated using receiver operating characteristic （ROC） curves， calibration curves， and decision curve analysis. ResultsThe final model incorporated eight predictors， namely uric acid， urea nitrogen， alkaline phosphatase， monoamine oxidase， alanine aminotransferase， glutathione， neutrophil percentage， and age. The model achieved areas under the curve （AUCs） of 0.800 （95%CI： 0.769-0.830）， 0.787 （95%CI： 0.738-0.836）， and 0.736 （95%CI： 0.667-0.835） in the training， internal validation， and external validation sets， respectively. The model demonstrated good calibration， and decision curve analysis showed clinical net benefit within the threshold probability range of 10%-80%. ConclusionThe developed model exhibits good discriminative ability and clinical utility， serving as an effective early screening tool for primary healthcare institutions.

ObjectiveTo investigate the in vivo anti-inflammatory effects of the triterpenoid saponin-enriched fraction Fr.B4 from the She medicine Clematis florida (C. florida) in a rat model of phenol-induced cervicitis and to preliminarily explore its potential mechanisms of action. MethodsThirty 6–8-week-old female SPF-grade SD rats were randomly assigned to three groups: control, cervicitis model, and C. florida treatment group, with 10 rats in each group. The model and C. florida treatment groups were induced with cervicitis by vaginal injection of 25% phenol gel (once every 2 d, for a total of three injections), and the vulva and cervix were examined to assess the effectiveness of model establishment. After successful modeling, the C. florida treatment group was administered Fr.B4 at 290 mg/kg daily by gavage (dissolved in normal saline), whereas the model group received an equal volume of normal saline; both treatments continued for 2 weeks. The control group received no modeling procedure and was administered normal saline for 2 weeks. After the last intervention, fresh feces and urine samples were collected from all rats. The rats were euthanized after anesthesia with 40 mg/kg Zoletil 50, and the serum and cervical tissue samples were harvested. ELISA was used to measure the levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6) in rat serum and cervical tissue. Hematoxylin and eosin (HE) staining was performed to observe the pathological changes in cervical tissue. Liquid chromatography-mass spectrometry was employed to analyze differential metabolites in feces and urine, followed by Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment and core metabolite analysis. 16S rDNA sequencing was used to assess the gut microbiota structure and diversity in each group. Statistical analysis was conducted using GraphPad Prism 9.0. ResultsCompared with the control group, rats in the model group exhibited cervical redness, swelling, and erosion, with significant increases in TNF-α, IL-1β, and IL-6 levels in both serum and cervical tissue (P<0.05 or P<0.01). Pathological examination of cervical tissue showed thickening of the squamous epithelium, infiltration of inflammatory cells, and edema. Compared with the model group, rats with C. florida treatment showed marked alleviation of cervicitis symptoms, with significantly reduced levels of pro-inflammatory cytokines in serum and cervical tissue (P<0.05 or P<0.01). Cervical tissue edema was alleviated, inflammatory cells were reduced, and squamous epithelium thickening was ameliorated. Metabolomics analysis revealed 346 and 564 differential metabolites in the feces and urine between the model and control groups, respectively. After treatment with Fr.B4, 236 and 451 metabolites in the feces and urine showed significant shifts toward control levels, involving pathways including cyclic adenosine monophosphate (cAMP) signaling, AMP-activated protein kinase (AMPK) signaling, and glutathione metabolism. Anti-inflammatory metabolites like boswellic acid and oleanolic acid were increased (P<0.01 or P<0.001). Gut microbiota analysis showed dysbiosis in the model group, with an imbalance in the Firmicutes/Bacteroidetes ratio. The Fr.B4 treatment remodeled the gut microbiota. The α-diversity of microbiota shifted toward that of the control group. Specific bacterial genera were found to correlate significantly with metabolites (P<0.05 or P<0.01). ConclusionThe triterpenoid saponin-enriched fraction Fr.B4 from She medicine C. florida may exert anti-cervicitis effects by reducing pro-inflammatory cytokine levels, modulating the gut microbiota balance, and remodeling metabolism.

Objective : To analyze the relationship between tongue volume, tongue position, dental and skeletal parameters in adult patients with different skeletal malocclusions, providing references for the etiology, diagnosis, and treatment of skeletal malocclusions. Methods: This study has been reviewed and approved by the Ethics Committee, and informed consent has been obtained from patients. Cone-beam computed tomography (CBCT) and cephalometric radiographs were collected from 60 adult patients, divided into three groups based on ANB angle values: skeletal Class I (0° < ANB < 4°), II (ANB > 4°), and III (ANB < 0°), with 20 cases in each group. Dental and skeletal parameters were measured using Dolphin software. Mimics software was used for 3D reconstruction of the tongue, oral cavity, and upper airway to measure tongue position, tongue volume, oral cavity volume, and upper airway volume, followed by statistical analysis. Results: The skeletal Class III group had significantly larger tongue and oral cavity volumes than the skeletal Class I and Class II groups (P = 0.02). Tongue length in the skeletal Class III group was also greater than in the skeletal Class I and Class II groups (P = 0.016). There was no significant difference in the ratio of tongue volume/oral cavity capacity among the three skeletal malocclusion groups (P > 0.05). Tongue volume was positively correlated with U1-SN and negatively correlated with overbite and overjet (P < 0.05). Additionally, tongue volume showed a significant positive correlation with Go-Gn and Pg-Np (P < 0.01), as well as with maxillary and mandibular dental arch width and basal bone arch width (P < 0.01). Upper airway volume was positively correlated with TT-VRL and TP-VRL (P < 0.05). Conclusion Patients with skeletal Class III malocclusion have larger tongue volumes and longer tongues. Patients with larger tongue volumes may also have larger, more forward-positioned mandibles. Patients with more posterior tongue positions may have smaller upper airway volumes. When developing orthodontic or orthognathic treatment plans, it is crucial to consider the relationship between tongue position, tongue volume, the jaws, and the airway to ensure optimal outcomes for both dental and orofacial function.

Objective To investigate the molecular mechanism by which salidroside inhibits the proliferation of gastric cancer(GC)cells through upregulation of miR-1343-3p.Methods RNA databases were used to screen for mRNAs associated with tumor proliferation and with miR-1343-3p,and exhibiting significant changes in their expression levels after salidroside treatment of human GC cells.Gene matching and immunoprecipitation of RNA-binding proteins were conducted to analyze the association between miR-1343-3p and SOX18.Immunocytochemistry was performed to determine the localization of SOX18 protein.The effect of salidroside on the proliferation of human GC cells(MGC-803 and AGS)was determined by CCK-8 assay.Human GC cells were divided into a blank control group and low-and high-dose salidroside groups.The expression of miR-1343-3p and SOX18 mRNA was measured by real-time quantitative fluorescence PCR(qPCR).The protein expression of SOX18 was measured by Western blot.GC cells were co-transfected with miR-1343-3p mimic and miR-1343-3p inhibitor,respectively,via LipofectamineTM 2000 liposomes.The expression of miR-1343-3p and SOX18 mRNA was measured by qPCR,and the protein expression of SOX18 was measured by Western blot.Results Through bioinformatic analysis,SOX18 was identified as a downstream target of miR-1343-3p.Gene alignment confirmed the presence of specific binding sites between the two genes,and immunoprecipitation of RNA-binding proteins validated the targeting relationship between them(P<0.05).Immunocytochemistry demonstrated the nuclear localization of SOX18 protein.CCK-8 assay findings demonstrated that salidroside significantly inhibited the proliferation of GC cells in a time-and dose-dependent manner.Compared with the blank control group,salidroside-treated GC cells showed decreased expression of both SOX18 mRNA and protein(P<0.05)and an increased miR-1343-3p expression(P<0.05).Compared with the control group,GC cells in the miR-1343-3p mimic group exhibited increased expression of miR-1343-3p and decreased expression of SOX18 mRNA and protein.In contrast,GC cells in the miR-1343-3p inhibitor group showed decreased expression of miR-1343-3p and increased expression of SOX18 mRNA and protein(all P<0.05).Conclusion Salidroside may inhibit the proliferation of GC cells by regulating the miR-1343-3p/SOX18 signaling axis and these regulators may present new potential therapeutic targets or biomarkers for gastric cancer.

Objective:To compare the differences in clinical characteristics among the patients at clinical high risk for bipolar disorder(CHR-BD),the patients with bipolar disorder(BD),and the healthy controls(HC)at low risk,and to provide the basis for the diognasis and treatment of CHR-BD.Methods:For the first time,the BD risk criteria and prospective structured assessment tools were jointly used in outpatients aged 16-30 years,and 43 CHR-BD patients were included to ensure the accuracy of the assessment.Meanwhile,33 BD patients and 32 HC subjects were also enrolled.The clinical symptoms,neurocognitive function,and global functional levels of the subjects in the three groups were evaluated using observer-rated and self-rated tools.The CHR-BD and BD groups were combined,and Logistic regression analysis was used to identify the independent influencing factors related to diagnostic status;Pearson or Spearman correlation analysis was used to analyze the correlations between the global functional levels and the symptoms or neurocognitive characteristics of the patients in CHR-BD and BD groups.Results:There were statistically significant differences in the scores of symptom and global functional level scales among HC,CHR-BD,and BD groups(P<0.05).Compared with HC group,the scores of mood symptoms(anxiety,depression,and mania/hypomania),psychotic symptoms,total affective temperament questionnaire scores,and some dimensions(cyclothymic,depressive,irritable,and anxious temperaments)in CHR-BD and BD groups were significantly increased(P<0.001),while the global functional levels were significantly decreased(P<0.001).Compared with BD group,the lowest global functional level score in the past year in CHR-BD group was significantly increased(P=0.022),while the current global functional level score was significantly decreased(P=0.005).No significant differences were observed in neurocognitive function scores among the three groups(P>0.05).The lowest global functional level score in the past year was an independent influencing factor for BD diagnosis[odds ratio(OR)=0.952,95%confidence interval(CI):0.917-0.988,P=0.010].In both CHR-BD and BD patients,the current global functional levels were negatively correlated with depressive(r=-0.417,P=0.005;r=-0.617,P<0.001)and anxiety symptoms(r=-0.360,P=0.018;r=-0.506,P=0.003).In BD patients,the current global functional level was negatively correlated with lifetime manic/hypomanic symptoms(r=-0.360,P=0.039),psychotic symptoms(r=-0.502,P=0.003),and affective temperament scores(r=-0.479,P=0.005),while the lowest global functional level in the past year was negatively correlated with lifetime manic/hypomanic symptoms(r=-0.391,P=0.024).Conclusion:CHR-BD patients share similar mood symptom characteristics with BD patients,and their global functional levels are negatively correlated with depressive and anxiety symptoms.BD patients exhibit worse lowest global functional levels in the past year,and their global functional levels are negatively correlated with manic/hypomanic symptoms.

Background The Inner Mongolia Autonomous Region is a vast area with a wide array of ecological environments, resulting in considerable regional variations in air pollution characteristics. Current research is limited by a scarcity of systematic, region-wide studies and risk assessments. Objective To assess the health risks associated with inhalation exposure to nine heavy metal and metalloid elements in atmospheric fine particulate matter (PM_2.5) for the population of the Inner Mongolia Autonomous Region. Methods From the 10th to the 16th of each month throughout 2023, atmospheric PM_2.5 samples were collected at designated monitoring sites in 12 leagues (cities) across the Inner Mongolia Autonomous Region to analyze the characteristics and trends in concentration. The health risk assessment model developed by the United States Environmental Protection Agency was employed to evaluate both the non-carcinogenic and carcinogenic risks associated with the heavy metal elements beryllium (Be), cadmium (Cd), chromium (Cr), hydrargyrum (Hg), plumbum (Pb), manganese (Mn), and nickel (Ni) and the metalloid elements stibium (Sb) and arsenic (As). Results In 2023, a total of 1206 valid PM_2.5 samples were analyzed from the Inner Mongolia Autonomous Region. The annual average PM_2.5 concentrations in Inner Mongolia, as well as in the cities of Ordos, Wuhai, and the Alxa League, all exceeded the national limit of 35 μg·m⁻³. The PM_2.5 concentrations across the leagues (cities) exhibited a clear seasonal variation, peaking in winter, followed by spring, and reaching a minimum in summer and autumn. The median PM_2.5 concentration in Ordos throughout the year was higher than that in the other leagues (cities) of the region. Concerning health risks, the non-carcinogenic risks associated with the 9 elements detected in each league (city) were all below 1, indicating acceptable levels. However, the non-carcinogenic risk values for Mn, Cr, and As were relatively high; specifically, Ordos City displayed the highest non-carcinogenic risk values for Mn (7.74×10⁻¹) and Cr (2.97×10⁻²), while Chifeng City recorded the highest value for As (2.34×10⁻³). The carcinogenic risk values for As, Cd, Cr, and Ni fell within the range of 1×10⁻⁹ to 1×10⁻⁵, representing an acceptable level. The health risks varied with age, and the elderly residents faced the highest non-carcinogenic and carcinogenic health risks. Conclusion While the carcinogenic and non-carcinogenic risks from heavy metals and metalloids within atmospheric PM_2.5 in the Inner Mongolia Autonomous Region are generally within acceptable limits, the potential risks that Mn, As, and Cr pose to the health of elderly people warrants particular attention, and Ordos and Chifeng cities exhibit notably higher health risks among other areas. It is recommended that regular, long-term monitoring be conducted, taking into account the specific conditions at monitoring sites across each league (city), and that targeted air quality management strategies be implemented to protect public health.