Background: and Purpose Ruptured intracranial aneurysms (RIA) are associated with a mortality rate of up to 40% in the Chinese population, highlighting the critical need for targeted treatment interventions for at-risk individuals. Although the impact of aldehyde dehydrogenase 2 (ALDH2) gene mutations on susceptibility to intracranial aneurysms (IA) is well documented, the potential connection between ALDH2 rs671 single-nucleotide polymorphism (SNP) and RIA remains unexplored. Given the increased prevalence of ALDH2 gene mutations among Chinese Han individuals, it is clinically relevant to investigate the link between ALDH2 rs671 SNP and IA rupture. Methods: A prospective study was conducted on 546 patients diagnosed with IA to investigate the association between ALDH2 rs671 SNP and the risk of IA rupture. Results: The ALDH2 rs671 SNP (ALDH2*2) was significantly more prevalent in patients with unruptured IA (UIA) than in those with RIA (32.56% vs. 18.58%, P=0.004). Multivariate logistic regression analysis revealed that people with the ALDH2 mutation (ALDH2*1/*2 and ALDH2*2/*2 gene type) had a significantly reduced odds ratio (OR=0.49; 95% confidence level [CI] 0.27–0.88; P=0.018) for RIAs. Age-specific subgroup analysis indicated that the ALDH2 mutation provided a stronger protective effect in individuals aged 60 years and above with IA compared to those under 60 years old (OR=0.38 vs. OR=0.52, both P<0.05). Conclusion The incidence of RIA was significantly higher in individuals with a normal ALDH2 gene (ALDH2*1/*1) than in those with an ALDH2 rs671 SNP (ALDH2*1/*2 or ALDH2*2/*2). ALDH2 rs671 SNP may serve as a protective factor against RIA in the Chinese Han population.

Background: and Purpose Ruptured intracranial aneurysms (RIA) are associated with a mortality rate of up to 40% in the Chinese population, highlighting the critical need for targeted treatment interventions for at-risk individuals. Although the impact of aldehyde dehydrogenase 2 (ALDH2) gene mutations on susceptibility to intracranial aneurysms (IA) is well documented, the potential connection between ALDH2 rs671 single-nucleotide polymorphism (SNP) and RIA remains unexplored. Given the increased prevalence of ALDH2 gene mutations among Chinese Han individuals, it is clinically relevant to investigate the link between ALDH2 rs671 SNP and IA rupture. Methods: A prospective study was conducted on 546 patients diagnosed with IA to investigate the association between ALDH2 rs671 SNP and the risk of IA rupture. Results: The ALDH2 rs671 SNP (ALDH2*2) was significantly more prevalent in patients with unruptured IA (UIA) than in those with RIA (32.56% vs. 18.58%, P=0.004). Multivariate logistic regression analysis revealed that people with the ALDH2 mutation (ALDH2*1/*2 and ALDH2*2/*2 gene type) had a significantly reduced odds ratio (OR=0.49; 95% confidence level [CI] 0.27–0.88; P=0.018) for RIAs. Age-specific subgroup analysis indicated that the ALDH2 mutation provided a stronger protective effect in individuals aged 60 years and above with IA compared to those under 60 years old (OR=0.38 vs. OR=0.52, both P<0.05). Conclusion The incidence of RIA was significantly higher in individuals with a normal ALDH2 gene (ALDH2*1/*1) than in those with an ALDH2 rs671 SNP (ALDH2*1/*2 or ALDH2*2/*2). ALDH2 rs671 SNP may serve as a protective factor against RIA in the Chinese Han population.

Background: and Purpose Ruptured intracranial aneurysms (RIA) are associated with a mortality rate of up to 40% in the Chinese population, highlighting the critical need for targeted treatment interventions for at-risk individuals. Although the impact of aldehyde dehydrogenase 2 (ALDH2) gene mutations on susceptibility to intracranial aneurysms (IA) is well documented, the potential connection between ALDH2 rs671 single-nucleotide polymorphism (SNP) and RIA remains unexplored. Given the increased prevalence of ALDH2 gene mutations among Chinese Han individuals, it is clinically relevant to investigate the link between ALDH2 rs671 SNP and IA rupture. Methods: A prospective study was conducted on 546 patients diagnosed with IA to investigate the association between ALDH2 rs671 SNP and the risk of IA rupture. Results: The ALDH2 rs671 SNP (ALDH2*2) was significantly more prevalent in patients with unruptured IA (UIA) than in those with RIA (32.56% vs. 18.58%, P=0.004). Multivariate logistic regression analysis revealed that people with the ALDH2 mutation (ALDH2*1/*2 and ALDH2*2/*2 gene type) had a significantly reduced odds ratio (OR=0.49; 95% confidence level [CI] 0.27–0.88; P=0.018) for RIAs. Age-specific subgroup analysis indicated that the ALDH2 mutation provided a stronger protective effect in individuals aged 60 years and above with IA compared to those under 60 years old (OR=0.38 vs. OR=0.52, both P<0.05). Conclusion The incidence of RIA was significantly higher in individuals with a normal ALDH2 gene (ALDH2*1/*1) than in those with an ALDH2 rs671 SNP (ALDH2*1/*2 or ALDH2*2/*2). ALDH2 rs671 SNP may serve as a protective factor against RIA in the Chinese Han population.

OBJECTIVES: This study aimed to explore the impact of cell spreading area on odontoblast polarization and differentiation using micropatterned surfaces ge-nerated by photolithography. METHODS: Micropatterned surfaces with differential adhesive properties were prepared using polyethylene glycol diacrylate (PEGDA)-ba-sed photolithography. Human dental pulp stem cells (hD-PSCs) were isolated into single cells and cultured on micropatterned surfaces with areas of 1 800, 2 700, and 3 600 μm². Immunofluorescence staining was used to observe cell morphology and analyze the relocating of the golgi apparatus and nucleus. Alkaline phosphatase staining was preformed to examine odontogenic differentiation. RESULTS: The hDPSCs were successfully isolated and cultured on micropatterned surfaces mimicking the morphology of polarized odontoblasts. Phalloidin staining confirmed that the isolated hDPSCs successfully recapitulated the morphology of predesigned micropatterns. Immunofluorescence staining showed that the polarization and differentiation levels of the hDPSCs with a 3600 μm² area were significantly higher than those with 1 800 and 2 700 μm² areas (P<0.05). CONCLUSIONS The polarization and differentiation of single hDPSCs increased with the cell areas on micropatterned surfaces.
Cell Differentiation ; Humans ; Dental Pulp/cytology* ; Odontoblasts/cytology* ; Stem Cells/cytology* ; Cells, Cultured ; Cell Polarity ; Surface Properties

Objective:To explore the safety and efficacy of Neuroform Atlas stent assisted coil embolization in intracranial wide-necked aneurysms, and analyze the risk factors for procedure-related complications.Methods:A retrospective analysis was performed; the clinical data of 367 patients with 374 intracranial wide-necked aneurysms accepted Neuroform Atlas stent assisted coil embolization from January 2021 to February 2024 were collected. Clinical prognosis, immediate postoperative and 6-12 months postoperative angiography, and procedure-related complications (including perioperative complications and complications during follow-up) were analyzed. Univariate and multivariate Logistic regression analyses were used to identify the independent risk factors for procedure-related complications.Results:Immediate postoperative Raymond-Roy Occlusion Classification (RROC) grading I was noted in 323 aneurysms (86.4%), grading II in 42 aneurysms (11.2%), and grading III in aneurysms (2.4%). Perioperative complications occurred in 26 patients (7.1%): 19 (5.2%) were ischemic complications, while 7 (1.9%) were hemorrhagic complications. A total of 260 aneurysms (69.5%) underwent follow-up angiography, including 229 aneurysms (88.1%) with RROC grading I, 25 aneurysms (9.6%) with grading II and 6 aneurysms (2.3%) with grading III. During the follow-up, 5 patients (1.9%) developed stent stenosis, but only 1 patient had transient ischemic attack, and all of them had boundless vessel occlusion. At the last follow-up, 10 patients (2.7%) had poor prognosis, including 8 (2.2%) with severe disabilities (7 with modified Rankin Scale [mRS] scores of 3 and 1 with mRS scores of 4), and 2 (0.5%) deaths (mRS scores of 6). Multivariate Logistic regression analysis showed that large aneurysms and posterior circulation aneurysms were independent risk factors for procedure-related complications ( OR=6.299, 95% CI: 1.131-35.094, P=0.036; OR=3.654, 95% CI: 1.478-9.035, P=0.005). Conclusion:Neuroform Atlas stent assisted coil embolization in intracranial wide-necked aneurysms is safe and feasible; patients with large aneurysms and posterior circulating aneurysms are more likely to have procedure-related complications.

Background and Objectives: Acute myocardial infarction (AMI) often occurs suddenly and leads to fatal consequences. Ferroptosis is closely related to the progression of AMI.However, the specific mechanism of ferroptosis in AMI remains unclear. Methods: We constructed a cell model of AMI using AC16 cells under oxygen and glucose deprivation (OGD) conditions and a mice model of AMI using the left anterior descending (LAD) ligation. The 3-(4, 5-dimethylthiazol-2-yl)-2, 5 diphenyltetrazolium bromide was employed to determine cell viability. The levels of lactate dehydrogenase, creatine kinase, reactive oxygen species (ROS), glutathione (GSH), malondialdehyde (MDA), and iron were measured using corresponding kits. Dual luciferase reporter gene assay, RNAbinding protein immunoprecipitation, and RNA pull-down were performed to validate the correlations among AC005332.7, miR-331-3p, and cyclin D2 (CCND2). Hematoxylin and eosin staining was employed to evaluate myocardial damage. Results: AC005332.7 and CCND2 were lowly expressed, while miR-331-3p was highly expressed in vivo and in vitro models of AMI. AC005332.7 sufficiency reduced ROS, MDA, iron, and ACSL4 while boosting the GSH and GPX4, indicating that AC005332.7 sufficiency impeded ferroptosis to improve cardiomyocyte injury in AMI. Mechanistically, AC005332.7 interacted with miR-331-3p, and miR-331-3p targeted CCND2. Additionally, miR-331-3p overexpression or CCND2 depletion abolished the suppressive impact of AC005332.7 on ferroptosis in OGD-induced AC16 cells. Moreover, AC005332.7 overexpression suppressed ferroptosis in mice models of AMI. Conclusions AC005332.7 suppressed ferroptosis in OGD-induced AC16 cells and LAD ligation-operated mice through modulating miR-331-3p/CCND2 axis, thereby mitigating the cardiomyocyte injury in AMI, which proposed novel targets for AMI treatment.

Objective:To construct the postgraduate teaching case database of rotation in department of cardiology, and to explore its application effect.Methods:The postgraduate teaching case base of rotation in department of cardiology was constructed during April 2020 to December 2020. A total of 32 graduate students rotating in Department of Cardiology of Affiliated Hospital of Guilin Medical University from January 2021 to April 2021 were selected and randomly divided into two groups. The routine group adopted the traditional teaching method, and the research group applied the teaching case base on this basis, both for one month. The examination results, the changes of clinical practice ability before and after the teaching, and the satisfaction with the teaching mode were compared between the two groups. SPSS 22.0 was used for t test and chi-square test. Results:The final results of the theoretical examination and practical operation examination of the two groups were higher than those of the entrance examination ( P<0.05), and the results of the theoretical examination and practical operation examination of the research group were higher than those of the routine group ( P<0.05). The scores of clinical practice ability of inquiry, case analysis, diagnosis, treatment and follow-up in the two groups after teaching were higher than those before teaching ( P<0.05), and the scores of clinical practice ability in the research group after teaching were higher than those in the routine group ( P<0.05). The satisfaction scores on improving examination results, enhancing clinical practice ability, deepening professional understanding and enhancing professional confidence of the teaching mode of the research group were higher than those of the routine group ( P<0.05). Conclusion:The construction and application of postgraduate teaching case base of cardiology rotation can improve the examination results, enhance the clinical practice ability, and achieve the satisfaction of postgraduates.

Objective To investigate the changes of left ventricular systolic and diastolic function before left ventricular morphologic changes in obstructive sleep apnea syndrome (OSAS) patients.Methods A total of 111 OSAS patients were divided into left ventricular hypertrophy (LVH) group (n=29) and non-LVH group (n=82).Meanwhile,50 healthy subjects were enrolled as normal control group.Routine echocardiography and two-dimensional speckle tracking imaging (2D-STI) were performed.The differences of conventional echocardiography and 2D-STI parameters were compared among the three groups.The correlations between echocardiography and clinical parameters were analyzed.Results Compared with those of the other 2 groups,left ventricular mass index (LVMI),diastolic thickness of interventricular septum (IVST),diastolic ventricular posterior wall thickness (PWT),left ventricular internal diastolic dimension (LVIDd),the ratio between early diastolic peak velocity of mitral valve and early diastolic velocity of mitral annular (E/e') and left atrial volume index (LAVI) increased (all P＜0.05),and mitral annular early diastolic velocity (e') at interventricular septum and lateral wall decreased in LVH group (all P＜0.05).The mitral annular systolic velocity (s') in LVH group was less than that in normal control group (P =0.013).Compared with those of the other 2 groups,left ventricular global longitudinal systolic strain (S) and early diastolic strain rate (SRE) decreased (all P＜0.05),and the ratio of early diastolic peak velocity of mitral valve to SRE (E/SRE) increased in LVH group (both P＜0.05).Compared with normal control group,systolic strain rate (SRS) decreased in LVH group (P=0.001).S,SRS,SRE in non-LVH group were less than those in normal control group (all P＜0.05),and E/SRE was higher than that in normal control group (P＜0.001).S,E/SRE were independently associated with apnea hypopnea index (both P＜0.05).LVMI was independently associated with mean arterial oxygen saturation (β =-0.299,t =-3.273,P =0.001).Conclusion OSAS can affect the structure and functions of left ventricular independently.The systolic and diastolic functions of left ventricular have been impaired before morphology changed.

Objective To investigate the early changes of left atrial structure and function using echocardiography in obstructive sleep apnea syndrome( OSAS) patients with and without left ventricular hypertrophy(LVH) . Methods Echocardiography was performed in 91 OSAS patients (64 without LVH , 27 with LVH) ,and the results were compared with those from age-matched and gender-matched controls ( n=40) . All subjects were examined with two-dimensional speckle tracking echocardiography ( 2D-STE) to obtain the apical four chamber and two chamber left atrium(LA) strain and strain rate curve image .Systolic strain and strain rate( Ss ,SRs) ,early diastolic strain and strain rate( Se ,SRe) ,late diastolic strain and strain rate(Sa ,SRa) were measured . Phasic LA volumes and empty fractions were calculated . The ratio of peak early diastolic mitral inflow and annulus velocity ( E/e′) was used to estimate left ventricular diastolic function . Results Compared with the control group ,LA volume ,LA stiffness index ,SRa and active empyting fraction ( AEF) increased ,Ss ,SRs ,Se ,SRe ,total empyting fraction ( TEF) and passive empyting fraction ( PEF) decreased in none LVH group ( P < 0 .05) . Importantly ,diastolic function was relatively normal in this subgroup without LVH( P > 0 .05) . Diastolic function decreased in LVH group ,and the changes of left atrial structure and function like above mentioned were more significant .The apnea-hypopnea index (AHI) was found to be negatively correlated with Ss ,SRs ,Se ,SRe ,TEF and PEF . Conclusions OSAS is associated with LA remodeling and dysfunction that occurs before the development of LVH and left ventricular diastolic dysfunction ,and it will be further aggravated along with the development of LVH .