霍山石斛对高脂诱导的LDLR基因敲除小鼠动脉粥样硬化和血管钙化的影响

目的 研究霍山石斛(DH)对高脂食物诱导的雄性低密度脂蛋白受体基因敲除(LDLR－/－)小鼠动脉粥样硬化(As)和血管钙化的影响,并初步探讨其作用机制。方法 LDLR－/－小鼠随机分为对照组和霍山石斛组(DH组)。喂养18周后对小鼠处以安乐死,收集血清、主动脉、肝脏等。分析血清中谷丙转氨酶(ALT)、谷草转氨酶(AST)、碱性磷酸酶(ALP)、总胆固醇(TC)、甘油三酯(TG)、高密度脂蛋白胆固醇(HDLC)和低密度脂蛋白胆固醇(LDLC)的水平;对全主动脉及其根部切片进行油红O染色,检测动脉粥样硬化斑块面积;主动脉根部切片分别做天狼猩红和茜素红S染色,分析斑块稳定性和血管钙化程度;再对肝脏及其冰冻切片进行检测,分析其脂质积累情况。结果 霍山石斛喂食LDLR－/－小鼠18周后,与对照组比较,DH组小鼠血清TG水平下降(P＜0.05),但不影响血清中转氨酶及其他脂质水平。与对照组比较,DH组小鼠全主动脉及主动脉根部的粥样硬化斑块面积均减少约20%(P＜0.05);斑块损伤区域的胶原纤维含量增加约70%(P＜0.05),从而提高斑块的稳定性,且斑块中坏死核心的发生发展也受到明显抑制;对主动脉根部切片的茜素红S染色发现,对照组主动脉根部钙化面积占比1.34%,而DH组主动脉根部钙化面积占比为0.88%,减少了约34%(P＜0.01)。结论 霍山石斛可以抑制动脉粥样硬化和血管钙化的发生发展。     

人主动脉瓣膜钙化过程中Th17/Treg细胞比率的变化

目的研究Th17/Treg细胞是否参与主动脉瓣膜钙化及其与瓣膜钙化发生相关的可能机制。方法人主动脉瓣膜组织分为3组(n=10):(1)对照组:瓣膜来自扩张型心肌病需心脏移植的受体,排除瓣膜组织病理改变者;(2)纤维化组:瓣膜来自严重主动脉瓣膜钙化需瓣膜置换术者,取远离瓣膜钙化部位,纤维化增生组织,排除风湿热及心内膜炎病史者;(3)钙化组:瓣膜来源同纤维化组,取瓣膜明显钙化组织。分别进行von kossa染色、免疫组织化学分析,用于进一步指导瓣膜组织分组;RT-PCR分析,检测瓣膜组织内Th17/Treg细胞浸润情况。结果对照组无Th17/Treg细胞浸润;纤维化组Th17细胞浸润明显高于钙化组(0.904±0.079比0.445±0.057,P<0.01);钙化组Treg细胞浸润明显高于纤维化组(0.900±0.058比0.396±0.032,P<0.01)。结论主动脉瓣膜钙化与纤维化组织中Th17/Treg细胞比率不同,调控Th17/Treg细胞分化趋势或许可以干预主动脉瓣膜钙化进程。     

冠脉旋磨术在冠状动脉钙化病变患者PCI治疗中的应用价值

目的:研究冠脉旋磨术(CRA)在冠状动脉钙化(CAC)病变患者经皮冠状动脉介入(PCI)治疗中的应用价值。方法:2016年6月~2016年12月于我院治疗,且需行PCI治疗的CAC病变患者104例被随机分为旋磨治疗组(52例,接受CRA)和球囊扩张组(52例,接受球囊扩张术),比较两组介入治疗指标、术中并发症发生率及随访1年内主要心血管不良事件(MACE)发生率。结果:两组术前最小管腔直径无显著差异(P=0.304)。与球囊扩张组比较,旋磨治疗组手术时间[(96.29±7.15)min比(72.96±5.76)min]、对比剂用量[(113.25±14.54)ml比(83.27±13.18)ml]、放射线暴露时间[(12.74±1.58)min比(9.07±1.26)min]、术中并发症发生率(26.92%比5.77%)显著降低,支架置入数量[(1.75±0.28)枚比(2.27±0.35)枚]、术后最小管腔直径[(3.15±0.53)mm比(4.31±0.86)mm]、病变残余狭窄<10%率(65.38%比94.23%)、手术即刻成功率(76.92%比98.08%)均显著升高(P均<0.01)。随访期间,旋磨治疗组MACE发生率显著低于球囊扩张组(13.46%比38.46%),P=0.004。结论:CRA能显著提高CAC病变患者PCI治疗手术成功率,降低术中并发症发生率,改善患者预后。     

Association of Epicardial Adipose Tissue With Progression of Coronary Artery Calcification Is More Pronounced in the Early Phase of Atherosclerosis: Results From the Heinz Nixdorf Recall Study

ObjectivesThis study sought to determine whether epicardial adipose tissue (EAT) volume predicts the progression of coronary artery calcification (CAC) score in the general population.BackgroundEAT predicts coronary events and is suggested to influence the development of atherosclerosis.MethodsWe included 3,367 subjects (mean age 59 ± 8 years; 47% male) from the population-based Heinz Nixdorf Recall study without known coronary artery disease at baseline. CAC was quantified from noncontrast cardiac electron beam computed tomography at baseline and after 5 years. EAT was defined as fat volume inside the pericardial sac and was quantified from axial computed tomography images. Association of EAT volume with CAC progression (log[CAC(follow-up) + 1] − log[CAC(baseline) + 1]) was depicted as percent progression of CAC + 1 per SD of EAT.ResultsSubjects with progression of CAC above the median had higher EAT volume than subjects with less CAC change (101.1 ± 47.1 ml vs. 84.4 ± 43.4 ml; p < 0.0001). In regression analysis, 6.3% (95% confidence interval [CI]: 2.3% to 10.4%; p = 0.0019) of progression of CAC + 1 was attributable to 1 SD of EAT, which persisted after adjustment for risk factors (6.1% [95% CI: 1.2% to 11.2%]; p = 0.014). For subjects with a CAC score of >0 to ≤100, progression of CAC + 1 by 20% (95% CI: 11% to 31%; p < 0.0001) was attributable to 1 SD of EAT. Effect sizes decreased with CAC at baseline, with no relevant link for subjects with a CAC score ≥400 (0.2% [95% CI: −3.5% to 4.2%]; p = 0.9). Likewise, subjects age <55 years at baseline showed the strongest association of EAT with CAC progression (20.6% [95% CI: 9.7% to 32.5%]; p < 0.0001). Interestingly, the effect of EAT on CAC progression was more pronounced in subjects with low body mass index (BMI), and decreased with degree of adiposity (BMI ≤25 kg/m²: 19.8% [95% CI: 9.2% to 31.4%]; p = 0.0001, BMI >40 kg/m²: 0.8% [95% CI: −26.7% to 38.9%]; p = 0.96).ConclusionsEAT is associated with the progression of CAC, especially in young subjects and subjects with low CAC score, suggesting that EAT may promote early atherosclerosis development.     

Coronary Artery Calcification and Family History of Myocardial Infarction in the Dallas Heart Study

ObjectivesThis study aimed to investigate the independent and joint associations between family history of myocardial infarction (FH) and coronary artery calcification (CAC) with incident coronary heart disease (CHD).BackgroundFH and CAC are associated with each other and with incident CHD. It is not known whether FH retains its predictive value after CAC results are accounted for.MethodsAmong 2,390 participants without cardiovascular disease enrolled in the Dallas Heart Study, we assessed FH (myocardial infarction in a first-degree relative) and prevalent CAC by electron-beam computed tomography. The primary outcome, a composite of CHD-related death, myocardial infarction, and percutaneous or surgical coronary revascularization, was assessed over a mean follow-up of 8.0 ± 1.2 years. The individual and joint associations with the CHD composite outcome were determined for FH and CAC.ResultsThe mean age of the population was 44 ± 9 years; 32% had FH and 47% had a CAC score of 0. In multivariate models adjusted for traditional risk factors, FH was independently associated with CHD (adjusted hazard ratio: 2.6; 95% confidence interval: 1.6 to 4.2; p < 0.001). Further adjustment for prevalent CAC did not diminish this association (adjusted hazard ratio: 2.6; 95% confidence interval: 1.6 to 4.2; p < 0.001). FH and CAC were additive: CHD event rates in those with both FH and CAC were 8.8% vs. 3.3% in those with prevalent CAC alone (p < 0.001). CHD rates were 1.9% in those with FH alone compared with 0.4% in those with neither FH nor CAC (p < 0.017). Among subjects without CAC, FH characterized a group with a more unfavorable cardiometabolic profile.ConclusionsFH provided prognostic information that was independent of and additive to CAC. Among those with CAC, FH identified subjects at particularly high short-term risk, and, among those without it, selected a group with an adverse risk-factor profile.     

肾元颗粒对db/db糖尿病肾病小鼠血管钙化的改善作用及其机制

目的：通过高磷诱导db/db糖尿病肾病（DN）小鼠血管钙化,探讨肾元颗粒对db/db DN小鼠血管钙化的改善作用及其可能机制。方法：将20只SPF级db/db小鼠随机分为模型组和肾元颗粒组（n=10）,同系背景野生型（WT）小鼠作为空白组（n=10）。给药12周后,取各组小鼠血清、肾脏和胸主动脉组织。ELISA法检测各组小鼠血清FGF23水平,HE和von Kossa法检测各组小鼠胸主动脉病理形态表现以及钙盐沉积情况,实时荧光定量PCR （Real-time PCR）法检测各组小鼠肾脏组织中KlothomRNA和胸主动脉组织中Pit-1、Runx2及SM22α mRNA表达水平,Western blotting法检测各组小鼠肾脏组织中Klotho蛋白和胸主动脉组织中Pit-1、Runx2及SM22α蛋白表达水平,免疫组织化学法检测各组小鼠胸主动脉组织中Pit-1蛋白表达水平,免疫荧光法检测各组小鼠胸主动脉组织中SM22α和Runx2蛋白表达水平。结果：与空白组比较,模型组小鼠血清FGF23水平明显升高（P<0.05）,肾脏组织中Klotho mRNA和蛋白表达水平明显降低（P<0.01）,胸主动脉组织中Pit-1和Runx2 mRNA及蛋白表达水平明显升高（P<0.01）,SM22α mRNA和蛋白表达水平明显降低（P<0.01）,胸主动脉组织中Pit-1和Runx2蛋白表达水平明显升高（P<0.01）,SM22α蛋白表达水平明显降低（P<0.01）。与模型组比较,肾元颗粒组小鼠血清FGF23水平降低（P<0.05）,肾脏组织中Klotho mRNA和蛋白表达水平明显升高（P<0.01）,胸主动脉组织中Pit-1和Runx2 mRNA及蛋白表达水平明显降低（P<0.01）,胸主动脉组织中SM22α mRNA和蛋白表达水平明显升高（P<0.01）。结论：肾元颗粒可通过上调小鼠肾脏组织中Klotho蛋白表达水平,减少Pit-1表达水平,抑制FGF23/Pit-1信号通路,调节血管平滑肌细胞（VSMC）的表型转化,达到血管保护作用。     

司维拉姆联合依帕司他治疗糖尿病肾病的临床效果

目的 司维拉姆联合依帕司他治疗糖尿病肾病的临床效果。方法 选择2013年1月-2015年12月榆林市第二医院收治的83例糖尿病肾病患者,随机分为两组。两组均采取血液透析治疗,对照组口服依帕司他治疗,每次50 mg,每天3次;观察组在对照组基础上联合服用司维拉姆治疗。两组均治疗3个月。检测两组治疗前后的炎性指标、脂代谢指标、血钙和血磷,并进行2年的随访。结果 观察组治疗后的肿瘤坏死因子-α（TNF-α）、白细胞介素-6（IL-6）、C反应蛋白（CRP）、低密度脂蛋白胆固醇（LDL-C）、总胆固醇（TC）、三酰甘油（TG）、甲状旁腺激素（iPTH）和血磷明显低于治疗前,同组治疗前后比较差异有统计学意义（P<0.05）;对照组治疗前后的各临床检测指标相比均无明显的差异;观察组的冠状动脉钙化率明显低于对照组,差异有统计学意义（P<0.05）。两组的2年生存率以及心血管事件病死率相比均无明显的差异。结论 司维拉姆联合依帕司他可以有效抑制糖尿病肾病患者的炎症反应,调节血脂水平,改善血管钙化情况,降低冠状动脉钙化发生率,有助于改善患者的预后。     

Investigation of the incidence of stylohyoid ligament calcifications with panoramic radiographs

Aim: This study examined and classified patients who were treated at the Faculty of Dentistry at Ankara University Dentistry to determine the incidence of different types of stylohyoid ligament calcification (SLC) using panoramic radiographs. In addition, it also assessed the possible causative symptoms and Eagle’s syndrome in cases of styloid process elongation. Methods: The study consisted of 2000 patients (1161 females and 839 males), aged 3–88 years, who were treated at our clinic. The panoramic radiographs were evaluated as part of this study. Results: Panoramic radiography examination revealed SLC in 1350 patients. Both‐sided (right and left), type 1 SLC was observed in 345 patients, while types 2–4 were found in 203, 418, and 384 patients, respectively. Conclusion: The incidence of SLC was found to be higher in female patients when compared to male patients. In addition, calcifications were seen more often at age 50–59 years, and the incidence of calcification was found to increase with age. Two Eagle’s syndrome cases were diagnosed among a total of 2000 patients. Finally, it was determined that the incidence of calcified stylohyoid ligament is higher in patients with systemic diseases.     

A young-onset frontal dementia with dramatic calcifications due to a novel CSF1R mutation

ABSTRACT

Neuroimaging and genomic analysis greatly aid in the identification of young-onset dementia antemortem. We present the case of a 33-year-old female with a 2-year rapid decline to dementia and immobility marked by personality change, executive deficits including compulsions, attention deficit, apraxia, Parkinsonism, and pyramidal signs. She had unique and dramatic calcifications and confluent white matter changes on imaging and was found to have a novel mutation in the colony stimulating factor 1 receptor gene causing adult-onset leukoencephalopathy with axonal spheroids and pigmented glia (ALSP). Here, we review ALSP and briefly discuss differential diagnoses.