Rate of intrusion of maxillary incisors in Class II Div 1 malocclusion using skeletal anchorage device and Connecticut intrusion arch

BackgroundNonsurgical correction of deep bite involves either extrusion of posterior teeth, intrusion of incisors, or combination of both. The introduction of skeletal anchorage device with microimplant provides near absolute anchorage without producing any untoward effects on anchor unit. Connecticut Intrusion Arch (CIA) provided an efficient system of intruding anterior segment without producing much adverse affects on anchor teeth.MethodsThe study comprised of 30 patients of Class II Div 1 malocclusion with overbite of >6 mm and required therapeutic extractions of all first premolars, randomly distributed into two groups. Group 1 was treated using orthodontic microimplants, while Group 2 treated with CIA. Lateral cephalograms were taken pre-intrusion (T1) and post-intrusion at the end of six months (T2).ResultsThe rate of intrusion was 0.51 and 0.34 mm/month for Group 1 and Group 2 respectively. The average amount of change in centroid point to PP distance and U1-SN angle was significantly higher in Group 1 compared to Group 2 (P < 0.001). The average amount of change in U6 to PP distance did not differ significantly between two study groups (P > 0.05).ConclusionThe amount of intrusion is significantly higher in SAD group. Although vertical molar positional change was higher in CIA group than the SAD group, it was not changed significantly in both treatment modalities. SAD group overall had better results and was easier in handling during intrusion.     

什么是合理的医疗卫生体系

医疗卫生体系是一个复杂的体系,医疗卫生体制改革也必然是一个复杂的系统工程。医疗卫生体系由医疗卫生保障体系、医疗卫生服务体系、医疗卫生资源提供体系及医疗卫生监管体系4个紧密相关的子系统构成。一个合理的医疗卫生体系应该是以人民健康为中心,在医疗卫生服务的提供与保障上兼顾公平与效率为原则的。建设合理有效的医疗卫生体系,其关键是抓好体系的能力建设、动力机制建设以及压力机制建设。     

人软骨糖蛋白-39对CIA大鼠淋巴细胞外增殖作用的研究

目的 观察人软骨糖蛋白-39( HCgp39)对胶原诱导型关节炎(CIA)大鼠淋巴细胞激活的影响,探讨其在类风湿关节炎(RA)发病中的作用.方法 建立CIA大鼠模型,分别在建模1、2、3、4、5、6、7、8周后,分离、培养大鼠脾淋巴细胞,CCK-8法检测HCgp39对淋巴细胞增殖的影响,ELISA法检测血浆中抗HCgp39抗体及COMP的分泌水平,分析指标之间相关性.结果 建模2周后,HCgp39抗原特异性T细胞与对照组比较出现明显增殖反应(P均＜0.01),与建模时间、抗HCgp39抗体水平显著正相关,与血管翳和滑膜炎症评分显著负相关.各组抗HCgp39抗体水平和COMP水平较对照组显著增高(P均＜0.01),且抗HCgp39抗体水平与建模时间及COMP呈显著正相关.结论 HCgp39可刺激CIA大鼠脾淋巴细胞的体外异常增殖,初步提示HCgp39抗原短肽在CIA早期及后续的发病过程中可能起着一定作用.     

T cell receptor signaling induced by an analog peptide of type II collagen requires activation of Syk

We have previously described an analog peptide of type II collagen (CII) that can suppress collagen-induced arthritis (CIA). This analog peptide represents CII_245–270, the immunodominant epitope of CII, but with substitutions at 260, 261, and 263 — CII_245–270 (A₂₆₀, B₂₆₁, and N₂₆₃) (A9). To elucidate the mechanisms responsible for suppression, we used mice transgenic for a collagen-specific T cell receptor (TCR). When we found that APCs pulsed with A9 failed to induce T cell phosphorylation of TCR-ζ and ZAP-70, we explored alternative signaling pathways. We determined that A9 instead induced phosphorylation of spleen tyrosine kinase (Syk). The importance of Syk was confirmed by the use of chemical Syk inhibitors, which blocked both cytokine secretion and activation of GATA-3 mediated by peptide A9. In summary, T cells use an alternative pathway in response to A9 that involves Syk. This novel T cell pathway may represent an important means for altering T cell phenotypes.     

uPAR反义RNA质粒对胶原型大鼠滑膜细胞外基质影响的初步研究

目的：初步探讨uPAR反义RNA表达质粒对CIA大鼠滑膜细胞外基质的影响。方法：50只雌性大鼠,其中10只为正常对照组,不做任何处理,其余40只建立Ⅱ型胶原诱导的大鼠类风湿性关节炎模型,分为4组,每组10只,为造模对照组、生理盐水治疗组、空质粒治疗组、重组质粒治疗组,后3组踝关节分别注射生理盐水、空质粒及uPAR反义RNA表达质粒,观察大鼠一般情况、关节炎指数,病理变化及免疫组织化学法检测踝关节滑膜uPAR、MMP-3的表达。结果：随着CIA免疫时间的延长,造模对照组、生理盐水治疗组、空质粒治疗组关节炎指数评分逐渐增加迅速,而重组质粒治疗组关节炎指数评分增加缓慢;与正常对照组比较,模型组大鼠滑膜,滑膜轻度增厚,滑膜新生血管开始增多,大量炎性细胞浸润、增生,免疫组织化学显示：模型对照组、生理盐水组及空质粒组之间无统计学意义（P〉0．05）,模型对照组、生理盐水组、空质粒组与重组质粒治疗组之间差异有统计学意义（P〈0．01）,MMP-3的表达正常大鼠与模型对照组比较,差异有统计学意义（P〈0．05）,模型对照组与重组质粒治疗组之间差异有统计学意义（P〈0．01）。结论：uPAR反义RNA表达质粒能抑制细胞外基质的降解,为类风湿性关节炎的治疗提供理论依据。     

Suppression of the onset and progression of collagen-induced arthritis in rats by QFGJS, a preparation from an anti-arthritic Chinese herbal formula

QFGJS is an herbal preparation, and its pronounced effectiveness in treating adjuvant-induced arthritis (AIA) has been previously demonstrated. We herein aimed to confirm its anti-arthritic effect on collagen-induced arthritis (CIA) in rats. CIA was established in female Wistar rats with intradermal injection of type II bovine collagen at the base of the tail of animals. CIA rats were treated daily with oral administration of different doses of QFGJS beginning on the day of the induction of arthritis (day 0, the prophylactic treatment) or on the day after the onset of arthritis (day 13, the therapeutic treatment) until day 30. The results showed that prophylactic treatment with QFGJS significantly suppressed the onset of arthritis, and therapeutic treatment with QFGJS markedly reduced paw swelling and ESR levels even in the established CIA. Radiologic and histopathologic changes in the arthritic joints were also significantly reduced in the QFGJS-treated versus vehicle-treated rats. Moreover, the serum levels of pro-inflammatory cytokines TNF-alpha, IL-1beta, and IL-6 were markedly lowered in the QFGJS-treated rats. Hence, our studies demonstrate the quality, safety, and effectiveness of QFGJS as an anti-arthritic agent, which makes QFGJS a strong candidate for further clinical trials on rheumatoid arthritis (RA) patients.     

Suppressive effects of Chelidonium majus methanol extract in knee joint, regional lymph nodes, and spleen on collagen-induced arthritis in mice

Chelidonium majus L. has multiple applications in Korean traditional medicine because of its anti-tumoral, cytotoxic, anti-inflammatory and anti-microbial activities and has long been known to have anti-inflammatory effects. However, no study on the anti-arthritic activity of Chelidonium majus has been reported in vivo. Rheumatoid arthritis (RA) is a systemic autoimmune disease with chronic inflammation characterized by hyperplasia of synovial cells in affected joints, which ultimately leads to the destruction of cartilage and bone. Cytokine production and gene expression were assessed during CIA (collagen-induced arthritis) model mice in knee joint, lymph node (LN), and spleen, using ELISA and competitive RT-PCR. DBA/1J mice were immunized with bovine type II collagen. After a second collagen immunization, mice were treated with CME orally at 400, 40mg/kg once a day for 4 weeks. The severity of arthritis within the knee joints was evaluated by histological assessment of cartilage destruction and pannus formation. Administration of CME significantly suppressed the progression of CIA and inhibited the production of TNF-alpha and IL-6 in spleen and lymph node. The erosion of cartilage was dramatically reduced in mouse knees after treatment with CME. In conclusion, our results demonstrates that CME significantly suppressed the progression of CIA and that this action was characterized by the decreased production of TNF-alpha, IL-6, IFN-gamma, B cells, gammadelta T cells (in spleen) and increased proportion of CD4+CD25+ regulatory T cells in vivo. In the serum of CME-treated mice, the levels of IgG and IgM RA factor were decreased.     

蒙药忠伦阿汤对胶原诱导性关节炎大鼠血清炎性细胞因子的影响

目的 探讨蒙药忠伦阿汤对类风湿关节炎(RA)模型大鼠抗Ⅱ型胶原(CⅡ)抗体及白细胞介素1(IL-1)、白细胞介素6(IL-6)、肿瘤坏死因子α(TNF-α)炎性细胞因子的影响.方法 取Wistar大鼠80只,随机选取68只造模,其余12只作为空白组,以牛Ⅱ型胶原皮下注射诱导建立胶原诱导性关节炎(CIA)大鼠模型,再将造模成功的62只大鼠随机分为模型组及忠伦阿汤低、中、高剂量组和雷公藤组各12只,剩余大鼠剔除.忠伦阿汤低、中、高剂量组分别予忠伦阿汤0.35g/kg、0.7g/kg、1.5g/kg,雷公藤组予雷公藤多苷片5mg/kg,空白组和模型组给予等体积生理盐水,各组灌胃给药6周后,采用酶联免疫吸附法(ELISA)测定抗CⅡ抗体、IL-1、IL-6、TNF-α的水平.结果 与空白组比较,模型组血清中抗CⅡ抗体、IL-1、IL-6、TNF-α含量均明显升高(P＜0.01),各药物组均可降低血清抗CⅡ抗体及炎性细胞因子的含量,忠伦阿汤中剂量组、高剂量组与雷公藤组在降低IL-1、IL-6、TNF-α水平方面差异无统计学意义(P＞0.05).结论 蒙药忠伦阿汤可能通过调节免疫,降低血清IL-1、IL-6及TNF-α的含量,减轻炎性细胞因子对关节炎的刺激作用,发挥干预类风湿关节炎的作用.     

阿克他利对Ⅱ型胶原性关节炎小鼠的治疗作用及部分机制研究

 目的 研究阿克他利(Acta)对小鼠Ⅱ型胶原性关节炎(CIA)的治疗作用。方法 采用Ⅱ型胶原(CⅡ)乳剂皮内注射诱导的小鼠CIA模型。在此基础上,检测小鼠足肿胀、免疫功能的改变,以及对CⅡ的迟发性变态反应(DTH)和血清中抗CⅡ抗体的测定,同时进行了病理组织学的检查。结果 Acta(10,30,90 mg·kg^-1)ig对CⅡ诱导的小鼠足肿胀有明显的抑制作用;体外研究发现,Acta(10,30,90 mg·kg^-1)能使CIA小鼠过高的ConA增殖反应和IL-2的产生恢复至接近正常,同时对CIA小鼠过高的IL-1产生有明显的抑制作用;Acta(10,30,90 mg·kg^-1)ig可以明显减轻CⅡ诱发迟发性变态反应(DTH),但Acta对CIA小鼠体内的抗体的产生无显著影响。病理学检查表明,Acta(10,30,90 mg·kg^-1)ig可以减轻CIA小鼠的骨膜增生和软骨破坏。结论 Acta对CIA小鼠具有治疗作用,该作用可能是通过细胞免疫调节实现的。