Cerebral amyloid angiopathy (CAA) is an age-dependent disease affecting older subjects. CAA is characterized by lobar intracerebral hemorrhage (ICH), lobar cerebral microbleeds (CMBs), nontraumatic subarachnoid hemorrhage, and cortical superficial siderosis (cSS), which is the main causes of spontaneous intracranial hemorrhage in the elderly. If a patient had experienced dementia, psychiatric symptoms, recurrent or multiple lobar hemorrhage, the possibility of CAA should be considered. Epilepsy can be associated with CAA. Literature studies had found that CAA-related inflammation are predisposing factors for the development of epilepsy. It is a unique subtype of CAA, which is a form of inflammation and a rare clinical manifestation of sporadic CAA. CAA-ri is a special type of central nervous system vasculitis. Once CAA patients had exhibited atypical clinical manifestations, such as headache, epilepsy, behavioral changes, focal neurological signs, consciousness impairment combined with asymmetric T2 weighted magnetic resonance imaging high signal lesions, clinicians had to consider it maybe CAA-ri. Although CAA- ri is rare, timely diagnosis is important because once seizure had occured, which may indicated the inflammation in CAA patients may had reached a very serious level. Therefore, timely identification and treatment are particularly important. Literature shows that most patients responded well to immunosuppressants. Because of its uncommon, researches on epilepsy in CAA mainly focused on case reports currently, and there were many controversies about its pathological mechanism, treatment and prognosis. This article mainly reviews the incidence rate , pathological mechanism, treatment and prognosis of epilepsy in CAA.
目的 探讨重组人p53腺病毒(recombinant human p53 adenovirus, rAd-p53)在脊柱转移瘤的治疗中的近期疗效。 方法 2006年6月-2009年8月，以经皮注射rAd-p53联合放疗及单独放疗方法治疗肺鳞状细胞癌来源脊柱转移瘤患者各18例，通过比较两组治疗前后的肿瘤体积变化评价疗效，观察两组治疗后肿瘤细胞坏死率情况，检测P53蛋白在癌组织中的表达以及血清中抗特异p53基因腺病毒抗体水平。 结果 联合治疗组疗效评定有效率为66.7%，高于单独放疗组的27.8%，差异有统计学意义(Plt;0.05)。联合治疗组可见明显肿瘤细胞坏死、P53蛋白表达阳性及血清中抗特异p53基因腺病毒抗体水平强阳性。 结论 rAd-p53基因治疗能抑制肿瘤生长，联合放疗可弥补单一放疗的不足，提高放疗的敏感性，有效治疗脊柱转移瘤。
Objective To study the effect of signal-selective parathyroid hormone (PTH) analogue peptide on Wnt signal ing factors in osteoblasts isolated from neonatal mouse, and provide theoretical basis for the mechanism of PTH’s function in bone metabolism. Methods Osteoblasts were isolated from calvaria of 2-3-day-old C57BL neonatal mouse and identified by alkal ine phosphatase (ALP) staining, and Alizarin red staining. The cells at passage 1 were divided into 4 groups: control group, PTH (1-34) group, G1R19 (1-34) group, and G1R19 (1-28) group. Then the medium was changed to α-MEM supplemented with 1%FBS. After 12 hours, trifluoroacetic acid or three peptides [(10 nmol/L PTH (1-34), 10 nmol/L G1R19 (1-34), and 100 nmol/L G1R19 (1-28)] were added into the culture medium. After 4 hours, the cells were washed gently ithcold PBS 3 times before total RNA was isolated. The expressions of Wnt related genes were measured by quantitative eal-time PCR. Results Most of the cells were polygonal and triangular; the cells were positive for ALP staining with blue cytoplasm at 14 days and the Al izarin red staining showed the formation of red mineral ized nodules in the special mineral ization induction medium at 28 days. The expressions of osteocalcin mRNA and Wnt5b mRNA in PTH (1-34) group, G1R19 (1-34) group, and G1R19 (1-28) group were significantly higher than those in control group (P lt; 0.05); the expression of Wnt2 mRNA was significantly lower than that in control group (P lt; 0.05); the expression of β-catenin mRNA in PTH (1-34) group was significantly higher than that in control group (P lt; 0.05); the expression of Wnt7b mRNA in PTH (1-34) group and G1R19 (1- 34) group was higher than that in control group, and the G1R19 (1-34) group was higher than PTH (1-34) group and G1R19 (1-28) group (P lt; 0.05). Conclusion In the Wnt-related factors, PTH (1-34) and G1R19 (1-34) affect mainly canonical Wnt signal factors, but the G1R19 (1-28) chiefly acts on non-canonical Wnt signal factors.