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 探討重組人p53腺病毒(recombinant human p53 adenovirus, rAd-p53)在脊柱轉移瘤的治療中的近期療效。 方法 2006年6月-2009年8月，以經皮注射rAd-p53聯合放療及單獨放療方法治療肺鱗狀細胞癌來源脊柱轉移瘤患者各18例，通過比較兩組治療前后的腫瘤體積變化評價療效，觀察兩組治療后腫瘤細胞壞死率情況，檢測P53蛋白在癌組織中的表達以及血清中抗特異p53基因腺病毒抗體水平。 結果 聯合治療組療效評定有效率為66.7%，高于單獨放療組的27.8%，差異有統計學意義(Plt;0.05)。聯合治療組可見明顯腫瘤細胞壞死、P53蛋白表達陽性及血清中抗特異p53基因腺病毒抗體水平強陽性。 結論 rAd-p53基因治療能抑制腫瘤生長，聯合放療可彌補單一放療的不足，提高放療的敏感性，有效治療脊柱轉移瘤。
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.