Experimental study on the immunosuppressive effects of gui zhi tang

In this paper the immunosuppressive effects of Gui Zhi Tang (a famous Chinese medicine) on the murine immune functions are reported. Varying dosages of Gui Zhi Tang administrated orally, i.p. and i.m. were able to inhibit the amounts of PFC, SRFC and the DTH response induced by BSA and the proliferation response of murine spleen cells to Con A and LPS. Further studies showed that Gui Zhi Tang had the inhibitory effect on Interleukin-2 production of murine spleen cells, which might be one of the mechanisms leading to the immunosuppressive effects of Gui Zhi Tang.     

用Alabama分析法比较安氏Ⅰ类错中国人与美国白人颅颌面结构差异

目的:研究中国安氏Ⅰ类错成人与美国安氏Ⅰ类错白人牙颌颅面形态结构的差异。方法:从西安市11所大学2098名新生中选取符合标准的101名(男53名、女48名)安氏Ⅰ类错样本。拍摄头颅定位X线片,用第四军医大学口腔医学院头影测量软件测量,用Alabama分析法与美国安氏Ⅰ类错白人颅颌面测量结果进行比较分析。结果:中国西安地区安氏Ⅰ类错成人上下颌突度大,面型较突;平面倾斜度、上下中切牙倾斜度及下中切牙至NB线距均较大;Y轴相对SN平面夹角增大,生长方向为后下。结论:与美国安氏Ⅰ类错白人比较,中国西安地区安氏Ⅰ类错成人颅面结构呈现颌骨突度大、下切牙唇倾及下颌趋向后下等特征。     

Atrophic dermatofibroma accompanied by aneurysmatic characteristics

A 40-year-old man presented a painful haemorrhagic plaque on his chest in the same location where a nodular lesion had been presented for many years. After 2 months, the plaque was replaced by a depressed lesion. The lesion diagnosed as an anetoderma was excised and the biopsy showed an atrophic dermatofibroma accompanied by aneurysmatic characteristics.     

Interleukin-18 Affects Local Cytokine Expression But Does Not Impact on the Development of Kidney Allograft Rejection

Interleukin-18 is predominantly a macrophage-derived cytokine with a key role in inflammation and cell-mediated immunity. Having previously demonstrated IL-18 upregulation in a rat model of kidney rejection, here we examined IL-18 in a fully MHC-mismatched murine model of acute kidney rejection using IL-18-deficient recipients (IL-18-/-) and animals administered neutralizing IL-18 binding protein (IL-18BP). Gene expression of IL-18 and its receptor were significantly upregulated in allografts compared to isografts, as was the cellular infiltrate (T cells and macrophages) (p < 0.001). Allografts developed kidney dysfunction (p < 0.05) and tubulitis (p < 0.01) not observed in controls. There was a significant reduction in gene expression of IL-18 downstream pro-inflammatory molecules (iNOS, TNFalpha and IFNgamma) in IL-18-/- recipients (p < 0.01), and IL-18BP-treated animals. The CD4+ infiltrate and IL-4 mRNA expression was greater in the IL-18-/- recipients than wild-type (WT) allografts and IL-18BP-treated animals (p < 0.05), suggesting a Th2-bias which was supported by IFNgamma and IL-4 ELISPOT data and an increased eosinophil accumulation (p < 0.001). Neither IL-18 deficiency nor neutralization prevented renal dysfunction or tubulitis. This study demonstrates increased production of IL-18 in murine kidney allograft rejection and provides evidence that IL-18-induced pathways of inflammation are active. However, neither IL-18 deficiency nor neutralization was protective against the development of allograft rejection.