Microcirculatory effects of experimental acute limb ischaemia-reperfusion.

BACKGROUND: The object of this study was to develop an animal model in which changes in microvascular haemodynamics and leucocyte-vessel wall interactions due to acute limb ischaemia-reperfusion (I/R) can be measured in the skin. Furthermore, it was investigated whether these changes are related to local muscle injury. METHODS: Male Lewis rats were subjected to unilateral limb ischaemia for 1 h (n = 8) or 2 h (n = 8) by cuff inflation, or to a sham protocol (n = 6). Intravital video microscopic measurements of leucocyte-vessel wall interactions, venular diameter, red blood cell velocity and reduced velocity (which is proportional to wall shear rate) were performed in skin venules before ischaemia and at 0.5, 1, 2, 3 and 4 h after the start of reperfusion. Oedema and leucocyte infiltration of ischaemic/reperfused skeletal muscle were quantified histologically. RESULTS: In skin venules, both 1 and 2 h of ischaemia induced a significant increase in leucocyte rolling (six and five times baseline, respectively; P < 0.05) and adherence during reperfusion (eight and four times baseline; P < 0.05). No significant increase in muscular leucocyte infiltration was detected. After an initial hyperaemic response of 180 per cent of baseline values (P < 0.05), blood flow decreased to about 60 per cent after 4 h of reperfusion in skin venules of both experimental groups. I/R induced tibial muscle oedema, the severity of which depended on the ischaemic interval (wet to dry ratio: control, 4.0; 1 h, 4.5 (P not significant); 2 h, 5.8 (P < 0.05)). CONCLUSION: A non-invasive animal model was developed that enables investigation of the consequences of acute limb I/R.     

清热解毒合剂的制备及质控研究

目的：研制清热解毒合剂,探讨制备工艺,研究质量控制标准。方法;研究该制剂的制备及质量控制方法,并做临床疗效观察。结果：制备工艺简单,质量可靠,且临床疗效明显。结论;该制剂制备工艺可行,质量标准可靠,治疗上呼吸道感染效果良好。     

若干莽草酸衍生物的合成和生物活性研究

虽然对莽草酸(shikimic acid)的研究由来已久,但只是在陆续发现了具有生物活性的乙二醛酶Ⅰ抑制剂(glyoxalase Ⅰinhibitor 1)和二(口恶)霉素(dioxolamycin 2)等含莽草酸类母核的天然产物后,才有合成莽草酸衍生物进行生物活性研究的报道,即由莽草酸甲酯合成乙二醛酶Ⅰ抑制剂的类似物3。     

CLONAL PROLIFERATION AND LONG-TERM CULTURE OF MALIGNANT LYMPHOMA CELLS UNDER SERUM-FREE CULTURE CONDITIONS

We developed a serum-free culture system that promoted the growth of B cell colonies in peripheral blood, bone marrow, lymph nodes and cerebrospinal fluid (CSF) from 7 out of 8 patients with non-Hodgkin's lymphomas of B cell type. The culture cells were pretreated with or without galactose oxi-dase (GO) prior to plating. Colony growth was best supported with BCGF. A moderate increment was observed with rIL-3, as well as rIL-1β and even to a lesser degree, by rlL-2, while B cell stimulating factor-2 (rBCSF-2) and rlL-1β did not show significant activity. rGM-CSF and rG-CSF had little effect, while rM-CSF enhanced the formation of lymphoma colonies. The cells from different patients had different requirements for Staphylococcus aureus protein A and GO pretreatment. It reflected the differences in activation and differentiation status and surface properties of lymphoma cells from different patients. The cells from CSF of one patient were successfully maintained in serum-free culture medium supplemented w     

A possible autocrine role for interleukin-6 in two lymphoma cell lines

Interleukin-6 (IL-6) is a growth factor with diverse biologic activity. Originally described as a T-cell product that enhances immunoglobulin (Ig) secretion in antigen-stimulated B cells, it also affects the growth of T cells, plasmacytomas, hybridomas, and hematopoietic stem cells. We report the expression and secretion of IL-6 by two lymphoma cell lines, OCI-LY3 and OCI-LY12. Addition of recombinant IL-6 stimulated their growth, whereas addition of polyclonal anti- recombinant IL-6 (anti-rIL-6) had a marked inhibitory effect on proliferation. These results suggest an autocrine role for IL-6 in the growth of these lymphoma cells in culture.     

白三烯拮抗剂ONO-1078对化学物质诱导大鼠皮肤微血管渗漏的抑制作用

大鼠皮内注射组胺、辣椒素和甲醛诱导皮肤微血管渗漏,白三烯拮抗剂ONO-1078剂量依赖性抑制这一反应,ID₅₀分别为1.98,1.78,2.23mg·kg^-1。与扑尔敏相比,对组胺的作用较弱,对辣椒素和甲醛的作用较强,地塞米松的作用强于ONOl078和扑尔敏。ONO-l078还抑制LTD4的作用,对大剂量组胺、缓激肽和P物质无明显作用。ONO-l078的作用可能与抑制感觉神经肽释放有关。     

A novel mutation L619F in the cardiac Na+ channel SCN5A associated with long-QT syndrome (LQT3): a role for the I-II linker in inactivation gating

Congenital long QT syndrome type 3 (LQT3) is caused by mutations in the gene SCN5A encoding the alpha-subunit of the cardiac Na(+) channel (Nav1.5). Functional studies of SCN5A mutations in the linker between domains III and IV, and more recently the C-terminus, have been shown to alter inactivation gating. Here we report a novel LQT3 mutation, L619F (LF), located in the domain I-II linker. In an infant with prolonged QTc intervals, mutational analysis identified a heterozygous missense mutation (L619F) in the domain I-II linker of the cardiac Na(+) channel. Wild-type (WT) and mutant channels were studied by whole-cell patch-clamp analysis in transiently expressed HEK cells. LF channels increase maintained Na(+) current (0.79 pA/pF for LF; 0.26 pA/pF for WT) during prolonged depolarization. We found a +5.8mV shift in steady state inactivation in LF channels compared to WT (WT, V(1/2)=-64.0 mV; LF, V(1/2)=-58.2 mV). The positive shift of inactivation, without a corresponding shift in activation, increases the overlap window current in LF relative to WT (1.09 vs. 0.58 pA/pF), as measured using a positive voltage ramp protocol (-100 to +50 mV in 2s). The increase in window current, combined with an increase in non-inactivating Na(+) current, may act to prolong the AP plateau and is consistent with the disease phenotype observed in patients. Moreover, the defective inactivation imposed by the L619F mutation implies a role for the I-II linker in the Na(+) channel inactivation process.     

Expression and alterations of different molecular form γ-glutamyl transferase and total RNA concentration during the carcinogenesis of rat hepatoma

ＩＮＴＲＯＤＵＣＴＩＯＮＣａｒｃｉｎｏｇｅｎｅｓｉｓｉｓｃｌｏｓｅｌｙｒｅｌａｔｅｄｗｉｔｈＤＮＡｓｙｎｔｈｅｓｉｓａｎｄｈｙｐｅｒｍｅｔａｂｏｌｉｓｍｏｆｎｕｃｌｅｉｃａｃｉｄ．γｇｌｕｔａｍｙｌｔｒａｎｓｆｅｒａｓｅ（ＧＧＴ,ＥＣ２．３．２．２...     

胃癌相关基因在癌前病变中的表达

目前认为癌的形成过程是多阶段、多过程的,包括多个连续的独立的事件,是多个遗传物质即基因积累改变的结果．与胃癌发生、发展有关的基因有3种：癌基因、抑癌基因、程序死亡基因．原癌基因的激活和抑癌基因的失活可使细胞增生,程序死亡基因的失活可能使细胞永生化,在胃癌的发生、发展的各个阶段,至少有两种以上的基因突变,他们各自发挥不同作用．研究胃癌相关基因在癌前病变中的表达,总结基因改变在癌变过程中的作用和地位．可以从分子水平揭开胃黏膜癌变的本质,进而明确胃癌发生、发展的分子机制．