Ascorbic acid (vitamin C) modulates the mutagenic effects produced by an alkylating agent in vivo

Recent reports suggest that ascorbic acid (vitamin C) inhibits tumorigenesis as well as exerts a protective effect against mutagenesis in vitro; however, there is no information on its ability to affect gene mutations induced in vivo. In this study, we have investigated the antimutagenic effects of ascorbic acid on the frequency of 6-thioguanine-resistant (6-TGr) T-lymphocytes produced in Fischer 344 rats dosed with the direct-acting alkylating agent, N-ethyl-N-nitrosourea (ENU). The freqeuncy of 6-TG^r T-lymphocytes from the spleen measured five weeks after ENU treatment indicated that ENU produced a substantial mutagenic response. Pretreatment and/or post-treatment of rats with ascorbic acid administered in the drinking water appeared to inhibit the response, but the inhibition was statistically significant only when data from the various dosing schedules were pooled. In addition, there was no clear dose-dependency to the inhibitory effect of ascorbic acid. To further evaluate the time effects of the vitamin supplement on ENU mutagenicity, rats were exposed to the mutagen together with ascorbic acid, which was given continuously for the entire duration of the experiment. At specific times after ENU treatment, the frequency of 6-TG^r T-cells was determined in lymphocytes isolated from the spleen and the thymus. Time-dependent increases in the frequency of 6-TG^r T-cells were observed with ENU treatment; ascorbic acid significantly reduced the ENU-mediated mutagenic responses, most dramatically in the spleen at weeks 6 and 8 (P < 0.0001), and to a lesser extent in the thymus (P < 0.01 at week 6 and P < 0.006 at week 8). Our data suggest that ascorbic acid intake affects the in vivo mutagenicity of ENU, a direct-acting mutagen/carcinogen, and that the reported inhibitory effects of the antioxidant on carcinogenesis may be partially mediated by its effects on mutagenesis. Although it is difficult to extrapolate from rodent studies to humans, the results presented suggest an explanation for epidemiological data that link vitamin C ingestion with decreased cancer risk. © 1994 Wiley-Liss, Inc.     

Laparoscopic splenectomy for isolated parenchymal splenic metastasis of ovarian cancer

Metastatic carcinoma of the spleen occurs in a setting of widespread malignant disease. Solitary parenchymal splenic metastasis of ovarian carcinoma is rare. We report a case of a 59-year-old woman who presented with an elevated serum CA125 level due to a solitary splenic metastasis after a long disease-free period. She was treated with laparoscopic splenectomy followed by chemotherapy. The literature contains 16 cases of solitary parenchymal splenic metastasis of ovarian carcinoma. Our case is the third case that was treated with laparoscopic splenectomy. We review the literature, and we focus on the laparoscopic approach in managing these cases.     

CO中毒致迟发性脑病大鼠脑内CD4+T淋巴细胞浸润及神经胶质酸性蛋白的表达

目的观察CO中毒致迟发性脑病（DNS）大鼠脑内CD4^＋T淋巴细胞浸润以及神经胶质酸性蛋白（GFAP）的表达情况，探讨CO中毒致DNS的病理过程。方法25只SD雄性大鼠随机分为对照组、染毒后3、7、10、20d组，每组5只。采用HE和免疫组织化学染色方法，观察染毒后各时间点大鼠脑内病理形态学变化，及CD4^＋T淋巴细胞浸润和GFAP的表达情况。结果HE染色结果显示：各染毒组在大脑皮层及海马均出现神经细胞不同程度的变性、坏死，染毒后7d组最重。免疫组织化学染色结果显示：对照组无CD4^＋T淋巴细胞浸润，有少量GFAP表达；各染毒组不同脑区CD4^＋T淋巴细胞、GFAP均有不同程度的浸润和表达。CD4^＋T淋巴细胞染毒后3d开始浸润，7d达峰值，两者在数量上差异有统计学意义（P〈0．01）。各组染毒后GFAP均有大量表达，随染毒时间延长表达数量呈上升趋势。结论CD4^＋T淋巴细胞可能参与了CO中毒致DNS的免疫病理过程，GFAP阳性细胞对CO中毒引发的DNS可能具有保护作用。     

Laparoscopic management of a ruptured giant epidermoid splenic cyst.

BACKGROUND: Epidermoid splenic cysts are uncommon lesions of the spleen. They are known to become symptomatic as a consequence of enlargement, infection, or rupture, the latter being an exceedingly rare complication traditionally treated with open splenectomy. We herein report a unique case of a giant epidermoid splenic cyst that ruptured spontaneously and was successfully treated with the laparoscopic approach. CONCLUSION: Laparoscopic surgery may be considered an initial treatment option in cases of very large epidermoid cysts even when rupture occurs.     

非控制性出血性休克低压复苏治疗效果的研究

目的　应用大鼠脾损伤非控制性出血性休克模型探讨低压及低压扩容复苏治疗非控制性出血性休克的可行性。方法　雄性Wistar大鼠 5 0只 ,在大鼠脾损伤模型复制成功后随机等分为 5组 ,组 1 :假手术组 ;组 2 :休克未处理组 ;组 3:常压复苏组 (急救期控制MAP在 80mmHg以上 ) ;组 4 :低压复苏组 (急救期控制MAP在 6 0mmHg±5mmHg) ;组 5 :低压扩容复苏组 (急救期输入硝普钠 5 μg·kg- 1 ·min- 1 ,同时输液控制MAP在 6 0mmHg± 5mmHg)。结果　 1～ 5组平均存活时间 (min)分别为 1 80、73.5 0± 8.0 4、1 1 4 .30± 31 .33、1 4 6 .70± 2 8.0 7和 1 71 .6 0± 1 5 .74 ,除组1、组 5外 (P =0 .0 6 71 ) ,其余各组间比较均有统计学意义 (P <0 .0 5 ) ;2～ 5组的急救期出血量 (ml·kg- 1 )分别为 :3.79± 1 .39、1 7.4 1± 8.88、8.6 7± 4 .5 9、1 0 .33± 4 .31 ,其中组 3出血量明显高于其他各组 (P <0 .0 1 ) ;组 4、组 5与组 2比较出血量明显增多 (P <0 .0 5 )。结论　在非控制性出血性休克治疗中 ,低压及低压复合适量硝普钠扩容复苏方法可改善组织代谢 ,提高生存时间 ,是更为理想的复苏方法     

维A酸对T淋巴细胞作用的研究进展

维A酸类药物广泛用于治疗各类皮肤病，且其适应证还在不断扩大。近年来越来越多的证据表明，维A酸具有免疫调节作用。首先，维A酸与皮肤免疫有密不可分的联系，其次，维A酸对机体T淋巴细胞的增殖、凋亡、趋化以及Th1／Th2细胞的极化都产生明显及确实的作用，但是维A酸发挥药理学作用涉及的蛋白调控、细胞因子分泌及信号传导的精确机制目前尚不清楚。     

部分性脾动脉栓塞治疗脾功能亢进

目的探讨脾功能亢进行脾部分栓塞时对门脉压力及外周血液变化的影响。方法对36例脾功能亢进患者,采用Seldinger's法经皮脾动脉超选择性插管造影,计数直径>1mm的脾内动脉血管数。用明胶海绵碎屑(1mm×1mm×1mm)或PVA颗粒实行脾动脉栓塞,栓塞上述血管的60%～80%,并进行1～36个月(平均20个月)临床随访观察对比手术前后门脉压力、血液成分的变化。结果平均门脉压力由4.05kPa降至2.51kPa,外周血液红细胞由2.0×1012/L升至4.20×1012/L,白细胞从3.2×109/L升至5.0×109/L,血小板从40×109/L升至150×109/L。食管静脉曲张引发上消化道出血4例中,术后3例未再出血。结论栓塞程度以脾血管数为计数单位,控制在60%～80%时,可较好地改善脾功能亢进患者外周血象、门静脉压力,减轻食管静脉曲张程度。     

Influence of impaired T- and B-cell compartments on efficacy of IVIg in dysimmune neuropathies

Autoimmune mechanisms are postulated to play a role in the development and progression of dysimmune neuropathies (DN). We investigated the relation between lymphocyte number and marker expression, and disease activity in 20 patients with DN under intravenous immunoglobulins (IVIg) treatment. B- and T-lymphocyte markers were studied by flow cytometry of the expression of CD5, CD25, CD23 and CD38 markers on B cells and of CD3, CD4 and CD8 markers, respectively. These parameters were compared with those obtained from matched healthy volunteers. The proportions of CD38+ B cells were higher in patients compared with those of controls. Proportions of activated CD4+ and CD8+ T cells were comparable in peripheral blood mononuclear cells of patients and controls, but a significant reduction of the absolute numbers of CD3+, CD4+ and CD8+ cells were observed in DN patients. The percentages of CD25+ memory T cells were instead significantly increased in DN patients. Lastly, T-cell reduction and the CD19/CD38 ratio over total B (CD19+) cells directly correlated with a poor response to IVIg therapy. In DN, whereas T-cell number is reduced, activated T and B cells are increased, thus suggesting an intrinsic defect of the immune response.     

Fluidity state of lymphocyte plasma membrane in malignant hyperthermia susceptible pigs and humans

Recent studies suggest that abnormalities occur at the lipid level in malignant hyperthermia susceptible humans and pigs. To test this hypothesis, we first investigated the physical state of plasma membranes of lymphocytes isolated from normal and malignant hyperthermia susceptible swine. In halothane-challenged pigs, malignant hyperthermia susceptibility was also assessed by ryanodine binding assay on purified sarcoplasmic reticulum membranes. The results clearly show that plasma membrane of lymphocytes from malignant hyperthermic pigs are significantly more fluid than controls. We then attempted to apply the same methodology to lymphocytes prepared from human patients previously diagnosed by the halothane and caffeine contracture test. In that case, there was no clear relationship between malignant hyperthermia susceptibility and the fluidity state of lymphocyte plasma membranes.