右半结肠癌No.206组淋巴结转移的观察研究

目的:分析右半结肠癌No.206组淋巴结转移的规律,为淋巴结的清扫提供临床参考。方法:回顾性收集2015年1月至2019年12月完成的111例右半结肠癌根治术患者的临床资料。观察指标:人口学特征、手术与术后恢复情况、术后病理学检查、随访及生存情况。结果:111例患者中男59例,女52例,中位年龄60岁。肿瘤部位回盲部9例,升结肠37例,结肠肝曲62例,横结肠右侧3例。患者均顺利完成右半结肠癌根治术,其中腹腔镜手术79例,开放手术8例,达芬奇手术24例;腹腔镜手术中1例中转开腹。手术时间110(98,115)min,术中出血量30(20,50)mL,术后肛门排便时间4(3,5)d,术后住院7(6,8)d。术后总并发症发生率9.9%(11/111),其中切口感染、脂肪液化5例,乳糜瘘5例,吻合口出血1例。病理标本肿瘤TNM分期Ⅰ期17例、Ⅱ期44例、Ⅲ期49例、Ⅳ期1例。淋巴结检出27(23,31)枚,阳性淋巴结检出0(0,2)枚,淋巴结转移率为44.14%(49/111)。No.206组淋巴结检出数为3(1,4)枚,阳性淋巴结检出数为0(0,0)枚,淋巴结转移率为0.9%(1/111)。术后102例(91.9%)获得随访,9例失访,随访7~65个月,中位随访时间23个月。5年总生存率86.3%,5年无病生存率73.4%。结论:右半结肠癌No.206组淋巴结转移率较低,如果术前或术中评估怀疑No.206组淋巴结转移或局部进展期肝曲结肠癌,建议清扫No.206组淋巴结。     

血栓闭塞性脉管炎患者血栓素、前列环素及血液流变学指标的检测分析

目的 :探讨血栓闭塞性脉管炎患者血栓素B2 、前列环素与血液流变学指标的变化及其与发病机制的关系。方法 :用放射免疫法测定TXA2 和PGI2 的代谢产物血栓素B2 (TXB2 )、6 酮 前列腺素F1α( 6 K PGF1α) ,LBY N6A自清洗旋转式粘度计测定血液流变学指标 ,并与对照组对比分析。结果 :血栓闭塞性脉管炎患者TXB2 ( 53.59± 83.2 1ng/L)、6 K PGF1α( 14 .50± 3.4 5ng/L) ,与对照组相比差异显著 ;全血高切粘度、低切粘度、血浆粘度及纤维蛋白原疾病组均高于对照组 ,差异具有统计学意义。结论 :血栓闭塞性脉管炎患者存在TXA2 /PGI2失衡 ,并与血液流变学的改变有密切关系     

益气通络方对大鼠短暂性脑缺血后海马DND的保护作用

目的 :探讨益气通络方对大鼠短暂性脑缺血后海马迟发性神经元死亡 (DND)的保护作用及其机制。方法 :用Pulsinelli四血管闭塞法制作全脑缺血模型。实验动物随机分为假手术对照组、脑缺血加生理盐水组和脑缺血加益气通络方组。缺血再灌 3天后进行HE染色、TUNEL染色。结果 :①HE染色 ,光镜下观察CA1区组织病理学变化 ,并用显微测微尺测量CA1区存活锥体细胞密度 (存活锥体细胞的个数 /mm) ,表明益气通络口服液组 ( 1 1 4 .5± 1 9.0 )与生理盐水组 ( 1 0 .5± 3.0 )比较 ,P <0 .0 1。②TUNEL染色 ,光镜下假手术组未见阳性结果 ,缺血再灌流加生理盐水组CA1区大部分锥体神经元发生凋亡 ( 1 2 4 .0± 1 1 .5) ,益气通络方组CA1区凋亡的锥体神经元明显减少 ( 2 4 .5± 3.0 ) ,存活细胞增多。结论 :益气通络方能够显著降低大鼠短暂性脑缺血后海马迟发性神经元死亡 ,抑制细胞凋亡可能是其临床疗效的机制之一。     

中药2号方抗肝纤维化的形态学和血清学实验研究

用猪血清腹腔注射法复制大鼠免疫性肝纤维化模型,用以清热利湿、补气健脾、养血活血为主要治法的中药２号方进行预防和治疗,用光镜观察肝脏ＨＥ、Ｍａｌｏｒｙ染色的变化,用电镜观察肝脏超微结构的变化,并检测了血清生物化学的变化。结果证明中药２号方有明显的改善肝功能和抗肝纤维化的作用     

<伤寒论>栀子豉汤证治剖析

《伤寒论》中以栀子豉汤为代表方的栀子豉汤类方,由于在理论上对其证治缺乏充分的认识,致使在临床上不能如桂枝剂、柴胡剂等经方那样发挥其应有的作用。本文提出栀子豉汤所治主证是热郁胃中所致的“心中懊”而非热扰胸膈的“虚烦”,而“心中懊”实乃胃中嘈杂。并进而分析了从热郁胃中至阳明腑实证与阳明湿热发黄证之间存在的内在病机演变过程,指出栀子豉汤是治疗阳明热证之第一法。     

大承气汤抗急性坏死性胰腺炎肺损伤的实验研究

为研究急性坏死性胰腺炎（ＡＮＰ）早期白细胞粘附强弱和肿瘤坏死因子（ＴＮＦ）的变化及其与肺损伤的关系,以及大承气汤能否减轻肺损伤的程度,将１４ 只家犬随机分成承气汤组（ｎ＝ ５,ＡＮＰ模型＋ 大承气汤治疗）,盐水组（ｎ＝ ５,ＡＮＰ模型＋ 生理盐水治疗）和假手术组（ｎ＝ ４）３ 组。术后在流室系统下观察白细胞与内皮细胞的粘附强弱,并测定血清及支气管肺泡灌洗液（ＢＡＬＦ）ＴＮＦ活性和肺损伤程度。结果显示：实验犬ＡＮＰ时白细胞粘附活性增强,外周血及ＢＡＬＦ中ＴＮＦ活性升高;承气汤组白细胞粘附活性低于盐水组（Ｐ＜ ０．０５）,血清及ＢＡＬＦ的ＴＮＦ活性低于盐水组（Ｐ＜ ０．０１）;承气汤组肺损伤程度轻于盐水组。结果提示：白细胞粘附和ＴＮＦ的过度分泌参与ＡＮＰ病理生理及肺损伤的发生,大承气汤能够减轻二者介导的肺损伤。     

《伤寒论》水气证治论析

就《伤寒论》水气的涵义、致病特点、形成与发病、证治等方面进行了分析和探讨。认为：水气是一个病理概念,具有病理产物和致病因素的双重性,其本质是体内停蓄之水,其致病过程具有动而不居的特点;痰饮、水肿、湿痹皆是水气为患。水气的形成机制是阳虚,阳不制阴。治疗以“温药和之”为常法,振奋阳气以祛除水气;非尽以温药和之为变法,攻逐、清热、滋阴皆在其中。     

口服Ⅱ号避孕药对血小板功能及血液凝固的影响

为了解口服Ⅱ号避孕药对血小板功能及血液凝固性的影响,本文对65名连续服药妇女进行了研究。她们的年龄为27～45(平均36.5)岁。服药期限1～17(平均6.7)年。测定项目有纤维蛋白原,血小板粘附率,血小板聚集率,Ⅷ因子相关抗原,抗凝血酶活力等。20例未服药妇女作对照。测定结果服药组血小板粘附率、聚集率及纤维蛋白原比对照组明显增高(P<0.001)。Ⅷ因子相关抗原略增高,但无统计学意义。抗凝血酶活力显著降低(P<0.001)。本文就急性心肌梗塞及血栓栓塞的潜在可能性等问题进行了讨论,并对预防此类并发症提出了建议。     

HLö 7 dimethanesulfonate,a potent bispyridinium-dioxime against anticholinesterases

HLö 7 dimethanesulfonate (1-[[[4-(aminocarbonyl)pyridinio] methoxy] methyl] -2,4-bis [(hydroxyimino) methyl]pyridinium dimethanesulfonate) is a broad-spectrum reactivator against highly toxic organophosphorus compounds. The compound was synthesized by a new route with the carcinogenic bis(chloromethyl)ether being substituted by the non-mutagenic bis(methylsulfonoxymethyl)ether. The very soluble dimethanesulfonate of obidoxime was also prepared by this way. HLö 7 dimethanesulfonate is the first water-soluble salt of HLö 7 that should be suitable for the wet/dry autoinjector technology, because aqueous solutions of HLö 7 are not very stable (calculated shelf-life 0.2 years when stored at 8°C, 1 M solution, pH 2.5). The crystalline preparation contains 96% of thesyn/syn-isomer, less than 2% of thesyn/anti-isomer and some minor identified by-products. HLö 7 was very efficient in reactivating acetylcholinesterase (AChE) blocked by organophosphates as long as ageing did not prevent dephosphylation. HLö 7 was superior to HI 6 (1-[[[4-(aminocarbonyl)pyridinio]methoxy]methyl]-2-[(hydroxyimino)methyl]pyridinium dichloride) in reactivating soman and sarin-inhibited AChE from erythrocytes, and literature data indicate that HLö 7 exceeds HI 6 by far in reactivating tabun-inhibited AChE. In atropine-protected, soman-poisoned mice HLö 7 was three times more potent than HI 6 (protective ratio 5 versus 2.5), and in sarin-poisoned mice HLö 7 was 10 times more potent than HI 6 (protective ratio 8 for both oximes). In atropine-protected guinea-pigs HLö 7 was less effective than HI 6 (protective ratio: 2.3 versus 5.2 for soman; 5.2 versus 6.8 for sarin; 4.3 versus 3.8 for tabun). The mean survival time of anaesthetized guinea-pigs exposed to 5 LD₅₀ soman (6.3 min) was increased by atropine (27 min) and atropine + HLö 7 (57 min). HLö 7 alone did not prolong the survival. The most impressive effect of HLö 7 was on respiration: 3 min after i.v. injection of HLö 7 and atropine, the depressed respiration increased rapidly to 60% of control and remained at that level during the observation period (60 min). With atropine alone, respiration recovered only slowly. Behavioural and physiologic parameters were determined in atropine-protected mice exposed to a sublethal soman dose. The running performance was significantly improved by HLö 7. Even central symptoms, e.g. hypothermia and convulsions, were decreased markedly by HLö 7 (evaluation 60 min after poisoning). The pharmacokinetic data for HLö 7 in male beagle dogs are similar to those of HI 6. After i.v. injection: t_1/2 = 5 min; t_1/2ß = 46 min; V_D = 0.24 1/kg; Cl_p1 = 3.7 ml x min^–1 x kg^–1; Cl_ren= 3.2 ml x min^–1 x kg^–1; renal excretion of unchanged HLö 7 = 86%. After i. m. injection: t_1/2abs = 14 min; t_1/2ß = 48 min; Vd = 0.27 1/kg; Cl_p1= 3.9 ml x min^–1 x kg^–1; Cl_ren= 2.7 ml x min^–1 x kg^–1; renal excretion of unchanged HLö 7 = 76%; bioavailability >95%. Plasma protein binding was <5%; HLö 7 did not permeate into red cells. A dose of 20 mol/kg was well tolerated both after i.v. and i.m. administration. In anaesthetized dogs (chloralose) HLö 7 i.v. (20 (imol/kg) showed marginal hypotensive effects, whereas 50 mol/kg resulted in decreased mean blood pressure (–15%) and blood flow (–30%) without reflex tachycardia. One out of four dogs developed a circulatory shock syndrome with anuria. Respiration varied only transiently. Blood gases and pH were not influenced. Similar cardiovascular effects were observed in anaesthetized (urethane) guinea-pigs. In isolated guinea-pig hearts (Langendorff) sinus and ventricular heart rate were not influenced by HLö 7 <500 M. HLö 7 antagonized both carbachol and nicotine effects. Red cell AChE was inhibited by HLö 7 by up to 50%; C₅₀ about 100 M. Previously, HLö 7 was shown to block ganglionic transmission (IC₅₀= 500 M), probably due to ion-channel blockade. These data indicate that HLö 7 combines ganglion blocking, anticholinergic and indirect cholinergic properties like other bispyridinium compounds. The results suggest that HLö 7 may be tolerated by man at a dose of 10 mol/kg. Vital functions are not expected to be impaired. At such a dose (250–500 mg), which can be injected by an autoinjector, HLö 7 is expected to be superior to HI 6.Part of thesis     

In situ demonstration of T cell subsets in atrophic parapsoriasis

It has been demonstrated recently in mycosis fungoides and lichen planus that T lymphocyte subsets may be identified in cutaneous lymphocytic infiltrates using the immunoperoxidase technic in conjunction with monoclonal antibodies produced by the technic of Kohler and Milstein. This communication describes the application of this technic to cutaneous lymphoid infiltrates of parapsoriasis in which T cell predominance has been demonstrated previously. The lymphoid infiltrates of six patients with atrophic parapsoriasis were examined by the indirect immunoperoxidase technic using monoclonal antibodies (from two commercial sources) directed against "helper" and "suppressor" T cell subsets. Both "helper" and "suppressor" cells (as defined by a positive reaction with monoclonal antibodies) could be identified in cutaneous infiltrates. "Helper" cells predominated, but in varying degrees among patients. The relevance of these findings in relation to the possible development of clinical mycosis fungoides from atrophic parapsoriasis is discussed. In addition, factors causing difficulty in the consistent identification of cell subtypes are discussed. These factors suggest that in the present state of imperfection, difficulty will be experienced in using this technic for the accurate quantification of percentages of lymphocyte subsets in tissue sections.U