瘦素及硬脂酰CoA去饱和酶-1在高脂饮食大鼠非酒精性脂肪肝发病中的作用

目的:研究瘦素及SCD-1在高脂饮食引起非酒精性脂肪肝形成及其药物治疗中的作用．方法:42只SD大鼠分成正常组、高脂组和干预组(自高脂饮食喂养8 wk起用罗格列酮进行干预16 wk)．酶联免疫法测定血清瘦素,RT-PCR实时荧光分析大鼠肝 SCD-1 mRNA与β-actin mRNA的比值．结果:肝组织HE染色显示高脂组大鼠肝脏内有弥漫性肝细胞脂肪变性,8 wk达到脂肪肝诊断标准．8,24 wk高脂组大鼠血清瘦素水平升高,与正常组相比有显著性差异(8 wk:5．29±1．83 μg／L vs 3．06±1．35 μg/L, P<0．05;24 wk:7．89±3．01 μg/L vs 3．09±1．52 μg/L, P<0．05);肝SCD-1 mRNA与β-actin mRNA的比值明显下降(8 wk:0．37±0．25 vs 0．82±0．34,P<0．05)．干预组与高脂组相比,血清瘦素水平下降(5．95±3．31 μg/L vs 7．89±3．01 g／L,P>0．05);肝SCD-1 mRNA表达明显增强(SCD-1/β-actin:1．02±0．11 vs 0．52±0．22,P<0．01)．结论:长期高脂饮食可导致血清瘦素水平升高,其通过下调肝SCD-1表达促进非酒精性脂肪肝的形成．罗格列酮可降低血清瘦素水平,上调肝SCD-1的表达,减轻因高脂饮食引起的非酒精性肝脂肪变．     

大鼠重症急性胰腺炎内毒素血症、细胞因子和一氧化氮的变化及善宁的治疗作用

目的:探讨内毒素血症、细胞因子和一氧化氮在重症急性胰腺炎(severe acuce pancreatitis, SAP)发展中的作用及善宁的治疗作用．方法:经胰管逆行注射15 g/L去氧胆酸钠建立SAP模型,给予善宁治疗,观察造模后各时间点血中内毒素(ET)、过氧化脂质(LPO), TNF-α,IL-6,一氧化氮(NO)的变化,并进行相关分析;于24 h后取胰腺组织,测定胰腺组织中LPO,TNF-α,IL-6和NO水平,同时进行相关分析及胰腺组织病理学检查．结果:与对照组比较,SAP组各时间点血浆 ET,LPO,TNF-α,IL-6,NO的水平明显升高 (P<0．01),其中ET,LPO,TNF-α和NO 6 h尤为显著(898±114 EU/L,24．58±1．23 μmol/L, 246．3±16．5 ng／L,162．8±10．9 mmol／L,P< 0．05 vs 12,24 h)．胰腺组织LPO,TNF-α,IL-6, NO的水平SAP组明显高于对照组(3．31±0．85 μmol/g vs 0．33±0．04 μmol/g,P<0．01:2．57± 0．14 ng/g vs 0．16±0．04 ng/g,P<0．01;85．6± 24．6 ng/g vs 32．5±5．7 ng/g,P<0．01;15．3± 1．2 mmol／g vs 6．6±1．4 mmol/g,P<0．01),光镜下胰腺组织病理损害明显．相关分析显示 SAP组血浆LPO,TNF-α,IL-6,NO水平分别与ET水平呈显著正相关(r=0．858,P<0．01:r =0．958,P<0．01;r=0．918,P<0．01;r=0．875, P<0．01)．善宁治疗后上述各指标均较SAP组明显改善(P<0．01)．结论:ET血症、细胞因子、NO等相互激发、相互促进,在SAP的发展中起着重要的协同作用．善宁能阻断这些损伤因子的连锁反应．     

大鼠急性胰腺炎早期肺损伤机制及前列腺素E1的保护作用

目的:探讨实验性急性胰腺炎(acute pancreatitis,AP)合并肺损伤的发生机制及前列腺素E1(PGE1)的保护作用．方法:健康成年SD大鼠78只,随机平均分为假手术组(SO组)、AP组和PGE1组,采用十二指肠闭袢法建立大鼠AP模型．PGE1组制模后即刻经颈静脉持续每分钟输入PGE160 ng／kg．观察胰腺和肺组织的病理组织学改变,测定血清淀粉酶、肺组织中性粒细胞髓过氧化物酶 (MPO)活性、脂质过氧化产物(LPO)水平及肺毛细血管通透性(LCP),免疫组织化学ABC法检测肺组织细胞黏附分子-1(ICAM-1)的表达．结果:制模后12和24 h,AP组大鼠胰腺和肺组织病理损伤持续加重,肺组织MPO(12 h: 5．65±0．80 vs 1．22±0．71 kat／g,P<0．01;24 h: 7．22±1．05 vs 1．48±0．57 kat／g,P<0．01)和 LPO(12 h:1．44±0．63 vs 0.38±0．07μmol／g． P<0．01;24 h:3．64±0．83 vs 0．44±0．15 μmol／ g,P<0．01)水平以及LCP(12 h:145．4±23．0 vs 47．3±5．5 μg／g组织湿重,P<0．01)明显高于SO组,AP组大鼠肺组织ICAM-1表达呈阳性或强阳性,而SO组呈阴性;与AP组比较, PGE1组的胰腺病理损伤虽未减轻,但肺组织 MPO(12 h:2．96±1．04 vs 5．65±0．80 kat／g, P<0．05;24 h:3．68±1．15 vs 7．22±1．05 kat／g, P<0．05)和LPO (12 h:0．86±0.34 vs 1．44± 0．63 μmol／g,P<0．05;24 h:1．69±0．45 vs 3．64 ±0．83 μmol／g,P<0．05)水平以及LCP(12 h: 105．9±23．9 vs 145．4±23．0 μg／g组织湿重, P<0．05)明显降低,ICAM-1表达下调．肺间质出血、水肿和中性粒细胞(PMN)浸润明显减轻．结论:肺组织ICAM-1过度表达、PMN浸润和氧自由基大量释放与AP早期肺损伤的发生关系密切．PGE1通过降低肺组织ICAM-1表达, 抑制PMN活化和氧自由基释放,从而减轻AP 早期肺损伤．     

丹酚酸B对MDA刺激的肝星状细胞增殖的抑制作用

目的:研究丹酚酸B的抗氧化性对大鼠肝星状细胞(HSC)的影响．方法:采用原位灌注法消化大鼠肝脏,108 g／L Nycodenz密度梯度离心,分离肝星状细胞,分别以不同浓度MDA／SAB处理细胞,MTT法观察细胞的增殖能力,2’,7’-二氯二氢荧光素 (DCFH)掺入反映细胞内氧化水平,Western blot检测增殖细胞核抗原(PCNA)蛋白含量, 免疫组化法检测血小板衍生的生长因子受体 (PDGFR)含量．结果:MDA刺激后,细胞增殖明显增强, MTT结果显示,吸光度与对照组相比显著升高(0．253±0．016 vs 0．213±0．004,P<0．05), 而1 μmol／L SAB(0．182±0．006,P<0．01)和 10 μmol／L SAB(0．179±0．006,P<0．01)均可以显著抑制MDA刺激的HSC增殖．Western blot显示,PCNA蛋白在MDA刺激后明显增加(1．72±0．026 vs 1．223±0．025,P<0．01),而 1和10 μmol／L SAB可显著抑制PCNA蛋白表达的升高(分别是1．080±0．040和1．066± 0．025,P<0．01)．MDA可明显刺激细胞PDGF 受体的表达(5．5±0．653 vs 对照组3．3±0．616, P<0．01),提高HSC细胞内氧化水平(荧光强度: 4．721±0．385 vs 对照组2．413±0．662,P<0．01), 10 μmol／L SAB则可抑制PDGF受体的表达(2．723±0．326)和降低细胞内的氧化水平 (3．324±0．264)(P<0．01)．结论:丹酚酸B可通过影响PDGF信号通路而抑制体外培养HSC的增殖,且这种抑制作用与丹酚酸B的抗氧化作用有关．     

黏附分子在沙利度胺所致大鼠肝纤维化中的作用机制

目的:观察沙利度胺对大鼠实验性肝纤维化的治疗效果并探讨其作用机制.方法:四氯化碳腹腔注射制备大鼠肝纤维化模型后,应用沙利度胺(100 mg/kg)ig分别治疗2、4、6 wk作为动态观察时相点.HE染色观察肝组织病理变化,放射免疫法检测血清透明质酸(HA)、层粘连蛋白(LN)、Ⅲ型前胶原(PC Ⅲ)和Ⅳ型胶原(CⅣ)的表达,免疫组织化学法检测细胞间黏附分子-1(ICAM-1)、血管细胞黏附分子-1(VCAM-1)和E-选择素(E-selectin)蛋白质的表达,逆转录聚合酶链反应法检测ICAM-1、VCAM-1和E-selectin mRNA的表达.结果:与肝纤维化组相比,沙利度胺治疗4wk、6 wk能显著降低大鼠肝组织纤维化积分,显著降低血清HA(176.6±7.5 μg/L,173.8±6.7 μg/L vs 486.9±12.4 μg/L)、LN(38.4±5.8 μg/L,34.7±7.3 μg/L vs 84.5±5.2 μg/L)、PC Ⅲ(44.3±5.5 μg/L,40.2±6.1 μg/L vs 65.0±5.6μg/L)、CⅣ(31.8±6.7 μg/L,30.4±5.7 μg/L vs 55.6±6.5 μg/L)的含量(P＜0.05),沙利度胺治疗2 wk 4 wk,6 wk组均可显著降低ICAM-1、VCAM-1和E-selectin蛋白和mRNA的表达(P＜0.05).结论:沙利度胺可通过下调ICAM-1、VCAM-1和E-selectin表达水平而发挥抗肝纤维化作用.     

中药通腑泻热方辅助治疗消化性溃疡急性穿孔并发脓毒症23例

目的:观察本法治疗消化性溃疡急性穿孔并发脓毒症的效果．方法:在常规手术和抗生素治疗基础上,给予中药通腑泻热方治疗本病23例,与常规治疗的 21例作随机对照观察．结果:与对照组比较,治疗组并发症发生率降低(肠梗阻5／23 vs 11／21,P<0．05;MODS: 2／23 vs 7／21,P<0．05),死亡率呈下降趋势,治疗后血浆内毒素(8．7±3．2 kEU／L vs 16．8± 4．5 kEU／L,P<0．01),TNF-α(23.3±8．6 ng／L vs 30．7±8．7 ng／L,P<0．01),IL-6(30．4±13．6 ng／ L vs 51．4±16．2 ng／L,P<0．01),IL-8(20．6± 9．4 ng／L vs 31．7±10．8 ng/L,P<0．01)均显著降低,IL-2(754．8±72．4 ng／L vs 600．8±65．8 ng.L, P<0．01)明显升高．结论:中药通腑泻热方能降低消化性溃疡急性穿孔并发脓毒症患者血中内毒素及促炎细胞因子水平,能提高与机体免疫功能直接相关的细胞因子,防治MODS,降低病死率．     

谷氨酰胺对大鼠肝脏缺血再灌注损伤时肝组织谷胱甘肽含量和Bcl-2、Bax蛋白表达的影响

目的:探讨谷氨酰胺(glutamine,Gln)对大鼠肝脏缺血再灌注损伤(HIRI)时肝组织谷胱甘肽(glutathione,GSH) 含量和细胞凋亡相关基因Bcl-2和Bax蛋白表达的影响．方法:将48只健康♂Wistar大鼠随机分为谷氨酰胺组 (G组)和对照组(C组)．预置中心静脉导管后经此输液通道分别注入谷氨酰胺溶液和生理盐水行预处理 (3 d)．采用Pringle法夹闭肝十二指肠韧带致肝脏缺血 30 min后,去夹恢复血流为再灌注．分别于再灌注后 1、24 h抽血检测ALT的水平,然后快速切取肝组织检测其还原型GSH的含量,切取部分肝组织用于组织病理学检查,并采用S-P免疫组织化学染色方法检测肝组织细胞凋亡相关基Bcl-2和Bax的蛋白表达情况．结果:再灌注后1、24 h,G组血清ALT水平皆显著低于C组(8．3±2．0 μkat／L vs 13．7±5．5 μkat／L,P<0．05; 2．9±2．5 μkat／L vs 9．1±4．3 μkat／L,P<0．01)．肝脏组织GSH的水平:再灌注后1、24 h,G组肝组织GSH水平皆明显高于C组(1216．09±152．78 μg／g vs 856．68± 117．64 μg/g,P<0．01;899．73±57．75 μg/g vs 800．50± 94．79 μg／g,P<0．05)．肝组织损害的病理学改变:G组明显轻于C组．再灌注后1、24 h,G组肝组织Bcl-2蛋白阳性表达率明显高于C组(100．0％ vs 37．5％,P<0．05; 87．5％ vs 25．0％,P<0．05);再灌注后1、24 h,G组肝组织Bax蛋白阳性表达率明显低于C组(25．0％ vs 87．5％,P<0．05;25．0％ vs 87．5％,P<0．05)．结论:Gln对大鼠HIRI具有保护作用,其作用机制可能与维持体内GSH含量和影响肝组织细胞凋亡相关基因 Bcl-2和Bax蛋白的表达有关．     

慢性乙醇中毒所致大鼠肝损伤和肝细胞凋亡

目的:研究肝细胞凋亡在实验性大鼠乙醇性肝病(ALD) 发生、发展中的作用．方法:给大鼠饮用220 g／L的乙醇,并结合540 g／L乙醇分次、少量灌胃的方法建立大鼠肝损伤模型;常规HE 染色,光镜观察大鼠病理学形态改变,用TUNEL法检测肝细胞凋亡,速率法检测血清ALT,AST水平．结果:灌乙醇5 wk大鼠肝脏出现轻到中度脂肪变性,脂滴为以大泡型为主的混合脂滴,脂变率为40％(8／20); 10 wk,85％(17／20)大鼠发生肝脂肪变,45％(9／20)大鼠出现乙醇性肝炎的病理变化．5,10 wk大鼠血清 ALT,AST均较同期对照组有显著升高(5 wk:1017 ±267 VS 550±133,P<0．05;1350±333 vs 967±150, P<0．05;10 wk:1500±267 vs 767±250．P<0．05;2167 ±533 vs 850±183,P<0．05);灌乙醇10 wk血清ALT, AST较5 wk升高(P<0．05),有统计学意义．5,10 wk大鼠 TUNEL指数分别为0．33±0．49％、2．03±1．61％,与同期对照组相比,5 wk无显著差异,10 wk有显著性差异 (P<0．05);灌乙醇10 wk TUNEL指数较5 wk高,有显著性差异(P<0．05)．按病理损伤程度,将实验组分成乙醇性肝炎(AH)组和乙醇性脂肪肝(AFL)组,结果显示AH 组TUNEL指数也较AFL组高(3．24±1．50％ vs 1．12± 0．63％,P<0．05),差异显著．结论:过量饮用乙醇可以引起中毒性肝脏疾病,饮用乙醇及持续时间与肝损伤的发生有密切关系．细胞凋亡在乙醇诱发肝损伤时可能起着重要作用．     

益肝康等活血化瘀中药抑制IL-1β刺激的HSC增殖及TIMP-1的表达

目的:探讨活血化瘀中药益肝康、丹参小复方、丹参对IL-1β刺激的活化的大鼠肝星状细胞(HSCs)增殖及基质金属蛋白酶抑制因子 mRNA(TIMP mRNA)表达的影响．方法:体外培养活化的大鼠HSC,随机分为8 组:对照组(A组)、IL-1β 10 μg/L(B组)、IL- 1β 10μg/L 益肝康2 g/L干预组(C组)、IL- 1β 10 μg/L 丹参小复方2g/L干预组(D组)、 IL-1β 10μg/L 丹参2g/L干预组(E组)、丹参 2 g／L(F组)、丹参小复方2 g/L(G组)、益肝康 2 g／L(H组)．加药后24 h．应用活细胞计数试剂盒-CCK-8检测各组HSC增殖,采用半定量 RT-PCR方法检测各组HSC TIMP-1 mRNA的表达．结果:A组HSC增殖和TIMP-1 mRNA表达强于F、G、H组(1．291±0．09 vs 1．055±0．105, 1±0．07,0．883±0．06,P<0．01:0．591±0．064 vs 0．493±0．088．0．458±0．076．0．356±0．046． P<0．05或P<0．01);H组HSC增殖和TIMP-1 mRNA表达低于F组和G组(P<0．05);B组HSC 增殖和TIMP-1 mRNA表达均明显强于A组 (1．575±0．017 vs 1.291±0,09,P<0．01;1．369± 0．097 vs 0．591±0．064,P<0．01)和C、D、E组 (1．575±0．017 vs 0．906±0．09,1．015±0．081, 1．097±0．038,P<0．01;1．369±0．097 vs 0．694 ±0．078,0．854±0．05,0．898±0．12,P<0．01);C 组HSC增殖和TIMP-1 mRNA表达低于D组和 E组(P<0．05)．结论:益肝康等活血化瘀中药能抑制IL-1β刺激的HSCs增殖及TIMP-1 mRNA表达,发挥其抗肝纤维化功效．益肝康抗肝纤维化作用强于丹参小复方和丹参单药．     

银杏天宝对大鼠实验性结肠炎抗氧化作用的影响

目的:在三硝基苯磺酸灌肠诱导大鼠实验性结肠炎模型中,研究银杏天宝(EGB)的治疗作用及其抗氧化损伤作用的机制.方法:应用三硝基苯磺酸(TNBS)/乙醇灌肠制备大鼠实验性结肠炎模型.实验设正常对照组,三硝基苯磺酸模型组,阳性药物对照组(5-ASA group,100 mg/kg),EGB组(200 mg/kg) 4组.观察大鼠肠组织大体形态和组织学评分.生化法检测大鼠肠组织超氧化物歧化酶(SOD),谷胱苷肽过氧化物酶(GSH-Px)活性及丙二醛(MDA),一氧化氮(NO)含量.免疫组化检测肠组织诱导型一氧化氮合酶(iNOS)蛋白的表达.结果:与模型组相比,EGB组结肠组织iNOS表达明显减少,NO、MDA明显降低(iNOS:19.60%±3.17% vs 81.36%±1.71%;NO:9.20±0.81μmol/g vs 14.77±1.34μmol/g;MDA:3.96±0_35 umol/g vs 6.06±0.39 umol/g;P<0.01):SOD、GSH-Px活性明显升高(SOD:32.52±1.82 kU/g vs 21.90±2.22 kU/g;GSH- Px:49.91±2.59 kU/g vs 41.26±2.90 kU/g;P<0.01).EGB能明显减少大鼠实验性结肠炎模型组大体形态和组织学评分(2.10±0.57vs 3.10±0.57:3.50±0.85 vs 4.7±0.82;P<0.01).结论:EGB可能通过抑制氧自由基反应,抗氧化损伤,抑制NO生成,来减轻结肠炎炎症反应.     

The immunoneuroendocrine role of melatonin

Abstract: A tight, physiological link between the pineal gland and the immune system is emerging from a series of experimental studies. This link might reflect the evolutionary connection between self-recognition and reproduction. Pinealectomy or other experimental methods which inhibit melatonin synthesis and secretion induce a state of immunodepression which is counteracted by melatonin. In general, melatonin seems to have an immunoenhancing effect that is particularly apparent in immunodepressive states. The negative effect of acute stress or immunosuppressive pharmacological treatments on various immune parameters are counteracted by melatonin. It seems important to note that one of the main targets of melatonin is the thymus, i.e., the central organ of the immune system. The clinical use of melatonin as an immunotherapeutic agent seems promising in primary and secondary immunodeficiencies as well as in cancer immunotherapy. The immunoenhancing action of melatonin seems to be mediated by T-helper cell-derived opioid peptides as well as by lymphokines and, perhaps, by pituitary hormones. Melatonin-induced-immuno-opioids (MHO) and lymphokines imply the presence of specific binding sites or melatonin receptors on cells of the immune system. On the other hand, lymphokines such as -γ-interferon and interleukin-2 as well as thymic hormones can modulate the synthesis of melatonin in the pineal gland. The pineal gland might thus be viewed as the crux of a sophisticated immunoneuroendocrine network which functions as an unconscious, diffuse sensory organ.     

Changes in connexin43, the gap junction protein of astrocytes, during development of the rat pineal gland

Abstract: The abundance of gap junctions between rat pineal astrocytes formed by connexin43 (Cx43) was studied during development. Levels and distribution of Cx43 were measured by immunoblotting and indirect immunofluorescence, respectively. The amount of Cx43 in cells located within the gland was low until about the 7th postnatal day and increased to adult values between the 14th and 21st days postpartum. Although astrocytes, recognized by their vimentin immunoreactivity, were scarce before birth, they were abundant by the 7th postnatal day suggesting that the low levels of Cx43 found at this age corresponded to a low expression of this protein. Localization of the immunoreactivity to Cx43 and vimentin showed a close correlation, indicating that mature or immature pineal astrocytes form gap junctions made of Cx43. Since Cx43 levels attained their adult values at about the time the innervation and the functional state of the gland reached maturity (2–3 weeks after birth), it is proposed that astrocyte gap junctions are involved in the function of the adult rat pineal gland.     

Conservative management of perforated duodenal diverticulum： A case report and review of the literature

Duodenal diverticula are a relatively common condition. They are asymptomatic, unless they become complicated, with perforation being the rarest but most severe complication. Surgical treatment is the most frequently performed approach. We report the case of a patient with a perforated duodenal diverticulum, which was diagnosed early and treated conservatively with antibiotics and percutaneous drainage of secondary retroperitoneal abscesses. We suggest this method could be an acceptable option for the management of similar cases, provided that the patient is in good general condition and without septic signs.     

Presence of immunoreactive growth hormone and prolactin in the ovine pineal gland

Abstract: The use of antisera raised against bovine growth hormone (GH) and ovine prolactin (PRL) enabled the detection of related immunoreactive (ir) sequences of proteins in ovine pineal tissue. The isolation of PRL-like ir-material was accomplished using a 0.25 M ammonium sulphate (pH 5.5) extraction followed by ethanol precipitation, whereas the resulting 2.0 M ammonium sulphate (pH 7.0) precipitate contained a GH-like immunoreactivity. Gel chromatography of the GH-like immunoreactivity (Sephadex G-100) indicated the presence of several GH-like fragments ranging in the M_r range of 7,000 to 55,000. Analyses of the PRL-like ir-material found in pineal tissue on HPLC using a TSK 545-DEAE column led to the resolution into a single peak of immunoreactivity. A single peak of activity was also observed following chromatofocusing and hydrophobic interaction chromatography of the ir-peak from the TSK 545-DEAE column. The PRL-like ir-material inhibited the binding of [¹²⁵I]ovine PRL-S14 to anti-ovine PRL antibodies without showing an affinity for binding to anti-rat PRL or anti-bovine GH antibodies. Scatchard analysis of the binding of pineal PRL-like ir-material and pituitary ovine PRL-S14 to liver membranes from day-20 pregnant rats revealed similar affinity constants (K_a of 4.7 ± 0.2 × 10⁹ M^-1). In addition, the replication of Nb 2 Node rat lymphoma cells was stimulated by pineal PRL-like ir-material, an effect known to be specific for lactogenic hormones. The pineal PRL-like immunoreactivity appeared on sodium dodecyl sulfate polyacrylamide gels as a single major band of M_r 24,000. The functional status of PRL-and GH-like ir-material in the ovine pineal remains to be determined, but evidence is presented that the overall protein synthesis rate of the rat pineal responded to circulating concentrations of PRL.     

N-acetyl-L-cysteine combined with mesalamine in the treatment of ulcerative colitis： Randomized,placebo-controlled pilot study

AIM： To evaluate the effectiveness and safety of oral N-acetyl-L-cysteine （NAC） co-administration with mesalamine in ulcerative colitis （UC） patients.
METHODS： Thirty seven patients with mild to moderate UC were randomized to receive a four-wk course of oral mesalamine （2.4 g/d） plus N-acetyl-L-cysteine （0.8 g/d） （group A） or mesalamine plus placebo （group B）. Patients were monitored using the Modified Truelove-Witts Severity Index （MTWSI）. The primary endpoint was clinical remission （MTWSI ≤ 2） at 4 wk. Secondary endpoints were clinical response （defined as a reduction from baseline in the MTWSI of ≥ 2 points） and drug safety. The serum TNF-α, interleukin-6, interleukin-8 and MCP-1 were evaluated at baseline and at 4 wk of treatment. RESULTS： Analysis per-protocol criteria showed clinical remission rates of 63% and 50% after 4 wk treatment with mesalamine plus N-acetyl-L-cysteine （group A） and mesalamine plus placebo （group B） respectively （OR = 1.71; 95% CI： 0.46 to 6.36; P = 0.19; NNT = 7.7）. Analysis of variance （ANOVA） of data indicated a significant reduction of MTWSI in group A （P = 0.046） with respect to basal condition without significant changes in the group B （P = 0.735） during treatment. Clinical responses were 66% （group A） vs 44% （group B） after 4 wk of treatment （OR = 2.5; 95% CI： 0.64 to 9.65; P = 0.11; NNT = 4.5）. Clinical improvement in group A correlated with a decrease of IL-8 and MCP-1. Rates of adverse events did not differ significantly between both groups.
CONCLUSION： In group A （oral NAC combined with mesalamine） contrarily to group B （mesalamine alone）, the clinical improvement correlates with a decrease of chemokines such as MCP-1 and IL-8. NAC addition not produced any side effects.     

Delorme's transrectal excision for internal rectal prolapse

Surgical therapy of functional outlet obstruction in patients with internal rectal intussusception may include abdominal, perineal, or transrectal procedures. Because abdominal procedures often result in significant physiologic impact but unrelieved constipation, the authors have elected Delorme's transrectal excision for management of these patients. Since a short-term placebo effect attends many therapies, this report describes results of transrectal excision only after a threeyear postoperative period. Delorme's transrectal excision of internal intussusception accomplished sustained symptomatic relief in over 70 percent of otherwise refractory constipated patients. The association of internal intussusception with other abnormalities underscores the importance of defining both anatomic and functional components when selecting patients whose constipation may require surgical therapy. Critical technical elements, surgical pitfalls, and potential complications of the procedure are discussed.Poster presentation at the meeting of The American Society of Colon and Rectal Surgeons, Toronto, Canada, June 11 to 16, 1989.     

The oral glucose tolerance test: A comparison of the time points on the basis of limit values,normal dispersion,and reproducibility

Summary Time points in the glucose tolerance test (GTT) are compared on the basis of limit values, dispersion within a reference population, and reproducibility. We suggest using the distance between a limit value and the median reference value as a measure of the magnitude of abnormality. The distance between 140 mg/100 ml and the median fasting plasma glucose value is chosen as a standard distance and limits for other points in the GTT are calculated to equal this standard distance of abnormality. We suggest that the probability of correctly interpreting an inividual result is directly related to the reproducibility of the test and inversely related to the percentage of the total range of values which is dispersed among the normal population. The ratio of reproducibility to percentage normal dispersion is proposed as an index of the probability of correctly interpreting an individual result. According to this index, the probability of correct interpretation varies in order: fasting plasma glucose concentration>3-h>2-h>0.5-h>1-h plasma glucose concentration.