基于声卡的肠鸣音采集系统的开发

肠鸣音是肠生理状态的反映,在临床急腹症的诊断中具有重要的意义,为了深入研究肠鸣音的产生机理,研制一个利用计算机集成声卡实现肠鸣音采样、在LabVIEW环境下开发的肠鸣音采集系统,它可以实现肠鸣音的实时采集,显示和二进制存储,为探索肠鸣音发生机理提供了详实的临床数据,同时也为搭建生理信号采集系统提供了便捷可行的解决方案。     

肠鸣音的采集与分析

本文介绍了对肠鸣音的采集与分析，由高灵敏度肠鸣音检测电路和微机可对肠鸣音进行灵敏，快速，方便的采集和时，频域定量分析，并精确，完整地显示，记录，存储分析结果，本文对几种肠鸣音的分析方法进行了讨论，并通过临床实验对肠鸣音的特点做出了总结。     

人体肠鸣音的记录和分析

作者介绍了利用仪器真实记录肠鸣音和分析肠鸣音的方法,并首次将控制论中的多相信息处理方法应用于肠鸣音信号分析中.通过对部分病例的记录分析,初步发现某些具有病理意义的结果,证明了肠鸣音临床诊断分析的可行性,为今后开展肠鸣音分析研究打下了基础.     

ICA在肠鸣音信号处理中的应用研究

目的:肠鸣音的去噪及时域特征提取.方法:本文首先分析了独立分量分析的基本原理,研究了FastICA算法,并给出了此算法的具体实现步骤.然后利用该方法对肠鸣音进行了处理,并用归一化平均香农能量分布提取了肠鸣音的时域特征.结果:上述方法有效地去除了肠鸣音信号中的噪声,发现正常音与异常音的时域特征存在典型差异.结论:肠呜音的检测和处理在胃肠道疾病的诊断治疗中具有重要的价值,实验结果可以看出独立分量分析在肠鸣音信号处理中是非常有效的.     

肠鸣音信号的自适应滤波及其特征提取方法研究

目的:肠鸣音的去噪和特征提取.方法:文中首先采用自适应干扰对消去除肠呜音中混叠的环境噪声,然后运用小波分析、归一化香农能量分布、功率谱密度估计等多种方法,从多个角度对肠鸣音进行分析处理,这些方法都致力于肠鸣音的特征提取和识别分类.结果:通过定性和定量分析,几种不同类型的肠鸣的特征值存在典型差异.结论:肠鸣音的检测和分析在胃肠道疾病的诊断治疗中具有重要的价值,利用上述方法能有效区分不同类型的肠鸣音,有助于肠道疾病的辅助诊断.     

穴位按摩配合耳穴压豆在改善肠息肉内镜下切除术后腹胀中的应用效果分析

目的:探究穴位按摩联合耳穴压豆对肠息肉内镜下切除术后腹胀患者的应用效果.方法:选取我科2019年3月至2021年3月期间收治的107例接受肠息肉内镜下切除术的患者作为研究对象,根据随机数字表法分为对照组(n=53)和观察组(n=54).对照组采用耳穴压豆法,观察组在对照组基础上增加穴位按摩,对比两组患者肠鸣音、腹胀缓解程、胃肠激素水平.结果:观察组术后1 h、术后2 h每分钟肠鸣音次数、腹胀程度、肠鸣音恢复时间、首次排气时间、腹胀完全缓解时间均低于对照组,胃泌素、胃动素、血管活性肠肽(Vasoactive intestinal peptide,VIP)水平均高于对照组(P<0.05).结论:对肠息肉内镜下切除术后患者行穴位按摩配合耳穴压豆干预,可有效改善降低患者腹胀程度,促进肠鸣音消失和肠道功能恢复.     

李氏忒菌病一例

李氏忒菌病一例陈光华，何坚娘患儿男婴，１个月，因发热、咳嗽、呕吐及腹泻４天于１９９１年８月１８日入院。入院时体温４０℃，热型不规则。双肺满布湿性音，肝肋下２ｃｍ，肠鸣音减弱。白细胞４．６×１０￣９／Ｌ，中性６３％，淋巴３６％。入院第５天开始出现黄疸，...     

小茴香热敷治疗腹部手术后肛门排气的效果研究

目的 观察小茴香热敷腹部促进腹部手术后肛门排气的疗效.方法 将478例患者分为试验组265例(小茴香热敷组),对照组213例(常规治疗护理组).观察记录两组病人的肠鸣音出现的时间及肛门排气的时间.结果 试验组肠鸣音出现时间及肛门排气时间均比对照组明显提前,差异有统计学意义.结论 小茴香热敷腹部操作简单,方便易行,能促进肠蠕动,无副作用.     

盲肠浆膜下位阑尾1例

盲肠浆膜下位阑尾１例王国平①刘利平①患者，女，２７岁，主因转移性右下腹痛２天入院。查体：Ｔ３７℃，体型较胖，急性病容。腹部平坦，右下腹腹肌略紧，ＭｅＢｕｒｎｅｙ点压痛阳性，反跳痛阳性，Ｍｕｒｐｈｙ′ｓ征阴性，无移动性浊音，肠鸣音正常。血液检验呈急性炎...     

先天性胸腹裂孔疝2例

例1，女，9个月。反复呕吐，发热、伴肛门停止排气排便4天。查体：营养发育良好好，无青紫，左胸略饱满，叩诊呈鼓音，左肺呼吸音减低，可闻及肠鸣音，腹部触之有空虚感。胸片示：纵隔右移，左胸腔内可见不规则充气肠袢影。胃肠造影示：左胸腔有含钡剂肠管影。在静脉复合麻醉下剖胸手术。术中见：疝人胸腔主要为小肠，部分结肠，肠段无坏死，给回纳腹腔，修补膈肌，痊愈出院。     

肠道菌群在高原低氧肠道损伤中的作用研究

目的　探讨肠道菌群在高原低氧环境中参与肠道损伤的作用机制。 方法　将20只C57 BL/6小鼠按1：1比例随机分为对照组和暴露组，建立6000 m高原低氧模型，造模成功后收集两组小鼠粪便、血液和近端结肠组织。采用16S rDNA测定粪便中肠道菌群结构；检测小鼠血液生化指标；HE和PAS染色观察结肠肠道黏膜结构的改变；RT-qPCR测定结肠组织ZO-1、Occludin、IL-6和TNFα的mRNA表达水平。 结果　与对照组相比，暴露组小鼠血细胞、血红蛋白和红细胞压积值显著升高，高原低氧模型建模成功；16 SrDNA结果显示肠道菌群紊乱、多样性下降，黏蛋白降解菌艾克曼菌，普雷沃氏菌、梭状芽胞杆菌XVIII等致病菌含量上升，短链脂肪酸产生菌罗斯氏菌、Odoribacter菌、Lachnospiracea菌、Butyricicoccus菌和欧氏菌等益生菌含量下降；HE和PAS染色结果显示结肠组织上皮连续性中断、腺体萎缩、隐窝变短、杯状细胞数量减少，提示肠道结构损伤且黏膜屏障破坏；结肠组织紧密连接蛋白Occludin和 ZO-1 mRNA表达水平下降，进一步暴露组小鼠肠道黏膜受损，炎症因子IL-6和TNFα 的mRNA表达量上升，可能与肠道炎症反应有关。 结论　高原低氧环境导致的肠道损伤可能与肠道菌群改变有关。肠道菌群紊乱、多样性下降，致病菌相对丰度上升，益生菌相对丰度下降，菌群的这些改变造成肠道黏膜损伤，引起肠道炎症，进而出现肠道损伤，最终导致高原肠道相关疾病。     

一种循环频率域内的心音包络合成方法

在循环频率域内分析心音的特性,提出一种新的心音包络合成方法.采用循环统计量,研究心音的循环平稳特性,把心音包络表示为循环频率的线性和,线性系数由循环谱估计.以心音分裂为例,进行包络提取仿真.在加性高斯白噪声和随机干扰环境下,对各种包络提取方法进行对比分析.仿真结果表明,心音包络可以在循环频率域内合成.心音具有显著的循环平稳特征,心音包络可以表示成循环频率的线性和.所提出的方法不仅对心音包络的合成与分解给出物理解释,而且具有一定的抗噪声和抗干扰能力.     

谷氨酰胺对急性肝损伤大鼠肠黏膜屏障的作用

目的 探讨谷氨酰胺(glutamine,GLN)对急性肝损伤大鼠肠黏膜屏障的作用.方法 61只清洁级Wistar大鼠随机分为3组:对照组、模型组、GLN干预组.采用脂多糖(lipopolysaccharide,LPS)和D-半乳糖胺(D-galactosamine,D-Gal)腹腔注射法建立急性肝损伤大鼠模型.检测血清丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)和总胆红素(TBiL)水平;光镜下及电镜下观察大鼠肝脏及肠道病理学改变;末端脱氧核苷酸转移酶(TdT)介导的缺口末端标记技术(TUNEL)检测细胞凋亡;高压液相离子色谱仪(HPLC-PED)检测大鼠肠黏膜通透性的改变.结果 模型组及GLN干预组大鼠死亡率差异无统计学意义(P>0.05);模型组及GLN干预组大鼠血清ALT、AST和TBIL水平差异无统计学意义(P>0.05);三组肠黏膜通透性差异无统计学意义(P>0.05);光镜下GLN干预组与模型组大鼠肝脏损伤程度差异无统计学意义;肠道未见明显病变;透射电镜下模型组和GLN干预组大鼠肝脏和肠道出现线粒体和细胞核等损伤,GLN干预组较模型组大鼠损伤轻;GLN干预组肝脏和肠道的凋亡指数(Apoptosis index,AI)显著低于模型组(P<0.05).结论 脂多糖可以造成D-半乳糖胺致敏大鼠急性肝损伤模型,造模前给予谷胺酰胺干预可能对于改善肝功能,保护肠黏膜的通透性,降低死亡率没有显著性作用.     

Effects of propofol on damage of rat intestinal epithelial cells induced by heat stress and lipopolysaccharides

Gut-derived endotoxin and pathogenic bacteria have been proposed as important causative factors of morbidity and death during heat stroke. However, it is still unclear what kind of damage is induced by heat stress. In this study, the rat intestinal epithelial cell line (IEC-6) was treated with heat stress or a combination of heat stress and lipopolysaccharide (LPS). In addition, propofol, which plays an important role in anti-inflammation and organ protection, was applied to study its effects on cellular viability and apoptosis. Heat stress, LPS, or heat stress combined with LPS stimulation can all cause intestinal epithelial cell damage, including early apoptosis and subsequent necrosis. However, propofol can alleviate injuries caused by heat stress, LPS, or the combination of heat stress and LPS. Interestingly, propofol can only mitigate LPS-induced intestinal epithelial cell apoptosis, and has no protective role in heat-stress-induced apoptosis. This study developed a model that can mimic the intestinal heat stress environment. It demonstrates the effects on intestinal epithelial cell damage, and indicated that propofol could be used as a therapeutic drug for the treatment of heat-stress-induced intestinal injuries.     

Neostigmine for the treatment of acute hepatic encephalopathy with acute intestinal pseudo-obstruction in a cirrhotic patient

We treated a 49-yr-old man with neostigmine, who had liver cirrhosis, acute hepatic encephalopathy, and acute intestinal pseudoobstruction. He was admitted in a state of hepatic confusion. On physical examination, the abdomen was distended; and bowel sound was absent. Plain abdomen film revealed multiple air-fluid levels and distention of bowel loops. Initially, we gave him lactulose enemas every 6 hr for one day without improvement in his mental state. Furthermore, he became to a state of coma. Therefore, we gave him 0.5 mg of neostigmine subcutaneously to improve his peristaltic movement, and 2 L of polyethylene glycol electrolyte solution through a nasogastric tube for 4 hr to reduce the production and absorption of gut-derived toxins of nitrogenous compounds. After these treatments, the venous ammonia level decreased to the normal range within 12 hr, and the coma disappeared after 2 days. We suggest that neostigmine may be one of the most effective treatments to initiate peristaltic movement and bowel cleansing in cirrhotic patients with acute hepatic encephalopathy and acute intestinal pseudoobstruction.     

益气滋阴通腑方对吗啡所致便秘小鼠肠道传输功能的影响

目的 研究益气滋阴通腑方对吗啡所致便秘小鼠肠道传输功能的影响。方法 将昆明种小鼠90只,随机分为6组,分别设为西沙比利组、模型组、空白组、中药高、中、低剂量组,每组15只。除空白组外,其余5组均予皮下注射吗啡,建立慢性传输型便秘（STC）模型。中药高、中、低剂量分别给于7.2、3.6、1.8 mg/（kg·d）益气滋阴通腑方颗粒剂浓缩液灌胃,模型组、空白组均予同等量次的蒸馏水注入胃内,各组均灌胃10 d。实验结束后,小鼠回盲部注入活性炭悬液,以检测小鼠肠道传输功能,在无张力状态下测量肠道全长及被墨汁染色的肠道长度,继而计算肠道推进率。结果 益气滋阴通腑方高、中、低各组均可改善肠动力障碍,与对照组比较,差异有统计学意义（P＜0.05）,但不同剂量组间比较,差异无统计学意义（P＞0.05）。中药各组与西沙比利组比较,效果接近,差异无统计学意义（P＞0.05）。但同时我们观察到,中药组的小鼠在整个实验过程中,无论是皮毛、精神状态、进食量,均明显好于西药组。结论 中药益气滋阴通腑方对吗啡所致便秘小鼠肠道传输功能障碍有明显改善作用,显著改善肠道动力,并可提高小鼠生存质量。     

Localization of the site of the murine IgG1 molecule that is involved in binding to the murine intestinal Fc receptor

Site-directed mutagenesis of a recombinant Fc hinge fragment has recently been used to localize the site of the murine IgG1 molecule that is involved in the control of catabolism (the “catabolic site”). In the current study, the effects of these CH2 and CH3 domain mutations (Ile 253 to Ala 253, His 310 to Ala 310, Gln 311 to Asn 311, His 433 to Ala 433 and Asn 434 to G1n 434) on intestinal transfer of Fc hinge fragments in neonatal mice have been analyzed. Studies using direct transfer and competition assays demonstrate that the mutations affect the transmission from intestinal lumen into serum in a way that correlates closely with the effects of the mutations on pharmacokinetics. Binding studies of several of the Fc hinge fragments to isolated neonatal brush borders have been used to confirm the in vivo transmission data. These analyses have resulted in the localization of the binding site for the intestinal transfer receptor, FcRn, to specific residues of the murine Fc hinge fragment. These residues are located at the CH2-CH3 domain interface and overlap with both the catabolic site and staphylococcal protein A (SpA) binding site. The pH dependence of IgG1 or Fc fragment binding to FcRn is consistent with the localization of the FcRn interaction site to a region of the Fc that encompasses two histidine residues (His 310 and His 433). To assess whether one or two FcRn binding sites per Fc hinge are required for intestinal transfer, a hybrid Fc hinge fragment comprising a heterodimer of one Fc hinge with the wild-type IgG1 sequence and a mutant Fc hinge with a defective catabolic site (mutated at His 310, G1n 311, His 433 and Asn 434) has been analyzed in direct and competition transmission assays. The studies demonstrate that the Fc hybrid is transferred with significantly reduced efficiency compared to the wild type Fc hinge homodimer and indicate that the binding to FcRn, and possibly subsequent transfer, is enhanced by the presence of two FcRn binding sites per Fc hinge fragment.     

Tolerance towards resident intestinal flora in mice is abrogated in experimental colitis and restored by treatment with interleukin-10 or antibodies to interleukin-12

There is now increasing evidence that hyperresponsiveness towards intestinal flora is a crucial event in the pathogenesis of inflammatory bowel disease (IBD). In support of this hypothesis, we recently described in humans that tolerance exists towards indigenous intestinal flora but is broken in active IBD lesions. In the present study, we have attempted to transfer this model into mice from different genetic backgrounds (BALB/c, SJL/J, C3H/HeJ). We found that mononuclear cells from spleen, small bowel and large bowel of mice do not proliferate, i.e. are tolerant when exposed to bacterial sonicates derived from autologous intestine (BsA) but do proliferate, i.e. are immune when exposed to bacterial sonicates derived from the heterologous intestine of syngenic littermates (BsH). Furthermore, we demonstrate that both local and systemic tolerance to BsA is broken in a murine model of chronic intestinal inflammation induced by the hapten reagent 2,4,6-trinitrobenzene sulfonic acid (TNBS), which mimics several important characteristics of Crohn's disease. Tolerance to BsA was restored and TNBS-induced colitis was abrogated in mice systemically treated with interleukin (IL)-10 or antibodies to IL-12. Treatment specifically restored tolerance to BsA, but did not suppress proliferation to BsH. In summary, we here report a new mouse model for the study of immunity and tolerance towards bacterial products. Our data suggest that tolerance to BsA is an important protective mechanism and that restoration of tolerance to resident intestinal flora by IL-10 and antibodies to IL-12 may be of potential therapeutic utility in patients with inflammatory bowel disease.     

谷氨酰胺防治急性肝衰竭大鼠肠道细菌移位实验研究

目的探讨谷氨酰胺（Gln）对急性肝衰竭（AHF）大鼠肠道细菌移位防治作用及机制。方法SD大鼠随机分成4组，对照组（A组），防治组（B组），治疗组（c组），模型组（D组）。B组、c组、D组腹腔注射D．氨基半乳糖（GaIN）建立急性肝功能不全大鼠模型。A组及D组予生理盐水灌胃。B组造模前两天予Gln灌胃防治，C组造模后一天Gln灌胃治疗。4d后处死动物。进行肝脏病理评分；观察肠系膜淋巴结细菌移位及平均组织含菌量、肠组织学改变；测量回肠绒毛高度和隐窝深度；检测血浆二胺氧化酶含量。结果B组和C组肝脏病理评分明显低于D组。B组肠系膜淋巴结细菌移位率低于D组，有显著性差异。B组、C组的血浆二胺氧化酶含量低于D组。B组显著低于C组。B组及C组的回肠绒毛高度和隐窝深度明显高于D组。B组明显高于C组，差异显著。结论谷氨酰胺可改善AHF大鼠的肠道黏膜屏障功能，减少AHF大鼠的肠道细菌移位的发生。     

Caspases-3, -8, and -9 are required for induction of epithelial cell apoptosis by enteropathogenic E. coli but are dispensable for increased paracellular permeability

Enteropathogenic Escherichia coli (EPEC) is an important cause of diarrhea, particularly among infants in developing countries. An increase in intestinal permeability due to EPEC infection has been suggested as a factor in the development of diarrhea. Abnormally high levels of programmed cell death (apoptosis) of intestinal epithelial cells can lead to increased intestinal permeability. The effects of EPEC on cell apoptosis remain incompletely understood. This study characterized the mechanisms of EPEC-induced epithelial apoptosis and examined whether this effect contributes to heightened permeability in an in vitro model of infection. We report that EPEC-induced apoptosis in T84 intestinal epithelial cells via a mechanism involving caspases-3, -6, -8, and -9, the cleavage of PARP, and oligonucleosome formation. In addition, EPEC time-dependently increased paracellular permeability as assessed by transepithelial resistance and the apical-to-basolateral movement of 3000 MW dextran. Furthermore, EPEC infection led to the cleavage and mislocalization of tight junctional ZO-1 and occludin. However, pharmacological inhibition of caspases did not prevent the EPEC-induced disruptions in epithelial barrier structure and function. Taken together, these results suggest that a caspase-dependent upregulation in epithelial cell apoptosis during EPEC infection occurs independent of impaired intestinal barrier function.