Fluid intake and industrial processing in apple juice induced chronic non-specific diarrhoea.

Dietary factors have been shown to contribute to the occurrence or persistence of chronic non-specific diarrhoea (CNSD). Among these are low dietary fat, high fluid consumption, and the consumption of apple juice. Prompted by the clinical impression that freshly pressed and unprocessed (''cloudy'') apple juice was less likely to induce diarrhoea than normal, enzymatically processed (''clear'') apple juice, both juices were compared in terms of carbohydrate malabsorption, gastric emptying, and effects on defecation patterns. Clear and cloudy apple juice differ in their fibre and non-absorbable monosaccharide and oligosaccharide contents. Ten healthy children aged 3.6 to 5.9 years ingested 10 ml/kg of clear and cloudy apple juice; in five of them it was enriched with 40 mg of [1-13C]-glycine. Clear apple juice resulted in increased (> or = 20 ppm) breath hydrogen excretion in 8/10, compared with 5/10 after cloudy apple juice; peak breath hydrogen was higher in the clear apple juice group (35 (4) and 18 (3) ppm, respectively). Gastric emptying as determined by means of labelled breath carbon dioxide (13CO2) excretion was similar with both juices. In a four week crossover clinical trial 12 children, formerly diagnosed as having CNSD, were given extra clear fluids (excluding fruit juices; > or = 50% over basal consumption), clear apple juice, or cloudy apple juice, for five day periods. Extra fluids and cloudy apple juice did not influence stool frequency and consistency compared with the basal period. In contrast, clear apple juice significantly promoted diarrhoea. It is suggested that, in addition to fructose, the increased availability of non-absorbable monosaccharides and oligosaccharides as a result of the enzymatic processing of apple pulp is an important aetiological factor in apple juice induced CNSD.     

枳■子黄酮类成分研究

从北枳（ＨｏｖｅｎｉａｄｕｌｃｉｓＴｈｕｎｂ）种子中首次分离并鉴定了４个黄酮类化合物，即双氢山奈酚（ｄｉｈｙｄｒｏｋａｅｍｐｆｅｒｏｌＩ）、槲皮素（ｑｕｅｒｃｅｔｉｎＩＩ）、（＋）３，３′，５′，５，７五羟基双氢黄酮［（＋）３，３′，５′，５，７ｐｅｎｔａｈｙｄｒｏｆｌａｖａｎｏｎｅＩＩ］和（＋）双氢杨梅黄素［（＋）ｄｉｈｙｄｒｏｍｙｒｉｃｅｔｉｎＩＶ］。其中ＩＩ为新化合物，Ｉ和ＩＶ为首次从该属植物中分到。     

Cu2+对神经肌肉接头传递的作用

Cu²⁺对间接刺激诱发大鼠隔肌的收缩及诱发小鸡颈二腹肌的收缩均产生浓度依赖性抑制作用。但Cu²⁺不影响膈神经的兴奋和传导,对直接刺激诱发膈肌收缩的抑制作用弱于间接刺激诱发膈肌收缩的抑制。Cu²⁺不影响小鸡颈二腹肌对Ach的敏感性。说明Cu²⁺主要作用于突触前膜阻滞神经肌接头的传递。Ca²⁺,L-半胱氨酸可拮抗Cu²⁺的阻滞提示Cu²⁺可能与突触前膜的SH基结合,影响Ca²⁺的跨膜内流,减少Ach的释放,阻滞神经肌接头的传递。     

热休克蛋白70对心脏移植大鼠供心心肌生化指标的影响

目的:观察应激情况下产生的热休克蛋白70对心脏移植大鼠供心心肌相关生化指标的影响。方法:实验于2006-04/09在青岛市市立医院中心实验室完成。①实验动物及分组:取成年SPF级雄性Wistar大鼠18只,按随机数字表法分为2组,每组9只。对照组腹腔注射生理盐水0.5mL,注射后24h取离体心脏,灌注HTK心脏保护液,并置于HTK液4℃保存3h后建立Langendorff离体心脏灌注模型,灌注K-H液2h。实验组腹腔注射重酒石酸去甲肾上腺素(溶于生理盐水中)3.1μmol/kg(0.53mg/kg),24h后取离体心脏,余处理步骤同对照组。②实验评估:应用全自动生化分析仪测定心肌肌酸激酶、乳酸脱氢酶含量;计算心肌肌酸激酶(乳酸脱氢酶)10min漏出率、心肌含水量;采用羟胺法测定超氧化物歧化酶活性,采用硫代巴比妥酸法测定丙二醛含量,采用双缩脲法测定组织蛋白含量;采用免疫组织化学法,以染色阳性面积占视野面积的百分比作为心肌组织热休克蛋白70的表达量。结果:18只大鼠全部进入结果分析,无脱失。①心肌组织热休克蛋白70含量:实验组高于对照组(t=17.96,P<0.01)。②相关生化指标:实验组大鼠心肌肌酸激酶、乳酸脱氢酶10min漏出率、心肌含水量及丙二醛含量显著均低于对照组(t=4.13～15.81,P<0.01),实验组大鼠心肌超氧化物歧化酶活性显著高于对照组(t=10.89,P<0.01)。结论:热休克蛋白70的高表达能减少氧自由基对供心心肌的损害,是热休克蛋白70发挥其供心心肌保护作用的可能途径之一。     

Test conditions greatly influence permeation of water soluble molecules through the intestinal mucosa: need for standardisation.

Permeability tests are widely used to investigate the pathogenesis of various gastrointestinal diseases including coeliac disease, infectious diarrhoea, and inflammatory bowel disease. In Crohn's disease they are used as activity parameters by some investigators. Lack of standardisation, however, makes it very difficult to compare data reported in different studies. The aim of this study was to gather permeation data in well controlled test conditions to standardise the methods. Nine healthy volunteers each received five consecutive permeability tests by mouth using polyethylene glycol-400 (PEG-400) and 51Cr-EDTA as probe molecules. The probes were dissolved in water, a glucose solution, a starch solution, a hyperosmolar lactulose-mannitol solution, and a liquid meal. A significantly decreased permeation for both probes was found when given with the hyperosmolar solution. The 51Cr-EDTA permeation was also decreased with water. The permeability index, 51Cr-EDTA/PEG-400, corrected for influencing factors, confirmed that the lactulose-mannitol solution and plain water yield lower values of macro-molecule permeation than starch, glucose or liquid meal. Hyperosmolarity was clearly accompanied by a decrease in permeability probably caused by reversed solvent drag. Interindividual variability of probe permeation and permeability index is very low with a standard liquid meal. It is proposed that for permeability studies a standard liquid meal is always used.     

Leukemia and lymphoma in ataxia telangiectasia

There is a large increase in lymphoid malignancy in A-T patients and a total absence of myeloid tumors. Penetrance of the tumor phenotype is about 10% to 15% by early adulthood. The increase in lymphoid malignancy includes both B- and T-cell tumors. However, young A-T patients do not show an increased susceptibility to cALL, and the UK data suggest that B-cell lymphoma occurs in older A-T children. T-cell tumors may occur at any age and may be T-ALL, T-cell lymphoma, or T- PLL; most strikingly, there may be a fourfold to fivefold increased frequency of T-cell tumors compared with that of B-cell tumors in these patients. If this is correct, it is possible that a significant proportion of all T-ALL/T-cell lymphoma in infants might be associated with undiagnosed A-T. The age range and sex predominance for T-ALL may be different for A-T and non-A-T patients and the age range for T-PLL may also be different in A-T and non-A-T patients. There is clearly some uncertainty concerning the ratio of T-cell to B-cell tumors in A- T, but this could be clarified by the publication of all tumors that occur in the disorder. In contrast, 8 of 9 tumors reported in NBS, which shows the same cellular features as A-T, were lymphomas and none was a leukemia. There are several indicators of genetic heterogeneity in A-T that suggest that not all patients are equally susceptible to all T-cell tumor types. Concordance for tumor type within individual families suggests that particular gene defects may be associated with particular tumor types. The logical extrapolation of this argument is that some patients may not have any increased risk for B-cell tumors at all or even to all T-cell types but only to a particular type of T-cell tumor. What is the cause of the increased predisposition to leukemia/lymphoma in A-T patients? There is no evidence that the immunodeficiency in A-T is related to this predisposition. One of the major findings in all A-T patients is the increase in V(D)J-mediated chromosome rearrangement observed in T lymphocytes. Particular chromosome translocations in T cells, involving a break in a TCR gene, are characteristically associated with either T-ALL or T-PLL in non-A-T patients. The majority of T-cell tumors in A-T are T-ALL and T-cell lymphoma, about which virtually nothing is known chromosomally, and the assumption is that the increased number of translocations leads to the increased level of these tumors. In older T patients, the expansion of specific translocation T-cell clones has been followed to the point to which they develop into T-PLL. All the evidence, therefore, suggests that the A-T mutation in the homozygous state allows a large increase in production of translocations formed at the time of V(D)J recombination, and this leads to the increased predisposition to leukemia. The general increased predisposition to T-cell tumors compared with B-cell tumors in A-T patients may be related to a preferential occurrence of translocations in T cells. Relatively little is known about translocations in circulating B lymphocytes in normal individuals, but A-T siblings have been shown to have clonal chromosome rearrangements of both B and T cells, simultaneously, although in these siblings the T-cell clones occupied all the T-cell compartment and the B-cell clones were small. An important inference from these facts is that the A-T defect preferentially affects immune system gene recombination in T cells rather than B cells. Recent evidence suggests that the V(D)J recombination machinery is not identical or is not regulated identically in T- and B-cell progenitors. This finding is consistent with the hypothesis that V(D)J rejoining in the majority, at least, of A-T patients may be preferentially deficient in T cells compared with B cells giving rise to the greatly increased number of translocations and T-cell tumors. Carbonari et al proposed that the recombination defect in A-T cells affected both Ig isotype switching and TCR rearrangeme