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61. Sulphated bile acids are excreted in urine in large amounts under cholestatic conditions.

62. Aggressive factors include gastric juice and bile salts which can reflux back into the stomach.

63. Studies in rats have shown that bile salts inhibit gastric emptying and prolongs intestinal transit time.

64. Daniel wanted to call out his shock, but the incoherent cry turned in his throat into a spurt of stomach bile.

65. It is usually as effective as surgery in treating bile duct stones and involves a shorter hospital stay.

66. He retched, and bile from his stomach poured from his open mouth.

67. It slid down the wall, leaving behind it a trail of dark brown juice, like bile.

68. Centrally administered neuropeptide Y caused a dose-dependent increase in bile flow that was associated with an increase in biliary bicarbonate output.

69. This pattern will continue until the regurgitation of bile causes hepatocellular damage.

70. It could so happen that slight bile acid malabsorption may or may not affect bile acid synthesis.

71. Only one of four studies in polyps has shown any increase in faecal bile acid excretion in this group.

72. In contrast, the unconjugated, carboxylic,(Sentence dictionary) bile acids are easily precipitated by calcium phosphate.

73. Furthermore, the higher concentrations used in this study reflect total bile salt concentrations in human colon.

74. Conversely, operations that divert bile away from the stomach will ameliorate dysplastic features induced by previous gastric surgery.

75. Likewise, the carcinogenic action of bile may be related to the duration of exposure of gastric mucosa to biliary carcinogens.

76. The bile acid concentration in faecal water also decreased with increasing dietary calcium, and this was not influenced by dietary phosphate.

77. Methylated bile acids were produced by reaction at room temperature for one hour and subsequently evaporated to dryness under nitrogen.

78. Paired hepatic and gall bladder bile samples were collected from 10 patients with cholesterol gall stones and six patients without gall stones.

79. However, the lack of bile flow into the intestines will result in neither urobilinogen nor urobilin being found in the feces.

80. Faecal bile acid loss in cystic fibrosis is unrelated to the presence of intraluminal fat or intestinal bacterial overgrowth.

81. Such obstruction to the flow of bile will cause the conjugated bilirubin to be regurgitated into the sinusoids and the general circulation.

82. Before the availability of endoscopic bile duct intervention surgical treatment was the usual approach to management.

83. Blood chemistry showed cholestatic liver enzymes and ultrasound showed dilated bile ducts.

84. Our technique and results of endoscopic treatment of bile duct injury after open cholecystectomy have been described in detail elsewhere.

85. The only patient given bile acid therapy who developed stone recurrence, stopped treatment after only two weeks because of side effects.

86. In general, a large proportion of bile duct injuries can be attributed to the learning experience of the surgeon.

87. Stool frequency and volume decreased and bile acid absorption increased after treatment.

88. Whole bile samples were collected anaerobically and into sterile tubes.

89. The SeHCAT test has made intestinal bile acid malabsorption much more easy to detect.

90. Cholesterol was added to increase the intestinal concentration of bile acids, because dietary cholesterol stimulates bile acid synthesis in rats.