The dye-dilution method for the determination of plasma volume presents several problems, one of which is the estimation of dye concentration in plasma.It is with this problem that the present paper is primarily concerned.The most frequently used dye is Evans blue, T 1824.The colorimetric estimation of this dye in plasma is open to a number of possible errors, particularly those introduced by opacity of the plasma and by the haemolysis of blood samples.Recently it has become possible quantitatively to extract Evans blue from plasma for estimation in watery solution (Allen and Orahovats, 1948; Allen, 1951 ; Korner, Morris, and Courtice, 1954; Bedwell, Patterson, and Swale, 1955).As a result of considerable experience with Korner, Morris, and Courtice's method, it has become apparent that certain details of technique are of critical importance.The purpose of this article is to describe a technique that has been found to give satisfactory results, with regard both to speed and to accuracy. MethodReagents.-Thefollowing are required: Evans blue, 0.5 g. / 100 ml., in distilled water (I.C.I.).Sodium chloride, 0.9 g. / 100 ml.Cellulose tissues (" kleenex "), double-thickness sheets of size 21{ x 17 cm.
Biochemical values in clinical medicine. Robert Duncan Eastham, Newcastle upon Tyne. Fifth edition. 175 × 100 mm. Pp. 237. 1975. Bristol: John Wright. £2 Get access Biochemical Values in Clinical Medicine. Robert DuncanEastham, Newcastle upon Tyne. Fifth edition. 175 × 100 mm. Pp. 237. 1975. Bristol: John Wright. £2. Michael Hobsley Michael Hobsley Search for other works by this author on: Oxford Academic Google Scholar British Journal of Surgery, Volume 62, Issue 12, December 1975, Page 987, https://doi.org/10.1002/bjs.1800621218 Published: 07 December 2005
Abstract The cause of abdominal pain need not necessarily reside in the viscera; the abdominal wall is another source of symptoms. Some causes of abdominal wall pain are obvious, e.g. hernias, but not so others such as nerve entrapment syndromes. This review is concerned with causes of abdominal wall pain which, although common, may be easily overlooked.
Abstract Of 574 patients with previously untreated, unremarkable parotid lumps, 194 proved to have pleomorphic adenomas and 73 adenolymphomas. ABO blood group details were available in 59 and 85 per cent of patients respectively. Smoking details were available in 84 per cent of a randomly chosen 46 per cent subgroup of patients with pleomorphic adenomas and in 86 per cent of all those with adenolymphomas. The incidences of smoking and of the ABO blood groups in these two diagnoses were compared with standard sources. There was no evidence that either histological diagnosis of parotid tumours was linked to an abnormal pattern of ABO blood groups. However, there was a much greater incidence of smoking among the adenolymphoma than in the pleomorphic adenoma group: only one of 63 patients with adenolymphoma as opposed to 31 of 75 with pleomorphic adenoma had never smoked, while the mean number of cigarettes smoked by each patient with an adenolymphoma was estimated to be 300 000 as opposed to 80 000 for those with pleomorphic adenoma.
Abstract The aim of this study was to identify the natural reservoir and route of transmission of Helicobacter pylori infection. Two hundred eight (208) dyspeptic patients (114 males, 94 females; peak age of cohort, 50–59.9 years) were recruited. Specimens were collected from saliva, supra‐ and subgingival dental plaque, tongue scrapings, and oropharyngeal swabs. At subsequent endoscopy, gastric antral biopsy was performed for the rapid urease test (RUT), microbiological culture, and, in some patients, histology. Gastric juice samples were aspirated, and in 50 patients duodenal aspirate was collected. Polymerase chain reaction (PCR) with primers targeted to the 16S rRNA sequence of H. pylori was also employed for each of the specimens. In those patients where H. pylori was detected from multiple sites (dental plaque, gastric juice, gastric biopsy, and duodenal aspirate), restriction endonuclease digestion with Hae III was performed to determine if they were epidemiologically linked. The results indicated that 15/208 patients (7%) tested positively for H. pylori by PCR in dental plaque; only 2 samples were positive by culture. In none of the other oral sites sampled was H. pylori detected by any test used in the study. Gastric juice and gastric biopsy specimens from 36/208 patients (17%) and 114/208 patients (55%), respectively, were positive by PCR. Duodenal aspirate from 6/50 patients (12%) also tested positively by PCR. All specimens tested by restriction endonuclease digestion with Hae III (15/15 patients) were positive in both antrat biopsy and gastric juice specimens, as well as 5 specimens from the duodenal aspirate. Four of the dental plaque strains had restriction patterns similar to those of the stomach and duodenal sites, providing evidence that these sites were infected with the same strain of H. pylori. In conclusion, the results suggest that H. pylori selects the gastric mucosa as its preferred site. The detection in dental plaque could indicate that the oral cavity may act as a reservoir or sanctuary for the organism. Whether H. pylori is a resident or transient oral microorganism is still unclear, although it is more likely to be transient in nature. Ann Periodontol 1998;3:276–280.
1. The electrolytes were measured in alkaline gastric juice from eleven subjects with various gastric disorders; seven of these subjects had histamine-fast anacidity. The aim was to investigate the relation between alkaline gastric aspirates and the alkaline component predicted by the two-component hypothesis of gastric secretion. 2. The electrolyte concentrations differed from one subject to another: decreasing concentrations of sodium, chloride and alkali were correlated with increasing potassium concentrations. 3. The observed variations were completely explicable in terms of dilution of gastric juice by saliva. It is therefore concluded that the uncontaminated gastric juice was similar in all subjects. 4. The purest specimens of alkaline gastric juice closely resembled the alkaline component predicted by the two-component hypothesis. It is unlikely that diffusion in exchange for primary acid secretion could have produced the same results.
Insulin stimulated gastric secretion was studied in 74 unoperated duodenal ulcer patients (DUs), (20 women and 54 men). Three indices of secretion were studied--observed volume, acid output, and volume of gastric juice corrected for pyloric loss and duodenal reflux (VG). These three measurements were expressed both as peak secretion and as secretion during the 1/2 to two hour period after insulin, and also both before and after standardisation for height, making 12 different indices in all. From the data a significant correlation between insulin-stimulated secretion and height in DUs was found. A method of standardising each patient9s secretion for height is described. We confirm a significantly higher insulin-stimulated secretion in men than in women and show that this difference can be explained by their difference in height. For each of the 12 indices of secretion, the range of secretion for the unoperated subjects was obtained. The same indices were measured in 155 postvagotomy patients, including 33 patients with recurrent DUs, and compared with the ranges of secretion established in the unoperated patients. Responses above the lower 95% tolerance limit of the preoperative range were designated positive and those below negative. The Hollander status was determined. It was found that the least satisfactory criterion was Hollander9s (7% false negative and 69% false positive). The best was 1/2-2 VG standardised for height (3% false negatives and 43% false positives). The improvement in predictably was significant at the 0-0005 level.
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