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Biomedical subjects

G Green

Publications and source records attributed to G Green.

At least 127 records · Page 7Linked to original sources
PubMed1978

Needle aspiration/biopsy of the spine in suspected disc infection.

Closed needle aspiration/biopsy was performed in 19 patients with suspected spinal disc space infection. A precise diagnosis was made, from the material obtained in 13 (68%); the infecting organism was isolated in 11 and malignant tumour diagnosed histologically in two. There were no important complications. The procedure which is described in detail is simple to perform and can be carried out early in the course of a patient's stay in hospital, thereby enabling prompt treatment.

Adolescent↗
PubMed1977

Effect of bile duct obstruction on pancreatic enzyme secretion and intestinal proteolytic enzyme activity in the rat.

The role of bile in regulation of intestinal proteolytic activity in rats was investigated by studying the effects of bile diversion and bile duct obstruction on pancreatic protease secretion and on recovery of protease from the intestine. Diversion of bile and pancreatic juice from the intestine caused a large increase in pancreatic enzyme secretion; replacement of bile partially suppressed this response. Bile duct obstruction resulted (3-4 days postobstruction) in a threefold increase in pancreatic juice chymotrypsin but caused a large decreases in intestinal trypsin and chymotrypsin activities and total proteolytic activity. Recovery of pancreatic juice protein (labeled with 14C) from intestinal contents was markedly decreased in bile duct obstruction, indicating a more rapid rate of degradation and absorption of pancreatic jucie protein. The evidence suggests that interruption of bile flow results in an accelerated rate of degradation of pancreatic proteolytic enzymes, and that the increase in pancreatic enzyme secretion is an adaptation to decreased intestinal proteolytic activity.

Animals↗
PubMed1977

Association of abnormal fibrin polymerisation with severe liver disease.

The frequent occurrence of abnormal fibrin polymerisation in patients with liver disease has recently been reported. To investigate this further, fibrin polymerisation was studied in 68 patients with cirrhosis or chronic active liver disease. Thirty-three of these patients demonstrated impairment of this phase of blood coagulation. When other tests of liver function were compared in patients demonstrating this abnormality and those in whom fibrin polymerisation was normal, it was found that the former group demonstrated significantly reduced albumin concentrations (p less than 0.0002), raised bilirubin and aspartate aminotransferase levels (p less than 0.0006 and less than 0.003 respectively), and greater prolongation of the one-stage prothrombin time (p less than 0.001) with more marked reduction in factor VII levels (p less than 0.002) compared with the latter patients. It is concluded that defective fibrin polymerisation occurring in patients with liver disease indicates the presence of severely impaired hepatocellular function. This might account for the grave prognosis reported in cirrhotic patients with abnormal fibrin polymerisation who also suffer bleeding from gastro-oesophageal varices.

Aspartate Aminotransferases↗
PubMed1976

A neutral collagenase from human gastric mucosa.

Biopsy specimens of human gastric mucosa, maintained in culture for 7 days in the absence of serum, released a collagen-degrading enzyme into the medium. The yield of active enzyme reached a maximum after 2-3 days, and viable tissue, capable of protein synthesis, was essential for its production. 2. At 25 degrees C the enzyme attacked undenatured collagen in solution, resulting in a 55% loss of specific viscosity and producing the two products TCA and TCB characteristic of neutral-collagenase action. 3. Electron microscopy of segment-long-spacing crystallites of these reaction products showed the exact cleavage locus of the collagen molecules to be between bands 43 and 44 (I-43). The larger TCA and smaller TCB products were fragments representing 77 and 23% respectively of the length of the collagen molecule. 4. Optimal enzyme activity was observed over the pH range 7.5-8.5 and a mol.wt. of approx. 38000 was derived from gel-filtration studies. 5. The enzyme was shown to be inhibited by the human serum proteins alpha2-macroglobulin and a smaller component of mol.wt. approx. 40000; alpha1-anti-trypsin was not inhibitory. 6. EDTA, 1, 10-phenanthroline, cysteine and dithiothreitol all inhibited collagenase activity. 7. The gastric enzyme has properties similar to other well characterized collagenases, but differences exist with respect to its molecular size and the site of attack on the collagen molecule.

Blood Proteins↗
PubMed1976

Abnormal fibrin polymerization in liver disease.

Although there have been isolated reports of an acquired abnormal fibrinogen in patients with liver disease, its frequency and clinical significance is not known. In this study 121 consecutive patients with a wide spectrum of hepatic disorders were screened for abnormal fibrin polymerization. A simple colorimetric method using Reptilase was employed. Of 32 patients with proven cirrhosis, 16 (50%) showed abnormal fibrin polymerization. The incidence in decompensated alcoholic cirrhosis was particularly high. The abnormality was also detected in all patients with acute liver failure and seven of 15 with chronic active liver disease. Clinical improvement often correlated with its disappearance. Two patients with primary liver cell tumours demonstrated the abnormal polymerization. In patients with bleeding oesophageal varices the detection of abnormal fibrin polymerization was associated with a poor prognosis. None of the patients with surgical obstructive jaundice (26) or miscellaneous liver disorders (37) had abnormal fibrin polymerization. The occurrence of abnormal fibrin polymerization in liver disease is more frequent than previously suspected and usually signifies severe primary hepatocellular dysfunction. Evidence is presented to support the presence of a primary abnormality of fibrinogen as the cause of impaired fibrin monomer polymerization.

Batroxobin↗
PubMed1976

Simple clinical method of measuring gastric emptying of solid meals.

The radioisotope techniques used for the measurement of gastric emptying of solid meals in man require complex and expensive scintiscanners of cameras. We have evaluated a simple technique which uses a fixed scintillation detector and compared the results with those obtained from a gamma camera. The rates and patterns of gastric emptying recorded by the two methods correlated well in both healthy volunteers (mean r= 0.95) and patients with duodenal ulcer (mean r =0.89). The scintillation detector provides a reliable and inexpensive method for measurement of gastric emptying of solid meals.

Duodenal Ulcer↗
PubMed1976

Factor VII as a marker of hepatocellular synthetic function in liver disease.

Factor VII levels have been measured in 100 patients with liver disease following parenteral vitamin K1 therapy. There was good agreement between specific factor VII measurements and the one-stage prothrombin time apart from six patients with compensated cirrhosis in whom the prothrombin time was prolonged despite the presence of normal factor VII levels. A mean activity of 58% was found in patients with cirrhosis. Cirrhotic patients with features of hepatic decompensation had a significantly lower mean level of activity (40%) than the "contrast" patients with surgical obstruction of the major bile ducts (93%). Patients with chronic active liver disease had moderate depression of factor VII levels and those with non-cirrhotic liver damage had mean activities similar to the contrast group. Factor VII levels could not be correlated with BSP retention but there was a correlation with serum albumin concentration. It is concluded that the prothrombin time using Quick test with a standardized thromboplastin showing good sensitivity to factor VII, eg, the Manchester reagent (BCT), provides a reliable index of coagulability in chronic liver disease, and specific factor VII assays are not indicated.

Cholestasis↗
PubMed1976

Automated approach to radioimmunoassays of somatotropin (human growth hormone) and insulin.

The adaptation of human somatotropin and insulin assays to the automated Centria radioimmunoassay system [Clin. Chem. 21, 1305 (1975)] is reported. For the somatotropin assay, reaction conditions include a borate/bovine serum albumin buffer (pH 8.4) AND 20-H Incubation at 4 degrees C. Assay results for clinical samples compared favorably (correlation coefficient = 0.930) with values obtained from a reference laboratory. The means determined for 92 patients' samples were 4.3 mug/liter (reference laboratory) and 5.1 mug/liter (Centria). Intra- and inter-run precision ranged from 3.2 to 15.9%. For the insulin assay, a phosphate/bovine serum albumin buffer (pH 7.4) is used, with a 20-h incubation at 4 degrees C. Previously analyzed insulin samples from a reference laboratory were determined by the Centria analyzer with excellent correlation (r = 0.965). Means for patients' samples were 43.0 milli (USP) units of insulin per liter (reference laboratory) and 47.5 milliunits of insulin per liter (Centria). In both assays an anionicexchange gel is used in the separation step. The criterion of parallelism, an indication of the validity of a radioimmunoassay, was satisfied in both assays. The Centria radioimmunoassay system offers the advantage of automating all the critical steps of these radioimmunoassays.

Autoanalysis↗
PubMed1975

Use of factor-VII-rich prothrombin complex concentrate in liver disease.

A prothrombin complex concentrate rich in factor VII has been used in the management of the clotting defect in thirteen patients with liver disease. Adequate correction of coagulation was achieved immediately after infusion in all cases. Within 4 hours there was some deterioration and by 24 hours the results approximated to pre-fusion values. Liver biopsies were performed without haemorrhagic complication in the immediate post-infusion period. There was no evidence of induced intravascular coagulation. Since other prothrombin complex concentrates have proved disappointing, both in their failure to correct the clotting defect and in their production of disseminated intravascular coagulation, this factor-VII-rich concentrate may be the treatment of choice in patients with liver disease who require temporary correction of their coagulation defect.

Blood Coagulation Disorders↗