Gallium scintigraphy in the diagnosis and management of multifocal Castleman's disease.
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Biomedical subjects
Publications and source records attributed to G Hamilton.
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The monoclonal HBA-71 antibody recognizes a Ewing's sarcoma associated antigen, which is also highly expressed on the cell surface of human cortical thymocytes and islets of Langerhans among normal tissues. The antibody was found to inhibit partially the growth of ES tumor cell lines and to trigger proliferation in thymocyte cultures. The influence of growth factors and the effect of the HBA-71 antibody was further investigated in the present study. The growth of ES tumor cells was demonstrated to be dependent on the presence of insulin-like growth factor I or insulin. The HBA-71 antibody (25 micrograms/ml) enhanced the growth stimulatory effect of IGF-I under serum-free conditions. The expression of the HBA-71 epitope is modulated positively by IGF-I and insulin and negatively by dexamethasone and human growth hormone in ES/PNET tumor cells and thymocytes. IGF-I either alone or in combination with HBA-71 stimulated the proliferation of thymocytes under serum-free conditions whereas in complete medium, IGF-I stimulated thymidine incorporation and the HBA-71 antibody either alone or in the presence of IGF-I showed inhibitory activity most likely due to down-regulation of the receptor. These data demonstrate the important role of IGF-I in the growth of ES/PNET tumor cells as well in the proliferative activity of HBA-71 positive normal thymocytes. The biological activity of IGF-I in malignant thymocytes, pancreas tumors, fetal muscle, brain, granulosa and Sertoli cells has been documented in the literature.(ABSTRACT TRUNCATED AT 250 WORDS)
Aspects of quality of life (symptoms, psychological well-being and activity) were evaluated by self-administered questionnaires in a 4 months randomized double-blind trial of titrated doses of verapamil slow release (n = 41) compared with nifedipine retard (n = 40). An untreated diastolic blood pressure of 95 to 115 mm Hg was required for inclusion in the trial. The mean age in both groups was 55 years. A significant difference between the two drugs was found in the average reporting of symptoms with an increase on nifedipine (p less than 0.01). The reporting of swollen ankles and flushing (p less than 0.05) increased on nifedipine, and nocturia (p less than 0.05) increased on verapamil. Measures of psychiatric morbidity tended to improve on verapamil and deteriorate on nifedipine. Only the change in cognitive function was significant between the drugs, being worse on nifedipine (p = 0.05). There was no difference between the two groups in the fall in diastolic blood pressure (average 18 mm Hg on nifedipine and 17 mm Hg on verapamil). There was a significantly greater fall in systolic blood pressure on nifedipine (23 mm Hg) compared with verapamil (13 mm Hg) (p less than 0.01). The two drugs differed in their effects on measures of quality of life. The improvements in symptomatic complaints and psychological well-being on verapamil may have been due to inclusion in a trial, although we cannot exclude the possibility of a drug effect. Conversely the increase in symptoms and self-assessed cognitive impairment on nifedipine were considered to be side-effects of the drug.
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Overexposed radiographs that have density measurements greater than three can yield diagnostic copies. An unexposed standard radiographic film is sandwiched between a completely black film and the film to be copied in a cassette with standard-speed rare earth intensifying screens. The fluorescence of the unblocked intensifying screen, induced by a measured x-ray dose from an x-ray machine, is the light source that exposes the film, yielding a negative copy. The negative can also be copied to produce a positive-phase radiographic image. The high degree of contrast achieved by this copy method regains the contrast scale that is lost on overexposure. It is capable of enhancing faint calcification and other low-contrast features of soft tissues.
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Intracellular pH (pHi) regulation is essential for basic functioning of the cell and activation of pHi regulatory mechanisms appears to be involved in the initial stage of cell division. Little is known about pHi regulation in human colonic carcinoma cells. We investigated SW-620 (CCL 227) cells, a cell-line derived from a human colonic adenocarcinoma. pHi changes were recorded by computer-assisted spectrofluorimetric monitoring of the pH-sensitive, fluorescent dye BCECF (2',7'-bis(carboxyethyl)- 5(6)carboxyfluorescein). Resting pHi in HEPES (N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid) buffered solution was 7.53 +/- 0.01. Intracellular acidification after an ammonium prepulse produced a pHi decline of 0.5 units and pHi returned to normal value in NaCl Ringer's. Both 1 mM amiloride and Na-free solution completely inhibited recovery for 8 minutes. This inhibition was reversible in NaCl Ringer's. Na-free solution led to a pHi decrease to 7.39 +/- 0.04 after 16 min, pHi was also lowered by 8 minute incubation of cells with 1 mM amiloride (7.40 +/- 0.02). In HCO3/CO2-buffered solution resting pHi was 7.42 +/- 0.01 (n = 35). Recovery from an acute acid load, induced by NH4 prepulse or switching from HEPES- to bicarbonate-buffered solution, was Na dependent, Cl independent, reversible and only partially blocked by 1 mM amiloride - pHi slowly recovered from 6.83 +/- 0.03 to 7.00 +/- 0.06 in 8 minutes. In the presence of amiloride and 200 microns H2DIDS (dihydro-4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid) pHi recovery was completely inhibited for 8 minutes. In Na-free solution pHi decreased from 7.44 +/- 0.04 to 7.29 +/- 0.03 within 8 minutes.(ABSTRACT TRUNCATED AT 250 WORDS)
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1. Aspects of quality of life (symptoms, psychological well-being and activity) were evaluated by self-administered questionnaires in a 4 month randomised double-blind trial of titrated doses of verapamil slow release (n = 41) compared with nifedipine retard (n = 40). An untreated diastolic blood pressure of 95-115 mm Hg was required for inclusion in the trial. 2. The mean age in both groups was 55 years. A significant difference between the two drugs was found in the average reporting of symptoms with an increase on nifedipine (P less than 0.01). The reporting of swollen ankles and flushing (P less than 0.05) increased on nifedipine, and nocturia (P less than 0.05) increased on verapamil. Measures of psychiatric morbidity tended to improve on verapamil and deteriorate on nifedipine. Only the change in cognitive function was significant between the drugs, being worse on nifedipine (P = 0.05). 3. There was no difference between the two groups in the fall in diastolic blood pressure (average 18 mm Hg on nifedipine and 17 mm Hg on verapamil). There was a significantly greater fall in systolic blood pressure on nifedipine (23 mm Hg) compared with verapamil (13 mm Hg) (P less than 0.01). 4. The two drugs differed in their effects on measures of quality of life. The improvements in symptomatic complaints and psychological well-being on verapamil may have been due to inclusion in a trial, although we cannot exclude the possibility of a drug effect. Conversely the increase in symptoms and self-assessed cognitive impairment on nifedipine were considered to be side-effects of the drug.
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