Doctor's compliance with compulsory reporting of occurrences.
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Biomedical subjects
Publications and source records attributed to P Reizenstein.
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The expression of adhesion molecules on blasts from 14 patients with acute myeloid leukemia (AML) was investigated by immunofluorescence and flow cytofluorometry. All tested blast populations expressed CD18/CD11a complex [leukocyte function antigen-1 (LFA-1)] and CD29 (very-late antigen (VLA)) and the majority were positive for CD54 [intercellular adhesion molecule-1 (ICAM-1), 78.6%] and CD56 [neural cell adhesion molecule (NCAM), 64.3%]. The expression of two other alpha chains of CD18/CD11b and CD11c varied considerably (64.3% and 42.8% of positive cases, respectively). Only one case (AML-M4) showed a weak expression of the activated platelet antigen CD41b. None of the tested blasts expressed the vitronectin receptor (CD61/CD51). No significant correlation between the expression of adhesion molecules and the FAB type of leukemia could be found. All tested blast populations were completely resistant to NK-mediated cytotoxicity and relatively resistant to LAK-mediated cytotoxicity in the standard 51Cr release assay. While no statistically significant correlation of the results in cytotoxicity assays with the expression of adhesion molecules or the expression of HLA-DR antigen could be observed, 2 out of 3 completely resistant cases lacked ICAM-1. These results show that even leukemic blasts which express all of the tested adhesion molecules can still be resistant to LAK-mediated cytotoxicity.
Twenty-four obese patients were studied before and 3, 6, and 12 months after gastric banding to see if the excessive weight reduction caused any dysfunction of the peripheral or central nervous system or both. Postoperatively the patients were assumed to be able to keep their intake to 800-1000 kcal/day together with a multivitamin supplement. Electromyography, electroneurography and vibratory thresholds were used to assess the peripheral, somatosensory and visual evoked potentials to assess the central nervous and synaptic functions. Regular clinical and neurological assessments were made as well as laboratory examinations including total potassium estimations to calculate lean body mass. The mean weight loss and the mean lean body mass reduction amounted to 20.5% and 18.4% at 3 months, and to 30.3% and 10.2% at 12 months, respectively. Electromyography showed signs of acute denervation in the anterior tibial muscle in one patient 3 and 6 months after operation, but restitution after 12 months despite continuous weight loss. In the left peroneal nerve the electroneurography showed a trend with slight successive reduction of the conduction velocity in the postoperative period. No abnormalities of the vibratory thresholds were found postoperatively. Somatosensory and visual evoked potentials were normal in all patients and no significant changes were observed during the postoperative period. The present study did not reveal any significant dysfunction of the peripheral or central nervous system as a result of excessive weight loss in obese adults undergoing weight reducing surgery.
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Results of five different methods (heme breakdown, mitotic indices, total marrow cellularity and different methods of labelling indices) to determine bone marrow cell growth are reviewed. Normal immature erythroblasts and myeloblasts have generation times of about 5-10 h. Erythroblasts in neoplastic conditions (the myelodysplastic syndrome and polycythemia vera) have generation times which are significantly prolonged, by 12-75 per cent, but this may not be true for myeloblasts, since total labelling indices are increased (from normal 3.9 to 11.2 per cent) in the myelodysplastic syndrome. In contrast, generation times in aplastic anemia are significantly shortened, by about 70-80 per cent. Normal mature erythroblasts and promyelocytes have generation times of about 24 h, and the malignant prolongation may be even greater.
Leukotriene (LT) formation was studied in ionophore A23187-stimulated white blood cell (WBC) preparations from patients with chronic myelogenous leukaemia (CML; n = 14), polycythaemia vera (PV; n = 10) and two control groups consisting of patients with non-malignant inflammatory disease (n = 4) and normal healthy donors (n = 25). The synthesized products were identified and quantitated using high-performance liquid chromatography combined with computerized UV-spectroscopy. White blood cell preparations from the CML patients produced more LTC4 (40.2 +/- 7.9 pmol/10(6) WBC, mean +/- SEM) than WBC from the healthy donors (9.0 +/- 1.8), P less than 0.0005. In contrast, the formation of LTB4 was normal and there was no increase in the total leukotriene synthesis (the sum of LTC4, LTB4, 20-OH-LTB4 and the delta 6-trans-isomers of LTB4). The ratio between leukotrienes C4 and B4 was strongly elevated in the CML group; 1.67 +/- 0.25 v. 0.37 +/- 0.07 in the controls, P less than 0.0005. No significant correlation was observed between the levels of LTC4 and the number of known LTC4 producing cells (such as monocytes, eosinophils and basophils) in the CML WBC preparations. In contrast, a correlation was found between the sum of neutrophilic granulocytes and metamyelocytes in these suspensions and the amount of LTB4 formed; r = 0.600, P less than 0.05. A number of other laboratory or clinical variables of the CML patients (including total white blood cell and platelet counts, differential counts, previous cytotoxic treatment, time from diagnosis, time from last treatment, post study survival and age) did not significantly correlate with the formation of leukotrienes. No abnormality in the production of LTB4 or LTC4 was observed in granulocyte and WBC preparations from the patients with polycythaemia vera and non-malignant inflammatory disease, respectively. The results indicate a selectively increased LTC4 producing capacity in CML.
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In a questionnaire study 140 subjects answered 4200 questions in 1980 and 1986. They consisted of patients with myeloma, acute leukemia, lung carcinoma, and non-malignant disease and their relatives. In 22 additional cases the questionnaire was not answered. The results show that myeloma patients are less content with the general care than leukemia patients (P less than 0.05). Similarly, relatives of decreased myeloma patients are less satisfied with the information given to them than relatives of deceased leukemia patients (P less than 0.001). The information has improved with time, however, since the patients were more satisfied in 1986 than in 1980 (P less than 0.001) and relatives of myeloma patients still alive were more satisfied than relatives of patients who had died earlier (P less than 0.001). The opinions of patients were similar to those of their relatives. However, the relatives of leukemia patients were even more satisfied with the contact with the medical staff than the patients themselves (P less than 0.05). As many as 10-30% of the relatives never gave up hope for their relative's survival. Only two out of 27 deaths were considered not dignified. The lung carcinoma patients reported a less good quality of life (P less than 0.001), and less satisfaction with the information given (P less than 0.01), than the hematological patients from the same year. Similarly, their attitude to the medical care improved less (P less than 0.01), and they were less content with the general care than the leukemia group (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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Earlier studies with individually phenotyped monoclonal antibody combinations and complement or lymphokine activated killer (LAK) cells showed that many acute myeloid leukemic cells were resistant to these cytotoxic agents when used singly. Therefore, a combination of both agents was studied. When the leukemic target cells were submitted to killer cells activated with 100 or 800 IU of recombinant interleukin-2 (rIL-2), only averages of 6.0 and 16.7% of the targets were killed respectively. When the remaining, refractory cells were confronted with a cocktail of individually phenotyped monoclonal antibodies and complement, an additional significant cell kill was obtained, but it amounted to only between 7.4 and 5.5% (for LAK-100 and LAK-800, respectively). In contrast, of the target cells initially refractory to the same cocktail of monoclonal antibodies, all were cross-resistant both to LAK-cells activated with 100 and to those activated with 800 IU of rIL-2. This cross-resistance was caused neither by sub-optimal LAK-cell activation, nor by antibody blocking of hypothetical LAK-cell receptors, since pre-incubation with monoclonal antibodies without complement did not inhibit LAK-cell cytotoxicity. Although only partial cross-resistance was found in the present study, it still remains that only a minority of the tumor cells could be killed. A higher in-vitro cell kill should be attempted prior to clinical trials in order to avoid clinical effects resembling those of a partial surgical tumor resection.