Urinary N2O as a measure of biologic exposure to nitrous oxide anaesthetic contamination.
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Biomedical subjects
Publications and source records attributed to K Nilsson.
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The urinary content of nitrous oxide was monitored during routine anaesthetic practice. There was a linear correlation with simultaneous measurements of technical exposure measured with a personal pump-bag sampling system (r = 0.99). Monitoring of urinary nitrous oxide with headspace extraction and gas chromatographic analysis is a simple and accurate mode of biological monitoring of exposure to nitrous oxide in the atmosphere.
The thromboplastin synthesis of the human monocytoid cell line U-937 and its two subclones designated U-937-3 and U-937-4 has been studied. U-937-4 seems by several functional criteria to represent a more advanced stage of monocyte differentiation than the original U-937. U-937-3 appears to be arrested at an even more immature stage than the original population. The basal thromboplastin activity was higher in U-937-4 than in U-937-3 or U-937 cells (7.0 +/- 1.9 (SEM), 1.0 +/- 0.2 and 1.6 +/- 0.6 units/mg protein, respectively) although not as high as in human normal monocytes (14.1 +/- 2.4). The thromboplastic expression of the two clones was maximal when cells were in logarithmic growth. Both clones responded with a weak to moderate thromboplastin synthesis upon addition of stimulants like phytohaemagglutinin (PHA), immune complexes or endotoxin. Thromboplastin production was also potentiated in the presence of lymphocytes. The supporting effect of lymphocytes was strong in the case of U-937-3 as well as in U-937 cells, but less pronounced in U-937-4 cells as it also is in human monocytes. The thromboplastin response after PHA stimulation was more rapid in U-937-4 cells (maximal after 4-8 h) than in U-937 or U-937-3 cells (12-16 h). Human monocytes also responds quickly to PHA (maximally 4 h). Total phospholipid content and the relative distribution of individual phospholipids were essentially similar in U-937-3, U-937-4 and U-937. With regard to thromboplastin production, U-937-4 cells seem to be more monocyte-like than the more immature cells U-937-3 and U-937. It is concluded that thromboplastin seems to be a useful marker for monocyte differentiation.
This paper reports the results of a 10-year follow-up of a pioneer group of 36 opiate addicts treated at a detoxification unit at St Lars Hospital in Lund in the years 1971-72. Sixteen of them are now ex-addicts. Their way out of addiction is described. The results show that there exists a turning process during which some kind of therapeutic action could be of considerable value. The ex-addicts go through a period in which they show signs of an identity conflict. During this period women seem more inclined to relapse than men. This stresses the importance of long-term therapeutic strategies.
The surface glycoprotein patterns of leukaemic B lymphocytes from 20 patients with clinically progressive or non-progressive chronic lymphocytic leukaemia (CLL) were investigated. Cells were labelled by the neuraminidase-galactose oxidase-tritiated sodium borohydride technique and the radioactive proteins were separated by polyacrylamide slab gel electrophoresis and visualized by fluorography. A total of 13 to 16 bands were detected. A common surface glycoprotein pattern for CLL cells was seen in all patients consisting of 7 proteins with the apparent molecular weights of 210, 200, 185, 150, 135, 110 and 90 kilodaltons, respectively. Interesting differences were, however, observed as cells from patients with progressive CLL in general lacked the glycoproteins 120, 72 and 67 K, which were found on cells from inactive CLL. The possible biological and clinical significance of these findings is discussed.
In a previous study, we demonstrated the existence in serum from patients with chronic lymphocytic leukaemia (CLL) of a cell-directed, heat-labile chemokinetic inhibitor of polymorphonuclear leucocytes (PMN). The aim of this investigation was to study the cellular origin of this inhibitor. Supernatants from short term cultured lymphocytes from 3 healthy persons and 5 patients with CLL, and from 16 different established human non-haematopoietic and haematopoietic cell lines were analyzed. Only the leukaemic B-lymphocytes from the CLL patients produced the inhibitor. The presence of the inhibitor was also demonstrated in supernatants from the fresh CLL cells from one CLL patient and a leukaemic cell line established from these cells using Epstein-Barr virus as the immortalizing agent. A lymphoblastoid cell line derived from the normal B-cells of the same CLL patient did not produce the chemokinetic inhibitor. We therefore conclude that the cellular origin of the heat-labile, cell-directed chemokinetic inhibitor of PMN migration is the CLL cell.
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The expression of major cell surface glycoproteins (sgp) of seven established human pulmonary small cell carcinoma (SCC) cell lines and two autologous non-neoplastic lymphoblastoid and fibroblastic cell lines were studied by the galactose oxidase tritiated sodiumborohydride labelling technique. The general sgp pattern of SCC cell lines was different from that of the autologous non-malignant cell lines and the various other normal and malignant hematopoietic cells, gliomas and melanomas previously studied by the same technique, thus confirming that the sgp pattern seems to represent a molecular "fingerprint" of various human cell types. The SCC cell lines could be subdivided into two major subgroups with respect to expression of characteristic sgps. One group of lines was characterized by having prominent sgp 52000 (52 K) Dalton (D), 50 KD, 40 KD, 34 KD and 10 KD. In the other group the major sgps had apparent molecular weights of 110 KD, 75 KD and 10 KD, respectively. In addition to these common basic "group specific" sgps each SCC line expressed individually distinct sgps.
The daily dietary consumption of refined sugar was studied in four equal-sized groups of 30 patients with Crohn's disease, ulcerative colitis (UC), irritable bowel syndrome (IBS), or minor orthopedic conditions. The latter group was matched for sex and age with the Crohn's disease group. The Crohn's disease patients consumed significantly more refined sugar (88.9 +/- 50.7 (SD) g/day) than the controls (64.3 +/- 45.6 g/day), the UC patients (64.3 +/- 38.7), or the IBS patients (59.9 +/- 33.3). Fifteen patients with Crohn's disease interviewed within 6 months of diagnosis consumed similar amounts of sugar (69.9 +/- 43.9) to those of the subjects in the other three groups. Fifteen other patients with Crohn's disease studied 7-36 months after diagnosis consumed significantly more refined sugar (107.9 +/- 41.2). These results indicate that the high sugar consumption in Crohn's disease is a secondary phenomenon without etiologic importance.
The radiation sensitivity of five human lymphoma cell lines has been investigated. All cell lines were originated from tumours clinically classified as histiocytic lymphomas. Using biochemical and immunologic techniques it was found that only one of them was a true histiocytic lymphoma. This cell line had an appreciable shoulder on the survival curve and capacity to repair sublethal damage. The survival curves of the other cell lines had no shoulders and the cells had nearly no capacity to repair sublethal damage. Taken together with previously published experimental and clinical observations the results indicate that tumours which by conventional diagnostic techniques are classified as histiocytic lymphomas are very heterogeneous in radiation sensitivity. It is possible that tumours of true histiocytic origin are more resistant to radiation than tumours of lymphocytic origin.
Some clones of the human histiocytic lymphoma line, U-937, were induced to differentiate into monocyte-like cells with loss of plating efficiency in agar by incubation with 0.1 to 10 nM 1 alpha,25-dihydroxycholecalciferol [1,25(OH)2D3]. At 1 nM, 40% of the cells of one sensitive clone exhibited differentiation after 2 days of incubation judging from assays for phagocytosis and capacity to reduce nitroblue tetrazolium. Induction appeared to occur by binding of the cholecalciferol to a specific cytoplasmic and/or nuclear receptor for 1,25(OH)2D3. However, the presence of this receptor was not sufficient for differentiation, since one clone which contained the receptor did not respond with differentiation upon addition of 1,25(OH)2D3. Differentiation induction did not require DNA synthesis but was blocked by agents which inhibit RNA or protein synthesis. It was also blocked by the calcium ionophore A 23187. A synergistic inducing effect was seen between 1,25(OH)2D3 and retinoic acid. In addition, the U-937 cells could be primed by a short incubation with 1,25(OH)2D3 to respond, with maturation, to the addition of agents which increase the intracellular level of cyclic adenosine 3':5'-monophosphate, such as prostaglandin E2, cholera toxin, and N6,O2'-dibutyryl adenosine 3':5'-monophosphate and which alone did not induce differentiation. Priming does not depend on the normal rate of RNA or protein synthesis, since it was not significantly inhibited by actinomycin D, cordycepin, or cycloheximide. It remains to be determined if unoccupied receptors for 1,25(OH)2D3 are present in fresh leukemia cells and if such cells can sometimes be induced to differentiate upon addition of cholecalciferol.
An important problem in the production of monoclonal antibodies is the large-scale cultivation of hybridoma cells in vitro. Fragility of cells and suboptimal in vitro cultivation methods have led to poor results in larger scale production up to now. To lower the mechanical stress on the cells we tried to entrap the cells into microspheres made of polymer material. In addition to other materials, agarose as embedding medium was investigated and results with hybridoma and other, non anchorage-dependent cell lines are given. The conclusion of the results is that encapsulation of living cells is possible and entrapped cells remain viable and continue to produce the desired substance for at least several weeks. The substances are secreted through the polymer matrix. Handling of microspheres is shown to be easy and simple fermentation apparatus may be used for the production on a reliable technical scale. Some problems remain unsolved, such as the determination of viable cell count within the microspheres and cultivation in columns which seems to be the simplest form of continuous production process.
The acute effects of cigarette smoking on fetal breathing movements and fetal movements were determined with a real-time ultrasound system in 10 healthy habitually smoking women in late gestation. The study was carried out for 1 hour before and 1 hour after the woman smoked a single cigarette. The maternal blood glucose concentration was maintained at a raised postprandial level through the study. After smoking, a significant increase in the rate of fetal breathing movements (P less than .05) appeared together with a reduction in the short time variability of the breath-to-breath intervals (P less than .05). The number of epochs without fetal breathing movements or fetal trunk and limb movements increased after smoking (P less than .05), indicating a change in the spacing of these fetal activities. The increased breathing rate and number of apneic epochs were both correlated to maternal nicotine levels. These observations suggest an acute influence on the fetal behavioral state of maternal smoking.
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The cytoplasmic glucocorticoid-receptor (GR) content was analyzed in peripheral leukocytes from 52 nonselected patients with chronic lymphocytic leukemia (CLL). Forty-six patients had measurable GR levels. Six patients lacking measurable GR and seven of eight patients with a low GR content had inactive disease. However, there was no significant difference in average GR content between patients with progressive or nonprogressive disease. Twelve GR-positive patients were treated with prednisolone as the sole medication. Seven patients responded, some in several treatment sessions. There was no correlation between GR-content and clinical response. Thus, in our experience, cytoplasmic GR measurement has only limited predictive value.
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Fresh neoplastic B cells from 14 untreated patients with naturally occurring B-cell leukemias were found to be susceptible to lysis by human natural killer (NK) cells. The observed lysis of the fresh, non-cultured, neoplastic B cells was mediated by a population of interferon-augmentable, FcR-positive, non-adherent lymphoid cells, which were also able to kill the "standard" NK target K562. A further finding was the correlation of NK susceptibility with disease activity in 11 patients with chronic lymphocytic (CLL) and one patient with lymphosarcoma cell leukemia (LSCL). Enriched neoplastic B cells from seven untreated patients with non-progressive CLL, whose disease activity was stable throughout the 6 month period of study, exhibited persistent and essentially unchanged NK susceptibility profiles. In contrast, four untreated patients with progressive CLL also had a measurable fraction of NK-susceptible, neoplastic targets, but these cells subsequently disappeared after successful cytoreductive therapy, and later re-emerged when these patients again developed progressive disease. Furthermore, one patient with LSCL was found to have persistent, measurable NK susceptibility in his tumor-enriched fraction after unsuccessful cytoreductive therapy. An additional finding in the peripheral blood of patients with chronic B-cell leukemias was the presence of significantly lower NK effector-cell activity against K562 as compared to normal donor peripheral blood lymphocytes (PBLs). The implications of these findings are discussed.
Normal and rheumatoid synovial cells have been analyzed in frozen sections and in suspension. HLA-DR-expressing, macrophage-like cells are demonstrated in normal synovial intima and in rheumatoid tissue. Suspended normal synoviocytes equaled peripheral blood non-T lymphocytes as stimulators of mixed lymphocyte reactions, whereas adherent rheumatoid synovial cells were extremely efficient as such stimulators and in presenting soluble antigens to autologous T lymphocytes. This HLA-DR-dependent T lymphocyte regulation might provide a cellular basis for the HLA-D haplotype-arthritis associations.