New onset of diabetes in FK 506 vs cyclosporine-treated kidney transplant recipients.
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Biomedical subjects
Publications and source records attributed to C Jensen.
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In the present study, we evaluated the relationship between 1. the volume and rate of dialysis outflow and subsequent inflow, 2. the patient's impression of the location of the catheter tip and 3. the stability of the catheter tip location. Thirteen patients were studied on 2 random occasions (periods 1 and 2). Inflow (L/min) was significantly faster than outflow (p less than 0.05). No catheter tips were located in the far upper part of the abdomen. Outflow with the catheter tip located in the middle part of the abdomen was significantly lower than with the tip located in the inferior quadrants (p less than 0.02). Two patients were able to feel the catheter tip at Period 1, and 4 at Period 2, but only 1 patient was able to state the exact location identical to fluoroscopy. Ninety-two percent of the fluoroscopic evaluations showed catheter tips located in the same anatomical regions in upright as well as supine positions. If vertical "neighbour" anatomical regions were included in the evaluation of the catheter tip migrations, all catheter tips were located at the same or the vertical "neighbour" region in the 2 study periods.
Developmental time and survival in larvae of the reduviid bug Triatoma infestans were studied in uninfected groups and in those exposed to a coprophagic infection with Blastocrithidia triatomae. Addition to young uninfected larvae of (a) different numbers of infected bugs, (b) infected and uninfected bugs, and (c) fresh or dry infectious feces were compared. Retardation of development was evident in groups given infected larvae or fresh feces. Mortality rates were correlated with infection rates and were higher in groups given more infected bugs, independent of the presence of uninfected bugs. Therefore, bugs did not discriminate between feces from infected and uninfected bugs, or they did not reject infectious feces. Dry feces had to be redissolved with fresh feces before infection was possible.
The pathogenic flagellate Blastocrithidia triatomae disrupts the digestion of Triatoma infestans; the midgut ultrastructure of bugs infected with the flagellate and of uninfected bugs is compared. Third or fourth instar larvae were dissected either unfed or 1 week after feeding. In all uninfected bugs extracellular membrane layers (e.m.l.) covered the apical microvillar border of the epithelial cells. Some midgut regions of bugs infected with B. triatomae appeared normal but often adjacent cells showed pathological effects. In affected cells the e.m.l. and the microvilli and finally the cells themselves were reduced or destroyed. Correlated with these observations of pathogenicity the method of attachment of parasites changed. When the e.m.l. were present only rarely were flagella found, but on extracellular membrane-free cells B. triatomae attached by flagellar enlargement to the microvillar border or, if this was reduced, to the apical host cell membrane. No hemidesmosome-like plaques were found at the attachment site. Although some flagella were inserted into the apical region of the cells no intracellular flagellates were observed.
Consecutive chest radiographs (n = 2,303) in 601 patients in the intensive care units (ICU) were analyzed with regard to main disease and indication. Two thirds of the patients were transferred for routine post-operative treatment, 14 per cent mainly for cardiopulmonary insufficiency. The remainder were referred because of various clinical conditions. The main indications for chest radiography were routine radiographic follow-up and/or control of the position of catheters, tubes, drainages etc. (50%). Obvious clinical indications appeared in only about 1/4 of the patients. When the patients were discharged from the ICU all chest radiographs were analyzed with regard to their predicted future value. Films considered not worth storing were removed and stored in a separate archive (57%). During a 15-month follow-up period none of the removed films were requested, indicating that a substantial number of films can be sorted out continuously. The possibility to reduce and to 'clinically compress' the amount of data in a future digital picture archive is emphasized.
The Klippel-Trenaunay-Weber (KTW) syndrome is a rare congenital syndrome of unknown etiology consisting of the triad: a large cutaneous naevus, congenital varicosities and hypertrophy of bones and soft tissues. A heterogenous group of vascular malformations may also occur. The case record of acute myelopathy in a patient aged 42 years with recognized KTW syndrome is presented. It is concluded that magnetic resonance imaging is indicated in cases of suspected intramedullary haemorrhage in patients with congenital vascular malformations.
The effect of lysophosphatidylserine on immunological histamine release has been studied in rat peritoneal mast cells actively sensitized with horse serum and in human basophils challenged with anti-IgE. In contrast to other lysophospholipids, lysophosphatidylserine enhances the immunological histamine release in rat mast cells. The effect shows the kinetics of a saturable process with an apparent Km for lysophosphatidylserine of 0.26 microM. A similar Km value (0.21 microM) is found when measuring the non-immunological histamine release activated by lysophosphatidylserine plus nerve growth factor. A comparison with phosphatidylserine shows that a half-maximal response to lysophosphatidylserine occurs at a concentration 4-times lower. In addition, the magnitude of the response is higher. At variance with rat mast cells, lysophosphatidylserine does not influence the histamine release elicited by immunological and non-immunological stimuli in human basophils. The histamine secretion in these cells is instead affected by a calcium ionophore or tetradecanoylphorbolacetate, a compound producing activation of protein kinase C.
Bacteria release histamine from human basophil leukocytes and mast cells. The release can be caused by an immunological (IgE-dependent) mechanism, but mostly we found a non-immunological (lectin-mediated) mechanism which indicates that mediator release triggered by bacteria can occur without the person being sensitized to the micro-organism in question. Both bacteria and bacterial products such as endotoxins potentiate basophil histamine release caused by allergens in allergic patients or by bacteria in persons sensitized to the micro-organisms. It is therefore tempting to speculate that bacteria and their products might be of importance for asthma by their capacity to release histamine and to potentiate mediator release.
The influence of exogenous addition of gangliosides on histamine release from human basophils and rat mast cells was examined in vitro. Gangliosides dose-dependently inhibited histamine release, and this inhibition was dependent on the ganglioside sialic acid content, since GT1b, having 3 sialic acid moieties, was more potent than gangliosides with 2 moieties (GD1a and GD1b), which again were more potent inhibitors than GM1 with one moiety. Asialo-GM1 was without effect. In high concentrations the gangliosides potentiated basophil histamine release. The modulation of histamine release was reflected in the sensitivity of the cells to extracellular calcium, since inhibition of the release could be counteracted by increasing the extracellular concentration of calcium.
The influence of the cell membrane content of sialic acid on basophil histamine release was examined in vitro in allergic patients and normal controls. Enzymatical removal of sialic acid enhanced histamine release induced by allergen and anti-IgE, whereas an increase in membrane sialic acid content by insertion of sialic acid containing gangliosides into the membrane inhibited the mediator release. The reduction in membrane sialic acid content abolished the inhibitory capacity of the calcium channel antagonist nimodipine, whereas the inhibition produced by verapamil and lanthanum was not affected. This difference, together with the previous finding that alterations in membrane sialic acid content is reflected in the cell sensitivity to extracellular calcium, suggest an interaction between membrane sialic acid and the calcium channels involved in basophil histamine release.
Histamine release from human basophils was inhibited by preincubation of the cells with a glucolipid mixture containing sialic acid-containing gangliosides. This was true for histamine release induced by anti-IgE, Concanavalin A and the calcium ionophore A23187, whereas the release induced by S. aureus Wood 46 was not affected. It was demonstrated that the inhibitory capacity of the glucolipid mixture could be attributed to the content of gangliosides, since no inhibition was obtained with cerebrosides or with gangliosides from which sialic acid was removed. Preincubation of the cells with the glucolipid mixture increased the sialic acid content of the cells, and this increase was attributed to an insertion of gangliosides into the cell membrane. The inhibition of histamine release was abolished by increasing the calcium concentration, which substantiates our previous findings that cell membrane sialic acid in basophil leukocytes is involved in the regulation of histamine release, possibly by a modulation of the transmembraneous calcium fluxes preceding histamine release.
Type I allergy against some common microorganisms was investigated in 14 patients with AIDS and 11 human immunodeficiency virus (HIV) antibody-positive homosexual men, and in a control group consisting of 13 heterosexual men without HIV antibodies. Basophil histamine release technique was used as a sensitive method to detect type I allergy against Candida albicans (CA), Herpes simplex virus type I (HSV-I) and cytomegalovirus (CMV). Of the 14 AIDS patients 11 (78%) showed significant histamine release when stimulated with CA, and HSV-I caused release in 10 (71%), whereas no response was obtained by CMV. In the group of HIV antibody-positive men only one released histamine when stimulated with CA and HSV-I and this patient also had lymphadenopathia. In contrast to these results, no release of histamine was obtained in the control group consisting of 13 heterosexual men. The histamine release caused by CA and HSV-I is mediated by an immunological reaction, since the release was abolished and regained by removal from and refixation to the cell surface of the cell-bound immunoglobulins. These results suggest an involvement of type I allergy as a pathogenetic co-factor in some infections in AIDS, and allergic type I reactions to CA and HSV-I might be an indicator for the presence of manifest AIDS.
A 5-year experience with postoperative acute acalculous cholecystitis is reported. The series concerns 9 male patients ranging in age from 28 to 69 years, with a mean age of 46 years. All underwent major surgical procedures and complications appeared in the postoperative course. Clinically, 89% of patients developed sepsis and 66% jaundice. Klebsiella pneumoniae was the microorganism most frequently isolated from the blood, intraabdominal and wound fluid collections. It is emphasized that the diagnosis of this form should be clinical and it should be immediately suspected whenever intraabdominal signs develop. A review of the international literature on the subject is presented. The etiology and pathogenetic mechanisms of postoperative acute acalculous cholecystitis are discussed.
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Histamine release from human basophils was investigated in vitro after removal of cell membrane sialic acid by three different sialidases. Pretreatment of the cells with sialidases from Cl. Perfringens, V. Cholera or Influenza virus A2 enhanced histamine release induced by subsequent stimulation of the cells with anti-IgE or the plant lectin Concanavalin A and caused a shift to the left of the dose-response curve for anti-IgE. The enhanced histamine release was reflected in a increased calcium sensitivity, thus suggesting that cell membrane sialic acid might be involved in the calcium fluxes preceeding histamine release. In higher doses the sialidase from Cl. Perfringens caused the cells to release histamine by itself, whereas the sialidases from V. Cholera and Influenza virus A2 in high doses inhibited the cell response to Concanavalin A.