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Biomedical subjects

P Larsson

Publications and source records attributed to P Larsson.

At least 127 records · Page 7Linked to original sources

Factors determining the uptake of persistent pollutants in an eel population (Anguila anguilla L.).

The distribution of persistent pollutants in an eel population from a eutrophic lake of southern Scandinavia was examined. The origin of PCBs, DDT, DDE and lindane found in the fish was most likely the atmosphere. The most important factors for uptake of the chlorinated hydrocarbons was age (exposure time), growth rate and fat content. The life cycle of the eel is unique with a stage in freshwater when energy reserves (fat stored in muscular tissue) and lipophilic pollutants are accumulated. This stage is followed by a long migration to the spawning areas in the Sargasso Sea when pollutants are released from the fat deposits. These two stages followed by a once-in-a-lifetime spawning behaviour, makes the eel especially vulnerable to persistent pollutants. The effects of persistent pollutants combined with the eel's unusual life cycle may explain the decline in the eel population in northern Europe in recent decades.

Journal Article↗

Flow cytometric deoxyribonucleic acid analysis in stage I renal cell carcinoma.

Tumor deoxyribonucleic acid (DNA) content was analyzed by flow cytometry in 60 consecutive patients with stage I renal cell carcinoma. Of 59 evaluable tumors 27 (46%) were homogeneously diploid, 1 (2%) was tetraploid and 31 (52%) were aneuploid. Of the 32 nondiploid tumors 25 were heterogeneous concerning ploidy. One of the 27 patients with diploid tumors had metastases compared to 5 of the 32 patients with nondiploid tumors (not significant). There was a significant difference in survival between patients with diploid and nondiploid tumors (p = 0.043). Neither nuclear grade, tumor cell type nor tumor size correlated with survival. Analysis of DNA content seems to predict survival significantly for patients with stage I renal cell carcinoma.

Adult↗

Ampicillin-aminoglycoside combinations as initial treatment for neonatal septicaemia or meningitis. A retrospective evaluation of 12 years' experience.

In a retrospective study covering the years 1975-1986, 341 episodes of invasive infections in 338 newborn infants were evaluated. Of the 365 pathogens isolated from blood and/or cerebrospinal fluid, 91% were sensitive to either ampicillin or aminoglycosides or both. Ampicillin resistance was mainly found in very low and low birthweight infants with late-onset infections, in which aerobic Gram-negative rods were common pathogens. In contrast, aminoglycoside resistance was common in early-onset infections, due to the dominance of group B streptococcal infections. The ampicillin-aminoglycoside combination had been given as initial treatment in 189 cases of septicaemia or meningitis. Treatment failed in 36 infections (20%), although all organisms were sensitive to one or both antibiotics. Treatment failed in 6 of 34 patients with meningitis but the failure was not related to ampicillin or aminoglycoside resistance. In conclusion, both in vitro and clinical results show that the ampicillin-aminoglycoside combination can be used as initial treatment of invasive infections in neonates.

Ampicillin↗

The serum reserve albumin concentration for monoacetyldiaminodiphenyl sulphone and auditory evoked responses during neonatal hyperbilirubinaemia.

Auditory brainstem evoked responses (ABR) were recorded in 9 neonates with hyperbilirubinaemia. Pathological recordings were found in two children showing absence of waves and prolonged latencies. There was no correlation between latencies to waves and the total serum bilirubin concentration. The serum reserve albumin concentration for monoacetyldiaminodiphenyl sulphone (MADDS) was, however, inversely related to the latencies in the ABR recordings. Our findings suggest that the binding properties of serum albumin contribute to the risk of bilirubin toxicity and that, in this study, the reserve albumin concentration for MADDS seemed to be of greater significance than the total bilirubin concentration.

Bilirubin↗

Sensory and motor blockade during epidural analgesia with 1%, 0.75%, and 0.5% ropivacaine--a double-blind study.

Levels of sensory (pinprick) and somatic motor blockade were measured in a double-blind study of 30 volunteers given single epidural injections of 1%, 0.75%, and 0.5% ropivacaine. Onset of analgesia was rapid with all concentrations (7-10 min). Maximal levels of analgesia were established 60 min after injection, with no significant differences in the maximal median cephalad spread. Duration of analgesia at the T-12 level and total duration were significantly longer with 1% and 0.75% than with 0.5% ropivacaine. Motor blockade was assessed by a quantitative method (measurements of isometric muscle force) and a qualitative method (modified Bromage scale). Onset of motor blockade measured by the quantitative method was significantly slower with 0.5% ropivacaine than with the higher concentrations. Maximal muscle weakness occurred 1-1.5 h after injection with all three concentrations. With increase in ropivacaine dose from 100 to 200 mg, the intensity and duration of motor blockade increased. Muscles involved in knee extension were blocked most, those of plantar flexion least. Recovery of motor function, assessed by the above-mentioned quantitative method, occurred simultaneously with the recovery of pinprick perception. Motor blockade registered by Bromage scale showed a slower onset for 0.5% ropivacaine than for the higher concentrations. Mean durations of grade 1 and 2 block were longest for the 1% solution. Motor blockade described by the Bromage scale showed only the first part of the regression phase. Full recovery of muscle strength (Bromage scale = 0) was attained 1.5-2.5 h earlier than assessed by the quantitative method. No adverse effects were registered.

Adult↗

Characteristics of spontaneously agglutinating Proteus mirabilis strains from bacteriuric patients.

Out of 210 Proteus mirabilis isolates from bacteriuric patients a total of eight spontaneously agglutinating strains were found. SDS-PAGE analysis of their lipopolysaccharides (LPS), the separation of polysaccharide fractions (PS) by gel filtration, and chemical characterization of PSs were performed. Out of the eight strains one S form and one mutant classified as Rc were detected. The remaining six strains were recognized as Ra and intermediate forms. When tested in a hematogenous infection model in mice, the P. mirabilis Rc mutant survived in kidneys for at least two weeks, while the Re mutant used as control was eliminated within 20 h after the challenge. These data indicated that strains of P. mirabilis may be pathogenic even if they express very incomplete LPS.

Adult↗

Homologous type II collagen-induced arthritis in rats. Characterization of the disease and demonstration of clinically distinct forms of arthritis in two strains of rats after immunization with the same collagen preparation.

Arthritis was induced in Lewis and DA rat strains after immunization with native homologous type II collagen (CII). Differences were noted in the clinical signs of arthritis in the 2 rat strains, which were immunized with the same arthritogenic preparation of CII. DA rats showed disease onset characterized by symmetric involvement of the interphalangeal joints of the hind feet. Lewis rats showed disease onset characterized by involvement of only the ankle or knee joints. Moreover, the arthritis tended to be chronic (i.e., persistent and variable redness and swelling seen in interphalangeal joints) in DA rats, but not in Lewis rats. Analysis of the delayed-type hypersensitivity reaction to CII and anti-CII autoantibody production demonstrated the presence of T cell, as well as B cell, reactivity to rat CII in both strains of rat. A spontaneous T cell reactivity to CII, as measured by rat CII-induced ear swelling, was observed in nonimmunized DA rats, but not in nonimmunized Lewis rats. The demonstration that clinical features of arthritis induced with identical arthritogenic stimuli are different depending on the genetic background of the affected animal may be relevant in understanding the heterogeneity of the clinical features of human inflammatory joint disease.

Animals↗

Disposition of 3H-aflatoxin B1 in mice: formation and retention of tissue bound metabolites in nasal glands.

Whole-body autoradiography with 3H-labelled aflatoxin B1 (3H-AFB1) in C57B1-mice showed a pronounced accumulation and retention of radioactivity in some nasal glands. At long survival intervals the labelling of the nasal glands was much higher than that of the liver. Experiments in vitro showed a capacity of the nasal glands to form tissue-bound 3H-AFB1-metabolites. Incubations in the presence of glutathione decreased the levels of tissue-bound 3H-AFB1-metabolites both in the liver and in the nasal glands, but the decrease was more pronounced in the former than in the latter tissue. The 3H-AFB1-metabolite-binding to the nasal glands in vitro was inhibited by the cytochrome P-450-inhibitor metyrapone and by CO- and N2-atmospheres indicating a cytochrome P-450-dependent bioactivation of the AFB1 in these glands. Cytochrome P-450 was shown to be present in the glands although at a much lower level than in the liver. The glands in the nose, which were shown to have this AFB1-metabolizing capacity, were the lateral nasal gland (Steno's gland) situated ventrally and laterally to the maxillary sinus and the large group of glands in the lateral nasal wall ventrally to the ostium of the maxillary sinus. Our results also indicated an AFB1-metabolizing capacity of the serous glands which are present in the anterior part of the nasal septum.

Aflatoxin B1↗

E. coli and urease-induced crystallisation in urine.

The effects of urine preinoculation with E. coli for 20 h on urease activities in urine have been studied in synthetic as well as human urine. The E. coli preinoculation increased pH in both synthetic and human urine. Urease enzymatic activity was enhanced in E. coli-preinoculated synthetic urine. The intraluminal urease-induced precipitation was increased in E. coli-preinoculated synthetic urine. The precipitation on glass rods, which more closely reflects crystal growth and aggregation, was reduced. The process of urease-induced crystallisation thus appears to be influenced by E. coli. In human urine, the effects of E. coli preinoculation were less uniform but a significantly increased urease-induced precipitation after E. coli preinoculation could be reproduced in human urine also.

Adult↗

Interleukin 4 induces synthesis of IgE and IgG4 in human B cells.

Interleukin (IL)4 has been shown to regulate the IgG subclasses and induce IgE production in splenic mouse B cells. Here we show that IL4 and phorbol 12-myristate 13-acetate (PMA) induce, on a per cell basis, very high IgE secretion in purified human B cells by using a mouse thymoma (EL4) co-culture method. In addition, a marked increase in the number of IgG4-producing cells was also observed. Furthermore, IL2 could synergize with IL4 and PMA in the production of IgE. By using limiting dilution analysis, a considerable increase in the precursor frequency for IgE was found when IL4 and PMA were added to cultures as compared to cultures with PMA only. This indicates that IL4 induces an isotype switch in human B cells.

Antibody Formation↗

In vivo treatment with anti-CD8 and anti-CD5 monoclonal antibodies alters induced tolerance to adjuvant arthritis.

Resistance (low dose tolerance) to adjuvant arthritis was induced by intradermal immunization with 10 micrograms Mycobacterium tuberculosis administered 5 and 3 weeks before induction of arthritis. With the purpose of determining phenotypes of cells which participate in the maintenance of the induced resistance to adjuvant arthritis, tolerized rats were treated with two different anti-T-cell monoclonal antibodies. In tolerized rats, it was shown that anti-CD8 (OX8) antibodies, which caused an elimination of CD8+ lymphoid cells as determined by immunofluorescence analysis, made the rats responsive to an arthritogenic challenge with mycobacteria. Nine of 19 (47.4%) rats developed the disease as compared with 2 of 18 (11.1%) (P less than 0.05) in the control antibody-treated group. Also, in vivo treatment with anti-CD5 (OX19) monoclonal antibodies made the rats responsive to an arthritogenic challenge with mycobacteria. Nine of 15 (60%) anti-CD5-treated rats developed the disease as compared with 2 of 18 (11.1%) (P less than 0.01) rats in the control group. Immunofluorescence analysis performed after anti-CD5 treatment showed a reduction of staining of CD5+ cells as well as a down-regulation of the staining intensity of CD5 cell surface receptors on the remaining CD5+ cells. These data indicate that CD8+- as well as CD5+ cells participate in the maintenance of low dose tolerance to adjuvant arthritis.

Animals↗

Concentrations of ceftazidime, tobramycin and ampicillin in the cerebrospinal fluid of newborn infants.

Thirty-five neonates with suspected septicaemia were randomized to treatment with tobramycin or ceftazidime, both in combination with ampicillin. Concentrations of antibiotics in the CSF were measured 1 h after the third, fourth or fifth injection. In 13 of 17 neonates tobramycin CSF concentrations were below 0.5 mg/l. Ceftazidime CSF concentrations ranged from 2.5 to 17 mg/l, which should be sufficient for treatment of infections with group B streptococci and most aerobic gram-negative bacilli but not all strains of Staphylococcus aureus. Ampicillin CSF concentrations ranged from 1 to 80 mg/l, which should be sufficient for treatment of meningitis caused by enterococci and Listeria monocytogenes, the most important neonatal pathogens not covered by ceftazidime.

Ampicillin↗

In vivo monoclonal antibody treatment with Ox19 (anti-rat CD5) causes disease relapse and terminates P2-induced immunospecific tolerance in experimental allergic neuritis.

The role of CD5+ lymphocytes in the recovery phase and on immunospecific protection against experimental allergic neuritis (EAN) was examined in Lewis rats by in vivo treatment with Ox19, a mouse anti-rat CD5 monoclonal antibody. Animals pretreated with the peripheral nerve basic protein P2 and thereby rendered resistant to the disease showed clinical signs of EAN after intraperitoneal (i.p.) Ox19 injection given at the same time as the rechallenge with neuritogenic doses of myelin in Freund's complete adjuvant. Non-pretreated rats recovered from signs of EAN developed a clinical relapse after i.p. Ox19 injections. Taken together, these data suggest an important regulatory role of the CD5 receptor in the immune response.

Animals↗

Metabolism of aflatoxin B1 in the bovine olfactory mucosa.

Carcinomas of the ethmoidal region of the nose are observed relatively frequently in cattle in several countries in tropical and subtropical latitudes. Viruses have been implicated as causative agents, but it has been observed that affected animals sometimes suffer from aflatoxicosis, and a role of aflatoxin B1 (AFB1) in the aetiology has also been proposed. We have examined whether the bovine nasal olfactory mucosa has a capacity to metabolize AFB1. The contents of cytochrome P-450 and cytochrome b5, and the NADPH cytochrome c reductase activity in the nasal olfactory mucosa have also been determined. Comparative experiments have been performed with the liver. Incubations with 3H-labelled AFB1 showed that the nasal olfactory mucosa has a much higher capacity than the liver to form lipid-soluble, water-soluble and tissue-bound AFB1-metabolites. High-resolution microautoradiography showed a strong localization of tissue-bound metabolites in the sustentacular cells in the apical portion of the olfactory surface epithelium and in Bowman's glands in the olfactory lamina propria mucosae. Especially in the sustentacular cells the labelling was preferentially located in the nuclei of the cells. Liquid chromatography of chloroform extracts of the nasal olfactory mucosa and the liver incubated with 3H-AFB1 showed formation of several metabolites. The dominating peak in both tissues was aflatoxin M1 (AFM1). However, the amount of AFM1 was higher in the nasal olfactory mucosa than in the liver, and the amounts and proportions of several other metabolites also differed markedly between the two tissues. The level of cytochrome P-450 in the nasal olfactory mucosa was found to be about one quarter of that in the liver, but the NADPH cytochrome c reductase activity was much higher in the nasal olfactory mucosa than in the liver. In addition, the cytochrome b5: cytochrome P-450 ratio was higher in the nasal olfactory mucosa than in the liver. The higher metabolism of AFB1 in the nasal olfactory mucosa than in the liver may be related to differences in the cytochrome P-450 isoenzyme profile. In addition, the microsomal electron transport to cytochrome P-450 may be facilitated by the high reductase: cytochrome P-450 ratio and the high cytochrome b5: cytochrome P-450 ratio in the nasal olfactory mucosa.(ABSTRACT TRUNCATED AT 400 WORDS)

Aflatoxin B1↗

Oestrogen is a potent immunomodulator of murine experimental rheumatoid disease.

Oestrogen has important modulatory effects on autoimmune diseases. Earlier studies, both in humans and in experimental models, have convincingly suggested that oestrogen exaggerates lupus disease and enhances autoantibody production in lupus. However, a general effect by oestrogen to stimulate auto-immune disease does not fit with recent findings in human rheumatoid arthritis and in certain experimental autoimmune models. Here it is shown that oestrogen treatment suppresses development of type II collagen induced arthritis in mice and rats, which is a T-cell dependent experimental model for human RA. The oestrogen-mediated effects are obtainable in physiological levels and both incidence and severity of disease can be suppressed. It is demonstrated that oestrogen has a dualistic effect on the immune system by suppressing antigen-specific T-cell dependent immune reactions while enhancing B-cell activities. On these grounds, we suggest that autoimmune diseases should be divided into two groups, one in which oestrogen accelerates disease progression and another in which oestrogen is beneficial.

Animals↗

Effects of purified protein derivative (PPD)-activated syngeneic epidermal cells on a PPD-specific rat T-helper cell line.

An important question in local immune regulation in the skin is how keratinocytes at inflammatory sites can modify a local T-cell response to antigens introduced via the skin. In the present study we investigated the effects of rat epidermal cells obtained from the site of a tuberculin reaction, on the proliferative response of a syngeneic purified protein derivative (PPD)-specific CD4+ T-cell line. Epidermal cell suspensions from the tuberculin-reactive ears contained 23-37% cells expressing class II transplantation antigens as judged by immunocytochemistry compared with 2-3% in normal epidermis. When comparing the capacity of these two different epidermal cell populations to induce a PPD-specific T-cell response in vitro, it was found that the PPD-reactive epidermal cells induced a lower T-cell response than did normal epidermal cells. This discrepancy cannot be explained by an infiltration of inflammatory cells into the epidermis of tuberculin-reactive ears. Our data indicate that epidermal cells modified during a delayed-type hypersensitivity reaction in vivo may suppress an antigen-specific T-cell proliferation.

Animals↗