[More respect for the family members. Study of patients and their relatives in psychiatric care].
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Biomedical subjects
Publications and source records attributed to K Johansson.
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The process and route of bacterial translocation from the gut after major liver resection remain unclear. In the present study enteric bacterial translocation, enterocyte ultrastructure in the ileum and colon, the process and route of bacterial invasion and the permeability of the cell membrane system and blood-tissue barrier were evaluated in rats receiving sham operation, and 70 or 90 per cent hepatectomy. The incidence of bacterial translocation to mesenteric lymph nodes was 80-100 per cent in rats 6 h after 70 per cent and 2-4 h after 90 per cent hepatectomy, and 80-100 per cent to the systemic circulation 2-4 h after 90 per cent hepatectomy but only 20 per cent to the portal vein. An increase in bacterial adherence to the intestinal surface, damage to the permeability of the cell membrane system and blood-tissue barrier, and pathological alterations in the ileum and colon developed, correlating with the extent of liver removed and the time that had passed after hepatectomy. Most translocating bacteria appeared in morphologically intact enterocytes with increased membrane permeability, in antigen-presenting cells and in submucosal lymphatics, but some bacteria were also seen within damaged enterocytes 4h after 90 per cent hepatectomy. These results indicate that altered permeability of the cell membrane system may be one of the earliest characteristics of challenged enterocytes, and that enteric bacteria translocate through both morphologically normal and abnormal enterocytes. Translocation occurred mainly into the lymphatics, bacteria either being 'carried' by antigen-presenting cells or entering by active invasion.
The Best's macular dystrophy (BMD) gene has previously been mapped to the 11q13 region. In this study, recombination data localizes the BMD gene to the 6-cM genetic interval between the markers Fc epsilon RI and D11S480/ROM1 in a large Swedish 12-generation BMD family. Mutation analyses of the candidate gene ROM1 did not reveal any mutations that could explain the disease phenotype. However, one recombination event between intragenic ROM1 polymorphisms and the BMD phenotype was detected. Therefore, it is highly unlikely that mutations in the ROM1 gene cause BMD. Identification of the disease gene will elucidate the pathophysiological mechanism in BMD, which may also be of importance in other retinopathies such as age-related macular degeneration.
An amalgam filling was inserted into the first upper molar of 12 rats and the animals were killed after 3-9 months. Tissue sections from the trigeminal ganglia and the brain stem were then investigated with a sensitive histochemical technique to trace mercury deposits. Within the trigeminal ganglia, nerve cells with mercury deposits were observed in seven out of 12 rats, whereas no mercury was detected in sections from the brain stem. The mechanism responsible for the accumulation of mercury in neurons of the trigeminal ganglia is discussed.
Obstructive jaundice is frequently associated with septic complications and enteric bacteria have been isolated from both the infectious focus and bile in jaundiced patients. The present study aimed to evaluate bacterial translocation and the influence of a macrophage-stimulant (muramyl tripeptide phosphatidylethanolamine) on bacterial translocation in obstructive jaundice. Male Sprague-Dawley rats were subjected to sham operation (n = 10) or common bile-duct ligation and transection (n = 35). Two weeks later, jaundiced animals received either physiological saline (n = 15), muramyl tripeptide phosphatidylethanolamine liposomes (n = 10) or placebo (empty) liposomes (n = 10) orally, while sham-operated rats received physiological saline, 48 h prior to evaluation of enteric bacterial translocation. Blood, bile and caecal contents were collected and cultured aerobically and anaerobically, as were tissue samples from the liver, spleen and mesenteric lymph nodes. Positive mesenteric lymph node cultures in animals with jaundice + saline (7/15; 47%) and jaundice + placebo liposomes (4/10; 40%) significantly differed (p < 0.05) from sham-operated animals (1/10; 10%) and muramyl tripeptide phosphatidylethanolamine treated animals (0/10). Caecal counts (CFU/g) of Escherichia coli, Lactobacilli and aerobic and microaerobic bacteria did not differ statistically among the groups, although the number of E. coli tended to be higher in jaundiced animals. Thus, liposomal muramyl tripeptide phosphatidylethanolamine inhibits bacterial translocation, probably by activating mucosal macrophages and enhancing reticuloendothelial system function in rats with biliary obstruction.
Laser Doppler flowmetry (LDF) was used for endoscopic measurement of regional blood flow in 20 patients who had undergone previous gastric resection for peptic ulcer. Twenty-five patients with intact stomach and normal endoscopic findings were used as controls. In resected patients, the degree of enterogastric reflux gastritis was assessed by subjective grading and by morphological examination of biopsies from the region of the gastroenterostomy. In patients with an intact stomach, the average blood flow was significantly higher in the body of the stomach compared to the antrum (p < 0.001), without any significant differences between the greater and lesser curvature. In resected patients, the average blood flow in the gastric body remnant was markedly higher than in the region of the gastroenterostomy, but also significantly higher than the corresponding area of the gastric body in patients with an intact stomach (p < 0.01). The degree of gastritis in the region of the stoma of resected patients was often overestimated on subjective endoscopic assessments compared to morphological biopsy examinations. The degree of histological gastritis was not significantly correlated to blood flow levels of the gastroenterostomy. It is concluded that low gastric wall perfusion, impeding mucosal defense, does not seem to be a major factor in the development of enterogastric reflux gastritis in the resected stomach.
When transfected into mouse splenic B cells stimulated with lipopolysaccharide (LPS) the expression of DNA vectors containing the chloramphenicol acetyl transferase gene under the control of a SP6 kappa promoter and the Ig heavy chain intron enhancer could be down-regulated 5- to 10-fold by treatment of the cells with anti-Ig prior to transfection. Exchanging the SP6 kappa promoter by minimal promoters consisting of an octamer or a SP1 motif linked to TATA box did not impair the anti-Ig induced down-regulation while inserting a rabbit beta-globin promoter did. The transcriptional regulation could be observed after replacing the Ig heavy chain intron enhancer with a SV40 enhancer, or duplicated minimal Ig heavy chain enhancers containing or lacking the octamer element. The down-regulation was not dependent on the level of transcriptional stimulation observed. A difference in Oct2 expression could neither be detected at the RNA nor protein level after treatment of LPS stimulated B cells with anti-Ig or phorbol-dibutyrate. Anti-Ig treatment, but not phorbol-di-butyrate treatment, induced increased levels of AP1 and NF kappa B transcription factors. Thus, either differentiation specific transcriptional control of Ig genes is exerted via transcription factors common to several distinct enhancers or via transcriptional adaptor molecules that can interact with several distinct DNA binding proteins.
Oct2-isoform expression in splenic B cells stimulated with lipopolysaccharide or lipopolysaccharide plus phorbol-di-butyrate was analysed by cDNA cloning. The frequency of Oct2-positive clones was 1/15,000 in both libraries. Two new isoforms were found that generate novel amino- or carboxy-terminal sequences. An isoform lacking exon 11 destroyed the carboxy-terminal leucin-zipper region and introduced a frame shift creating a novel, proline-rich carboxy terminus. A new exon containing a highly basic region (4c) was characterized, between exons 4 and 5. This exon was inserted between glutamine-rich regions 2 and 3, carboxy terminal of a tentative leucine-zipper structure. In addition, a new combination isoform containing Oct2a's amino terminal insert (exon 7a) and Oct2b's carboxy terminal insert (exon 13) was found that created a novel large isoform, Oct2ab. More frequent use of the classical Oct2a and Oct2b isoforms was observed in the lipopolysaccharide-stimulated B cells, while a preference for the Oct2ab and Oct2ba isoforms was observed in lipopolysaccharide plus phorbol-di-butyrate-treated cells.
In order to determine the influence of phospholipid on abdominal biomaterial-induced bacterial translocation (BT), phsophatidylcholine (PC) or phosphatidylinositol (PI) was administered orally or intraperitoneally in rats with intraperitoneal implantation of 7-cm2 rubber drain pieces. Two days after surgery, the incidence of translocation to mesenteric lymph nodes and liver significantly decreased, the adherence of 3H-labeled Escherichia coli to the ileal mucosa was significantly inhibited and the phagocytic and bactericidal capacity of peritoneal macrophages increased in animals with PC or PI administered orally, but not intraperitoneally, as compared with rats without phospholipid administration. Scanning electron microscopy revealed a coating layer on the surface of the intestinal mucosa in phospholipid-gavaged rats. Thus, the results in the present study imply that oral, but not intraperitoneal, PC of PI administration reduces enteric BT induced by intraperitoneal drain implantation.
BACKGROUND AND PURPOSE: In a randomized study of hemiparetic stroke patients with a median age of 75 years, functional recovery was significantly better in those who received additional sensory stimulation (n = 38), including electrostimulation, than in control patients (n = 40) given the same physiotherapy and occupational therapy; group differences for balance, mobility, and activities of daily living were significant. The present study was designed to investigate postural control in patients who survived more than 2 years after stroke onset. METHODS: The 48 survivors (mean, 2.7 years; range, 2.0 to 3.8 years), 22 from the treatment group and 26 from the control group, were compared with 23 age-matched healthy subjects. Subjects were perturbed by vibrators applied to calf muscles or with galvanic vestibular stimulation. We evaluated postural control in terms of sway variances or sway velocities and the dynamics of postural control as a feedback system using system identification with a model previously validated for human postural control. RESULTS: Significantly more patients of the treatment group than of the control group maintained stance during perturbations (P < .01). Among patients capable of maintaining stance during perturbation, the control patients were characterized by significant divergence from normal values in two of the three characteristic parameters of dynamic postural control (ie, swiftness and stiffness; P < .05) compared with the treatment subgroup or age-matched subjects. CONCLUSIONS: The course of sensory stimulation enhanced recovery of postural function, an enhancement still significant 2 years after the lesion and treatment. The differences and near normalization of characteristic parameters of dynamic postural control among treated patients suggest that improved recovery after sensory stimulation may be achieved by patients regaining normal or near normal dynamics of human postural control.
In a five-generation selection experiment, separate lines of standard mink (Mustela vison) were subjected to selection for litter size at 3 wk (F line), body weight in September (BS line), underfur density (P line), or combined selection for litter size and body weight (I line). One unselected line served as a control (C line). The present paper focuses on correlated responses to selection regarding fertility and fitness traits, fur quality, and body size traits. Genetic and environmental parameters were estimated with REML (Restricted Maximum Likelihood) techniques using a multi-trait, reduced animal model in a derivative-free way. Genetic and phenotypic correlations were estimated from four subsets of data consisting of 1) female September weight, litter size, and kit mortality; 2) body size traits; 3) September weight and fur traits graded on live mink; and 4) fur traits graded on live mink and skins. September weight was found to be negatively correlated with fertility and fitness traits as well as with fur traits. Selection for underfur density resulted in an improvement in guard hair quality and in general impression of the fur and almost eliminated the fur defect metallic sheen.
Puberty traits of 740 Yorkshire gilts from a selection experiment were analyzed. Heritabilities were estimated to be .32 for pubertal age, .23 for length of proestrus, .16 for length of standing estrus, .29 for ability to show standing reflex, and .24 for intensity of vulvar symptoms. Genetic correlations between length of proestrus, intensity of vulvar symptoms, and ability to show standing reflex were positive. There seemed to be a negative genetic correlation between percentage of lean and intensity of vulvar symptoms. There were negative genetic correlations between growth rate and length of standing estrus, and between growth rate and ability to show standing reflex.
Recently a new hemostatic disorder has been described which appears to be an important risk factor for familial thromboembolism. The disorder is characterized by a poor anticoagulant response to activated Protein C (APC) and has been shown to be due to lack of an APC cofactor activity which is a property of factor V. A kit for determining the response of plasma samples towards addition of APC in an APTT-based assay--COATEST APC Resistance-has been evaluated on 35 coagulation instruments in a multicenter study involving 32 laboratories. A lyophilized normal plasma and identical plasma aliquotes from 20 individuals, one of whom had a borderline resistance to APC, were analysed in each laboratory and the sensitivity of each plasma to APC was determined as the ratio between the clotting times obtained in the presence and absence of APC (APC ratio). The plasma from the individual with a borderline resistance to APC activity was correctly classified as the lowest responder in each laboratory, with an APC ratio in the range 1.6-2.4. In comparison, plasmas from individuals with a pronounced response to APC activity resulted in APC ratios above 3.4 in most cases. Interestingly, although the actual APT time for a plasma from a given individual showed a more than 10s difference due to the type of instrumentation used, the variation in the APC ratio was limited. A similar discrimination was also obtained from evaluation of the actual prolongation of the clotting time in the presence of APC.(ABSTRACT TRUNCATED AT 250 WORDS)
Co-transfection of expression vectors for c-myc or myn down-regulated the expression from a reporter plasmid containing the chloramphenicol-acetyl-transferase (CAT) gene, under the control of an immunoglobulin kappa promoter and the immunoglobulin heavy-chain enhancer. The effect was dose-dependent and an additive effect was seen when both expression vectors were transfected simultaneously. Deletion mutants lacking the leucine zipper region of c-myc were unable to down-regulate the transcription from the reporter construct. Reporter genes where the immunoglobulin enhancer had been exchanged with a SV40 enhancer or an immunoglobulin minimal enhancer were still down-regulated by a cotransfection with c-myc expression vectors. A minimal promoter containing an octamer motif responded to myc expression while a minimal promoter containing a SP1 motif did not. No direct interactions between myc, myn and Oct proteins could be detected either by band-shift analysis, or by co-translation in vitro followed by precipitation with SP6 kappa promoter bound to magnetic carriers. Furthermore, B cells from mice transgenic for myc showed aberrant expression of transcription factors.
The healing characteristics of polymer-coated Dacron grafts with or without heparin-bonding and collagen-coated Dacron grafts are compared with standard knitted Dacron grafts by implanting eight of each graft into pig iliac arteries. The grafts were implanted at random bilaterally with end-to-side anastomoses. The grafts were explanted after 1, 2 and 4 weeks and prepared for histological evaluation by in vivo fixation. Graft segments were investigated by light microscopy, scanning electron microscopy and transmission electron microscopy. The endothelial coverage, intimal thickness and healing characteristics were subjected to one-way analysis of variance. One week after surgery endothelial-like cells appeared close to the anastomoses and after 2 weeks a clear growing endothelial edge was observed in the collagen-coated grafts. After 4 weeks' implantation all grafts were patent and endothelial cells covered the grafts to a various extent. Collagen-coated grafts had significantly greater endothelial cell coverage compared with Dacron and polymer-coated grafts without heparin bonding (P < 0.05). Evaluation by transmission electron microscopy revealed the luminal coverage of the collagen-coated grafts to consist of organized smooth muscle cells and endothelial cells containing Weibel-Palade bodies. The smooth muscle cells in the other grafts were less organized and were covered by endothelial cells to a lesser degree. No differences were noted regarding the inflammatory response of the graft materials and no further positive effects were encountered by the addition of heparin to the polymer coating. The study demonstrates that various coating procedures and surface modulation of knitted Dacron grafts produce a graft which is impervious to blood but still allows tissue incorporation.(ABSTRACT TRUNCATED AT 250 WORDS)
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Molecular genetic studies have identified disease-causing mutations at codon 717 of the amyloid protein precursor gene in families with early-onset Alzheimer's disease. Recently, we reported a new mutation at codon 670/671 in a large Swedish family with Alzheimer's disease. The mutation results in two amino acid changes at the N-terminal of the beta-amyloid region. In the present study, we screened for the APP 670/671 mutation in sufferers from 31 other Swedish families with Alzheimer's disease using PCR and restriction enzyme digestion. The mutation was found only in the family previously reported and not in any other family. It is concluded that this mutation is a rare cause of familial Alzheimer's disease in Sweden.
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