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1.
  • Adamsson, I, et al. (creator_code:aut_t)
  • Microbial ecology and treatment of Helicobacter pylori infections : Review
  • 2000
  • record:In_t: Journal of chemotherapy. - 1120-009X .- 1973-9478. ; 12:1, s. 5-16
  • swepub:Mat_researchreview_t (swepub:level_refereed_t)abstract
    • The aims of the present study were to investigate the ecological disturbances caused by four different anti-H. pylori regimens, to compare different methods for diagnosing H. pylori, and to study the genetic variability of H. pylori. The patients included in the study were all treated at the Center of Gastroenterology, Huddinge University Hospital, Karolinska Institute. All patients were H. pylori-positive before entering the study, confirmed by rapid urease test, histology, culture and urea breath test or PCR. Treatment regimens included in the study were omeprazole alone (OP), in combination with amoxicillin (OA), in combination with amoxicillin and metronidazole (OAM) and in combination with clarithromycin and metronidazole (OCM). Samples from the mouth (saliva and dental plaque), stomach (biopsies from the gastric mucosa in the corpus and in the antrum) and the intestine (feces) were collected before, during and after treatment. The oral microflora was challenged by the three treatment regimens including antimicrobial agents, with the emergence of resistant streptococci and staphylococci in the OCM group. Bacterial strains in the gastric mucosa increased in numbers during treatment in all treatment groups, probably due to the pH rise, which provides a better environment for the commensal microflora. This overgrowth was especially pronounced during treatment with omeprazole alone (OP), possibly due to the fact that a concomitant suppression exerted by the antimicrobial agents occurred in the other treatment groups. H. pylori was, on the other hand, suppressed during treatment in all treatment groups, possibly due to a direct effect of omeprazole and to the colonization resistance expressed by the normal microflora, An emergence of resistant commensal strains in the gastric mucosa was seen in the OCM and the OAM groups. The intestinal microflora was most altered in the OAM and the OCM groups, with persistent disturbances in the OCM group 4 weeks after treatment. The frequency of resistant Enterococcus spp, (OCM), Enterobacteriaceae spp, (OA and OAM) and Bacteroides spp, (OCM) was increased during and after treatment. Different detection methods for H. pylori were compared and PCR was shown to have higher sensitivity than other routine diagnostic tests. The patients in the present study seemed to be colonized with a single strain of H. pylori. Treatment failures in patients treated with OAM were caused by recrudescence. These four patients with relapsing H. pylori infection, were shown to be reinfected with the original H. pylori strain, indicating that H. pylori escapes treatment by a thus far unknown mechanism.
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3.
  • Aeluri, Madhu, et al. (creator_code:aut_t)
  • An Intramolecular Heck Approach To Obtain 17-Membered Macrocyclic Diversity and the Identification of an Antiangiogenesis Agent from a Zebrafish Assay
  • 2013
  • record:In_t: European Journal of Organic Chemistry. - : Wiley. - 1434-193X .- 1099-0690. ; :19, s. 3955-3958
  • swepub:Mat_article_t (swepub:level_refereed_t)abstract
    • We report a practical and modular approach to obtain two different types of 17-membered ring macrocyclic compounds through an intramolecular Heck reaction. These macrocyclic compounds are functionalized, that is, they contain two contiguous stereogenic hydroxy functional groups and an amino acid moiety in the macrocyclic ring skeleton. The macrocycles were then screened against a zebrafish assay to determine the antiangiogenesis activity of these small molecules. Macrocyclic compound 2.2a was identified as a potent inhibitor at 2.5 M, whereas its acyclic precursor and the other related macrocyclic compounds did not show any effect.
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4.
  • Agvald-Öhman, C, et al. (creator_code:aut_t)
  • Anaerobic bacteria commonly colonize the lower airways of intubated ICU patients
  • 2003
  • record:In_t: Clinical Microbiology and Infection. - : Elsevier BV. - 1198-743X .- 1469-0691. ; 9:5, s. 397-405
  • swepub:Mat_article_t (swepub:level_refereed_t)abstract
    • Objectives To investigate respiratory tract colonization by aerobic and anaerobic bacteria in mechanically ventilated patients. Methods Bacterial colonization of the stomach and the respiratory tract was qualitatively and quantitatively analyzed over time in 41 consecutive mechanically ventilated patients in a Swedish intensive care unit (ICU), with special emphasis on elucidation of the role of anaerobic bacteria in the lower respiratory tract. Samples were taken from the oropharynx, gastric juice, subglottic space and trachea within 24 h (median 14 h) of intubation, and then every third day until day 18 and every fifth day until day 33. Results The patients were often heavily colonized with microorganisms not considered to belong to a healthy normal oropharyngeal and gastric flora on admission to the ICU. A majority harbored enterococci, coagulase-negative staphylococci and Candida spp. in at least one site on day 1. Anaerobic bacteria, mainly peptostreptococci and Prevotella spp., were isolated from subglottic and/or tracheal secretions in 59% of the patients. Different routes of tracheal colonization for different groups of microorganisms were found. Primary or concomitant colonization of the oropharynx with staphylococci, enterococci, enterobacteria and Candida was often seen, while Pseudomonas spp., other non-fermenting Gram-negative rods and several anaerobic species often primarily colonized the trachea, indicating exogenous or direct gastrointestinal routes of colonization. Conclusions Mechanically ventilated patients were heavily colonized in their lower airways by potential pathogenic microorganisms, including a high load of anaerobic bacteria. Different routes of colonization were shown for different species.
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5.
  • Agvald-Öhman, C, et al. (creator_code:aut_t)
  • Multiresistant coagulase-negative staphylococci disseminate frequently between intubated patients in a multidisciplinary intensive care unit
  • 2004
  • record:In_t: Critical Care. - : Springer Science and Business Media LLC. - 1364-8535 .- 1466-609X. ; 8:1, s. R42-R47
  • swepub:Mat_article_t (swepub:level_refereed_t)abstract
    • Introduction The intensive care unit is burdened with a high frequency of nosocomial infections often caused by multiresistant nosocomial pathogens. Coagulase-negative staphylococci (CoNS) are reported to be the third causative agent of nosocomial infections and the most frequent cause of nosocomial bloodstream infections. CoNS are a part of the normal microflora of skin but can also colonize the nasal mucosa, the lower airways and invasive devices. The main aim of the present study was to investigate colonization and the rate of cross-transmissions of CoNS between intubated patients in a multidisciplinary intensive care unit. Materials and methods Twenty consecutive patients, ventilated for at least 3 days, were included. Samples were collected from the upper and lower airways. All samples were cultured quantitatively and CoNS were identified by morphology and biochemical tests. A total of 199 CoNS isolates from 17 patients were genetically fingerprinted by pulsed-field gel electrophoresis in order to identify clones and to monitor dissemination within and between patients. Results An unexpected high number of transmission events were detected. Five genotypes were each isolated from two or more patients, and 14/20 patients were involved in at least one and up to eight probable transmission events. Conclusions A frequent transmission of CoNS was found between patients in the intensive care unit. Although transmission of bacteria does not necessarily lead to infection, it is nevertheless an indication that infection control measures can be improved.
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6.
  • Akre, O, et al. (creator_code:aut_t)
  • Body size and testicular cancer
  • 2000
  • record:In_t: Journal of the National Cancer Institute. - : Oxford University Press (OUP). - 0027-8874 .- 1460-2105. ; 92:13, s. 1093-1096
  • swepub:Mat_article_t (swepub:level_refereed_t)
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7.
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8.
  • Alheim, Katarina, et al. (creator_code:aut_t)
  • Identification of a functional glucocorticoid response element in the promoter of the cylcin-dependant kinase inhibitor p57(Kip2)
  • 2003
  • record:In_t: Journal of Molecular Endocrinology. - : Bioscientifica. - 0952-5041 .- 1479-6813. ; 30:3, s. 359-368
  • swepub:Mat_article_t (swepub:level_refereed_t)abstract
    • Glucocorticoids are known regulators of the cell cycle, normally exerting an anti-proliferative effect. We have previously shown that glucocorticoids stimulate expression of p57(Kip2), a member of the Cip/Kip family of cyclin-dependent kinase inhibitors which, in some cell types, may account for the anti-proliferative responses seen after glucocorticoid treatment. The induction of p57(Kip2) involves primary transcriptional effects where no de novo protein synthesis is necessary, suggesting a direct interaction of the glucocorticoid receptor with the p57(Kip2) gene. In this study we have identified a functional glucocorticoid response element (GRE), located 5 kilo bases (kb) upstream of the transcription start site in the human P57(Kip2) promoter. This GRE was functional also when isolated, suggesting a direct transcriptional effect of the glucocorticoid receptor. Furthermore, mutation of this GRE abolished glucocorticoid induction of the reporter gene, whereas mutation of a nearby Sp1 site did not. Using electrophoretic mobility shift assays, we have shown that the -5 kb p57(Kip2) promoter GRE was able to compete with a well-known GRE for glucocorticoid receptor binding. Sequence comparisons with the mouse genome showed that this GRE is highly conserved, further strengthening the biological importance of this site. All these data emphasize the involvement of this GRE in the glucocorticoid-mediated induction of p57(Kip2) expression.
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9.
  • Appelgren, Henrik, et al. (creator_code:aut_t)
  • Distinct centromere domain structures with separate functions demonstrated in live fission yeast cells
  • 2003
  • record:In_t: Journal of Cell Science. - : The Company of Biologists. - 0021-9533 .- 1477-9137. ; 116:19, s. 4035-4042
  • swepub:Mat_article_t (swepub:level_refereed_t)abstract
    • Fission yeast (Saccharomyces pombe) centromere DNA is organized in a central core region flanked on either side by a region of outer repeat (otr) sequences. The otr region is known to be heterochromatic and bound by the Swi6 protein whereas the central core region contains an unusual chromatin structure involving the histone H3 variant Cnp1 (S. pombe CENP-A). The central core is the base for formation of the kinetochore structure whereas the flanking region is important for sister centromere cohesion. We have previously shown that the ultrastructural domain structure of S. pombe centromeres in interphase is similar to that of human centromeres. Here we demonstrate that S. pombe centromeres are organized in cytologically distinct domains even in mitosis. Fluorescence in situ hybridization of fixed metaphase cells revealed that the otr regions of the centromere were still held together by cohesion even after the sister kinetochores had separated. In live cells, the central cores and kinetochores of sister chromosomes could be distinguished from one Another when they were subjected to mitotic tension. The function of the different centromeric domains was addressed. Transacting mutations affecting the kinetochore (nuf2) central core domain (mis6) and the heterochromatin domain (rik1) were analyzed in live cells. In interphase, both nuf2 and mis6 caused declustering of centromeres from the spindle pole body whereas centromere clustering was normal in rik1 despite an apparent decondensation defect. The declustering of centromeres in mis6 cells correlated with loss the Ndc80 kinetochore marker protein from the centromeres. Interestingly the declustered centromeres were still restricted to the nuclear periphery thus revealing a kinetochore-independent peripheral localization mechanism for heterochromatin. Time-lapse microscopy of live mis6 and nuf2-1 mutant cells in mitosis showed similar severe misaggregation phenotypes whereas the rik1 mutants showed a mild cohesion defect. Thus, S. pombe centromeres have two distinguishable domains even during mitosis, and our functional analyses support the previous observations that the kinetochore/central core and the heterochromatin domains have distinct functions both in interphase and mitosis.
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10.
  • Arabi, Azadeh, et al. (creator_code:aut_t)
  • Accumulation of c-Myc and proteasomes at the nucleoli of cells containing elevated c-Myc protein levels
  • 2003
  • record:In_t: Journal of Cell Science. - : The Company of Biologists. - 0021-9533 .- 1477-9137. ; 116:9, s. 1707-1717
  • swepub:Mat_article_t (swepub:level_refereed_t)abstract
    • c-Myc is a predominately nuclear transcription factor that is a substrate for rapid turnover by the proteasome system. Cancer-related mutations in c-Myc lead to defects in its degradation and thereby contribute to the increase in its cellular level that is associated with the disease. Little is known about the mechanisms that target c-Myc to the proteasomes. By using a GFP fusion protein and live analysis we show that c-Myc shuttles between the nucleus and cytoplasm and thus it could be degraded in either compartment. Strikingly, at elevated levels of expression c-Myc accumulates at nucleoli in some cells, consistent with saturation of a nucleolus-associated degradation system in these cells. This idea is further supported by the observation that proteasome inhibitor treatment causes accumulation of c-Myc at the nucleoli of essentially all cells. Under these conditions c-Myc is relatively stably associated with the nucleolus, as would be expected if the nucleolus functions as a sequestration/degradation site for excess c-Myc. Furthermore, during elevated c-Myc expression or proteasome inhibition, nucleoli that are associated with c-Myc also accumulate proteasomes. c-Myc and proteasomes co-localise in intranucleolar regions distinct from the dense fibrillar component of the nucleolus. Based on these results we propose a model for c-Myc downregulation where c-Myc is sequestered at the nucleoli. Sequestration of c-Myc is accompanied by recruitment of proteasomes and may lead to subsequent degradation.
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