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991.
Aim of work Evaluation of suitability and safety of venous port implantation with catheter insertion via the right internal jugular vein in oncology patients.Patients and methods One hundred one totally implantable venous ports were placed in 100 patients with malignancies from January 1, 2003 until March 31, 2005. Catheter of venous port was preferably inserted via the right internal jugular vein. We recorded a number of successful implantations using this venous approach and the rate of complications during the procedure and follow-up.Main results Ninety-seven catheters (96%) of totally implantable venous ports were inserted via the right internal jugular vein in 96 patients, and only in four cases were we not able to access this vein. We had no complications related to catheter insertion via the right internal jugular vein. Follow-up was made in all 96 patients with a total access days of 41 in 151 days (mean: 407 days). Premature catheter removal was required in six (6.2%, 0.144 per 1,000 access days) due to complications: three catheter dislocations/malfunctions (3.1%, 0.072 per 1,000 access days), one port-related sepsis, one pocket port infection, and one decubitus over port (1%, 0.024 per 1,000 access days). Six venous ports were removed after completion of the treatment at the patient’s request.Conclusion The placement of totally implantable venous ports with catheter insertion via the right internal jugular vein has a high success rate without any early complications. Follow-up also demonstrates a low incidence of late complications requiring port removal. 相似文献
992.
Richard Hopkins Wenwei Xiang Damien Marlier Veonice Bijin Au Qianting Ching Lynn Xue Wu Rujun Guan Bernett Lee Whay-Kuang Chia Who-Whong Wang Joseph Wee Joanna Ng Rachael Cheong Shuting Han Axel Chu Chit Lai Chee Timothy Shuen Michael Podinger John E. Connolly 《Molecular therapy》2021,29(2):734-743
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993.
Schulze-Bahr E Neu A Friederich P Kaupp UB Breithardt G Pongs O Isbrandt D 《The Journal of clinical investigation》2003,111(10):1537-1545
The cardiac pacemaker current I(f) is a major determinant of diastolic depolarization in sinus nodal cells and has a key role in heartbeat generation. Therefore, we hypothesized that some forms of "idiopathic" sinus node dysfunction (SND) are related to inherited dysfunctions of cardiac pacemaker ion channels. In a candidate gene approach, a heterozygous 1-bp deletion (1631delC) in exon 5 of the human HCN4 gene was detected in a patient with idiopathic SND. The mutant HCN4 protein (HCN4-573X) had a truncated C-terminus and lacked the cyclic nucleotide-binding domain. COS-7 cells transiently transfected with HCN4-573X cDNA indicated normal intracellular trafficking and membrane integration of HCN4-573X subunits. Patch-clamp experiments showed that HCN4-573X channels mediated I(f)-like currents that were insensitive to increased cellular cAMP levels. Coexpression experiments showed a dominant-negative effect of HCN4-573X subunits on wild-type subunits. These data indicate that the cardiac I(f) channels are functionally expressed but with altered biophysical properties. Taken together, the clinical, genetic, and in vitro data provide a likely explanation for the patient's sinus bradycardia and the chronotropic incompetence. 相似文献
994.
Genomic imbalances in drug-resistant T-cell acute lymphoblastic CEM leukemia cell lines 总被引:1,自引:0,他引:1
Efferth T Verdorfer I Miyachi H Sauerbrey A Drexler HG Chitambar CR Haber M Gebhart E 《Blood cells, molecules & diseases》2002,29(1):1-13
Ten T-cell acute lymphoblastic (T-ALL) CEM cell lines selected for resistance toward methotrexate (CEM/MTX60PGA, CEM/MTX140LV, CEM/MTX1500LV, CEM/MTX5000PGA, CEM/MTXR1, CEM/MTXR2, and CEM/MTXR3), doxorubicin (CEM/ADR5000), vincristine (CEM/VCR1000), or hydroxyurea (CEM/HUR90), respectively, and parental drug-sensitive CCRF-CEM cells were analyzed using comparative genomic hybridization. Most genomic imbalances were not specific for drug resistance, as they were found in both parental and drug-resistant lines. Three aberrations were common to all or most cell lines analyzed: dim(5q35), dim(9p21p24), and enh(20q). We were concerned on those imbalances which were specifically present in drug-resistant but not in drug-sensitive cells. All methotrexate-resistant cell lines were characterized by an enhancement or an amplification of 5q13. The methotrexate resistance-conferring dihydrofolate reductase (DHFR) gene is located at this locus. Gain of DHFR was verified by PCR analyses. CEM/MTX60PGA, CEM/MTX140LV, CEM/MTX1500LV, and CEM/MTX5000PGA showed enh(14q21qter) and CEM/MTX5000PGA amp(5p13p15.2). These two loci harbor the methylenetetrahydrofolate dehydrogenase (MTHFD1) and 5'-methyltetrahdrofolate-homocysteine methyltransferase reductase (MTRR) genes, both of which are involved in folate metabolism. Their gain indicates a role in methotrexate resistance. A loss of 4q35 was found in CEM/MTXR2, CEM/MTXR3, and CEM/ADR5000 where the proapoptotic caspase-3 gene is located. The thioredoxin (TXN) locus 9q31 was enhanced in CEM/ADR5000 and CEM/MTX5000PGA cells. 2p22pter was increased in hydroxyurea-resistant CEM/HUR90 cells. Ribonucleotide reductase polypeptide M2 (RRM2), which confers resistance to hydroxyurea, resides at this locus. Other specific genomic imbalances in drug-resistant cell lines were dim(1p36.5), enh(4p), dim(8p22pter), enh(12p13), dim(17p), enh(18q12), enh(21q22.2), dim(21q22.2), and dim(22q13). All genomic imbalances were subjected to hierarchical cluster analysis and clustered image mapping to identify profiles of chromosomal aberrations in the cell lines. The obtained dendrograms allowed separation of imbalances common to all or most cell lines from other more individual aberrations. Furthermore, methotrexate-resistant cell lines clustered together. Our future efforts will be directed toward those imbalances which implicate still unknown candidate drug resistance genes. 相似文献
995.
Kahmann L Uciechowski P Warmuth S Plümäkers B Gressner AM Malavolta M Mocchegiani E Rink L 《Rejuvenation research》2008,11(1):227-237
Aging is associated with low-grade inflammation on the one hand and mild zinc deficiency on the other. These conditions contribute to decreased immune functions, resulting in increased incidences of infections and autoimmune diseases. The aim of this study was to give more insight into the question, to what extent is low-grade inflammation caused by zinc deficient status. Here we report the effect of improved intracellular zinc status on low-grade inflammatory activity in 19 healthy elderly subjects. Our experiments show that adjustment of labile zinc by moderate zinc supplementation reduces spontaneous cytokine release and defects in termination of inflammatory activity. This results in reduced amounts of unspecific preactivated T cells and leads to improved T cell response upon mitogenic stimulation. Therefore, in contrast to other anti-inflammatory drugs, zinc does not suppress, but improves immune reaction upon pathogen invasion. These results suggest that mildly zinc-deficient, healthy elderly subjects might benefit from moderate zinc supplementation due to a more balanced immune response with reduced incidences of infections and autoimmune diseases. 相似文献
996.
The aim of the study was to evaluate morphologic alterations of microvessels quantitatively and objectively in patients with
various connective tissue diseases (CTD) by means of histomorphometry. Standardized histomorphometrical examination of dermal
microvessels was performed by means of interactive semi-automated image analysis in specimens obtained by the technique of
capillaroscopically guided nailfold biopsy in 31 patients with various CTD and 8 controls without CTD. Histomorphometry revealed
a significant enlargement, an increased dysmorphia and a diminished number of microvessels as well as an increased papillary
area in CTD-patients compared to controls. The most severe alterations of microvessels were seen in scleroderma and MCTD,
whereas in SLE the morphometrically observed changes were less impressive. By means of histomorphometry morphological changes
of the microvasculature can be analyzed quantitatively and objectively. Since differences regarding nature and extent of the
microvascular injury between particular conditions can be disclosed by the technique, this approach may be a useful tool to
identify distinct patterns of microangiopathy in the various types of CTD. 相似文献
997.
Barbara Hoffmann Susanne Moebus Andreas Stang Eva-Maria Beck Nico Dragano Stephan M?hlenkamp Axel Schmermund Michael Memmesheimer Klaus Mann Raimund Erbel Karl-Heinz J?ckel 《European heart journal》2006,27(22):2696-2702
AIMS: Long-term exposure to urban air pollution may accelerate atherogenesis and increase cardiopulmonary mortality. We aim to examine the relationship between the long-term residential exposure to traffic and prevalence of coronary heart disease (CHD). METHODS AND RESULTS: We used baseline data from the German Heinz Nixdorf RECALL study, a population-based, prospective cohort study. For 3399 participants from two cities, we assessed the long-term personal traffic exposure and background air pollution, comparing residents living within 150 m of major roads with those living further away. The principal outcome variable was clinically manifest CHD. We evaluated the association with multivariable logistic regression, controlling for background air pollution and individual level risk factors. Of 3399 participants, 242 (7.1%) had CHD. The crude odds ratio (OR) for prevalence of CHD at high traffic exposure was significantly elevated (1.62, 95%CI 1.12-2.34) and rose to 1.85 (95%CI 1.21-2.84) after adjusting for cardiovascular risk factors and background air pollution. Subgroup analysis showed stronger effects for men (OR 2.33, 95%CI 1.44-3.78), participants younger than 60 years (OR 2.67, 95%CI 1.24-5.74) and never-smokers (OR 2.72, 95%CI 1.40-5.29). CONCLUSION: This study provides epidemiological evidence that the long-term exposure to traffic-related emissions may be an important risk factor for CHD. 相似文献
998.
999.
Marcel Kunadt Katrin Eckermann Anne Stuendl Jing Gong Belisa Russo Katrin Strauss Surya Rai Sebastian Kügler Lisandro Falomir Lockhart Martin Schwalbe Petranka Krumova Luis M. A. Oliveira Mathias Bähr Wiebke Möbius Johannes Levin Armin Giese Niels Kruse Brit Mollenhauer Ruth Geiss-Friedlander Albert C. Ludolph Axel Freischmidt Marisa S. Feiler Karin M. Danzer Markus Zweckstetter Thomas M. Jovin Mikael Simons Jochen H. Weishaupt Anja Schneider 《Acta neuropathologica》2015,129(5):695-713
1000.
Sven M?bius-Winkler Nicolas Majunke Marcus Sandri Norman Mangner Axel Linke Gregg W Stone Ingo D?hnert Gerhard Schuler Peter B Sick 《World journal of cardiology》2015,7(2):65-75
Transcatheter closure of the left atrial appendage has been developed as an alternative to chronic oral anticoagulation for stroke prevention in patients with atrial fibrillation, and as a primary therapy for patients with contraindications to chronic oral anticoagulation. The promise of this new intervention compared with warfarin has been supported by several, small studies and two pivotal randomized trial with the Watchman Device. The results regarding risk reduction for stroke have been favourable although acute complications were not infrequent. Procedural complications, which are mainly related to transseptal puncture and device implantation, include air embolism, pericardial effusions/tamponade and device embolization. Knowledge of nature, management and prevention of complications should minimize the risk of complications and allow transcatheter left atrial appendage closure to emerge as a therapeutic option for patients with atrial fibrillation at risk for cardioembolic stroke. 相似文献