Karolinska University Hospital

Stockholm, Sweden

Karolinska University Hospital

Stockholm, Sweden

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News Article | April 24, 2017
Site: www.biosciencetechnology.com

To support healthcare and scientific research groups with high quality cytological cell samples, the National Clinical Cytology Biobank at the Karolinska Institute in Stockholm (Sweden) has invested in 2D coded sample storage tubes and sample handling equipment from Micronic to provide traceable, high integrity storage of its valuable gynecological cell samples. The Clinical Cytology Biobank was opened in August 2011 and installed at the Department of Laboratory Medicine of the Karolinska University Hospital. The biobank houses more than 800,000 biological cell samples. Nasrin Perskvist, National Coordinator and Director of the Clinical Cytology Biobank, commented “As of 2013, we have a national reach. Fourteen of the twenty county councils have now implemented the Clinical Cytology Biobank at their laboratories. This means that throughout Sweden, more than 90 percent of the liquid-based cytological cell samples are processed for biobanking. The total number of cell samples stored within this common platform is more than 1.3 million.” She added, “To safeguard and track our valuable samples, we carefully evaluated different sample storage suppliers and selected Micronic 0.75ml 2D coded tubes together with 1D barcoded storage racks, split TPE push caps and the Univo Manual/Electric Capper.” Micronic 0.75ml sample storage tubes are manufactured from medical grade, ultra-low binding polypropylene, in a certified Class 7 cleanroom environment ensuring they exhibit absolute product consistency, near zero contaminants and are RNase/DNase free. The tubes resist many organic solvents (DMSO, methanol, dichloromethane), may be autoclaved, withstand gamma rays used for sterilization and can be repeatedly freeze-thawed. A unique 2D code non-detachable laser etched onto the bottom of each tube provides an easy and unambiguous means of storing and identifying samples. The split TPE push caps can be pierced multiple times with a robotic tip without losing sealing performance.

GAITHERSBURG, Md., April 13, 2017 (GLOBE NEWSWIRE) -- OpGen, Inc. (NASDAQ:OPGN) today announced that five posters featuring its technologies will be presented at the 27th European Congress of Clinical Microbiology and Infectious Diseases (ECCMID) being held April 22-25, 2017 in Vienna, Austria. Among them will be a poster presentation titled “Prediction of antibiotic resistance in Escherichia Coli from resistance genes” by Dr. Terry Walker, Senior Vice President of Research and Development at OpGen. The presentation will highlight preliminary results supporting OpGen’s efforts to develop and commercialize a rapid and highly accurate test that predicts antibiotic resistance using resistance gene detection and the bioinformatics capabilities of the Acuitas Lighthouse® Knowledgebase. The OpGen booth location is 32B. The details for the presentations at ECCMID are as follows: Poster title: Prediction of antibiotic resistance in Escherichia coli from resistance genes Presenter: T. Walker, OpGen Date and time: Tuesday, April 25 from 12:54 - 12:59 pm CEST Location: Poster Area Poster number: #EP0938 Abstract number: #4182 Session info: Direct detection methods Poster title: Use of the Acuitas Resistome Test to detect and type carbapenemase producing organisms (CPOs): A pilot study Presenter:  G. Vanstone, Royal Free London NHS Foundation Trust Date and time: Saturday, April 22 from 3:30 - 4:30 pm CEST Location: Poster Area Poster number: #P0387 Abstract number: #6205 Session info: Detection of resistant pathogens Poster title: Rapid outbreak detection of multi-drug resistant organisms using resistance genes profiles Presenter: W. Chang, OpGen Date and time: Saturday, April 22 from 8:45 am - 3:30 pm CEST Location: Poster Area Poster number: #EV0483 Abstract number: #5396 Session info: Resistance surveillance & epidemiology: Gram-negatives Poster title: Evaluation of QuickFISH and the Sepsityper assays for early identification of aetiological agents in bloodstream infection in a clinical routine setting Presenter: A. Pernestig, Systems Biology Research Centre, University of Skövde Date and time: Monday, April 24 from 1:30 - 2:30 pm CEST Location: Poster Area Poster number: #P1561 Abstract number: #1166 Session info: Diagnostic microbiology Poster title: Seven years of clinical experience with the Yeast Traffic Light PNA FISH: assay performance and implications on antifungal therapy Presenter: V. Özenci, Karolinska University Hospital Date and time: Sunday, April 23 from 1:30 - 2:30 pm CEST Location: Poster Area Poster number: #P0969 Abstract number: #5533 Session info: Diagnostic mycology I About OpGen OpGen, Inc. is harnessing the power of informatics and genomic analysis to provide complete solutions for patient, hospital and network-wide infection prevention and treatment. Learn more at www.opgen.com and follow OpGen on Twitter and LinkedIn.

Elekta (EKTA-B.ST) today announced that its Leksell®Vantage™ Stereotactic System*, the company's next-generation system for target localization and coordinate referencing for precision neurosurgery will be highlighted at Elekta booth 2139 at the American Association of Neurological Surgeons (AANS) Annual Meeting, April 22-26 in Los Angeles. Leksell Vantage head frame is constructed of a novel epoxy composite and is designed to improve imaging quality, speed and patient comfort in neurosurgery procedures. Vantage received CE Mark clearance in March 2017 and will be used this month in clinical practice for the first time in Europe at University Hospital La Timone (Marseilles, France), The Academic Medical Center (Amsterdam, the Netherlands), The National Hospital for Neurology and Neurosurgery, Queens Square (London, England) and Karolinska University Hospital (Stockholm, Sweden). The system is currently pending 510(k) clearance with the U.S. Food and Drug Administration. "Our Leksell Stereotactic System has been helping clinicians achieve outstanding patient outcomes for more than 60 years, and Vantage improves upon this gold standard platform to deliver uncompromising accuracy in stereotactic imaging and treatment," says Jesper Söderqvist, Vice President Neuroscience Portfolio at Elekta. "With potential for faster imaging, more efficient workflow, reduced artifacts and a better overall user experience, Leksell Vantage is a welcome advancement for physicians and their patients." Leksell Gamma Knife featured in more than 15 abstracts In addition to Vantage, Elekta will highlight its Leksell Gamma Knife® radiosurgery system. The most clinically studied stereotactic radiosurgery platform, Gamma Knife was highlighted in more than 15 scientific presentations at AANS, including: The posters for Abstracts #1837 and #2022 are available through the AANS conference app. "The inclusion of more than 15 data abstracts at this major neurosurgery conference underscores the fundamental role that Gamma Knife plays today in the treatment of cancer and other complex neurological disorders," says Söderqvist. "These studies also highlight the potential of Gamma Knife to enable the treatment regimens of tomorrow, offering the enhanced radiation targeting and sparing of healthy tissue that is essential for optimum care and outcomes." Additional data presented during the conference (Abstract #2331) confirmed that Elekta's Leksell Gamma Knife was the most frequently mentioned SRS system in a comprehensive clinical literature review with 11,638 citations out of 13,539 articles retrieved. Gamma Knife was also the most frequently cited SRS system in neurosurgical indications, including brain metastases (n=1037), arteriovenous malformation (n=734) and spinal metastases (n=184). For more information on Gamma Knife, visit Elekta booth 2139 at AANS 2017 or www.gammaknife.com. *Leksell® Vantage™ Stereotactic System is pending 510(k) clearance and not available for sale or distribution in the United States. For further information, please contact: Gert van Santen, Group Vice President Corporate Communications, Elekta AB Tel: +31 653 561 242, e-mail: gert.vansanten@elekta.com Time zone: CET: Central European Time This information was brought to you by Cision http://news.cision.com The following files are available for download: To view the original version on PR Newswire, visit:http://www.prnewswire.com/news-releases/elekta-to-highlight-continued-innovation-in-stereotactic-neurosurgery-with-leksell-vantage-stereotactic-system-at-aans-300444156.html

Lippitz B.E.,Karolinska University Hospital
The Lancet Oncology | Year: 2013

Active, but dysfunctional, immune responses in patients with cancer have been studied in several tumour types, but owing to the heterogeneity of cancer theories of common reaction mechanisms seem to be obsolete. In this Review of published clinical studies of patients with cancer, expression and interplay of the following cytokines are examined: interleukin 2, interleukin 6, interleukin 8, interleukin 10, interleukin 12, interleukin 18, tumour necrosis factor α (TNFα), transforming growth factor β (TGFβ), interferon-γ, HLA-DR, macrophage migration inhibitory factor (MIF), and C-X-C motif chemokine receptor 4 (CXCR4). Clinical data were analysed in a non-quantitative descriptive manner and interpreted with regard to experimentally established physiological cytokine interactions. The clinical cytokine pattern that emerged suggests that simultaneous immunostimulation and immunosuppression occur in patients with cancer, with increased concentrations of the cytokines MIF, TNFα, interleukin 6, interleukin 8, interleukin 10, interleukin 18, and TGFβ. This specific cytokine pattern seems to have a prognostic effect, since high interleukin 6 or interleukin 10 serum concentrations are associated with negative prognoses in independent cancer types. Although immunostimulatory cytokines are involved in local cancer-associated inflammation, cancer cells seem to be protected from immunological eradication by cytokine-mediated local immunosuppression and a resulting defect of the interleukin 12-interferon-γ-HLA-DR axis. Cytokines produced by tumours might have a pivotal role in this defect. A working hypothesis is that the cancer-specific and histology-independent uniform cytokine cascade is one of the manifestations of the underlying paraneoplastic systemic disease, and this hypothesis links the stage of cancer with both the functional status of the immune system and the patient's prognosis. Neutralisation of this cytokine pattern could offer novel and so far unexploited treatment approaches for cancer. © 2013 Elsevier Ltd.

Andersson U.,Karolinska University Hospital | Tracey K.J.,Feinstein Institute for Medical Research
Annual Review of Immunology | Year: 2011

A key question in immunology concerns how sterile injury activates innate immunity to mediate damaging inflammation in the absence of foreign invaders. The discovery that HMGB1, a ubiquitous nuclear protein, mediates the activation of innate immune responses led directly to the understanding that HMGB1 plays a critical role at the intersection of the host inflammatory response to sterile and infectious threat. HMGB1 is actively released by stimulation of the innate immune system with exogenous pathogen-derived molecules and is passively released by ischemia or cell injury in the absence of invasion. Established molecular mechanisms of HMGB1 binding and signaling through TLR4 reveal signaling pathways that mediate cytokine release and tissue damage. Experimental strategies that selectively target HMGB1 and TLR4 effectively reverse and prevent activation of innate immunity and significantly attenuate damage in diverse models of sterile and infection-induced threat. © 2011 by Annual Reviews. All rights reserved.

Telomerase activation through induction of its catalytic component telomerase reverse transcriptase (TERT) expression is essential for malignant transformation. TERT promoter mutations namely C228T and C250T that stimulate TERT transcription and telomerase activation have recently been identified in many human malignancies. We thus determined these mutations and their biological and clinical implications in thyroid carcinomas in the present study. The TERT promoter was sequenced in 10 thyroid cancer cell lines and 144 tumors from 20 patients with anaplastic thyroid carcinoma (ATC), 51 with papillary thyroid carcinoma (PTC), 36 with follicular thyroid carcinoma (FTC), and 37 with medullary thyroid carcinoma (MTC). We identified C228T or C250T mutation in 6/8 of ATC cell lines, as well as in tumor tissue from 10/20, 13/51, 8/36 and 0/37 patients with ATC, PTC, FTC and MTC, respectively. In PTC patients, these mutations were exclusively present in the group with age >45 years (P<0.0001), and highly correlated shorter telomeres (P<0.0001) and distant metastasis (P=0.028). The previous radioactivity exposure did not induce the mutation. The presence of C228T or C250T was an independent predictor associated with shorter disease-related survival (DRS) in the entire cohort (P<0.0001), as well as among patients >45 years (P=0.021). ATC patients carrying the mutation survived shorter than those without mutations, although not statistically significant (P=0.129). The TERT promoter mutation was associated with overall survival (P=0.038) and DRS (P=0.058) of FTC patients. Taken together, age- and shorter telomere-dependent TERT promoter mutations occur frequently in follicular cell-derived thyroid carcinoma (ATC, PTC and FTC) but not in parafollicular cell-originated MTC, and may serve as a marker for aggressive disease and poor outcome.

Renne T.,Karolinska University Hospital
Seminars in Immunopathology | Year: 2012

The contact system is a plasma protease cascade that is initiated by coagulation factor XII activation on cardiovascular cells. The system starts procoagulant and proinflammatory reactions, via the intrinsic pathway of coagulation or the kallikrein-kinin system, respectively. The biochemistry of the contact system in vitro is well understood, however, its in vivo functions are just beginning to emerge. Data obtained in genetically engineered mice have revealed an essential function of the contact system for thrombus formation. Severe deficiency in contact system proteases impairs thrombus formation but does not reduce the hemostatic capacity of affected individuals. The system is activated by an inorganic polymer, polyphosphate that is released from activated platelets. Excessive inherited activation of the contact system causes a life-threatening swelling disorder, hereditary angioedema. Activation of the contact system by pathogens contributes to leakage in bacterial infections. Mast-cell-derived heparin triggers contact-system-mediated edema formation with implications for allergic disease states. Here we present an overview about the plasma contact system in occlusive and inflammatory disease and its contribution to health and pathology. © Springer-Verlag 2011.

Increasing evidence suggests that tumor-initiating cells (TICs), also called cancer stem cells, are partly responsible for resistance to DNA-damaging treatment. Here we addressed if such a phenotype may contribute to radio- and cisplatin resistance in non-small cell lung cancer (NSCLC). We showed that four out of eight NSCLC cell lines (H125, A549, H1299 and H23) possess sphere-forming capacity when cultured in stem cell media and three of these display elevated levels of CD133. Indeed, sphere-forming NSCLC cells, hereafter called TICs, showed a reduced apoptotic response and increased survival after irradiation (IR), as compared with the corresponding bulk cell population. Decreased cytotoxicity and apoptotic signaling manifested by diminished poly (ADP-ribose) polymerase (PARP) cleavage and caspase 3 activity was also evident in TICs after cisplatin treatment. Neither radiation nor cisplatin resistance was due to quiescence as H125 TICs proliferated at a rate comparable to bulk cells. However, TICs displayed less pronounced G2 cell cycle arrest and S/G2-phase block after IR and cisplatin, respectively. Additionally, we confirmed a cisplatin-refractory phenotype of H125 TICs in vivo in a mouse xenograft model. We further examined TICs for altered expression or activation of DNA damage repair proteins as a way to explain their increased radio- and/or chemotherapy resistance. Indeed, we found that TICs exhibited increased basal γH2AX (H2A histone family, member X) expression and diminished DNA damage-induced phosphorylation of DNA-dependent protein kinase (DNA-PK), ataxia telangiectasia-mutated (ATM), Krüppel-associated protein 1 (KAP1) and monoubiquitination of Fanconi anemia, complementation group D2 (FANCD2). As a proof of principle, ATM inhibition in bulk cells increased their cisplatin resistance, as demonstrated by reduced PARP cleavage. In conclusion, we show that reduced apoptotic response, altered DNA repair signaling and cell cycle perturbations in NSCLC TICs are possible factors contributing to their therapy resistance, which may be exploited for DNA damage-sensitizing purposes.

Andersson U.,Karolinska University Hospital | Tracey K.J.,Feinstein Institute for Medical Research
Annual Review of Immunology | Year: 2012

The reasoning that neural reflexes maintain homeostasis in other body organs, and that the immune system is innervated, prompted a search for neural circuits that regulate innate and adaptive immunity. This elucidated the inflammatory reflex, a prototypical reflex circuit that maintains immunological homeostasis. Molecular products of infection or injury activate sensory neurons traveling to the brainstem in the vagus nerve. The arrival of these incoming signals generates action potentials that travel from the brainstem to the spleen and other organs. This culminates in T cell release of acetylcholine, which interacts with α7 nicotinic acetylcholine receptors (α7 nAChR) on immunocompetent cells to inhibit cytokine release in macrophages. Herein is reviewed the neurophysiological basis of reflexes that provide stability to the immune system, the neural-and receptor-dependent mechanisms, and the potential opportunities for developing novel therapeutic devices and drugs that target neural pathways to treat inflammatory diseases. © 2012 by Annual Reviews. All rights reserved.

The lack of significant treatment and prevention progress highlights the need for a more expanded strategy. Given the robust association between socioeconomic factors and obesity, combined with new insights into how socioeconomic disadvantage affects both behaviour and biology, a new causal model is proposed. The model posits that psychological and emotional distress is a fundamental link between socioeconomic disadvantage and weight gain. At particular risk are children growing up in a disharmonious family environment, mainly caused by parental socioeconomic disadvantage, where they are exposed to parental frustrations, relationship discord, a lack of support and cohesion, negative belief systems, unmet emotional needs and general insecurity. Without adequate resilience, such experiences increase the risk of psychological and emotional distress, including low self-esteem and self-worth, negative emotions, negative self-belief, powerlessness, depression, anxiety, insecurity and a heightened sensitivity to stress. These inner disturbances eventually cause a psycho-emotional overload, triggering a cascade of weight gain-inducing effects including maladaptive coping strategies such as eating to suppress negative emotions, chronic stress, appetite up-regulation, low-grade inflammation and possibly reduced basal metabolism. Over time, this causes obesity, circular causality and further weight gain. Tackling these proposed root causes of weight gain could potentially improve both treatment and prevention outcomes. © 2014 The Author. obesity reviews © 2014 World Obesity.

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