tbuckley/cabot-search huggingface dataset:
Thrombotic Thrombocytopenic Purpura after Allogeneic Hematopoietic Stem Cell Transplantation: A Complication Still Frequent and Responsible of Severe Outcome.
Authors: Cornelio Uderzo, Haidi Sangalli, Sonia Bonanomi, Giuseppe Morreale, Edoardo Lanino, Claudio Annaloro, Aldo Della Volpe, Paolo Alessandrino, Mario Lazzarino, Mila Renoldi, Paolo Ferrari, Massimo Iacobelli, Alessandro Busca, Franco Locatelli, Adriana Balduzzi, Attilio Rovelli
Journal: Blood (2005)
512. The Cytokine Release Syndrome Crucially Contributes to the Anti-Leukemic Effects of CD44v6 CAR-T Cells
Authors: Margherita Norelli, Monica Casucci, Barbara Camisa, Laura Falcone, Aurore Saudemont, Luigi Naldini, Fabio Ciceri, Claudio Bordignon, Chiara Bonini, Attilio Bondanza
Journal: Molecular Therapy (2016)

Background: Despite the remarkable clinical results of CD19 CAR-T cells in B-cell leukemias, their long-term efficacy is limited by the emergence of CD19-loss escape variants. Moreover, whether the cytokine release syndrome (CRS) is necessary for durable remissions is a matter of debate. Currently available xenograft models in NSG mice are not suited for studying the antitumor effects of CAR-T cells beyond 3-4 weeks, because of xenograft-versus-host disease (X-GVHD). Moreover, since NSG mice lack functional myeloid cells, the CRS does not develop. Aim: To verify whether the CRS contributes to the antileukemic effects of CAR in an innovative xenotolerant mouse model.Results: NSG mice triple transgenic for human IL-3, GM-CSF and SCF (NSG-3GS) were sub-lethally irradiated and injected intra-liver with human HSCs soon after birth, enabling an accelerated and better balanced lympho-hematopoietic reconstitution compared with NSG mice. Reconstituting human T cells were single CD4+/CD8+ T cells, representing all memory sub-populations. After ex vivo isolation and activation with CD3/CD28-beads and IL-7/IL-15, NSG-3GS T cells were transduced with a CD44v6 CAR, retaining an early-differentiated (stem-cell/central-memory) phenotype and full antitumor functionality against acute myeloid leukemia (AML). NSG-3GS-derived CD44v6 CAR T cells were subsequently infused in tumor-bearing secondary recipients previously humanized with autologous HSCs. CAR-T cells persisted in vivo for at least 6 months and mediated durable leukemia remissions (P<0.001 vs controls) in the absence of X-GVHD. Tumor clearance associated with an acute malaise syndrome, characterized by high fevers and a surge in human IL-6 levels, which was lethal in 30% of the mice. Differently from CD19 CAR-T cells, the CRS by CD44v6 CAR-T cells was significantly anticipated (3 vs 8 days), coinciding with human CD44v6+ monocyte depletion. In humanized mice, previous myeloid-cell depletion by clodronate administration completely prevented this syndrome, but associated with late leukemia relapses. Conversely, mice developing the CRS entered a state of durable and profound remission, as demonstrated by prolonged observation times and secondary transplantation. Conclusions: By using an innovative xenotolerant mouse model, we have demonstrated that the CRS is needed for sustained antileukemic effects by CD44v6 CAR-T cells.
Effects of neuromuscular blockers on transpulmonary pressures in moderate to severe acute respiratory distress syndrome
Authors: Christophe Guervilly, Magali Bisbal, Jean Marie Forel, Malika Mechati, Samuel Lehingue, Jeremy Bourenne, Gilles Perrin, Romain Rambaud, Melanie Adda, Sami Hraiech, Elisa Marchi, Antoine Roch, Marc Gainnier, Laurent Papazian
Journal: Intensive Care Medicine (2016)
Sinus floor elevation procedures to enable implant placement and integration: techniques, biological aspects and clinical outcomes
Authors: Stefan Lundgren, Giovanni Cricchio, Mats Hallman, Måns Jungner, Lars Rasmusson, Lars Sennerby
Journal: Periodontology 2000 (2016)

Abstract Implant treatment in an atrophied edentulous posterior maxilla constitutes a challenge for the therapeutic team. The authors of the present study acknowledge that modern micro‐rough surface implants in lengths of about 8–10 mm or longer and of different brands are similarly successful. Consequently, the authors propose that the use of different sinus floor elevation techniques should be considered when &lt; 8 mm of bone is available below the maxillary sinus. The type of sinus floor elevation technique selected is mainly based on residual vertical bone height, marginal bone width, local intrasinus anatomy and the number of teeth to be replaced, although other factors (such as surgical training and surgical experience) may have an impact. It is proposed that a transcrestal sinus floor elevation approach can be considered as a first‐choice method for single tooth gaps in situations with sufficient width for implant placement and a residual bone height of 5–8 mm, while lateral sinus floor elevation, with or without grafting materials, is indicated when &lt; 5 mm of bone is available and when several teeth are to be replaced. With regard to time of implant placement, a one‐stage procedure is preferred provided that high primary stability can be ensured.
Comparison of Leishmania typing results obtained from 16 European clinical laboratories in 2014
Authors: Gert Van der Auwera, Aldert Bart, Carmen Chicharro, Sofia Cortes, Leigh Davidsson, Trentina Di Muccio, Jean-Claude Dujardin, Ingrid Felger, Maria Grazia Paglia, Felix Grimm, Gundel Harms, Charles L. Jaffe, Monika Manser, Christophe Ravel, Florence Robert-Gangneux, Jeroen Roelfsema, Seray Töz, Jaco J. Verweij, Peter L. Chiodini
Journal: Eurosurveillance (2016)

Leishmaniasis is endemic in southern Europe, and in other European countries cases are diagnosed in travellers who have visited affected areas both within the continent and beyond. Prompt and accurate diagnosis poses a challenge in clinical practice in Europe. Different methods exist for identification of the infecting Leishmania species. Sixteen clinical laboratories in 10 European countries, plus Israel and Turkey, conducted a study to assess their genotyping performance. DNA from 21 promastigote cultures of 13 species was analysed blindly by the routinely used typing method. Five different molecular targets were used, which were analysed with PCR-based methods. Different levels of identification were achieved, and either the Leishmania subgenus, species complex, or actual species were reported. The overall error rate of strains placed in the wrong complex or species was 8.5%. Various reasons for incorrect typing were identified. The study shows there is considerable room for improvement and standardisation of Leishmania typing. The use of well validated standard operating procedures is recommended, covering testing, interpretation, and reporting guidelines. Application of the internal transcribed spacer 1 of the rDNA array should be restricted to Old World samples, while the heat-shock protein 70 gene and the mini-exon can be applied globally.
Human Innate Lymphoid Cell Subsets Possess Tissue-Type Based Heterogeneity in Phenotype and Frequency
Authors: Yannick Simoni, Michael Fehlings, Henrik N. Kløverpris, Naomi McGovern, Si-Lin Koo, Chiew Yee Loh, Shawn Lim, Ayako Kurioka, Joannah R. Fergusson, Choong-Leong Tang, Ming Hian Kam, Koh Dennis, Tony Kiat Hon Lim, Alexander Chung Yaw Fui, Chan Weng Hoong, Jerry Kok Yen Chan, Maria Curotto de Lafaille, Sriram Narayanan, Sonia Baig, Muhammad Shabeer, Sue-Anne Ee Shiow Toh, Henry Kun Kiaang Tan, Rosslyn Anicete, Eng-Huat Tan, Angela Takano, Paul Klenerman, Alasdair Leslie, Daniel S.W. Tan, Iain Beehuat Tan, Florent Ginhoux, Evan W. Newell
Journal: Immunity (2016)
Xanthohumol Induces Apoptosis in B-CLL In Vitro by Sustained Endoplasmic Reticulum Stress and Inhibition of NFκ-B.
Authors: Sofie Lust, Barbara Vanhoecke, Mireille Van Gele, Mary Kaileh, Jerina Boelens, Martine Poelman, Wim VandenBerghe, Jan Philippé, Fritz Offner
Journal: Blood (2006)
Abstract 1006: Celastrol modulated Taz and induced cell apoptosis in vitro
Authors: Shuren Wang
Journal: Cancer Research (2015)

Abstract Celastrol is derived from the Chinese medicinal plant Tripterygium wilfordii, which has attracted great attention for its potent anticancer effects. Celastrol has been found to inhibit the proliferation, induce apoptosis, and suppress invasion/migration and angiogenesis both in vitro and in vivo. In our current study, we treated the HEK293 cells with the Celastrol(0.75μM) for 24h and found that Celastrol could reduce the expression of TAZ in HEK293 cells. To better evaluate the effect of TAZ on HEK293 cells, cell growth curve and colony formation assay were performed. HEK293/TAZ and HEK293/control cells were plated at a density of 50 cells/mm2 in triplicate for 5 days and HEK293/TAZ and HEK293/control cells were seeded into six-well plates of 500 cells/well for two weeks. The result showed that HEK293/TAZ grew obviously faster and could form more colonies than HEK293/control cells. To further address the effect of TAZ in vivo, equal numbers(1.5×106) of HEK293/TAZ and HEK293/control cells were injected bilateral subcutaneously into nude mice. The mice were sacrificed 40 days after injection. We found that the latency of tumor formation in nude mice injected with HEK293/TAZ cells was shorter than the tumor injected with HEK293/control cells. Furthermore, HEK293/TAZ cells could lead to a larger tumor size compared to the HEK293/control cells. Our data indicated that the overexpression of TAZ could significantly promote cell proliferation in vitro and in vivo. Furthermore, after HEK293/TAZ and HEK293/control cells were treated with Celastrol(0.75μM) for 24h, the data showed that the less PARP cleavage was definitely observed in HEK293/TAZ cells than HEK293/control cells by Western blotting. Moreover, 18.9% of HEK293/TAZ cells were TUNEL-positive, compared with 83.2% of HEK293/control cells after Celastrol treatment(0.75μM, 24h). Our data indicated that overexpression of TAZ could overcome partially the cell apoptosis induced by Celastrol in vitro. In summary, our finding prompts that Celastrol could suppress growth of tumor cells through the modulation of TAZ, and the mechanism how TAZ plays its function needs to be further explored. Citation Format: Shuren Wang. Celastrol modulated Taz and induced cell apoptosis in vitro. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 1006. doi:10.1158/1538-7445.AM2015-1006
The Activation of Stat3 by the Stk Receptor Tyrosine Kinase Requires Src Kinases and Gab2, and Is Essential for Friend Virus Induced, Epo-Independent Growth of Primary Erythroid Cells.
Authors: Shuang Ni, Hami Heal, Jie Xu, Robert Paulson, Pamela H. Correll
Journal: Blood (2004)
Abstract 943: The critical role of CDK2 activation in determining the differential sensitivity of cell lines to Chk1 and Wee1 inhibitors
Authors: Nandini Sakurikar, Ruth Thompson, Ryan Montano, Alan Eastman
Journal: Cancer Research (2015)

Abstract Anticancer DNA damaging agents activate checkpoints that halt the cell cycle to prevent further DNA replication and mitosis until the damage has been repaired. One of the important regulatory proteins activated in this pathway is Checkpoint kinase 1 (Chk1). Hence, Chk1 inhibitors have emerged as promising novel therapeutics. In clinical trials, Chk1 inhibitors are primarily being evaluated in combination with various DNA damaging agents. However, Chk1 inhibitors also show single agent activity in a subset of cell lines, and this provides a unique therapeutic opportunity to target these tumors. The goal of this study is to define the mechanism of this sensitivity, and identify biomarkers that would permit selection of appropriate patients for clinical trials. From screening a large panel of cancer cell lines, we observed that 15% were sensitive to the Chk1 inhibitor MK-8776, with rapid (&amp;lt;6 h) induction of DNA double-strand breaks (DSB) in S phase cells. Most of the resistant cell lines were sensitive to the Wee1 inhibitor, MK-1775 (AZD1775), while all the cell lines were sensitive to the Wee1/Myt1 dual inhibitor, PD-166285. Wee1 suppresses activation of CDK1 and CDK2, suggesting that MK-1775-mediated activation of one or other (or both) of these kinases leads to DSB. MK-8776 did not activate CDK1, so we hypothesized that activation of CDK2 was critical. To differentiate between the role of CDK1 and CDK2 in cell lines sensitive or resistant to MK-8776, we used inhibitors to CDK1/2. We found that CVT-313 was a selective inhibitor of CDK2 at low concentrations, but that Ro-3306 failed to discriminate between these two kinases in cells. CVT-313 prevented DSB and the associated phosphorylation of histone-H2AX induced by MK-8776 and MK-1775. Cyclin E is a direct target of CDK2; phosphorylation of cyclin E leads to its degradation which was only observed in sensitive cells and prior to the formation of DSB. The acute cytotoxicity was dependent on cyclin A rather than cyclin E, as siRNA-mediated knockdown of cyclin A but not cyclin E, prevented DSB. We conclude that activation of cyclin A/CDK2 determines the sensitivity of cells to MK-8776. Resistance to MK-8776 results from failure to activate CDK2, presumably through failure to activate the upstream CDC25A phosphatase. MK-1775 can circumvent this resistance by directly activating CDK2. The untimely and abnormal activation of CDK2 is then cytotoxic to cancer cells. Citation Format: Nandini Sakurikar, Ruth Thompson, Ryan Montano, Alan Eastman. The critical role of CDK2 activation in determining the differential sensitivity of cell lines to Chk1 and Wee1 inhibitors. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 943. doi:10.1158/1538-7445.AM2015-943
Abstract 3031: Replication stress and DNA damage promote genomic instability in near-tetraploid colorectal cancer cells
Authors: Isabel Quintanilla, Darawalee Wangsa, Markus Brown, Amaia Ercilla, Greg Klus, Maria Vila, Juan José Lozano, Zoltan Szallsi, Neus Agell, Antoni Castells, Thomas Ried, Jordi Camps
Journal: Cancer Research (2015)

Abstract Aneuploidy represents a hallmark of most solid tumours, and potentially has a causal role in carcinogenesis. Also, cancer cells exhibit high rates of chromosome missegregation, which leads to chromosomal instability (CIN). However, a large amount of tumours present near-triploid karyotypes likely to go through a tetraploid transient stage. Here, by using DLD-1 isogenic diploid and tetraploid cell lines generated by single cell FACS-sorting, we aimed at exploring how polyploidization affects cellular functions and whether tetraploid per se generates CIN in a genomically stable background. First, gene expression and subsequent gene set enrichment analysis revealed that genes involved in the machinery of the DNA synthesis and replication, such as MCM2 and RRM2, and genes involved in cell cycle, were significantly upregulated in near-tetraploid cells compared to their diploid counterparts. Functionally, polyploidy cells exhibited replication stress, as indicated by higher levels of pCHK1, RPA and 53BP1 foci, which resulted in increased DNA damage in S- and M-phase. In addition, tetraploid cells displayed impaired proliferative capabilities as a consequence of a cell cycle delay confirmed by BrdU pulse and flow cytometry. Furthermore, near-tetraploid clones showed a higher amount of intracellular karyotypic heterogeneity due to the higher frequency of micronuclei formation compared to their diploid counterparts. In fact, polyploid cells displayed an increased tendency of abnormal anaphase events, including lagging chromosomes and acentric fragments. Interestingly, these heterogeneous cellular populations showed strengthen migratory capabilities and preliminary experiments suggested an increment in tumor invasiveness too. Taken together, our data suggest that near-tetraploid cells systematically undergo replication stress, which can be responsible for the increased levels of genomic instability. Citation Format: Isabel Quintanilla, Darawalee Wangsa, Markus Brown, Amaia Ercilla, Greg Klus, Maria Vila, Juan José Lozano, Zoltan Szallsi, Neus Agell, Antoni Castells, Thomas Ried, Jordi Camps. Replication stress and DNA damage promote genomic instability in near-tetraploid colorectal cancer cells. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 3031. doi:10.1158/1538-7445.AM2015-3031
Abstract 551: Identification of gene-expression biomarkers in urine pathology specimens for the detection of bladder cancer
Authors: Karen B. Chapman, Liqun Qiu, Jennifer Kidd, Aparna Baxi, Markus D. Lachter, Joseph Wagner, Dorothy L. Rosenthal, Matthew T. Olson
Journal: Cancer Research (2015)

Abstract Bladder cancer recurrence screening is typically managed with a combination of urine cytology and cystoscopy, each with its inherent caveats. Cystoscopy is generally considered the gold standard for diagnosing bladder cancer and can yield a valuable biopsy, but is too invasive and expensive for routine screening and surveillance. Voided urine cytology is inexpensive and readily available, but lacks the desired level of sensitivity. Furthermore, up to 20% of urine cytology specimens fall into one of two indeterminate categories that require follow-up testing, typically in the form of an invasive cystoscopy procedure. With the goal of developing a urine-based molecular test for bladder cancer recurrence surveillance, we examined gene expression biomarkers in urine cytopathology specimens. 90 patient urine samples were analyzed: 45 high-grade urothelial carcinoma (HG-UC) and 45 benign samples. All patient samples were submitted to the Johns Hopkins Cytopathology Department for evaluation for bladder cancer via urine cytology. The samples represent patients undergoing bladder cancer recurrence screening and patients without a prior history of bladder cancer presenting with hematuria. The urine sediments were stored in liquid based cytology solution at 4°C for a period of 7 - 10 days, during which time the cytopathology diagnosis was determined from a portion of the sample. Post-diagnosis, the pathology sample “leftover” was analyzed for gene expression. RNA was extracted, amplified and microarray analysis was performed and a panel of molecular biomarkers was identified. Individual genes in this panel discriminate between HG-UC and benign in this training set with an average ROC of 0.86 (p &amp;lt;0.0001) while a combined panel of 10 genes yields a ROC of 0.97 (p &amp;lt;0.0001). Differential expression of some of the individual genes from the panel was confirmed by qPCR. Additional evaluation of this gene panel in a validation set is ongoing and results from this validation study will be discussed. Citation Format: Karen B. Chapman, Liqun Qiu, Jennifer Kidd, Aparna Baxi, Markus D. Lachter, Joseph Wagner, Dorothy L. Rosenthal, Matthew T. Olson. Identification of gene-expression biomarkers in urine pathology specimens for the detection of bladder cancer. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 551. doi:10.1158/1538-7445.AM2015-551
Immunohistochemical Analysis of the Expression of the B- Cell Markers BCL-6, MUM1/IRF4, CD79A and Transcription Factors BOB.1 and OCT.2 in Classical Hodgkin Lymphoma.
Authors: S. Valsami, D. Rontogianni, V. Pappa, T. Economopoulos, F. Kontsioti, E. Papageorgiou, J. Dervenoulas, T. Karmiris, I. Kaitsa, V. Giannopoulou, D. Pektassidis, E. Nikiforakis, S. A. Raptis
Journal: Blood (2005)
Hemocompatibility of Superhemophobic Titania Surfaces
Authors: Sanli Movafaghi, Victoria Leszczak, Wei Wang, Jonathan A. Sorkin, Lakshmi P. Dasi, Ketul C. Popat, Arun K. Kota
Journal: Advanced Healthcare Materials (2016)

The hemocompatibility of superhemophobic surfaces is investigated and compared with that of hemophobic surfaces and hemophilic surfaces. This analysis indicates that only those superhemophobic surfaces with a robust Cassie–Baxter state display significantly lower platelet adhesion and activation. It is envisioned that the understanding gained through this work will lead to the fabrication of improved hemocompatible, superhemophobic medical implants. As a service to our authors and readers, this journal provides supporting information supplied by the authors. Such materials are peer reviewed and may be re-organized for online delivery, but are not copy-edited or typeset. Technical support issues arising from supporting information (other than missing files) should be addressed to the authors. Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.
Alemtuzumab and Rituximab in the treatment of refractory autoimmune Cytopenias.
Authors: David Gomez-Almaguer, Manuel Solano-Genesta, Olga Cantu-Rodriguez, Cesar Homero Gutierrez-Aguilar, Jose Carlos Jaime-Perez, Luz Carmen Tarin-Arzaga, Miguel Angel Gomez-Guijosa
Journal: Blood (2009)
Is Serum Albumin Associated With Guillain-Barré Syndrome Outcomes?
Authors: Richard A. C. Hughes
Journal: JAMA Neurology (2016)

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Utlilizing Mutant Mice To Dissect Immune Bone Marrow Failure: Markedly Reduced Cytotoxicity of Lymphocytes from Fas- and Fas Ligand-Deficient Mice in Lymph Node Cell-Mediated Aplastic Anemia.
Authors: Stephanie O. Omokaro, Felicia M. Ellison, Keyvan Keyvanfar, Jichun Chen, Neal S. Young
Journal: Blood (2007)
Chronic Renal Insufficiency in Japanese Patients with Paroxysmal Nocturnal Hemoglobinuria (PNH): Improvement with Eculizumab Treatment in the Long-Term Follow-up of the AEGIS Study.
Authors: Yuzuru Kanakura, Kazuma Ohyashiki, Tsutomu Shichishima, Shinichiro Okamoto, Kiyoshi Ando, Haruhiko Ninomiya, Tatsuya Kawaguchi, Shinji Nakao, Hideki Nakakuma, Jun-ichi Nishimura, Taroh Kinoshita, Camille Bedrosian, Marye Ellen Valentine, Keiya Ozawa, Mitsuhiro Omine
Journal: Blood (2009)