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A reporting system for endometrial cytology: Cytomorphologic criteria—Implied risk of malignancy 下载免费PDF全文
Niki Margari M.D. Ph.D. Abraham Pouliakis Ph.D. Dionysios Anoinos M.D. Ph.D. Emmanouil Terzakis M.D. Ph.D. Nikolaos Koureas M.D. Charalampos Chrelias M.D. George Marios Makris M.D. Assimakis Pappas M.D. Ph.D. Evripidis Bilirakis M.D. Ph.D. Christina Goudeli M.D. Vasileia Damaskou M.D. Nicolaos Papantoniou M.D. Ioannis Panayiotides M.D. Petros Karakitsos M.D. 《Diagnostic cytopathology》2016,44(11):888-901
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Evripidis Kaltsonoudis Eleftherios Pelechas Paraskevi V. Voulgari Alexandros A. Drosos 《Seminars in arthritis and rheumatism》2019,48(4):597-602
Objectives
To estimate the size of unmet needs in the treatment of early Rheumatoid Arthritis (eRA), using all the conventional synthetic disease-modifying antirheumatic drugs (csDMARDs) and/or biological DMARDs (bDMARDs) in a long-term observational study.Materials and methods
538 patients with eRA were evaluated. The 2010 ACR/EULAR classification criteria were used. All patients were csDMARDs and bDMARDs-naive with disease duration less than one year. They were treated according to EULAR and ACR recommendations for RA. All the csDMARDs and bDMARDs were used. Clinical, laboratory findings with the disease activity score-28 and treatment decisions were all recorded as well as adverse drug reactions, reason of therapy termination, disease complications and comorbidities.Results
Methotrexate (58%) and Infliximab (37%) where the first csDMARD and bDMARD choice respectively. During follow-up, 14 patients were lost and 7 developed comorbidities. The final results are referred to 517 patients. Among those, 66% were treated with csDMARDs as monotherapy or in combination therapy with sustained low disease activity (LDA). However, 3.2% from this group neither achieved LDA, nor received bDMARDs, due to comorbidities. On the other hand, 34% were treated with bDMARDs with or without csDMARDs. The majority of them demonstrated sustained LDA. From this group, 17.7% never achieved LDA, despite that they switched and received all bDMARDs. Thus, 20.9% of our patients never achieved LDA.Conclusions
Using the current recommendations for RA therapy we successfully treated the majority of our patients. However, we found that the size of gap and the unmet needs for treatment is about 20%. 相似文献5.
LaBelle JL Katz SG Bird GH Gavathiotis E Stewart ML Lawrence C Fisher JK Godes M Pitter K Kung AL Walensky LD 《The Journal of clinical investigation》2012,122(6):2018-2031
Cancer cells subvert the natural balance between cellular life and death, achieving immortality through pathologic enforcement of survival pathways and blockade of cell death mechanisms. Pro-apoptotic BCL-2 family proteins are frequently disarmed in relapsed and refractory cancer through genetic deletion or interaction-based neutralization by overexpressed antiapoptotic proteins, resulting in resistance to chemotherapy and radiation treatments. New pharmacologic strategies are urgently needed to overcome these formidable apoptotic blockades. We harnessed the natural killing activity of BCL-2-interacting mediator of cell death (BIM), which contains one of the most potent BH3 death domains of the BCL-2 protein family, to restore BH3-dependent cell death in resistant hematologic cancers. A hydrocarbon-stapled peptide modeled after the BIM BH3 helix broadly targeted BCL-2 family proteins with high affinity, blocked inhibitory antiapoptotic interactions, directly triggered proapoptotic activity, and induced dose-responsive and BH3 sequence-specific cell death of hematologic cancer cells. The therapeutic potential of stapled BIM BH3 was highlighted by the selective activation of cell death in the aberrant lymphoid infiltrates of mice reconstituted with BIM-deficient bone marrow and in a human AML xenograft model. Thus, we found that broad and multimodal targeting of the BCL-2 family pathway can overcome pathologic barriers to cell death. 相似文献
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Lanitis E Poussin M Hagemann IS Coukos G Sandaltzopoulos R Scholler N Powell DJ 《Molecular therapy》2012,20(3):633-643
Cancer regression by gene-modified T cells bearing a chimeric antigen receptor (CAR) exodomain of mouse origin can be limited by the induction of transgene immunogenicity resulting in poor persistence and function in vivo. The development of functionally-active CAR of human origin can address this issue. Here, we constructed and evaluated fully human anti-mesothelin CARs comprised of a human mesothelin-specific single-chain antibody variable fragment (P4 scFv) coupled to T cell signaling domains. Primary human T cells expressing P4 CAR specifically produced proinflammatory cytokines, degranulated and exerted potent cytolytic functions when cultured with mesothelin-expressing tumors in vitro. P4 CAR T cells also mediated bystander killing of mesothelin-negative cancer cells during coculture. CAR reactivity was not abrogated by soluble tumor-secreted or recombinant mesothelin protein even at supraphysiological levels. Importantly, adoptive transfer of P4 CAR-expressing T cells mediated the regression of large, established tumor in the presence of soluble mesothelin in a xenogenic model of human ovarian cancer. Thus, primary human T cells expressing fully human anti-mesothelin CAR efficiently kill mesothelin-expressing tumors in vitro and in vivo and have the potential to overcome the issue of transgene immunogenicity that may limit CAR T cell trials that utilize scFvs of mouse origin. 相似文献
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Novel Assessment (BlueDop) Device for Detection of Lower Limb Arterial Disease: A Prospective Comparative Study 下载免费PDF全文
Ali Kordzadeh MBBS MSc MD VA‐BC Mekhola Hoff MRCS PhD Evripidis Tokidis MBBS David H. King BSc MSc Tom Browne FRCS Ioannis Prionidis FRCS PhD 《Journal of ultrasound in medicine》2018,37(3):763-768
According to National Institute of Clinical Excellence guidelines, the ankle‐brachial pressure index coupled with a full clinical evaluation has been the mainstay of detecting peripheral arterial disease on its suspicion. However, this technique is not free of its own limitations in calcified arteries, ulcerative and diabetic patients. We introduce a new, novel, and effective assessment device (BlueDop) with a minimal learning curve that could overcome such barriers and serve as a valid replacement in perihospital settings. 相似文献
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Whelan RS Konstantinidis K Wei AC Chen Y Reyna DE Jha S Yang Y Calvert JW Lindsten T Thompson CB Crow MT Gavathiotis E Dorn GW O'Rourke B Kitsis RN 《Proceedings of the National Academy of Sciences of the United States of America》2012,109(17):6566-6571
The defining event in apoptosis is mitochondrial outer membrane permeabilization (MOMP), allowing apoptogen release. In contrast, the triggering event in primary necrosis is early opening of the inner membrane mitochondrial permeability transition pore (mPTP), precipitating mitochondrial dysfunction and cessation of ATP synthesis. Bcl-2 proteins Bax and Bak are the principal activators of MOMP and apoptosis. Unexpectedly, we find that deletion of Bax and Bak dramatically reduces necrotic injury during myocardial infarction in vivo. Triple knockout mice lacking Bax/Bak and cyclophilin D, a key regulator of necrosis, fail to show further reduction in infarct size over those deficient in Bax/Bak. Absence of Bax/Bak renders cells resistant to mPTP opening and necrosis, effects confirmed in isolated mitochondria. Reconstitution of these cells or mitochondria with wild-type Bax, or an oligomerization-deficient mutant that cannot support MOMP and apoptosis, restores mPTP opening and necrosis, implicating distinct mechanisms for Bax-regulated necrosis and apoptosis. Both forms of Bax restore mitochondrial fusion in Bax/Bak-null cells, which otherwise exhibit fragmented mitochondria. Cells lacking mitofusin 2 (Mfn2), which exhibit similar fusion defects, are protected to the same extent as Bax/Bak-null cells. Conversely, restoration of fused mitochondria through inhibition of fission potentiates mPTP opening in the absence of Bax/Bak or Mfn2, indicating that the fused state itself is critical. These data demonstrate that Bax-driven fusion lowers the threshold for mPTP opening and necrosis. Thus, Bax and Bak play wider roles in cell death than previously appreciated and may be optimal therapeutic targets for diseases that involve both forms of cell death. 相似文献
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Bourkiza R Sykakis E Parmar DN 《Journal of cataract and refractive surgery》2012,38(6):1114-5; author reply 1115