tbuckley/cabot-search huggingface dataset:
CD4 and CD8 T cells mediate distinct lethal meningoencephalitis in mice challenged with Tacaribe arenavirus
Authors: Derek DC Ireland, Cecilia Tami, Joao Pedras-Vasconcelos, Daniela Verthelyi
Journal: Cellular and Molecular Immunology (2016)

Neonates are at increased risk of viral encephalopathies that can result in neurological dysfunction, seizures, permanent disability and even death. The neurological damage results from the combined effect of the virus and the immune response it elicits, thus finding tools to facilitate viral clearance from central nervous system (CNS) while minimizing neuron damage remains a critical challenge. Neonatal mice inoculated intraperitoneally with Tacaribe virus (TCRV) develop seizures, hindlimb paralysis and death within 15 days of inoculation. TCRV localizes to the CNS within days of challenge, primarily infecting astrocytes in the cerebellum and brain stem. We show that infection leads to inflammation, T cell and monocyte infiltration into the cerebellar parenchyma, apoptosis of astrocytes, neuronal degeneration and loss of Purkinje cells. Infiltrating antigen-specific T cells fail to clear the virus but drive the disease, as T-cell-deficient CD3ɛ KO mice survive TCRV infection with minimal inflammation or clinical manifestations despite no difference in CNS viral loads in comparison with T-cell sufficient mice. CD8+ T cells drive the pathology, which even in the absence of CD4+ T-cell help, infiltrate the parenchyma and mediate the apoptotic loss of cerebellar astrocytes, neurodegeneration and loss of Purkinje cells resulting in loss of balance, paralysis and death. CD4+ T cells are also pathogenic inducing gliosis and inflammation in the cerebellum and cerebrum that are associated with wasting and death several weeks after CD4+ T-cell transfer. These data demonstrate distinct pathogenic effects of CD4+ and CD8+ T cells and identify them as possible therapeutic targets.
After phrenology: Time for a paradigm shift in cognitive science
Authors: Paul Benjamin Badcock, Annemie Ploeger, Nicholas Brian Allen
Journal: Behavioral and Brain Sciences (2016)

Anderson (2014) uses an impressive, consolidating review of the literature to argue for major changes in cognitive science. Arguably, however, much of what he proposes is not particularly new. He also neglects important predictive coding approaches that call his perspective of the brain into question, and his misconstrual of evolutionary psychology devalues an influential paradigm that promises to complement his own.
Determinants of Complete Resection of Thymoma by Minimally Invasive and Open Thymectomy: Analysis of an International Registry
Authors: Bryan M. Burt, Xiaopan Yao, Joseph Shrager, Alberto Antonicelli, Sukhmani Padda, Jonathan Reiss, Heather Wakelee, Stacey Su, James Huang, Walter Scott
Journal: Journal of Thoracic Oncology (2016)
A Reanalysis of Study of Prostate-Specific Antigen Testing Among Urologists
Authors: Quoc-Dien Trinh
Journal: JAMA Internal Medicine (2016)

Michael E. Zavaski, MD; Christian P. Meyer, MD; Jesse D. Sammon, DO; Julian Hanske, MD; Soham Gupta; Maxine Sun, MPH; Quoc-Dien Trinh, MD
Defining recurrence of nonmelanoma skin cancer after Mohs micrographic surgery: Report of the American College of Mohs Surgery Registry and Outcomes Committee
Authors: Justin J. Leitenberger, Howard Rogers, John C. Chapman, Ian A. Maher, Matthew C. Fox, Chris B. Harmon, Evans C. Bailey, Peter Odland, Ashley Wysong, Tim Johnson, Oliver J. Wisco
Journal: Journal of the American Academy of Dermatology (2016)
Aspirin and Cancer Risk
Authors: Diana I. Brixner, David D. Stenehjem, Cornelia Ulrich
Journal: JAMA Oncology (2016)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA Oncology HomeNew OnlineCurrent IssueFor Authors Podcast Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA Oncology journal
제 7 차 춘계학술대회 초록집 : 구연 ; 한국인에서 간암발생의 위험요인 및 개인별 간암 발생 예측 모형
Authors: 정재연, 한광협, 안상훈, 백용한, 송건훈, 전재윤, 문영명, 송기준, 김동기, 서일
Journal: Clinical and Molecular Hepatology (2001)
Identification of Gulf War Syndrome: Methodological Issues and Medical Illnesses-Reply
Authors: Robert W. Haley
Journal: JAMA (1997)

<h3>In Reply.</h3> —We thank Drs Gordon, Schlesinger, and Kaires for their comments from their clinical experience with Gulf War veterans. Regarding Dr Schlesinger's suggestion to test for muscle enzymes, we measured creatine kinase levels in our case-control study, but did not find a difference between the cases with our syndrome 3 and the controls. During clinical testing of 20 veterans, Dr Amato et al<sup>1</sup>found several patients with neuromuscular symptoms, elevated levels of creatine kinase, and abnormalities on muscle biopsy, but attributed the symptoms to psychological stress. The suggestion of Drs Engel and Jing to include a control group of veterans of the same era not deployed to the Persian Gulf region was accomplished in our case-control study; characteristics of the deployed and nondeployed control groups were shown in Table 2 of that article. We agree that repeating the study with larger number of veterans would strengthen its findings. We would welcome the formation
Miscarriage following dengue virus 3 infection in the first six weeks of pregnancy of a dengue virus-naive traveller returning from Bali to Italy, April 2016
Authors: Maurizio Zavattoni, Francesca Rovida, Giulia Campanini, Elena Percivalle, Antonella Sarasini, Graziella Cristini, Lina Rachele Tomasoni, Francesco Castelli, Fausto Baldanti
Journal: Eurosurveillance (2016)

We report miscarriage following dengue virus (DENV)-3 infection in a pregnant woman returning from Bali to Italy in April 2016. On her arrival, the woman had fever, rash, asthenia and headache. DENV RNA was detected in plasma and urine samples collected the following day. Six days after symptom onset, she had a miscarriage. DENV RNA was detected in fetal material, but in utero fetal infection cannot be demonstrated due to possible contamination by maternal blood.
Surgical Management of Choledocholithiasis
Authors: Feng Shen, Timothy M. Pawlik
Journal: JAMA Surgery (2016)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA Surgery HomeNew OnlineCurrent IssueFor Authors Podcast Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA Surgery journal
Neutrophils and tissue damage: is hypoxia the key to excessive degranulation?
Authors: Andrew E Williams, Rachel C Chambers
Journal: Thorax (2016)

Neutrophils are the first innate immune cells recruited into sites of infection and inflammation, and although they are critical for host defence against microbial pathogens, they have also been associated with local tissue damage. Predominant neutrophilic inflammation is a key hallmark of many respiratory diseases, and the release of proteinases and reactive oxygen species (ROS) from primed neutrophils has been implicated in mediating the damage to surrounding tissue.1 Inflammation is further accompanied by severe hypoxia (lack of oxygen) within the affected tissue, and is a characteristic of both acute and chronic lung diseases, such as acute respiratory distress syndrome (ARDS),2 COPD3 and cystic fibrosis (CF).4 Considering that tissue hypoxia is part of a normal inflammatory response, innate immune cells such as neutrophils and macrophages possess important cellular and molecular mechanisms that enable them to function effectively at low oxygen concentrations.5

There is considerable interplay between the molecular pathways that regulate hypoxia and inflammation. In previous studies, mice exposed to hypoxic conditions (5% O2 for 1 hour) demonstrated increased levels of interleukin 6 (IL-6), tumour necrosis factor and IL-1 in both serum and isolated macrophages.6 In humans, increased levels of IL-6, IL-1RA and C-reactive protein were detected in serum after volunteers experienced three overnight stays at altitude.7 Moreover, infiltrating neutrophils directly increase their oxygen consumption in order to assemble the nicotinamide adenine dinucleotide phosphate oxidase complex that generates ROS and, in conjunction with superoxide dismutase and myeloperoxidase (MPO), hydrogen peroxide (H2O2) and hypochlorous acid (HClO), thereby depleting local levels of oxygen.8 ,9 Neutrophils are also thought to influence the tissue microenvironment during episodes of hypoxia. For example, neutrophil migration across epithelia increases the transcriptional activity of hypoxia-inducible genes in epithelial cells, which in turn influence the …
Подвижник земской медицины на Екатеринославщине — ​Днепропетровщине (часть 2)
Authors: М. Chaban, Z. Shevtsova, V. Haponov
Journal: GASTROENTEROLOGY (2016)

Представлены жизненный путь и профессиональная деятельность Петра Сочинского — земского врача, общественного деятеля, коллекционера, фольклориста, мецената, действительного члена Екатеринославской ученой архивной комиссии, который внес весомый вклад в развитие земской медицины и сохранение памятников истории и культуры на Приднепровье.
O043 : The FNDC5 rs3480 is protective on the steatosis and fibrosis in patients with NAFLD
Authors: R. Anty, Y.L. Liu, A. Iannelli, S. Patouraux, C. Canivet, I. Ben-Amor, A.-S. Schneck, M.-C. Saint-Paul, J. Gugenheim, C. Day, A. Daly, A. Tran, P. Gual, Q. Anstee
Journal: Journal of Hepatology (2015)
Environmental Risk Factors of Inhibitor in Mild/Moderate Hemophilia A Patients Included in the FranceCoag Network
Authors: Roseline d'Oiron, Virginie Demiguel, Annie Borel-Derlon, Ségolène Donadel-Claeyssens, Jenny Goudemand, Benoît Guillet, Yves Gruel, Valérie Roussel-Robert, Fabienne Volot, Thierry Calvez
Journal: Blood (2011)
Case 7-1977
Authors: Earle W. Wilkins, James J. Galdabini
Journal: New England Journal of Medicine (1977)

Presentation of CaseA 39-year-old woman was admitted to the hospital because of a mass in the neck.She was well until three months previously, when a chronic, nonproductive cough developed; six weeks later the cough worsened. One month before entry a swelling developed in the lower anterior portion of the neck over a period of three hours, accompanied by a low-grade fever and sweats. A thyroid scan demonstrated that the mass was extrinsic to the thyroid gland; the 24-hour radioiodine uptake and thyroxine level were normal. One day before admission purulent material was aspirated from the mass; stained smears . . .
Association Between Gene Expression Profiles and Commonly Mutated Genes In The Hematopoietic Stem Cells Of Patients With Myelodysplastic Syndromes
Authors: Andrea Pellagatti, Moritz Gerstung, Elli Papaemmanuil, Luca Malcovati, Aristoteles Giagounidis, Matteo G Della Porta, Martin Jadersten, Amit Verma, Paresh Vyas, Sally Killick, Eva Hellstrom-Lindberg, Mario Cazzola, Peter J. Campbell, Jacqueline Boultwood
Journal: Blood (2013)
Feasibility of conducting home-based clinical trials in patients with advanced pancreatic cancer.
Authors: A. P. Abernethy, L. S. Schwartzberg, D. Li, D. Scott, M. Hensley
Journal: Journal of Clinical Oncology (2010)

e14647 Background: Frail individuals with declining performance status, and people with very advanced cancer, are frequently excluded from clinical trials, making it difficult to test new therapeutics intended to improve longevity or quality of life (QOL) in the advanced cancer and palliative care settings. Is it feasible to conduct these trials at home and adhere to Good Clinical Practice (GCP)? Methods: KLT-PANC-001 is a 2:1 randomized study of gemcitabine (G) with or without Kanglaite (K) injection (extract of coix seed, a traditional Chinese medicine) in metastatic pancreatic cancer. Each 4-week cycle requires K infusions over >2 hours, 5 days weekly for 3 weeks (then 1 week off); G is infused in a clinic-based facility on days 1, 8, 15. After establishing infusion safety, K is administered in clinic or at home by GCP-trained nurses. Laboratory data are collected with standardized kits. Home patient-reported QOL and symptoms (PROs) are collected using tablet computers assigned to each patient. Results: 22 participants have been enrolled with metastatic pancreatic cancer. For 7 participants randomized to G, all infusions were received as intended except for protocol-related exclusions. 15 participants were randomized to K+G and 14 chose home infusions. Despite the intensive KLT treatment program, compliance with scheduled doses remained high and comparable between clinic and home settings; see Table: K+G compliance with planned doses (% of scheduled infusions administered on time), by cycle week, for all treatment cycles. Focusing on week 3 of the treatment cycle (most burdensome) 81-100% of intended pain PROs were collected in clinic, 86-92% at home. Conclusions: Home-based infusions by GCP-trained staff and data collection using patient-specific tablet computers can facilitate intensive clinical trials intended to enroll ill patients with advanced cancer. Protocol compliance with scheduled infusions and data collection was high. Treatment cycle week Proportion received in clinic (doses scheduled) Proportion received in home (doses scheduled) Week 1 94% (59) 94% (149) Week 2 87% (39) 91% (149) Week 3 87% (71) 92% (108) Author Disclosure Employment or Leadership Position Consultant or Advisory Role Stock Ownership Honoraria Research Funding Expert Testimony Other Remuneration Kanglaite, Inc. Kanglaite, Inc.
<i>MEF2D</i>-<i>BCL9</i> Fusion Gene Is Associated With High-Risk Acute B-Cell Precursor Lymphoblastic Leukemia in Adolescents
Authors: Kyogo Suzuki, Yusuke Okuno, Nozomu Kawashima, Hideki Muramatsu, Tatsuya Okuno, Xinan Wang, Shinsuke Kataoka, Yuko Sekiya, Motoharu Hamada, Norihiro Murakami, Daiei Kojima, Kotaro Narita, Atsushi Narita, Hirotoshi Sakaguchi, Kimiyoshi Sakaguchi, Nao Yoshida, Nobuhiro Nishio, Asahito Hama, Yoshiyuki Takahashi, Kazuko Kudo, Koji Kato, Seiji Kojima
Journal: Journal of Clinical Oncology (2016)

Purpose Acute lymphoblastic leukemia (ALL) makes up a significant proportion of all pediatric cancers, and relapsed ALL is a leading cause of cancer-associated deaths in children. Identification of risk factors and druggable molecular targets in ALL can lead to a better stratification of treatments and subsequent improvement in prognosis. Patients and Methods We enrolled 59 children with relapsed or primary refractory ALL who were treated in our institutions. We primarily performed RNA sequencing (RNA-seq) using patients’ leukemic cells to comprehensively detect gene fusions and analyze gene expression profiles. On the basis of results obtained by RNA-seq, we performed genetic validation, functional analysis, and in vitro drug sensitivity testing using patients’ samples and an exogenous expression model. Results We identified a total of 26 gene fusions in 22 patients by RNA-seq. Among these, 19 were nonrandom gene fusions already described in ALL, and four of the remaining seven involved identical combination of MEF2D and BCL9. All MEF2D-BCL9–positive patients had B-cell precursor immunophenotype and were characterized as being older in age, being resistant to chemotherapy, having very early relapse, and having leukemic blasts that mimic morphologically mature B-cell leukemia with markedly high expression of HDAC9. Exogenous expression of MEF2D-BCL9 in a B-cell precursor ALL cell line promoted cell growth, increased HDAC9 expression, and induced resistance to dexamethasone. Using a primary culture of leukemic blasts from a patient, we identified several molecular targeted drugs that conferred inhibitory effects in vitro. Conclusion A novel MEF2D-BCL9 fusion we identified characterizes a novel subset of pediatric ALL, predicts poor prognosis, and may be a candidate for novel molecular targeting.
Potential survival benefit of adjuvant sunitinib in high risk uveal melanoma.
Authors: Matias Emanuel Valsecchi, Marlana M. Orloff, Inna Chervoneva, Carol L Shields, Jerry A Shields, Erin Sharpe-Mills, Michael J. Mastrangelo, Takami Sato
Journal: Journal of Clinical Oncology (2015)

e20046 Background: Patients with high-risk uveal melanoma have up to 70% chances of developing distant metastases. There is no US FDA-approved adjuvant treatment able to reduce that risk and prolong survival. We aimed to compare overall survival (OS) in high-risk patients who received adjuvant sunitinib with institutional historical controls. Methods: A cohort of patients who received adjuvant sunitinib for at least 6 months was compared with institutional historical controls patients who had similar demographic as well as high-risk features, including: A) – monosomy-3 and 8q amplification (M3-8qA) in the primary tumor by cytogenetic analysis or class II by molecular analysis; B) – monosomy-3 and large tumor size (T3 or 4 by AJCC TNM). Patients in the control group were diagnosed during the same period of time (2007 - 2013) but did not receive any adjuvant treatment. Primary endpoint was OS and was evaluated using Kaplan-Meier survival curves and Cox proportional hazards model. Results: A total of 105 Caucasian patients were included; median follow-up was 34.5 months (range 0.25 – 82 months). There were 50 patients who received sunitinib. Median age was 55 (29 – 69 years old) and 46% were males. Fifty five historical controls, with the same high risk factors, were found in our database. The median age was 58 (21 – 70 years old) and 51% were males. Patients in the sunitinib group had worse cytogenetic features (M3-8qA 78% vs. 47%; P = .001) but smaller tumor sizes (T3-4 56% vs. 80%; P = .01). There were a total of 19 deaths; 3 (6%) in the sunitinib and 16 (29%) in the control group, respectively. Estimated 5-year survival rate was 91% (95% CI: 82 –100%) in the sunitinib group and 61% (95% CI: 47 – 79%) in the non-adjuvant control group. OS was significantly longer in the sunitinib group (HR = 0.267, 95% CI: 0.077 – 0.925, P = 0.037) and this remained significant after being individually adjusted by cytogenetic status, tumor size, age and gender. No meaningful interactions were detected. Conclusions: In this retrospective study, the use of sunitinib in the adjuvant setting was associated with better OS. Current ongoing clinical trials are testing this hypothesis.
Self- and Parent/Proxies-Reported Health-Related Quality Of Life In Children and Adolescents With Bleeding Disorders: Cross Sectional Investigation and Comparison With Healthy Siblings and Healthy Peers
Authors: Neuner Bruno, Sylvia von Mackensen, Susan Halimeh, Susanne Holzhauer, Robert Klamroth, Karin Kurnik, Anne Kruempel, Michael Fruewald, Henning Krampe, Ulrike Nowak-Goettl
Journal: Blood (2013)
Multi-omics analysis of primary glioblastoma cell lines shows recapitulation of pivotal molecular features of parental tumors
Authors: Shai Rosenberg, Maïté Verreault, Charlotte Schmitt, Justine Guegan, Jeremy Guehennec, Camille Levasseur, Yannick Marie, Franck Bielle, Karima Mokhtari, Khê Hoang-Xuan, Keith Ligon, Marc Sanson, Jean-Yves Delattre, Ahmed Idbaih
Journal: Neuro-Oncology (2016)

Glioblastoma (GBM) is the deadliest primary brain cancer in adults. Emerging innovative therapies hold promise for personalized cancer treatment. Improving therapeutic options depends on research relying on relevant preclinical models. In this line we have established in the setting of the GlioTex project (GBM and Experimental Therapeutics) a GBM patient-derived cell line (GBM-PDCL) library. A multi-omic approach was used to determine the molecular landscape of PDCL and the extent to which they represent GBM tumors. Single nucleotide polymorphism array, expression arrays, exome sequencing, and RNA sequencing were used to measure and compare the molecular landscapes of 20 samples representing 10 human GBM tumors and paired GBM-PDCLs. Copy number variations were similar for a median of 85% of the genome and for 59% of the major focal events. Somatic point mutations were similar in a median of 41%. Mutations in GBM driver and "druggable" genes were maintained in 67% of events. Mutations that were not conserved in the PDCL were mainly low allelic fraction and/or non-driver mutations. Based on RNA expression profiling, PDCLs cluster closely to their parental tumor with overexpression of pathways associated with cancer progression in PDCL. Overall, PDCLs recapitulate pivotal molecular alterations of paired-parental tumors supporting their use as a preclinical model of GBM. However, some driver aberrations are lost or gained in the passage from tumor to PDCL. Our results support using PDCL as a relevant preclinical model of GBM. Further investigations of changes between PDCLs and their parental tumor may provide insights into GBM biology.
Amelioration of Idiopathic Pneumonia Syndrome (IPS) and GVHD by KGF-Pretreatment Is Partly Mediated Via a STAT-6-Dependent Pathway in the Host.
Authors: Angela Panoskaltsis-Mortari, Andrew Price, Kevin Tram, Rita McFadden, Michael J. Ehrhardt, Michael J. Grusby, Bruce R. Blazar
Journal: Blood (2006)
Widespread transneuronal propagation of α-synucleinopathy triggered in olfactory bulb mimics prodromal Parkinson’s disease
Authors: Nolwen L. Rey, Jennifer A. Steiner, Nazia Maroof, Kelvin C. Luk, Zachary Madaj, John Q. Trojanowski, Virginia M.-Y. Lee, Patrik Brundin
Journal: The Journal of Experimental Medicine (2016)

Parkinson's disease (PD) is characterized by the progressive appearance of intraneuronal Lewy aggregates, which are primarily composed of misfolded α-synuclein (α-syn). The aggregates are believed to propagate via neural pathways following a stereotypical pattern, starting in the olfactory bulb (OB) and gut. We hypothesized that injection of fibrillar α-syn into the OB of wild-type mice would recreate the sequential progression of Lewy-like pathology, while triggering olfactory deficits. We demonstrate that injected α-syn fibrils recruit endogenous α-syn into pathological aggregates that spread transneuronally over several months, initially in the olfactory network and later in distant brain regions. The seeded inclusions contain posttranslationally modified α-syn that is Thioflavin S positive, indicative of amyloid fibrils. The spreading α-syn pathology induces progressive and specific olfactory deficits. Thus, we demonstrate that propagating α-syn pathology triggered in the OB is functionally detrimental. Collectively, we have created a mouse model of prodromal PD.