tbuckley/cabot-search huggingface dataset:
The Future of <i>JAMA Dermatology</i>
Authors: Kanade Shinkai
Journal: JAMA Dermatology (2018)

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 Dermatology 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 Dermatology journal
Corrigendum to ‘Design and optimization of PLGA microparticles for controlled and local delivery of Neuregulin-1 in traumatic spinal cord injury’. [Journal of Controlled Release 261(2017) 147–162]
Authors: Kallivalappil T. Santhosh, Arsalan Alizadeh, Soheila Karimi-Abdolrezaee
Journal: Journal of Controlled Release (2018)
Subacute Progressive Ptosis, Ophthalmoplegia, Gait Instability, and Cognitive Changes
Authors: Jessica Lin, Jacob C. Pellinen, Steven L. Galetta
Journal: JAMA Neurology (2018)

A 70-year-old woman with long-term tobacco use presented with 2 weeks of bilateral ptosis and binocular horizontal diplopia and moderate exotropia, severe bilateral ptosis, impaired bilateral adduction and vertical ductions, and impaired convergence. What is your diagnosis?
Caspase recruitment domain 6 protects against hepatic ischemia/reperfusion injury by suppressing ASK1
Authors: Juan-Juan Qin, Wenzhe Mao, Xiaozhan Wang, Peng Sun, Daqing Cheng, Song Tian, Xue-Yong Zhu, Ling Yang, Zan Huang, Hongliang Li
Journal: Journal of Hepatology (2018)
Medical Attention Seeking After Transient Ischemic Attack and Minor Stroke Before and After the UK Face, Arm, Speech, Time (FAST) Public Education Campaign
Authors: Frank J. Wolters, Linxin Li, Sergei A. Gutnikov, Ziyah Mehta, Peter M. Rothwell
Journal: JAMA Neurology (2018)

<h3>Importance</h3> Risk of major stroke is high during the hours and days after transient ischemic attack (TIA) and minor stroke but is substantially reduced by urgent medical treatment. Public education campaigns have improved the response after major stroke, but their association with behavior after TIA and minor stroke is uncertain. The number of potentially preventable early recurrent strokes in patients who delay or fail to seek medical attention is unknown. <h3>Objective</h3> To investigate the association of public education with delays and failure in seeking medical attention after TIA and minor stroke. <h3>Design, Setting, and Participants</h3> Prospective population-based study of all patients with TIA or stroke who sought medical attention between April 1, 2002, and March 31, 2014, registered at 9 general practices in Oxfordshire, United Kingdom. Data analysis took place from July 1, 2013, to March 2, 2015. <h3>Exposures</h3> Face, Arm, Speech, Time (FAST) public education campaign in the United Kingdom. <h3>Main Outcomes and Measures</h3> Number of early recurrent strokes in patients who delayed or failed to seek medical attention, as well as the odds of seeking urgent attention after TIA and minor stroke before vs after initiation of the public education campaign. <h3>Results</h3> Among 2243 consecutive patients with first TIA or stroke (mean [SD] age, 73.6 [13.4] years; 1126 [50.2%] female; 96.3% of white race/ethnicity), 1656 (73.8%) had a minor stroke or TIA. After the FAST campaign, patients with major stroke more often sought medical attention within 3 hours (odds ratio [OR], 2.56; 95% CI, 1.11-5.90;<i>P</i> = .03). For TIA and minor stroke, there was no improvement in use of emergency medical services (OR, 0.79; 95% CI, 0.50-1.23;<i>P</i>for interaction = .03 vs major stroke) or time to first seeking medical attention within 24 hours (OR, 0.75; 95% CI, 0.48-1.19;<i>P</i>for interaction = .006 vs major stroke). Patient perception of symptoms after TIA and minor stroke was associated with more urgent behavior, but correct perception declined after the FAST campaign (from 37.3% [289 of 774] to 27.6% [178 of 645]; OR, 0.64; 95% CI, 0.51-0.80;<i>P</i> &lt; .001). One hundred eighty-eight patients had a stroke within 90 days of their initial TIA or stroke, of whom 93 (49.5%) followed unheeded TIAs for which no medical attention was sought, similar before and after the FAST campaign (43 of 538 [8.0%] before vs 50 of 615 [8.1%] after,<i>P</i> = .93). <h3>Conclusions and Relevance</h3> This study suggests that in contrast to major stroke, extensive FAST-based public education has not improved the response to TIA and minor stroke in the United Kingdom, emphasizing the need for campaigns that are tailored to transient and less severe symptoms.
Treatment and outcome patterns in European patients with Waldenström's macroglobulinaemia: a large, observational, retrospective chart review
Authors: Christian Buske, Shalal Sadullah, Efstathios Kastritis, Alessandra Tedeschi, Ramón García-Sanz, Lukasz Bolkun, Xavier Leleu, Wolfgang Willenbacher, Roman Hájek, Monique C Minnema, Mei Cheng, Elizabeth Bilotti, Thorsten Graef, Meletios A Dimopoulos
Journal: The Lancet Haematology (2018)
Abstract 408: Evidence of DLL4, NNAT, and SLC35C2 in suppression of breast cancer initiation, growth, and metastasis
Authors: Cody Plasterer, Angela Lemke, Dana Murphy, Carmen Bergom, Amit Joshi, Hallgeir Rui, Michael J. Flister
Journal: Cancer Research (2018)

Abstract Breast cancer affects 1 in 8 women, resulting in 40,000 deaths annually. In most cases, a single cause of breast cancer cannot be found, but rather multiple environmental and genetic factors contribute to overall disease susceptibility. This, combined with complex gene interaction in both malignant tumor cells and nonmalignant tumor microenvironment (TME) cells, poses significant challenges in sifting through the many variants that contribute to the ~31% of breast cancer risk that is heritable. Here, we narrowed the regions associated with breast cancer risk on rat chromosome 3 (RNO3) by introgressing portions of RNO3 derived from the BN rat (protective strain) onto the genomic background of the SS rat (susceptible strain). These SS.BN3 congenics were then phenotyped for DMBA-induced mammary tumor incidence, latency, and multiplicity, which revealed two loci in close proximity that contribute to mammary tumor risk: chr3:95-130Mb (QTL1) and chr3: 154-177Mb (QTL2). By comparing these data with a previous study (Flister et al. Breast Cancer Res Treat. 2017 Aug;165(1):53-64.), we concluded that QTL1 is dependent on the host TME, whereas QTL2 directly modifies breast tumorigenesis and cancer cell proliferation. By combining the congenic mapping studies with genomic and transcriptomic sequencing, and functional analysis, we have now localized the top three candidate modifiers on RNO3: DLL4 (QTL1; TME modifier), NNAT (QTL2; cancer cell modifier), and SLC35C2 (QTL2; cancer cell modifier). Collectively, these data demonstrate the effects of several novel breast cancer modifiers, as well as highlight the potential interactions between modifiers of the malignant cancer cells and the nonmalignant host TME. Citation Format: Cody Plasterer, Angela Lemke, Dana Murphy, Carmen Bergom, Amit Joshi, Hallgeir Rui, Michael J. Flister. Evidence of DLL4, NNAT, and SLC35C2 in suppression of breast cancer initiation, growth, and metastasis [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 408.
Неалкогольна жирова хвороба печінки в дітей: сучасний погляд на можливості діагностики та лікування (I частина)
Authors: Yu.M. Stepanov, А.Ye. Abaturov, N.Yu. Zavgorodnia, I.Yu. Skyrda
Journal: GASTROENTEROLOGY (2020)

На цей час неалкогольна жирова хвороба печінки (НАЖХП) визнана провідною нозологічною формою в структурі хронічних дифузних захворювань печінки в дітей та підлітків у промислово розвинутих країнах світу. НАЖХП асоціюється з абдомінальним ожирінням, інсулінорезистентністю, порушенням толерантності до вуглеводів та дисліпідемією, тобто має тісний зв’язок з метаболічним синдромом та є його проявом. Дані досліджень свідчать, що НАЖХП пов’язана з підвищенням рівня загальної смертності та ймовірності формування серцево-судинних захворювань, що не залежить від наявності класичних факторів ризику розвитку атеросклерозу. Спостереження за перебігом захворювання протягом 20 років дозволило встановити скорочення терміну виживаності хворих на НАЖХП порівняно з очікуваним показником у загальній популяції, прогресування ступеня фіброзу у 80 % випадках спостережень, розвиток декомпенсованих форм цирозу печінки з потребою в трансплантації органа в 6 % хворих. Схильність до прогресування структурних змін печінки з розвитком термінальних стадій захворювання — цирозу й гепатоцелюлярної карциноми, висока ймовірність розвитку кардіоваскулярних ускладнень, можливість запобігання прогредієнтному перебігу за умов своєчасного терапевтичного втручання обумовлюють необхідність ранньої діагностики НАЖХП у дітей.Провідними конституціональними факторами ризику розвитку НАЖХП, які модифікуються, у дітей вважаються ожиріння та інсулінорезистентність.Механізм розвитку й прогресування НАЖХП є складним і багатофакторним процесом. У даний час існують дві провідні концепції, що пояснюють патогенез НАЖХП, — теорія двох ударів та теорія багатьох паралельних ударів.НАЖХП у дітей не має певних клінічних ознак і є випадковою знахідкою в асимптомних пацієнтів. Маніфестація захворювання найчастіше відбувається у віці понад 10 років. У клінічній картині НАЖХП у дітей превалюють неспецифічні симптоми: загальна слабкість, швидка втомлюваність, виснажливість.У клінічній практиці зазвичай першим кроком у діагностиці захворювання є виявлення підвищених рівнів печінкових трансаміназ та/або сонографічних ознак стеатозу при рутинному ультразвуковому дослідженні.Установлення діагнозу НАЖХП є можливим за відсутності ознак іншої природи ураження печінки, насамперед вірусного, аутоімунного й медикаментозно індукованого гепатиту.
Therapeutic equivalence of two formulations of calcipotriol-betamethasone ointment: a multicentre, randomized, double-blind study in adult patients with chronic plaque psoriasis
Authors: N. Habjanic, R. Koytchev, R. Yankova, M. Kerec-Kos, D. Grabnar-Peklar
Journal: British Journal of Dermatology (2018)
Phase I and Biomarker Study of Plerixafor and Bevacizumab in Recurrent High-Grade Glioma
Authors: Eudocia Q. Lee, Dan G. Duda, Alona Muzikansky, Elizabeth R. Gerstner, John G. Kuhn, David A. Reardon, Lakshmi Nayak, Andrew D. Norden, Lisa Doherty, Debra LaFrankie, Jennifer Stefanik, Trupti Vardam, Katrina H. Smith, Christine McCluskey, Sarah Gaffey, Tracy T. Batchelor, Rakesh K. Jain, Patrick Y. Wen
Journal: Clinical Cancer Research (2018)

Abstract Purpose: Although antiangiogenic therapy for high-grade glioma (HGG) is promising, responses are not durable. Correlative clinical studies suggest that the SDF-1α/CXCR4 axis may mediate resistance to VEGFR inhibition. Preclinical data have demonstrated that plerixafor (a reversible CXCR4 inhibitor) could inhibit glioma progression after anti-VEGF pathway inhibition. We conducted a phase I study to determine the safety of plerixafor and bevacizumab in recurrent HGG. Patients and Methods: Part 1 enrolled 23 patients with a 3 × 3 dose escalation design to a maximum planned dose of plerixafor 320 μg/kg subcutaneously on days 1 to 21 and bevacizumab 10 mg/kg intravenously on days 1 and 15 of each 28-day cycle. Cerebrospinal fluid (CSF) and plasma samples were obtained for pharmacokinetic analyses. Plasma and cellular biomarkers were evaluated before and after treatment. Part 2 enrolled 3 patients and was a surgical study to determine plerixafor's penetration in tumor tissue. Results: In Part 1, no dose-limiting toxicities were seen at the maximum planned dose of plerixafor + bevacizumab. Treatment was well tolerated. After plerixafor 320 μg/kg treatment, the average CSF drug concentration was 26.8 ± 19.6 ng/mL. Plerixafor concentration in resected tumor tissue from patients pretreated with plerixafor was 10 to 12 μg/g. Circulating biomarker data indicated that plerixafor + bevacizumab induces rapid and persistent increases in plasma SDF-1α and placental growth factor. Progression-free survival correlated with pretreatment plasma soluble mesenchymal–epithelial transition receptor and sVEGFR1, and overall survival with the change during treatment in CD34+ progenitor/stem cells and CD8 T cells. Conclusions: Plerixafor + bevacizumab was well tolerated in HGG patients. Plerixafor distributed to both the CSF and brain tumor tissue, and treatment was associated with biomarker changes consistent with VEGF and CXCR4 inhibition. Clin Cancer Res; 24(19); 4643–9. ©2018 AACR.
Diagnosis and management of pseudohypoparathyroidism and related disorders: first international Consensus Statement
Authors: Giovanna Mantovani, Murat Bastepe, David Monk, Luisa de Sanctis, Susanne Thiele, Alessia Usardi, S. Faisal Ahmed, Roberto Bufo, Timothée Choplin, Gianpaolo De Filippo, Guillemette Devernois, Thomas Eggermann, Francesca M. Elli, Kathleen Freson, Aurora García Ramirez, Emily L. Germain-Lee, Lionel Groussin, Neveen Hamdy, Patrick Hanna, Olaf Hiort, Harald Jüppner, Peter Kamenický, Nina Knight, Marie-Laure Kottler, Elvire Le Norcy, Beatriz Lecumberri, Michael A. Levine, Outi Mäkitie, Regina Martin, Gabriel Ángel Martos-Moreno, Masanori Minagawa, Philip Murray, Arrate Pereda, Robert Pignolo, Lars Rejnmark, Rebecca Rodado, Anya Rothenbuhler, Vrinda Saraff, Ashley H. Shoemaker, Eileen M. Shore, Caroline Silve, Serap Turan, Philip Woods, M. Carola Zillikens, Guiomar Perez de Nanclares, Agnès Linglart
Journal: Nature Reviews Endocrinology (2018)

This Consensus Statement covers recommendations for the diagnosis and management of patients with pseudohypoparathyroidism (PHP) and related disorders, which comprise metabolic disorders characterized by physical findings that variably include short bones, short stature, a stocky build, early-onset obesity and ectopic ossifications, as well as endocrine defects that often include resistance to parathyroid hormone (PTH) and TSH. The presentation and severity of PHP and its related disorders vary between affected individuals with considerable clinical and molecular overlap between the different types. A specific diagnosis is often delayed owing to lack of recognition of the syndrome and associated features. The participants in this Consensus Statement agreed that the diagnosis of PHP should be based on major criteria, including resistance to PTH, ectopic ossifications, brachydactyly and early-onset obesity. The clinical and laboratory diagnosis should be confirmed by a molecular genetic analysis. Patients should be screened at diagnosis and during follow-up for specific features, such as PTH resistance, TSH resistance, growth hormone deficiency, hypogonadism, skeletal deformities, oral health, weight gain, glucose intolerance or type 2 diabetes mellitus, and hypertension, as well as subcutaneous and/or deeper ectopic ossifications and neurocognitive impairment. Overall, a coordinated and multidisciplinary approach from infancy through adulthood, including a transition programme, should help us to improve the care of patients affected by these disorders. This Consensus Statement gives recommendations for the diagnosis and management of patients with pseudohypoparathyroidism and related disorders. A coordinated and multidisciplinary approach from infancy through adulthood is recommended to improve the care of these patients.
PD-1 Inhibitory Receptor Downregulates Asparaginyl Endopeptidase and Maintains Foxp3 Transcription Factor Stability in Induced Regulatory T Cells
Authors: Chaido Stathopoulou, Arunakumar Gangaplara, Grace Mallett, Francis A. Flomerfelt, Lukasz P. Liniany, David Knight, Leigh A. Samsel, Rolando Berlinguer-Palmini, Joshua J. Yim, Tania C. Felizardo, Michael A. Eckhaus, Laura Edgington-Mitchell, Jonathan Martinez-Fabregas, Jinfang Zhu, Daniel H. Fowler, Sander I. van Kasteren, Arian Laurence, Matthew Bogyo, Colin Watts, Ethan M. Shevach, Shoba Amarnath
Journal: Immunity (2018)
Endocrine Late Effects in Survivors of Cancer in Adolescence and Young Adulthood
Authors: Mette Vestergaard Jensen, Kathrine Rugbjerg, Sofie de Fine Licht, Christoffer Johansen, Kjeld Schmiegelow, Klaus Kaae Andersen, Jeanette Falck Winther
Journal: JAMA Network Open (2018)

As survival rates from cancer have improved dramatically over the last decades, there is a need to explore the long-term consequences. Adolescents and young adults with cancer are at risk for several therapy-related late effects; however, these have not been studied extensively.To investigate the lifetime risks of endocrine late effects of cancer and cancer treatment in adolescent and young adult cancer survivors.This Danish, nationwide, population-based cohort study was conducted from January 1, 1976, through December 31, 2009, and included follow-up from January 1, 1977, through December 31, 2010. A total of 32 548 one-year cancer survivors diagnosed at ages 15 to 39 years were identified using the Danish Cancer Registry and 188 728 cancer-free comparison participants matched by year of birth and sex were randomly chosen from the Danish Civil Registration system. Analyses were performed from July 3, 2015, to February 27, 2018.Individuals in the survivor cohort were diagnosed with a first primary cancer at ages 15 to 39 years and received treatment according to recommendations and guidelines at time of diagnosis.By linkage to the National Patient Register, all hospital contacts for endocrine diseases were identified, and standardized hospitalization rate ratios (RRs) and absolute excess risks (AERs) were calculated.A total of 32 548 adolescent and young adult 1-year cancer survivors (14 021 [43.1%] male) in the Danish Patient Registry were followed up for 379 157 person-years (median [range]: 10 [0-34] years) and 188 728 cancer-free participants (82 669 [43.8%] male) for comparison were followed up for 2 958 994 person-years (median [range]: 15 [0-34] years). A total of 2129 survivors (6.5%) had at least 1 hospital contact for an endocrine disease, while 1232.0 (3.8%) were expected, yielding a statistically significant increased RR of 1.73 (95% CI, 1.65-1.81). The RRs were highest for testicular hypofunction (75.12; 95% CI, 45.99-122.70), ovarian hypofunction (14.65; 95% CI, 8.29-25.86), and pituitary hypofunction (11.14; 95% CI, 8.09-15.34). The leading reasons for hospital contacts were thyroid disease (38.0% of total AER), testicular dysfunction (17.1% of total AER), and diabetes (14.4% of total AER). Leukemia survivors were at a high risk for any endocrine disease (RR, 3.97; 95% CI, 3.10-5.09), while Hodgkin lymphoma survivors (RR, 3.06; 95% CI, 2.62-3.57) had the highest disease-specific excess risk for hypothyroidism (AER, 362 per 100 000 person-years; 95% CI, 280-443 per 100 000 person-years).The increased risk for endocrine diseases in adolescent and young adult cancer survivors indicates the need for counseling and follow-up, and could guide future preventive measures and surveillance strategies. Additional studies are required to determine exact associations between treatment regimens and endocrine diseases.
Efficacy and Safety of High-Dose Rifampin in Pulmonary Tuberculosis. A Randomized Controlled Trial
Authors: Gustavo E. Velásquez, Meredith B. Brooks, Julia M. Coit, Henry Pertinez, Dante Vargas Vásquez, Epifanio Sánchez Garavito, Roger I. Calderón, Judith Jiménez, Karen Tintaya, Charles A. Peloquin, Elna Osso, Dylan B. Tierney, Kwonjune J. Seung, Leonid Lecca, Geraint R. Davies, Carole D. Mitnick
Journal: American Journal of Respiratory and Critical Care Medicine (2018)

We examined whether increased rifampin doses could shorten standard therapy for tuberculosis without increased toxicity.To assess the differences across three daily oral doses of rifampin in change in elimination rate of Mycobacterium tuberculosis in sputum and frequency of rifampin-related adverse events.We conducted a blinded, randomized, controlled phase 2 clinical trial of 180 adults with new smear-positive pulmonary tuberculosis, susceptible to isoniazid and rifampin. We randomized 1:1:1 to rifampin at 10, 15, and 20 mg/kg/d during the intensive phase. We report the primary efficacy and safety endpoints: change in elimination rate of M. tuberculosis log10 colony-forming units and frequency of grade 2 or higher rifampin-related adverse events. We report efficacy by treatment arm and by primary (area under the plasma concentration-time curve [AUC]/minimum inhibitory concentration [MIC]) and secondary (AUC) pharmacokinetic exposure.Each 5-mg/kg/d increase in rifampin dose resulted in differences of -0.011 (95% confidence interval, -0.025 to +0.002; P = 0.230) and -0.022 (95% confidence interval, -0.046 to -0.002; P = 0.022) log10 cfu/ml/d in the modified intention-to-treat and per-protocol analyses, respectively. The elimination rate in the per-protocol population increased significantly with rifampin AUC0-6 (P = 0.011) but not with AUC0-6/MIC99.9 (P = 0.053). Grade 2 or higher rifampin-related adverse events occurred with similar frequency across the three treatment arms: 26, 31, and 23 participants (43.3%, 51.7%, and 38.3%, respectively) had at least one event (P = 0.7092) up to 4 weeks after the intensive phase. Treatment failed or disease recurred in 11 participants (6.1%).Our findings of more rapid sputum sterilization and similar toxicity with higher rifampin doses support investigation of increased rifampin doses to shorten tuberculosis treatment. Clinical trial registered with www.clinicaltrials.gov (NCT 01408914) .