tbuckley/cabot-search huggingface dataset:
Antenatal nutritional supplementation and autism spectrum disorders in the Stockholm youth cohort: population based cohort study
Authors: Elizabeth A DeVilbiss, Cecilia Magnusson, Renee M Gardner, Dheeraj Rai, Craig J Newschaffer, Kristen Lyall, Christina Dalman, Brian K Lee
Journal: BMJ (2017)

Abstract Objective To determine whether nutritional supplementation during pregnancy is associated with a reduced risk of autism spectrum disorder (ASD) with and without intellectual disability in offspring. Design Observational prospective cohort study using multivariable logistic regression, sibling controls, and propensity score matching. Setting Stockholm County, Sweden. Participants 273 107 mother-child pairs identified through population registers. The study sample was restricted to children who were aged 4 to 15 years by the end of follow-up on 31 December 2011 and were born between 1996 and 2007. Exposures Multivitamin, iron, and folic acid supplement use was reported at the first antenatal visit. Main outcome measure Diagnosis of ASD with and without intellectual disability in children determined from register data up to 31 December 2011. Results Prevalence of ASD with intellectual disability was 0.26% (158 cases in 61 934) in the maternal multivitamin use group and 0.48% (430 cases in 90 480) in the no nutritional supplementation use group. Maternal multivitamin use with or without additional iron or folic acid, or both was associated with lower odds of ASD with intellectual disability in the child compared with mothers who did not use multivitamins, iron, and folic acid (odds ratio 0.69, 95% confidence interval 0.57 to 0.84). Similar estimates were found in propensity score matched (0.68, 0.54 to 0.86) and sibling control (0.77, 0.52 to 1.15) matched analyses, though the confidence interval for the latter association included 1.0 and was therefore not statistically significant. There was no consistent evidence that either iron or folic acid use were inversely associated with ASD prevalence. Conclusions Maternal multivitamin supplementation during pregnancy may be inversely associated with ASD with intellectual disability in offspring. Further scrutiny of maternal nutrition and its role in the cause of autism is recommended.
Second-line tivantinib (ARQ 197) vs placebo in patients (Pts) with MET-high hepatocellular carcinoma (HCC): Results of the METIV-HCC phase III trial.
Authors: Lorenza Rimassa, Eric Assenat, Markus Peck-Radosavljevic, Vittorina Zagonel, Marc Pracht, Elena Rota Caremoli, Philippe Mathurin, William Proctor Harris, Luigi Bolondi, Maria Reig, Nevena Damjanov, Bruno Daniele, Camillo Porta, Vincenzo Mazzaferro, Giovanni Abbadessa, Brian E. Schwartz, Maria Lamar, Terri Robin Goldberg, Armando Santoro, Jordi Bruix
Journal: Journal of Clinical Oncology (2017)

4000 Background: Tivantinib (T), a selective, oral MET inhibitor, improved overall survival (OS) and progression-free survival (PFS) versus placebo (P) in a phase II study in MET-High HCC pts. Methods: This randomized, placebo-controlled phase III trial (NCT01755767) enrolled pts with: advanced HCC; Child Pugh A; ECOG PS ≤1; adequate bone marrow, liver, kidney functions; no liver transplant; radiographic disease progression (PD) after or intolerance to sorafenib; tumor MET-High (MET ≥2+ in ≥50% of tumor cells) by centralized immunohistochemistry. Pts were randomly assigned 2:1 to oral T or P, stratified by vascular invasion (VI), extrahepatic spread (ES), AFP ( &lt; / &gt; 200ng/mL), treated until PD or unacceptable toxicity. Response (RECIST 1.1) was evaluated by CT / MRI every 8 weeks. Primary endpoint of OS and secondary endpoints including PFS and safety were assessed in the intent-to-treat (ITT) population. Results: From Dec 2012 to Dec 2015, 1209 pts were consented in Australia, the Americas, Europe, New Zealand: 589 MET-High, 43 initially randomized at the dose of 240mg BID, then reduced due to high neutropenia rate, 340 randomized at 120mg BID: 226 to T, 114 to P (ITT population). Characteristics of pts were balanced between arms: 306 (90%) male; median age: 67; PS 0: 207 (61%); VI: 117 (34%); ES: 197 (58%); AFP ≤200: 195 (57%); radiographic PD on sorafenib: 275 (81%). Median OS (95% CI) was 8.4 months (m) (6.8-10.0) in T, 9.1 m (7.3-10.4) in P, HR = 0.97 (0.75-1.25), P = 0.81. Median PFS (95% CI) was 2.1 m (1.9-3.0) in T, 2.0 m (1.9-3.6) in P, HR = 0.96 (0.75-1.22), P = 0.72. No OS difference was seen in pts with VI (HR 1.19, 0.79-1.79), ES (HR 1.09, 0.78-1.52), AFP &gt; 200ng/mL (HR 1.00, 0.71-1.41). Grade (G) &gt; 3 AEs were 55.6% in T, 55.3% in P. In T, most common G &gt; 3 AEs were ascites (7.1%), general deterioration (5.8%), anemia (4.9%); most common serious AE was general deterioration (4.9%). Deaths within 30 days of last dose were 22.1% on T vs 15.8% on P (most common causes: general deterioration 3.5%, hepatic failure 2.6%). Conclusion: Tivantinib at the 120mg BID dose did not improve OS or PFS over placebo in patients with advanced MET-High HCC who failed previous treatment with sorafenib. Clinical trial information: NCT01755767.
Extracellular Matrix Proteomics Reveals Interplay of Aggrecan and Aggrecanases in Vascular Remodeling of Stented Coronary Arteries
Authors: Gonca Suna, Wojciech Wojakowski, Marc Lynch, Javier Barallobre-Barreiro, Xiaoke Yin, Ursula Mayr, Ferheen Baig, Ruifang Lu, Marika Fava, Robert Hayward, Chris Molenaar, Stephen J. White, Tomasz Roleder, Krzysztof P. Milewski, Pawel Gasior, Piotr P. Buszman, Pawel Buszman, Marjan Jahangiri, Catherine M. Shanahan, Jonathan Hill, Manuel Mayr
Journal: Circulation (2017)

Extracellular matrix (ECM) remodeling contributes to in-stent restenosis and thrombosis. Despite its important clinical implications, little is known about ECM changes post-stent implantation.Bare-metal and drug-eluting stents were implanted in pig coronary arteries with an overstretch under optical coherence tomography guidance. Stented segments were harvested 1, 3, 7, 14, and 28 days post-stenting for proteomics analysis of the media and neointima.A total of 151 ECM and ECM-associated proteins were identified by mass spectrometry. After stent implantation, proteins involved in regulating calcification were upregulated in the neointima of drug-eluting stents. The earliest changes in the media were proteins involved in inflammation and thrombosis, followed by changes in regulatory ECM proteins. By day 28, basement membrane proteins were reduced in drug-eluting stents in comparison with bare-metal stents. In contrast, the large aggregating proteoglycan aggrecan was increased. Aggrecanases of the ADAMTS (a disintegrin and metalloproteinase with thrombospondin motifs) family contribute to the catabolism of vascular proteoglycans. An increase in ADAMTS-specific aggrecan fragments was accompanied by a notable shift from ADAMTS1 and ADAMTS5 to ADAMTS4 gene expression after stent implantation. Immunostaining in human stented coronary arteries confirmed the presence of aggrecan and aggrecan fragments, in particular, at the contacts of the stent struts with the artery. Further investigation of aggrecan presence in the human vasculature revealed that aggrecan and aggrecan cleavage were more abundant in human arteries than in human veins. In addition, aggrecan synthesis was induced on grafting a vein into the arterial circulation, suggesting an important role for aggrecan in vascular plasticity. Finally, lack of ADAMTS-5 activity in mice resulted in an accumulation of aggrecan and a dilation of the thoracic aorta, confirming that aggrecanase activity regulates aggrecan abundance in the arterial wall and contributes to vascular remodeling.Significant differences were identified by proteomics in the ECM of coronary arteries after bare-metal and drug-eluting stent implantation, most notably an upregulation of aggrecan, a major ECM component of cartilaginous tissues that confers resistance to compression. The accumulation of aggrecan coincided with a shift in ADAMTS gene expression. This study provides the first evidence implicating aggrecan and aggrecanases in the vascular injury response after stenting.
GW28-e1067 Urotensin II induces endothelial-mesenchymal transition of cardiac microvascular endothelial cells via endoplasmic reticulum stress
Authors: Yonggang Zhang, Jinyao Zhong, Yuqiang Cui, Da Chen, Lihua Ji, Fan Zheng, Xiaoying Zheng, Wenbin Xia
Journal: Journal of the American College of Cardiology (2017)
REM Sleep Behavior Disorder
Journal: JAMA (1994)

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 HomeNew OnlineCurrent IssueFor Authors Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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 journal
Prognostic value of NK and T-lymphocyte markers in operable non-small cell lung cancer (NSCLC)
Authors: M. Skrzypski, A. Szymanowska-Narloch, A. Kowalczyk, A. Maciejewska, M. Marczyk, J. Polańska, W. Biernat, W. Rzyman, J. Jassem
Journal: Annals of Oncology (2017)
Precision medicine for the treatment of metastatic uveal melanoma: A pilot study
Authors: S. Leyvraz, M. Schuette, D.T. Rieke, T. Kessler, S. Ochsenreither, V. Amstislavskiy, T. Risch, C. Wierling, K. Joehrens, C.A. Peuker, M. Lamping, S. Burock, G. Poch, F. Kiecker, R. Schaefer, B. Lange, H. Lehrach, A. Joussen, U. Keilholz, M.-L. Yaspo
Journal: Annals of Oncology (2017)
Neoplasms and Other Lesions of the Eye Induced by Ultraviolet Radiation in Strain A Mice
Authors: Stuart W. Lippincott, Harold F. Blum
Journal: JNCI Journal of the National Cancer Institute (1943)

Neoplasms and Other Lesions of the Eye Induced by Ultraviolet Radiation in Strain A Mice Get access Stuart W. Lippincott, Stuart W. Lippincott formerly passed assistant surgeon (R) Search for other works by this author on: Oxford Academic PubMed Google Scholar Harold F. Blum Harold F. Blum senior pharmacologist National Cancer Institute, National Institute of Health, United States Public Health Service Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 3, Issue 5, June 1943, Pages 545–554, https://doi.org/10.1093/jnci/3.5.545 Published: 01 June 1943
Vacunación BCG selectiva en un país con baja incidencia de tuberculosis
Authors: V Romanus
Journal: Eurosurveillance (2006)

En 1975, Suecia cambio de una politica de vacunacion rutinaria por la BCG para todos los recien nacidos a una vacunacion selectiva de los grupos de mas riesgo. El informe siguiente evalua la politica actual teniendo en cuenta la situacion de la tuberculosis en Suecia durante el periodo de 1989 a 2005. Durante este periodo la poblacion sueca cambio, con un numero y una proporcion creciente de inmigrantes, que vienen particularmente de paises con una elevada prevalencia de tuberculosis. La cobertura vacunal de la BCG disminuyo de mas del 95% antes de 1975 a menos del 2% entre 1976 y 1980, antes de aumentar de nuevo a un nivel cercano al 16% (correspondiendo al 88% aproximadamente de los grupos de riesgo recomendados para la vacunacion). La proporcion creciente de pacientes nacidos fuera de Suecia respecto al total de casos en el pais y la elevada incidencia especifica por edad en los grupos de edad fertil de la poblacion nacida en el extranjero, muestran que se debe seguir con la vacunacion selectiva para los ninos de familias procedentes de paises con incidencia elevada de tuberculosis. Se estima en 0,5 casos por 100.000 personas por ano la incidencia acumulada de tuberculosis en las 30 cohortes nacidas en Suecia despues de 1974 y seguidas hasta finales de 2004. 
Suecia sigue formando parte de los paises con menor incidencia de tuberculosis, lo que representa un riesgo minimo de infeccion para la mayoria de los ninos nacidos de padres suecos. El aumento de la tuberculosis observado en 2005, atribuido en parte a un brote en una guarderia, subraya las graves consecuencias de los diagnosticos retrasados. 
La accion mas importante para prevenir la tuberculosis infantil es intensificar la busqueda activa de casos, eliminando las fuentes de infeccion, para prevenir la transmision a la poblacion infantil, asi como una deteccion y tratamiento precoz de los ninos infectados para prevenir el desarrollo de la tuberculosis diseminada.
Thrombin-activatable fluorescent peptide incorporated gold nanoparticles for dual optical/computed tomography thrombus imaging
Authors: Sung-Pil Kwon, Sangmin Jeon, Sung-Hoon Lee, Hong Yeol Yoon, Ju Hee Ryu, Dayil Choi, Jeong-Yeon Kim, Jiwon Kim, Jae Hyung Park, Dong-Eog Kim, Ick Chan Kwon, Kwangmeyung Kim, Cheol-Hee Ahn
Journal: Biomaterials (2017)
Reframing non-communicable diseases
Authors: Lavanya Vijayasingham, Pascale Allotey
Journal: The Lancet Global Health (2017)

In reframing non-communicable diseases (NCDs) as socially transmitted conditions bound by common upstream drivers, Luke Allen and Andrea Feigl (July, 2017),1Allen LN Feigl AB Reframing non-communicable diseases as socially transmitted conditions.Lancet Glob Health. 2017; 5: e644-e646Summary Full Text Full Text PDF PubMed Scopus (47) Google Scholar suggest a strong focus on the causative aspects of social context. We suggest a conceptual extension: if social factors drive the prevalence of these conditions, then social factors drive their lived consequences and course. This is not a new idea. Social drivers and contexts influence NCD course, severity, and quality of life. Even congenital and degenerative conditions, which Allen and Feigl suggest are imperfectly captured by the term socially transmitted, are subject to the influences of social context in how they are managed. Clinically similar cases of NCDs translate into different consequences, depending on individual circumstances at the micro, meso, and macro levels of context, where the contrast of disease consequences is especially evident between high-income and low-income countries.2Allotey P Reidpath D Kouamé A Cummins R The DALY, context and the determinants of the severity of disease: an exploratory comparison of paraplegia in Australia and Cameroon.Soc Sci Med. 2003; 57: 949-958Crossref PubMed Scopus (79) Google Scholar As social consequences, we use the example of the work lives of individuals with NCDs, with a view that these consequences are the interplay of individual, organisational, and sociostructural factors. Consider: the differences in access to medicines and finances that enable individuals with NCDs to manage their condition, and consequently their continued employability; the protective structures that buffer against the cumulative health, economic, and social disadvantage of living with an NCD; and the various sociostructural resources, opportunities, and capabilities needed by an individual with an NCD to be resilient to risk and detriment. The resultant experiences and outcomes reflect the imposition of local social architecture and processes. We declare no competing interests. Reframing non-communicable diseases as socially transmitted conditionsIn a Comment (February, 2017),1 we argued that action on the conditions currently referred to as non-communicable diseases (NCDs) may be hampered by the inadequacy of their label. We received a remarkable amount of feedback on this suggestion, and in this Comment we synthesise the responses garnered from a Lancet Facebook poll, Correspondence letters,2–5 and a related GHD Online discussion . We also propose a new definition based on shared social drivers. Full-Text PDF Open Access
Multiplatform assay to classify formalin-fixed paraffin-embedded (FFPE) colorectal cancer (CRC) samples into molecular subtypes with mutational profiles
Authors: E. Fontana, C. Ragulan, D. Cunningham, S. Hulkki-Wilson, F. Sclafani, G. Nyamundanda, K. Eason, R. Begum, I. Chong, C. Peckitt, M.A. Bali, J. Oates, D. Watkins, S. Rao, M. Hubank, A. Wotherspoon, N. Valeri, I. Chau, N. Starling, A. Sadanandam
Journal: Annals of Oncology (2017)
Response to eLetter: ‘Discussion of methotrexate dosage’ by Maguire <i>et al</i>
Authors: Mary Safy, J W G Jacobs, Nicole D Ijff, J W J Bijlsma, J M van Laar, Maria J H de Hair
Journal: Annals of the Rheumatic Diseases (2017)

In their letter to the editor ‘Discussion of Methotrexate Dosage’, Maguire et al 1 raised three issues regarding our recent paper.2 We appreciate their interest in our study and will address these issues here.

First, regarding the methotrexate dosage, we reiterate what we have discussed in the discussion section of our paper: ‘As in the post-trial follow-up period, the controlled situation was lost and treatment was open to the rheumatologists, long-term outcomes in our study may have been influenced by the use of different antirheumatic drugs’. We did not …
Improved Algorithmic Complexity for the 3SEQ Recombination Detection Algorithm
Authors: Ha Minh Lam, Oliver Ratmann, Maciej F Boni
Journal: Molecular Biology and Evolution (2017)

Identifying recombinant sequences in an era of large genomic databases is challenging as it requires an efficient algorithm to identify candidate recombinants and parents, as well as appropriate statistical methods to correct for the large number of comparisons performed. In 2007, a computation was introduced for an exact nonparametric mosaicism statistic that gave high-precision P values for putative recombinants. This exact computation meant that multiple-comparisons corrected P values also had high precision, which is crucial when performing millions or billions of tests in large databases. Here, we introduce an improvement to the algorithmic complexity of this computation from O(mn3) to O(mn2), where m and n are the numbers of recombination-informative sites in the candidate recombinant. This new computation allows for recombination analysis to be performed in alignments with thousands of polymorphic sites. Benchmark runs are presented on viral genome sequence alignments, new features are introduced, and applications outside recombination analysis are discussed.
Pathologic Stimulus Determines Lineage Commitment of Cardiac C-kit <sup>+</sup> Cells
Authors: Zhongming Chen, Wuqiang Zhu, Ingrid Bender, Wuming Gong, Il-Youp Kwak, Amritha Yellamilli, Thomas J. Hodges, Natsumi Nemoto, Jianyi Zhang, Daniel J. Garry, Jop H. van Berlo
Journal: Circulation (2017)

Background: Although cardiac c-kit + cells are being tested in clinical trials, the circumstances that determine lineage differentiation of c-kit + cells in vivo are unknown. Recent findings suggest that endogenous cardiac c-kit + cells rarely contribute cardiomyocytes to the adult heart. We assessed whether various pathological stimuli differentially affect the eventual cell fates of c-kit + cells. Methods: We used single-cell sequencing and genetic lineage tracing of c-kit + cells to determine whether various pathological stimuli would result in different fates of c-kit + cells. Results: Single-cell sequencing of cardiac CD45 - c-kit + cells showed innate heterogeneity, indicative of the existence of vascular and mesenchymal c-kit + cells in normal hearts. Cardiac pressure overload resulted in a modest increase in c-kit-derived cardiomyocytes, with significant increases in the numbers of endothelial cells and fibroblasts. Doxorubicin-induced acute cardiotoxicity did not increase c-kit-derived endothelial cell fates but instead induced cardiomyocyte differentiation. Mechanistically, doxorubicin-induced DNA damage in c-kit + cells resulted in expression of p53. Inhibition of p53 blocked cardiomyocyte differentiation in response to doxorubicin, whereas stabilization of p53 was sufficient to increase c-kit-derived cardiomyocyte differentiation. Conclusions: These results demonstrate that different pathological stimuli induce different cell fates of c-kit + cells in vivo. Although the overall rate of cardiomyocyte formation from c-kit + cells is still below clinically relevant levels, we show that p53 is central to the ability of c-kit + cells to adopt cardiomyocyte fates, which could lead to the development of strategies to preferentially generate cardiomyocytes from c-kit + cells.
Determination of polysomy of chromosome 17 (C17) in immunohistochemistry (IHC) and FISH-negative HER2/neu breast cancer
Authors: elena Martinez-Navarro, manuel sureda, ramon manzano, Jeronimo forteza, francisco Fernandez-Morejon, carlos dussan, begona vazquez, joseba rebollo, antonio brugarolas
Journal: Cancer Research (2008)

197   Preliminary evidence suggests that a subset of breast cancer patients with no detectable expression of HER2/neu by IHC and no amplification by FISH may still benefit from trastuzumab treatment (Proc ASCO 2007 #511). Recently, a correlation between the copy numbers of C17 and trastuzumab efficacy has also been suggested (Proc ASCO 2007 #1009). At the present time the incidence of polysomy of C17 in breast cancer without HER2/neu overexpression or gene copy amplification is not known.  Breast cancer specimens processed at the Pathology Department of the USP Hospital San Jaime, Torrevieja, Spain, and defined as negative (0, 1+), or indetermined (2+) by IHC (HercepTest™, DAKO) were evaluated by FISH with specific probes for detection of Her-2/neu gene and centromeric region of C17 (HER2 FISH pharmDx™), in order to evaluate either amplification of Her2/neu gene and/or polysomy of C17.  From January 2007 to November 2007, 24 formalin-fixed paraffin-embedded tissue blocks and 1 PAP smear cytology of infiltrating breast carcinoma were evaluated. Two cases showed IHC 3+. Two cases showed IHC 2+ and 21cases IHC 0 or 1+. Amplification of HER2-neu gene (HER2/CEP17>2) without polysomy of C17 was detected only in the 2 IHC 2+ cases. Among the 21 IHC 0 or 1+ cases, polysomy of C17 (CEN17/nucleus>2.5) has been found in 4 (19 %).  Conclusion: Polysomy of C17 in the absence of HER2 gene copy amplification and protein overexpression has been found in around 20% of infiltrating breast cancers. Clinical significance of this finding must be adequately stablished in future studies.
PACE4 Undergoes an Oncogenic Alternative Splicing Switch in Cancer
Authors: Frédéric Couture, Robert Sabbagh, Anna Kwiatkowska, Roxane Desjardins, Simon-Pierre Guay, Luigi Bouchard, Robert Day
Journal: Cancer Research (2017)

Abstract Inhibition of PACE4, a proprotein convertase that is overexpressed in prostate cancer, has been shown to block cancer progression in an androgen-independent manner. However, the basis for its overexpression and its growth-inhibitory effects are mitigated and uncertain. Here, we report that PACE4 pre-mRNA undergoes DNA methylation–sensitive alternative splicing of its terminal exon 3′ untranslated region, generating an oncogenic, C-terminally modified isoform (PACE4-altCT). We found this isoform to be strongly expressed in prostate cancer cells, where it displayed an enhanced autoactivating process and a distinct intracellular routing that prevented its extracellular secretion. Together, these events led to a dramatic increase in processing of the progrowth differentiation factor pro-GDF15 as the first PACE4 substrate to be identified in prostate cancer. We detected robust expression of PACE4-altCT in other cancer types, suggesting that an oncogenic switch for this proenzyme may offer a therapeutic target not only in advanced prostate cancer but perhaps also more broadly in human cancer. Cancer Res; 77(24); 6863–79. ©2017 AACR.