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Institution

Tufts University

EducationMedford, Massachusetts, United States
About: Tufts University is a education organization based out in Medford, Massachusetts, United States. It is known for research contribution in the topics: Population & Poison control. The organization has 32800 authors who have published 66881 publications receiving 3451152 citations. The organization is also known as: Tufts College & Universitatis Tuftensis.


Papers
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Journal ArticleDOI
TL;DR: The development of effective synthesis methods and the identification of suitable stabilizers and promoters are expected to lead to the increasing application of atomically dispersed noble metal catalysts for practical processes characterized by efficient resource utilization and cost savings.
Abstract: Our aim in this review is to assess key recent findings that point to atomically dispersed noble metals as catalytic sites on solid supports, which may be viewed as ligands bonded to the metal. Both zeolites and open metal oxide supports are considered; the former offer the advantages of uniform, crystalline structures to facilitate fundamental understanding, and the latter offer numerous advantages in applications. The notion of strong interactions between metals and supports has resurfaced in the recent literature to explain how subnanometer clusters and even atoms of noble metals such as platinum and gold survive under often harsh reaction conditions on some supports, such as ceria and perovskites. Individual cations of platinum, palladium, rhodium, or other metals anchored to supports through M–O bonds can be formed on these supports in configurations that are stable and catalytically active for several reactions illustrated here, notably, oxidation and reduction. The development of effective synthesi...

460 citations

Journal ArticleDOI
TL;DR: The rate of missed acute myocardial infarction in the emergency department was only 1.9%, but death or potentially lethal complications occurred in 25% of missed AMI patients, and another 25% might have been prevented had patients who were recognized to have ischemic heart disease by the physician in the ED been admitted.

459 citations

Journal ArticleDOI
TL;DR: This study provides the first detailed analysis of the anatomical, electrophysiological and molecular properties of Martinotti cells located in different neocortical layers and proposed that MCs are crucial interneurones for feedback inhibition in and between neocorticals layers and columns.
Abstract: Whole-cell patch-clamp recordings followed by histochemical staining and single-cell RT-PCR were obtained from 180 Martinotti interneurones located in layers II to VI of the somatosensory cortex of Wistar rats (P13-P16) in order to examine their anatomical, electrophysiological and molecular properties. Martinotti cells (MCs) mostly displayed ovoid-shaped somata, bitufted dendritic morphologies, and axons with characteristic spiny boutons projecting to layer I and spreading horizontally across neighbouring columns more than 1 mm. Electron microscopic examination of MC boutons revealed that all synapses were symmetrical and most synapses (71%) were formed onto dendritic shafts. MCs were found to contact tuft, apical and basal dendrites in multiple neocortical layers: layer II/III MCs targeted mostly layer I and to a lesser degree layer II/III; layer IV MCs targeted mostly layer IV and to a lesser degree layer I; layer V and VI MCs targeted mostly layer IV and layer I and to a lesser degree the layer in which their somata was located. MCs typically displayed spike train accommodation (90%; n = 127) in response to depolarizing somatic current injections, but some displayed non-accommodating (8%) and a few displayed irregular spiking responses (2%). Some accommodating and irregular spiking MCs also responded initially with bursts (17%). Accommodating responses were found in all layers, non-accommodating mostly in upper layers and bursting mostly in layer V. Single-cell multiplex RT-PCR performed on 63 MCs located throughout layers II-VI, revealed that all MCs were somatostatin (SOM) positive, and negative for parvalbumin (PV) as well as vasoactive intestinal peptide (VIP). Calbindin (CB), calretinin (CR), neuropeptide Y (NPY) and cholecystokinin (CCK) were co- expressed with SOM in some MCs. Some layer-specific trends seem to exist. Finally, 24 accommodating MCs were examined for the expression of 26 ion channel genes. The ion channels with the highest expression in these MCs were (from highest to lowest); Cabeta1, Kv3.3, HCN4, Cabeta4, Kv3.2, Kv3.1, Kv2.1, HCN3, Caalpha1G, Kv3.4, Kv4.2, Kv1.1 and HCN2. In summary, this study provides the first detailed analysis of the anatomical, electrophysiological and molecular properties of Martinotti cells located in different neocortical layers. It is proposed that MCs are crucial interneurones for feedback inhibition in and between neocortical layers and columns.

459 citations

Journal ArticleDOI
10 Dec 1999-Science
TL;DR: These two mouse models provide the means to address fundamental aspects of disease development and to test therapeutic strategies, and demonstrate that loss of the wild-type Nf1 allele is rate-limiting in tumor formation.
Abstract: Neurofibromatosis type 1 (NF1) is a prevalent familial cancer syndrome resulting from germ line mutations in the NF1 tumor suppressor gene. Hallmark features of the disease are the development of benign peripheral nerve sheath tumors (neurofibromas), which can progress to malignancy. Unlike humans, mice that are heterozygous for a mutation in Nf1 do not develop neurofibromas. However, as described here, chimeric mice composed in part of Nf1-/- cells do, which demonstrates that loss of the wild-type Nf1 allele is rate-limiting in tumor formation. In addition, mice that carry linked germ line mutations in Nf1 and p53 develop malignant peripheral nerve sheath tumors (MPNSTs), which supports a cooperative and causal role for p53 mutations in MPNST development. These two mouse models provide the means to address fundamental aspects of disease development and to test therapeutic strategies.

459 citations

Journal ArticleDOI
Richard Anney1, Richard Anney2, Stephan Ripke3, Stephan Ripke4  +211 moreInstitutions (77)
TL;DR: A significant genetic correlation with schizophrenia and association of ASD with several neurodevelopmental-related genes such as EXT1, ASTN2, MACROD2, and HDAC4 is identified and identified.
Abstract: Background: Over the past decade genome-wide association studies (GWAS) have been applied to aid in the understanding of the biology of traits. The success of this approach is governed by the underlying effect sizes carried by the true risk variants and the corresponding statistical power to observe such effects given the study design and sample size under investigation. Previous ASD GWAS have identified genome-wide significant (GWS) risk loci; however, these studies were of only of low statistical power to identify GWS loci at the lower effect sizes (odds ratio (OR) <1.15). Methods: We conducted a large-scale coordinated international collaboration to combine independent genotyping data to improve the statistical power and aid in robust discovery of GWS loci. This study uses genome-wide genotyping data from a discovery sample (7387 ASD cases and 8567 controls) followed by meta-analysis of summary statistics from two replication sets (7783 ASD cases and 11359 controls; and 1369 ASD cases and 137308 controls). Results: We observe a GWS locus at 10q24.32 that overlaps several genes including PITX3, which encodes a transcription factor identified as playing a role in neuronal differentiation and CUEDC2 previously reported to be associated with social skills in an independent population cohort. We also observe overlap with regions previously implicated in schizophrenia which was further supported by a strong genetic correlation between these disorders (Rg = 0.23; P=9 ×10−6). We further combined these Psychiatric Genomics Consortium (PGC) ASD GWAS data with the recent PGC schizophrenia GWAS to identify additional regions which may be important in a common neurodevelopmental phenotype and identified 12 novel GWS loci. These include loci previously implicated in ASD such as FOXP1 at 3p13, ATP2B2 at 3p25.3, and a ‘neurodevelopmental hub’ on chromosome 8p11.23. Conclusions: This study is an important step in the ongoing endeavour to identify the loci which underpin the common variant signal in ASD. In addition to novel GWS loci, we have identified a significant genetic correlation with schizophrenia and association of ASD with several neurodevelopmental-related genes such as EXT1, ASTN2, MACROD2, and HDAC4.

458 citations


Authors

Showing all 33110 results

NameH-indexPapersCitations
Walter C. Willett3342399413322
Frank B. Hu2501675253464
Ralph B. D'Agostino2261287229636
John Q. Trojanowski2261467213948
Peter Libby211932182724
David Baltimore203876162955
Eric B. Rimm196988147119
Lewis C. Cantley196748169037
Bernard Rosner1901162147661
Charles A. Dinarello1901058139668
William B. Kannel188533175659
Scott M. Grundy187841231821
John P. A. Ioannidis1851311193612
David H. Weinberg183700171424
Joel Schwartz1831149109985
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
2023100
2022467
20213,334
20203,065
20192,806
20182,618