gebhart/patrepeval huggingface dataset:
Structure of human steroid 21-hydroxylase genes. (1986)

We have determined the structure of cDNA and two genomic genes encoding steroid 21-hydroxylase [21-OHase; steroid 21-monooxygenase; steroid, hydrogen-donor:oxygen oxidoreductase (21-hydroxylating); EC 1.14.99.10]. If this cytochrome P-450 enzyme is defective, cortisol cannot be synthesized, resulting in congenital adrenal hyperplasia. The cDNA encoding this enzyme is 2.0 kilobases long, and the encoded protein is predicted to contain 494 amino acid residues with a molecular weight of 55,000. This enzyme is at most 28% homologous to other P-450 enzymes that have been studied. The 21-OHase genomic genes, which are located in the HLA major histocompatibility complex on chromosome 6, each contain 10 exons. This structure is distinct from other characterized P-450 genes, which contain 7 or 9 exons. Studies of individuals with homozygous deletions of the 21-OHase A or B genes suggest that only the B gene encodes an active enzyme. This is confirmed by the finding that the A gene has an 8-base deletion within codons 110-112, resulting in a frameshift that brings a stop codon into the reading frame at codon 130. A second frameshift and a nonsense mutation occur downstream. In contrast, the sequence of the exons of the B gene is identical to the cDNA sequence. The 21-OHase A gene is, therefore, a pseudogene.
Age-Dependent Reduction in Serum Melatonin Concentrations in Healthy Human Subjects (1982)

Serum melatonin concentrations were determined by RIA in 81 healthy humans, aged 1–92 yr. The daytime (0900–1100 h) serum levels of melatonin decreased progressively with advancing age. No sex difference was noted. The nocturnal rise of serum melatonin in the aged group was significantly reduced compared with that in the young group. These results suggest that serum melatonin may be secreted under the agerelated neural control of pineal metabolism.
An Oncogene-Induced DNA Damage Model for Cancer Development (2008)

Of all types of DNA damage, DNA double-strand breaks (DSBs) pose the greatest challenge to cells. One might have, therefore, anticipated that a sizable number of DNA DSBs would be incompatible with cell proliferation. Yet recent experimental findings suggest that, in both precancerous lesions and cancers, activated oncogenes induce stalling and collapse of DNA replication forks, which in turn leads to formation of DNA DSBs. This continuous formation of DNA DSBs may contribute to the genomic instability that characterizes the vast majority of human cancers. In addition, in precancerous lesions, these DNA DSBs activate p53, which, by inducing apoptosis or senescence, raises a barrier to tumor progression. Breach of this barrier by various mechanisms, most notably by p53 mutations, that impair the DNA damage response pathway allows cancers to develop. Thus, oncogene-induced DNA damage may explain two key features of cancer: genomic instability and the high frequency of p53 mutations.
A Large-Scale Evaluation of Acoustic and Subjective Music-Similarity Measures (2004)

June 01 2004 A Large-Scale Evaluation of Acoustic and Subjective Music-Similarity Measures Adam Berenzweig, Adam Berenzweig LabROSA Columbia University New York, New York 10027 USA alb63@columbia.edu Search for other works by this author on: This Site Google Scholar Beth Logan, Beth Logan HP Labs One Cambridge Center Cambridge, Massachusetts 02142–1612 USA beth.logan@hp.com Search for other works by this author on: This Site Google Scholar Daniel P.W. Ellis, Daniel P.W. Ellis LabROSA Columbia University New York, New York 10027 USA dpwe@ee.columbia.edu Search for other works by this author on: This Site Google Scholar Brian Whitman Brian Whitman HP Labs One Cambridge Center Cambridge, Massachusetts 02142–1612 USAMusic, Mind & Machine Group MIT Media Lab Cambridge, Massachusetts 02139–4307 USAbwhitman@media.mit.edu Search for other works by this author on: This Site Google Scholar Author and Article Information Adam Berenzweig LabROSA Columbia University New York, New York 10027 USA alb63@columbia.edu Beth Logan HP Labs One Cambridge Center Cambridge, Massachusetts 02142–1612 USA beth.logan@hp.com Daniel P.W. Ellis LabROSA Columbia University New York, New York 10027 USA dpwe@ee.columbia.edu Brian Whitman HP Labs One Cambridge Center Cambridge, Massachusetts 02142–1612 USAMusic, Mind & Machine Group MIT Media Lab Cambridge, Massachusetts 02139–4307 USAbwhitman@media.mit.edu Online ISSN: 1531-5169 Print ISSN: 0148-9267 © 2004 Massachusetts Institute of Technology2004 Computer Music Journal (2004) 28 (2): 63–76. https://doi.org/10.1162/014892604323112257 Cite Icon Cite Permissions Share Icon Share Facebook Twitter LinkedIn Email Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Search Site Citation Adam Berenzweig, Beth Logan, Daniel P.W. Ellis, Brian Whitman; A Large-Scale Evaluation of Acoustic and Subjective Music-Similarity Measures. Computer Music Journal 2004; 28 (2): 63–76. doi: https://doi.org/10.1162/014892604323112257 Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All ContentAll JournalsComputer Music Journal Search Advanced Search This content is only available as a PDF. © 2004 Massachusetts Institute of Technology2004 Article PDF first page preview Close Modal You do not currently have access to this content.
Lung Cancer Risk Reduction After Smoking Cessation: Observations From a Prospective Cohort of Women (2003)

The risk for lung cancer is increased for both current and former smokers compared with never smokers and declines for former smokers with increasing duration of abstinence. The decline in excess lung cancer risk among former smokers is prolonged compared with other studies, especially for adenocarcinoma and for heavy smokers, suggesting that more emphasis should be placed on smoking prevention and lung cancer chemoprevention.
Ultraviolet Irradiation Blocks Cellular Responses to Transforming Growth Factor-β by Down-regulating Its Type-II Receptor and Inducing Smad7 (2001)

Transforming growth factor-beta (TGF-beta) is a multi-functional cytokine that regulates cell growth and differentiation. Cellular responses to TGF-beta are mediated through its cell surface receptor complex, which activates transcription factors Smad2 and Smad3. Here we report that UV irradiation of mink lung epithelial cells causes near complete inhibition of TGF-beta-induced Smad2/3-mediated gene expression. UV irradiation inhibited TGF-beta-induced phosphorylation of Smad2 and subsequent nuclear translocation and DNA binding of Smad2/3. Specific cell surface binding of TGF-beta was substantially reduced after UV irradiation. This loss of TGF-beta binding resulted from UV-induced down-regulation of TGF-beta type II receptor (T beta RII) mRNA and protein. UV irradiation significantly inhibited T beta RII promoter reporter constructs, indicating that UV reduction of T beta RII expression involved transcriptional repression. In contrast to its effects on T beta RII, UV irradiation rapidly induced Smad7 mRNA and protein. Smad7 is known to antagonize activation of Smad2/3 and thereby block TGF-beta-dependent gene expression. UV irradiation stimulated Smad7 promoter reporter constructs, indicating that increased Smad7 expression resulted, at least in part, from increased transcription. Overexpression of Smad7 protein to the level induced by UV irradiation inhibited TGF-beta-induced gene expression 30%. Maintaining T beta RII levels by overexpression of T beta RII prevented UV inhibition of TGF-beta responsiveness. Taken together, these data indicate that UV irradiation blocks cellular responsiveness to TGF-beta through two mechanisms that impair TGF-beta receptor function. The primary mechanism is down-regulation of T beta RII, and the secondary mechanism is induction of Smad7.
High-speed spelling with a noninvasive brain–computer interface (2015)

The past 20 years have witnessed unprecedented progress in brain-computer interfaces (BCIs). However, low communication rates remain key obstacles to BCI-based communication in humans. This study presents an electroencephalogram-based BCI speller that can achieve information transfer rates (ITRs) up to 5.32 bits per second, the highest ITRs reported in BCI spellers using either noninvasive or invasive methods. Based on extremely high consistency of frequency and phase observed between visual flickering signals and the elicited single-trial steady-state visual evoked potentials, this study developed a synchronous modulation and demodulation paradigm to implement the speller. Specifically, this study proposed a new joint frequency-phase modulation method to tag 40 characters with 0.5-s-long flickering signals and developed a user-specific target identification algorithm using individual calibration data. The speller achieved high ITRs in online spelling tasks. This study demonstrates that BCIs can provide a truly naturalistic high-speed communication channel using noninvasively recorded brain activities.
Immunoregulation by interleukin-12 (1996)

Interleukin-12 (IL-12) is a heterodimeric cytokine produced primarily by antigen-presenting cells (monocytes, macrophages, dendritic cells, and B cells). Its production is stimulated by bacteria, bacterial products, and intracellular parasites and enhanced by priming with granulocyte-macrophage colony-stimulating factor (CM-CSF) and interferon-gamma (IFN-gamma) or inhibited by IL-10. The major biological activity of IL-12 is on T and natural killer (NK) cells in which it increases cytokine production, proliferation, and cytotoxicity. Its production occurs several hours after exposure to infections agents, which induces a rapid production of IFN-gamma by NK and later by T cells. This IFN-gamma potentiates antigen-presenting cell functions important in clearing infections agents (phagocytosis, oxidative burst, and production of nitrous oxide) and also increases further production of IL-12. IL-12 has been clearly demonstrated to be important in the generation of CD4 and CD8 type 1 T cells both in vivo and in vitro. Our data reveals that IL-12 primes naive T cells for high IFN-gamma and IL-10 production, whereas IL-4 is required for IL-4 priming, thus suggesting that these genes and possibly others are independently regulated. IL-12 is therefore involved in the skewing of cytokine production toward a type 1 and has been implicated in being involved in selective mechanisms of established T cells. It is now becoming clear that the IL-12 acts as both a proinflammatory cytokine and an immunomodulator and therefore bridges the innate and adaptive immune responses.
Kinetic Characterization of the Glycosyltransferase Module of Staphylococcus aureus PBP2 (2005)

We report the heterologous overexpression and purification of Staphylococcus aureus PBP2 and demonstrate efficient glycan polymerization from lipid II in vitro. S. aureus PBP2 is the first purified gram-positive class A penicillin-binding protein to show good transglycosylase activity. This enables further studies on this important class of enzymes.
HDL and the Inflammatory Response Induced by LDL-Derived Oxidized Phospholipids (2001)

Oxidation of low density lipoprotein (LDL) phospholipids containing arachidonic acid at the sn-2 position occurs when a critical concentration of "seeding molecules" derived from the lipoxygenase pathway is reached in LDL. When this critical concentration is reached, the nonenzymatic oxidation of LDL phospholipids produces a series of biologically active, oxidized phospholipids that mediate the cellular events seen in the developing fatty streak. Normal high density lipoprotein (HDL) contains at least 4 enzymes as well as apolipoproteins that can prevent the formation of the LDL-derived oxidized phospholipids or inactivate them after they are formed. In the sense that normal HDL can prevent the formation of or inactivate these inflammatory LDL-derived oxidized phospholipids, normal HDL is anti-inflammatory. HDL from mice that are genetically predisposed to diet-induced atherosclerosis became proinflammatory when the mice are fed an atherogenic diet, injected with LDL-derived oxidized phospholipids, or infected with influenza A virus. Mice that were genetically engineered to be hyperlipidemic on a chow diet and patients with coronary atherosclerosis, despite normal lipid levels, also had proinflammatory HDL. It is proposed that LDL-derived oxidized phospholipids and HDL may be part of a system of nonspecific innate immunity and that the detection of proinflammatory HDL may be a useful marker of susceptibility to atherosclerosis.
Induced Abortion and the Risk of Breast Cancer (1997)

Induced abortions have no overall effect on the risk of breast cancer.
The Chemistry of Hortiamine and 6-Methoxyrhetsinine1 (1961)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTThe Chemistry of Hortiamine and 6-Methoxyrhetsinine1Irwin J. Pachter, Richard J. Mohrbacher, and David E. ZachariasCite this: J. Am. Chem. Soc. 1961, 83, 3, 635–642Publication Date (Print):February 1, 1961Publication History Published online1 May 2002Published inissue 1 February 1961https://pubs.acs.org/doi/10.1021/ja01464a032https://doi.org/10.1021/ja01464a032research-articleACS PublicationsRequest reuse permissionsArticle Views207Altmetric-Citations24LEARN ABOUT THESE METRICSArticle Views are the COUNTER-compliant sum of full text article downloads since November 2008 (both PDF and HTML) across all institutions and individuals. These metrics are regularly updated to reflect usage leading up to the last few days.Citations are the number of other articles citing this article, calculated by Crossref and updated daily. Find more information about Crossref citation counts.The Altmetric Attention Score is a quantitative measure of the attention that a research article has received online. Clicking on the donut icon will load a page at altmetric.com with additional details about the score and the social media presence for the given article. Find more information on the Altmetric Attention Score and how the score is calculated. Share Add toView InAdd Full Text with ReferenceAdd Description ExportRISCitationCitation and abstractCitation and referencesMore Options Share onFacebookTwitterWechatLinked InRedditEmail Other access optionsGet e-Alertsclose Get e-Alerts
Automated 3D geometric reasoning in Computer Assisted joint reconstructive surgery (2009)

Computer Assisted Orthopedic Surgery (CAOS) employing information and computer graphics technologies for preoperative planning, intraoperative navigation, and for guiding or performing surgical interventions, has received very little attention for bone tumor surgery applications. We have developed a CAOS system called OrthoSYS, driven by geometric reasoning algorithms to visualize tumor size, shape, and plan for resection according to the tumor's spread, starting from a 3D model reconstructed from CT images. Anatomical landmarks on bone are automatically identified and labeled, useful for registering patient model with virtual model during surgery and also as a reference for tumor resection and prosthesis positioning. The thickness of bone stock remaining after tumor resection is automatically analyzed to choose the best modular stem and fix the prosthesis. A method for prosthesis components selection using fuzzy logic has been developed to assist the surgeons. The medial axis of the long bones and anatomical landmarks are used for positioning the prosthesis in virtual planning and verification in the intraoperative stage. A set of anatomical metrics have been developed to measure the effectiveness of the prosthetic replacement of bone.
Flow cytometric characterization of perfused human bone marrow cultures: Identification of the major cell lineages and correlation with the CFU‐GM assay (2003)

The data showed that CD71 and CD13 antibodies separate the autofluorescent cells into two populations but do not separate hematopoietic cells into specific phenotypic populations. The data also showed that the number of CD13+/++Lin- cells correlated with the number of CFU-GM. These data present the initial step toward detailed phenotypic analysis of ex vivo expanded human BM MNC cultures.
Molecular Mechanisms of Thyroid Hormone-stimulated Steroidogenesis in Mouse Leydig Tumor Cells (1999)

Using a mouse Leydig tumor cell line, we explored the mechanisms involved in thyroid hormone-induced steroidogenic acute regulatory (StAR) protein gene expression, and steroidogenesis. Triiodothyronine (T3) induced a approximately 3.6-fold increase in the steady-state level of StAR mRNA which paralleled with those of the acute steroid response ( approximately 4.0-fold), as monitored by quantitative reverse transcriptase-polymerase chain reaction assay and progesterone production, respectively. The T3-stimulated progesterone production was effectively inhibited by actinomycin-D or cycloheximide, indicating the requirement of on-going mRNA and protein synthesis. T3 displayed the highest affinity of [125I]iodo-T3 binding and was most potent in stimulating StAR mRNA expression. In accordance, T3 significantly increased testosterone production in primary cultures of adult mouse Leydig cells. The T3 and human chorionic gonadotropin (hCG) effects on StAR expression were similar in magnitude and additive. Cells expressing steroidogenic factor 1 (SF-1) showed marginal elevation of StAR expression, but coordinately increased T3-induced StAR mRNA expression and progesterone levels. In contrast, overexpression of DAX-1 markedly diminished the SF-1 mRNA expression, and concomitantly abolished T3-mediated responses. Noteworthy, T3 augmented the SF-1 mRNA expression while inhibition of the latter by DAX-1 strongly impaired T3 action. Northern hybridization analysis revealed four StAR transcripts which increased 3-6-fold following T3 stimulation. These observations clearly identified a regulatory cascade of thyroid hormone-stimulated StAR expression and steroidogenesis that provides novel insight into the importance of a thyroid-gonadal connection in the hormonal control of Leydig cell steroidogenesis.
Electrospun Fibrous Mats on Lithographically Micropatterned Collectors to Control Cellular Behaviors (2012)

Spatial arrangement of multiple cell types plays a critical role in maintaining the viability of cells and functionality of tissues. Micropatterning has been used to fabricate scaffolds to modulate cell distribution, growth, and functions for reconstructing the anisotropy in native tissues. In the current study, a glass substrate patterned with an electrically conductive circuit was prepared by lithography as a collector for electrospinning. Densely packed fibers were deposited on the top of silver strips and patterned fibrous mats were obtained with distinct ridge and groove areas. Orthogonal alignment was shown for fibers in the ridge and groove areas, and the pattern feature and fiber alignment were well maintained in the ridge during incubation of cells with patterned fibrous mats. Sequential confocal laser scanning from the top of cell-loaded fibrous mats indicated that a larger number of cells were spread in the ridge than that in the groove areas, and cells penetrated into the fibrous mats in the ridge. Microscopic observation and immunofluorescent staining indicated that cells and collagen deposition appeared to have distinct patterns on the fibrous scaffold and aligned along the directionality of fibers with an elongated morphology. It is concluded that lithography can provide the design flexibility of collectors with micrometer-scale precision patterning, and cells can be confined to precise locations, sizes, and shapes by the use of micropatterned fibrous scaffolds without any adverse effect on the cell viability and function. The results suggest the potential of patterned electrospun fibrous mats to construct complex tissues of well organized multiple cell types and with spatially distributed extracellular matrices.
Emerging Signaling Pathways in Hepatocellular Carcinoma (2012)

Signaling pathways have become a major source of targets for novel therapies in hepatocellular carcinoma (HCC). Survival benefits achieved with sorafenib, a multikinase inhibitor, are unprecedented and underscore the importance of improving our understanding of how signaling networks interact in transformed cells. Numerous signaling modules are de-regulated in HCC, including some related to growth factor signaling (e.g., IGF, EGF, PDGF, FGF, HGF), cell differentiation (WNT, Hedgehog, Notch), and angiogenesis (VEGF). Intracellular mediators such as RAS and AKT/MTOR may also play a role in HCC development and progression. Different molecular mechanisms have been shown to induce aberrant pathway activation. These include point mutations, chromosomal aberrations, and epigenetically driven down-regulation. The use of novel molecular technologies such as next-generation sequencing in HCC research has enabled the identification of novel pathways previously underexplored in the HCC field, such as chromatin remodeling and autophagy. Considering recent failures of molecular therapies in advanced clinical trials (e.g., sunitinib, brivanib), survey of these and other new pathways may provide alternative therapeutic targets.
Quantification of cellular volume and sub-cellular density fluctuations: comparison of normal peripheral blood cells and circulating tumor cells identified in a breast cancer patient (2012)

Cancer metastasis, the leading cause of cancer-related deaths, is facilitated in part by the hematogenous transport of circulating tumor cells (CTCs) through the vasculature. Clinical studies have demonstrated that CTCs circulate in the blood of patients with metastatic disease across the major types of carcinomas, and that the number of CTCs in peripheral blood is correlated with overall survival in metastatic breast, colorectal, and prostate cancer. While the potential to monitor metastasis through CTC enumeration exists, the basic physical features of CTCs remain ill defined and moreover, the corresponding clinical utility of these physical parameters is unknown. To elucidate the basic physical features of CTCs we present a label-free imaging technique utilizing differential interference contrast (DIC) microscopy to measure cell volume and to quantify sub-cellular mass-density variations as well as the size of subcellular constituents from mass-density spatial correlations. DIC measurements were carried out on CTCs identified in a breast cancer patient using the high-definition (HD) CTC detection assay. We compared the biophysical features of HD-CTC to normal blood cell subpopulations including leukocytes, platelets (PLT), and red blood cells (RBCs). HD-CTCs were found to possess larger volumes, decreased mass-density fluctuations, and shorter-range spatial density correlations in comparison to leukocytes. Our results suggest that HD-CTCs exhibit biophysical signatures that might be used to potentially aid in their detection and to monitor responses to treatment in a label-free fashion. The biophysical parameters reported here can be incorporated into computational models of CTC-vascular interactions and in vitro flow models to better understand metastasis.