gebhart/patrepeval huggingface dataset:
Mirror-image DNA (1991)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTMirror-image DNAHidehito Urata, Keiko Shinohara, Emiko Ogura, Yoshiaki Ueda, and Masao AkagiCite this: J. Am. Chem. Soc. 1991, 113, 21, 8174–8175Publication Date (Print):October 1, 1991Publication History Published online1 May 2002Published inissue 1 October 1991https://pubs.acs.org/doi/10.1021/ja00021a057https://doi.org/10.1021/ja00021a057research-articleACS PublicationsRequest reuse permissionsArticle Views410Altmetric-Citations68LEARN 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
Genomic Profiling of MicroRNA and Messenger RNA Reveals Deregulated MicroRNA Expression in Prostate Cancer (2008)

MicroRNAs are small noncoding RNAs that regulate the expression of protein-coding genes. To evaluate the involvement of microRNAs in prostate cancer, we determined genome-wide expression of microRNAs and mRNAs in 60 primary prostate tumors and 16 nontumor prostate tissues. The mRNA analysis revealed that key components of microRNA processing and several microRNA host genes, e.g., MCM7 and C9orf5, were significantly up-regulated in prostate tumors. Consistent with these findings, tumors expressed the miR-106b-25 cluster, which maps to intron 13 of MCM7, and miR-32, which maps to intron 14 of C9orf5, at significantly higher levels than nontumor prostate. The expression levels of other microRNAs, including a number of miR-106b-25 cluster homologues, were also altered in prostate tumors. Additional differences in microRNA abundance were found between organ-confined tumors and those with extraprostatic disease extension. Lastly, we found evidence that some microRNAs are androgen-regulated and that tumor microRNAs influence transcript abundance of protein-coding target genes in the cancerous prostate. In cell culture, E2F1 and p21/WAF1 were identified as targets of miR-106b, Bim of miR-32, and exportin-6 and protein tyrosine kinase 9 of miR-1. In summary, microRNA expression becomes altered with the development and progression of prostate cancer. Some of these microRNAs regulate the expression of cancer-related genes in prostate cancer cells.
Asynchronous arithmetic for VLSI neural systems (1987)

A computational style is described that mimics that of a biological neural network. Circuit forms of neural and synaptic functions are presented, and results of simulation and fabrication are reported.
Small Maf Proteins Heterodimerize with Fos and May Act as Competitive Repressors of the NF-E2 Transcription Factor (1995)

The maf oncogene encodes a bZip nuclear protein which recognizes sequences related to an AP-1 site either as a homodimer or as heterodimers with Fos and Jun. We describe here a novel maf-related gene, mafG, which shows extensive homology with two other maf-related genes, mafK and mafF. These three maf-related genes encode small basic-leucine zipper proteins lacking the trans-activator domain of v-Maf. Bacterially expressed small Maf proteins bind to DNA as homodimers with a sequence recognition profile that is virtually identical to that of v-Maf. As we have previously described, the three small Maf proteins also dimerize with the large subunit of NF-E2 (p45) to form an erythroid cell-specific transcription factor, NF-E2, which has distinct DNA-binding specificity. This study shows that the small Maf proteins can also dimerize among themselves and with Fos and a newly identified p45-related molecule (Ech) but not with v-Maf or Jun. Although the small Maf proteins preferentially recognize the consensus NF-E2 sequence as heterodimers with either NF-E2 p45, Ech, or Fos, these heterodimers seemed to be different in their transactivation potentials. Coexpression of Fos and small Mafs could not activate a promoter with tandem repeats of the NF-E2 site. These results raise the possibility that tissue-specific gene expression and differentiation of erythroid cells are regulated by competition among Fos, NF-E2 p45, and Ech for small Maf proteins and for binding sites.
Controlling interlayer diffusion to achieve sustained, multiagent delivery from layer-by-layer thin films (2006)

We present the fabrication of conformal, hydrolytically degradable thin films capable of administering sustained, multiagent release profiles. Films are constructed one molecular layer at a time by using the layer-by-layer, directed-deposition technique; the subsequent hydrolytic surface erosion of these systems results in the release of incorporated materials in a sequence that reflects their relative positions in the film. The position of each species is determined by its ability to diffuse throughout the film architecture, and, as such, the major focus of this work is to define strategies that physically block interlayer diffusion during assembly to create multicomponent, stratified films. By using a series of radiolabeled polyelectrolytes as experimental probes, we show that covalently crosslinked barriers can effectively block interlayer diffusion, leading to compartmentalized structures, although even very large numbers of ionically crosslinked (degradable or nondegradable) barrier layers cannot block interlayer diffusion. By using these principles, we designed degradable films capable of extended release as well as both parallel and serial multiagent release. The ability to fabricate multicomponent thin films with nanoscale resolution may lead to a host of new materials and applications.
Self-Immolative Polymers (2008)

Smart polymers are special kinds of polymeric molecules that respond to external stimuli. We have developed a novel smart polymer designed to sequentially disassemble into its building blocks upon initiation by a triggering event at the polymer head. The polymer structure is based on a polyurethane backbone that disassembles through a domino-like, 1,6-elimination and decarboxylation reactions. We synthesized a self-immolative polymer that amplifies a single cleavage reaction into multiple release of fluorogenic molecules and confirmed the head-to-tail disassembly concept. These polymers can be used to prepare highly sensitive molecular sensors with large signal-to-noise ratios. The sensors should be useful for the detection of a wide range of biological and chemical activities through use of the appropriate trigger at the polymer head.
Subresolution placement using infrared image alignment to the computer-aided design database for backside probing and editing (2001)

As more integrated circuits are packaged in controlled collapse chip connection format, internal debug tools need to image devices through their silicon packaging. Infrared (IR) optical systems make through-silicon imaging possible, but navigation becomes challenging because IR resolution is often lower than positioning accuracy required for design debug. We perform subresolution image alignment between computer-aided design (CAD) and IR images to obtain the required placement accuracy. Our goal is to automate and improve CAD-based IR navigation for silicon-side probing and editing. Using our alignment algorithm, which combines equalization, oversampling, and cross correlation, we demonstrate the ability to achieve 0.1 μm placement accuracy with a 1 μm resolution optical system.
Involvement of the Y-1 receptor subtype in the regulation of luteinizing hormone secretion by neuropeptide Y in rats (1992)

The present experiments were designed to investigate structure-function relationships, and identify the receptor subtype and postreceptor cellular mechanisms that mediate the ovarian hormone-dependent, excitatory, and inhibitory effects of neuropeptide Y (NPY) on LH release in female rats. Intracerebroventricular administration of NPY decreased plasma concentrations of LH in ovariectomized, hormonally untreated rats but stimulated LH release in ovariectomized rats pretreated with estradiol benzoate and progesterone. A similar dual response was also obtained after administration of NPY2-36. However, deletion of additional amino acids at the N terminus, as in NPY5-36, NPY11-36, NPY16-36, and NPY25-36, rendered the peptides inactive. An N-terminal fragment, NPY1-24-amide, and a discontinuous NPY analog, NPY1-4-epsilon-amino-caproic acid-25-36, similarly failed to influence LH release. The analog [Leu31,Pro34]NPY, a preferential agonist at the Y-1 NPY receptor subtype, also elicited the dual LH responses, but the preferential Y-2 receptor agonist, NPY13-36, was completely inactive. Further, only the peptides that stimulated LH release in vivo, i.e. NPY, NPY2-36, and [Leu31,Pro34]NPY, also stimulated the release of LHRH from median eminence fragments of steroid-primed rats in vitro, and the excitatory effect of [Leu31,Pro34] NPY was blocked by a noncompetitive NPY receptor antagonist, D-myo-inositol-1,2,6-trisphosphate. With the exception of NPY1-24-amide, all of the NPY fragments tested bound specifically to NPY binding sites in hypothalamic membrane preparations, but the highest binding affinities were found for the peptides that evoked biological responses in the in vivo and in vitro tests. Further analysis of the mode of action of NPY showed that the stimulation of LHRH release in vitro was unaffected by omission of Ca2+ from the incubation medium, but was prevented by two antagonists of intracellular Ca2+ mobilization, 3,4,5-trimethoxybenzoic acid 8-(diethylamino)octyl ester and ryanodine. Inhibition of prostaglandin synthesis with indomethacin blocked the stimulatory effect of the alpha 1-adrenergic agonist methoxamine on LHRH release, but not the increase produced by NPY.(ABSTRACT TRUNCATED AT 400 WORDS)
Genetic Neurodegenerative Diseases: The Human Illness and Transgenic Models (1998)

Review The neurodegenerative disorders, a heterogeneous group of chronic progressive diseases, are among the most puzzling and devastating illnesses in medicine. Some of these disorders, such as Alzheimer's disease, amyotrophic lateral sclerosis, the prion diseases, and Parkinson's disease, can occur sporadically and, in some instances, are caused by inheritance of gene mutations. Huntington's disease is acquired in an entirely genetic manner. Transgenic mice that express disease-causing genes recapitulate many features of these diseases. This review provides an overview of transgenic mouse models of familial amyotrophic lateral sclerosis, familial Alzheimer's disease, and Huntington's disease and the emerging insights relevant to the underlying molecular mechanisms of these diseases.
Laterality in the Histological Effects of Injections of Amyloid-β 25-35 into the Amygdala of Young Fischer Rats (1997)

We have observed that single amyloid-β 25–35 (Aβ) injections (5.0 nmol) into the right amygdala of rats produce progressive cytoskeletal and astrogliotic reactions not only within the amygdala, but also in distal brain regions that project to the amygdala. To determine if these effects are potentiated by bilateral injections, we injected Aβ (5.0 nmol) into the left and right amygdala of young male Fischer rats. Animals were sacrificed 32 days postoperatively. Bilateral infusions of Aβ induced significant neuronal shrinkage, tau-2 neuronal staining, and reactive astrocytosis within the right amygdala and/or hippocampus, compared with vehicle-treated rats. Surprisingly, the same brain regions within the left hemisphere were significantly less affected even though no differences were observed between the left and right amygdala in the size of Congored-positive Aβ deposits. Unilateral injections of Aβ into the left amygdala led to significant histological changes in the right amygdala and hippocampus, but not in the same brain regions within the left hemisphere. These results suggest a laterality in the histopathological effects of Aβ in male Fischer rats. Identification of the cause for the lateralized effect of Aβ may prove valuable for understanding the etiology of Alzheimer disease and provide possible therapeutic strategies designed to slow the progression of the disease.
Generalized Helicoids for Modeling Hair Geometry (2011)

Abstract In computer graphics, modeling the geometry of hair and hair‐like patterns such as grass and fur remains a significant challenge. Hair strands can exist in an extensive variety of arrangements and the choice of an appropriate representation for tasks such as hair synthesis, fitting, editing, or reconstruction from samples, is non‐trivial. To support such applications we present a novel mathematical representation of hair based on a class of minimal surfaces called generalized helicoids. This representation allows us to characterize the geometry of a single hair strand, as well as of those in its vicinity, by three intuitive curvature parameters and an elevation angle. We introduce algorithms for fitting piecewise generalized helicoids to unparameterized hair strands, and for interpolating hair between these fits. We showcase several applications of this representation including the synthesis of different hair geometries, wisp generation, hair interpolation from samples and hair‐style parametrization and reconstruction from real hair data.
Animal Models of Fibrotic Lung Disease (2013)

Interstitial lung fibrosis can develop as a consequence of occupational or medical exposure, as a result of genetic defects, and after trauma or acute lung injury leading to fibroproliferative acute respiratory distress syndrome, or it can develop in an idiopathic manner. The pathogenesis of each form of lung fibrosis remains poorly understood. They each result in a progressive loss of lung function with increasing dyspnea, and most forms ultimately result in mortality. To better understand the pathogenesis of lung fibrotic disorders, multiple animal models have been developed. This review summarizes the common and emerging models of lung fibrosis to highlight their usefulness in understanding the cell-cell and soluble mediator interactions that drive fibrotic responses. Recent advances have allowed for the development of models to study targeted injuries of Type II alveolar epithelial cells, fibroblastic autonomous effects, and targeted genetic defects. Repetitive dosing in some models has more closely mimicked the pathology of human fibrotic lung disease. We also have a much better understanding of the fact that the aged lung has increased susceptibility to fibrosis. Each of the models reviewed in this report offers a powerful tool for studying some aspect of fibrotic lung disease.
Surgery for recurrent ovarian cancer. (2000)

Recurrent ovarian cancer is associated with a poor long-term prognosis and optimal management for this problem is not well defined. The benefits of primary surgical cytoreduction in prolonging survival rates in advanced ovarian cancer have prompted examination of the potential role of secondary cytoreductive surgery in patients with recurrent disease or disease that progresses or stabilizes during primary adjuvant chemotherapy. No randomized clinical trials have been performed to evaluate secondary surgery in these settings. Based on available data, secondary surgery does not appear to improve survival in patients whose disease progresses or stabilizes during primary adjuvant chemotherapy and therefore is not recommended. The most promising experience with secondary surgery has been in patients with recurrent disease following optimal primary surgical resection with a recurrence-free interval of at least 1 year. While secondary surgery is feasible, it has not yet been proven to improve survival, as similar survival rates have been reported using chemotherapy alone. Consequently, it is critical to minimize the risk of morbidity through careful patient selection when secondary surgery is used.
Three-dimensional holographic disks (1994)

We describe optical disks that store data holographically in three dimensions by using either angle multiplexing or wavelength multiplexing. Data are stored and retrieved in parallel blocks or pages, and each page consists of approximately 10(6) bits. The storage capacity of such disks is derived as a function of disk thickness, pixel size, page size, and scanning parameters. The optimum storage density is approximately 120 bits/µm(2).
Optimum bit allocation and accurate rate control for video coding via ρ-domain source modeling (2002)

We present a new framework for rate-distortion (R-D) analysis, where the coding rate R and distortion D are considered as functions of /spl rho/ which is the percentage of zeros among the quantized transform coefficients. Previously (see He, Z. et al., Int. Conf. Acoustics, Speech and Sig. Proc., 2001), we observed that, in transform coding of images and videos, the rate function R(/spl rho/) is approximately linear. Based on this linear rate model, a simple and unified rate control algorithm was proposed for all standard video coding systems, such as MPEG-2, H.263, and MPEG-4. We further develop a distortion model and an optimum bit allocation scheme in the /spl rho/ domain. This bit allocation scheme is applied to MPEG-4 video coding to allocate the available bits among different video objects. The bits target of each object is then achieved by our /spl rho/-domain rate control algorithm. When coupled with a macroblock classification scheme, the above bit allocation and rate control scheme can also be applied to other video coding systems, such as H.263, at the macroblock level. Our extensive experimental results show that the proposed algorithm controls the encoder bit rate very accurately and improves the video quality significantly (by up to 1.5 dB).
Increased Risk of Recurrence After Hormone Replacement Therapy in Breast Cancer Survivors (2008)

After extended follow-up, there was a clinically and statistically significant increased risk of a new breast cancer event in survivors who took HT.
Connecting Chromosomes, Crisis, and Cancer (2002)

Cancer is a disease of impaired genome stability. The molecular forces that maintain genome integrity and sense altered chromosome structure are invariably subverted in cancer cells. Here, we explore the contrasting contributions of telomeres in the initiation and suppression of cancer and review the evidence supporting a role for telomere dysfunction as a mechanism driving the radical chromosomal aberrations that typify cancer genomes. Recent work suggests that passage of cells through crisis in the setting of deactivated DNA damage checkpoints provides a mutational mechanism that can generate the diverse genetic alterations required for cancer initiation. A greater understanding of telomere-induced crisis and the cell's crisis management mechanisms should guide the rational development of new therapeutics for cancer and other disorders.
Plasma 24-metabolite Panel Predicts Preclinical Transition to Clinical Stages of Alzheimer’s Disease (2015)

We recently documented plasma lipid dysregulation in preclinical late-onset Alzheimer's disease (LOAD). A 10 plasma lipid panel, predicted phenoconversion and provided 90% sensitivity and 85% specificity in differentiating an at-risk group from those that would remain cognitively intact. Despite these encouraging results, low positive predictive values limit the clinical usefulness of this panel as a screening tool in subjects aged 70-80 years or younger. In this report, we re-examine our metabolomic data, analyzing baseline plasma specimens from our group of phenoconverters (n = 28) and a matched set of cognitively normal subjects (n = 73), and discover and internally validate a panel of 24 plasma metabolites. The new panel provides a classifier with receiver operating characteristic area under the curve for the discovery and internal validation cohort of 1.0 and 0.995 (95% confidence intervals of 1.0-1.0, and 0.981-1.0), respectively. Twenty-two of the 24 metabolites were significantly dysregulated lipids. While positive and negative predictive values were improved compared to our 10-lipid panel, low positive predictive values provide a reality check on the utility of such biomarkers in this age group (or younger). Through inclusion of additional significantly dysregulated analyte species, our new biomarker panel provides greater accuracy in our cohort but remains limited by predictive power. Unfortunately, the novel metabolite panel alone may not provide improvement in counseling and management of at-risk individuals but may further improve selection of subjects for LOAD secondary prevention trials. We expect that external validation will remain challenging due to our stringent study design, especially compared with more diverse subject cohorts. We do anticipate, however, external validation of reduced plasma lipid species as a predictor of phenoconversion to either prodromal or manifest LOAD.
Vascular Disrupting Agents: A Novel Mechanism of Action in the Battle Against Non-Small Cell Lung Cancer (2009)

Targeting vasculature, essential in oxygen and nutrient supply, represents a new frontier in the treatment of cancer. Apart from angiogenesis inhibitors that compromise the formation of new blood vessels, a second class of vascular disrupting agents (VDAs) targets endothelial cells and pericytes of the already established tumor vasculature, resulting in tumor ischemia and necrosis. VDAs have been divided into two types: ligand-directed VDAs and small molecules. Ligand-directed VDAs consist of targeting and effector moieties that are linked together. Their clinical efficacy appears limited because of cost and a lack of specificity and toxicity. Small molecules include two classes: the synthetic flavonoids, which work through induction of local cytokine production, and the tubulin-binding agents. The aim of this review is to discuss the hypothesized molecular mechanisms of action of VDAs and their early preclinical and clinical results, emphasizing ASA404, combretastatin A-4 disodium phosphate, ABT-751, and NPI-2358, reported in the treatment of non-small cell lung cancer, which is the leading cause of cancer death worldwide, and also to discuss future developments in this cancer population.