gebhart/patrepeval huggingface dataset:
AG alpha 1 is the structural gene for the Saccharomyces cerevisiae alpha-agglutinin, a cell surface glycoprotein involved in cell-cell interactions during mating. (1989)

We have cloned the alpha-agglutinin structural gene, AG alpha 1, by the isolation of alpha-specific agglutination-defective mutants, followed by isolation of a complementing plasmid. Independently isolated alpha-specific agglutination-defective mutations were in a single complementation group, consistent with biochemical results indicating that the alpha-agglutinin is composed of a single polypeptide. Mapping results suggested that the complementation group identified by these mutants is allelic to the ag alpha 1 mutation identified previously. Expression of AG alpha 1 RNA was alpha specific and inducible by a-factor. Sequences similar to the consensus sequences for positive control by MAT alpha 1 and pheromone induction were found upstream of the AG alpha 1 initiation codon. The AG alpha 1 gene could encode a 650-amino-acid protein with a putative signal sequence, 12 possible N-glycosylation sites, and a high proportion of serine and threonine residues, all of which are features expected for the alpha-agglutinin sequence. Disruption of the AG alpha 1 gene resulted in failure to express alpha-agglutinin and loss of cellular agglutinability in alpha cells. An Escherichia coli fusion protein containing 229 amino acids of the AG alpha 1 sequence was recognized by an anti-alpha-agglutinin antibody. In addition, the ability of this antibody to inhibit agglutination was prevented by this fusion protein. These results indicate that AG alpha 1 encodes alpha-agglutinin. Features of the AG alpha 1 gene product suggest that the amino-terminal half of the protein contains the a-agglutinin binding domain and that the carboxy-terminal half contains a cell surface localization domain, possibly including a glycosyl phosphatidylinositol anchor.
The New Kid on the Block: RET in Lung Cancer (2013)

RET has recently been identified as a potential new oncogenic driver in a subset of patients with non-small cell lung cancer (NSCLC). In this issue of Cancer Discovery, Drilon and colleagues report preliminary trial data with a RET inhibitor in RET fusion-positive NSCLC, validating RET as a therapeutic target in lung cancer.
Wearable Health Devices—Vital Sign Monitoring, Systems and Technologies (2018)

Wearable Health Devices (WHDs) are increasingly helping people to better monitor their health status both at an activity/fitness level for self-health tracking and at a medical level providing more data to clinicians with a potential for earlier diagnostic and guidance of treatment. The technology revolution in the miniaturization of electronic devices is enabling to design more reliable and adaptable wearables, contributing for a world-wide change in the health monitoring approach. In this paper we review important aspects in the WHDs area, listing the state-of-the-art of wearable vital signs sensing technologies plus their system architectures and specifications. A focus on vital signs acquired by WHDs is made: first a discussion about the most important vital signs for health assessment using WHDs is presented and then for each vital sign a description is made concerning its origin and effect on heath, monitoring needs, acquisition methods and WHDs and recent scientific developments on the area (electrocardiogram, heart rate, blood pressure, respiration rate, blood oxygen saturation, blood glucose, skin perspiration, capnography, body temperature, motion evaluation, cardiac implantable devices and ambient parameters). A general WHDs system architecture is presented based on the state-of-the-art. After a global review of WHDs, we zoom in into cardiovascular WHDs, analysing commercial devices and their applicability versus quality, extending this subject to smart t-shirts for medical purposes. Furthermore we present a resumed evolution of these devices based on the prototypes developed along the years. Finally we discuss likely market trends and future challenges for the emerging WHDs area.
Heterogeneity of the sympathetic innervation of rat interscapular brown adipose tissue via intercostal nerves (1982)

The interscapular brown adipose tissue (IBAT) of cold-acclimated white rats was partially denervated by cutting in most cases four of the five intercostal nerves going to one of its two bilaterally located, lobular pads. After 24 h the functional ability and the degree of residual sympathetic innervation of the pads and of their lobes were assessed (in separate groups of rats): the former by measuring tissue blood flow as an index of sympathetically mediated calorigenesis during exposure of the animals to -6 degrees C, the latter by measuring the residual noradrenaline (NA) content of the tissue. Only the four anterior intercostal nerves contributed significantly to the sympathetic innervation of IBAT pads. On average their contributions were unequal, but there was considerable variation between rats in the relative contribution of each nerve. The measurements on lobes of the pads indicated that the sympathetic fibers supplied by a given intercostal nerve were not distributed uniformly throughout the pad. For example, measurements of NA indicated that on average the fibers of the fourth nerve were four times as abundant in the lateral lobe as in the posterior lobe. But at this level of analysis also there was wide variation between rats. The variation in the participation of each intercostal nerve in the sympathetic innervation of rat IBAT and in the distribution of each nerve's fibers to different parts of the IBAT pad could be of genetic origin or it could reflect a considerable degree of flexibility during development of the innervation of IBAT. Because of the observation variation, it is suggested that if functional responses of IBAT evoked by electrical stimulation of intercostal nerves are to be recorded from a highly localized area of tissue, stimulation of all the nerves probably would be required to obtain responses that are consistent between animals.
Cytochrome P450 1B1: A Novel Anticancer Therapeutic Target (2005)

Cytochrome P450 (CYP)1B1 is overexpressed in tumor cells and is also recognized as a biomarker of the tumor phenotype. This review highlights the tremendous potential of this enzyme as a novel cancer therapeutic target. The range of therapeutic strategies including immunotherapeutics, CYP1B1-activated prodrugs and CYP1B1 inhibitors, that are currently being developed to exploit the presence and activity of CYP1B1 in tumor cells is outlined. The therapeutic strategy, which is at the most advanced stage of development, is a CYP1B1-based vaccine which has already successfully completed a Phase I clinical trial.
Alternative Models of Knowledge Production: a Step Forward in Information Literacy as a Liberal Art (2006)

Cytogenetic and dermatoglyphic features were studied in a family in which the mongoloid propositus inherited a 13-15/21 translocation chromosome from his father. Seven other healthy male carriers scattered throughout the pedigree produced nine chromosomally normal children and five carrier children in addition to the mongoloid propositus. These results show that carrier males do not necessarily produce an unusually large proportion of carrier children as previous reports would indicate. Dermatoglyphic studies showed that translocation carriers in this family have neither significantly more centralized nor less centralized palmar axial triradii than non-carrier relatives. No direct evidence was therefore found for the hypothesis that an allele is present on chromosome 21 which influences the height of the triradius.
Ion Trap Mass Spectrometry (1991)

RETURN TO ISSUEPREVNewsNEXTIon Trap Mass SpectrometryR. GRAHAM COOKS, GARY L. GLISH, SCOTT A. MCLUCKEY, and RAYMOND E. KAISERView Author Information Purdue University Oak Ridge National Laboratory Eli Lilly & Co.Cite this: Chem. Eng. News 1991, 69, 12, 26–41Publication Date (Print):March 25, 1991Publication History Published online10 November 2010Published inissue 25 March 1991https://pubs.acs.org/doi/10.1021/cen-v069n012.p026https://doi.org/10.1021/cen-v069n012.p026newsACS PublicationsCopyright © 1991 American Chemical SocietyArticle Views90Altmetric-Citations100LEARN 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 options SUBJECTS:Ions,Mass spectrometers Get e-Alerts
Effect of Electrode and Electrolyte Modification on the Performance of One‐Chamber Solid Oxide Fuel Cell (1999)

A one‐chamber solid oxide fuel cell (working in a methane‐air mixture) with yttria‐stabilized zirconia (YSZ) electrolyte was modified by adding oxide to the anode (Pt) and cathode (Au). It was determined that the addition of to both electrodes significantly improved the cell discharge characteristics. The short‐circuit current density of a cell using 15 wt % added to the Pt and 20 wt % added to the Au was about 50 times larger than that of a cell using Pt and Au electrodes. Moreover, the cell performance was enhanced further when 1 wt % was doped into the YSZ electrolyte. Microstructural observations of the YSZ electrolyte/electrodes interfaces indicated that both the electrode porosity and the contact areas between electrodes and YSZ electrolyte increased markedly for the Pt and Au electrodes. In addition, the electrocatalytical property of added in the electrodes may also contribute to the improved cell performance. © 1999 The Electrochemical Society. All rights reserved.
Privatization of the Urban Land Market in Shanghai (1997)

After the initiation of the privatization program of land use rights in China, land markets began to rapidly develop. This is undoubtedly due to a market mechanism finally being established to allocate land according to economic principles. However, the socialist practice of planned allocation for land leaves behind a land use pattern that affects the privatization of land market to a certain degree. In this study, a major land market in Asia-Shanghai, China-is examined in order to ascertain how the merging of the old land use pattern and the new market system for land use rights produces both opportunities and constraints in the process of privatization.
Enforced cytokinesis without complete nuclear division in embryonic cells depleting the activity of DNA topoisomerase IIα (2003)

Our results indicate that topo IIalpha has an essential role in the early stages of mouse development and that depletion of topo IIalpha from the embryonic cells causes incomplete nuclear division followed by enforced cytokinesis.
A vaccine strategy against AIDS: An HIV gp41 peptide immunization prevents NKp44L expression and CD4 + T cell depletion in SHIV-infected macaques (2008)

We previously showed that a gp41 peptide (3S) induces expression of a natural killer (NK) ligand (NKp44L) on CD4+ T cells during HIV-1 infection and that those cells are highly sensitive to NK lysis. In HIV-infected patients, anti-3S antibodies are associated with the maintenance of CD4+ T cell counts close to their baseline values, and CD4+ T cells decrease with the antibody titer. This study sought to determine whether anti-3S immunization could prevent NKp44L expression on these CD4+ T cells in vivo and inhibits the subsequent decline in CD4+ T cell counts by immunizing macaques with 3S and then infecting them with simian HIV(162P3). The results show that anti-3S antibodies inhibited NKp44L expression and NK activity and cytotoxicity. They also decreased the apoptosis rate of CD4+ T cells in peripheral blood and lymph nodes. These data raise questions about the pathogenesis of HIV and present opportunities for both preventive and therapeutic HIV vaccine strategies.
Detection of two forms of GP330. Their role in Heymann nephritis. (1993)

Heymann nephritis is characterized by glomerular immune deposits that contain a glycoprotein called gp330. The deposits are believed to result from shedding of immune complexes formed on podocytes. Complexes are also shed from proximal tubule cells, when antibodies combine with gp330 on the cell surface. We performed the present study to investigate what portion of the gp330 molecule is shed, using a rabbit antiserum against a peptide deduced to be in the cytoplasmic domain of gp330, as well as a rabbit antiserum and two monoclonal antibodies that recognize extracellular epitopes of gp330. The anti-cytoplasmic peptide antiserum precipitated from Fx1A (a crude renal cortical membrane preparation), a protein with a mass of about 440 kd that was reactive with two monoclonal anti-gp330 antibodies. (In our experiments, the protein called gp330 generally has a mass estimated to be about 440 kd.) The anti-cytoplasmic peptide antiserum also reacted with a truncated gp330 protein produced in transfected COS cells. Immunohistochemical studies showed that all the antibodies recognized the same group of epithelial cells. However, as seen in immunoultrastructural studies of proximal tubules, the anti-cytoplasmic peptide antiserum reacted only with components at the base of microvilli, whereas the anti-gp330 ectodomain antibodies identified material not only at the base, but over the surface of microvilli as well. In rats with Heymann nephritis, glomerular deposits and material shed into tubule lumens reacted with antibodies against extracellular epitopes of gp330, but not with the anti-cytoplasmic peptide antiserum. We propose that there are two forms of gp330 on the cell surface of proximal renal tubules. One form is restricted to coated pit regions at the base of microvilli and has a cytoplasmic domain containing a sequence deduced from a partial complementary DNA encoding gp330. The other form is present over microvilli (and possibly at the base of microvilli as well) and lacks the cytoplasmic domain deduced from the complementary DNA. The complexes that are shed in Heymann nephritis contain either a portion of gp330 cleaved from the full-length molecule or a form of gp330 that lacks the cytoplasmic domain.
Effects of micro-nutrients and major nutrients on natural phytoplankton populations (1980)

Six experiments were carried out with natural phytoplankton populations grown under simulated natural conditions, in an attempt to assess the gross effects of major nutrient and micronutrient perturbations upon the growth and species composition of these populations. Water was collected from Yaquina Bay, Oregon, and filtered into twenty-litre growth containers. Some of this water was treated with activated carbon to remove a portion of the trace metals and trace organics. Various combinations of major nutrients, micro-nutrients, and chelators were added to these cultures. Inoculation was with unfiltered bay water, at a ratio of 1:1000. Incubation was in outdoor tanks of water circulating from the bay, under natural sunlight. The major nutrients and micro-nutrients appeared to have fundamentally different effects on the growth and species composition of phytoplankton. The micro-nutrients had marked effects on the species composition of the phytoplankton populations, while major nutrients had minimal effects on species composition. The micro-nutrients also had substantial effects on population growth rates, lag periods, and final yields. The major nutrients had a substantial effect only on final yields.
Genetics of Influenza Viruses (2002)

Influenza A viruses contain genomes composed of eight separate segments of negative-sense RNA. Circulating human strains are notorious for their tendency to accumulate mutations from one year to the next and cause recurrent epidemics. However, the segmented nature of the genome also allows for the exchange of entire genes between different viral strains. The ability to manipulate influenza gene segments in various combinations in the laboratory has contributed to its being one of the best characterized viruses, and studies on influenza have provided key contributions toward the understanding of various aspects of virology in general. However, the genetic plasticity of influenza viruses also has serious potential implications regarding vaccine design, pathogenicity, and the capacity for novel viruses to emerge from natural reservoirs and cause global pandemics.
Differential localization and expression of the Cdk9 42k and 55k isoforms (2004)

Cdk9, a member of the cyclin-dependent kinase family, is the catalytic subunit of P-TEFb, a protein kinase complex that stimulates transcriptional elongation. Cdk9, complexed with its regulatory partner cyclin T1, serves as the cellular mediator of the transactivation function of the HIV Tat protein. There are two known isoforms of Cdk9: a 42 kDa protein (42k, originally identified as PITALRE) and a more recently identified 55 kDa form (55k). To investigate possible functional differences between the two isoforms, we examined their kinase activities, their subcellular distributions, and their expression levels in primary cells relevant to HIV infection. Both isoforms were found to hyper-phosphorylate the carboxyl-terminal domain of the largest subunit of RNA polymerase II and displayed identical phosphorylation patterns with 144 peptide substrates. Epitope-tagged transiently-expressed Cdk9 42k localized diffusely in the nucleoplasm, while Cdk9 55k accumulated in the nucleolus. In primary undifferentiated monocytes, Cdk9 55k expression was not detected although 42k was present at high levels; however, 55k expression was induced upon macrophage differentiation. In primary lymphocytes, the levels of 55k decreased or remained steady following activation, while the levels of 42k increased. The promoter for 42k was significantly stronger than that of 55k in HeLa cells, and only the 42k promoter was responsive to activation signals in primary lymphocytes. These results indicate that expression of the 42k and 55k isoforms is differentially regulated and suggest that functional differences between the 42k and 55k isoforms of Cdk9 are likely to depend on access to substrates based on their differential subcellular localization and expression patterns.
Purification and Bioactivity of Recombinant Human Glucagon-like Peptide-1 (2002)

To produce recombinant human glucagon-like peptide-1 (rhGLP-1) and study on its biological activityt, 6 oligonucleotide fragments were synthesized according to the codon of hGLP-1 cDNA. The hGLP-1 cDNA was constructed by the procedure of annealing and ligation with oligonucleotide fragments. The recombinant plasmid containing hGLP-1 cDNA was transformed into E. coli BL21(DE3) and expressed significantly by induction of IPTG. The fusion protein was purified from lysates with glutathione-Sepharose 4B affinity chromatography. The rhGLP-1 was obtained following a series of purification steps such as cutting with CNBr, QAE-Sepharose F F and HPLC. ESI mass spectrometry showed that the molecular weight was 3355.0 as expected. The biological activity of rhGLP-1 in rat model suggested that plasma glucose level was significantly lower after adminstration of rhGLP-1 in combination with glucose comparing with glucose alone.
Efficacy of an Anti-transferrin Receptor 1 Antibody Against AIDS-related Non-Hodgkin Lymphoma (2015)

The transferrin receptor 1 (TfR1), also known as CD71, is a target for antibody-based cancer immunotherapy due to its high expression on the surface of cancer cells and its ability to internalize. We have previously developed a mouse/human chimeric IgG3 specific for human TfR1 genetically fused to avidin, as a vector to deliver biotinylated anticancer agents into malignant cells. However, we found that this fusion protein (ch128.1Av), and to a lesser extent the same antibody without avidin (ch128.1), exhibits direct cytotoxic activity in vitro against certain malignant hematopoietic cells through the induction of TfR1 degradation and lethal iron starvation. Importantly, both ch128.1 and ch128.1Av have also shown significant anticancer activity in 2 xenograft models of the B-cell malignancy multiple myeloma. It is interesting to note that ch128.1 exhibited superior anticancer activity in both models compared with ch128.1Av, even against malignant cells that show no sensitivity to ch128.1 in vitro. In the present study, we evaluated the efficacy of ch128.1 against an AIDS-related human Burkitt lymphoma cell line (2F7) to determine if ch128.1 can eliminate these cells in vitro and in an in vivo model of AIDS-related non-Hodgkin lymphoma (AIDS-NHL). Even though 2F7 cells expressed high TfR1 levels, these cells lacked sensitivity to the cytotoxicity induced by ch128.1 in vitro. However, ch128.1 showed significant anticancer activity against these AIDS-NHL cells in vivo by significantly prolonging the survival of immunodeficient mice bearing 2F7 tumors. Therefore, ch128.1 warrants further study as a candidate for the treatment of AIDS-NHL and other B-cell malignancies.
β-Catenin Up-regulates Atoh1 Expression in Neural Progenitor Cells by Interaction with an Atoh1 3′ Enhancer (2009)

Atoh1, a basic helix-loop-helix transcription factor, plays a critical role in the differentiation of several epithelial and neural cell types. We found that beta-catenin, the key mediator of the canonical Wnt pathway, increased expression of Atoh1 in mouse neuroblastoma cells and neural progenitor cells, and baseline Atoh1 expression was decreased by siRNA directed at beta-catenin. The up-regulation of Atoh1 was caused by an interaction of beta-catenin with the Atoh1 enhancer that could be demonstrated by chromatin immunoprecipitation. We found that two putative Tcf-Lef sites in the 3' enhancer of the Atoh1 gene displayed an affinity for beta-catenin and were critical for the activation of Atoh1 transcription because mutation of either site decreased expression of a reporter gene downstream of the enhancer. Tcf-Lef co-activators were found in the complex that bound to these sites in the DNA together with beta-catenin. Inhibition of Notch signaling, which has previously been shown to induce bHLH transcription factor expression, increased beta-catenin expression in progenitor cells of the nervous system. Because this could be a mechanism for up-regulation of Atoh1 after inhibition of Notch, we tested whether siRNA to beta-catenin prevented the increase in Atoh1 and found that beta-catenin expression was required for increased expression of Atoh1 after Notch inhibition.
Unified on-chip memory allocation for SIMT architecture (2014)

The popularity of general purpose Graphic Processing Unit (GPU) is largely attributed to the tremendous concurrency enabled by its underlying architecture -- single instruction multiple thread (SIMT) architecture. It keeps the context of a significant number of threads in registers to enable fast ``context switches" when the processor is stalled due to execution dependence, memory requests and etc. The SIMT architecture has a large register file evenly partitioned among all concurrent threads. Per-thread register usage determines the number of concurrent threads, which strongly affects the whole program performance. Existing register allocation techniques, extensively studied in the past several decades, are oblivious to the register contention due to the concurrent execution of many threads. They are prone to making optimization decisions that benefit single thread but degrade the whole application performance.