gebhart/patrepeval huggingface dataset:
Vigilin interacts with <scp>CCCTC</scp>‐binding factor (<scp>CTCF</scp>) and is involved in <scp>CTCF</scp>‐dependent regulation of the imprinted genes <i>Igf2</i> and <i>H19</i> (2014)

CCCTC ‐binding factor ( CTCF ), a highly conserved zinc finger protein, is a master organizer of genome spatial organization and has multiple functions in gene regulation. Mounting evidence indicates that CTCF regulates the imprinted genes Igf2 and H19 by organizing chromatin at the Igf2 / H19 locus, although the mechanism by which CTCF carries out this function is not fully understood. By yeast two‐hybrid screening, we identified vigilin, a multi‐ KH ‐domain protein, as a new partner of CTCF . Subsequent coimmunoprecipitation and glutathione S ‐transferase pulldown experiments confirmed that vigilin interacts with CTCF . Moreover, vigilin is present at several known CTCF target sites, such as the promoter regions of c‐myc and BRCA 1 , the locus control region of β‐globin, and several regions within the Igf2 / H19 locus. In vivo depletion of vigilin did not affect CTCF binding; however, knockdown of CTCF reduced vigilin binding to the H19 imprinting control region. Furthermore, ectopic expression of vigilin significantly downregulated Igf2 and upregulated H19 , whereas depletion of vigilin upregulated Igf2 and downregulated H19 , in HepG2, CNE 1 and HeLa cells. These results reveal the functional relevance of vigilin and CTCF , and show that the CTCF –vigilin complex contributes to regulation of Igf2 / H19 . Structured digital abstract CTCF physically interacts with Vigilin by two hybrid ( View interaction ) CTCF physically interacts with L31 by two hybrid ( View interaction ) CTCF physically interacts with CHD1L by two hybrid ( View interaction ) CTCF physically interacts with Ral A by two hybrid ( View interaction ) CTCF physically interacts with DDX17 by two hybrid ( View interaction ) CTCF physically interacts with ND4 by two hybrid ( View interaction ) CTCF physically interacts with Vigilin by pull down ( View interaction ) CTCF physically interacts with Vigilin by anti bait coimmunoprecipitation ( 1 , 2 )
An economical and versatile synthesis of 5,8-dialkoxy-2-acetyl-3,4-dihydronaphthalenes: key precursors for the synthesis of chiral anthracyclines (1983)

5,8-Diacetoxy-2-acetyl-3,4-dihydronaphthalene, prepared by a new route from the Diels–Alder adduct of buta-1,3-diene and p-benzoquinone, is selectively deacetylated (Cs2CO3 in tetrahydrofuran or K2CO3 in dimethyl sulphoxide) to intermediates suitable for use in chiral anthracycline synthesis.
Neuropathological Diagnostic Criteria for Creutzfeldt‐Jakob Disease (CJD) and Other Human Spongiform Encephalopathies (Prion Diseases) (1995)

Neuropathological diagnostic criteria for Creutzfeldt-Jakob disease (CJD) and other human transmissible spongiform encephalopathies (prion diseases) are proposed for the following disease entities: CJD--sporadic, iatrogenic (recognised risk) or familial (same disease in 1st degree relative): spongiform encephalopathy in cerebral and/or cerebellar cortex and/or subcortical grey matter; or encephalopathy with prion protein (PrP) immunoreactivity (plaque and/or diffuse synaptic and/or patchy/perivacuolar types). Gerstmann-Sträussler-Scheinker disease (GSS) (in family with dominantly inherited progressive ataxia and/or dementia): encephalo(myelo)pathy with multicentric PrP plaques. Familial fatal insomnia (FFI) (in member of a family with PRNP178 mutation): thalamic degeneration, variable spongiform change in cerebrum. Kuru (in the Fore population). Without PrP data, the crucial feature is the spongiform change accompanied by neuronal loss and gliosis. This spongiform change is characterised by diffuse or focally clustered small round or oval vacuoles in the neuropil of the deep cortical layers, cerebellar cortex or subcortical grey matter, which might become confluent. Spongiform change should not be confused with non-specific spongiosis. This includes status spongiosus ("spongiform state"), comprising irregular cavities in gliotic neuropil following extensive neuronal loss (including also lesions of "burnt-out" CJD), "spongy" changes in brain oedema and metabolic encephalopathies, and artefacts such as superficial cortical, perineuronal, or perivascular vacuolation; focal changes indistinguishable from spongiform change may occur in some cases of Alzheimer's and diffuse Lewy body diseases. Very rare cases might not be diagnosed by these criteria. Then confirmation must be sought by additional techniques such as PrP immunoblotting, preparations for electron microscopic examination of scrapie associated fibrils (SAF), molecular biologic studies, or experimental transmission.
First demonstration of microphonic control of a superconducting cavity with a fast piezoelectric tuner (2004)

Superconducting cavities exhibit a high susceptibility to mechanical vibrations due to their narrow bandwidth of operation. The resulting modulation of the resonance frequency (typical amplitudes are, in the absence of mechanical dampers, a few tens of Hz at a modulation frequency of up to a few hundred Hz) can exceed the cavity bandwidth leading to a perturbation of the amplitude and phase of the accelerating field, which can be controlled only at the expense of rf power. It is therefore highly desirable to control the resonance frequency of the cavity with a fast controller. A fast mechanical tuner based on piezoelectric or magnetostrictive actuator appears very attractive, since its tuning is done simply by a micrometric deformation of the resonator geometry. In the past these tuners have been limited by mechanical resonances in the transfer function to a modulation bandwidth of about 1 Hz. With modem control theory and high speed DSPs and FPGAs it is now possible to design complex controllers which allow high gain up to several hundred Hz. In this paper we present first results of fast microphonics piezoelectric control for a superconducting quarter wave resonator. Microphonics at 42 Hz (inner conductor) are controlled despite a large mechanical resonance a 662 Hz in the actuator transfer function.
Expanded Cytotoxic T-cell Lymphocytes Target the Latent HIV Reservoir (2015)

Enhanced human immunodeficiency virus (HIV)-specific immunity may be required for HIV eradication. Administration of autologous, ex vivo expanded, virus-specific, cytotoxic T-lymphocytes derived from HIV-infected patients on suppressive antiretroviral therapy (HXTCs) are a powerful tool for proof-of-concept studies. Broadly specific, polyclonal HXTCs resulting from ex vivo expansion demonstrated improved control of autologous reservoir virus compared to bulk CD8(+) T cells in viral inhibition assays. Furthermore, patient-derived HXTCs were able to clear latently infected autologous resting CD4(+) T cells following exposure to the latency-reversing agent, vorinostat. HXTCs will be ideal reagents to administer with precise control in future in vivo studies in combination with latency-reversing agents.
[Simulated annealing based phase correction of interferogram in Fourier transform imaging spectrometer]. (2011)

Phase correction is one of the key technologies in the spectrum recovery of the Fourier transform imaging spectrometer. The present paper proposes a correction method based on simulated annealing algorithm to calculate phase error, which overcomes the disadvantage of the existing methods that can not correct the interferogram with noise. The method determines the phase optimum solution by controlling the phase decrease function, attaining objective function value by correcting interferogram data with random phase value generated in the phase range, and determining the objective function increment in accordance with the Metropolis criterion. The simulation result of the algorithm indicates that the optimized phase error is less than 0.5%, and both the error accuracy and stability of the spectrum-recovered relative spectrum is less than 1%, which is a great improvement compared with the existing algorithm.
Tumor necrosis factor-alpha acutely inhibits insulin signaling in human adipocytes: implication of the p80 tumor necrosis factor receptor. (1998)

Tumor necrosis factor (TNF)-alpha is postulated to play a major role in the pathogenesis of obesity-linked insulin resistance, probably resulting from an interaction with insulin signaling pathways. This cross talk has now been investigated in human adipocytes at the level of phosphatidylinositol (PI) 3-kinase, and the TNF receptors (TNFRs) mediating these processes have been identified. Equilibrium binding studies using human adipocytes from mammary tissue indicated the presence of two populations of TNFR with apparent affinity constants of 13 pmol/l and 1.6 nmol/l, respectively. Interaction of TNF-alpha with insulin signaling was determined by quantification of insulin receptor substrate (IRS)-1-associated PI 3-kinase activity. Under control conditions, PI 3-kinase was activated about 10-fold in response to insulin (10[-7] mol/l, 5 min). Preincubation of adipocytes with 5 nmol/l TNF-alpha for 15 min resulted in a 60-70% reduction of insulin action, reaching a stable inhibition (40%) after longer incubation with the cytokine. The inhibitory action of TNF-alpha was dose-dependent, already detectable at 10 pmol/l, and was correlated to inhibition of tyrosine phosphorylation of IRS-1 with an unaltered autophosphorylation of the insulin receptor beta-subunit. The modulation of insulin signaling by TNF-alpha was found to be paralleled by a comparable inhibition of insulin-stimulated glucose transport. An agonistic TNFR1 antibody completely mimicked the inhibitory action of TNF-alpha on insulin signaling, whereas at 100 pmol/l TNF-alpha, a nonagonistic p80 TNFR antibody, was shown to ameliorate the inhibitory action of the cytokine. These findings indicate that in human adipocytes, low concentrations of TNF-alpha induce a rapid inhibition of insulin signaling at the level of PI 3-kinase. We suggest that under these conditions, the p80 TNFR is essential for initiating the intracellular cross talk that involves signaling by the p60 TNFR.
A fast and high efficiency buck converter with Switch-On-Demand Modulator for wide load range applications (2011)

This paper presents a buck converter with a switch-on-demand modulator (SOM) for achieving a fast transient response, small voltage ripple, and high power efficiency over a wide load range. Switching power MOS on or off depending on the energy demand of the load circuit results in a hybrid operation of pulse width modulation (PWM) and pulse frequency modulation (PFM). The proposed buck converter uses 90nm CMOS process and can achieve a transient response time of less than 2µs and a voltage ripple of 18mV at a load current range of 10mA∼500mA with a power efficiency above 88%.
The Research on Hot Compression Mechanism of Light Alloy (2012)

In this research, in order to explore the main mechanism of direct and two-stage compression in as-cast light alloy, the mechanical property, microstructure evolution and the flowing of second phase particles were studied, before and after deformation. Then, the influence of the strain volume in first stage on flowing stress of the second stage deformation also was researched.
Low-copy-number T7 vectors for selective gene expression and efficient protein overproduction in<i>Escherichia coli</i> (1994)

A set of low-copy-number vectors (pPD) has been constructed that permit selective gene expression and high-level protein overproduction in Escherichia coli, based on the bacteriophage T7 RNA polymerase/T7 promoter system. These plasmids carry a chloramphenicol resistance gene (cat) as a selective marker and an extended multiple cloning site for convenient gene cloning. Their replication is mediated by ori sequences derived from the low-copy-number vector pSC101. The efficient T7 gene 10 promoter present on these vectors allows selective and high-level transcription of cloned genes carrying their own translational initiation signals. In addition, low-copy-number T7 vectors were constructed that permit expression of genes lacking their own transcription and translation initiation elements by providing a ribosome binding site, an ATG start codon and a multiple cloning site devised for the cloning in all three reading frames. The pPD expression vectors were used to achieve high-level overproduction of the E. coli integral outer membrane protein Tsx, and the cytoplasmic enzymes beta-galactosidase (beta Gal) and UTP:alpha-D-glucose-1-phosphate uridylyltransferase (GalU). The characteristics of these low-copy-number T7 expression vectors should prove very useful for the cloning and high-level overexpression of genes whose gene products are deleterious to the E. coli host.
Rad6 is a Potential Early Marker of Melanoma Development (2014)

Melanoma is the leading cause of death from skin cancer in industrialized countries. Several melanoma-related biomarkers and signaling pathways have been identified; however, their relevance to melanoma development/progression or to clinical outcome remains to be established. Aberrant activation of Wnt/β-catenin pathway is implicated in various cancers including melanoma. We have previously demonstrated Rad6, an ubiquitin-conjugating enzyme, as an important mediator of β-catenin stability in breast cancer cells. Similar to breast cancer, β-catenin-activating mutations are rare in melanomas, and since β-catenin signaling is implicated in melanoma, we examined the relationship between β-catenin levels/activity and expression of β-catenin transcriptional targets Rad6 and microphthalmia-associated transcription factor-M (Mitf-M) in melanoma cell models, and expression of Rad6, β-catenin, and Melan-A in nevi and cutaneous melanoma tissue specimens. Our data show that Rad6 is only weakly expressed in normal human melanocytes but is overexpressed in melanoma lines. Unlike Mitf-M, Rad6 overexpression in melanoma lines is positively associated with high molecular weight β-catenin protein levels and β-catenin transcriptional activity. Double-immunofluorescence staining of Rad6 and Melan-A in melanoma tissue microarray showed that histological diagnosis of melanoma is significantly associated with Rad6/Melan-A dual positivity in the melanoma group compared to the nevi group (P=.0029). In contrast to strong β-catenin expression in normal and tumor areas of superficial spreading malignant melanoma (SSMM), Rad6 expression is undetectable in normal areas and Rad6 expression increases coincide with increased Melan-A in the transformed regions of SSMM. These data suggest a role for Rad6 in melanoma pathogenesis and that Rad6 expression status may serve as an early marker for melanoma development.
Effect of formaldehyde‐containing drugs on human dental pulp evaluated by enzyme histochemical technique (1976)

The in vivo effect of formaldehyde on pulp tissue in short-term studies cannot be established by using routine histologic techniques because the tissue is exposed to a fixative in vivo as well as during the histologic preparation. The pulps of permanent premolars were amputated and zinc oxide with 4% formaldehyde or formocresol was used as wound dressing. The observation periods varied from 1 to 16 d. After extraction the teeth were freeze-sectioned, freeze-dried and then incubated for histochemical demonstration of some oxidative and hydrolytic enzymes. A demarcated border between apically stained and cervically nonstained pulp tissue was found in sections incubated for oxidative enzymes. When formocresol, which has a high concentration of formaldehyde, was used, the border was situated closer to the apex. This was also the case when the observation period was increased. The incubation for lactate dehydrogenase gave a high staining intensity. Thus the use of frozen sections in combination with the histochemical method for the demonstration of lactate dehydrogenase appears to be suitable for the study of the penetration of formaldehyde in pulp tissue in short-term studies.
687. Therapeutic Correction of an LCA-Causing Splice Defect in the CEP290 Gene by CRISPR/Cas-Mediated Genome Editing (2015)

Leber congenital amaurosis (LCA) comprises a genetically heterogeneous group of early-onset retinal disorders characterized by severe loss of vision in the first years of life. Approximately 30% of LCA patients harbor mutations in the CEP290 gene, which codes for a centrosomal protein involved in ciliogenesis and ciliary trafficking in the photoreceptors. While AAV-mediated gene therapy is showing promise in clinical trials for RPE65-associated LCA, the size of CEP290 exceeds the limit for efficient packaging in AAV. Thus, alternative approaches to treat CEP290 associated LCA are needed. Here, we report a gene editing approach in which the CRISPR/Cas9 system is used to modify the endogenous CEP290 locus and restore normal function of the gene. The most common mutation in CEP290 is the IVS26 c. 2991+1655 A>G mutation. This point mutation in intron 26 of the gene generates a novel splice donor, resulting in aberrant splicing and the inclusion of an extra 128bp cryptic exon into the coding sequence of the transcript. Using the S. aureus CRISPR/Cas9 system, we employed a dual-cut approach in which two gRNAs are used to induce a pair of double strand breaks and excise the region of DNA containing the mutation. We screened gRNA pairs in primary fibroblasts derived from LCA patients harboring homozygous IVS26 mutations and identified pairs capable of generating targeted deletions with high efficiency. Using qRT-PCR, we showed that deletion of the mutation results in increased expression of wildtype CEP290 and concomitant decrease in expression of the aberrantly spliced mutant RNA species. Genome-wide specificity profiling allows for assessment of potential off-target modifications induced by the gRNAs and informs selection of optimal gRNA pairs for further study. Assays to assess ciliogenesis, as well as molecular characterization of gene editing in patient-derived photoreceptor precursor cells, demonstrate phenotypic correction in the relevant cell population. The use of the S. aureus CRISPR/Cas9 system enables efficient packaging of the Cas9 gene, as well as two gRNA genes, into a single AAV vector and provides a method for delivery of this system into patient photoreceptors.
Collagenase in the lower respiratory tract of patients with adult respiratory distress syndrome. (1985)

Collagenase activity in the bronchoalveolar lavage (BAL) of patients with adult respiratory distress syndrome (ARDS) was measured against Type I collagen (17 patients) and against Type III collagen (13 patients). Serine protease activity was also measured against Type III collagen (13 patients). Type I collagenase activity was detectable in 12 of 17 and Type III collagenase was detectable in 12 of 13 patients with ARDS. The 10 control subjects had no detectable Types I or III collagenase activity. Total and differential white cell counts were analyzed in the lavage fluid. Although the total counts did not differ between patients with ARDS and control subjects, the percentage of neutrophils was increased more than 25-fold and the percentage of macrophages was reduced almost 10-fold in the ARDS patients. Serial collagenase activity was followed in 1 ARDS survivor. In this patient Type III collagenase activity peaked before the Type I collagenase activity or serine protease activity reached their maximums. Both the latter enzyme activities paralleled the total recoverable cells in the BAL.
[Effect of TGF-beta1 stimulation on the smad signal transduction pathway of human peritoneal mesothelial cells]. (2004)

The SMAD signal transduction pathway of HPMCs can be specifically activated by TGF-beta1 and influence the process of human peritoneal fibrosis. With the stimulation of TGF-beta1, the protein and mRNA expressions of SMAD 7 (an inhibitor of SMAD pathway) significantly increase as a result of feedback.
<i>AdCD40L</i> Immunogene Therapy for Bladder Carcinoma—The First Phase I/IIa Trial (2010)

To our knowledge, this is the first report on immunogene therapy in bladder cancer and the first using AdCD40L in vivo. Local AdCD40L gene therapy was safe, boosted immune activation, and should be further evaluated as a single or an adjuvant therapy for urothelial malignancies.
Kinetic studies of the enzymic dopamine β-hydroxylation reaction (1968)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTKinetic studies of the enzymic dopamine β-hydroxylation reactionMenek. Goldstein, Tong Hyub. Joh, and Thomas Q. GarveyCite this: Biochemistry 1968, 7, 8, 2724–2730Publication Date (Print):August 1, 1968Publication History Published online1 May 2002Published inissue 1 August 1968https://pubs.acs.org/doi/10.1021/bi00848a005https://doi.org/10.1021/bi00848a005research-articleACS PublicationsRequest reuse permissionsArticle Views136Altmetric-Citations105LEARN 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
Exoskeleton for forearm pronation and supination rehabilitation (2005)

Loss of function after SCI, ABI or stroke has a marked affect on ones quality of life. Return of function has been a long-standing goal of physical and occupational therapy. Repeated motor practice has been identified as crucial for motor recovery. The development of a robotic device for neuromotor rehabilitation and upper extremity neuromuscular system recovery is described. The actuator mechanism allows free motion when possible, and provides programmable therapeutic levels of resistance. The sensor system allows characterization of the applied forces, and accurate measurement of the range of motion of the joint. The control system provides real time feedback of actuator commands based on sensor data, calibration routines, and operational modes.