gebhart/patrepeval huggingface dataset:
Grid Friendly Appliance Controllers to Increase the Dynamic Stability of Networked Resiliency-based Microgrids (2018)

Microgrids provide the ability to maintain service to critical end-use loads when utility service is not available. Despite their ability to increase resiliency, they can have high capital and operating costs; this can be compounded by the complexities associated with low inertia systems. One option to mitigate the costs is to more effectively engage the assets within the microgrids, specifically the end-use loads. Previous work has shown that by using Grid Friendly™ Appliance controllers, it is possible to increase the dynamic stability of multiple microgrids during switching transients, without the need to oversize generation assets or to install energy storage devices. Building on the previous work, this paper will present a method for determining the set-points of decentralized controllers, accounting for the different characteristics and sizes of loads, to facilitate multiple microgrid switching operations. By effectively engaging the end-use load as a resource, the switching operations necessary to network low inertia microgrids for resiliency applications can be supported without the need to oversize generation assets or for energy storage.
Nonspecific esterase of B lymphocytes from a case of chronic lymhocytic leukemia and of normal T lymphocytes: similar constellations of isoenzymes (1982)

Lymphocytes from a case of B-cell chronic lymphocytic leukemia (CLL) were obtained in a highly purified state from a therapeutic leukapheresis preparation. The CLL lymphocytes showed a fine, scattered, granular pattern of nonspecific esterase cytochemical reactivity with either alpha-naphthyl acetate (alpha NA) or alpha-naphthyl butyrate (alpha NB) substrate as opposed to the more focal pattern of control (T) lymphocytes. Nonspecific esterase of CLL lymphocytes and normal control lymphocytes was equally resistant to inhibition by fluoride ion. Extractable nonspecific esterases from the CLL lymphocytes and from purified normal T lymphocytes were indistinguishable in regard to specific activity, substrate specificity, pH optima, and zymogram profiles on polyacrylamide gel electrophoresis at pH 9.5 and pH 4.0. Zymograms of alpha NA esterase and alpha NB esterase prepared by isoelectric focusing were also similar, with no unequivocal differences. These results are consistent with recent reports that B lymphocytes contain detectable nonspecific esterase and suggest that the B lymphocytes from this case of CLL contained a constellation of isoenzymes similar to that of normal T lymphocytes. This is interpreted as a reflection of the close kinship of these cells.
Analysis of the isomer ratios of polymethylated-DOTA complexes and the implications on protein structural studies (2016)

A rigidified and symmetrical polymethylated 1,4,7,10-tetraazacyclododecane-1,4,7,10-tetraacetic acid (DOTA) ligand bearing four SSSS methyl groups in both the tetraaza ring and the acetate arms (SSSS-SSSS-M4DOTMA) was prepared. The isomer ratio of SSSS-SSSS-M4DOTMA complexed with a series of lanthanide ions was carefully investigated using RP-HPLC and NMR. A square antiprismatic (SAP) configuration was exclusively observed for the early lanthanides, while the twisted square antiprismatic (TSAP) geometry was preferred as the lanthanide ion size decreases. The late lanthanides preferentially adopted the TSAP geometry. One of the pendant arms was modified with a pyridyl disulfide group (SSSS-SSSS-M8SPy) for cysteine attachment and displayed a similar isomer trend as the parent compound, Ln-SSSS-SSSS-M4DOTMA. Covalent attachment to the ubiquitin S57C mutant showed resonances whose intensities are in agreement with the isomeric population observed by RP-HPLC. Furthermore, the NOE experiments combined with quantum chemical calculations have unequivocally demonstrated that the SAP of Pr-SSSS-SSSS-M4DOTMA and Pr-SSSS-SSSS-M8SPy, as well as the TSAP of Yb-SSSS-SSSS-M8SPy are more stable than their corresponding isomers.
Blockade of the Wnt/.BETA.-Catenin Pathway Attenuates Bleomycin-Induced Pulmonary Fibrosis (2011)

Idiopathic pulmonary fibrosis (IPF) is a progressive fibrotic lung disease and characterized by abnormal growth of fibroblasts and lung scarring. While the pathogenesis of IPF is not clearly understood, activation of transforming growth factor-β (TGF-β) and disruption of alveolar basement membrane seem to play important roles in leading to excess disruption of the matrix, which is associated with activated matrix metalloproteinase (MMP) and aberrant proliferation of myofibroblasts. The Wnt/β-catenin pathway is an important regulator of cellular proliferation and differentiation and abnormal activation of Wnt/β-catenin signal was observed in IPF. We examined whether inhibition of the Wnt/β-catenin pathway could attenuate pulmonary fibrosis in a bleomycin-induced murine model of pulmonary fibrosis. Pulmonary fibrosis was induced in C57BL/6N mice by intratracheal instillation of bleomycin. To inhibit the Wnt/β-catenin pathway, small interfering RNA (siRNA) for β-catenin was administered into trachea 2 h before bleomycin instillation and every 48 h afterward until sacrifice on day 14. The level of β-catenin expression was increased in the epithelial cells of bleomycin-administered mice. Intratracheal treatment with β-catenin siRNA significantly reduced β-catenin expression, pulmonary fibrosis and collagen synthesis in bleomycin-administered mice compared with controls, with no significant effect on the inflammatory response. The β-catenin-targeted siRNA also significantly decreased the levels of MMP-2 (P<0.01) and TGF-β (P<0.01) expression in the lung tissue. Blockade of the Wnt/β-catenin pathway by β-catenin siRNA decreased bleomycin-induced pulmonary fibrosis in the murine model. These findings suggest that targeting Wnt/β-catenin signaling may be an effective therapeutic approach in the treatment of IPF.
Ezh2, the histone methyltransferase of PRC2, regulates the balance between self-renewal and differentiation in the cerebral cortex (2010)

Multipotent progenitor cells of the cerebral cortex balance self-renewal and differentiation to produce complex neural lineages in a fixed temporal order in a cell-autonomous manner. We studied the role of the polycomb epigenetic system, a chromatin-based repressive mechanism, in controlling cortical progenitor cell self-renewal and differentiation. We found that the histone methyltransferase of polycomb repressive complex 2 (PCR2), enhancer of Zeste homolog 2 (Ezh2), is essential for controlling the rate at which development progresses within cortical progenitor cell lineages. Loss of function of Ezh2 removes the repressive mark of trimethylated histone H3 at lysine 27 (H3K27me3) in cortical progenitor cells and also prevents its establishment in postmitotic neurons. Removal of this repressive chromatin modification results in marked up-regulation in gene expression, the consequence of which is a shift in the balance between self-renewal and differentiation toward differentiation, both directly to neurons and indirectly via basal progenitor cell genesis. Although the temporal order of neurogenesis and gliogenesis are broadly conserved under these conditions, the timing of neurogenesis, the relative numbers of different cell types, and the switch to gliogenesis are all altered, narrowing the neurogenic period for progenitor cells and reducing their neuronal output. As a consequence, the timing of cortical development is altered significantly after loss of PRC2 function.
Cholinergic activity of acetylenic imidazoles and related compounds (1991)

A series of acetylenic imidazoles related to oxotremorine (1a) were prepared and evaluated as cholinergic agents with in vitro binding assays and in vivo pharmacological tests in mice. 1-[4-(1H-Imidazol-1-yl)-2-butynyl]-2-pyrrolidinone (1b) was a cholinergic agonist with one-half the potency of oxotremorine. Analogues of 1b with a 5- or 2-methyl substituent in the imidazole ring (compounds 1c and 1g) were cholinergic partial agonists. Analogues of 1b with a methyl substituent at the 5-position in the pyrrolidinone ring (7b) or at the alpha-position in the acetylenic chain (8b) were antagonists. Various analogues of these imidazole acetylenes where the pyrrolidinone ring was replaced by an amide, carbamate, or urea residue were prepared. Several compounds which contained 5-methylimidazole as the amine substituent were partial agonists. The activities of the imidazole compounds are compared with those of the related pyrrolidine and dimethylamine analogues. Agonist and antagonist conformations for these compounds at muscarinic receptors are proposed.
Acidosis-Induced Coronary Arteriolar Dilation Is Mediated by ATP-Sensitive Potassium Channels in Vascular Smooth Muscle (1996)

Although a decrease in extravascular pH has been suggested to be involved in coronary flow regulations during hypoxia, ischemia, and increased metabolic demand of the heart, its vasomotor control mechanism has not been elucidated. To examine the effect of acidosis of vasomotor tone, porcine coronary arterioles (40 to 110 microns) were isolated, cannulated, and pressurized to 60 cm H2O intraluminal pressure without flow for in vitro study. Acidosis (pH 7.4 to 7.0) was produced by adding HCl to the extravascular solution. The involvement of potassium channels in the vasomotor response to acidosis was evaluated by using BaCl2 (100 mumol/L, nonspecific potassium channel inhibitor), glibenclamide (5 mumol/L, ATP-sensitive potassium channel inhibitor), and iberiotoxin (100 nmol/L, calcium-activated potassium channel inhibitor). To determine whether endothelial hyperpolarization contributes to the acidosis-induced dilation, the pH-diameter relation of the vessel was examined under a high intraluminal concentration of KCl (40 mmol/L). The involvement of nitric oxide and prostaglandins was assessed by using NG-monomethyl-L-arginine (L-NMMA, 10 mumol/L) and indomethacin (10 mumol/L), respectively. To evaluate the role of endothelium in the acidosis-induced dilation, the pH-diameter relation was studied after endothelial removal. All vessels developed a similar level of spontaneous tone (internal diameter, 75 +/- 4 microns [approximately 69 +/- 1% of maximum diameter) and dilated to HCl in dose-dependent manner. Glibenclamide completely abolished vasodilation to a mild level of acidosis (pH 7.2 to 7.3) and attenuated the vasodilation by 70% at pH 7.0. Acidosis-induced dilation was also inhibited by BaCl2 but not by iberiotoxin. L-NMMA, indomethacin, and intraluminal KCl did not alter the pH-diameter relation. Vasodilation to acidosis of the endothelium-denuded vessels was identical to that of the endothelium-intact vessels. In addition, glibenclamide attenuated the acidosis-induced arteriolar dilation of endothelium-denuded vessels. These results suggest that the opening of ATP-sensitive potassium channels in vascular smooth muscle mediates the coronary arteriolar dilation during acidosis.
A Comparison of Single-Level Fusions With and Without Hardware (1991)

During a 47-month period, 68 patients were studied prospectively to compare single-level lumbar fusion with and without adjunctive pedicular fixation. Fusion indications were disabling back pain for a minimum of 6 months, inability to work, and failed conservative care. Twenty-nine patients fused without hardware and 39 fused with VSP fixation in identical procedures. All patients were evaluated according to fusion success, perceived pain, and return to work. Pseudarthrosis was demonstrated in 58.6% of the noninstrumented group. No pseudarthroses were noted in instrumented patients. Pain improvement in the nonhardware group was 41.4%, and in the hardware group, 76.9%. Return to work was 31% and 72% in each group, respectively. The fusion rate for patients exhibiting single-level disc disease improves with spinal fixation.
Purification and Characterization of Human Mitochondrial Transcription Factor 1 (1988)

We purified to near homogeneity a transcription factor from human KB cell mitochondria. This factor, designated mitochondrial transcription factor 1 (mtTF1), is required for the in vitro recognition of both major promoters of human mitochondrial DNA by the homologous mitochondrial RNA polymerase. Furthermore, it has been shown to bind upstream regulatory elements of the two major promoters. After separation from RNA polymerase by phosphocellulose chromatography, mtTF1 was chromatographed on a MonoQ anion-exchange fast-performance liquid chromatography column. Analysis of mtTF1-containing fractions by sodium dodecyl sulfate-polyacrylamide gel electrophoresis revealed a single major polypeptide with an Mr of approximately 25,000. Centrifugation in analytical glycerol gradients indicated a sedimentation coefficient of approximately 2.5 S, consistent with a monomeric 25-kilodalton protein. Finally, when the 25-kilodalton polypeptide was excised from a stained sodium dodecyl sulfate-polyacrylamide gel and allowed to renature, it regained DNA-binding and transcriptional stimulatory activities at both promoters. Although mtTF1 is the only mitochondrial DNA-binding transcription factor to be purified and characterized, its properties, such as a high affinity for random DNA and a weak specificity for one of its target sequences, may typify this class of regulatory proteins.
A Novel γ-Hydroxybutyrate Dehydrogenase (2003)

In plants, gamma-aminobutyrate (GABA), a non-protein amino acid, accumulates rapidly in response to a variety of abiotic stresses such as oxygen deficiency. Under normoxia, GABA is catabolized to succinic semialdehyde and then to succinate with the latter reaction being catalyzed by succinic semialdehyde dehydrogenase (SSADH). Complementation of an SSADH-deficient yeast mutant with an Arabidopsis cDNA library enabled the identification of a novel cDNA (designated as AtGH-BDH for Arabidopsis thaliana gamma-hydroxybutyrate dehydrogenase), which encodes a 289-amino acid polypeptide containing an NADP-binding domain. Constitutive expression of AtGHBDH in the mutant yeast enabled growth on 20 mm GABA and significantly enhanced the cellular concentrations of gamma-hydroxybutyrate, the product of the GHDBH reaction. These data confirm that the cDNA encodes a polypeptide with GHBDH activity. Arabidopsis plants subjected to flooding-induced oxygen deficiency for up to 4 h possessed elevated concentrations of gamma-hydroxybutyrate as well as GABA and alanine. RNA expression analysis revealed that GHBDH transcription was not up-regulated by oxygen deficiency. These findings suggest that GHBDH activity is regulated by the supply of succinic semialdehyde or by redox balance. It is proposed that GHBDH and SSADH activities in plants are regulated in a complementary fashion and that GHBDH and gamma-hydroxybutyrate function in oxidative stress tolerance.
Transcription Factor Stat5 Synergizes with Androgen Receptor in Prostate Cancer Cells (2008)

The molecular mechanisms underlying progression of prostate cancer to the hormone-independent state are poorly understood. Signal transducer and activator of transcription 5a and 5b (Stat5a/b) is critical for the viability of human prostate cancer cells. We have previously shown that Stat5a/b is constitutively active in high-grade human prostate cancer, but not in normal prostate epithelium. Furthermore, activation of Stat5a/b in primary human prostate cancer predicted early disease recurrence. We show here that transcription factor Stat5a/b is active in 95% of clinical hormone-refractory human prostate cancers. We show for the first time that Stat5a/b synergizes with androgen receptor (AR) in prostate cancer cells. Specifically, active Stat5a/b increases transcriptional activity of AR, and AR, in turn, increases transcriptional activity of Stat5a/b. Liganded AR and active Stat5a/b physically interact in prostate cancer cells and, importantly, enhance nuclear localization of each other. The work presented here provides the first evidence of synergy between AR and the prolactin signaling protein Stat5a/b in human prostate cancer cells.
Fluoroscopically triggered contrast-enhanced three-dimensional MR angiography with elliptical centric view order: application to the renal arteries. (1997)

With this fluoroscopically triggered MR angiographic technique, high-quality, arterial phase, relatively motion immune angiograms can be routinely obtained.
Use of the Penumbra System 054 plus Low Dose Thrombolytic Infusion for Multifocal Venous Sinus Thrombosis (2012)

Multifocal cerebral venous sinus thrombosis (CVST) has a high mortality rate especially when patients present with stupor or coma. Medical treatment including anticoagulation raises concerns about the associated high risk of intracerebral hemorrhage. Treatment of multifocal CVST with mechanical thrombectomy devices and local tPA infusion have previously been reported. However, these devices may have technical limitations. Success of the new-generation aspiration thrombectomy device like the Penumbra system has been reported in few cases of isolated CVST without the use of chemical thrombolysis. We describe two cases in which mechanical thrombectomy were used in conjunction with intra-sinus tPA infusion. Both cases were complicated and failed initial anticoagulation. Penumbra 054 was used in both cases. The Penumbra 054 is a novel device that has a bigger lumen which provides compatibility with other microcatheters, if additional therapies are required. The larger internal diameter of this catheter also allows for stronger thrombo-aspiration, potentially effecting more rapid sinus recanalization. Both cases showed remarkable clinical recovery without any major complications. This is the first reported simultaneous use of the Penumbra system 054 along with tPA infusion. New devices such as the Penumbra system may offer additional therapeutic options in the treatment of multifocal CVST.
An Evaluation of Croscarmellose as a Tablet Disintegrant in Direct Compression Systems (1982)

The disintegrant actions of croscarmellose type A (Ac-Di-Sol, FMC Corp.) and croscarmellose type B (CLD-2, Buckeye Cellulose Corp.) have been compared to that of corn starch in direct compression tablets in which microcrystalline cellulose (Avicel PH101, FMC Corp.) was the matrix. Two types of formulations were examined using either pyridoxine or hydrochlorothiazide as drug. The data clearly shows that both forns of croscarmellose are markedly superior to corn starch and are active at quite low concentrations. The CLD-2 may promote more rapid dissolution in some systems than Ac-Di-Sol.
THE DETECTION OF LINKAGE IN TETRAD ANALYSIS (1953)

STABLISHING the existence of linkage between genes at two loci is a E distinct problem from estimating map-distance once genes are known to be linked.This paper considers two questions that concern linkage detection in organisms with genetically analyzable tetrads.First, what criterion is best for establishing linkage when tetrad segregations are analyzedl?And second, what are the advantages of tetrads compared to random single strands for indicating linkage?
The Antibody-Mediated Targeted Delivery of Interleukin-15 and GM-CSF to the Tumor Neovasculature Inhibits Tumor Growth and Metastasis (2007)

Tumor-targeting immunocytokines represent a new class of anticancer pharmaceutical agents, which often display a superior therapeutic index compared with the corresponding unconjugated cytokines. In this article, we have studied the anticancer properties of interleukin-15 (IL-15) and granulocyte macrophage colony-stimulating factor (GM-CSF), fused to the human antibody fragment scFv(L19), specific to the EDB domain of fibronectin, a marker of angiogenesis. The immunocytokines L19-IL-15 and L19-GM-CSF were expressed in mammalian cells and purified to homogeneity, revealing no loss of cytokine activity in in vitro assays. Furthermore, the ability of the two immunocytokines to selectively localize to tumors in vivo was confirmed by biodistribution analysis with radioiodinated protein preparations. L19-IL-15 and L19-GM-CSF displayed a potent antitumor activity both in s.c. and in metastatic F9 and C51 murine models of cancer in immunocompetent mice. This therapeutic action was superior compared with IL-15-based and GM-CSF-based fusion proteins, containing antibodies of irrelevant specificity in the mouse, which were used as non-tumor-targeting controls. For both L19-IL-15 and L19-GM-CSF immunocytokines, CD8(+) T cells seemed to mostly contribute to the therapeutic action as shown by in vivo cell depletion experiments. The results presented in this article are of clinical significance, considering the fact that the sequence of EDB is identical in mouse and man and that the tumor-targeting ability of the L19 antibody has been extensively shown in clinical trials in patients with cancer.
SNX9 Regulates Dynamin Assembly and Is Required for Efficient Clathrin-mediated Endocytosis (2005)

Dynamin, a central player in clathrin-mediated endocytosis, interacts with several functionally diverse SH3 domain-containing proteins. However, the role of these interactions with regard to dynamin function is poorly defined. We have investigated a recently identified protein partner of dynamin, SNX9, sorting nexin 9. SNX9 binds directly to both dynamin-1 and dynamin-2. Moreover by stimulating dynamin assembly, SNX9 stimulates dynamin's basal GTPase activity and potentiates assembly-stimulated GTPase activity on liposomes. In fixed cells, we observe that SNX9 partially localizes to clathrin-coated pits. Using total internal reflection fluorescence microscopy in living cells, we detect a transient burst of EGFP-SNX9 recruitment to clathrin-coated pits that occurs during the late stages of vesicle formation and coincides spatially and temporally with a burst of dynamin-mRFP fluorescence. Transferrin internalization is inhibited in HeLa cells after siRNA-mediated knockdown of SNX9. Thus, our results establish that SNX9 is required for efficient clathrin-mediated endocytosis and suggest that it functions to regulate dynamin activity.
Mutations in the tau gene that cause an increase in three repeat tau and frontotemporal dementia (2003)

The majority of cases with frontotemporal dementia (FTD) have no tau deposition in the brain, yet mutations in the tau gene lead to a similar clinical phenotype with insoluble tau depositing in neuropathological lesions. We report two tau gene mutations at positions +19 and +29, in the intronic sequences immediately following the stem loop structure in exon 10, which segregate with FTD. Exon-trapping experiments showed that these gene mutations alter the splicing out of exon 10 and produce an increase in tau isoforms with three microtubule binding domains (three repeat tau). Mutagenesis experiments demonstrated that the +19 mutation was responsible for the increase in three repeat tau, possibly by altering an intron silencer modulator sequence element found at this region of the gene. Microtubule binding experiments revealed a significant decrease in microtubule assembly with increasing amounts of three and decreasing amounts of four repeat tau. Brain autopsy was available in one case. Analysis of the type of soluble tau isoforms revealed an increase in three repeat tau and an absence of tau isoforms with exon 3 inserts. No insoluble tau was isolated in the tissue fractions, consistent with the absence of tau-positive histopathology. There was also an increase in tau degradation products suggestive of increased proteolysis. This increase in tau breakdown products was associated with TUNEL- and activated caspase-3-positive neurons identified histologically. These studies show that increases in soluble three repeat tau can be responsible for FTD in cases with tau gene mutations in the intronic region immediately adjacent to the stem loop in exon 10. These cases of FTD have tau isoforms (without exon 3 inserts) that do not form abnormal aggregates and appear more prone to proteolysis. The increase in tau proteolysis was associated with increased evidence of apoptosis. This mechanism of neurodegeneration may be more applicable to the majority of FTD cases, which do not accumulate insoluble tau deposits.