gebhart/patrepeval huggingface dataset:
Oriented Attachment and Membrane Reconstitution of His-Tagged CytochromecOxidase to a Gold Electrode:  In Situ Monitoring by Surface-Enhanced Infrared Absorption Spectroscopy (2004)

A novel concept is introduced for the oriented incorporation of membrane proteins into solid supported lipid bilayers. Recombinant cytochrome c oxidase solubilized in detergent was immobilized on a chemically modified gold surface via the affinity of its histidine-tag to a nickel-chelating nitrilo-triacetic acid (NTA) surface. The oriented protein monolayer was reconstituted into the lipid environment by detergent substitution. The individual steps of the surface modification, including (1) chemical modification of the gold support, (2) adsorption of the protein, and (3) reconstitution of the lipid bilayer, were followed in situ by means of surface-enhanced infrared absorption spectroscopy (SEIRAS) and accompanied by normal-mode analysis. The high surface sensitivity of SEIRAS allows for the identification of each chemical reaction process within the monolayer at the molecular level. Finally, full functionality of the surface-tethered cytochrome c oxidase was demonstrated by cyclic voltammetry after binding of the natural electron donor cytochrome c.
Direct Sulfhydrylation for Methionine Biosynthesis in Leptospira meyeri (1998)

ABSTRACT A gene library of the Leptospira meyeri serovar semaranga strain Veldrat S.173 DNA has been constructed in a mobilizable cosmid with inserts of up to 40 kb. It was demonstrated that a Leptospira DNA fragment carrying metY complemented Escherichia coli strains carrying mutations in metB . The latter gene encodes cystathionine γ-synthase, an enzyme which catalyzes the second step of the methionine biosynthetic pathway. The metY gene is 1,304 bp long and encodes a 443-amino-acid protein with a molecular mass of 45 kDa as determined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. The deduced amino acid sequence of the Leptospira metY product has a high degree of similarity to those of O -acetylhomoserine sulfhydrylases from Aspergillus nidulans and Saccharomyces cerevisiae . A lower degree of sequence similarity was also found with bacterial cystathionine γ-synthase. The L. meyeri metY gene was overexpressed under the control of the T7 promoter. MetY exhibits an O -acetylhomoserine sulfhydrylase activity. Genetic, enzymatic, and physiological studies reveal that the transsulfuration pathway via cystathionine does not exist in L. meyeri , in contrast to the situation found for fungi and some bacteria. Our results indicate, therefore, that the L. meyeri MetY enzyme is able to perform direct sulfhydrylation for methionine biosynthesis by using O -acetylhomoserine as a substrate.
A New Family of Chiral Binaphthyl‐Derived Cyclophane Receptors: Complexation of Pyranosides (1995)

Even in the presence of a protic solvent (up to 20% v/v CD3OD) the optically active cyclophane tetraanion in (R,R,R,R)-1 binds to carbohydrates such as 1-O-octyl-β-D-glycopyranoside. In addition, neutral cyclophanes with similarly highly organized cavities are suitable binders in chloroform. The macrocycles are synthesized by Glaser–Hay coupling of novel chiral diethynylated 1,1'-binaphthyl monomers.
Bovine Herpesvirus 5 Glycoprotein E Is Important for Neuroinvasiveness and Neurovirulence in the Olfactory Pathway of the Rabbit (2000)

Glycoprotein E (gE) is important for full virulence potential of the alphaherpesviruses in both natural and laboratory hosts. The gE sequence of the neurovirulent bovine herpesvirus 5 (BHV-5) was determined and compared with that of the nonneurovirulent BHV-1. Alignment of the predicted amino acid sequences of BHV-1 and BHV-5 gE open reading frames showed that they had 72% identity and 77% similarity. To determine the role of gE in the differential neuropathogenesis of BHV-1 and BHV-5, we have constructed BHV-1 and BHV-5 recombinants: gE-deleted BHV-5 (BHV-5gEDelta), BHV-5 expressing BHV-1 gE (BHV-5gE1), and BHV-1 expressing BHV-5 gE (BHV-1gE5). Neurovirulence properties of these recombinant viruses were analyzed using a rabbit seizure model (S. I. Chowdhury et al., J. Comp. Pathol. 117:295-310, 1997) that distinguished wild-type BHV-1 and -5 based on their differential neuropathogenesis. Intranasal inoculation of BHV-5 gEDelta and BHV-5gE1 produced significantly reduced neurological signs that affected only 10% of the infected rabbits. The recombinant BHV-1gE5 did not invade the central nervous system (CNS). Virus isolation and immunohistochemistry data suggest that these recombinants replicate and spread significantly less efficiently in the brain than BHV-5 gE revertant or wild-type BHV-5, which produced severe neurological signs in 70 to 80% rabbits. Taken together, the results of neurological signs, brain lesions, virus isolation, and immunohistochemistry indicate that BHV-5 gE is important for efficient neural spread and neurovirulence within the CNS and could not be replaced by BHV-1 gE. However, BHV-5 gE is not required for initial viral entry into olfactory pathway.
High-Performance One-Body Core/Shell Nanowire Supercapacitor Enabled by Conformal Growth of Capacitive 2D WS2 Layers (2016)

Two-dimensional (2D) transition-metal dichalcogenides (TMDs) have emerged as promising capacitive materials for supercapacitor devices owing to their intrinsically layered structure and large surface areas. Hierarchically integrating 2D TMDs with other functional nanomaterials has recently been pursued to improve electrochemical performances; however, it often suffers from limited cyclic stabilities and capacitance losses due to the poor structural integrity at the interfaces of randomly assembled materials. Here, we report high-performance core/shell nanowire supercapacitors based on an array of one-dimensional (1D) nanowires seamlessly integrated with conformal 2D TMD layers. The 1D and 2D supercapacitor components possess "one-body" geometry with atomically sharp and structurally robust core/shell interfaces, as they were spontaneously converted from identical metal current collectors via sequential oxidation/sulfurization. These hybrid supercapacitors outperform previously developed any stand-alone 2D TMD-based supercapacitors; particularly, exhibiting an exceptional charge-discharge retention over 30,000 cycles owing to their structural robustness, suggesting great potential for unconventional energy storage technologies.
Phosphotyrosine profiling identifies the KG-1 cell line as a model for the study of FGFR1 fusions in acute myeloid leukemia (2006)

The 8p11 myeloproliferative syndrome (EMS) is associated with translocations that disrupt the FGFR1 gene. To date, 8 fusion partners of FGFR1 have been identified. However, no primary leukemia cell lines were identified that contain any of these fusions. Here, we screened more than 40 acute myeloid leukemia cell lines for constitutive phosphorylation of STAT5 and applied an immunoaffinity profiling strategy to identify tyrosine-phosphorylated proteins in the KG-1 cell line. Mass spectrometry analysis of KG-1 cells revealed aberrant tyrosine phosphorylation of FGFR1. Subsequent analysis led to the identification of a fusion of the FGFR1OP2 gene to the FGFR1 gene. Small interfering RNA (siRNA) against FGFR1 specifically inhibited the growth and induced apoptosis of KG-1 cells. Thus, the KG-1 cell line provides an in vitro model for the study of FGFR1 fusions associated with leukemia and for the analysis of small molecule inhibitors against FGFR1 fusions.
LDL-receptor mutations in Europe (2004)

Familial hypercholesterolemia (FH) is a clinical definition for a remarkable increase of cholesterol serum concentration, presence of xanthomas, and an autosomal dominant trait of either increased serum cholesterol or premature coronary artery disease (CAD). The identification of the low-density lipoprotein (LDL)-receptor (LDLR) as the underlying cause and its genetic characterization in FH patients revealed more insights in the trafficking of LDL, which primarily transports cholesterol to hepatic and peripheral cells. Mutations within LDLR result in hypercholesterolemia and, subsequently, cholesterol deposition in humans to a variable degree. This confirms the pathogenetic role of LDLR and also highlights the existence of additional factors in determining the phenotype. Autosomal dominant FH is caused by LDLR deficiency and defective apolipoprotein B-100 (APOB), respectively. Heterozygosity of the LDLR is relatively common (1:500). Clinical diagnosis is highly important and genetic diagnosis may be helpful, since treatment is usually effective for this otherwise fatal disease. Very recently, mutations in PCSK9 have been also shown to cause autosomal dominant hypercholesterolemia. For autosomal recessive hypercholesterolemia, mutations within the so-called ARH gene encoding a cellular adaptor protein required for LDL transport have been identified. These insights emphasize the crucial importance of LDL metabolism intra- and extracellularly in determining LDL-cholesterol serum concentration. Herein, we focus on the published European LDLR mutation data that reflect its heterogeneity and phenotypic penetrance.
31‐2: See‐through Image Blurring of Transparent OLED Display: Diffraction Analysis and OLED Pixel Optimization (2016)

A calculation method was proposed to accurately simulate blurred see‐through image for transparent OLED display. Error between calculated and actual images were only 5.6% and 5.7% in terms of pattern's characteristic and MTF respectively. Then OLED pixel structure was optimized and significantly suppressed see‐through image blurring was actually verified.
The contrasting roles of ICE family proteases and interleukin-1beta in apoptosis induced by trophic factor withdrawal and by copper/zinc superoxide dismutase down-regulation. (1996)

We compare here the mechanisms of apoptotic death of PC12 cells induced by down-regulation of Cu2+,Zn2+ superoxide dismutase (SOD1) and withdrawal of trophic support (serum/nerve growth factor). Our previous results indicated that the initiating causes of death are different in each paradigm. However, bcl-2 rescues cells in either paradigm, suggesting common downstream elements to the cell death pathway. To determine whether the ICE [interleukin 1beta converting enzyme] family of proteases, which is required for apoptosis on trophic factor withdrawal, is also required for apoptosis induced by oxidative stress, we have developed a novel peptide inhibitor that mimics the common catalytic site of these enzymes and thereby blocks their access to substrates. This differs from the more usual pseudosubstrate approach to enzyme inhibition. Blockade of ICE family proteases by either this inhibitor or by a permeant competitive ICE family antagonist rescues PC12 cells from apoptotic death following apoptosis induced by down-regulation of SOD1, as well as from trophic factor/nerve growth factor deprivation. SOD1 down-regulation results in an increase in interleukin 1beta (IL- 1beta) production by the cells, and cell death under these conditions can be prevented by either blocking antibodies against IL-1beta or the IL-1 receptor antagonist (IL-1Ralpha). In contrast, trophic factor withdrawal does not increase IL-1beta secretion, and the blocking antibody failed to protect PC12 cells from trophic factor withdrawal, whereas the receptor antagonist was only partially protective at very high concentrations. There were substantial differences in the concentrations of pseudosubstrate inhibitors which rescued cells from SOD1 down-regulation and trophic factor deprivation. These results suggest the involvement of different members of the ICE family, different substrates, or both in the two different initiating causes of cell death.
Regulation of antigen-specific IgE, IgG1, and mast cell responses to ingested allergen by mucosal tolerance induction (1997)

Mucosal administration of soluble protein Ags results in profound immunologic nonresponsiveness, characterized by reduced production of Th1 and Th2 cytokines and concomitant suppressed Ig production. It has been suggested that Th2 cells are required for the induction and maintenance of this tolerogenic state. In this study, we show that oral tolerance induction abrogates subsequent Th2-driven Ag-specific IgE and IgG1 responses, while intranasal tolerance induction only blocks the production of IgE, but not IgG1. Consistent with suppressed IgE serum levels, elevated IFN-gamma production was observed in the spleens of tolerized mice. Moreover, both oral and intranasal tolerance induction were found to inhibit intestinal mast cell responses upon subsequent priming and intragastric provocation. Transfer of total splenocytes or purified CD4+, but not CD8+, T cells from intranasally tolerized mice clearly suppressed ongoing Ag-specific IgE, but not IgG1, responses in primed recipients. In addition, coadministration of IFN-gamma-neutralizing Abs completely blocked the transfer of suppression to primed recipients. These results show that Th2 cells can be subjected to tolerance induction, by inducing cross-regulatory, IFN-gamma-producing CD4+ T cells. Moreover, our results point out differences in the regulation of T cell-dependent Ag-specific IgE and IgG1 responses.
Design of a 3-dimension FPGA (2005)

Thesis (S.M.)--Massachusetts Institute of Technology, Dept. of Electrical Engineering and Computer Science, 2005.
Symbolic computation of digital filter transfer function using MATLAB (2003)

We present an original software DFSYM for symbolic computation of transfer function of digital filters and linear time-invariant discrete-time Systems. The software uses standard MATLAB commands and MATLAB SYMBOLIC TOOLBOX. The transfer function is derived directly from the filter schematic created by DrawFilt. DFSYM finds transfer function of filters with arbitrary real or complex coefficients. Filter designers, practitioners, students, researchers, educators and scientists can use DFSYM to evaluate, validate, document or verify the existing filter realizations or to explore, get insight to and optimize the filters they work on.
Analytical methods for lignin characterization - Differential scanning calorimetry (2006)

Results of a round robin on lignin thermal analyses are reported. Six laboratories have conducted thermal analyses of four lignin types to determine their c(p) values and softening points, and to study the thermal behaviour, materials endo- and exotherms included. The lignin types examined were wood Kraft lignin, steam explosion lignin, bagasse lignin, and lignosulfonates. Thermal analyses were carried out over the 20900 degrees C temperature range, at a heating rate of 10 degrees C/min, under both inert (nitrogen) and oxidative (air/oxygen) atmosphere. Six different types of thermal analyzers (DSC and TG equipment) were tested. A lignin chemical reactivity test was also considered. Several laboratories identified similar lignin softening temperatures for some of the samples, yet, generally, the results attained are characterised by a high variability of the lignin types and analytical protocols applied in the six laboratories. The different results have been mainly attributed to the "history" of the material, e.g., whether the samples were completely dried before the experiments.
Relationship between Adipose PolyamineConcentrations and Triacylglycerol SyntheticEnzymes in Lean and Obese Zucker Rats (1996)

Previous studies from our laboratory demonstrate that polyamines, namely spermine and spermidine, stimulate adipose triacylglycerol formation from the sn-glycerol-3-phosphate pathway by activation of several enzymes from this pathway, including sn-glycerol-3-phosphate acyltransferase, Mg(2+)-dependent phosphatidate phosphohydrolase and diacylglycerol acyltransferase. Since obesity in Zucker rats was associated with increased accumulation of adipocyte triacylglycerols, we have examined the relationship between changes in the activities of various triacylglycerol synthetic enzymes and the endogenous concentrations of spermine and spermidine in the adipose tissues from lean and obese animals. As compared with lean rats, the adipocytes from obese rats showed a 4-fold rise in the concentration of spermine and spermidine which was accompanied by 4- to 14-fold increases in the activities of various triacylglycerol synthetic enzymes, including Mg(2+)-dependent phosphatidate phosphohydrolase. These studies suggest that obesity in Zucker rats is associated with the activation of various adipose triacylglycerol synthetic enzymes resulting from increased concentrations of endogenous spermine and spermidine.
The Lysine 831 of Vascular Endothelial Growth Factor Receptor 1 Is a Novel Target of Methylation by SMYD3 (2007)

We previously identified SMYD3 as a histone methyltransferase and showed that its expression was elevated in colorectal, hepatocellular, and breast carcinomas. In the investigation of methyltransferase activity of SMYD3, we have found that vascular endothelial growth factor receptor 1 (VEGFR1) was also methylated by SMYD3. We further identified the methylated residue at VEGFR1 lysine 831, which is located in the kinase domain and is conserved among VEGFR1 orthologues. We also found that the lysine is followed by serine, which is conserved among some of the methylation targets of histone methyltransferases. Furthermore, methylation of VEGFR1 enhanced its kinase activity in cells. These data should be helpful for the profound understanding of the biological role of SMYD3 and regulatory mechanisms of VEGFR1. Additionally our finding may facilitate the development of strategies that may inhibit the progression of cancer cells.
Transcriptional activation by herpes simplex virus type 1 VP16 in vitro and its inhibition by oligopeptides. (1994)

VP16 is a herpes simplex virus (HSV)-encoded transcriptional activator protein that is essential for efficient viral replication and as such may be a target for novel therapeutic agents directed against viral gene expression. We have reconstituted transcriptional activation by VP16 in an in vitro system that is dependent on DNA sequences from HSV immediate-early gene promoters and on protein-protein interactions between VP16 and Oct-1 that are required for VP16 activation in vivo. Activation increased synergistically with the number of TAATGARAT elements (the cis-acting element for VP16 activation in vivo) upstream of the core promoter, and mutations of this element that reduce Oct-1 or VP16 DNA binding reduced transactivation in vitro. A VP16 insertion mutant unable to interact with Oct-1 was inactive, but, surprisingly, a deletion mutant lacking the activation domain was approximately 65% as active as the full-length protein. The activation domains of Oct-1 were necessary for activation in reactions containing the VP16 deletion mutant, and they contributed significantly to activation by full-length VP16. Addition of a GA-rich element present in many HSV immediate-early gene enhancers synergistically stimulated VP16-activated transcription. Finally, oligopeptides that are derived from a region of VP16 thought to contact a cellular factor known as HCF (host cell factor) and that inhibit efficient VP16 binding to the TAATGARAT element also specifically inhibited VP16-activated, but not basal, transcription. Amino acid substitutions in one of these peptides identified three residues that are absolutely required for inhibition and presumably for interaction of VP16 with HCF.
Evolution of CRISPR RNA recognition and processing by Cas6 endonucleases (2013)

In many bacteria and archaea, small RNAs derived from clustered regularly interspaced short palindromic repeats (CRISPRs) associate with CRISPR-associated (Cas) proteins to target foreign DNA for destruction. In Type I and III CRISPR/Cas systems, the Cas6 family of endoribonucleases generates functional CRISPR-derived RNAs by site-specific cleavage of repeat sequences in precursor transcripts. CRISPR repeats differ widely in both sequence and structure, with varying propensity to form hairpin folds immediately preceding the cleavage site. To investigate the evolution of distinct mechanisms for the recognition of diverse CRISPR repeats by Cas6 enzymes, we determined crystal structures of two Thermus thermophilus Cas6 enzymes both alone and bound to substrate and product RNAs. These structures show how the scaffold common to all Cas6 endonucleases has evolved two binding sites with distinct modes of RNA recognition: one specific for a hairpin fold and the other for a single-stranded 5'-terminal segment preceding the hairpin. These findings explain how divergent Cas6 enzymes have emerged to mediate highly selective pre-CRISPR-derived RNA processing across diverse CRISPR systems.
3D-QSAR CoMFA and CoMSIA Study on Benzodipyrazoles as Cyclin Dependent Kinase 2 Inhibitors (2008)

Cyclin dependent kinase 2 (CDK2) has appeared as an important drug target over the years with a multitude of therapeutic potentials. With the intention of designing compounds with enhanced inhibitory potencies against CDK2, the 3D-QSAR CoMFA and CoMSIA study on benzodipyrazoles series is presented here. The developed models showed a strong correlative and predictive capability having a cross validated correlation co-efficient of (r(2)(cv)) 0.699 for CoMFA and 0.794 for CoMSIA models. A very good conventional and predicted correlation co-efficients were also obtained: CoMFA (r(2)(ncv), r(2)(pred): 0.883, 0.754), CoMSIA (0.937, 0.815). The models were found to be statistically robust and are expected to be of an aid to design and/or prioritize drug likes for synthesis.
Transmission of mitochondrial DNA following assisted reproduction and nuclear transfer (2006)

Mitochondria are the organelles responsible for producing the majority of a cell's ATP and also play an essential role in gamete maturation and embryo development. ATP production within the mitochondria is dependent on proteins encoded by both the nuclear and the mitochondrial genomes, therefore co-ordination between the two genomes is vital for cell survival. To assist with this co-ordination, cells normally contain only one type of mitochondrial DNA (mtDNA) termed homoplasmy. Occasionally, however, two or more types of mtDNA are present termed heteroplasmy. This can result from a combination of mutant and wild-type mtDNA molecules or from a combination of wild-type mtDNA variants. As heteroplasmy can result in mitochondrial disease, various mechanisms exist in the natural fertilization process to ensure the maternal-only transmission of mtDNA and the maintenance of homoplasmy in future generations. However, there is now an increasing use of invasive oocyte reconstruction protocols, which tend to bypass mechanisms for the maintenance of homoplasmy, potentially resulting in the transmission of either form of mtDNA heteroplasmy. Indeed, heteroplasmy caused by combinations of wild-type variants has been reported following cytoplasmic transfer (CT) in the human and following nuclear transfer (NT) in various animal species. Other techniques, such as germinal vesicle transfer and pronuclei transfer, have been proposed as methods of preventing transmission of mitochondrial diseases to future generations. However, resulting embryos and offspring may contain mtDNA heteroplasmy, which itself could result in mitochondrial disease. It is therefore essential that uniparental transmission of mtDNA is ensured before these techniques are used therapeutically.