gebhart/patrepeval huggingface dataset:
Low-Temperature Coupling of Methane (1996)

Introduction Methane is the main component of natural gas and its utilization amounts to ca. 1.7 × 109 tons of oil equivalent per year [1]. Since the present reserve of methane is located in remote places, its transportation is a major problem. Methane coupling to form C2+ hydrocarbons is, therefore, of a primary importance because before transportation methane should be converted into hydrocarbons with higher boiling points, such as ethane, propane, etc. The catalytic conversion of methane can be carried out in several ways which have excellently been reviewed in Refs. 1 and 2. Basically, three routes exist: (i) the indirect route in which methane is first converted into syngas in presence of water (steam reforming), CO2 (carbon dioxide reforming), or oxygen (partial oxidation) and the resultant syngas can be utilized in the traditional way; (ii) direct coupling in the presence of oxygen (oxidative coupling of methane, OCM) or hydrogen (two-step polymerization); and (iii) direct conversion in the presence of oxygen to oxygenates (CH3OH, HCOH), in the presence of Cl2, HCI to methane chlorides, in the presence of ammonia to HCN, etc.
Formation of HeH+ from Low-Energy Collisions of Metastable Helium and Molecular Hydrogen (1972)

A merging-beams technique has been used to study HeH+ formation resulting from the interaction of a composite beam of He(21S) and He (23S) with a beam of H2. The experiments were conducted over a range of interaction energy W from 0.05 to 10 eV. It was learned that the dominant process for producing HeH+ is the rearrangement ionization reaction He*+H2→HeH++H+e, where He* represents the metastable helium. The experiment consisted of measuring the lab-energy distributions of HeH+. Relative and absolute cross sections were obtained from these distributions. The distributions indicate that, in the center-of-mass system, most of the HeH+ is scattered in the direction of the incident He*. The energies associated with the HeH+ at the peaks of these distributions are very close to those expected for spectator stripping. Conservation of energy for the reaction can only be achieved by assuming that the electron carries away a substantial portion of the available energy. It is shown that the two-step model He*+H2→He+H2+†+e→HeH++H+e (where † indicates ground-state or vibrationally excited H2+) satisfactorily explains the measured lab-energy distributions near W=0.05 eV but does not agree completely with the results for W≥ 2 eV.
Chemical and Sensory Effects of Microorganisms on Grape Musts And Wine (1966)

Techniques were developed for the infection and decay of grapes by monofungus cultures. Blends of up to 40% juice from decayed Thompson Seedless grapes and the balance from uninfected fruit were fermented by standard enological procedures. <i>Botrytis cinerea, Rhizopus arrhizus, Aspergillus niger</i> and <i>A. flavus</i> had little or no effect on the volatile acidity of either the musts or wines. However, volatile acidity of musts and wines was raised when grapes were decayed by combinations of <i>Acetobacter roseus</i> and <i>Saccharomyces cereviseae</i> with <i>A. niger, R. arrhizus</i> or <i>B. cinerea</i>; but very little by combinations which included <i>A. flavus</i>. The fixed total acid of the musts and wines was raised only by <i>A. niger</i>, which also lowered the pH of the wines. Wines which did not ferment to dryness were those with appreciable volatile acidity. There were no marked differences in the amount of residual reducing sugar. There was an inverse relation between alcohol and the volatile acid content of the wines. As determined by the Folin-Denis method, wines from grapes decayed by <i>A. flavus</i> were much higher in tannin-like materials than wines from unaffected grapes or from grapes decayed by the other three fungi. These wines had an unusual yellow-pink color.
Synthesis and Properties of a Water‐Soluble Single‐Walled Carbon Nanotube–Poly(m‐aminobenzene sulfonic acid) Graft Copolymer (2004)

Abstract Poly( m ‐aminobenzene sulfonic acid) (PABS), was covalently bonded to single‐walled carbon nanotubes (SWNTs) to form a water‐soluble nanotube–polymer compound (SWNT–PABS). The conductivity of the SWNT–PABS graft copolymer was about 5.6 × 10 –3 S cm –1 , which is much higher than that of neat PABS (5.4 × 10 –7 S cm –1 ). The mid‐IR spectrum confirmed the formation of an amide bond between the SWNTs and PABS. The 1 H NMR spectrum of SWNT–PABS showed the absence of free PABS, while the UV/VIS/NIR spectrum of SWNT–PABS showed the presence of the interband transitions of the semiconducting SWNTs and an absorption at 17 750 cm –1 due to the PABS addend.
Mechanisms of impaired mitochondrial energy metabolism in acute and chronic neurodegenerative disorders (2007)

Altered mitochondrial energy metabolism contributes to the pathophysiology of acute brain injury caused by ischemia, trauma, and neurotoxins and by chronic neurodegenerative disorders such as Parkinson's and Huntington's diseases. Although much evidence supports that the electron transport chain dysfunction in these metabolic abnormalities has both genetic and intracellular environmental causes, alternative mechanisms are being explored. These include direct, reversible inhibition of cytochrome oxidase by nitric oxide, release of mitochondrial cytochrome c, oxidative inhibition of mitochondrial matrix dehydrogenases and adenine nucleotide transport, the availability of NAD for dehydrogenase reactions, respiratory uncoupling by activities such as that of the permeability transition pore, and altered mitochondrial structure and intracellular trafficking. This review focuses on the catabolism of neuronal NAD and the release of neuronal mitochondrial NAD as important contributors to metabolic dysfunction. In addition, the relationship between apoptotic signaling cascades and disruption of mitochondrial energy metabolism is considered in light of the fine balance between apoptotic and necrotic neural cell death.
Selective Hydrolysis of Phosphate Esters, Nitrophenyl Phosphates and UpU, by Dimeric Zinc Complexes Depends on the Spacer Length (1995)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTSelective Hydrolysis of Phosphate Esters, Nitrophenyl Phosphates and UpU, by Dimeric Zinc Complexes Depends on the Spacer LengthWilliam H. Chapman Jr. and Ronald BreslowCite this: J. Am. Chem. Soc. 1995, 117, 20, 5462–5469Publication Date (Print):May 1, 1995Publication History Published online1 May 2002Published inissue 1 May 1995https://pubs.acs.org/doi/10.1021/ja00125a005https://doi.org/10.1021/ja00125a005research-articleACS PublicationsRequest reuse permissionsArticle Views1237Altmetric-Citations214LEARN 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
Functional Genomic Analysis of Type II IL-1β Decoy Receptor: Potential for Gene Therapy in Human Arthritis and Inflammation (2002)

Gene expression arrays show that human epithelial cells and human arthritis-affected cartilage lack detectable amounts of mRNA for IL-1 antagonizing molecules: IL-1Ra and IL-1RII, but constitutively express IL-1. Functional genomic analysis was performed by reconstituting human IL-1RII expression in various IL-1RII-deficient cell types to examine its antagonist role using gene therapy approaches. Adenovirus-expressing IL-1RII when transduced into human and bovine chondrocytes, human and rabbit synovial cells, human epithelial cells, and rodent fibroblasts expressed membrane IL-1RII and spontaneously released functional soluble IL-1RII. The IL-1RII(+) (but not IL-1RII(-)) cells were resistant to IL-1beta-induced, NO, PGE(2), IL-6, and IL-8 production or decreased proteoglycan synthesis. IL-1RII inhibited the function of IL-1 in chondrocytes and IL-1- and TNF-alpha-induced inflammatory mediators in human synovial and epithelial cells. IL-1RII(+) chondrocytes were more resistant to induction of NO and PGE(2) by IL-1beta compared with IL-1RII(-) cells incubated with a 10-fold (weight) excess of soluble type II IL-1R (sIL-1RII) protein. In cocultures, IL-1RII(+) synovial cells released sIL-1RII, which in a paracrine fashion protected chondrocytes from the effects of IL-1beta. Furthermore, IL-1RII(+) (but not IL-1RII(-)) chondrocytes when transplanted onto human osteoarthritis-affected cartilage in vitro, which showed spontaneous release of sIL-1RII for 20 days, inhibited the spontaneous production of NO and PGE(2) in cartilage in ex vivo. In summary, reconstitution of IL-1RII in IL-1RII(-) cells using gene therapy approaches significantly protects cells against the autocrine and paracrine effects of IL-1 at the signaling and transcriptional levels.
Confining Light to Deep Subwavelength Dimensions to Enable Optical Nanopatterning (2009)

In the past, the formation of microscale patterns in the far field by light has been diffractively limited in resolution to roughly half the wavelength of the radiation used. Here, we demonstrate lines with an average width of 36 nanometers (nm), about one-tenth the illuminating wavelength lambda1 = 325 nm, made by applying a film of thermally stable photochromic molecules above the photoresist. Simultaneous irradiation of a second wavelength, lambda2 = 633 nm, renders the film opaque to the writing beam except at nodal sites, which let through a spatially constrained segment of incident lambda1 light, allowing subdiffractional patterning. The same experiment also demonstrates a patterning of periodic lines whose widths are about one-tenth their period, which is far smaller than what has been thought to be lithographically possible.
Reaction Mechanism in Aromatic Heterocyclic Compound. I. The Reactions of N-Alkoxypyridinium Derivarives (1959)

N-Alkoxypyridinium derivatives were reacted with potassium cyanide and 2- and 4-cyanopyridines were obtained as the reaction product. This reaction was proved to be a universal reaction for quaternary salts of N-oxides of pyridine and substituted pyridines including quinoline and isoquinoline. A mechanism for this reaction was proposed.
Dual Roles for Coactivator Activator and its Counterbalancing Isoform Coactivator Modulator in Human Kidney Cell Tumorigenesis (2008)

Coactivator activator (CoAA) has been reported to be a coactivator that regulates steroid receptor-mediated transcription and alternative RNA splicing. Herein, we show that CoAA is a dual-function coregulator that inhibits G(1)-S transition in human kidney cells and suppresses anchorage-independent growth and xenograft tumor formation. Suppression occurs in part by down-regulating c-myc and its downstream effectors ccnd1 and skp2 and causing accumulation of p27/Kip1 protein. In this cellular setting, CoAA directly represses the proto-oncogene c-myc by recruiting HDAC3 protein and decreasing both the acetylation of histone H3 and the presence of RNA polymerase II on the c-myc promoter. Interestingly, a splicing isoform of CoAA, coactivator modulator (CoAM), antagonizes CoAA-induced G(1)-S transition and growth inhibition by negatively regulating the mRNA levels of the endogenous CoAA isoform. In addition, we found that expression of CoAA protein is significantly decreased in human renal cell carcinoma compared with normal kidney. Our study presents evidence that CoAA is a potential tumor suppressor in renal carcinoma and that CoAM is a counterbalancing splice isoform. This is, thus far, the only example of a nuclear receptor coregulator involved in suppression of kidney cancer and suggests potentially significant new roles for coregulators in renal cancer biology.
Anchoring and scaffold proteins for kinases and phosphatases. (1997)

Many hormones mediate their intracellular actions by triggering signal transduction pathways that alter the phosphorylation state of key regulatory proteins. Protein phosphorylation is a reversible process involving two classes of signaling enzymes: protein kinases, which catalyze the transfer of phosphate from ATP onto substrate proteins, and phosphoprotein phosphatases, which perform the dephosphorylation step. To insure tight control of hormonally initiated phosphorylation events, the activity of multifunctional kinases and phosphatases is precisely regulated and responds to fluctuations in diffusible second messengers such as Ca2+, phospholipid, and cAMP. Another mechanism that contributes to their regulation is to restrict the location of these enzymes to certain subcellular compartments. Subcellular targeting enhances the selectivity of serine/threonine phosphatases and kinases by favoring their accessibility to certain substrate proteins. Compartmentalization is achieved through a "targeting moiety," which is defined as that part of a phosphatase or kinase that directs the catalytic subunit to a certain subcellular environment. The targeting moiety restricts the location of a phosphatase or kinase through association with a "targeting locus." These are often structural membrane proteins, cytoskeletal components, or cellular organelles. Targeting subunits for the type I phosphatase and protein kinase C have been identified; however, the focus of this chapter centers around a family of anchoring proteins, called AKAPs, that localize the type II cAMP-dependent protein kinase (PKA). Structure-function analysis suggest that each anchoring protein binds to the RII dimer through a conserved amphipathic helix region and is tethered to specific subcellular sites via association of a targeting domain with structural proteins or cellular organelles. Peptides patterned after the amphipathic region have been used to probe the functional significance of PKA anchoring inside cells and have begun to be established by that disruption RII/AKAP interaction in vivo has concomitant effects on certain PKA-mediated phosphorylation events. In addition, multivalent binding proteins such as AKAP79 and AKAP250 have been characterized and appear to serve as platforms for the assembly of kinase/phosphatase signaling complexes. Collectively, these studies suggest that the AKAPs represent a growing family of regulatory proteins that provide a molecular architecture that organizes the intracellular location of a single or multiple multifunctional kinase.
DETERGENT SOLUBILISATION OF BABOON HISTOCOMPATIBILITY ANTIGENS AND THEIR USE IN PROLONGING LIVER ALLOGRAFT SURVIVAL (1975)

Histocompatibility antigens have been solubilised from baboon spleen cell membranes by brief exposure to sodium deoxycholate (DOC). Preparations contained a high molecular weight species (DOCH-Ag) excluded by Sephadex G-200, and a low molecular weight species (DOCL-Ag) which eluted in the included fraction (molecular weight 46,000). The low molecular weight antigen was stable and was not sedimented by high speed centrifugation even after dialysis against a low molar salt solution. It elicited a delayed-type hypersensitivity response in sensitised baboons but not in normal animals. DOCL-Ag cultured in vitro with sensitised allogeneic lymphocytes produced a 1.3- to 24.9-fold stimulation, whereas when cultured with normal lymphocytes the maximum stimulation index was 2. Intravenous administration of donor DOCL-Ag (2 mg/kg) at the time of transplantation and without additional immunosuppression significantly prolonged the mean survival time of baboon liver allografts. The same treatment with donor DOCH-Ag did not prolong graft survival.
Human squamous cell carcinoma lines express oncofetal 44-kd polypeptide defined by monoclonal antibody to mouse fetus (1988)

Most primary human carcinomas uniformly express an oncofetal epitope which has not been demonstrated previously in established human carcinoma cell lines. We successfully derived several low-passage cell lines of human squamous cell carcinoma (SCC) from head and neck tumors using an in vitro adaptation procedure, characterized these lines, and examined them for expression of a 44-kilodalton (kD) polypeptide (PP) oncofetal antigen (OFA) at the cell surface. Newly established an in vitro-passaged SCC cells retained characteristic microvilli, numerous desmosomes and tonofilaments, abundant rough endoplasmic reticulum, osmophilic keratohyaline granules, and other features of the primary SCC cells. These new cell lines and two long-term, established SCC lines (FaDu and Detroit 562) displayed OFA at the cell surface, as determined by flow cytometry using monoclonal antibody (MoAb) 115. While the FaDu and Detroit 562 lines exhibited aneuploidy during flow cytometric analysis, the new, low-passage SCC lines that we developed remained diploid as were the primary SCC cells from which they were derived. We propose that the expression of a 44-kD OFA is a common feature of human SCC. This marker may prove useful in the detection and treatment of these tumors.
Slit2 inhibits glioma cell invasion in the brain by suppression of Cdc42 activity (2009)

Acquisition of insidious invasiveness by malignant glioma cells involves multiple genetic alterations in signaling pathways. Slit2, a chemorepulsive factor, controls cell migration of neuronal and glial cells during development and inhibits chemotaxic migration of various types of cells in vitro. However, the role of Slit2 in vitro remains controversial, and the biological significance of Slit2 expression in cancer cell invasion in vivo has not yet been determined. In the present study, we characterized the effects of Slit2 expression on the migration and invasion of invasive glioma cells in vitro and in vivo. By reverse transcriptase polymerase chain reaction (PCR) analyses, Slit2 was found to be expressed at lower levels in primary glioma specimens and invasive glioma cells compared with normal human brain cells and astrocytes. Ectopic expression of Slit2 or treatment with recombinant Slit2 on glioma cells attenuates cell migration and invasion through inhibition of Cdc42 activity in vitro. Cellular depletion of Robo1, a cognate receptor for Slit2, prevented Slit2 inhibition of Cdc42 activity and glioma cell migration. In vivo, expression of Slit2 by invasive SNB19 glioma cells markedly inhibited glioma cell infiltration into the brain of mice. Moreover, impediment of glioma cell invasion by Slit2 did not affect the expression of N-cadherin and beta-catenin in glioma cells. These results provide the first evidence demonstrating that Slit2-Robo1 inhibits glioma invasion through attenuating Cdc42 activity in vitro and in the brain. Understanding the mechanisms of Slit2-Robo1 inhibition of glioma cell invasion will foster new treatments for malignant gliomas.
A Family of Putative Chloride Channels from Arabidopsis and Functional Complementation of a Yeast Strain with a CLC Gene Disruption (1996)

We have cloned four novel members of the CLC family of chloride channels from Arabidopsis thaliana. The four plant genes are homologous to a recently isolated chloride channel gene from tobacco (CLC-Nt1; Lurin, C., Geelen, D., Barbier-Brygoo, H., Guern, J., and Maurel, C. (1996) Plant Cell 8, 701-711) and are about 30% identical in sequence to the most closely related CLC-6 and CLC-7 putative chloride channels from mammalia. AtCLC transcripts are broadly expressed in the plant. Similarly, antibodies against the AtCLC-d protein detected the protein in all tissues, but predominantly in the silique. AtCLC-a and AtCLC-b are highly homologous to each other ( approximately 87% identity), while being approximately 50% identical to either AtCLC-c or AtCLC-d. None of the four cDNAs elicited chloride currents when expressed in Xenopus oocytes, either singly or in combination. Among these genes, only AtCLC-d could functionally substitute for the single yeast CLC protein, restoring iron-limited growth of a strain disrupted for this gene. Introduction of disease causing mutations, identified in human CLC genes, abolished this capacity. Consistent with a similar function of both proteins, the green fluorescent protein-tagged AtCLC-d protein showed the identical localization pattern as the yeast ScCLC protein. This suggests that in Arabidopsis AtCLC-d functions as an intracellular chloride channel.
Filamentous coliphage M13 as a cloning vehicle: insertion of a HindII fragment of the lac regulatory region in M13 replicative form in vitro. (1977)

A HindII restriction fragment comprising the Escherichia coli lac regulatory region and the genetic information for the alpha peptide of beta-galactosidase (beta-D-galactosidegalactohydrolase, EC. 3.2.1.23) has been inserted into 1 of the 10 Bsu I cleavage sites of M13 by blunt end ligation. A stable hybrid phage was isolated and identified by its ability to complement the lac alpha function. Further characterization of the hybrid phage includes retransformation studies, agarose gel electrophoresis, DNA-DNA hybridization, and heteroduplex mapping. The insertion point has been localized at 0.083 map unit on thewild-type circular map-i.e., within the intergenic region. The results prove that part of the intergenic region is nonessential and that the phage can be used as a cloning vehicle.
On joint transmitter and receiver optimization for multiple-input-multiple-output (MIMO) transmission systems (1994)

The problem of joint transmitter and receiver optimization for MIMO systems under the mean-squared error (MSE) criterion is revisited. We address the general problem of N (number of users) /spl ne/M (number of channel inputs) /spl ne/P (number of channel outputs) when the system is Nyquist bandlimited and obtain analytical solutions for the optimal transmit-receive pair. Next, we demonstrate how the above result is directly applicable to the problem where the system has excess bandwidth, thereby generalizing the results of Salz (1985). In conclusion, several numerical examples are included to demonstrate the performance gains obtainable with jointly optimized MIMO systems vis-a-vis systems based only on receiver optimization.< <ETX xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">&gt;</ETX>