gebhart/patrepeval huggingface dataset:
Behavior of antithrombin III isoforms on immobilized heparins. Evidence that the isoforms bind to different numbers of low-affinity heparin sites. (1988)

Antithrombin III exists in plasma as major and minor isoforms differing in affinity for heparin. The nature of the binding of each purified isoform to immobilized heparins was investigated. Unfractionated, mixed-affinity heparin bound each isoform with both high affinity and concentration-dependent low affinity. The isoforms were resolved when filtered through low-affinity heparin (heparin repeatedly passed over immobilized antithrombin III) columns. Following chemical modification of a specific tryptophan residue required for heparin binding, each isoform failed to bind to either low-affinity or mixed-affinity heparin-agarose, but elution of the modified higher-affinity isoform was retarded on both gels. Because the modified lower-affinity isoform eluted with the similarly sized bovine serum albumin in these experiments, the difference in isoform affinity for heparin appears to be the result of a unique, secondary heparin-binding site in the higher-affinity isoform that can bind a heparin site with low affinity for antithrombin III. This interpretation was supported by the chromatographic behavior of the isoforms on mixed-affinity agarose during reverse gradient elution. Two other populations of each of the tryptophan-modified isoforms were identified. Since these isoforms bound tightly to mixed-affinity heparin-agarose but eluted at lower salt concentrations than the corresponding unmodified isoforms, both isoforms may contain additional secondary sites that interact weakly with heparin. A general model of heparin-antithrombin III interaction is proposed in which a high-affinity heparin site initially interacts with a primary site on antithrombin III. The subsequent conformational change leads to a cooperative, entropy-driven association between secondary sites on the protein and low-affinity sites on heparin, stabilizing antithrombin III in its activated form.
Nitrogen catabolite repression of asparaginase II in Saccharomyces cerevisiae (1980)

The biosynthesis of asparaginase II in Saccharomyces cerevisiae is subject to strong catabolite repression by a variety of nitrogen compounds. In the present study, asparaginase II synthesis was examined in a wild-type yeast strain and in strains carrying gdhA, gdhCR, or gdhCS mutations. The following effects were observed: (i) In the wild-type strain, the biosynthesis of asparaginase II was strongly repressed when either 10 mM ammonium sulfate or various amino acids (10 mM) served as the source of nitrogen. (ii) In a yeast strain carrying the gdhA mutation, asparaginase II was synthesized at fully derepressed levels when 10 mM ammonium sulfate was the source of nitrogen. When amino acids (10 mM) served as the nitrogen source, asparaginase II synthesis was strongly repressed. (iii) In a strain carrying the gdhCR mutation, the synthesis of asparaginase II was partially (30 to 40%) derepressed when either 10 mM ammonium sulfate or amino acids were present in the medium. (iv) In a yeast strain containing both gdhA and gdhCR mutations, asparaginase II synthesis was fully derepressed when 10 mM ammonium sulfate was the nitrogen source and partially derepressed when 10 mM amino acids were present. (v) Yeast strains carrying the gdhCS mutation were indistinguishable from the wild-type strain with respect to asparaginase II synthesis.
Collagen-Induced Arthritis in Mice: Synergistic Effect of E. Coli Lipopolysaccharide Bypasses Epitope Specificity in the Induction of Arthritis with Monoclonal Antibodies to Type II Collagen (1995)

DBA/1 mice develop a chronic peripheral arthritis after immunization with type II collagen termed collagen-induced arthritis. We have localized the main arthritogenic determinants of CB11, a CNBr-generated arthritogenic fragment of chick type II collagen (CII), using 3 smaller peptide fragments of CB11 generated by endoproteinase LysC, LysC1 (CII 124-290), LysC2 (CII 291-374) and LysC3 (CII 375-402) and a panel of monoclonal antibodies (mAb) specific to CB11. MAb specific to the arthritogenic region of CB11 were also used to study the synergistic effect of E. coli lipopolysaccharide (LPS) on antibody-mediated arthritis in naive DBA/1 mice. LysC2 contained a minimum essential arthritogenic fragment of type II collagen: LysC2 induced arthritis by active immunization, also, a combination of four mAb specific to LysC2 passively transferred arthritis to naive mice. A single i.p. injection of LPS (50 micrograms/mouse) reduced the threshold values of the arthritogenic dose of mAb from 1 mg to 50 micrograms/clone per mouse, and decreased the number of mAb required for inducing arthritis from 4 to 2 clones. These observations suggest that LysC2, an 84 amino acid residue fragment, contains the main arthritogenic determinants within chick CB11. Importantly, LPS, a strong inducer of pro-inflammatory cytokines, negates the required multiple epitope specificity of autoantibodies in the passive transfer model and acts synergistically in the induction of arthritis by autoantibody.
Azimuthal anchoring transition of nematic liquid crystals on self-assembled monolayers formed from odd and even alkanethiols (1996)

A first order orientational transition, characterized by a 90\ifmmode^\circ\else\textdegree\fi{} azimuthal rotation of the surface easy direction, is reported for nematic liquid crystals (NLCs) anchored on self-assembled monolayers (SAMs). The SAMs are formed from alkanethiols [$\mathrm{C}{\mathrm{H}}_{3}{(\mathrm{C}{\mathrm{H}}_{2})}_{n\ensuremath{-}1}\mathrm{SH};5&lt;~n&lt;~16$] on obliquely deposited films of gold. The anchoring of the NLC is uniform and planar; the azimuthal orientation of the nematic director is, however, perpendicular to the direction of deposition of gold on SAMs formed from alkanethiols with odd chain lengths ($n=\mathrm{odd}$) and is parallel to the direction of deposition of gold on SAMs formed from alkanethiols with even ($n=\mathrm{even}$) chain lengths.
An Electric Artificial Heart for Clinical Use (1990)

Advances in microelectronics, high-strength magnets, and control system design now make replacement of the heart using an implantable, electrically powered pump feasible. The device described herein is a compact, dual pusher plate unit with valved polyurethane sac-type ventricles positioned at either end. The power unit consists of a small, brushless direct current motor and a motion translator. A microprocessor control system is used to regulate heart beat rate and provide left-right output balance. Bench studies lasting for as long as 1 year have been performed. Heart replacement with the electric heart has been performed in 18 calves since 1984. The longest survivor lived for more than 7 months. Among the causes of termination were component failure, thromboembolic complications, and bleeding. No major problem has been identified that precludes prolonged use of the electric heart. In the future the patient with end-stage heart disease will have an electric artificial heart as one therapeutic option.
10 Gbit/s repeaterless transmission over 258 km employing 24 ps RZ pulses (1996)

Summary form only given. A 10 Gbit/s RZ transmission system with large loss budget is described and the repeaterless transmission employing short pulses of 24-ps-wide over 258 km is also discussed. The configurations of a 10 Gbit/s RZ transmitter and a receiver are depicted. At the transmitter, a monolithically integrated MQW-DFB-LD/MQW-EA modulator produced 24-ps-wide transform-limited pulses at 10-GHz repetition rate. The signal power was boosted to + 22 dBm by a booster EDFA. No SBS-suppressing circuits were employed, because the SPM-induced spectral broadening could suppress the SBS effectively. At the receiver, a low-noise optical pre-amplifier was followed by a wide-band optical filter.
In-band spectrum sensing in cognitive radio networks (2008)

In a cognitive radio network (CRN), in-band spectrum sensing is essential for the protection of legacy spectrum users, with which the presence of primary users (PUs) can be detected promptly, allowing secondary users (SUs) to vacate the channels immediately. For in-band sensing, it is important to meet the detectability requirements, such as the maximum allowed latency of detection (e.g., 2 seconds in IEEE 802.22) and the probability of mis-detection and false-alarm. In this paper, we propose an effcient periodic in-band sensing algorithm that optimizes sensing-frequency and sensing-time by minimizing sensing overhead while meeting the detectability requirements. The proposed scheme determines the better of energy or feature detection that incurs less sensing overhead at each SNR level, and derives the threshold aRSSthreshold on the average received signal strength (RSS) of a primary signal below which feature detection is preferred. We showed that energy detection under lognormal shadowing could still perform well at the average SNR < SNRwall [1] when collaborative sensing is used for its location diversity. Two key factors affecting detection performance are also considered: noise uncertainty and inter-CRN interference. aRSSthreshold appears to lie between -114.6 dBm and -109.9 dBm with the noise uncertainty ranging from 0.5 dB to 2 dB, and between -112.9 dBm and -110.5 dBm with 1~6 interfering CRNs.
Chondroitin sulfate and hyaluronic acid (500-730 kda) inhibit stromelysin-1 synthesis in human osteoarthritic chondrocytes. (2005)

Chondroitin sulfate (CS) and 500-730 kDa hyaluronic acid (HA) are symptomatic slow-acting drugs for the treatment of osteoarthritis (OA). In addition, a growing body of evidence suggests a role for CS and this specific HA as modifiers of the course of OA. The therapeutic efficacy of CS and HA lies in their different mechanisms of action. Stromelysin-1 (metalloprotease-3 [MMP-3]) is a cartilage proteolytic enzyme, which induces cartilage destruction and acts as a mediator of the inflammatory response. However, there are few studies evaluating the in vitro effect of CS and HA on MMP-3 synthesis in human chondrocyte cultures from OA patients. Thus, the aim of the present study was to analyze the effect of CS and HA (500-730 kDa) on MMP-3 synthesis induced by interleukin-1beta (IL-1beta) in chondrocytes from patients with hip OA. Chondrocyte cultures were incubated for 48 h with IL-1beta (2.5 ng/ml) in the absence or presence of different HA 500-730 kDa (Hyalgan, Bioibérica Farma, Barcelona, Spain) concentrations, or alternatively, CS (Condro.san, Bioibérica Farma) at concentrations of 10, 50, 100, 150, 200 and 1,000 microg/ml. The results revealed that both CS and HA (500-730 kDa) inhibited MMP-3 synthesis induced by IL-1beta in human OA chondrocytes. Specifically, CS and HA (500-730 kDa) reduced MMP-3 expression levels at all tested concentrations. Therefore, our study provides new data on the mechanism of action of these drugs, which could help to explain their clinical efficacy in OA patients.
Identification of Epitopes and Immunodominant Regions on the MICA Protein Defined by Alloantibodies From Kidney Transplant Patients (2009)

The presence of anti-MICA Abs could be an important marker for diagnosis because of their contribution to the outcome of the graft, regardless of presence of anti-HLA Abs. Additionally, the identification of epitopes revealed the in vivo antigens of the transplant and is spurring the development of new matching strategies to reduce the incidence of acute and chronic rejection.
Modification by adenosine of the effect of adriamycin on myocardial cells in culture. (1979)

The cardiotoxic effects of Adriamycin (ADM) were studied utilizing mammalian myocardial cells in culture as a model system. ADM inhibited cell growth and the rhythmic contractions characteristic of these cells. Because a possible involvement of energy metabolism in the action of ADM was suggested previously, the adenylate energy charge and phosphorylcreatine mol fraction were determined in the ADM-treated cells. The adenylate energy charge was found to be significantly decreased, while the phosphorylcreatine mol fraction was not. Such disparity suggests an inhibition of creatine phosphokinase. The addition of 1 mM adenosine to the myocardial cell cultures markedly increased the adenosine triphosphate concentration but not the adenylate charge. In the ADM-treated cells, the addition of adenosine increased both the adenosine triphosphate concentration and the adenylate charge, and, concomitant with this increase, the functional integrity of the cells in terms of percentage of beating cells and rate of contractions was maintained.
Palladium(II) Complexes of a Sterically Bulky, Benzannulated N-Heterocyclic Carbene with Unusual Intramolecular C−H···Pd and Ccarbene···Br Interactions and Their Catalytic Activities (2006)

The sterically bulky carbene precursor 1,3-diisopropylbenzimidazolium bromide (iPr2-bimyH+Br-) (A) has been prepared by an improved method in 84% yield. Reaction of A with Pd(OAc)2 and NaBr gave the dimeric Pd(II) benzimidazolin-2-ylidene complex [PdBr2(iPr2-bimy)]2 (1), which can be easily cleaved by CH3CN, another equivalent of salt A, and triphenylphosphine to afford the novel benzannulated monocarbene complexes trans-[PdBr2(CH3CN)(iPr2-bimy)] (2), (iPr2-bimyH)[PdBr3(iPr2-bimy)] (3), trans-[PdBr2(iPr2-bimy)(Ph3P)] (trans-4), and cis-[PdBr2(iPr2-bimy)(Ph3P)] (cis-4), respectively. All compounds have been fully characterized by multinuclei NMR spectroscopies and mass spectrometries (FAB, ESI). X-ray diffraction studies on single crystals of 1−3 and cis-4 revealed a square planar geometry and a fixed orientation of the N-isopropyl substituents with the C−H group pointing to the metal center to maximize C−H···Pd interactions. The large downfield shift of the C−H protons in the 1H NMR spectrum compared to the precursor A indicates that these C−H···Pd interactions are retained in solution and better described as weak hydrogen bonds, rather than as agostic interactions. Furthermore, the molecular structures of especially complexes 2 and 3 clearly show a bending of the bromo ligands toward the carbene carbon atom in order to maximize intramolecular Ccarbene···Br interactions. The nature of these interactions can be attributed to a form of back-bonding to the formally vacant p-orbital of the Ccarbene atom with the electron density originating from the bromo ligands' lone pairs. A detailed study on the trans−cis isomerization of the mixed NHC−phosphine complexes 4 revealed that a cis arrangement in such complexes is thermodynamically favored. Furthermore, a preliminary catalytic study shows that complex 1 is highly active in the Suzuki−Miyaura coupling of aryl bromides and chlorides in pure water as environmentally benign solvent.
Bean Ribonuclease‐Like Pathogenesis‐Related Protein Genes (Ypr10) Display Complex Patterns of Developmental, Dark‐Induced and Exogenous‐Stimulus‐Dependent Expression (1996)

The intracellular pathogenesis-related (PR) proteins of common bean (Phaseolus vulgaris L.) are encoded by a highly polymorphic family of at least 20 genes. One member, the Ypr10*c gene, has been isolated and characterised. The deduced amino acid sequence of the encoded protein, PR-10, exhibits similarities to tree-pollen allergens, to food allergens from celery and apple and to ginseng ribonuclease peptide sequences. We show by RNA blot analysis that the Ypr10 gene family, including Ypr10*c, is strongly expressed in bean roots. In leaves Ypr10 transcript levels are low in young and mature stages but are elevated during senescence and in diseased states. Dark treatment of leaves causes strong induction of Ypr10 transcripts, which is reversible by light, and diurnal rhythms of transcript accumulation during the night are observed. Ypr10 genes are responsive to external stimuli related to pathogen-defence such as glutathione or salicylic acid. Transcriptional activity of a Ypr10*c promoter-beta-glucuronidase fusion gene in transgenic tobacco was observed in roots, in developing xylem and phloem of stems, and in the blade of senescent leaves, with highest levels at the onset of senescence. The most striking characteristic of developmental expression was the specific localisation of beta-glucuronidase activity in the transmitting tract of styles in flowers at anthesis. Feeding of various pathogen-related and stress-related stimuli to young tobacco leaves led to accumulation of GUS activity in leaf blades. We identify considerable spatio-temporal similarities between reported expression patterns of Ypr10 genes and ribonuclease genes, which, together with the significant sequence similarity to the ginseng ribonuclease, support the hypothesis of a ribonuclease function for PR-10 proteins and allow the prediction of possible biological roles.
Inhibition of rat mammary gland chemical carcinogenesis by dietary dehydroepiandrosterone or a fluorinated analogue of dehydroepiandrosterone. (1991)

The chemopreventive efficacy of p.o. administered dehydroepiandrosterone (DHEA), DHEA plus N-(4-hydroxyphenyl)retinamide (4-HPR), or 16 alpha-fluoro-5-androsten-17-one (DHEA analogue 8354) was examined in rats treated with N-methyl-N-nitrosourea (MNU; 50 mg/kg body weight, i.v.) at 50 days of age. Semipurified diet (AIN-76A) containing each steroid alone, or DHEA plus 4-HPR, was administered during initiation (-1 week to +1 week post-MNU), promotion/progression (+1 week post-MNU to termination), or both phases (-1 week post-MNU to termination) of the carcinogenic process. Neither DHEA nor DHEA analogue 8354 (0.2%, w/w) significantly affected the initiation of mammary cancer when administered alone; however, DHEA (0.2%, w/w) plus 4-HPR (1 mmol/kg diet) significantly reduced cancer multiplicity (26%) when given during initiation. All three treatments were strongly effective when given during promotion/progression, significantly reducing mammary cancer multiplicity by 77% (DHEA), 84% (DHEA/4-HPR), and 66% (DHEA analogue 8354), relative to carcinogen controls. Cancer incidence was significantly inhibited by DHEA (33% inhibition) and DHEA/4-HPR (24% reduction) during promotion/progression. However, the most effective chemopreventive treatment encompassed both phases of carcinogenesis. Thus, under these conditions, DHEA (0.2% or 0.1%, w/w) reduced cancer incidence (52% and 32% reductions, respectively) and multiplicity (91% and 86% reductions, respectively). Further reduction in mammary cancer incidence was observed in animals that received DHEA (both doses) plus 4-HPR (1 and 0.5 mmol/kg diet, respectively). DHEA analogue 8354 (0.2% or 0.1%, w/w) given for the duration of the study reduced only cancer multiplicity (61% and 56% reductions, respectively). Tumor-related mortality was significantly lower in rats that received long-term treatment with DHEA or DHEA/4-HPR, when compared with carcinogen controls. Except for a slight, but significant, postcarcinogen decrease in the mean body weights of rats treated concomitantly with DHEA (plus or minus 4-HPR) and MNU, additional gross manifestations of steroid-induced toxicity were not observed.
PP.14.18 (2015)

Objective: To elucidate whether tetrahydrobiopterin(BH4)could induce improve left ventricular diastolic function through phosphoinositide-3 kinase/phosphorylated protein kinase B (PI3K/p-Akt)signaling pathway in hypertensive mice. Design and method: Ninety male C57BL/6 mice were randomly divided into two groups:sham-operation group(n = 40);deoxycorticosterone acetate(DOCA)-salt group(n = 50).After two weeks,sham-operation group was divided into:SHAM group(n = 20)and BH4 group(n = 20);DOCA-salt group was divided into DOCA group(n = 22)and DOCA+BH4 group(n = 22).The blood pressure measurements were performed three weeks later.Cardiac function were assessed by echocardiography and hemodynamic parameters.The myocardial cyclic guanosinc monophosphate (cGMP), malondialdehyde(MDA),superoxide dism-utase(SOD) and nitric oxide(NO) were detected by ELISA.The levels of BH4 and dihydrobiopterin (BH2)were tested by high-performance liquid chromatography(HPLC).PI3K,Akt and p-Akt protein expression were determined by Western blot. Results: Three weeks after coarctation,comparing with the SHAM group,systolic blood pressure (SBP)and diastolic blood pressure(DBP)were significantly increased in DOCA-salt hypertension group(all P < 0.001).The parameters of left ventricular diastolic function were significantly decreased.The levels of BH4 and BH2 were reduced(all P < 0.001).cGMP,SOD and NO were declined significantly,MDA was augmented markedly.In addition,the PI3K and Akt(Ser473)protein phosphorylation in DOCA group were significantly down-regulated.Treatment with BH4 effectively decreased SBP,improved left ventricular diastolic function,augmented SOD,PI3K and p-Akt(Ser473) in DOCA group. Conclusions: These results suggested that BH4 could improve left ventricular diastolic function in hypertensive mice possibly through PI3K/p-Akt signaling pathway.
In vivo antitumor activity of anti-CD3-induced activated killer cells. (1989)

This study investigates the potential of the alpha CD3-induced killer cells for use in adoptive immunotherapy of tumor growth. The alpha CD3-induced, activated, killer cells (CD3-AK) were generated in DBA/2 (H-2d) splenocytes by preactivation with alpha CD3 and were then cultured in the presence (CD3-AK [alpha CD3+]) or absence (CD3-AK [alpha CD3-]) of alpha CD3. The conventional lymphokine-activated killer (LAK) cells were induced by culturing DBA/2 splenocytes with purified human recombinant interleukin 2. Testing their in vitro cytotoxicity against syngeneic mastocytoma P815, CD3-AK (alpha CD3+) cells gave the highest levels of cytotoxicity and were 20-fold higher than LAK cells and 200-fold higher than CD3-AK (alpha CD3-) cells. However, the cytotoxic activity of LAK or CD3-AK (alpha CD3-) cells was augmented by preincubating them with alpha CD3 for 3 h; then, the difference in cytotoxic activity was reduced from 20- to 4-fold and from 200- to 2-fold, respectively. The in vivo antitumor activity of these killer cells paralleled the in vitro activity. In tests using tumor neutralization experiments, 80-100% of the mice that were challenged with 1 x 10(2) P815 cells remained tumor free after receiving 5 x 10(6) CD3-AK (alpha CD3+) cells. When the challenge dose increased to 1 x 10(3) and to 1 x 10(4) cells, giving CD3-AK (alpha CD3+) cells slowed down the rate of tumor growth but only 20% of the mice remained tumor free. The untreated LAK cells or CD3-AK (alpha CD3-) cells did not induce any protection. After preincubation with alpha CD3 for 3 h, the CD3-AK (alpha CD3-) cells provided protection in 30% of the challenged mice. The phenotype of effectors for mediating the in vitro and in vivo antitumor activities was found to be Thy1+, CD4-, and CD8+ cells. Flow microfluorometry analysis showed that the higher levels of cytotoxic activity obtained with CD3-AK (alpha CD3+) cells could not be simply explained by the increase of CD8+ cells, and the cytotoxic activity of individual CD3-AK (alpha CD3+) cells appeared to be much higher than that of the LAK cells. After tumor growth was established for 1-2 days, giving CD3-AK (alpha CD3+) cells slowed down the rate of tumor growth, and 20% of the mice remained tumor free. These results indicate that CD3-AK cells may be used in the immunotherapy of tumor growth.(ABSTRACT TRUNCATED AT 400 WORDS)
A Convenient Synthesis of L-(S)-Glyceraldehyde Acetonide from L-Ascorbic Acid (1986)

L-S)-glyceraldehyde acetonide is easily obtained from L-ascorbic acid by three-step procedure. Since the aldehyde is rather unstable in pure form it is more convenient to use it as an aqueous solution. It was used to synthesize L-(R)-glycerol acetonide, monocyclic-ß-lactams, and olefins (by Wittig reaction).