gebhart/patrepeval huggingface dataset:
Routing of multipoint connections (1988)

The author addresses the problem of routing connections in a large-scale packet-switched network supporting multipoint communications. He gives a formal definition of several versions of the multipoint problem, including both static and dynamic versions. He looks at the Steiner tree problem as an example of the static problem and considers the experimental performance of two approximation algorithms for this problem. A weighted greedy algorithm is considered for a version of the dynamic problem which allows endpoints to come and go during the life of a connection. One of the static algorithms serves as a reference to measure the performance of the proposed weighted greedy algorithm in a series of experiments.< <ETX xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">&gt;</ETX>
Molecular cloning and sequence analysis of cDNA encoding human cholesterol 7α‐hydroxylase (1990)

A complete cDNA clone encoding human cholesterol 7 alpha-hydroxylase has been isolated using a rat P-450ch7 alpha cDNA insert [(1989) FEBS Lett. 257, 97-100] as a probe and totally sequenced. The cDNA contained 1512-base pair open reading frame encoding 504 amino acid residues (Mr 57,630), 39-base pair 5'-untranslated region 1322-base pair 3'-ultranslated region including 20 nucleotides of poly A tail in the total length of 2873 base pairs. The deduced amino acid sequence showed 82% similarity to rat P-450ch7 alpha. Unique amino acid residues were observed in putative binding domains for heme and steroid which are highly conserved in most steroidogenic P-450s.
Subgenomic RNAs of Lelystad virus contain a conserved leader-body junction sequence (1993)

During the replication of Lelystad virus in alveolar lung macrophages, a 3'-coterminal nested set of six subgenomic RNAs (RNA2 to RNA7) is formed. These contain a common leader sequence derived from the 5' non-coding region of the genomic RNA. In this study, the sequence of the junction sites, i.e. the sites where the leader sequence joins to the body of the subgenomic RNA, was determined for all six subgenomic RNAs. For each subgenomic RNA, six to nine cDNA clones were isolated by means of reverse transcription and PCR. The nucleotide sequence at the junction site was identical for all eight cDNA clones derived from subgenomic RNA4. However, heterogeneity was observed in the nucleotide sequence surrounding the junction sites of the cDNA clones derived from subgenomic RNAs 2, 3, 5, 6 and 7. This heterogeneity suggests that the fusion of the leader to the body of the subgenomic RNA may be imprecise. The junction sites of the six subgenomic RNAs had a conserved sequence motif of six nucleotides (UCAACC or a highly similar sequence). The distance between the junction site and the translation initiation codon of the downstream open reading frame varied from nine to 83 nucleotides.
Silicon-on-Insulator Wafer Bonding-Wafer Thinning Technological Evaluations (1989)

The realization of wafer-scale Silicon-on-Insulator by Van der Waals wafer bonding and subsequent thinning of one of the wafers is described for 100 mm wafers. The bonding of two silicon wafers is brought about by Van der Waals forces which are found to be sufficiently strong for a tight bond at wafer distances of less than 1 nm. This condition requires wafer surfaces which are extremely flat and free of dust particles. Usually the bonding susceptibility is enhanced by a short polishing step. Van der Waals bonding (dipole bonding) is sufficiently strong to withstand the thinning procedure, but bonding is often enhanced by an anneal step (chemical bonding) before thinning. Four thinning procedures are described: 1. Electroless chemical thinning: Selective etching of highly doped bulk material of an active wafer using an electrochemically controlled HF–HNO 3 –HAc–H 2 O etchant down to a low-dope, low etch-rate epilayer. 2. Chemical thinning: Electrochemically controlled chemical etching of p-type bulk material of an active wafer down to a p/n junction, where electrochemical passivation of an n-type silicon epilayer occurs. 3. Thinning down to a tribochemical polish stop: In this technique an active wafer is polished until grooves filled with Si 3 N 4 are encountered. The removal rate then becomes small while SOI remains in the areas between the grooves. 4. Polish without stopper: By adapting the existing optical polishing technology, extreme control of flatness and parallelism of wafer surfaces can be achieved. It then becomes possible to polish homogeneously down to SOI layers a few microns thick over a 100 mm wafer. In procedures 1 and 2 an acceptable surface quality is obtained by applying a final tribochemical polishing step. Experimental results of the four technologies are presented. In these technologies, tribochemical polishing is crucial. The necessity of this polishing technology as an off-line facility is discussed in the broader context of ICs of the future.
Three Dimensional Analysis for Texture of Corroded Surface by Using of Image Processing Techniques (1996)

The surface textures of corroded materials gave us important information to understand corrosion mechanisms. Various methods to measure these corrosion shapes were already reported. These methods were briefly explained in this article and the characteristics of these were summarized. Especially, a stereo image processing technique which can derive three dimensional feature of a corroded specimen is explained in detail. And the future trends of the analysis of corroded shapes are introduced briefly.
Enhanced BRET technology for the monitoring of agonist-induced and agonist-independent interactions between GPCRs and β-arrestins (2010)

The bioluminescence resonance energy transfer (BRET) technique has become extremely valuable for the real-time monitoring of protein-protein interactions in live cells. This method is highly amenable to the detection of G protein-coupled receptor (GPCR) interactions with proteins critical for regulating their function, such as β-arrestins. Of particular interest to endocrinologists is the ability to monitor interactions involving endocrine receptors, such as orexin receptor 2 or vasopressin type II receptor. The BRET method utilizes heterologous co-expression of fusion proteins linking one protein of interest (GPCR) to a bioluminescent donor enzyme, a variant of Renilla luciferase, and a second protein of interest (β-arrestin) to an acceptor fluorophore. If in close proximity, energy resulting from oxidation of the coelenterazine substrate by the donor will transfer to the acceptor, which in turn fluoresces. Using novel luciferase constructs, we were able to monitor interactions not detectable using less sensitive BRET combinations in the same configuration. In particular, we were able to show receptor/β-arrestin interactions in an agonist-independent manner using Rluc8-tagged mutant receptors, in contrast to when using Rluc. Therefore, the enhanced BRET methodology has not only enabled live cell compound screening as we have recently published, it now provides a new level of sensitivity for monitoring specific transient, weak or hardly detectable protein-protein complexes, including agonist-independent GPCR/β-arrestin interactions. This has important implications for the use of BRET technologies in endocrine drug discovery programs as well as academic research.
Social Serendipity: Proximity Sensing and Cueing (2004)

We describe a system that detects wireless devices, queries a centralized server that links the devices with their owners&amp;apos; online profiles, and instigates serendipitous interactions. The system is currently running on Symbian mobile phones that support Bluetooth and is comprised of two applications. The initial application, BlueAware, senses unique Bluetooth identifiers (BTIDs) and logs them to a text file. The Serendipity application queries a server with a discovered BTID, and the server associates the BTID with an individual&amp;apos;s online profile. A similarity metric is generated between the two people and depending on both users&amp;apos; settings, the server alerts them of their proximity and common interests. The system enables a suite of additional applications including the facilitation of networking in conference and business environments, the augmentation of current models of airborne pathogen dissemination, and the provision of a novel dating service.
Structure-activity relationships in luteinizing hormone-releasing hormone (1976)

Three analogs of luteinizing hormone-releasing hormone (LH-RH) of the structure less than Glu-His-Trp-Ser-Tyr-Gly-Gly-Leu-Arg-Pro-Gly-NH2, involving substitutions inpositions 1, 3, and 8 with nonprotein amino acids, have been synthesized by the solid-phase method. They are [pyro-L-alpha-(1-aminoadipic)]-LH-RH, [3-(2-naphthyl)-L-Ala3]-LH-RH, and [delta-N-i-Pr-L-Orn8]-LH-RH. Their LH-RH activities in vivo were 12.5, 51.8, and 3.7% that of LH-RH, respectively, in the assay using ovariectomized, estrogen- and progesterone-treated rats. In a test based upon subcutaneous injection into immature male rats, [3-(2-naphthyl)-Ala3]-LH-RH released 1.2 times as much LH and 0.8 times as much FSH as synthetic LH-RH.
Interactions of soluble CD59 with the terminal complement complexes. CD59 and C9 compete for a nascent epitope on C8. (1993)

Human CD59-Ag is a glycophosphoinositol lipid-anchored inhibitor of the membrane attack complex of complement (MAC). We have examined the interactions of CD59 with the terminal complement complexes using soluble CD59 purified from human urine (CD59U). CD59U bound to SC5b-8, SC5b-9, and MAC complexes when present during their formation. When SC5b-8, SC5b-9, and MAC were allowed to perform, progressively less 125I-CD59U bound to the complexes. Terminal SC5b-9 complexes isolated from activated sera no longer bound CD59U, indicating that the binding sites had become inaccessible in the fully assembled SC5b-9 complex. Unlike acylated myocardial CD59 (CD59H) neither CD59U nor PIPLC-treated CD59H became incorporated into poly-C9 complexes, suggesting that the interaction of CD59 with C9 requires the lipid anchor. Human C9 and heterologous C9 from guinea pig serum, as well as the YTH53.1 anti-CD59 mAb, inhibited the binding of CD59U to SC5b-8. On the other hand, soluble CD59U did not inhibit binding of C9 to SC5b-8, although CD59E has been shown to limit the number of C9 molecules entering into MAC. This suggests that two interaction sites between C5b-8 and C9 exist: one conferring the initial binding of C9 into the C5b-8 complex, and a second directing the insertion of C9 into the lipid bilayer. The latter interaction is the prerequisite for C9 polymerization and the target for interference by CD59.
Gut Motility and Transit Changes in Patients Receiving Long‐Term Methadone Maintenance (1998)

This study was conducted to survey gut motility and transit in 19 volunteers receiving methadone maintenance who were opioid-dependent, and to measure the oral-cecal transit time in these individuals using the lactulose hydrogen breath test. None of these patients reported constipation problems before use of illicit drugs. During current long-term methadone therapy, 58% of patients experienced some degree of constipation, and two of these 19 patients reported that constipation was a very serious problem. Mean +/- standard deviation (SD) oral-cecal transit time in these individuals was 159+/-49.2 minutes, which is significantly longer than the transit time recorded in two previous studies of healthy volunteers (P < 0.01). These results indicate that tolerance to opioids does not appear to extend to gastrointestinal motility and transit. It seems that patients receiving long-term methadone therapy are a good model for use in evaluating gastrointestinal effects of opioid antagonists.
Phospholipase C-linked receptors regulate the ATP-sensitive potassium channel by means of phosphatidylinositol 4,5-bisphosphate metabolism (1999)

In the COS7 cells transfected with cDNAs of the Kir6.2, SUR2A, and M(1) muscarinic receptors, we activated the ATP-sensitive potassium (K(ATP)) channel with a K(+) channel opener and recorded the whole-cell K(ATP) current. The K(ATP) current was reversibly inhibited by the stimulation of the M(1) receptor, which is linked to phospholipase C (PLC) by the G(q) protein. The receptor-mediated inhibition was observed even when protein kinase C (PKC) was inhibited by H-7 or by chelating intracellular Ca(2+) with 10 mM 1, 2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetate (BAPTA) included in the pipette solution. However, the receptor-mediated inhibition was blocked by U-73122, a PLC inhibitor. M(1)-receptor stimulation failed to inhibit the K(ATP) current activated by the injection of exogenous phosphatidylinositol 4,5-bisphosphate (PIP(2)) through the whole-cell patch pipette. The receptor-mediated inhibition became irreversible when the replenishment of PIP(2) was blocked by wortmannin (an inhibitor of phosphatidylinositol kinases), or by including adenosine 5'-[beta,gamma-imido]triphosphate (AMPPNP, a nonhydrolyzable ATP analogue) in the pipette solution. In inside-out patch experiments, the ATP sensitivity of the K(ATP) channel was significantly higher when the M(1) receptor in the patch membrane was stimulated by acetylcholine. The stimulatory effect of pinacidil was also attenuated under this condition. We postulate that stimulation of PLC-linked receptors inhibited the K(ATP) channel by increasing the ATP sensitivity, not through PKC activation, but most probably through changing PIP(2) levels.
COMPATIBILITY OF INSECTICIDES WITH ENTOMOPATHOGENIC FUNGI <em>Beauveria bassiana</em> AND <em>Metarhizium anisopliae</em> (2017)

Insecticide use has produced negative impact by affecting the non-target predatory organisms in nature, one of which is the entomopathogenic fungi, Beauveria bassiana and Metarhizium anisopliae. Interactions occur, however, between insecticides and the entomopathogens. The combination of insecticides at a low dose and an entomopathogenic fungus can work synergistically to increase pest insect mortality. This combination is particularly advantageous because it decreases the insecticide dose applied, reduces environmental contamination, and decreases pest resistance. The study purpose was to determine the compatible working insecticide dose and the entomopathogenic fungi B. basiana and M. anisopliae. The experimental design applied completely randomized design consisting of 15 treatments and four replicates. There were five types of insecticides with three different doses each (0.5 × Dose of Field (DF), 1 × DF, and 2 × DF), whereas the fungal isolates included B. basiana and M. anisopliae. The parameters observed were the germination percentage of conidia, the percentage of inhibition, and the number of conidia.ml-1. Data were analyzed using ANOVA (5% error rate). The mean values were analyzed by DMRT p &lt; 0.05. Deltamethrin 0.5 x DF, and imidacloprid 0.5 x DF demonstrated the highest conidial germination in B. basiana and M. anisopli, respectively. Insecticides showing the highest vegetative growth on B. basiana and M. anisopliae at 7 DAI was imidacloprid 0.5 x DF, while at 14 DAI was imidacloprid 0.5 x DF and chlorphyrifos 2 x DF, respectively. The highest conidial production of the fungi was triggered by imidacloprid 0.5 x DF. Based on compatibility calculation, imidacloprid 0,5 x DF worked with B. basiana (BI: 67.77) and M. anisopliae (BI: 67.16).
Pregnancy-Induced Noncoding RNA (PINC) Associates with Polycomb Repressive Complex 2 and Regulates Mammary Epithelial Differentiation (2012)

Pregnancy-induced noncoding RNA (PINC) and retinoblastoma-associated protein 46 (RbAp46) are upregulated in alveolar cells of the mammary gland during pregnancy and persist in alveolar cells that remain in the regressed lobules following involution. The cells that survive involution are thought to function as alveolar progenitor cells that rapidly differentiate into milk-producing cells in subsequent pregnancies, but it is unknown whether PINC and RbAp46 are involved in maintaining this progenitor population. Here, we show that, in the post-pubertal mouse mammary gland, mPINC is enriched in luminal and alveolar progenitors. mPINC levels increase throughout pregnancy and then decline in early lactation, when alveolar cells undergo terminal differentiation. Accordingly, mPINC expression is significantly decreased when HC11 mammary epithelial cells are induced to differentiate and produce milk proteins. This reduction in mPINC levels may be necessary for lactation, as overexpression of mPINC in HC11 cells blocks lactogenic differentiation, while knockdown of mPINC enhances differentiation. Finally, we demonstrate that mPINC interacts with RbAp46, as well as other members of the polycomb repressive complex 2 (PRC2), and identify potential targets of mPINC that are differentially expressed following modulation of mPINC expression levels. Taken together, our data suggest that mPINC inhibits terminal differentiation of alveolar cells during pregnancy to prevent abundant milk production and secretion until parturition. Additionally, a PRC2 complex that includes mPINC and RbAp46 may confer epigenetic modifications that maintain a population of mammary epithelial cells committed to the alveolar fate in the involuted gland.
Uric acid, a natural scavenger of peroxynitrite, in experimental allergic encephalomyelitis and multiple sclerosis (1998)

Uric acid, the naturally occurring product of purine metabolism, is a strong peroxynitrite scavenger, as demonstrated by the capacity to bind peroxynitrite but not nitric oxide (NO) produced by lipopolysaccharide-stimulated cells of a mouse monocyte line. In this study, we used uric acid to treat experimental allergic encephalomyelitis (EAE) in the PLSJL strain of mice, which develop a chronic form of the disease with remissions and exacerbations. Uric acid administration was found to have strong therapeutic effects in a dose-dependent fashion. A regimen of four daily doses of 500 mg/kg uric acid was required to promote long-term survival regardless of whether treatment was initiated before or after the clinical symptoms of EAE had appeared. The requirement for multiple doses is likely to be caused by the rapid clearance of uric acid in mice which, unlike humans, metabolize uric acid a step further to allantoin. Uric acid treatment also was found to diminish clinical signs of a disease resembling EAE in interferon-gamma receptor knockout mice. A possible association between multiple sclerosis (MS), the disease on which EAE is modeled, and uric acid is supported by the finding that patients with MS have significantly lower levels of serum uric acid than controls. In addition, statistical evaluation of more than 20 million patient records for the incidence of MS and gout (hyperuricemic) revealed that the two diseases are almost mutually exclusive, raising the possibility that hyperuricemia may protect against MS.
Nucleic Acids Research annual Database Issue and the NAR online Molecular Biology Database Collection in 2009 (2008)

The current issue of Nucleic Acids Research includes descriptions of 179 databases, of which 95 are new. These databases (along with several molecular biology databases described in other journals) have been included in the Nucleic Acids Research online Molecular Biology Database Collection, bringing the total number of databases in the collection to 1170. In this introductory comment, we briefly describe some of these new databases and review the principles guiding the selection of databases for inclusion in the Nucleic Acids Research annual Database Issue and the Nucleic Acids Research online Molecular Biology Database Collection. The complete database list and summaries are available online at the Nucleic Acids Research web site (http://nar.oxfordjournals.org/).
Sequencing and characterization of the sdaB gene from Escherichia coli K‐12 (1993)

The sdaB gene which codes for the second L-serine deaminase (L-SD) of Escherichia coli K-12 has been sequenced and shown to be very similar to the sdaA gene which codes for the first L-serine deaminase. sdaB is transcribed in rich medium, particularly in the absence of glucose, and is under the control of catabolite activator protein. A mutation which established expression of the sdaB gene and synthesis of L-serine deaminase 2 in minimal medium has been demonstrated to result in a change in the ribosome-binding site of the sdaB gene.
Sequence heterogeneity of PsaA, a 37-kilodalton putative adhesin essential for virulence of Streptococcus pneumoniae (1996)

psaA encodes a 37-kDa putative pneumococcal surface adhesin. Although its complete nucleotide sequence has been determined, its contribution to the pathogenicity of Streptococcus pneumoniae has not previously been assessed. In this study, we used a PCR-amplified internal fragment of the psaA gene from S. pneumoniae type 2 strain D39 cloned in pVA891, to direct the construction of D39 derivatives in which the psaA gene had been specifically interrupted, by insertion-duplication mutagenesis. Two independent D39 psaA mutants (PsaA-(1) and PsaA-(2)) were significantly less virulent (as judged by intranasal or intraperitoneal challenge of mice) than either the wild-type D39 strain or a derivative of PsaA-(1) in which the psaA gene had been reconstituted by back-transformation with an intact copy of the cloned gene. pVA891-directed mutagenesis of an open reading frame (designated ORF3) immediately 3' to psaA or insertion of pVA891 between psaA and ORF3 had no impact on intranasal virulence. However, a small but significant difference in virulence was observed between these two derivatives and the parental D39 strain in a low-dose intraperitoneal challenge model, suggesting that the ORF3 product may also contribute to pathogenesis. Adherence of PsaA-(1) to A549 cells (type II pneumocytes) was only 9% of that for D39, while the ORF3-negative strain exhibited intermediate adherence (23%). This is the first functional evidence that PsaA is an adhesin. Sequence analysis of the psaA gene from D39 indicated significant deviation from that previously published for the homolog from S. pneumoniae R36A. The deduced amino acid sequences of mature PsaA from the two strains had only 81% homology, with the bulk of the variation occurring in the amino-terminal portion.
Long-term stability of coagulation variables: Protein S as a biomarker for preanalytical storage-related variations in human plasma (2009)

Long-term stability of coagulation variables: Protein S as a biomarker for preanalytical storage-related variations in human plasma -
The Preclinical Properties of a Novel Group II Metabotropic Glutamate Receptor Agonist LY379268 (2007)

Activation of group II metabotropic glutamate (mGlu2/3) receptors reduces excessive glutamate release that is often associated with neurodegenerative and psychiatric disorders. This finding encouraged the search for potent and selective agonists as potential therapeutic agents. The search led to the discovery of LY379268 {(-)-2-oxa-4-aminobicyclo[3.1.0]hexane-4,6-dicarboxylic acid}, which is a highly potent and systemically available mGlu2/3 receptor agonist. LY379268 was effective in several animal models of stroke, epilepsy, drug abuse, schizophrenia, and pain. Suppression of motor activity is the major side effect of LY379268. Upon repeated administration tolerance develops to this side effect, while the therapeutic effects of LY379268 remain. To date, no clinical data with LY379268 are available. This review article summarizes the preclinical pharmacology of LY379268.