gebhart/patrepeval huggingface dataset:
Delayed healing of muscle after injection of bupivicaine and steroid. (1990)

The purpose of this study was to evaluate the histologic changes that occur in an area of rat skeletal muscle injected with a local anesthetic and steroid combination. Thirty adult male laboratory rats were assigned to one of six groups. Group 1 received bupivicaine injected into the right gastrocnemius muscle; Group 2 received procaine; Group 3 received bupivicaine and triamcinolone; Group 4 received procaine and triamcinolone; Group 5 received triamcinolone; and Group 6 received normal saline. Animals were sacrificed at 24 hours and at 1, 2, 3, and 4 weeks. The saline, steroid, and procaine groups showed minimal tissue reaction. The procaine/steroid group had focal areas of inflammation at 24 hours but none on subsequent evaluations. The bupivicaine group showed moderate localized necrosis of muscle fibers and a mild inflammatory cell response at 24 hours. Regeneration of muscle fibers was seen at 1 week, and at 3 weeks the tissue had returned to normal. The bupivicaine/steroid group showed extensive localized necrosis of muscle fibers with a heavy inflammatory cell response at 24 hours. These areas of necrosis persisted throughout the 4-week post-injection period, although some muscle fiber regeneration and fibrosis were also noted. This study shows that bupivicaine produces more tissue reaction than procaine and that the addition of steroid to bupivicaine increases the initial tissue damage and prolongs the healing phase.
Pharmacological characterization of antagonists of the C5a receptor (1999)

1. Potent and highly selective small molecule antagonists have recently been developed by us for C5a receptors (C5aR) on human polymorphonuclear leukocytes (PMN). In this study we compared a new cyclic antagonist, F-[OPdChaWR], with an acyclic derivative, MeFKPdChaWr, for their capacities to bind to C5aR on human PMN and human umbilical artery membranes. We also compared their inhibition of myeloperoxidase (MPO) secretion from human PMNs and their inhibition of human umbilical artery contraction induced by human recombinant C5a. 2. In both PMNs and umbilical artery, the cyclic and acyclic C5a antagonists displayed insurmountable antagonism against C5a. There were differences in selectivities for the C5aR with F-[OPdChaWR] (pKb 8.64+/-0.21) being 30 times more potent than MeFKPdChaWr (pKb 7.16+/-0.11, P<0.05) in PMNs, but of similar potency (pKb 8.19+/-0.38 vs pKb 8.28+/-0.29, respectively) in umbilical artery. This trend was also reflected in their relative binding affinities, both antagonists having similar affinities (-logIC50 values) for C5aR in umbilical artery membranes (F-[OPdChaWR], 7.00+/-0.46; MeFKPdChaWr, 7.23+/-0.17), whereas in PMN membranes the C5aR affinity of the cycle F-[OPdChaWR] (7.05+/-0. 06) was four times higher than that of acyclic MeFKPdChaWr (6.43+/-0. 24, P<0.05). 3. In summary, the results reveal that these antagonists are insurmountable in nature against C5a for C5aR on at least two human cell types, and the differences in relative receptor binding affinities and antagonistic potencies against C5a are consistent with differences in receptors within these cell types. The nature of these differences is yet to be elucidated.
Laparoscopic Approach for A Small Intestinal Penetration Caused by a Chicken Bone : A Case Report (2009)

症例は52歳, 男性. 右下腹部痛で当院を受診し, 急性虫垂炎の疑いで入院となった. 血液検査では軽度の炎症所見のみであったが, 腹部CTで小腸内にhigh densityな線状の異物を認めた. 小腸異物による穿通と診断し手術を行った. 腹腔鏡で腹腔内の検索を行うと回腸の一部に発赤を認めた. 発赤部位の直上で小開腹を行い小腸を切開し異物を摘出した. 異物はV字型の骨様であり形状と本人の食事歴より鶏骨と判断した. 術後経過は良好で術後6日目に退院した. 消化管異物の症例に対する腹腔鏡アプローチは広範囲に腹腔内の観察が行え, 最小限の創で処置が可能である. 病状に応じてはファーストチョイスになりうると考えられる.
Automatic conditioning of speech signals (1968)

As a part of the larger problem of providing speech input to a computer in a communications system, before either digital buffering, vocoding, or programmed recognition of the speech signals is performed, automatic conditioning of the input signal can significantly improve system performance. The signal conditioning sub-system described in this paper is intended to provide a constant-amplitude signal of the best quality possible from an uncontrolled speech source such as a telephone line, and to indicate the beginning and continued presence of a speech utterance. A fast-acting wide-range automatic level control is used both to compensate for the average strength of the received signal and to remove the word and phrase amplitude dynamics so that the amplitude-controlled signal is contained in a minimum dynamic range. The presence of an utterance is detected by comparison of the logarithm of signal amplitude to an automatic variable threshold set by the logarithm of the input noise as measured during the absence of signal, thus achieving a constant SNR threshold. The functions described for conditioning can be implemented with analog circuits without the aid of signal delay.
Structure and chromosomal localization of human arachidonate 12-lipoxygenase gene. (1992)

Arachidonate 12-lipoxygenase introduces a molecular oxygen into the C-12 position of arachidonic acid to produce 12(S)-hydroperoxy-5,8,10,14-eicosatetraenoic acid. With the aid of cDNA probes for the enzyme, we isolated overlapping lambda clones encompassing the human 12-lipoxygenase gene and flanking regions from a human genomic library. The gene consists of 14 exons with 13 introns and spans approximately 15 kilobases of DNA. All the exon-intron junctions conform to the GT/AG rule. Neither a typical TATA box nor a CAAT box was found in approximately 1-kb sequence of 5'-upstream region of the translation initiation site. However, this region contains several regulatory elements including four GC boxes, two CACCC boxes, three AP-2 binding sequences, and a glucocorticoid-responsive element. The major transcription initiation site was determined by primer-extension analysis as an adenosine residue at 306 bases upstream from the translation initiation codon. The chromosomal localization of the human 12-lipoxygenase gene was examined by fluorescence in situ hybridization, and the gene was assigned to the sub-band p13.1 of chromosome 17.
Neurite outgrowth on muscle cell surfaces involves extracellular matrix receptors as well as Ca2+-dependent and -independent cell adhesion molecules. (1987)

To identify the molecules on the neuronal surface that mediate axonal growth on myotubes, we have examined neurite formation by ciliary neurons grown on myotubes in the absence or presence of specific antibodies. Dramatic inhibition of neurite outgrowth was seen only when antibodies blocked simultaneously the functions of two cell adhesion molecules--neural cell adhesion molecule (N-CAM) and neural Ca2+-dependent CAM (N-Cal-CAM)--and the neuronal receptors for several extracellular matrix (ECM) proteins. Although the antibody used to block ECM receptors (JG22) has been shown to eliminate almost all neurite growth on ECMs, it had only small effects on neurite growth on myotubes, reducing somewhat the length of neurites. Similarly, antibodies to the two CAMs, when used alone, had no detectable effects on neurite length and, when used together, had only small inhibitory effects on neurite growth. Combination of anti-ECM receptor (JG22) with antibodies to either CAM, however, greatly shortened the length of neurites. These results imply that ECM receptors and the CAMs N-CAM and N-Cal-CAM are major macromolecules used by neuronal growth cones for interactions with myotubes. Each provides a distinct mechanism for regulating growth cone motility.
Right ventricular lead implantation facilitated by a guiding sheath in a patient with severe chamber dilatation with tricuspid regurgitation. (2011)

Implantation of pacemakers can be challenging in the context of dilated cardiac chambers and valvular regurgitation. We report a difficult case of single chamber pacemaker implantation in a patient with restrictrive cardiomyopathy resulting in grossly enlarged atria and severe tricuspid regurgitation. In this situation, use of a slittable guiding sheath, more typically used for coronary sinus lead implantation, greatly facilitated rapid and stable deployment of the right ventricular lead.
Antispasmodics. II. Esters of Basic Bicyclic Alcohols* (1952)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTAntispasmodics. II. Esters of Basic Bicyclic Alcohols*L. H. Sternbach and S. KaiserCite this: J. Am. Chem. Soc. 1952, 74, 9, 2219–2221Publication Date (Print):May 1, 1952Publication History Published online1 May 2002Published inissue 1 May 1952https://pubs.acs.org/doi/10.1021/ja01129a020https://doi.org/10.1021/ja01129a020research-articleACS PublicationsRequest reuse permissionsArticle Views605Altmetric-Citations34LEARN 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
Mutual coupling effects in multi-user massive MIMO base stations (2012)

We analyze the effects of mutual coupling and spatial correlation on the performance of multi-user MIMO systems having a large number of antenna elements at the base station (`large-scale' MIMO or `massive' MIMO). We show that these effects set a practical limit on the maximum number of antennas that can be packed into any given physical base station size, above which no further spectral efficiency gain is achieved. Different antenna elements such as dipoles, patches and dual-polarized patches are considered.
TRAIL: not just for tumors anymore? (2012)

Since the discovery of TNF-related apoptosis-inducing ligand (TRAIL) and its network of receptors, the majority of attention has focused on the clinical potential of manipulating this pathway in cancer therapy. However, the widespread expression of TRAIL under inflammatory conditions and the ability to induce both apoptotic and prosurvival signaling pathways has suggested that TRAIL plays broader roles in regulating immune processes. Two new studies now show that expression of TRAIL by neutrophils in the lung facilitates defenses against bacterial pathogens, whereas expression of TRAIL by cells within arterioles exacerbates vascular disease. These differentiating results highlight that the context of TRAIL signaling can determine whether the outcome is beneficial or pathogenic for the host.
Agonists at metabotropic glutamate receptors presynaptically inhibit EPSCs in neonatal rat hippocampus. (1991)

1. The effects of metabotropic glutamate receptor agonists on excitatory synaptic transmission in the CA1 region of rat hippocampal slices (11-30 days) were studied using extracellular and whole-cell patch-clamp recording techniques. 2. Trans-1-amino-1,3-cyclopentanedicarboxylic acid (trans-ACPD; 25-100 microM) reversibly depressed excitatory postsynaptic currents (EPSCs) without affecting presynaptic fibre excitability or EPSC reversal potential. 3. Ibotenate (25 microM) or L-glutamate (250 microM), in the presence of the N-methyl-D-aspartate (NMDA) receptor antagonist, D-2-amino-5-phosphonovaleric acid (APV, 50-75 microM), depressed the EPSC amplitude while inducing no detectable inward current. L-2-Amino-4-phosphonobutyrate (L-AP4, 25-100 microM), the phosphonic derivative of glutamate, also depressed EPSC amplitude and caused no detectable inward current. 4. The NMDA receptor-mediated component of the EPSC recorded in the presence of the non-NMDA receptor antagonist, 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 20-30 microM) was depressed by trans-ACPD, L-AP4, or quisqualate (1-2 microM). 5. The response to ionophoretic application of alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) was unaffected by trans-ACPD or L-AP4 although the simultaneously recorded EPSC was strongly depressed. In addition, paired-pulse facilitation (50-75 ms interstimulus interval) was reversibly enhanced by trans-ACPD or L-AP4. These results indicate that the depression of synaptic transmission likely was mediated by a presynaptic 'autoreceptor'. 6. The effects of trans-ACPD or L-AP4 on synaptic transmission decreased significantly over ages 12-30 days and were minimal in adult (greater than 80 days) slices. 7. The depression of synaptic transmission caused by trans-ACPD or L-AP4 was not altered following the induction of long-term potentiation (LTP). 8. The results indicate that metabotropic glutamate receptor agonists suppress excitatory synaptic transmission in CA1 pyramidal cells by an action at a presynaptic site. This effect is developmentally regulated and is maximally expressed during the first postnatal month.
BENZOQUINOLINES II. SYNTHESIS OF SOME NEW BENZO[h] PYRIMIDO [4′,5′:4,5]THIENO[2,3-b]QUINOLINE DERIVATIVES AND RELATED FUSED HEXACYCLIC SYSTEMS (2000)

Abstract Reaction of 8-amino-7-(2 furyl)-5,6-dihydrobenzo[h]thieno[2,3-b]quinoline-9-carbonitrile (3a) with phenyl isothiocyanate, triethyl orthoformate, ethylenediamine and/or sodium azide afforded benzo[h]thieno[2,3-b]quinolines 4,7,20 and 25 respectively. Cyclization of thiourea derivative 4 furnished thioxopyrimidine derivative 5. The dithioxopyrimidine 6 was prepared by reaction of 3a with carbon disulfide. On treatment of 7 with hydrazine hydrate, 10-amino-7-(2-furyl)-11-imino-5,6,10,11-tetrahydrobenzo[h]pyrimido[4′,5′:4,5]thieno [2,3-b]quinoline (8) was obtained. Compounds 8,20 and 25 were used as key intermediates in the synthesis of the fused hexacyclic compounds 9–19, 21–24 and 26–28 respectively. 8-Amino-7-(2-furyl)-5,6-dihydrobenzo[h]thieno[2,3-b]quinoline-9-carboxamide (3b) was reacted with some reagents, namely triethyl orthoformate, benzaldehyde, carbon disulfide, phenyl isothiocyanate, and/or acetic anhydride to give the corresponding benzo[h]pyrimido [4′,5′: 4,5]thieno[2,3-b]quinolines 29, 30, 31, 32 and 34. Compound 29 underwent some sequence reactions to give 37–42. Some of the prepared compounds were tested in vitro for their antibacterial and antifungal activities.
Mantle dynamics, element recycling, and magma genesis beneath the Kermadec Arc‐Havre Trough (2002)

New geochemical and isotopic data are presented for lavas from three sites in the Havre Trough‐Lau Basin back arc and six volcanoes along the Kermadec arc. The back arc basalts range from MORB‐like to arc‐like in composition and contain a variable contribution from the underlying slab. The least contaminated MORB‐like back arc lavas from 24°–29°S are low degree partial melts of a source with Pacific MORB isotopic characteristics. A transition occurs at 30°S between the strongly depleted northern Kermadec (and Tonga) arc lavas and the mildly depleted southern Kermadec arc lavas. This transition does not correlate with changes in the back arc extension rate or width but may reflect inhibited mantle wedge replenishment behind the shallower‐dipping northern Kermadec‐Tonga slab. Northern Kermadec lavas require mixing between two components: (1) depleted Havre Trough mantle and (2) fluid derived from altered MORB crust with a slight input of sediment lead. Inter‐volcano differences in fluid compositions probably reflect local variations on the subducting slab rather than mineralogical variation in the mantle wedge. Southern Kermadec lavas require an additional component: (3) Pacific sediment melt. This sediment melt is only detected where the subduction rate is &lt;7 cm/year, and requires thermal heating of the slab to &gt;650°C before passing through the sub‐arc melt generation zone.
Alleviating transcript insufficiency caused by Friedreich's ataxia triplet repeats (2000)

Expanded GAA.TTC trinucleotide repeats in intron 1 of the frataxin gene cause Friedreich's ataxia (FRDA) by reducing frataxin mRNA levels. Insufficient frataxin, a nuclear encoded mitochondrial protein, leads to the progressive neurodegeneration and cardiomyopathy characteristic of FRDA. Previously we demonstrated that long GAA.TTC tracts impede transcription elongation in vitro and provided evidence that the impediment results from an intramolecular purine.purine.pyrimidine DNA triplex formed behind an advancing RNA polymerase. Our model predicts that inhibiting formation of this triplex during transcription will increase successful elongation through GAA.TTC tracts. Here we show that this is the case. Oligodeoxyribonucleotides designed to block particular types of triplex formation provide specific and concentration-dependent increases in full-length transcript. In principle, therapeutic agents that selectively interfere with triplex formation could alleviate the frataxin transcript insufficiency caused by pathogenic FRDA alleles.
A Bacillus amyloliquefaciens ChbB protein binds β- and α-chitin and has homologues in related strains The GenBank/NCIB accession number for the sequence reported in this paper is AF181997. (2001)

A small (19.8 kDa) protein was identified in Bacillus amyloliquefaciens ALKO 2718 cultures during growth in the presence of yeast extract and chitin, but not with glucose. The protein targets beta-chitin best, then alpha-chitin, but barely any other polysaccharide. This described chitin-binding protein (ChbB) is the first of its type from a Bacillus strain and cross-reacts with antibodies raised against the Streptomyces alpha-chitin-binding protein CHB1. Using reverse genetics, the chromosomal chbB gene of strain ALKO 2718 was identified, cloned and sequenced. ChbB shares several motifs with the alpha-chitin-binding proteins CHB1 and CHB2 of Streptomyces and CBP21 of Serratia marcescens predominantly targeting beta-chitin. Synthesis was repressed by glucose and the presence of cre boxes suggests catabolite control. Using PCR, Southern hybridization and anti-ChbB antibodies, the presence of a chbB gene, as well as of a ChbB protein homologue, was ascertained in several tested B. amyloliquefaciens strains, but not in Bacillus subtilis 168. Contrary to B. subtilis 168, all B. amyloliquefaciens strains secreted varying amounts of enzymic activity, degrading carboxymethyl chitin coupled with Remazol brilliant violet.
A shuttle vector which facilitates the expression of transfected genes inTrypanosoma cruzi and Leishmania (1992)

A Trypanosoma cruzi expression vector has been constructed using sequences derived from the flanking regions of the glyceraldehyde 3-phosphate dehydrogenase (gGAPDH) genes. The neomycin phosphotransferase (neor) gene was incorporated as a selectable marker. Using electroporation we have introduced this vector into both T. cruzi and Leishmania cells and conferred G418 resistance. Transformation is mediated by large extrachromosomal circular elements composed of head-to-tail tandem repeats of the vector. The transformed phenotype is stable for at least 6 months in the absence of G418 and can be maintained during passage through the T. cruzi life-cycle. Foreign genes inserted into an expression site within the vector (pTEX) can be expressed at high levels in transformed cells. To our knowledge this paper describes the first trypanosome shuttle vector and the first vector which functions in both trypanosomes and Leishmania.
Autoantibodies to malondialdehyde-modified epitope in connective tissue diseases and vasculitides (1995)

Malondialdehyde (MDA), a peroxidative end-product released during polyunsaturated fatty acid degradation, reacts strongly with lysine residues of cellular proteins. MDA-modified proteins become immunogenic and may elicit specific autoantibody formation. We hypothesized that systemic diseases in which inflammatory events occur, could be an interesting model for studying oxidative stress. A few studies have suggested that MDA-modified proteins may exist in systemic diseases, and that autoantibodies to MDA-modified structures might reflect this oxidative process. Autoantibodies to MDA-modified epitope(s) were therefore assayed in sera of patients with systemic lupus erythematosus (SLE, n = 29), scleroderma (SCL, n = 11), giant cell arteritis (GCA, n = 11), periarteritis nodosa (PAN, n = 10), rheumatoid arthritis (RA, n = 9), and healthy subjects (HS, n = 32). Significantly increased anti-MDA-modified epitope(s) autoantibodies were found in patients with SLE and also in other systemic diseases such as PAN and SCL. Autoantibodies to MDA-modified epitope(s) were predominantly of IgM isotype, with low levels of IgG and no IgA activity. In SLE, anti-MDA-modified epitope(s) autoantibody titres correlated strongly with systemic lupus activity measure (SLAM, r = 0.702, P = 0.0001), anti-nuclear antigen autoantibodies (ANA, r = 0.4, P = 0.029), IgG anti-cardiolipin (r = 0.558, P = 0.03) and the steroid drug regimen (r = 0.52, P = 0.004). Autoantibodies to MDA-modified epitope(s) may reflect oxidative modifications occurring in systemic diseases, and might be useful as clinical markers of SLE activity if further investigated.
NKX6.1 Promotes PDX-1-Induced Liver to Pancreatic β-Cells Reprogramming (2010)

Reprogramming adult mammalian cells is an attractive approach for generating cell-based therapies for degenerative diseases, such as diabetes. Adult human liver cells exhibit a high level of developmental plasticity and have been suggested as a potential source of pancreatic progenitor tissue. An instructive role for dominant pancreatic transcription factors in altering the hepatic developmental fate along the pancreatic lineage and function has been demonstrated. Here we analyze whether transcription factors expressed in mature pancreatic β-cells preferentially activate β-cell lineage differentiation in liver. NKX6.1 is a transcription factor uniquely expressed in β-cells of the adult pancreas, its potential role in reprogramming liver cells to pancreatic lineages has never been analyzed. Our results suggest that NKX6.1 activates immature pancreatic markers such as NGN-3 and ISL-1 but not pancreatic hormones gene expression in human liver cells. We hypothesized that its restricted capacity to activate a wide pancreatic repertoire in liver could be related to its incapacity to activate endogenous PDX-1 expression in liver cells. Indeed, the complementation of NKX6.1 by ectopic PDX-1 expression substantially and specifically promoted insulin expression and glucose regulated processed hormone secretion to a higher extent than that of PDX-1 alone, without increasing the reprogrammed cells. This may suggest a potential role for NKX6.1 in promoting PDX-1 reprogrammed cells maturation along the β-cell-like lineage. By contrast, NKX6.1 repressed PDX-1 induced proglucagon gene expression. The individual and concerted effects of pancreatic transcription factors in adult extra-pancreatic cells, is expected to facilitate developing regenerative medicine approaches for cell replacement therapy in diabetics.