gebhart/patrepeval huggingface dataset:
Rodent Anterior Ischemic Optic Neuropathy (rAION) Induces Regional Retinal Ganglion Cell Apoptosis with a Unique Temporal Pattern (2008)

rAION results in later RGC death than in traumatic optic nerve damage models. Apoptosis, measured by FITC-annexin, occurs maximally in the second to third week after infarct. Cleaved caspase-3 activation confirms that after rAION, RGCs undergo apoptosis by the caspase activation pathway. The regional pattern in dying RGCs after rAION implies that a measure of retinotopic organization occurs in the rodent optic nerve. The prolonged period from insult to death suggests that the window for successful treatment after ON infarct may be longer than previously recognized.
Protein Kinase C Isotypes Controlled by Phosphoinositide 3-Kinase Through the Protein Kinase PDK1 (1998)

Phosphorylation sites in members of the protein kinase A (PKA), PKG, and PKC kinase subfamily are conserved. Thus, the PKB kinase PDK1 may be responsible for the phosphorylation of PKC isotypes. PDK1 phosphorylated the activation loop sites of PKCzeta and PKCdelta in vitro and in a phosphoinositide 3-kinase (PI 3-kinase)-dependent manner in vivo in human embryonic kidney (293) cells. All members of the PKC family tested formed complexes with PDK1. PDK1-dependent phosphorylation of PKCdelta in vitro was stimulated by combined PKC and PDK1 activators. The activation loop phosphorylation of PKCdelta in response to serum stimulation of cells was PI 3-kinase-dependent and was enhanced by PDK1 coexpression.
Erectile dysfunction and radiation therapy for prostate cancer (2006)

The number of patients diagnosed with early stage prostate cancer (PC) has increased dramatically, because of routine prostate-specific antigen testing in the recent years and the possibility for cure of early disease. Radiation therapy is together with radical prostatectomy the most effective treatment for localized disease. Incidence of erectile dysfunction (ED) after radiotherapy (RT) reported in the literature vary from 6% to 84% after external-beam RT to 0–51% after brachytherapy. Most of these studies are retrospective, the definition of ED is variable and sexual functioning is frequently assessed by asking only one question. Already in the 1980s it was suggested that post-radiation ED was attributable to vascular damage. More recently, a strong relationship between radiation dose and volume of the penile bulb has been found. Though, a multifactorial etiology has to be considered taking into account pre-treatment erectile function. If radiation induces vascular damage that causes ED, any means of reducing the dose to the pelvic vascular structures would likely decrease ED. Patients need to be informed about the availability of effective treatments such as PDE5-I, intracavernosal injection and vacuum devices. Le nombre de diagnostics précoces de cancer de la prostate (PC) a augmenté considérablement depuis que les techniques de dépistages par le PSA sont devenues courantes et qu'il existe une possibilité de traitement des cancers débutants. La radiothérapie avec la prostatectomie radicale sont les traitements les plus efficaces lorsque la maladie est localisée. L'incidence du dysfonctionnement érectile (DE) après radiothérapie dans la littérature varie de 6 à 84 % après radiothérapie externe à 0 à 51 % après curiethérapie. La plupart de ces études sont rétrospectives, la définition de l'ED y est variable et le fonctionnement sexuel est souvent évalué par une seule question. Déjà dans les années 1980, on attribuait la DE après radiothérapie à des dommages vasculaires. Plus récemment, une corrélation entre la dose irradiée et le volume du bulbe a été démontrée. Ainsi, doit-on envisager une origine multifactorielle prenant en compte le fonctionnement érectile avant traitement. Si la radiothérapie induit des lésions vasculaires responsables de la DE, tous moyens mis en œuvre pour réduire la dose d'irradiation vers les structures vasculaires devraient diminuer la fréquence de la DE. Les patients doivent être informés de la disponibilité de traitements efficaces comme les IPDE5, les injections intracaverneuses et les vacuum.
Catalytic Site Components Common to Both Splicing Steps of a Group II Intron (1994)

The splicing of group II introns occurs in two steps involving substrates with different chemical configurations. The question of whether these two steps are catalyzed by a single or two separate active sites is a matter of debate. Here, certain bases and phosphate oxygen atoms at conserved positions in domain V of a group II self-splicing intron are shown to be required for catalysis of both splicing steps. These results show that the active sites catalyzing the two steps must, at least, share common components, ruling out the existence of two completely distinct active sites in group II introns.
Two-Stage Dispersion Polymerization toward Monodisperse, Controlled Micrometer-Sized Copolymer Particles (2004)

We describe a two-stage dispersion polymerization process to prepare monodisperse micrometer-sized polymer particles in which problematic reagents, such as functional monomers and cross-linkers that commonly disrupt the particle-forming process, were added to the reaction after the nucleation stage was complete. Comonomers added after this point became incorporated into the particles without disturbing the final particle size and size distribution. In this way dye-labeled or functional group-containing micrometer-sized particles with a very narrow size distribution were prepared. By varying the amount of monomer added in the second stage, the final particle diameter could be controlled precisely. Most important of all, this synthetic strategy allowed us to prepare cross-linked particles containing up to 3 mol % cross-linking agent.
Comprehensive genomic profiling aids in treatment of a metastatic endometrial cancer (2018)

<i>FGFR</i>-<i>TACC</i> fusions, including <i>FGFR3</i>-<i>TACC3</i>, have been identified as potential oncogenic drivers and actionable alterations in a number of different cancer types. The clinical relevance of <i>FGFR3-TACC3</i> fusions in endometrial cancer has not yet been described. Formalin-fixed, paraffin-embedded metastatic endometrial carcinoma from the spleen and peritoneum were sent for comprehensive genomic profiling (CGP) using the FoundationOne platform as part of a prospective tumor genomic profiling protocol. We report the identification of an <i>FGFR3</i>-<i>TACC3</i> fusion in a case of metastatic endometrioid endometrial cancer. Other potentially actionable alterations detected in this specimen included <i>PIK3CA</i> T1025S and an uncharacterized rearrangement involving <i>TSC2</i> The patient initially received an FGFR inhibitor as an investigational agent and experienced stable disease with complete resolution of a pelvic nodule; however, treatment had to be discontinued because of intolerable side effects. A PET/CT scan nearly 3 mo after discontinuation showed disease progression. She subsequently received the mTOR inhibitor, temsirolimus, later accompanied by letrozole, and achieved stable disease. Clinical benefit was attributed to the mTOR inhibitor as tumor stained negative for estrogen receptor. Temsirolimus was discontinued after >17 mo because of disease progression. FGFR inhibitors may have clinical benefit in the treatment of endometrial carcinoma with <i>FGFR3</i>-<i>TACC3</i> fusions. Additionally, clinical benefit from an mTOR inhibitor may reflect a response to targeting the alteration in <i>PIK3CA</i> or <i>TSC2</i> More research is needed to understand the activity of <i>FGFR3-TACC3</i> fusions on tumors and to discover additional therapeutic options for endometrial carcinoma patients with this gene fusion.
Rhizobium meliloti anthranilate synthase gene: cloning, sequence, and expression in Escherichia coli (1989)

We determined the DNA sequence of the Rhizobium meliloti gene encoding anthranilate synthase, the first enzyme of the tryptophan pathway. Sequences similar to those seen for the two subunits of the enzyme as found in all other procaryotic species studied are present in a single open reading frame of 729 codons. This apparent gene fusion joins the C terminus of the large subunit (TrpE) to the N terminus of the small subunit (TrpG) through a short connecting segment. We designate the fused gene trpE(G). The gene is flanked by a typical rho-independent terminator at the 3' end and a complex regulatory region at the 5' end resembling those of operons under transcriptional attenuation control. The location of the promoter was determined by S1 nuclease protection, using Rhizobium mRNA. Although this promoter was inactive in Escherichia coli, mutations eliciting activity were easily obtained. One of these was a C----T change at position -9 in the -10 region. The +1 position of the mRNA is the first base of the initiation codon of the leader peptide, implying that unlike trpE(G), which has a normal Shine-Dalgarno sequence, the leader peptide gene lacks a ribosome-binding site.
Genomic cloning and promoter analysis of macrophage inflammatory protein (MIP)-2, MIP-1 alpha, and MIP-1 beta, members of the chemokine superfamily of proinflammatory cytokines (1993)

Macrophage inflammatory protein (MIP)-2, MIP-1 alpha, and MIP-1 beta all belong to the newly recognized "chemokine" superfamily of structurally related, activation-inducible cytokines with inflammatory and growth regulatory activities. We report the isolation and sequencing of genomic clones for murine MIP-2 and murine MIP-1 beta, and analyze their regulatory sequences in comparison with each other and with several other members of the chemokine family. The murine (mu)MIP-2 genomic clone displays the canonical four exon/three intron structure typical of other genes in the chemokine alpha subfamily (e.g., IL-8). Potential cis regulatory elements in the proximal promoter region were highly conserved between muMIP-2 and its three most closely related human homologs: human (hu)GRO-alpha, huGRO-beta, and huGRO-gamma. A mouse macrophage cell line, RAW 264.7, was transfected with a growth hormone reporter construct driven by a proximal fragment of the muMIP-2 5' promoter, and nested deletion mutant analysis localized the LPS responsive element to a region that contains a conserved NF kappa B consensus motif and lies 51 to 70 bp 5' from the transcription start site. In contrast to that of MIP-2, the muMIP-1 beta genomic clone exhibited the three exon/two intron structure characteristic of the chemokine beta family members (e.g., MCP-1). A comparison of the promoters for muMIP-1 beta and muMIP-1 alpha reveals a conserved CK-1 element, but transient expression studies in RAW 264.7 macrophages with proximal fragments of either the muMIP-1 beta or the muMIP-1 alpha 5' promoter fused to a human growth hormone reporter gene link LPS-inducibility in both to promoter segments near to, but not identical with, the consensus CK-1 sequence. Proximal 5' promoter fragments cloned from both the MIP-1 alpha and MIP-1 beta genes unexpectedly conferred constitutive expression on the fused reporter gene sequences in macrophage-like cells, but initial 5' deletion analysis did not link this responsiveness to known sequence motifs. The muMIP-1 beta promoter, but not the muMIP-1 alpha promoter, was constitutively active in B16 mouse melanoma cells, and both promoters were active in the myelomonocytic cell line WEHI 3B(A)d-, the muMIP-1 alpha promoter being three times stronger.
Serologic Response to Cell Wall Mannoproteins and Proteins ofCandida albicans (1998)

The cell wall of Candida albicans not only is the structure in which many biological functions essential for the fungal cells reside but also is a significant source of candidal antigens. The major cell wall components that elicit a response from the host immune system are proteins and glycoproteins, the latter being predominantly mannoproteins. Both the carbohydrate and protein moieties are able to trigger immune responses. Although cell-mediated immunity is often considered to be the most important line of defense against candidiasis, cell wall protein and glycoprotein components also elicit a potent humoral response from the host that may include some protective antibodies. Proteins and glycoproteins exposed at the most external layers of the wall structure are involved in several types of interactions of fungal cells with the exocellular environment. Thus, coating of fungal cells with host antibodies has the potential to influence profoundly the host-parasite interaction by affecting antibody-mediated functions such as opsonin-enhanced phagocytosis and blocking the binding activity of fungal adhesins for host ligands. In this review, the various members of the protein and glycoprotein fraction of the C. albicans cell wall that elicit an antibody response in vivo are examined. Although a number of proteins have been shown to stimulate an antibody response, for some of these species the response is not universal. On the other hand, some of the studies demonstrate that certain cell wall antigens and anti-cell wall antibodies may be the basis for developing specific and sensitive serologic tests for the diagnosis of candidasis, particularly the disseminated form. In addition, recent studies have focused on the potential for antibodies to cell wall protein determinants to protect the host against infection. Hence, a better understanding of the humoral response to cell wall antigens of C. albicans may provide the basis for the development of (i) effective procedures for the serodiagnosis of disseminated candidiasis and (ii) novel prophylactic (vaccination) and therapeutic strategies for the management of this type of infection.
Genome-Wide Association Analysis Identifies Candidate Genes Associated with Iron Deficiency Chlorosis in Soybean (2011)

Iron deficiency chlorosis (IDC) is a significant yield-limiting problem in several major soybean [Glycine max (L.) Merr.] production regions in the United States. Soybean plants display a variety of symptoms that range from a slight yellowing of the leaf to interveinal chlorosis, to stunted growth that reduces yield. The objective of this analysis was to employ single nucleotide polymorphism (SNP)-based genome-wide association mapping to uncover genomic regions associated with IDC tolerance. Two populations [2005 (n = 143) and 2006 (n = 141)] were evaluated in replicated, multilocation IDC trials. After controlling for population structure and individual relatedness, and selecting statistical models that minimized false positives, 42 and 88 loci, with minor allele frequency >10%, were significant in 2005 and 2006, respectively. The loci accounted for 74.5% of the phenotypic variation in IDC in2005 and 93.8% of the variation in 2006. Nine loci from seven genomic locations were significant in both years. These loci accounted for 43.7% of the variation in 2005 and 47.6% in 2006. A number of the loci discovered here mapped at or near previously discovered IDC quantitative trait loci (QTL). A total of 15 genes known to be involved in iron metabolism mapped in the vicinity (>500 kb) of significant markers in one or both populations.
Retention of a type II surface membrane protein in the endoplasmic reticulum by the Lys-Asp-Glu-Leu sequence. (1992)

Soluble luminal proteins of the endoplasmic reticulum (ER) are known to be retained by a tetrapeptide retention signal, KDEL. We report in this communication that the KDEL sequence when appended to the carboxy terminus of a cell surface membrane protein, dipeptidyl peptidase IV (DPPIV), resulted in its retention in the endoplasmic reticulum of transfected Madin-Darby canine kidney cells as assessed by indirect immunofluorescence. Selective surface biotinylation revealed that about 90-95% of the expressed DPPIV was retained in the ER. Appendance of the sequence KDEV did not, however, result in ER retention, illustrating the functional specificity of the retention signal. The ER retention was not due to misfolding of the mutant protein, as the mutant proteins remained enzymatically active. Our data suggest that the KDEL receptor is able to recognize and recycle type II membrane proteins containing a carboxyl-terminal KDEL sequence and postulates the existence of such yet to be identified endogenous proteins.
Finite Element Models for the Viscoelasticity of Open-Cell Polyurethane Foam (2006)

Finite Element Analysis (FEA) was used to model viscoelastic effects in the compression of polyurethane (PU) foam. Modelling of the impact compression of foam cubes predicted that a compressed region propagated through the sample, causing step increases in the stress traces. Modelling of head impacts on gymnastic ‘crash’ mats, made of PU chip foam, revealed that the majority, but not all, of the energy losses could be attributed to the polymer viscoelasticity. The Gibson-Ashby micromechanics model was used to show that the hysteresis in a viscoelastic foam could be higher than in the parent polymer. A wet Kelvin foam, with a better foam geometry, was then used for viscoelastic analysis. The lattice of uniform-sized cells, in a Body Centred Cubic array, were compressed in the [111] direction. With the PU treated as a linear viscoelastic material, the predicted hysteresis in the cyclic stress-strain curve was slightly smaller than that measured for a PU flexible foam.
Coding and cell-loss recovery in DCT-based packet video (1993)

The applications of discrete cosine transform (DCT)-based image- and video-coding methods in the asynchronous transfer mode (ATM) environment are considered. Coding and reconstruction mechanisms are jointly designed to achieve a good compromise among compression gain, system complexity, processing delay, error-concealment capability, and reconstruction quality. The Joint Photographic Experts Group (JPEG) and Motion Picture Experts Group (MPEG) algorithms for image and video compression are modified to incorporate block interleaving in the spatial domain and DCT coefficient segmentation in the frequency domain to conceal the errors due to packet loss. A new algorithm is developed that recovers the damaged regions by adaptive interpolation in the spatial, temporal, and frequency domains. The weights used for spatial and temporal interpolations are varied according to the motion content and loss patterns of the damaged regions. When combined with proper layered transmission, the proposed coding and reconstruction methods can handle very high packet-loss rates at only a slight cost in compression gain, system complexity, and processing delay.< <ETX xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">&gt;</ETX>
Effects of WAY100635, a selective 5-HT1A-receptor antagonist on the micturition-reflex pathway in the rat (2001)

5-Hydroxytryptamine (5-HT) receptors in the central nervous system have been implicated in the control of micturition. The present study was undertaken to evaluate the effects of a selective 5-HT 1A -receptor antagonist { N-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]- N-(2-pyridinyl)cyclohexanecarboxamide trihydrochloride (WAY100635)} on the micturition-reflex pathway in urethane-anesthetized female Wistar rats. Rhythmic isovolumetric bladder contractions evoked by bladder distension were abolished by 0.3- to 3-mg/kg iv or 30- to 100-μg intrathecal (it) administration of WAY100635 in a dose-dependent manner for periods of 3–15 min. Intrathecal injection of WAY100635 was effective only if injected at the L6-S1 spinal cord level, but not at the thoracic or cervical cord levels. WAY100635 (30–100 μg it) significantly reduced the amplitude of bladder contractions evoked by electrical stimulation of the pontine micturition center. However, the field potentials in the rostral pons evoked by electrical stimulation of pelvic nerve were not affected by intrathecal or intravenous injection of WAY100635. These results suggest that 5-HT 1A receptors at the L6-S1 level of the spinal cord have an important role in the tonic control of the descending limb of the micturition-reflex pathway in the rat.
INTERACTION OF ANTIGENS AND ANTIBODIES AT MUCOSAL SURFACES (1997)

Infections often involve the mucosal surfaces of the body, which form a boundary with the outside world. This review focuses on immunoglobulin A (IgA) antibodies because IgA is the principal mucosal antibody class. IgA is synthesized by local plasma cells and has a specific polymeric immunoglobulin receptor-mediated transport mechanism for entry into the secretions. By serving as an external barrier capable of inhibiting attachment of microbes to the luminal surface of the mucosal epithelial lining, IgA antibodies form the first line of immune defense. In addition to this traditional mode of extracellular antibody function, recent evidence suggests that IgA antibodies can also function in a nontraditional fashion by neutralizing viruses intracellularly, if a virus is infecting an epithelial cell through which specific IgA antibody is passing on its way to the secretions. IgA antibodies are also envisaged as providing an internal mucosal barrier beneath the mucosal lining. Antigens intercepted by IgA antibodies here can potentially be ferried through the epithelium and thereby excreted. In addition to the polymeric immunoglobulin receptor on mucosal epithelial cells, IgA antibodies can bind to receptors on a variety of leukocytes and have been shown, in some experimental systems, to be capable of activating the alternative complement pathway, making IgA antibodies potential participants in inflammatory reactions. Although the relationship of IgA antibodies to inflammation is not entirely clear, the bias presented is that IgA is basically noninflammatory, perhaps even anti-inflammatory. According to this view, the major role of the Fc portion of IgA antibodies is to transport IgA across mucosal epithelial cells and not, as in the case of the other classes of antibody, to activate secondary phenomena of the kind that contribute to inflammation. Because of IgA's key role as an initial barrier to infection, much current research in mucosal immunology is directed toward developing new vectors and adjuvants that can provide improved approaches to mucosal vaccines. Finally, because of advances in monoclonal antibody technology, topical application of antibodies to mucosal surfaces has significant potential for preventing and treating infections.
Apoptosis in atheroclerosis: implications for plaque destabilization. (2004)

An increasing body of evidence from both animal models and human specimens suggests that apoptosis or programmed cell death is a major event in the pathophysiology of atherosclerosis. Although the significance of apoptosis in atherosclerosis remains unclear, it has been proposed that apoptotic cell death contributes to plaque instability, rupture and thrombus formation. In this study, we have outlined some of our most recent results concerning initiation of apoptosis in atherosclerosis with a special focus on oxidative DNA and RNA damage. Furthermore, we provide a detailed picture of the pro- and anti-apoptotic genes/proteins that are involved during the initiation of cell death in atherosclerotic plaques by using a combination of established immunohistochemical stainings and recent molecular biology techniques. Our data suggest that smooth muscle cells and macrophages in atherosclerotic plaques express a different panel of apoptosis-related genes in response to proapoptotic stimuli. Although this may seem a promising starting-point for the development of anti-atherogenic drugs, it remains to be determined whether modulation of apoptosis can become a clinically important approach to influence plaque progression.
当“偷窥”走起 (2013)

你有“（被）偷窥”癖吗？这样的问题问出口，十有八九会被人扔鸡蛋。但当发（刷）微博、上传照片、上传视频成为我们生活不可或缺的一部分时，我们不由得发现许多人其实已在“（被）偷窥”的道路上越走越远。