gebhart/patrepeval huggingface dataset:
Peritoneal healing and adhesion formation/reformation (2001)

Intra-abdominal adhesion formation and reformation after surgery is a cause of significant morbidity, resulting in infertility and pain. The understanding of the pathogenesis of adhesion formation and reformation especially at the cellular and molecular level can help to further develop more effective treatments for the prevention of adhesion formation and reformation. Following an injury to the peritoneum, fibrinolytic activity over the peritoneal surface decreases, leading to changes in the expression and synthesis of various cellular mediators and in the remodelling of the connective tissue. The cellular response to peritoneal injury and adhesion formation and reformation are reviewed. Analysis of the available literature data on the cellular mediators in the peritoneal fluid showed variation in results from different investigators. The potential sources of variability and error are examined. It is still unclear if there is significant individual variation in the peritoneal response to injury.
Silver 2: toxicity in mammals and how its products aid wound repair (2002)

The second article examining the role of this metallic element in a wound environment discusses toxicity in individual cells, animals and humans and considers how different silver-based dressings assist in wound healing.
Repression of 92-kDa Type IV Collagenase Expression by MTA1 Is Mediated through Direct Interactions with the Promoter via a Mechanism, Which Is Both Dependent on and Independent of Histone Deacetylation (2003)

Although the expression of the metastases-associated gene MTA1 correlates with tumor metastases, its role in regulating type IV collagenase expression is unknown. Enforced MTA1 expression in HT1080 cells reduced basal and 12-myristate 13-acetate-induced 92-kDa type IV collagenase (MMP-9) protein/mRNA levels. DNase I hypersensitivity and PstI accessibility assays revealed multiple regions of the MMP-9 promoter (-650/-450 and -120/+1), showing reduced hypersensitivity in the MTA1-expressing cells. Chromatin immunoprecipitation assays demonstrated MTA1 binding to the distal region, which spans several regulatory cis elements. Co-immunoprecipitation and chromatin immunoprecipitation assay experiments revealed histone deacetylase 2 (HDAC2)-MTA1 protein-protein interactions and the MTA1-dependent recruitment of HDAC2 to the distal MMP-9 promoter region, yielding diminished histone H3/H4 acetylation. However, HDAC2 binding and H3/H4 acetylation at the proximal MMP-9 region were unaffected by MTA1 expression. Furthermore, trichostatin treatment only partially relieved MTA1-repressed MMP-9 expression, indicating a HDAC-insensitive component possibly involv ing the nucleosome-remodeling Mi2 activity, which was recruited to the promoter by MTA1. In summary, (a) MMP-9 adds to a short list of MTA1-regulated genes, which so far only includes c-myc and pS2, and (b) MTA1 binds to the MMP-9 promoter, thereby repressing expression of this type IV collagenase via histone-dependent and independent mechanisms.
Mutator phenotypes in human colorectal carcinoma cell lines. (1994)

Recent studies have revealed that tumors in patients with hereditary nonpolyposis colon cancer are associated with high-frequency alterations of microsatellite sequences. To investigate the mechanisms and consequences of this form of genetic instability, we identified three colorectal carcinoma cell lines that express dinucleotide-repeat instability like that found in hereditary nonpolyposis colon cancer tumors and show increased rates of spontaneous mutation at selectable loci. However, the pattern of hypermutation in these cell lines differed significantly. In one line (HCT116), microsatellite mutations occurred at a remarkably high rate (approximately 10(-2) mutations per cell per generation), whereas this rate was considerably lower in the two other lines (DLD-1 and HCT15). The rate of mutation at the locus encoding hypoxanthine guanine phosphoribosyltransferase was substantially elevated (200- to 600-fold) in all three tumor cell lines, yet the types of mutations arising differed. A specific frame-shift hotspot accounted for 24% of hypoxanthine guanine phosphoribosyltransferase mutations in HCT116. The frequency of mutations at this site was reduced significantly in DLD-1 and HCT15 lines. These data suggest that the mutatw phenotypes in the colorectal carcinoma cell lines could be the consequence of mutator genes affecting different repair or error-avoidance pathways.
Catalytic asymmetric synthesis of optically active 2-alkanols via hydrosilylation of 1-alkenes with a chiral monophosphine-palladium catalyst (1991)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTCatalytic asymmetric synthesis of optically active 2-alkanols via hydrosilylation of 1-alkenes with a chiral monophosphine-palladium catalystYasuhiro Uozumi and Tamio HayashiCite this: J. Am. Chem. Soc. 1991, 113, 26, 9887–9888Publication Date (Print):December 1, 1991Publication History Published online1 May 2002Published inissue 1 December 1991https://pubs.acs.org/doi/10.1021/ja00026a044https://doi.org/10.1021/ja00026a044research-articleACS PublicationsRequest reuse permissionsArticle Views3113Altmetric-Citations301LEARN 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-AlertscloseSupporting Info (1)»Supporting Information Supporting Information Get e-Alerts
Synergistic activation of the rat growth hormone promoter by Pit-1 and the thyroid hormone receptor. (1992)

The rat GH (rGH) gene is expressed in the pituitary in a highly tissue-specific manner. A pituitary-specific transcription factor, Pit-1 (or GHF-1), and other, more tissue-general factors, including the thyroid hormone receptor (T3R), are important for regulating rGH promoter activity. The relative roles of Pit-1, T3R, and protein kinases in the activation of the rGH promoter were studied. Each component was supplied individually or in combination with the others to human monocyte U937 cells. The transfected rGH promoter was inactive in these cells even when it was cotransfected with either Pit-1 or T3R expression vectors. The rGH promoter carried in a truncated pUC vector could be activated by expression of the T3R if the cells were cultured with inducers of protein kinase-A (forskolin) and protein kinase-C [phorbol 12-myristate 13-acetate (PMA)] activity. By contrast, the PMA- and forskolin-dependent activation of the rGH promoter by Pit-1 expression was comparatively insignificant unless 1) the sequences deleted from the pUC vector (including a putative site for the transcription factor AP1) were restored to the plasmid carrying the rGH promoter; or 2) the T3R was coexpressed, which led to a marked synergistic response. These results indicate the relative inactivity of Pit-1 in isolation from other factors. Activation by forskolin and PMA did not require de novo protein synthesis. The synergistic activation by Pit-1 and the T3R was enhanced, but was not dependent upon, thyroid hormone (T3). The T3-dependent effect operated predominately through a thyroid hormone response element located up-stream of the two Pit-1-binding sites within the rGH promoter, whereas the T3-independent effect did not require any of the known T3R-binding sites on the rGH promoter. These results suggest a role for the more tissue-general T3R and protein kinases in the activation of the rGH promoter. They demonstrate the synergistic interplay between the T3R and Pit-1, underscore the dependence of Pit-1 action on other transcription factors, and implicate Pit-1 as a cofactor, rather than the dominant factor, influencing the tissue-specific expression of the rGH promoter.
Activation of the c-Src tyrosine kinase is required for the induction of mammary tumors in transgenic mice. (1994)

Transgenic mice expressing the polyomavirus (PyV) middle T oncogene in the mammary epithelium develop multifocal mammary tumors that metastasize with high frequency. The potent transforming activity of PyV middle T antigen can, in part, be attributed to its ability to associate with and to activate a number of c-Src family tyrosine kinases (c-Src, c-Yes, and Fyn). As a first step toward assessing the role of individual c-Src family tyrosine kinases in PyV middle T antigen-induced mammary tumorigenesis, we have crossed transgenic mice carrying the mouse mammary tumor virus (MMTV)/PyV middle T antigen fusion gene with mice bearing a disrupted c-src proto-oncogene. In contrast to the rapid tumor progression seen in the original MMTV/PyV middle T antigen strains, mice expressing the transgene in the absence of functional c-Src rarely developed mammary tumors. After long latency, these mice did eventually develop abnormal hyperplastic mammary tissue. This growth disturbance was correlated with elevated expression of the PyV middle T antigen and the activation of the PyV middle T antigen-associated c-Yes tyrosine kinase. However, transgenic mice expressing the PyV middle T antigen in the mammary epithelium of wild-type or Yes-deficient mice developed multifocal mammary tumors with comparable kinetics. Taken together, these findings suggest that c-Src tyrosine kinase activity is required for PyV middle T antigen-induced mammary tumorigenesis and also illustrate an in vivo genetic approach to the dissection of mitogenic signal transduction pathways.
Nucleic Acid Aptamers as Potential Therapeutic and Diagnostic Agents for Lymphoma (2013)

Lymphomas are cancers that arise from white blood cells and usually present as solid tumors. Treatment of lymphoma often involves chemotherapy, and can also include radiotherapy and/or bone marrow transplantation. There is an un-questioned need for more effective therapies and diagnostic tool for lymphoma. Aptamers are single stranded DNA or RNA oligonucleotides whose three-dimensional structures are dictated by their sequences. The immense diversity in function and structure of nucleic acids enable numerous aptamers to be generated through an iterative <i>in vitro</i> selection technique known as Systematic Evolution of Ligands by EXponential enrichment (SELEX). Aptamers have several biochemical properties that make them attractive tools for use as potential diagnostic and pharmacologic agents. Isolated aptamers may directly inhibit the function of target proteins, or they can also be formulated for use as delivery agents for other therapeutic or imaging cargoes. More complex aptamer identification methods, using whole cancer cells (Cell-SELEX), may identify novel targets and aptamers to affect them. This review focuses on recent advances in the use of nucleic acid aptamers as diagnostic and therapeutic agents and as targeted delivery carriers that are relevant to lymphoma. Some representative examples are also discussed.
cDNA cloning and transcriptional mapping of nine polyadenylylated RNAs encoded by the genome of human respiratory syncytial virus. (1983)

We have isolated cDNA clones representing nine unique poly(A)+ RNAs transcribed from the genome of human respiratory syncytial virus, a paramyxovirus. A cDNA library was constructed by using poly(A)+ RNA from virus-infected cells as template and the Escherichia coli plasmid pBR322 as vector. Viral cDNA clones were identified by hybridization with cDNA probes prepared from viral genomic RNA. The viral clones were grouped into nine different families by hybridization with individual size-selected reverse transcripts representing the major classes of poly(A)+ RNA from virus-infected cells. The largest clone from each family was selected for analysis. These nine clones, molecular sizes ranging from 520 to 2,600 base pairs, were shown to be unrelated on the basis of reciprocal hybridization using dot-blots. These cDNA clones were then used as hybridization probes to analyze intracellular viral RNAs that had been separated by gel electrophoresis and transferred to diazobenzyloxymethyl-paper. All nine clones hybridized with intracellular viral genomic RNA, confirmation of virus specificity. Nine unique intracellular viral poly(A)+ RNAs were identified [molecular sizes ranging from 720 to 7,500 nucleotides, including poly(A)]. Comparison of the sizes of these major RNAs and the cDNA clones indicated that a number of the clones represented nearly complete copies of the corresponding RNAs. Several other intracellular viral poly(A)+ RNAs appeared to be polycistronic by the criteria of molecular weights and homologies to various combinations of cDNA clones. The sizes and sequence contents of these polycistronic RNAs were used to prepare a transcriptional map whose significance is discussed.
Function of the htrB High Temperature Requirement Gene of Escherichia coli in the Acylation of Lipid A (1996)

By assaying lysates of Escherichia coli generated with the hybrid lambda bacteriophages of an ordered library (Kohara, Y., Akiyama, K., and Isono, K. (1987) Cell 50, 495-508), we identified two clones (lambda232 and lambda233) capable of overexpressing the lauroyl transferase that functions after 3-deoxy-D-manno-octulosonic acid (Kdo) addition in lipid A biosynthesis (Brozek, K. A., and Raetz, C. R. H. (1990) J. Biol. Chem. 265, 15410-15417). The E. coli DNA inserts in lambda232 and lambda233 suggested that a known gene (htrB) required for rapid growth above 33 degrees C might encode the lauroyl transferase. Using the intermediate (Kdo)2-lipid IVA as the laurate acceptor, extracts of strains with transposon insertions in htrB were found to contain no lauroyl transferase activity. Cells harboring hybrid htrB+ plasmids overproduced transferase activity 100-200-fold. The overproduced transferase was solubilized with a non-ionic detergent and purified further by DEAE-Sepharose chromatography. With lauroyl acyl carrier protein as the donor, the purified enzyme rapidly incorporated one laurate residue into (Kdo)2-lipid IVA. The rate of laurate incorporation was reduced by several orders of magnitude when either one or both Kdos were absent in the acceptor. With a matched set of acyl-acyl carrier proteins, the enzyme incorporated laurate 3-8 times faster than decanoate or myristate, respectively. Transfer of palmitate, palmitoleate, or R-3-hydroxymyristate was very slow. Taken together with previous studies, our findings indicate that htrB encodes a key, late functioning acyltransferase of lipid A biosynthesis.
Hospital-Onset Infections: A Patient Safety Issue (2002)

Hospital-onset infections, particularly those involving the urinary tract, lung, and bloodstream, are common and costly and cause substantial morbidity. This article analyzes the case of a 78-year-old man with lung cancer who died after developing hospital-onset pneumonia and urinary catheter-related infection during hospitalization for elective removal of a cerebellar metastasis. The field of infection control could benefit by adopting several approaches advocated by patient safety adherents, such as root-cause analysis. For example, hospital-onset infections that are implicated as attributable causes of death should perhaps be reviewed by local infection control teams regardless of the institution's overall infection rates. The patient safety movement can also learn from the traditions of infection control and hospital epidemiology. Specifically, applying infection control-based practices to safety problems may enhance safety. Such practices include establishing clear definitions of adverse events, standardizing methods for detecting and reporting events, creating appropriate rate adjustments for case-mix differences, instituting evidence-based intervention programs, and relying on skilled professionals to promote ongoing improvements in care.
Studies of multibaseline spaceborne interferometric synthetic aperture radars (1990)

The authors have utilized a set of Seasat synthetic aperture radar (SAR) data that were obtained in nearly repeat ground-track orbits to demonstrate the performance of spaceborne interferometric SAR (INSAR) systems. An assessment of the topography measurement capability is presented. A phase measurement error model is described and compared with the data obtained at various baseline separations and signal-to-noise ratios. Finally, the implications of these results on future spaceborne INSAR design are discussed.< <ETX xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">&gt;</ETX>
Toward fault-tolerant quantum computation without concatenation (2001)

It is known that quantum error correction via concatenated codes can be done with exponentially small failure rate if the error rate for physical qubits is below a certain accuracy threshold. Other, unconcatenated codes with their own attractive features such as improved accuracy threshold, local operations, have also been studied. By iteratively distilling a certain two-qubit entangled state it is shown how to perform an encoded Toffoli gate, important for universal computation, on codes whose C-NOT operation is bitwise. For certain codes, over a very large range of block sizes, this technique requires at most one concatenation.
Nonlinear air-to-fuel ratio and engine speed control for hybrid vehicles (2003)

Internal combustion spark ignition engine management systems regulate the fuel, spark, and idle air subsystems to achieve sufficient engine performance at acceptable fuel economy and tailpipe emission levels. Engine control units also monitor other engine processes, using a suite of sensors, and periodically check the system actuators' operation to satisfy legislated onboard diagnostics. The majority of production engines regulate the air-to-fuel ratio using a speed-density, or air-flow, control strategy. In this approach, the mass of air drawn into a given cylinder is calculated using the engine speed, manifold absolute pressure, and inlet air temperature. Based on the air mass, appropriate fuel amounts are injected to achieve stoichiometric operation. However, the wide range of operating conditions, inherent induction process nonlinearities, and gradual component degradations due to aging have prompted research into model-based algorithms. In this paper, a nonlinear model-based control strategy will be proposed for simultaneous air-to-fuel ratio control and speed tracking in hybrid electric vehicles. The motivation for engine speed management resides in the integrated control of the engine and a continuously variable transmission for increased efficiency. The proposed backstepping controller uses an observer to reduce the inputs to manifold air mass (e.g., manifold absolute pressure and inlet air temperature) and engine speed. The underlying engine model describes the air intake, fuel injection, and rotational dynamics. For comparison purposes, an existing multisurface sliding mode controller and an integrated speed-density air-to-fuel controller with attached engine speed regulation have been implemented. The performance of each controller is studied using an analytical engine model with representative numerical results presented and discussed to provide insight into the overall performances.
The effect of angiostatin on vascular leakage and VEGF expression in rat retina (2004)

Angiostatin is a potent angiogenic inhibitor. The present study identified a new activity of angiostatin: reducing vascular leakage, which is associated with diabetic macular edema, tumor growth and inflammation. An intravitreal injection of angiostatin significantly reduced retinal vascular permeability in rats with oxygen-induced retinopathy and in those with streptozotocin-induced diabetes, but not in normal rats. Consistent with its effect on permeability, angiostatin downregulated vascular endothelial growth factor (VEGF) expression in the retina in both the rat models but not in normal controls. These results suggest that the effect of angiostatin on vascular leakage is mediated, at least in part, through blockade of VEGF overexpression.
Comorbid generalized anxiety disorder and its association with quality of life in patients with major depressive disorder (2017)

The comorbidity of major depressive disorder (MDD) and generalized anxiety disorder (GAD) is common and often predicts poorer outcomes than either disorder alone. This study aimed to examine the prevalence of comorbid GAD and its association with quality of life (QOL) among MDD patients. A total of 1225 psychiatric outpatients were screened using the Hospital Anxiety and Depression Scale (HADS). Those who scored ≥8 on the HADS were interviewed using DSM-IV criteria by two senior psychiatrists. Patients diagnosed with MDD were further assessed using the 9-item Patient Health Questionnaire, Social Support Rating Scale, Pittsburgh Sleep Quality Index, and World Health Organization QOL Scale, brief version (WHOQOL-BREF). Ultimately, 667 patients were diagnosed with MDD, of 71.7% of whom had GAD. Compared to those with MDD alone, comorbid patients had lower scores on the physical (38.64 ± 10.35 vs.36.54 ± 12.32, P = 0.026) and psychological (35.54 ± 12.98 vs. 30.61 ± 14.66, P < 0.001) domains of the WHOQOL-BREF. The association between comorbid GAD and poor QOL on the two domains remained statistically significant in the multiple linear regression (unstandardized coefficients: -1.97 and -4.65, P < 0.001). In conclusion, the prevalence of comorbid GAD in MDD patients is high, and co-occurring GAD may exacerbate impaired physical and psychological QOL in Chinese MDD patients.
HIF1α and pancreatic β‐cell development (2012)

During early embryogenesis, the pancreas shows a paucity of blood flow, and oxygen tension, the partial pressure of oxygen (pO(2)), is low. Later, the blood flow increases as β-cell differentiation occurs. We have previously reported that pO(2) controls β-cell development in rats. Here, we checked that hypoxia inducible factor 1α (HIF1α) is essential for this control. First, we demonstrated that the effect of pO(2) on β-cell differentiation in vitro was independent of epitheliomesenchymal interactions and that neither oxidative nor energetic stress occurred. Second, the effect of pO(2) on pancreas development was shown to be conserved among species, since increasing pO(2) to 21 vs. 3% also induced β-cell differentiation in mouse (7-fold, P<0.001) and human fetal pancreas. Third, the effect of hypoxia was mediated by HIF1α, since the addition of an HIF1α inhibitor at 3% O(2) increased the number of NGN3-expressing progenitors as compared to nontreated controls (9.2-fold, P<0.001). In contrast, when we stabilized HIF1α by deleting ex vivo the gene encoding pVHL in E13.5 pancreas from Vhl floxed mice, Ngn3 expression and β-cell development decreased in such Vhl-deleted pancreas compared to controls (2.5 fold, P<0.05, and 6.6-fold, P<0.001, respectively). Taken together, these data demonstrate that HIF1α exerts a negative control over β-cell differentiation.