gebhart/patrepeval huggingface dataset:
Attenuation of chronic hypoxic pulmonary hypertension by simvastatin (2003)

The 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) have been shown to improve multiple normal endothelial cell functions and inhibit vascular wall cell proliferation. We hypothesized that one such agent, simvastatin, would attenuate chronic hypoxic pulmonary hypertension. Male adult Sprague-Dawley rats were exposed (14 days) to normoxia (N), normoxia plus once-a-day administered simvastatin (20 mg/kg ip) (NS), hypoxia (10% inspired O2 fraction) (H), or hypoxia plus simvastatin (HS). Mean pulmonary artery pressure, measured in anesthetized, ventilated rats with an open-chest method, was reduced from 25 +/- 2 mmHg in H to 18 +/- 1 in HS (P < 0.001) but did not reach normoxic values (12 +/- 1 mmHg). Similarly, right ventricular/left ventricular plus interventricular septal weight was reduced from 0.53 +/- 0.02 in the H group to 0.36 +/- 0.02 in the HS group (P < 0.001). The increased hematocrit in H (0.65 +/- 0.02) was prevented by simvastatin treatment (0.51 +/- 0.01, P < 0.001). Hematocrit was similar in N versus NS. Alveolar vessel muscularization and medial thickening of vessels 50-200 microM in diameter induced by hypoxia were also significantly attenuated in the HS animals. Lung endothelial nitric oxide synthase (eNOS) protein expression in the HS group was less than H (P < 0.01) but was similar in N versus NS. We conclude that simvastatin treatment potently attenuates chronic hypoxic pulmonary hypertension and polycythemia in rats and inhibits vascular remodeling. Enhancement of lung eNOS expression does not appear to be involved in mediating this effect.
Detection and formation mechanism of micro-defects in ultrafine pitch Cu—Cu direct bonding (2016)

In this paper, Cu–Cu interconnects with ultrafine pad pitches of 6 μm, 8 μm, and 15 μm are implemented on the 12 inch wafers by a direct bonding process. Defects are not found by traditional non-destructive (NDT) c-mode scanning acoustic microscopy (c-SAM). However, cross sectional observation of bonding interfaces reveals that micro-defects such as micro seams are located at SiO2 bonding interfaces. In order to examine the micro-defects in the ultra-fine pitch direct bonding process by the NDT technology, a novel defect-enlarged approach is proposed. The bonded dies are first annealed in an N2 oven at 300 °C for a few hours and then cooled quickly in air. The c-SAM scanning images show large defects at the place where nothing can be detected by c-SAM before this treatment. Cross sectional observation of the bonding interfaces indicates that these defects consist of large size micro seams at the SiO2 bonding interface, especially near Cu pads with an ultrafine pitch of 6 μm. However, these large defects disappear after several hours at room temperature, observed by c-SAM. It is inferred that the disappearance of these defects inspected by the defect-enlarged approach results from the combination of intrinsic micro seams and weak bonds in the silicon oxide layer. Then the underlying physical mechanism of these micro-defects is proposed, which is influenced by Cu pad surface topology and bonding models.
Polymer additives mixture analysis using pulsed-field gradient NMR spectroscopy (1998)

The analysis of mixtures is a problem commonly faced in analytical chemistry. In this work, pulsed-field gradient NMR (PFG-NMR) experiments were used to analyze mixtures of polymer additives and simple polymer solutions. PFG-NMR experiments were also utilized to determine diffusion coefficients of the individual components of a mixture and in this way facilitate resonance assignments. This strategy is particularly useful for molecules containing isolated protons that are not amenable to the standard two-dimensional NMR experiments based on J-coupling. PFG-NMR was also used to edit the NMR spectra of polymer solutions by eliminating the resonances of fast-diffusing components such as low molecular weight additives or residual solvent. Diffusion ordered spectroscopy (DOSY) was used for the analysis of the PFG-NMR data. The DOSY method produces a two-dimensional spectrum that correlates chemical shift with the calculated diffusion coefficient, and simplifies the analysis of many complex mixtures. For well resolved resonances, the correct diffusion coefficient is unambiguously determined. The DOSY analysis was able to resolve the diffusion coefficients of most of the components in the mixtures examined. However, in some cases of overlapped resonances and components with similar diffusion coefficients, a single diffusion coefficient was determined which was the weighted average of the two components. ©1998 John Wiley & Sons, Ltd.
Posttherapy pathologic stage predicts survival in patients with esophageal carcinoma receiving preoperative chemoradiation (2005)

Posttherapy pathologic stage was the best available predictor of outcome for patients with locoregional carcinoma of the esophagus or esophagogastric junction who underwent chemoradiation therapy followed by esophagectomy. The findings in the current study supported the concept of downstaging by preoperative therapy.
Efficient Nitrogen Ring-Expansion Process Facilitated by in Situ Hemiketal Formation. An Asymmetric Schmidt Reaction (1995)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTEfficient Nitrogen Ring-Expansion Process Facilitated by in Situ Hemiketal Formation. An Asymmetric Schmidt ReactionVijaya Gracias, Gregory L. Milligan, and Jeffrey AubeCite this: J. Am. Chem. Soc. 1995, 117, 30, 8047–8048Publication Date (Print):August 1, 1995Publication History Published online1 May 2002Published inissue 1 August 1995https://pubs.acs.org/doi/10.1021/ja00135a036https://doi.org/10.1021/ja00135a036research-articleACS PublicationsRequest reuse permissionsArticle Views1688Altmetric-Citations85LEARN 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 (2)»Supporting Information Supporting Information Get e-Alerts
Pulsewidth modulation control of electronic ballast for dimming control of fluorescent lamps (2002)

The design of a resonant-inverter for the control of high efficiency lamps is presented. The topology of the circuit is a full-bridge parallel resonant-converter that switches at fixed frequency, and incorporates a pulsewidth modulation (PWM) method to control the output power. Expressions are provided that are fundamental for the design and the understanding of the operational principle. With a proposed lamp model and using it as the load of the inverter, the circuit operation is analysed. The experimental results of the design are compared with calculations and HSPICE simulations.
Lysine acetyltransferase 8 is involved in cerebral development and syndromic intellectual disability (2019)

Epigenetic integrity is critical for many eukaryotic cellular processes. An important question is how different epigenetic regulators control development and influence disease. Lysine acetyltransferase 8 (KAT8) is critical for acetylation of histone H4 at lysine 16 (H4K16), an evolutionarily conserved epigenetic mark. It is unclear what roles KAT8 plays in cerebral development and human disease. Here, we report that cerebrum-specific knockout mice displayed cerebral hypoplasia in the neocortex and hippocampus, along with improper neural stem and progenitor cell (NSPC) development. Mutant cerebrocortical neuroepithelia exhibited faulty proliferation, aberrant neurogenesis, massive apoptosis, and scant H4K16 propionylation. Mutant NSPCs formed poor neurospheres, and pharmacological KAT8 inhibition abolished neurosphere formation. Moreover, we describe KAT8 variants in 9 patients with intellectual disability, seizures, autism, dysmorphisms, and other anomalies. The variants altered chromobarrel and catalytic domains of KAT8, thereby impairing nucleosomal H4K16 acetylation. Valproate was effective for treating epilepsy in at least 2 of the individuals. This study uncovers a critical role of KAT8 in cerebral and NSPC development, identifies 9 individuals with KAT8 variants, and links deficient H4K16 acylation directly to intellectual disability, epilepsy, and other developmental anomalies.
Double stranded DNA sequencing as a choice for DNA sequencing (1988)

Journal Article Double stranded DNA sequencing as a choice for DNA sequencing Get access Hong Zhang, Hong Zhang Search for other works by this author on: Oxford Academic PubMed Google Scholar Randy Scholl, Randy Scholl 1Genetics Department, Ohio State UniversityColumbus, OH 43210, USA Search for other works by this author on: Oxford Academic PubMed Google Scholar John Browse, John Browse Search for other works by this author on: Oxford Academic PubMed Google Scholar Chris Somerville Chris Somerville Search for other works by this author on: Oxford Academic PubMed Google Scholar Nucleic Acids Research, Volume 16, Issue 3, 11 February 1988, Page 1220, https://doi.org/10.1093/nar/16.3.1220 Published: 11 February 1988 Article history Accepted: 23 October 1987 Published: 11 February 1988
Evidence of Interaction Network Evolution by Whole-Genome Duplications: A Case Study in MADS-Box Proteins (2006)

Recent investigations on metazoan transcription factors (TFs) indicate that single-gene duplication events and the gain and loss of protein domains are 2 crucial factors in shaping their protein-protein interaction networks. Plant genomes, on the other hand, have a history of polyploidy and whole-genome duplications (WGDs), and thus, their study helps to understand whether WGDs have also had a significant influence on protein network evolution. Here we investigate the evolution of the interaction network in the well-studied MADS domain MIKC-type proteins, a TF family which plays an important role in both the vegetative and the reproductive phases of plant life. We combine phylogenetic reconstruction, protein domain analysis, and interaction data from different species. We show that, unlike previously analyzed interaction networks, the MIKC-type protein network displays a characteristic topology, with overall high inter-subfamily connectivity, shared interactors between paralogs, and conservation of interaction patterns across species. The evaluation of the number of MIKC-type proteins at key time points throughout the evolution of land plants in the lineage leading to Arabidopsis suggested that most duplicates were retained after each round of WGD. We provide evidence that an initial network, formed by 9-11 homodimerizing proteins interacting with each other, existed in the common ancestor of all seed plants. This basic structure has been conserved after each round of WGD, adding layers of paralogs with similar interaction patterns. We thus present the first model where we can show that a network of eukaryotic TFs has evolved via rounds of WGD. Furthermore, we found that in subfamilies in which the K domain is most diverged, the interactions with other subfamilies have been largely lost. We discuss the possibility that such a high proportion of genes were retained after each WGD because of their capacity to form higher order complexes involving proteins from different subfamilies. The simultaneous duplications allowed for the conservation of the quantitative balance between the constituents and facilitated sub- and neofunctionalization through differential expression of whole units.
Component of Human Complement (C'3) (1969)

A B S T R A C T A kindred has been investigated in which seven individuals were found to have half-normal serum concentrations of the third component of complement (C'3). This partial deficiency was transmitted as an autosomal dominant trait. Affected individuals were entirely healthy. Hemolytic complement titers were slightly reduced but immune adherence titers and reagent titrations of the classical complement components were normal. Examination for C'3 allotypes revealed that all affected individuals had patterns resembling those of homozygotes. Analysis of the inheritance of C'3 structural genes disclosed that the most likely mechanism for partial C'3 deficiency in this family was nonexpression of one allele.
Using Clickstream Data to Predict WWW Usage (2018)

The purpose of this study is to consider the determinants of World Wide Web (WWW) usage using clickstream data. Clickstream data is a natural byproduct of a user accessing WWW pages, and refers to the sequence of pages visited and the time these pages were viewed. A key component of this study is a large scale empirical analysis of clickstream data from a representative sample of PC owning households in the U.S. This sample comes from Media Metrix's PC Meter using a nationwide panel of over 5,000 households during 1997 and 1998. A primary finding of this research is that demographics are not a primary driver of web usage. While it is true that access to the WWW is influenced by demographic characteristics, the best way to predict current usage is to use information about past usage, and not use demographics. Additionally, we show there is a great deal of diversity in the usage of individual sites. These findings imply that if managers really want to learn how to fulfill the promise of interactivity on the WWW they need to learn how to capture and use their customers' clickstreams.
The Myth of Measurable Disease in Ovarian Cancer: Revisited (2009)

There are well-documented and serious limitations associated with analyzing measurable disease in ovarian cancer as a sole primary endpoint in clinical trials, as this focus requires the presence of individual tumor masses of sufficient size and distinctive shape to image. An alternative highly rational strategy adds the routine monitoring of validated serum tumor markers (e.g., CA-125), which can more adequately define changes in "tumor volume" associated with small nonvisualized macroscopic and diffuse microscopic cancer.
Optical properties of conducting polymers (1988)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTOptical properties of conducting polymersA. O. Patil, A. J. Heeger, and Fred WudlCite this: Chem. Rev. 1988, 88, 1, 183–200Publication Date (Print):January 1, 1988Publication History Published online1 May 2002Published inissue 1 January 1988https://pubs.acs.org/doi/10.1021/cr00083a009https://doi.org/10.1021/cr00083a009research-articleACS PublicationsRequest reuse permissionsArticle Views6185Altmetric-Citations896LEARN 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
In vitro generation of CD83+ human blood dendritic cells for active tumor immunotherapy. (1997)

There is increasing clinical interest in dendritic cells that are capable of initiating antitumor immune responses. Dendritic cells cultured from human blood mononuclear cells using granulocyte/macrophage colony-stimulating factor (GM-CSF) and interleukin-4 (IL-4) are competent for antigen uptake but express relatively low levels of costimulatory molecules and thus correspond to immature resident tissue dendritic cells. In this study we took advantage of the new dendritic cell-specific marker CD83, which is expressed by mature dendritic cells, to delineate the maturation of cultured human blood dendritic cells. Although dendritic cells cultured with GM-CSF and IL-4 contained transcripts for CD83 as determined by reverse transcription PCR, CD83 protein was barely detectable by flow cytometry, confirming that dendritic cells obtained with this system are immature. However, treatment of dendritic cells with tumor necrosis factor-alpha (TNF-alpha) significantly increased the levels of CD83 transcripts and induced CD83 protein expression in dendritic cells. In contrast to the initiation of dendritic cell culture, which was facilitated by high cell density (5 x 10(6) cells/mL), differentiation into CD83+ dendritic cells required a low cell concentration (0.5 x 10(6) cells/mL). At higher cell density (1 x 10(6) cells/mL), CD83 expression was suppressed and was almost completely prevented at 2 x 10(6) cells/mL. Induction of CD83 expression was accompanied by a strong upregulation of the costimulator B7-2 (CD86) on dendritic cells. While untreated CD83(-) dendritic cells efficiently internalized fluoresceinated Dextran, TNF-alpha treated CD83+ dendritic cells excluded these molecules, confirming that maturation of dendritic cells was associated with the silencing of the antigen-capturing machinery. Morphologically, CD83+ dendritic cells presented with pronounced cytoplasmic projections (veils) characteristic of mature dendritic cells. In summary, we show that cell density critically regulates dendritic cell development. Knowledge of the appropriate conditions for dendritic cell generation and maturation will be important in clinical immunotherapy settings.
A potential mechanism of "cross-talk" between the p55 tumor necrosis factor receptor and Fas/APO1: proteins binding to the death domains of the two receptors also bind to each other. (1996)

The p55 tumor necrosis factor (TNF) receptor and Fas/APO1 induce cell death via distinct regions in their intracellular domains. Three cytoplasmic proteins that bind to these receptor regions have been identified recently. One, MORT1 (also called FADD), binds to Fas/APO1 but not to p55-R; another, TRADD, binds to the p55 TNF receptor but not to Fas/APO1; and the third, RIP, binds weakly to both receptors. The regions within these proteins that are involved in binding to the receptors and the receptor regions to which they bind share a common sequence motif, that of the "death domain." This study shows that the death domain motifs in MORT1, TRADD, and RIP bind effectively to each other, a mode of binding that may allow "cross-talk" between the functional expression of the p55 TNF receptor and Fas/APO1.
Colicin V can be produced by lactic acid bacteria (1999)

Colicin V is a small, proteinaceous bacterial toxin, produced by many strains of Escherichia coli and other members of the Enterobacteriaceae, that fits the definition of class II bacteriocins of Gram-positive bacteria. Export of colicin V is dependent on specific ABC (ATP-binding cassette) secretion proteins which recognize a double-glycine-type leader peptide on the immature colicin V bacteriocin. Replacement of the colicin V leader peptide by a signal peptide from the signal sequence-dependent bacteriocin divergicin A allowed expression of colicin V in lactic acid bacteria. This system may serve as a model for the heterologous expression of other small bacteriocins active against Gram-negative bacteria and other antibacterial peptides from lactic acid bacteria.
Proteomic analysis of seminal plasma from asthenozoospermia patients reveals proteins that affect oxidative stress responses and semen quality (2009)

Asthenozoospermia (AS) is a common cause of human male infertility. In one study, more than 80% of the samples from infertile men had reduced sperm motility. Seminal plasma is a mixture of secretions from the testis, epididymis and several male accessory glands, including the prostate, seminal vesicles and Cowper's gland. Studies have shown that seminal plasma contains proteins that are important for sperm motility. To further explore the pathophysiological character of AS, we separated the seminal plasma proteins from AS patients and healthy donors using sodium dodecyl sulfate polyacrylamide gel electrophoresis and in-gel digestion, and then subjected the proteins to liquid chromatography-mass spectrometry (LC-MS/MS) analysis. A total of 741 proteins were identified in the seminal plasma, with a false discovery rate of 3.3%. Using spectral counting, we found that 45 proteins were threefold upregulated and 56 proteins were threefold downregulated in the AS group when compared with the control. Most of these proteins originated from the epididymis and prostate. This study identified a rich source of biomarker candidates for male infertility and indicates that functional abnormalities of the epididymis and prostate can contribute to AS. We identified DJ-1-a protein that has been shown elsewhere to be involved in the control of oxidative stress (OS)-as a downregulated protein in AS seminal plasma. The levels of DJ-1 in AS seminal plasma were about half of those in the control samples. In addition, the levels of reactive oxygen species were 3.3-fold higher in the AS samples than in the controls. Taken together, these data suggest that downregulation of DJ-1 is involved in OS in semen, and therefore affects the quality of the semen.
Determinants of anti-vascular action by combretastatin A-4 phosphate: role of nitric oxide (2000)

The anti-vascular action of the tubulin binding agent combretastatin A-4 phosphate (CA-4-P) has been quantified in two types of murine tumour, the breast adenocarcinoma CaNT and the round cell sarcoma SaS. The functional vascular volume, assessed using a fluorescent carbocyanine dye, was significantly reduced at 18 h after CA-4-P treatment in both tumour types, although the degree of reduction was very different in the two tumours. The SaS tumour, which has a higher nitric oxide synthase (NOS) activity than the CaNT tumour, showed approximately 10-fold greater resistance to vascular damage by CA-4-P. This is consistent with our previous findings, which showed that NO exerts a protective action against this drug. Simultaneous administration of CA-4-P with a NOS inhibitor, N(omega)-nitro-L-arginine (L-NNA), resulted in enhanced vascular damage and cytotoxicity in both tumour types. Administration of diethylamine NO, an NO donor, conferred protection against the vascular damaging effects. Following treatment with CA-4-P, neutrophil infiltration into the tumours, measured by myeloperoxidase (MPO) activity, was significantly increased. Levels of MPO activity also correlated with the levels of vascular injury and cytotoxicity measured in both tumour types. Neutrophilic MPO generates free radicals and may therefore contribute to the vascular damage associated with CA-4-P treatment. MPO activity was significantly increased in the presence of L-NNA, suggesting that the protective effect of NO against CA-4-P-induced vascular injury may be, at least partially, mediated by limiting neutrophil infiltration. The data are consistent with the hypothesis that neutrophil action contributes to vascular injury by CA-4-P and that NO generation acts to protect the tumour vasculature against CA4-P-induced injury. The protective effect of NO is probably associated with an anti-neutrophil action.