gebhart/patrepeval huggingface dataset:
Vascular endothelial growth factor (VEGF) in endometriosis (1998)

Angiogenesis is likely to be involved in the pathogenesis of endometriosis. According to the transplantation theory, when the exfoliated endometrium is attached to the peritoneal layer, the establishment of a new blood supply is essential for the survival of the endometrial implant and development of endometriosis. From the known angiogenic factors, vascular endothelial growth factor (VEGF) has emerged as a pivotally important regulator of normal angiogenesis and pathological neovascularization. The VEGF protein was evaluated immunohistochemically in the eutopic endometrium of 10 women without endometriosis (group I) at laparoscopy and the eutopic endometrium and peritoneal endometriotic lesions of 43 women with endometriosis (group II). VEGF histological scores were 9.7 +/- 4.3 and 4.0 +/- 2.6 respectively in the epithelium and stroma of the eutopic endometrium of group I women, and 10.3 +/- 2.3 and 3.6 +/- 2.3 respectively in women of group II. In red lesions, the VEGF scores were 11.1 +/- 3.0 in the epithelium and 5.1 +/- 3.0 in the stroma, and in black lesions were 8.6 +/- 2.7 and 1.6 +/- 1.6, respectively. Significantly lower values were observed in black lesions as compared with eutopic endometrium and red lesions, the values of which were similar. Scores were also evaluated according to the phase of the cycle. In eutopic as well as ectopic endometrium, no significant cyclic variations were observed throughout the cycle. However, VEGF content was found to be higher in the eutopic glandular epithelium of women with endometriosis during the late secretory phase, possibly suggesting a more likely tendency to implant. In contrast, significantly higher VEGF content was noted in red lesions as compared with black lesions. During all phases of the cycle, the VEGF content in stromal cells of red lesions was higher than in black lesions. Similarities in VEGF content were observed in the glandular epithelium of the eutopic endometrium of women with endometriosis and red lesions, suggesting that endometriosis probably arises from the peritoneal seeding of viable endometrial cells during retrograde menstruation and that red lesions can be considered as the first stage of implantation. After the attachment phase, the high VEGF levels could provoke an increase in the subperitoneal vascular network and facilitate implantation and viability in the retroperitoneal space. Lower VEGF levels in black lesions explain the decrease in both stromal vascularization, followed by fibrosis and inactivation of the implant.
PKCδ-Induced PU.1 Phosphorylation Promotes Hematopoietic Stem Cell Differentiation to Dendritic Cells (2010)

Human CD34(+) hematopoietic stem cells (HSCs) exhibit the potential to differentiate into a variety of specialized blood cells. The distinct intracellular mechanisms that control cell fate and lineage commitment of these multipotent cells are not well defined. In this study, we investigate and modulate the signaling processes during HSC differentiation toward myeloid dendritic cells (mDCs). DC differentiation induced by the cytokines Granulocyte macrophage colony-stimulating factor (GM-CSF) and Interleukin-4 (IL-4) led to activation of the Extracellular-signal-regulated kinase (ERK), protein kinase C (PKC), and Janus kinase (JAK)/Signal Transducer and Activator of Transcription (STAT) but not the SAPK/c-Jun NH(2) -terminal kinase and p38 mitogen-activated protein kinase signaling pathways. From the activated signaling pathways the PKC isoform δ was found to phosphorylate the transcription factor PU.1, which is described as one of the key factors for myeloid HSC differentiation. On molecular level, PKCδ regulated PU.1 activity by affecting its transactivation activity, whereas its DNA binding activity remained unaffected. This was accompanied by PKCδ-induced phosphorylation of the PU.1 transactivation domain. Furthermore, treatment with PKC- and ERK1/2-specific signaling inhibitors impaired both HSC differentiation toward mDCs as well as phosphorylation-mediated transactivation activity of PU.1. Taken together, these results provide new insights into the molecular mechanisms promoting the differentiation process of HSCs toward mDCs and introduce the PKC isoform δ as critical mediator.
High-Throughput Time-Resolved FRET Reveals Akt/PKB Activation as a Poor Prognostic Marker in Breast Cancer (2014)

Dysregulation of the Akt/PKB pathway has been associated with poor prognosis in several human carcinomas. Current approaches to assess Akt activation rely on intensity-based methods, which are limited by the subjectivity of manual scoring and poor specificity. Here, we report the development of a novel assay using amplified, time-resolved Förster resonance energy transfer (FRET), which is highly specific and sensitive and can be adapted to any protein. Using this approach to analyze primary breast tissue microarrays, we quantified levels of activated pAkt at a spatial resolution that revealed molecular heterogeneity within tumors. High pAkt status assessed by amplified FRET correlated with worse disease-free survival. Our findings support the use of amplified FRET to determine pAkt status in cancer tissues as candidate biomarker for the identification of high-risk patients.
Compiling Fortran 90D/HPF for Distributed Memory MIMD Computers (1994)

This paper describes the design of the Fortran90D/HPF compiler, a source-to-source parallel compiler for distributed memory systems being developed at Syracuse University. Fortran 90D/HPF is a data parallel language with special directives to specify data alignment and distributions. A systematic methodology to process distribution directives of Fortran 90D/HPF is presented. Furthermore, techniques for data and computation partitioning, communication detection and generation, and the run-time support for the compiler are discussed. Finally, initial performance results for the compiler are presented. We believe that the methodology to process data distribution, computation partitioning, communication system design, and the overall compiler design can be used by the implementors of compilers for HPF.
Fe3O4 Magnetic Nanoparticles as Peroxidase Mimetics and Their Applications in H2O2 and Glucose Detection (2008)

Artificial enzyme mimetics are a current research interest because natural enzymes bear some serious disadvantages, such as their catalytic activity can be easily inhibited and they can be digested by proteases. A very recently study reported by Yan et al. has proven that Fe(3)O(4) magnetic nanoparticles (MNPs) exhibit an intrinsic enzyme mimetic activity similar to that found in natural peroxidases, though MNPs are usually thought to be biological and chemical inert (Gao, L. Z.; Zhuang, J.; Nie, L.; Zhang, J. B.; Zhang, Y.; Gu, N.; Wang, T. H.; Feng, J.; Yang, D. L.; Perrett, S.; Yan, X. Y. Nat. Nanotechnol. 2007, 2, 577-583). In the present work, we just make use of the novel properties of Fe(3)O(4) MNPs as peroxidase mimetics reported by Yan et al. to detect H(2)O(2). The Fe(3)O(4) MNPs were prepared via a coprecipitation method. The as-prepared Fe(3)O(4) MNPs were then used to catalyze the oxidation of a peroxidase substrate 2,2'-azino-bis(3-ethylbenzo-thiazoline-6-sulfonic acid) diammonium salt (ABTS) by H(2)O(2) to the oxidized colored product (see eq 1) which provides a colorimetric detection of H(2)O(2). As low as 3 x 10(-6) mol/L H(2)O(2) could be detected with a linear range from 5 x 10(-6) to 1 x 10(-4) mol/L via our method. More importantly, a sensitive and selective method for glucose detection was developed using glucose oxidase (GOx) and the as-prepared Fe(3)O(4) MNPs. The detection platforms for H(2)O(2) and glucose developed in the present work not only further confirmed that the Fe(3)O(4) MNPs possess intrinsic peroxidase-like activity but also showed great potential applications in varieties of simple, robust, and easy-to-make analytical approaches in the future.
HLA-B*5801 allele as a genetic marker for severe cutaneous adverse reactions caused by allopurinol (2005)

Allopurinol, a commonly prescribed medication for gout and hyperuricemia, is a frequent cause of severe cutaneous adverse reactions (SCAR), which include the drug hypersensitivity syndrome, Stevens-Johnson syndrome, and toxic epidermal necrolysis. The adverse events are unpredictable and carry significant morbidity and mortality. To identify genetic markers for allopurinol-SCAR, we carried out a case-control association study. We enrolled 51 patients with allopurinol-SCAR and 228 control individuals (135 allopurinol-tolerant subjects and 93 healthy subjects from the general population), and genotyped for 823 SNPs in genes related to drug metabolism and immune response. The initial screen revealed strong association between allopurinol-SCAR and SNPs in the MHC region, including BAT3 (encoding HLA-B associated transcript 3), MSH5 (mutS homolog 5), and MICB (MHC class I polypeptide-related sequence B) (P < 10(-7)). We then determined the alleles of HLA loci A, B, C, and DRB1. The HLA-B*5801 allele was present in all (100%) 51 patients with allopurinol-SCAR, but only in 20 (15%) of 135 tolerant patients [odds ratio 580.3 (95% confidence interval, 34.4-9780.9); corrected P value = 4.7 x 10(-24)] and in 19 (20%) of 93 of healthy subjects [393.51 (23.23-6665.26); corrected P value = 8.1 x 10(-18)]. HLA alleles A*3303, Cw*0302, and DRB1*0301 were in linkage disequilibrium and formed an extended haplotype with HLA-B*5801. Our results indicated that allopurinol-SCAR is strongly associated with a genetic predisposition in Han Chinese. In particular, HLA-B*5801 allele is an important genetic risk factor for this life-threatening condition.
c-Jun NH2-terminal Kinase-mediated Activation of Interleukin-1β Converting Enzyme/CED-3-like Protease during Anticancer Drug-induced Apoptosis (1997)

Upon treatment with various anticancer drugs, myeloid leukemia U937 cells undergo apoptosis. In this study, we found that either etoposide (VP-16) or camptothecin (CPT) activated c-Jun N-terminal kinase 1/stress-activated protein kinase (JNK1/SAPK), transient c-jun expression, and ICE (interleukin-1beta converting enzyme)/CED-3-like proteases in U937 cells. Phorbol ester-resistant U937 variant, UT16 cells, displayed a decreased susceptibility to apoptosis induced by these drugs. The drugs did not cause JNK1 activation, c-jun expression, nor activation of ICE/CED-3-like proteases in UT16 cells. As reported previously, benzyloxycarbonyl-Asp-CH2OC(O)-2,6-dichlorobenzene (Z-Asp), a preferential inhibitor of ICE/CED-3-like proteases, blocked the apoptosis of U937 cells. Interestingly, however, Z-Asp did not inhibit JNK1 activation in either VP-16- or CPT-treated U937 cells. The JNK1 antisense oligonucleotides diminished protein expression of JNK1 and inhibited drug-induced apoptosis of U937 cells, whereas sense control oligonucleotides did not. Consistent with this observation, the antisense oligonucleotide-treated cells did not respond to VP-16 or CPT with Z-Asp-sensitive proteases. These results indicate that JNK1 triggers the DNA damaging drug-induced apoptosis of U937 cells by activating Z-Asp-sensitive ICE/CED-3-like proteases.
Gas chromatography multiphoton ionization Fourier transform mass spectrometry (1985)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTGas chromatography multiphoton ionization Fourier transform mass spectrometryThomas M. Sack, David A. McCrery, and Michael L. GrossCite this: Anal. Chem. 1985, 57, 7, 1290–1295Publication Date (Print):June 1, 1985Publication History Published online1 May 2002Published inissue 1 June 1985https://pubs.acs.org/doi/10.1021/ac00284a027https://doi.org/10.1021/ac00284a027research-articleACS PublicationsRequest reuse permissionsArticle Views79Altmetric-Citations38LEARN 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
Altered states: Involvement of phosphorylated CagA in the induction of host cellular growth changes by Helicobacter pylori (1999)

Helicobacter pylori , present in half of the world’s population, is a very successful pathogen. It can survive for decades in the human stomach with few obvious consequences to the host. However, it is also the cause of gastric diseases ranging from gastritis to ulcers to gastric cancer and has been classified a type 1 carcinogen by the World Health Organization. We have previously shown that phosphorylation of a 145-kDa protein and activation of signal transduction pathways are associated with the attachment of H. pylori to gastric cells. Here we identify the 145-kDa protein as the H. pylori CagA protein. We also show that CagA is necessary to induce a growth-factor-like phenotype (hummingbird) in host gastric cells similar to that induced by hepatocyte growth factor (HGF). Additionally, we identify a second cellular phenotype induced after attachment by H. pylori, which we call SFA (stress fiber associated). SFA is CagA independent and is produced by type I and type II H. pylori .
Proton magnetic resonance study of polydeoxyriboadenylic acid (1971)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTProton magnetic resonance study of polydeoxyriboadenylic acidJames L. Alderfer and Stanford L. SmithCite this: J. Am. Chem. Soc. 1971, 93, 26, 7305–7314Publication Date (Print):December 1, 1971Publication History Published online1 May 2002Published inissue 1 December 1971https://pubs.acs.org/doi/10.1021/ja00755a031https://doi.org/10.1021/ja00755a031research-articleACS PublicationsRequest reuse permissionsArticle Views66Altmetric-Citations13LEARN 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
The multimedia fax-MIME gateway (1994)

New standards may help bridge the rapidly growing communities of the Internet and facsimile machine users. One of these is the Internet standard proposed in July 1992 which provides enhanced capabilities for e-mail. This new standard, Multipurpose Internet Mail Extensions (MIME), lets users exchange multiple-media mail messages over the Internet. The fax-MIME gateway takes advantage of these developments to offer fax services to Internet users and Internet services to multimedia fax users.< <ETX xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">&gt;</ETX>
Space division multiple access (SDMA) for robust ad hoc vehicle communication networks (2002)

Proposes a robust, self-organizing architecture for mobile ad hoc networks. The network architecture, space division multiple access (SDMA), relies on user location information and provides users access to the communication channel based on their location. SDMA divides the geographical space, where users are located, into smaller spaces. The key element of the design is a one-to-one map between the space division and the bandwidth division of time slots, frequency division, etc. Therefore, SDMA is compatible with any multiple access scheme such as TDMA, FDMA, and CDMA. The system requirement is the user information of its location and a priori knowledge of the one-to-one map of location to the bandwidth division. The scheme is self-starting and self-maintaining. It provides collision-free access to the communication medium for the users and facilitates communication address resolution amongst the users. In addition, SDMA guarantees delay-bounded communication. The paper presents the SDMA architecture and discusses its advantages and disadvantages. Moreover, enhanced SDMA is suggested to increase bandwidth efficiency.
Regulation of a TRPM7-like Current in Rat Brain Microglia (2003)

Non-excitable cells use Ca2+ influx for essential functions but usually lack voltage-gated Ca2+ channels. The main routes of Ca2+ entry appear to be store-operated channels or Ca2+-permeable non-selective cation channels, of which the magnesium-inhibited cation (or magnesium-nucleotide-regulated metal cation) current has received considerable recent attention. This current appears to be produced by one of the recently cloned transient receptor potential (TRP) channels, TRPM7. In this study of rat microglia, we identified TRPM7 transcripts and a prevalent current with the hallmark biophysical and pharmacological features of TRPM7. This is the first identification of a TRPM7-like current in the brain. There is little known about how members of the TRPM sub-family normally become activated. Using whole-cell patch clamp recordings from rat microglia, we found that the TRPM7-like current activates spontaneously after break-in and that the current and its activation are inhibited by elevated intracellular Mg2+ but not affected by cell swelling or a wide range of intracellular Ca2+ concentrations. The TRPM7-like current in microglia appears to depend on tyrosine phosphorylation. It was inhibited by several tyrosine kinase inhibitors, including a peptide (Src 40-58) that was shown previously to inhibit Src actions, but not by inactive drugs or peptide analogues. The current did not depend on the cell activation state; i.e. it was the same in microglia recently removed from the brain or when cultured under a wide range of conditions that favor the resting or activated state. Because TRPM7 channels are permeable to Ca2+, this current may be important for microglia functions that depend on elevations in intracellular Ca2+.
A method of small object detection and tracking based on particle filters (2008)

In this paper an efficient method of small object localization is proposed that integrates detection and tracking. The system is initialized using a strong detector and then it locates the object over time using a weak detector and a temporal tracker. Both of strong and weak detectors are based on foreground-background segmentation. The strong detector is created from shape analysis of foreground blobs and used to trigger the object tracker. The weak detector is built with outputs from the foreground detection likelihood and integrated into the trackerpsilas observation likelihood. In the particle filter-based object tracker, motion estimation is embedded to generate a better proposal distribution and a mixture model is tailored to handle the ambiguity of template matching due to cluttered background. As a case study, the proposed scheme is applied to ball detection and tracking in soccer game videos. Promising results are presented to illustrate the proposed method effectively handles heavy clutter, occlusion and motion blur.
Targeted therapy for the treatment of imatinib-resistant chronic myeloid leukemia: A pharmacogenetic analysis (2005)

Background/Aims Chronic myeloid leukemia (CML) is driven by the enzymatic activity of BCR-ABL, a tyrosine kinase that is selectively inhibited by imatinib. However, a subset of patients develop resistance. BMS-354825 retains in vitro activity against 14 out of 15 imatinib-resistant forms of BCR-ABL in the nanomolar concentration range. BMS-354825 is currently undergoing analysis in a phase I clinical trial of imatinib-resistant or -intolerant CML cases. We sought to determine if a correlation exists between specific kinase domain mutation and response to BMS-354825. Methods Fifteen patients were included in the analysis. All had a diagnosis of Philadelphia chromosome-positive CML, and were either imatinib-resistant or -intolerant. Sequencing of the BCR-ABL kinase domain was performed prior to treatment. The achievement of a complete hematologic response was correlated with BCR-ABL genotype. Results Preliminary analysis suggests a strong correlation between response and absence of the T315I mutation, and no significant response in cases of the T315I mutant. These data corroborate our preclinical results, and identify the T315I mutation as a potentially major component of clinical resistance to BMS-354825. Conclusions These studies suggest an evolving role for patient-specific therapy based upon the specific genotype of the target gene in human cancers treated with the burgeoning class of small molecule kinase inhibitors, and warrant confirmatory analysis in a larger cohort of patients. Clinical Pharmacology & Therapeutics (2005) 77, P17–P17; doi: 10.1016/j.clpt.2004.11.066
Peptides Constrained by an Aliphatic Linkage between Two CαSites:  Design, Synthesis, and Unexpected Conformational Properties of ani,(i+4)-Linked Peptide (2001)

A novel route for the synthesis of cyclic peptides constrained by an aliphatic bridge between two C(alpha)sites, using a triply orthogonal protecting group strategy, is described. The synthesis of the orthogonally protected bis-amino acid 1, via an enantioselective route utilizing the Schöllkopf and Evans methodologies, is first described. This is then incorporated into a short, alanine-rich peptide 13, using a novel triply orthogonal protecting group strategy to couple first one, then the other, amino acid moiety in such a way that an aliphatic bridge is formed between the i and i + 4 positions. Unexpectedly, the resulting constrained peptide does not adopt a helical conformation: instead, it is shown by CD at low temperature to adopt a left-handed type II beta-turn conformation in aqueous media and a right-handed type I beta-turn conformation in TFE.
A Multipath QoS Routing with Route Stability for Mobile Ad Hoc Networks (2010)

AbstractMultihop wireless networks have emerged recently as an evolution of wireless network technology and are likely to be the integral part of future communication environment. In this context, support for quality of service (QoS) is becoming an inherent necessity rather than an additional feature of the network. This paper presents a route stability-based multipath QoS routing protocol for mobile ad hoc networks to support throughput and delay sensitive real-time applications in these networks. We incorporate a hop-by-hop admission control and a soft resource reservation scheme in a route discovery process to ensure QoS assurance to real-time applications. Further, a simple route stability model is utilized during both route discovery and maintenance phases for selecting QoS routes with higher stability. The reliability of the multiple QoS routes is improved through node disjointness and stability properties of the discovered routes. Following an effective QoS violation detection and route maintenance...