gebhart/patrepeval huggingface dataset:
Assessment of Minimal Residual Disease in Standard-Risk AML (2016)

The presence of minimal residual disease, as determined by quantitation of NPM1-mutated transcripts, provided powerful prognostic information independent of other risk factors. (Funded by Bloodwise and the National Institute for Health Research; Current Controlled Trials number, ISRCTN55675535.).
Selection rules for singlet-oxygen reactions. Concerted addition reactions (1969)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTSelection rules for singlet-oxygen reactions. Concerted addition reactionsDavid R. KearnsCite this: J. Am. Chem. Soc. 1969, 91, 24, 6554–6563Publication Date (Print):November 1, 1969Publication History Published online1 May 2002Published inissue 1 November 1969https://pubs.acs.org/doi/10.1021/ja01052a003https://doi.org/10.1021/ja01052a003research-articleACS PublicationsRequest reuse permissionsArticle Views581Altmetric-Citations136LEARN 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
Novel anticancer prodrugs of butyric acid. 2 (1992)

The antitumor activity of novel prodrugs butyric acid was examined. The in vitro effect of the compounds on induction of cytodifferentiation and on inhibition of proliferation and clonogenicity showed that (pivaloyloxy)methyl butyrate (1a) (labeled AN-9) was the most active agent. SAR's suggested that its activity stemmed from hydrolytically released butyric acid. In vivo, 1a displayed antitumor activity in B16F0 melanoma primary cancer model, manifested by a significant increase in the life span of the treated animals. Murine lung tumor burden, induced by injection of the highly metastatic melanoma cells (B16F10.9), was decreased by 1a. It also displayed a significant therapeutic activity against spontaneous metastases which were induced by 3LL Lewis lung carcinoma cells. Moreover, 1a has the advantage of low toxicity, with an acute LD50 = 1.36 +/- 0.1 g/kg (n = 5). These results suggest that 1a is a potential antineoplastic agent.
A Meta-Analytic Review of Double-Blind, Placebo-Controlled Trials of Antidepressant Efficacy of Omega-3 Fatty Acids (2007)

Although our meta-analysis showed significant antidepressant efficacy of omega-3 PUFAs, it is still premature to validate this finding due to publication bias and heterogeneity. More large-scale, well-controlled trials are needed to find out the favorable target subjects, therapeutic dose of EPA, and the composition of omega-3 PUFAs in treating depression.
Cooperative Inhibition of Renal Cancer Growth by Anti-Epidermal Growth Factor Receptor Antibody and Protein Kinase A Antisense Oligonucleotide (1998)

The combination of anti-EGFR MAb C225 and ited cooperative antiproliferative effects and cooperative antitumor effects on EGFR and PKAI-expressing human renal cancer cell lines.
Integrated Pipeline for Mass Spectrometry-Based Discovery and Confirmation of Biomarkers Demonstrated in a Mouse Model of Breast Cancer (2007)

Despite their potential to impact diagnosis and treatment of cancer, few protein biomarkers are in clinical use. Biomarker discovery is plagued with difficulties ranging from technological (inability to globally interrogate proteomes) to biological (genetic and environmental differences among patients and their tumors). We urgently need paradigms for biomarker discovery. To minimize biological variation and facilitate testing of proteomic approaches, we employed a mouse model of breast cancer. Specifically, we performed LC-MS/MS of tumor and normal mammary tissue from a conditional HER2/Neu-driven mouse model of breast cancer, identifying 6758 peptides representing >700 proteins. We developed a novel statistical approach (SASPECT) for prioritizing proteins differentially represented in LC-MS/MS datasets and identified proteins over- or under-represented in tumors. Using a combination of antibody-based approaches and multiple reaction monitoring-mass spectrometry (MRM-MS), we confirmed the overproduction of multiple proteins at the tissue level, identified fibulin-2 as a plasma biomarker, and extensively characterized osteopontin as a plasma biomarker capable of early disease detection in the mouse. Our results show that a staged pipeline employing shotgun-based comparative proteomics for biomarker discovery and multiple reaction monitoring for confirmation of biomarker candidates is capable of finding novel tissue and plasma biomarkers in a mouse model of breast cancer. Furthermore, the approach can be extended to find biomarkers relevant to human disease.
Multicellular spheroids: a three‐dimensionalin vitroculture system to study tumour biology (1998)

The growth of tumour cells as three-dimensional multicellular spheroids in vitro has led to important insights in tumour biology, since properties of the in vivo-tumour such as proliferation or nutrient gradients, can be studied under controlled conditions. While this review starts with an update of recent data on spheroid monocultures, especially concerning tumour microenvironment and therapeutic modalities, the main emphasis is put on the spectrum of heterologous cultures which have evolved in previous years. This type of culture includes tumour cell interaction with endothelial, fibroblast or immunocompetent cells. The relation of the spheroid culture model to other types of three-dimensional culture and our critical evaluation and presentation of the technical aspects of growing and analysing spheroids are included in the text. These topics are chosen to help the experimental pathologist design experiments with tumour spheroids and to stimulate discussion.
Blood and Marrow Transplantation (BMT) in Adult ACUTE Leukemia Patients in Cuba: Current Results and Future Opportunities through International Collaboration (2017)

In low-middle-income countries (LMIC) cancer care is limited by lack of patients' access to care and/or unaffordable cost of treatment. In contrast with many other LMIC, in Cuba any standard treatment for acute leukemias, including BMT, is available for free. However, laboratories do not always provide immunophenotypic, cytogenetic or molecular tests to support the diagnosis or the management of leukemias, and BMT centers do not have access to international donor registries. In this retrospective study we analyzed the results of BMT in adult acute leukemia patients transplanted at the Hermanos Ameijeiras Hospital in Havana (Cuba) from June 1986 to January 2016. A total of 101 consecutive cases (83 acute myeloid leukemia [AML] and 18 acute lymphoblastic leukemia [ALL]) were transplanted. Eligibility criteria for BMT included: age >16 and <60; achievement of morphologic complete remission and no severe comorbidities according to standard BMT criteria. Patients who had an HLA matched related donor (MRD) received an allogeneic BMT, whereas all the others received an autologous BMT. Stem cell source was fresh bone marrow in 80% of patients, fresh G-CSF mobilized peripheral blood (PBSC) in 19%, and only 1 cord blood transplant was attempted in a patient without a MRD. Of 83 AML patients, 36 received an allogeneic (AML-allo) and 47 an autologous (AML-auto) stem cell transplant. Median age in AML-allo and AML-auto groups was 37 (range:22-54) and 36 (range: 18-58) years, respectively. Median follow-up was 50.4 months (range:1-288) in AML-allo and 50.7 months (range: 1-324) in AML-auto. This is in part due to the policy that patients from outside Havana return to their primary hematologist within 1-2 years after transplant. In addition, some patients left Cuba soon after transplant. Of 36 AML-allo 36% died of transplant-related-mortality (TRM) and 25% of relapse. On the contrary, of 47 AML-auto 17% died of TRM and 40% of relapse. Overall survival (OS) was 38% in AML-allo and 42% in AML-auto. Of 18 ALL patients, 7 received an allogeneic (ALL-allo) and 11 and autologous (ALL-auto) transplant. Median age in the two groups was 36 (range: 18-47) and 27 (range:17-34) years, respectively. Of 7 ALL-allo cases, 1 died of TRM and 3 of relapse (OS 43%). Of 11 ALL-auto cases 4 patients died, all due to relapse (OS 64%). In conclusion, BMT is available for acute leukemia patients in Cuba. Despite limited resources, we envision that through an active collaboration with UIC the BMT program at the Hermanos Ameijeiras Hospital may: improve disease risk assessment of patients through cytogenetic and molecular technologies, implement stem cell cryopreservation, initiate haploidentical transplantation for patients without a MRD, apply reduced intensity conditioning regimens in elderly patients. Support of training and development of research infrastructures remain of key importance in global BMT.
Identification of Klebsiella pneumoniae virulence determinants using an intranasal infection model (2005)

Klebsiella pneumoniae is a Gram-negative enterobacterium that has historically been, and currently remains, a significant cause of human disease. It is a frequent cause of urinary tract infections and pneumonia, and subsequent systemic infections can have mortality rates as high as 60%. Despite its clinical significance, few virulence factors of K. pneumoniae have been identified or characterized. In this study we present a mouse model of acute K. pneumoniae respiratory infection using an intranasal inoculation method, and examine the progression of both pulmonary and systemic disease. Wild-type infection recapitulates many aspects of clinical disease, including significant bacterial growth in both the trachea and lungs, an inflammatory immune response characterized by dramatic neutrophil influx, and a steady progression to systemic disease with ensuing mortality. These observations are contrasted with an infection by an isogenic capsule-deficient strain that shows an inability to cause disease in either pulmonary or systemic tissues. The consistency and clinical accuracy of the intranasal mouse model proved to be a useful tool as we conducted a genetic screen to identify novel virulence factors of K. pneumoniae. A total of 4800 independent insertional mutants were evaluated using a signature-tagged mutagenesis protocol. A total of 106 independent mutants failed to be recovered from either the lungs or spleens of infected mice. Small scale independent infections proved to be helpful as a secondary screening method, as opposed to the more traditional competitive index assay. Those mutants showing verified attenuation contained insertions in loci with a variety of putative functions, including a large number of hypothetical open reading frames. Subsequent experiments support the premise that the central mechanism of K. pneumoniae pathogenesis is the production of a polysaccharide-rich cell surface that provides protection from the inflammatory response.
Time to digital converter based on a 2-dimensions Vernier architecture (2009)

A novel 2-dimension Vernier Time to digital converter (TDC) is presented. The proposed architecture reduces drastically the number of delay stage required by linear TDCs minimizing the power consumption and the area of the design. A 7 bits TDC prototype realized in 65 nm CMOS technology is presented. The chip has a resolution of 4.8 ps with a power consumption of 1.7 mW at a conversion rate of 50 Msps.
Absence of DICER1, CTCF, RPL22, DNMT3A, TRRAP, IDH1 and IDH2 hotspot mutations in patients with various subtypes of ovarian carcinomas (2014)

Cancer is caused by multiple genetic alterations within cells. Recently, large-scale sequencing has identified frequent ribonuclease type III (<i>DICER1</i>), CCCTC-binding factor (<i>CTCF</i>), ribosomal protein L22 (<i>RPL22</i>), DNA (cytosine-5-)-methyltransferase 3α (<i>DNMT3A</i>), transformation/transcription domain-associated protein (<i>TRRAP</i>), isocitrate dehydrogenase (<i>IDH</i>)1 and <i>IDH2</i> hotspot mutations in diverse types of cancer. However, it remains largely unknown whether these mutations also exist in ovarian carcinomas. In the present study, a collection of 251 patients with distinct subtypes of ovarian carcinomas were recruited and sequenced for the presence of these hotspot mutations. However, no mutations in the seven genes were detected in the samples. These negative results, together with certain recent reports, indicate that the hotspot mutations in the <i>CTCF, RPL22, DNMT3A, TRRAP, IDH1</i> and <i>IDH2</i> genes may not be actively involved in the carcinogenesis of ovarian carcinoma. Of note, the <i>DICER1</i> mutation frequency in Sertoli-Leydig cell tumor in the present study was significantly lower compared to prior observation, and therefore, it is speculated that this discrepancy may be mainly due to the small sample size analyzed in the study. In addition, among these samples, frequent polymerase (DNA directed) ε, catalytic subunit (<i>POLE1</i>) and ring finger protein 43 (<i>RNF43</i>) mutations were identified in endometrioid and mucinous ovarian carcinomas, respectively; thus <i>DICER1, CTCF, RPL22, DNMT3A, TRRAP, IDH1</i> and <i>IDH2</i> hotspot mutations may not play synergistic roles with <i>POLE1</i> or <i>RNF43</i> mutations in the carcinogenesis of endometrioid or mucinous ovarian carcinomas.
The Optimal Duration of Anticoagulant Therapy for Venous Thrombosis (1995)

Over the past 20 years, the results of well-designed randomized trials in patients with deep-vein thrombosis have provided reliable information about the treatment of this common disorder. Patients with deep-vein thrombosis should receive adequate doses of heparin for a minimum of five days.13 When heparin is stopped, patients should continue to receive oral anticoagulant therapy; the incidence of recurrent deep-vein thrombosis in the first three months is over 25 percent without such treatment, but less than 4 percent among treated patients.4,5 Progress has been made in determining the optimal intensity of oral anticoagulant therapy,6 but the optimal duration . . .
Comparative genomic hybridization analysis detects frequent, often high-level, overrepresentation of DNA sequences at 3q, 5p, 7p, and 8q in human non-small cell lung carcinomas. (1997)

Comparative genomic hybridization analysis was used to identify chromosomal imbalances in 20 non-small cell lung carcinoma (NSCLC) biopsies and cell lines. The chromosome arms most often overrepresented were 3q (85%), 5p (70%), 7p (65%), and 8q (65%), which were observed at high copy numbers in many cases. Other common overrepresented sites were 1q, 2p, and 20p. DNA sequence amplification was often observed, with the most frequent site being 3q26 (six cases). Other recurrent sites of amplification included 8q24, 3q13, 3q28-qter, 7q11.2, 8p11-12, 12p12, and 19q13.1-13.2. The most frequent underrepresented segment was 3p21 (50%); other recurrent sites of autosomal loss included 8p21-pter, 15q11.2-13, 5q11.2-15, 9p, 13q12-14, 17p, and 18q21-qter. These regions of copy number decreases are also common sites of allelic loss, further implicating these sites as locations of tumor suppressor genes. Although some of the overrepresented segments harbor known or suspected oncogenes/growth-regulatory genes, we have identified 3q and 5p as new sites that are very frequently overrepresented in NSCLC. These findings could represent entry points for the identification of novel amplified DNA sequences that may contribute to the development or progression of NSCLC.
Cytokeratin and protein expression patterns in squamous cell carcinoma of the oral cavity provide evidence for two distinct pathogenetic pathways (2016)

Squamous cell carcinoma (SCC) of the oral cavity is a morphological heterogeneous disease. Various cytokeratin (CK) expression patterns with different prognostic values have been described, but little is known concerning the underlying biological cell mechanisms. Therefore, the present study investigated 193 cases of oral SCCs using immunohistochemistry for α/β/γ-catenin, glucose transporter 1, caspase-3, X-linked inhibitor of apoptosis protein, hypoxia inducible factor-1α, carbonic anhydrase 9, heat shock protein (hsp) 70, mast/stem cell growth factor receptor, p21, p27, p16, p53, B-cell lymphoma 6, epidermal growth factor receptor, cyclin D1 and CK1, 5/6, 8/18, 10, 14 and 19. Expression patterns were analyzed with biomathematical permutation analysis. The present results revealed a significant association between the expression of low-molecular weight CK8/18 and 19 and a high-tumor grade, β and γ-catenin expression, deregulated cell cycle proteins and a predominant localization of the tumor on the floor of the mouth. By contrast, expression of high-molecular weight CK1, 5/6, 10 and 14 was significantly associated with the expression of p21 and hsp70. In conclusion, the current study presents evidence for the existence of two parallel pathogenetic pathways in oral SCCs, characterized by the expression of low- and high-molecular weight CKs. Additional studies are required to demonstrate the extent that these results may be used to improve therapeutic regimens.
Novel Phosphamide Additive to Improve Thermal Stability of Solid Electrolyte Interphase on Graphite Anode in Lithium-Ion Batteries (2013)

In this communication, a novel electrolyte additive, N,N-diallyic-diethyoxyl phosphamide (DADEPA), is described for the first time to improve the thermal stability of lithiated graphite anode in Li-ion batteries. The differential scanning calorimetry (DSC) measurement demonstrated that when the graphite was lithiated in the 5% DADEPA-containing electrolyte, the heat generation decreased sharply by half as compared with the reference, whereas the onset temperature for the main exothermic process was postponed by 20 °C. Electrochemical and XPS analyses indicated that the distinctive improvement in thermal safety came from a new interfacial chemistry, in which phosphorus-containing ingredients was embedded during the initial forming of the interphase.
Oncostatin M Regulates the Synthesis and Turnover of gp130, Leukemia Inhibitory Factor Receptor α, and Oncostatin M Receptor β by Distinct Mechanisms (2001)

The cytokine receptor subunits gp130, leukemia inhibitory factor receptor alpha (LIFRalpha), and oncostatin M receptor beta (OSMRbeta) transduce OSM signals that regulate gene expression and cell proliferation. After ligand binding and activation of the Janus protein-tyrosine kinase/STAT and mitogen-activated protein kinase signal transduction pathways, negative feedback processes are recruited. These processes attenuate receptor action by suppression of cytokine signaling and by down-regulation of receptor protein expression. This study demonstrates that in human fibroblasts or epithelial cells, OSM first decreases the level of gp130, LIFRalpha, and OSMRbeta by ligand-induced receptor degradation and then increases the level of the receptors by enhanced synthesis. The transcriptional induction of gp130 gene by OSM involves STAT3. Various cell lines expressing receptor subunits to the different interleukin-6 class cytokines revealed that only LIFRalpha degradation is promoted by activated ERK and that degradation of gp130, OSMRbeta, and a fraction of LIFRalpha involves mechanisms that are separate from signal transduction. These mechanisms include ligand-mediated dimerization, internalization, and endosomal/lysosomal degradation. Proteosomal degradation appears to involve a fraction of receptor subunit proteins that are ubiquitinated independently of ligand binding.
Transcranial Direct Current Stimulation and Visual Perception (2008)

Membrane potentials and spike sequences represent the basic modes of cerebral information processing. Both can be externally modulated in humans by quite specific techniques: transcranial direct current stimulation (tDCS) and repetitive transcranial magnetic stimulation (rTMS). These methods induce reversible circumscribed cortical excitability changes, either excitatory or inhibitory, outlasting stimulation in time. Experimental pharmacological interventions may selectively enhance the duration of the aftereffects. Whereas rTMS induces externally triggered changes in the neuronal spiking pattern and interrupts or excites neuronal firing in a spatially and temporally restricted fashion, tDCS modulates the spontaneous firing rates of neurons by changing resting-membrane potential. The easiest and most common way of evaluating the cortical excitability changes is by applying TMS to the motor cortex, since it allows reproducible quantification through the motor-evoked potential. Threshold determinations at the visual cortex or psychophysical methods usually require repeated and longer measurements and thus more time for each data set. Here, results derived from the use of tDCS in visual perception, including contrast as well as motion detection and visuo-motor coordination and learning, are summarised. It is demonstrated that visual functions can be transiently altered by tDCS, as has been shown for the motor cortex previously. Up- and down-regulation of different cortical areas by tDCS is likely to open a new branch in the field of visual psychophysics.
Broad Antiproliferative Effects of Benidipine on Cultured Human Mesangial Cells in Cell Cycle Phases (2002)

Benidipine markedly inhibited the proliferation of mesangial cells, at both the G0/G1 and G1/S phases, and it might be effective to suppress the progression of mesangioproliferative glomerular diseases.
Carbon monoxide-induced suspended animation protects against hypoxic damage in Caenorhabditis elegans (2004)

Oxygen deprivation is a major cause of cellular damage and death. Here we demonstrate that Caenorhabditis elegans embryos, which can survive both in anoxia (<0.001 kPa O(2)) by entering into suspended animation and in mild hypoxia (0.25-1 kPa O(2)) through a hypoxia-inducible factor 1-mediated response, cannot survive in intermediate concentrations of oxygen, between 0.01 and 0.1 kPa O(2). Moreover, we show that carbon monoxide can protect C. elegans embryos against hypoxic damage in this sensitive range. Carbon monoxide can also rescue the hypoxia-sensitive mutant hif-1(ia04) from lethality in hypoxia. This work defines the oxygen tensions over which hypoxic damage occurs in C. elegans embryos and demonstrates that carbon monoxide can prevent this damage by inducing suspended animation.