gebhart/patrepeval huggingface dataset:
Chains and Grains in Interstellar Space (1987)

The intriguing abundance of long linear carbon chain molecules in dark clouds such as TMC1 and in circumstellar shells such as that surrounding IRC+10216 are still not understood. Recent radioastronoray studies are beginning to confirm that more saturated analogues of the carbon chain species are not abundant. Recent laboratory studies indicate that when carbon vapour nucleates to form particles, linear chains and spheroidal shell molecules also form probably as intermediates. The results appear to have consequences as far as the formation, structures and spectroscopic properties of interstellar grains are concerned, in particular those ejected from cool carbon stars.
Microbiology and treatment of halitosis (2002)

The prevalence of oral malodor is probably high in the United States, although precise epidemiological data are missing. The many thousands of individuals who experience oral malodor from the overgrowth of proteolytic, anaerobic bacteria on their tongue surfaces can be successfully treated by a regimen that includes tongue brushing, toothbrushing and possibly the usage of mouthrinses containing various agents. Several candidate mouthrinses containing essential oils (Listerine), ZnCl2, or an oil, water and cetylpyridum chloride mouthrinse have reduced the organoleptic scores of individuals with moderate levels of oral malodor in the absence of tongue brushing. Very few long-term data beyond 6 weeks of usage are available. Anecdotal evidence suggests that other agents such as chlorine dioxide may be helpful. These mouthrinses should be marketed as oral deodorants that are analogous in purpose to the usage of deodorant soaps to control and/or eliminate body malodors. In this way the mouthrinse could be considered as a cosmetic by the FDA, provided that there are data on the safety of the various ingredients in the mouthrinse. Mouthrinses containing zinc ions are able to reduce the levels of volatile sulfur compounds by converting these volatile compounds to non-volatile, and therefore, non-malodorous zinc sulfides, and this mode of action would appear to support a cosmetic claim.
Phase I study of paclitaxel and carboplatin: implications for trials in head and neck cancer. (1995)

An ongoing phase I and pharmacokinetic trial of paclitaxel (Taxol; Bristol-Myers Squibb Company, Princeton, NJ) in combination with carboplatin is evaluating the maximum tolerated dose (MTD) of a 3-hour paclitaxel infusion combined with fixed doses of carboplatin in previously treated and untreated patients with a variety of advanced cancers. A patient's previous treatment status determines the fixed carboplatin dose: target area under the concentration-time curves of 4.0 and 4.5 mg.min/mL in previously treated and untreated patients, respectively. Studies 1 and 2 entered previously treated patients to establish the paclitaxel MTD without and with cytokine support: study 1 established 135 mg/m2 paclitaxel as the MTD without such support. In study 2, granulocyte colony-stimulating factor is administered, and the MTD has not yet been reached with paclitaxel doses of 135 mg/m2 to 230 mg/m2 assessed thus far and 250 mg/m2 now being evaluated. Objective responses have been seen in three of five patients with squamous cell carcinoma of the head and neck and in patients with non-small cell lung cancer and metastatic cancer of unknown primary site as well. Myelosuppression has been the dose-limiting toxicity, although significant nausea and vomiting and myalgia have been documented occasionally. Paclitaxel apparently has nonlinear pharmacokinetics with a beta half-life of 6.7 hours (SD +/- 1.3 hours). Future trials of paclitaxel/carboplatin will address the management of squamous cell carcinoma of the head and neck and non-small cell carcinoma of the lung.
A novel protein with RNA-binding motifs interacts with ataxin-2 (2000)

Spinocerebellar ataxia type 2 (SCA2) is caused by expansion of a polyglutamine tract in ataxin-2, a protein of unknown function. Using the yeast two-hybrid system, we identified a novel protein, A2BP1 (ataxin-2 binding protein 1) which binds to the C-terminus of ataxin-2. Northern blot analysis showed that A2BP1 was predominantly expressed in muscle and brain. By immunocfluorescent staining, A2BP1 and ataxin-2 were both localized to the trans -Golgi network. Immunocytochemistry showed that A2BP1 was expressed in the cytoplasm of Purkinje cells and dentate neurons in a pattern similar to that seen for ataxin-2 labeling. Western blot analysis of subcellular fractions indicated enrichment of A2BP1 in the same fractions as ataxin-2. Sequence analysis of the A2BP1 cDNA revealed an RNP motif that is highly conserved among RNA-binding proteins. A2BP1 had striking homology with a human cDNA clone, P83A20, of unknown function and at least two copies of A2BP1 homologs are found in the Caenorhabditis elegans genome database. A2BP1 and related proteins appear to form a novel gene family sharing RNA-binding motifs.
Sensors and switches from supramolecular chemistry (1995)

The first page of this article is displayed as the abstract.
Realization of the Hadamard Multiplex Advantage Using a Programmable Optical Mask in a Dispersive Flat-Field Near-Infrared Spectrometer (2000)

Spectrometry and hyperspectral imaging are finding numerous applications for micro-optoelectromechanical systems (MOEMS). A type of MOEMS device in the form of a digital micromirror array (DMA) has been made commercially available by Texas Instruments USA for projector display applications. We use this device as a spatial light modulator (SLM) in a new type of flat-field, near-infrared dispersive spectrometer (NIRDMAS). Attributes of the DMA used in this manner are presented for discussion. Features that make a DMA attractive for spectrometry and imaging are described. A brief introduction to Hadamard transform (HT) techniques is presented to show that the DMA may be the best Hadamard encoding mask yet developed. A comparison of a conventional raster scanning (CRS) scan and a Hadamard transform spectrometry (HTS) scan with respect to the Hadamard multiplex advantage using a nonphoton noise-limited, single-element detector is presented. A signal-to-noise ratio comparison using four spectral lines from a mercury-argon calibration lamp demonstrates that the theoretical noise reduction is approached for the HTS scan compared to the CRS scan. Some future applications of MOEMS in spectrometry and hyperspectral imaging are suggested.
Proximity-Dependent Inhibition in Escherichia coli Isolates from Cattle (2011)

We describe a novel proximity-dependent inhibition phenotype of Escherichia coli that is expressed when strains are cocultured in defined minimal media. When cocultures of "inhibitor" and "target" strains approached a transition between logarithmic and stationary growth, target strain populations rapidly declined >4 log CFU per ml over a 2-h period. Inhibited strains were not affected by exposure to conditioned media from inhibitor and target strain cocultures or when the inhibitor and target strains were incubated in shared media but physically separated by a 0.4-μm-pore-size membrane. There was no evidence of lytic phage or extracellular bacteriocin involvement, unless the latter was only present at effective concentrations within immediate proximity of the inhibited cells. The inhibitory activity observed in this study was effective against a diversity of E. coli strains, including enterohemorrhagic E. coli serotype O157:H7, enterotoxigenic E. coli expressing F5 (K99) and F4 (K88) fimbriae, multidrug-resistant E. coli, and commensal E. coli. The decline in counts of target strains in coculture averaged 4.8 log CFU/ml (95% confidence interval, 4.0 to 5.5) compared to their monoculture counts. Coculture of two inhibitor strains showed mutual immunity to inhibition. These results suggest that proximity-dependent inhibition can be used by bacteria to gain a numerical advantage when populations are entering stationary phase, thus setting the stage for a competitive advantage when growth conditions improve.
Interferon‐γ binds to heparan sulfate by a cluster of amino acids located in the C‐terminal part of the molecule (1991)

Using three different approaches (domain mapping with monoclonal antibodies, limited enzymatic digestion and competition with synthetic peptides), we demonstrated that a cluster of basic amino acids on interferon-gamma is involved in its binding to heparan sulfate. This cluster (Lys125-Arg131) is localized in the C-terminal part of IFN-gamma. Once bound to heparin sulfate, IFN-gamma is protected against protease attack.
Macrolide–ketolide inhibition of MLS‐resistant ribosomes is improved by alternative drug interaction with domain II of 23S rRNA (2000)

The macrolide antibiotic erythromycin and its 6-O-methyl derivative (clarithromycin) bind to bacterial ribosomes primarily through interactions with nucleotides in domains II and V of 23S rRNA. The domain II interaction occurs between nucleotide A752 and the macrolide 3-cladinose moiety. Removal of the cladinose, and substitution of a 3-keto group (forming the ketolide RU 56006), results in loss of the A752 interaction and an approximately 100-fold drop in drug binding affinity. Within domain V, the key determinant of drug binding is nucleotide A2058 and substitution of G at this position is the major cause of drug resistance in some clinical pathogens. The 2058G mutation disrupts the drug-domain V contact and leads to a further > 25 000-fold decrease in the binding of RU 56006. Drug binding to resistant ribosomes can be improved over 3000-fold by forming an alternative and more effective contact to A752 via alkyl-aryl groups linked to a carbamate at the drug 11/12 position (in the ketolide antibiotics HMR 3647 and HMR 3004). The data indicate that simultaneous drug interactions with domains II and V strengthen binding and that the domain II contact is of particular importance to achieve binding to the ribosomes of resistant pathogens in which the domain V interaction is perturbed.
T cell‐based targeted immunotherapies for patients with multiple myeloma (2014)

Despite high-dose chemotherapy followed by autologs stem-cell transplantation as well as novel therapeutic agents, multiple myeloma (MM) remains incurable. Following the general trend towards personalized therapy, targeted immunotherapy as a new approach in the therapy of MM has emerged. Better progression-free survival and overall survival after tandem autologs/allogeneic stem cell transplantation suggest a graft versus myeloma effect strongly supporting the usefulness of immunological therapies for MM patients. How to induce a powerful antimyeloma effect is the key issue in this field. Pivotal is the definition of appropriate tumor antigen targets and effective methods for expansion of T cells with clinical activity. Besides a comprehensive list of tumor antigens for T cell-based approaches, eight promising antigens, CS1, Dickkopf-1, HM1.24, Human telomerase reverse transcriptase, MAGE-A3, New York Esophageal-1, Receptor of hyaluronic acid mediated motility and Wilms' tumor gene 1, are described in detail to provide a background for potential clinical use. Results from both closed and on-going clinical trials are summarized in this review. On the basis of the preclinical and clinical data, we elaborate on three encouraging therapeutic options, vaccine-enhanced donor lymphocyte infusion, chimeric antigen receptors-transfected T cells as well as vaccines with multiple antigen peptides, to pave the way towards clinically significant immune responses against MM.
FBXO31 determines poor prognosis in esophageal squamous cell carcinoma (2011)

Cyclin D1 plays important roles in esophageal squamous cell carcinoma (ESCC) cases by amplification of the 11q13.3 locus. FBXO31 is a subunit of the SCF ubiquitin ligase, which targets cyclin D1 for degradation. In this study, we clarified the clinical significance of FBXO31 and characterized the association between cyclin D1 and FBXO31 in ESCC cases. Total RNA was extracted from tumor tissues obtained from 68 ESCC patients who underwent surgical resection. FBXO31 expression levels were determined by quantitative RT-PCR, and both FBXO31 and cyclin D1 protein expression and localization were evaluated by immunohistochemistry (IHC). Furthermore, using CGH and gene expression array data of another subset, we validated the association between cyclin D1 genomic amplification and FBXO31 expression levels. Higher FBXO31 expression levels significantly correlated with depth of tumor invasion and clinical stage (P<0.05). In addition, the FBXO31 high expression group showed a significantly poorer prognosis than the low expression group (P<0.001). Multivariate analysis indicated that FBXO31 expression was an independent prognostic factor [relative risk (RR): 1.79, confidence interval (CI): 1.14-3.01, P=0.01]. Using IHC, concordant expression was observed between cyclin D1 and FBXO31 in the nucleus and cytoplasm, respectively. CGH array indicated that cases having cyclin D1 with increased copy number were significantly associated with elevated FBXO31 expression levels (P<0.05). FBXO31 could be a novel and robust prognostic marker for ESCC.
Epigenetic Characteristics and Development of Embryos Cloned from Donor Cells Treated by Trichostatin A or 5-aza-2′-deoxycytidine1 (2003)

Development to blastocyst following nuclear transfer is dependent on the donor cell's ability to reprogram its genome to that of a zygote. This reprogramming step is inefficient and may be dependent on a number of factors, including chromatin organization. Trichostatin A (TSA; 0-5 microM), a histone deacetylase inhibitor, was used to increase histone acetylation and 5-aza-2'-deoxycytidine (5-aza-dC; 0-5 microM), a DNA methyl-transferase inhibitor, was used to decrease methylation of chromatin in donor cells in an attempt to improve their reprogrammability. Adult fibroblast cells treated with 1.25 or 5 microM TSA had elevated histone H3 acetylation compared to untreated controls. Cells treated with 0.3 microM 5-aza-dC had decreased methylation compared to untreated controls. Both drugs at 0.08 microM caused morphological changes of the donor cells. Development to blastocysts by embryos cloned from donor cells after 0.08 or 0.3 microM 5-aza-dC treatments was lower than in embryos cloned from untreated control cells (9.7% and 4.2%, respectively, vs. 25.1%), whereas 0.08 microM TSA treatment of donor cells increased blastocyst development compared to controls (35.1% vs. 25.1%). These results indicate that partial erasure of preexisting epigenetic marks of donor cells improves subsequent in vitro development of cloned embryos.
Polyvalency: A promising strategy for drug design (2008)

Abstract The simultaneous binding of multiple ligands on one entity to multiple receptors on another can result in an affinity that is significantly greater than that for the binding of a single ligand to a single receptor. This concept of “polyvalency” can be used to design molecules that are potent inhibitors of toxins and pathogens. We describe the design of potent polyvalent inhibitors that neutralize anthrax toxin in vivo as well as our attempts to elucidate the relationship between inhibitor structure and activity. We also highlight promising future avenues for research in polyvalent drug design. Biotechnol. Bioeng. 2008;101: 429–434. © 2008 Wiley Periodicals, Inc.
DNA Hypomethylation Arises Later in Prostate Cancer Progression than CpG Island Hypermethylation and Contributes to Metastatic Tumor Heterogeneity (2008)

Hypomethylation of CpG dinucleotides in genomic DNA was one of the first somatic epigenetic alterations discovered in human cancers. DNA hypomethylation is postulated to occur very early in almost all human cancers, perhaps facilitating genetic instability and cancer initiation and progression. We therefore examined the nature, extent, and timing of DNA hypomethylation changes in human prostate cancer. Contrary to the prevailing view that global DNA hypomethylation changes occur extremely early in all human cancers, we show that reductions in (5me)C content in the genome occur very late in prostate cancer progression, appearing at a significant extent only at the stage of metastatic disease. Furthermore, we found that, whereas some LINE1 promoter hypomethylation does occur in primary prostate cancers compared with normal tissues, this LINE1 hypomethylation is significantly more pronounced in metastatic prostate cancer. Next, we carried out a tiered gene expression microarray and bisulfite genomic sequencing-based approach to identify genes that are silenced by CpG island methylation in normal prostate cells but become overexpressed in prostate cancer cells as a result of CpG island hypomethylation. Through this analysis, we show that a class of cancer testis antigen genes undergoes CpG island hypomethylation and overexpression in primary prostate cancers, but more so in metastatic prostate cancers. Finally, we show that DNA hypomethylation patterns are quite heterogeneous across different metastatic sites within the same patients. These findings provide evidence that DNA hypomethylation changes occur later in prostate carcinogenesis than the CpG island hypermethylation changes and occur heterogeneously during prostate cancer progression and metastatic dissemination.
Expression of αvβ8 integrin on dendritic cells regulates Th17 cell development and experimental autoimmune encephalomyelitis in mice (2010)

Th17 cells promote a variety of autoimmune diseases, including psoriasis, multiple sclerosis, rheumatoid arthritis, and inflammatory bowel disease. TGF-β is required for conversion of naive T cells to Th17 cells, but the mechanisms regulating this process are unknown. Integrin αvβ8 on DCs can activate TGF-β, and this process contributes to the development of induced Tregs. Here, we have now shown that integrin αvβ8 expression on DCs plays a critical role in the differentiation of Th17 cells. Th17 cells were nearly absent in the colons of mice lacking αvβ8 expression on DCs. In addition, these mice and the DCs harvested from them had an impaired ability to convert naive T cells into Th17 cells in vivo and in vitro, respectively. Importantly, mice lacking αvβ8 on DCs showed near-complete protection from experimental autoimmune encephalomyelitis. Our results therefore suggest that the integrin αvβ8 pathway is biologically important and that αvβ8 expression on DCs could be a therapeutic target for the treatment of Th17-driven autoimmune disease.
Judging a Protein by More Than Its Name: GSK-3 (2001)

As knowledge of cellular signal transduction has accumulated, general truisms have emerged, including the notion that signaling proteins are usually activated by stimuli and that they, in turn, mediate the actions of specific agonists. Glycogen synthase kinase-3 (GSK-3) is an unusual protein-serine kinase that bucks these conventions. This evolutionarily conserved protein kinase is active in resting cells and is inhibited in response to activation of several distinct pathways, including those acting by elevation of 3′ phosphorylated phosphatidylinositol lipids and adenosine 3′-5′-monophosphate (cAMP). In addition, GSK-3 is distinctly regulated by, and is a core component of, the Wnt pathway. This review describes the unique characteristics of this decidedly oddball protein kinase in terms of its diverse biological functions, plethora of targets, role in several human diseases, and consequential potential as a therapeutic target.
IL-8 Production in Human Lung Fibroblasts and Epithelial Cells Activated by the Pseudomonas Autoinducer N -3-Oxododecanoyl Homoserine Lactone Is Transcriptionally Regulated by NF-κB and Activator Protein-2 (2001)

The destructive pulmonary inflammation associated with Pseudomonas aeruginosa colonization is caused, in part, by the production of the chemokine IL-8, which recruits neutrophils into the lung. The Pseudomonas autoinducer, N-3-oxododecanoyl homoserine lactone (3-O-C12-HSL), is a small lipid-soluble molecule that is essential in the regulation of many P. aeruginosa virulence factors, but little is known about how it affects eukaryotic cells. In this report we demonstrate that 3-O-C12-HSL is a potent stimulator of both IL-8 mRNA and protein from human fibroblasts and epithelial cells in vitro. The IL-8 produced from these 3-O-C12-HSL-stimulated cells was found to be functionally active by inducing the chemotaxis of neutrophils. To determine a mechanism for this IL-8 induction, deletion constructs of the IL-8 promoter were examined. It was found that the DNA region between nucleotides -1481 and -546 and the transcription factor NF-kappaB were essential for the maximal induction of IL-8 by 3-O-C12-HSL. This was confirmed by EMSAs, where 3-O-C12-HSL induced a shift with both AP-2 and NF-kappaB consensus DNA. The activation of NF-kappaB and subsequent production of IL-8 were found to be regulated by a mitogen-activated protein kinase pathway. These findings support the concept that the severe lung damage that accompanies P. aeruginosa infections is caused by an exuberant neutrophil response stimulated by 3-O-C12-HSL-induced IL-8. Understanding the mechanisms of 3-O-C12-HSL activation of lung structural cells may provide a means to help control lung damage during infections with P. aeruginosa.
Nonvolatile ferroelectric-gate field-effect transistors using SrBi2Ta2O9/Pt/SrTa2O6/SiON/Si structures (1999)

We report fabrication and characterization of p-channel metal–ferroelectric-metal–insulator–semiconductor (MFMIS) field-effect transistors (FETs) using the Pt/SrBi2Ta2O9/Pt/SrTa2O6/SiON/Si structures. It is shown that SrTa2O6/SiON stacked layer is suitable as an “I” layer in the MFMIS structure, because the SrTa2O6/SiON/Si structure has low leakage current and good interface properties. We also show that by using a small MFM capacitor on a large MIS structure, a large memory window of 3.0 V can be obtained. Furthermore, it is found that the data retention characteristics have been improved for Pt/SrBi2Ta2O9/Pt/SrTa2O6/SiON/Si MFMIS-FETs.
Regorafenib Inhibits Colorectal Tumor Growth through PUMA-Mediated Apoptosis (2014)

Our results demonstrate a key role of PUMA in mediating the anticancer effects of regorafenib in colorectal cancer cells. They suggest that PUMA induction can be used as an indicator of regorafenib sensitivity, and also provide a rationale for manipulating the apoptotic machinery to improve the therapeutic efficacy of regorafenib and other targeted drugs.
INICIA HOY EL VII TALLER DE ACTUALIZACION BIOQUIMICA (1981)

CON EL PROPOSITO DE ACTUALIZAR LOS CONOCIMIENTOS EN BIOQUIMICA, ASI COMO COMENTAR E INTERCAMBIAR EXPERIENCIAS DOCENTES Y DE APRENDIZAJE EN ESE CAMPO, EL DEPARTAMENTO DE BIOQUIMICA DE LA FACULTAD DE MEDICINA DE LA UNAM, EN COORDINACION CON LA DIRECCION GENERAL DE INVESTIGACION CIENTIFICA Y SUPERACION ACADEMICA DE LA SEP, INICIARAN A PARTIR DE HOY LOS TRABAJOS DEL VIII TALLER DE ACTUALIZACION BIOQUIMICA A CELEBRARSE EN EL CENTRO VACACIONAL OAXTEPEC, EN EL ESTADO DE MORELOS; ASI LO DIO A CONOCER EL DOCTOR ENRIQUE PINA GARZA, JEFE DE ESE DEPARTAMENTO DE BIOQUIMICA.
High Growth Rate in Atomic Layer Deposition of TiO2 thin films by UV Irradiation (2011)

The exposure effect of the reaction surface to ultraviolet (UV) light was studied for atomic layer deposition (ALD) of TiO2 films from Ti(OiPr)4 and H2O at 260°C. UV light was irradiated on the reaction surface after the purge step of Ti-precursor and oxygen source, respectively. UV irradiation on the reaction surface resulted in a higher growth rate of the TiO2 films compared to the thermal ALD. The growth rate of anatase TiO2 increased by a factor of 2 to about 0.25 nm/cycle while the surface roughness was reduced. UV-light induced increase of the number of chemisorption sites is discussed as the possible mechanism.