gebhart/patrepeval huggingface dataset:
A Highly Sensitive Fluorescent Sensor for Palladium Based on the Allylic Oxidative Insertion Mechanism (2007)

Although palladium catalysts are powerful reagents in organic synthesis, hazardous palladium is often found in reaction products even after purifications. Thus, the detection of palladium is an important process in the production of fine chemicals and active pharmaceutical ingredients. We have developed a highly sensitive fluorescent sensor that is capable of detecting 1 ng of palladium quantitatively with the naked eye. Using this method, we were able to selectively detect palladium contamination in aspirin tablets (10 ppm Pd in 1 mg aspirin; mixed in the laboratory for this study), on the surface of flasks previously exposed to palladium, and in rocks containing palladium.
Accelerated epithelial cell senescence in IPF and the inhibitory role of SIRT6 in TGF-β-induced senescence of human bronchial epithelial cells (2010)

Reepithelialization of remodeled air spaces with bronchial epithelial cells is a prominent pathological finding in idiopathic pulmonary fibrosis (IPF) and is implicated in IPF pathogenesis. Recent studies suggest that epithelial senescence is a risk factor for development of IPF, indicating such reepithelialization may be influenced by the acceleration of cellular senescence. Among the sirtuin (SIRT) family, SIRT6, a class III histone deacetylase, has been demonstrated to antagonize senescence. We evaluated the senescence of bronchiolization in association with SIRT6 expression in IPF lung. Senescence-associated β-galactosidase staining and immunohistochemical detection of p21 were performed to evaluate cellular senescence. As a model for transforming growth factor (TGF)-β-induced senescence of abnormal reepithelialization, we used primary human bronchial epithelial cells (HBEC). The changes of SIRT6, p21, and interleukin (IL)-1β expression levels in HBEC, as well as type I collagen expression levels in fibroblasts, were evaluated. In IPF lung samples, an increase in markers of senescence and SIRT6 expression was found in the bronchial epithelial cells lining cystically remodeled air spaces. We found that TGF-β induced senescence in primary HBEC by increasing p21 expression, and, whereas TGF-β also induced SIRT6, it was not sufficient to inhibit cellular senescence. However, overexpression of SIRT6 efficiently inhibited TGF-β-induced senescence via proteasomal degradation of p21. TGF-β-induced senescent HBEC secreted increased amounts of IL-1β, which was sufficient to induce myofibroblast differentiation in fibroblasts. These findings suggest that accelerated epithelial senescence plays a role in IPF pathogenesis through perpetuating abnormal epithelial-mesenchymal interactions, which can be antagonized by SIRT6.
Dynamics of Synthesis, Translation, and Degradation of trp Operon Messenger RNA in E. coli (1969)

We have been interested in those factors other than repression which control the extent of protein biosynthesis directed by bacterial genes. These factors include the frequency with which each gene is transcribed, the number of ribosomes which translate each messenger RNA (mRNA), and the functional (as well as chemical) lifetime of the messenger molecule.
Deficiency of a leukocyte surface glycoprotein (LFA-1) in two patients with Mo1 deficiency. Effects of cell activation on Mo1/LFA-1 surface expression in normal and deficient leukocytes. (1984)

Mo1, a phagocyte surface glycoprotein heterodimer, is involved in a number of phagocyte adhesion functions such as binding and ingestion of serum-opsonized particles, zymosan-induced degranulation, and superoxide generation. Deficiency of this antigen in humans has been associated with increased susceptibility to recurrent bacterial infections. The beta subunit of Mo1 is shared by another surface glycoprotein named LFA-1, which is involved in lymphocyte proliferation, cytolytic T cell, and natural killing activities. Two unrelated patients with Mo1 deficiency were found to be deficient in LFA-1 as well as in the common beta subunit. Investigation of lymphocyte functions in these two patients revealed normal mixed leukocyte culture-generated cytolytic T cell and natural killing activities and significantly reduced proliferative response to phytohemagglutinin. LFA-1-deficient cells also proliferated in response to soluble antigen and different alloantigens. These responses were partially blocked by anti-LFA-1 antibody. Whereas LFA-1 was undetectable by immunofluorescence and immunoprecipitation on the patients' resting T cells, significantly reduced (approximately 5% of normal) but detectable amounts of the heterodimeric LFA-1 antigen were found on mitogen and alloantigen-activated T cells. On granulocytes, Mo1 surface expression was also dependent on the state of cellular activation. The amount of surface Mo1 present on resting normal granulocytes increased by 3-10-fold following exposure to stimuli that induced degranulation, suggesting the presence of a major intracellular pool for this antigen. Analysis of subcellular fractions from granulocytes showed that intracellular Mo1 is located primarily in the specific granule fraction. Activated granulocytes had little or no increase in their surface expression of LFA-1 antigen. Deficient granulocytes had significantly increased numbers of Mo1 antigen expressed on the surface following stimulation with calcium ionophore (1 microM). However, the amount expressed continued to be significantly reduced compared with normal cells. Quantitation of surface Mo1 on granulocytes exposed to calcium ionophore (1 microM) showed that both parents in one family but only the mother in the other family had significantly reduced levels of Mo1, suggesting heterogeneity in the inheritance of this disorder. Whereas LFA-1 deficiency on lymphocytes was associated with normal alloantigen-induced cytolytic T cell and natural killing activities in these two patients, functions which were in part dependent on small amounts of detectable LFA-1 antigen, the Mo1 deficiency state led to significant defects in phagocyte adhesion functions. Hence, the clinical symptoms associated with this combined deficiency state reflect a more profound phagocyte than lymphocyte disorder.
The rfaE Gene from Escherichia coli Encodes a Bifunctional Protein Involved in Biosynthesis of the Lipopolysaccharide Core Precursor ADP- l - glycero - d - manno -Heptose (2000)

ABSTRACT The intermediate steps in the biosynthesis of the ADP- l - glycero - d - manno -heptose precursor of inner core lipopolysaccharide (LPS) are not yet elucidated. We isolated a mini-Tn 10 insertion that confers a heptoseless LPS phenotype in the chromosome of Escherichia coli K-12. The mutation was in a gene homologous to the previously reported rfaE gene from Haemophilus influenzae . The E. coli rfaE gene was cloned into an expression vector, and an in vitro transcription-translation experiment revealed a polypeptide of approximately 55 kDa in mass. Comparisons of the predicted amino acid sequence with other proteins in the database showed the presence of two clearly separate domains. Domain I (amino acids 1 to 318) shared structural features with members of the ribokinase family, while Domain II (amino acids 344 to 477) had conserved features of the cytidylyltransferase superfamily that includes the aut gene product of Ralstonia eutrophus . Each domain was expressed individually, demonstrating that only Domain I could complement the rfaE ::Tn 10 mutation in E. coli , as well as the rfaE543 mutation of Salmonella enterica SL1102. DNA sequencing of the rfaE543 gene revealed that Domain I had one amino acid substitution and a 12-bp in-frame deletion resulting in the loss of four amino acids, while Domain II remained intact. We also demonstrated that the aut ::Tn 5 mutation in R. eutrophus is associated with heptoseless LPS, and this phenotype was restored following the introduction of a plasmid expressing the E. coli Domain II. Thus, both domains of rfaE are functionally different and genetically separable confirming that the encoded protein is bifunctional. We propose that Domain I is involved in the synthesis of d - glycero - d - manno -heptose 1-phosphate, whereas Domain II catalyzes the ADP transfer to form ADP- d - glycero - d - manno -heptose.
Little role of anti-gB antibodies in neutralizing activity of patient's sera with human cytomegalovirus (HCMV) infection (2000)

Human cytomegalovirus (HCMV) gB is known to play important roles in cell surface attachment, virion penetration, spread of infection from cell to cell, and provocation of neutralizing antibody. This study was performed to determine the role of anti-HCMV gB antibody in overall neutralizing response in patients with HCMV infection and healthy control with past infection. HCMV gB was stably expressed in 293 cells. With the stable cell line expressing gB as a specific immunosorbent, anti-gB antibody was removed from the current and past HCMV-infected sera and the remaining neutralizing activity was measured by plaque assay. It was shown that 19-50% of the total virus-neutralizing activity of sera with past HCMV infections was derived from anti-gB antibody, but anti-gB antibody had little effect on the total serum virus-neutralizing activity in patients currently infected with HCMV. This result suggests that neutralizing antibody to HCMV gB may reflect disease status.
Molecular cloning and analysis of a gene coding for the Bowman-Birk protease inhibitor in soybean. (1984)

We have constructed cDNA clones from size-selected mRNA of developing soybean seeds to identify genes encoding the Bowman-Birk protease inhibitor. Recombinant clones containing sequences coding for the Bowman-Birk inhibitor were identified by mRNA hybrid selected translation and immunoprecipitation. The nucleotide sequence of the insert of plasmid pB38 corresponds to the mRNA for the Bowman-Birk inhibitor, although it is missing a portion of the coding sequence at the 5' end. Northern hybridization analysis of total RNA isolated from developing soybean seeds showed that the mRNA for the inhibitor is approximately 450 nucleotides long and that it accumulates early in embryogeny. Southern hybridization analysis of restriction enzyme-digested soybean nuclear DNA indicated that the gene encoding the Bowman-Birk inhibitor is not highly reiterated in the genome. We have isolated a gene encoding the Bowman-Birk inhibitor from a soybean genomic library constructed in Charon 4A. DNA sequence analysis of the genomic clone reveals that it is similar, although not identical, to the cDNA clone and that it contains no intervening sequences.
City lights (2003)

City Lights are space-efficient fisheye techniques that provide contextual views along the borders of windows and subwindows that describe unseen objects in all directions. We present a family of techniques that use a range of graphical dimensions to depict varied information about unseen objects. City Lights can be used alone or in conjunction with scrollbars, 2D overview+detail, and interaction techniques such as zoomable user interfaces.
Quinolinic acid in patients with systemic lupus erythematosus and neuropsychiatric manifestations. (1996)

To evaluate the relationship between quinolinic acid, a neuroactive metabolite of L-tryptophan, and neuropsychiatric manifestations of systemic lupus erythematosus (SLE).Forty specimens of cerebrospinal fluid (CSF) were obtained from 39 patients with SLE who were evaluated for 40 episodes of neuropsychiatric dysfunction. The diagnosis of the neuropsychiatric dysfunction was determined clinically. CSF and serum specimens were analyzed for levels of quinolinic acid without knowledge of the clinical diagnosis.Neuropsychiatric dysfunction attributed to SLE (NPSLE) was confirmed in 30 patient-episodes (Group 1), whereas in the other 10 (Group 2) other etiologies were felt to explain their CNS dysfunction. The median levels of CSF quinolinic acid for Group 1 (232.5 nmol/l) were significantly higher than those for Group 2 (median 38.2 nmol/l) (p < 0.014). CSF and serum quinolinic acid levels correlated significantly (p < 0.003) but there was not correlation between CSF quinolinic acid and CSF protein concentrations or white blood cell counts.We conclude that elevated quinolinic acid levels in the CSF and serum may be associated with NPSLE and could possibly play a role in its pathogenesis.
Repeat courses of intravenous alefacept in patients with chronic plaque psoriasis provide consistent safety and efficacy (2003)

Repeat courses of alefacept were well tolerated, and subsequent retreatment courses were at least as effective as the initial course of therapy.
On the Mechanism of the Biosynthesis of Prostaglandins E1 and F1α (1967)

The mechanism of the conversion of 8,11,14-eicosatrienoic acid into prostaglandin E1 (PGEl) and prostaglandin F1, (PGFI,) has been studied.Incubation of [13~-~H,3-"C]and [13~-3H ,3J*C]8,11,14-eicosatrienoic acids showed that the hydrogen removed from C-13 during the conversion into PGEl and PGFI, has the L configuration.The conversion of [13~-3H ,3J4C]8, 11,14-eicosatrienoic acid into PGEl is accompanied by a hydrogen isotope effect.No conversion of [ 2 J*C]lSL-hydroperoxy -8(cis), ll(cis) ,13(trans) -eicosatrienoic acid or [2-'*C]lSL-hydroxy-8(cis), ll(cis) , lJ(frans)eicosatrienoic acid into PGEl or PGFI, could be detected.Incubations of [9-3H ,3J4C]8,11 ,14-eicosatrienoic acid revealed that PGF1, is not formed via PGEl in the system used.The mechanistic implications of the results obtained are discussed.It is suggested that 11-peroxy-8,12,14-eicosatrienoic acid is the first intermediate in the conversion.The peroxy acid is cyclized into an endoperoxide, which is eventually transformed into PGEl or PGF,, by independent reactions.
Hydrogen Storage in Microporous Metal–Organic Frameworks with Exposed Metal Sites (2008)

Owing to their high uptake capacity at low temperature and excellent reversibility kinetics, metal-organic frameworks have attracted considerable attention as potential solid-state hydrogen storage materials. In the last few years, researchers have also identified several strategies for increasing the affinity of these materials towards hydrogen, among which the binding of H(2) to unsaturated metal centers is one of the most promising. Herein, we review the synthetic approaches employed thus far for producing frameworks with exposed metal sites, and summarize the hydrogen uptake capacities and binding energies in these materials. In addition, results from experiments that were used to probe independently the metal-hydrogen interaction in selected materials will be discussed.
Regulation of endosomal motility and degradation by amyotrophic lateral sclerosis 2/alsin (2009)

Dysfunction of alsin, particularly its putative Rab5 guanine-nucleotide-exchange factor activity, has been linked to one form of juvenile onset recessive familial amyotrophic lateral sclerosis (ALS2). Multiple lines of alsin knockout (ALS2(-/-)) mice have been generated to model this disease. However, it remains elusive whether the Rab5-dependent endocytosis is altered in ALS2(-/-) neurons. To directly examine the Rab5-mediated endosomal trafficking in ALS2(-/-) neurons, we introduced green fluorescent protein (GFP)-tagged Rab5 into cultured hippocampal neurons to monitor the morphology and motility of Rab5-associated early endosomes. Here we report that Rab5-mediated endocytosis was severely altered in ALS2(-/-) neurons. Excessive accumulation of Rab5-positive vesicles was observed in ALS2(-/-) neurons, which correlated with a significant reduction in endosomal motility and augmentation in endosomal conversion to lysosomes. Consequently, a significant increase in endosome/lysosome-dependent degradation of internalized glutamate receptors was observed in ALS2(-/-) neurons. These phenotypes closely resembled the endosomal trafficking abnormalities induced by a constitutively active form of Rab5 in wild-type neurons. Therefore, our findings reveal a negatively regulatory mechanism of alsin in Rab5-mediated endosomal trafficking, suggesting that enhanced endosomal degradation in ALS2(-/-) neurons may underlie the pathogenesis of motor neuron degeneration in ALS2 and related motor neuron diseases.
Elaboration et caractérisation de micro- et nano-composites alumine-zircone pour application orthopédique (2006)

Ce travail de thèse a pour objectif l'élaboration et la caractérisation de micro- et nano-composites alumine-zircone appliqués aux têtes fémorales de prothèses de hanches. Les micro-composites ont été élaborés par dispersion atomisation, puis pressage. La dispersion électrostérique a permis de déterminer le taux de dispersant (Darvan C) optimal, pour l'alumine et les zircones (pure et yttriée). Ce taux est de 0.25 wt%. Cependant, ce type de stabilisation s'est montrée moins efficace que la stabilisation électrostatique, comme en témoignet des agrégats de zircone caractérisés au sein des suspensions par des mesures de rhéologie, et par MEB dans les microstructures des composites frittés. En revanche, par dispersion électrostatique, il est possible d'obtenir des composites homogènes, soit à pH 4,5 pour un mélange d'alumine et de zircone pure ou yttriée, soit à pH 11, pour un mélange d'alumine et de zircone pure. Les micro-composites denses sont caractérisés en terme de propriétés mécaniques, résistance au vieillissement, propriétés biologiques et tribologiques. Pour éviter tout vieillissement, nous avons montré qu'il est nécessaire de proscrire tout agrégat de zircone de la microstructure et d'utiliser un taux de zircone à 16 vol%. Les tests mécaniques d'indentation Vickers, par la méthode d'Anstis, nous ont permis de déterminer les seuils de propagation des fissures de nos différentes nuances, et de sélectionner une nuance contenant 10 vol% de zircone pure. Les caractéristiques en frottement sont par ailleurs comparables à celles des têtes en alumine (référence pour cette application). L'absence de cytotoxicité de notre composite en présence de fibroblastes et d'ostéoblastes a été démontrée par des tests MTT. Enfin, l'élaboration de nanocomposites a nécessité des techniques d'élaboration particulières (dispersion, coulage, et frittage SPS). Le nanocomposite obtenu présente des tailles de grains d'alumine et de zircone de 200nm et 95nm, pour une densité de 98%. Les propriétés mécaniques d'un tel nanocomposite, évaluées par indentation (méthode d'Anstis), se sont avérées similaires à celles d'un composite microstructuré
Local administration of 7 beta-hydroxycholesteryl-3-oleate inhibits growth of experimental rat C6 glioblastoma. (1994)

The effect of 7 beta-hydroxycholesteryl-3-oleate on rat brain C6 glioblastoma cells was studied. Three days after the inoculation of 2 x 10(5) C6 cells into the frontal cortex of 6-day-old Wistar rats, two types of liposomes [consisting of either phosphatidylcholine and monosialoganglioside (PG:GM1, 10:1 mol/mol) only, or containing 7 beta-hydroxycholesterol, 7 beta-hydroxycholesteryl-3-oleate, 7 alpha-hydroxycholesteryl-3-oleate, or 7-ketocholesteryl-3-oleate] were injected into the xenograft. Ten days later, the animals were sacrificed, the tumors were stained with cresyl violet or hematoxylin/eosin, their volumes determined by image analysis, and their development followed by magnetic resonance imaging. The mean (+/- SE) tumor volume was 4.4 +/- 1.0 mm3. The injection of liposomes without oxysterol had no effect on tumor growth, whereas injection of liposomes containing 7 beta-hydroxycholesteryl-3-oleate (36 nmol) gave rise to a marked decrease in tumor volume (from 4.4 +/- 1.0 to 0.7 +/- 0.4 mm3). Seven nmol had no effect on tumor growth, 72 nmol were as efficient as 36 nmol, and 144 nmol attenuated the tumor volume by 50% only. Liposomes containing 72 nmol of oleic acid enhanced the tumor volume 4-fold. These findings were confirmed by magnetic resonance imaging. Thus, following induction of tumors in both the right and left sides of the cortex and treatment of the right side, magnetic resonance imaging indicated a significant decrease in tumor volume on the right side only. When C6 cells and 7 beta-hydroxycholesteryl-3-oleate were simultaneously injected, tumors did not develop in 80% of the animals. The clearance of [3H]7 beta-hydroxycholesteryl-3-oleate, of which 75% was converted to cholesterol, reached 99% after 48 h. Other oxysterols did not affect the tumor volume except that 7-keto-cholesteryl-3-oleate decreased the tumor volume by 50%. Thus, the 3-fatty acyl ester and 7 beta-hydroxyl groups are apparently required for the antitumor growth effect. Taken together, these data suggest that 7 beta-hydroxycholesteryl-3-oleate might be useful for local glioblastoma chemotherapy.
In Situ Selection of Lead Compounds by Click Chemistry:  Target-Guided Optimization of Acetylcholinesterase Inhibitors (2005)

The target-guided, in situ click chemistry approach to lead discovery has been successfully employed for discovering acetylcholinesterase (AChE) inhibitors by incubating a selected enzyme/tacrine azide combination with a variety of acetylene reagents that were not previously known to interact with the enzyme's peripheral binding site. The triazole products, formed by the enzyme, were identified by HPLC-mass spectrometry analysis of the crude reaction mixtures. The target-guided lead discovery search was also successful when performed with reagent mixtures containing up to 10 components. From 23 acetylene reagents, the enzyme selected two phenyltetrahydroisoquinoline (PIQ) building blocks that combined with the tacrine azide within the active center gorge to form multivalent inhibitors that simultaneously associate with the active and peripheral binding sites. These new inhibitors are up to 3 times as potent as our previous phenylphenanthridinium-derived compounds, and with dissociation constants as low as 33 femtomolar, they are the most potent noncovalent AChE inhibitors known. In addition, the new compounds lack a permanent positive charge and aniline groups and possess fewer fused aromatic rings. Remarkably, despite the high binding affinity, the enzyme displayed a surprisingly low preference for one PIQ enantiomer over the other.
Enfermedad cerebrovascular y estado nutricional (2007)

Background: It is recognized the importance of malnutrition as a cause of morbidity and mortality in medical and surgical affections. The nutritional assessment of the patient should be based on a correct evaluation of different aspects. Objective: To assess the nutritional state of patients affected by cerebrovascular diseases in its ischemic form and the incidence of complications and deaths. Methods: A randomized simple and open clinical trial which is also prospective and longitudinal, not controlled by placebos that included 80 patients with a tomographed-clinical diagnosis of cerebral infarction admitted at the Higher Institute of Military Medicine during 2005. Clinical and dietary record, weight, size, daily assessments of the immunological performance by means of peripheral count of lymphocytes were analyzed. Results: Out of the total, 90 per cent of the patients had a weight loss lesser than 10 % of the ideal weight and, the 10% made evident a discrete increasing of weight. Patients with complications presented higher per cent of loss of weight and higher figures of urinary nitrogen. The higher per cent of loss of weight and the lowest lymphocytes count were found in patients with septic complications. An abbaissement in adequate nutritional parameters was found in deceased patients. Significant differences in the report of the initial malnourished patient’s complication existed. Conclusions: It was evident the relationship between the evolution of the cerebrovascular disease and the nutritional state which is conditioned by the appearance of complications with emphasis on sepsis. That’s why it is necessary to pay special attention to the nutrition of patients with neuroictus.