gebhart/patrepeval huggingface dataset:
Simultaneous conversion of Pd-PPh3 and B-H to B-PPh2 under exceedingly mild conditions. Crystal and molecular structure of PdPPh3Cl{7-SMe-8-Me-11-PPh2-7,8-C2B9H10} (1991)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTSimultaneous conversion of Pd-PPh3 and B-H to B-PPh2 under exceedingly mild conditions. Crystal and molecular structure of PdPPh3Cl{7-SMe-8-Me-11-PPh2-7,8-C2B9H10}Francesc Teixidor, Jaume Casabo, Antonio M. Romerosa, Clara Vinas, Jordi Rius, and Carles MiravitllesCite this: J. Am. Chem. Soc. 1991, 113, 26, 9895–9896Publication Date (Print):December 1, 1991Publication History Published online1 May 2002Published inissue 1 December 1991https://pubs.acs.org/doi/10.1021/ja00026a049https://doi.org/10.1021/ja00026a049research-articleACS PublicationsRequest reuse permissionsArticle Views134Altmetric-Citations32LEARN ABOUT THESE METRICSArticle Views are the COUNTER-compliant sum of full text article downloads since November 2008 (both PDF and HTML) across all institutions and individuals. These metrics are regularly updated to reflect usage leading up to the last few days.Citations are the number of other articles citing this article, calculated by Crossref and updated daily. Find more information about Crossref citation counts.The Altmetric Attention Score is a quantitative measure of the attention that a research article has received online. Clicking on the donut icon will load a page at altmetric.com with additional details about the score and the social media presence for the given article. Find more information on the Altmetric Attention Score and how the score is calculated. Share Add toView InAdd Full Text with ReferenceAdd Description ExportRISCitationCitation and abstractCitation and referencesMore Options Share onFacebookTwitterWechatLinked InRedditEmail Other access optionsGet e-AlertscloseSupporting Info (1)»Supporting Information Supporting Information Get e-Alerts
Anti- <i>Saccharomyces cerevisiae</i> and antineutrophil cytoplasmic antibodies as predictors of inflammatory bowel disease (2005)

ASCA and pANCA may predict development of inflammatory bowel disease years before the disease is clinically diagnosed.
Secondary Disease in Rat Radiation Chimeras<xref ref-type="fn" rid="FN2">2</xref><xref ref-type="fn" rid="FN3">3</xref> (1964)

Rats were treated with homologous bone marrow following nearly lethal and lethal X irradiation. About 60 percent of the animals survived beyond the 4th week. In the rat-strain combination used, secondary disease developed during the 2d and 3d month in about 30 percent of the survivors, with emaciation and skin lesions as the principal symptoms. Surprisingly, colitis and diarrhea, prominent and consistent symptoms of secondary disease in the other species so far investigated, were never found, even in fatal secondary disease of the rat. There was no evidence of hemolytic anemia. The administration of homologous lymphoid cells provoked a faster, somewhat modified secondary syndrome with much higher mortality. In these rats, histologic lesions of the intestinal mucosa were found, but no colitis or diarrhea. Homologous bone marrow was also administered after median lethal radiation doses, which resulted in a temporarily functioning graft. A detrimental effect of such grafts, as described for certain mouse-strain combinations (“the MLD effect”), was not found.
Isolation of directed evolution mutants of chloroperoxidase resistant to suicide inactivation by primary olefins (2000)

Abstract Wild‐type chloroperoxidase catalyzes the efficient chiral epoxidation of secondary olefins but is rapidly inactivated in a mechanism‐based suicide reaction when incubated with hydrogen peroxide and primary olefins. Directed evolution mutants of chloroperoxidase have now been isolated that are resistant to suicidal inactivation. Plasmid vectors containing error‐prone copies of the chloroperoxidase gene and a hygromycin B resistance marker gene have been used to transform Caldariomyces fumago spheroplasts and produce mutant libraries. The mutant library clones were screened for their ability to resist mechanism‐based inactivation by allylbenzene. Four generations of PCR‐based random mutagenesis and screening yielded mutants that were completely resistant to the suicide‐inactivation reaction. Rather surprisingly, the fourth generation mutant developed enhanced epoxidation activity in addition to resistance to allylbenzene inactivation. These initial results suggest that the directed evolution technique can be used to produce chloroperoxidase variants that can further exploit the potential of chloroperoxidase for the synthesis of chiral intermediates.
Peripheral vs. Central Blockade of the Renin-Angiotensin System in Spontaneously Hypertensive Rats: Comparison of Novel AT1 Receptor Antagonist TCV-116 with Angiotensin Converting Enzyme Inhibitor Delapril. (1993)

In the present study, we evaluated the hemodynamic and metabolic profiles derived from oral administration of the angiotensin converting enzyme inhibitor, delapril 50mg/kg/day, and the non-peptide angiotensin II type I (AT1) receptor antagonist, TCV-116 1mg/kg/day, for five days, to try to discriminate AT1 receptor-related responses from the depressor properties of chronic treatment with delapril in spontaneously hypertensive rats (SHRs). Both TCV-116 and delapril oral administrations significantly decreased blood pressure without any changes in heart rate. Delapril induced dipsogenic response and natriuresis associated with augmentation of urinary catecholamine excretion, while TCV-116 did not cause any changes in these variables. Neither delapril nor TCV-116 changed urinary excretion of prostaglandin (PG) E2 and 6-keto PG F1α. We also examined the effects of centrally administered angiotensin converting enzyme inhibitor and AT1 receptor antagonist to determine the central role of these drugs.Either the active metabolite of delapril, delapril-M1 1 mg/kg/day, or the active form of TCV-116, CV-11974 0.1mg/kg/day, were administered intracerebroventricularly for five days. Both treatments significantly decreased the blood pressure, in association with augmentation of the baroreceptor reflex control of heart rate, in response to phenylephrine injection. These findings suggest that the depressor properties of orally administered delapril are more complex than those of TCV-116, while central blockade by both angiotensin converting enzyme and AT1 receptor decreases blood pressure in part through baroreceptor sensitization. (Hypertens Res;1993 16: 239-246)
Effects of chronic beta-adrenergic blockade on exercise training in dogs (1988)

To assess the role of beta-adrenergic stimulation in cardiovascular conditioning we examined the effects of a beta-adrenergic blocker, propranolol, in mongrel dogs during an 8-wk treadmill-training program. Seven dogs were trained without a drug (NP), six were trained on propranolol 10 mg.kg-1.day-1 (P), and five served as caged controls (C). Effective beta-adrenergic blockade was documented by a decrease in peak exercise heart rate of 54 +/- 11 (SE) beats/min (P less than 0.05) and a one-log magnitude of increase in the isoproterenol-heart rate dose-response curve. Testing was performed before drug treatment or training and again after training without the drug for 5 days. Submaximal exercise heart rate decreased similarly in both NP and P (-26 +/- 4 NP vs. -25 +/- 9 beats/min P, P less than 0.05 for both) but peak heart rate decreased only with NP (-33 +/- 9 beats/min, P less than 0.05). Treadmill exercise time increased similarly in both groups: 3.4 +/- 0.6 min in NP and 3.0 +/- 0.2 min in P (both P less than 0.05). Blood volume also increased after training in both groups: 605 +/- 250 ml (26%) in NP and 377 +/- 140 ml (17%) in P (both P less than 0.05). Submaximal exercise arterial lactates were reduced similarly in both groups but peak exercise lactate was reduced more in NP (-1.4 +/- 0.3 NP vs -0.3 +/- 0.12 mmol/l P, P less than 0.05). Lactate threshold increased in both groups but the increase was greater in NP (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
The demethylation of griseofulvin by fungi (1961)

Research Article| July 01 1961 The demethylation of griseofulvin by fungi B Boothroyd; B Boothroyd 1Glaxo Laboratories Limited, Sefton Park, Stoke Poges, Bucks Search for other works by this author on: This Site PubMed Google Scholar EJ Napier; EJ Napier 1Glaxo Laboratories Limited, Sefton Park, Stoke Poges, Bucks Search for other works by this author on: This Site PubMed Google Scholar GA Somerfield GA Somerfield 1Glaxo Laboratories Limited, Sefton Park, Stoke Poges, Bucks Search for other works by this author on: This Site PubMed Google Scholar Biochem J (1961) 80 (1): 34–37. https://doi.org/10.1042/bj0800034 Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Facebook Twitter LinkedIn MailTo Cite Icon Cite Get Permissions Citation B Boothroyd, EJ Napier, GA Somerfield; The demethylation of griseofulvin by fungi. Biochem J 1 July 1961; 80 (1): 34–37. doi: https://doi.org/10.1042/bj0800034 Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All ContentAll JournalsBiochemical Journal Search Advanced Search This content is only available as a PDF. © 1961 The Biochemical Society1961 Article PDF first page preview Close Modal You do not currently have access to this content.
Autistic effector T cells in mice with a point mutation in the LAT adaptor fail to respond to Listeria monocytogenes infection (2005)

The adaptor protein linker for activation of T cells (LAT) is an important transducer of extracellular T cell stimuli. In mice with a point mutation in LAT (LatY136F), TCR signaling is substantially compromised and LatY136F T cells are unresponsive to CD3 cross-linking in vitro. Nevertheless, LatY136F mice develop a polyclonal lymphoproliferation of CD4(+) T cells, which display a T(h)2-polarized effector phenotype. In this study, LatY136F mice were infected with the intracellular bacterium Listeria monocytogenes and the antigen-specific responses of T cells were determined. Both CD4(+) and CD8(+) LatY136F T cells were unresponsive to L. monocytogenes infection. In contrast, when CD4(+) T cells from wild-type mice were adoptively transferred into LatY136F hosts, they responded normally to L. monocytogenes, indicating that the LatY136F milieu permits T(h)1 responses. Furthermore, we analyzed whether the infection would influence the capacity of LatY136F CD4(+) T cells to produce IL-4 and IFN-gamma. While L. monocytogenes infection results in T(h)1-type T cell responses in wild-type animals, we found that it did not shift the strong T(h)2 polarization of LatY136F T cells towards a T(h)1 pattern. In conclusion, our results suggest that the activation and T(h)2 polarization of the LatY136F CD4(+) T cells is not influenced by infection with an intracellular pathogen known to induce robust T(h)1 responses, and is thus likely driven by T cell intrinsic mechanisms.
Common waterhemp (Amaranthus rudis) interference in corn (2004)

Knowing the interference potential of common waterhemp in corn could be beneficial in planning waterhemp management strategies. In 2000, 2001, and 2002, field studies were conducted to examine both early- and late-season common waterhemp interference in corn. Early-season interference was determined by removing common waterhemp at the VE (vegetative emergence), V4 (four visible leaf collars), V6, V8, V10, V12, and V14 growth stages of corn for the entire season, and late-season interference was determined by allowing common waterhemp to emerge and compete from the VE, V4, V6, V8, V10, V12, and V14 corn growth stages. The interference potential of common waterhemp varied between the year 2000 and the combined years of 2001–2002. This is probably due to differences in precipitation in May and June in these two environments (297 mm in 2000 compared with 198 mm in 2001–2002). An excess of 590 g m−2 of dry matter and 13,000 and 1,200 seeds per female plant were produced when common waterhemp emerged at V4 and V6 corn, respectively, the 2 yr that corn was drought stressed. When corn was not moisture stressed, common waterhemp that emerged at V4 and V6 corn produced less than 220 g m−2 and less than 500 seeds per female plant. Season-long common waterhemp interference reduced corn yield 74% in 2 yr of the study and 11% in the third. Early-season common waterhemp interference began at V6 corn, with a 4 and 23% yield loss in 2000 and 2001–2002, respectively. Common waterhemp interference from late-season emergence reduced corn yield when emergence occurred before the V8 corn growth stage. Taking into account early- and late-season common waterhemp interference. the critical common waterhemp–free period was around the V6 corn stage to optimize corn yield.
Chlorination of Titanium Oxycarbonitride Produced by Carbothermal Nitridation of Rutile (2008)

Titanium oxycarbonitride was produced by carbothermal nitridation of rutile. Mixtures consisting of titania and graphite with different carbon to titanium dioxide molar ratios were pressed into pellets and subsequently heated under nitrogen atmosphere at 1450 °C. Titanium oxycarbonitride was chlorinated in a horizontal tube furnace using chlorine and Cl2−N2 gas mixture. Effects of furnace temperature, chlorine partial pressure, gas flow rate, and particle size on the rate and extent of chlorination were examined. The chlorination was ignited at 150−200 °C. Chlorine partial pressure in Cl2−N2 gas mixture, gas flow rate, and particle size affected the chlorination rate, while the effect of particle size was insignificant. Extent of chlorination of titanium oxycarbonitride produced with carbon-to-titania molar ratio at 2.5 was close to 100% after 40 min of reaction.
Role of Toll-Like Receptor 4 in the Proinflammatory Response to <i>Vibrio cholerae</i> O1 El Tor Strains Deficient in Production of Cholera Toxin and Accessory Toxins (2005)

Following intranasal inoculation, Vibrio cholerae KFV101 (DeltactxAB DeltahapA DeltahlyA DeltartxA) colonizes and stimulates tumor necrosis factor alpha and interleukin 1beta (IL-1beta) in mice, similar to what occurs with isogenic strain P4 (DeltactxAB), but is less virulent and stimulates reduced levels of IL-6, demonstrating a role for accessory toxins in pathogenesis. Morbidity is enhanced in C3H/HeJ mice, indicating that Toll-like receptor 4 is important for infection containment.
Mechanisms of Inactivation of γ-Aminobutyric Acid Aminotransferase by 4-Amino-5-fluoro-5-hexenoic Acid (1996)

An investigation of the mechanisms of inactivation of the pyridoxal 5‘-phosphate (PLP)-dependent pig brain γ-aminobutyric acid (GABA) aminotransferase by 4-amino-5-fluoro-5-hexenoic acid (2), a monofluorinated analogue of the anticonvulsant drug vigabatrin, is described. Inactivation of [3H]PLP-reconstituted GABA aminotransferase with 2 followed by denaturation released the coenzyme in two forms, one as PLP and the other in a modified form in the ratio 7:3. All enzyme activity was lost upon inactivation by 2, but about 30% of the activity returned upon incubation with PLP, consistent with the formation and release of 30% of the coenzyme in a modified form, as noted above. Inactivation of GABA aminotransferase with [2-3H]-2 followed by gel filtration resulted in the attachment of 0.7 equiv of tritium to the enzyme, even though complete inactivation occurred. This also is consistent with the above results that about 30% of inactivation is the result of release of a modified coenzyme, leaving 30% of the enzyme as its apoenzyme form. Isolation and mass spectral analysis of the modified coenzyme gave peaks consistent with a modified coenzyme formed from a reaction with the inactivator (27). Denaturation of the enzyme containing 0.7 equiv of radioactivity from the above experiment led to release of 0.2−0.3 equiv of the radioactivity as γ-acetyl-GABA (20). Treatment of the denatured enzyme with sodium periodate generated 0.2−0.25 equiv of succinic acid, leaving 0.15 equiv of radioactivity still covalently bound to the enzyme. Analysis of amine metabolites shows the formation of 0.5 equiv of 20. Analysis of the nonamine metabolites resulted in the identification of 1 equiv of 4-oxo-5-hexenoic acid (24). After inactivation, 2.6 ± 0.1 equiv of fluoride ions was detected, consistent with the loss of 1 fluoride ion to produce inactivation, 1 fluoride ion to generate the 4-oxo-5-hexenoic acid, and 0.5 fluoride ion released in the production of γ-acetyl-GABA. Normal transamination also occurs; 6.3 ± 0.6 transamination events occurred during inactivation, as measured by the conversion of [14C]-α-ketoglutarate to [14C]glutamate. These results indicate that there are, at least, three different inactivation mechanisms in effect (Schemes 4-6). All of these mechanisms begin with Schiff base formation between 2 and the active site PLP followed by removal of the γ-proton and elimination of the fluoride ion. It is from this conjugated allene intermediate (17) that all of the inactivation pathways and metabolites result, except for the normal transamination product. The partition ratio, the amount of inactivator converted to a product per inactivation event, is about 8; 6.5 transaminations, 0.5 conversion to 20, and 1.0 conversion to 24 per 1.0 inactivation event.
Abstract 20670: Coronary Microembolization During Transfemoral Transcatheter Aortic Valve Implantation: An Intracoronary Doppler Study (2014)

Background: A postprocedural increase of the serum troponin I concentration (TnI) reflects myocardial injury and occurs frequently during transcatheter aortic valve implantation (TAVI). Periprocedural coronary microembolization is a potential cause of such injury. We therefore evaluated each step of the transfemoral TAVI procedure for coronary embolization using intracoronary Doppler (ICD) in the left anterior descending (LAD) artery. Methods: 15 high-risk patients with severe, symptomatic aortic valve stenosis (age 79 ± 45 yrs; EuroScore 17 ± 4%) who underwent transfemoral TAVI using the balloon-expandable Edwards bioprosthesis were included. ICD examinations were recorded and evaluated off-line for high-intensity transient signals (HITS). Perioperative concentrations of TnI were serially measured within the first 72 h after TAVI, and a cardiac MRI with late gadolinium-enhancement (LGE) was performed within 7 days. Results: HITS were detected in all patients (figure 1), mostly during the initial crossing of the native valve and positioning of the prosthesis with subsequent implantation. TnI peaked at 24 h after TAVI (3.17 ng/ml), and LGE was observed in only one single case. There was no correlation between amount of HITS and TnI area under the curve in the first 72 h after TAVI. Conclusions: Procedural HITS were detected by ICD in all patients undergoing transfemoral TAVI. The highest amount of HITS was observed during initial valve passage and positioning of the prosthesis with subsequent implantation. However, no association was found between the number of HITS and myocardial injury, as reflected by increased serum TnI concentrations or LGE on cardiac MRI.
Metal ion-mediated regulation of heme oxygenase induction in cultured avian liver cells. (1982)

The induction of heme oxygenase (EC 1.14.99.3) in response to various metal treatments was investigated in monolayer cultures of chick embryo liver cells maintained in a chemically defined serum-free medium. The most potent heme oxygenase-inducing action was exhibited by CO2+, Cd2+, Sb3+, As3+, and Au1+ followed by lesser induction observed with Cu2+, Fe2+, and Fe3+. Mn2+, Ni2+, Se4+, Sn2+, and Zn2+ were without effect. In contrast to the marked inducing effect of Co2+ on heme oxygenase, Co-protoporphyrin IX decreased the enzyme activity in a dose-dependent manner. Addition of Zn2+ (20 microM) to Co2+-treated liver cell cultures revealed a striking ability of Zn2+ to block completely Co2+-induced heme oxygenase. Simultaneous addition of Mn2+ (50 microM) to Co2+-treated cells also blocked Co2+-induced heme oxygenase (approximately 50%). These findings in tissue culture confirm those made earlier in whole animals (Drummond, G. S., and Kappas, A. (1979) Proc. Natl. Acad. Sci. U. S. A. 76, 5331-5335) and indicate that these effects of Zn2+ and Mn2+ are exerted directly in liver cells. Addition of cysteine (400 microM) to the cultures also inhibited heme oxygenase induction by Co2+ substantially. Cycloheximide and actinomycin D blocked the induction of heme oxygenase, indicating that increased heme oxygenase activity by metal treatment is dependent on fresh RNA and protein synthesis. The half-life of the enzyme was calculated to be approximately 15 h after treatment with cycloheximide. These findings provide further evidence that metal ions can regulate heme oxygenase synthesis directly in isolated liver cells and that the metal-metal interactions which lead to blockade of the enzyme induction do not involve extrahepatic tissues.
Isolation of candidate genes of Friedreich`s ataxia on chromosome 9q13 (1994)

Friedreich`s ataxia (FRDA) is an autosomal recessive degenerative disease involving the central and peripheral nervous system and the heart. The mutated gene in FRDA has recently been localized within a 450 Kb interval on chromosome 9q13 between the markers D9S202/FR1/FR8. We have been able to confirm such localization for the disease gene by analysis of extended haplotype in consanguineous families. Cases of loss of marker homozygosity, which are likely to be due to ancient recombinations, have been found to involve D9S110, D9S15, and D9S111 on the telomeric side, and FR5 on the centromeric side, while homozygosity was always found for a core haplotype including D9S5, FD1, and D9S202. We constructed a YAC contig spanning the region between the telomeric markers and FR5, and cosmids have been obtained from the YACs. In order to isolate transcribed sequences from the FRDA candidate region we are utilizing a combination of approaches, including hybridization of YACs and cosmids to an arrayed human heart cDNA library, cDNA direct selection, and exon amplification. A transcribed sequence near the telomeric end of the region has been isolated by cDNA direct selection using pooled cosmids as genomic template and primary human heart, muscle, brain, liver and placenta cDNAsmore » as cDNA source. We have shown this sequence to be the human equivalent of ZO-2, a tight junction protein previously described in the dog. No mutations of this gene have been found in FRDA subjects. Additional cDNA have recently been isolated and they are currently being evaluated.« less
PPARγ‐Independent Side Effects of Thiazolidinediones on Mitochondrial Redox State in Rat Isolated Hearts (2015)

The effect of anti‐diabetic thiazolidinediones (TZDs) on contributing to heart failure and cardiac ischemia/reperfusion (IR) injury is controversial. Peroxisome proliferator‐activated receptor‐gamma (PPARγ) agonists are under scrutiny because of concerns about their cardiovascular safety. Acute administration of rosiglitazone, for example, was reported to differentially aggravate IR injury in a consomic rat heart model. In this study we investigated the effect of select TZDs on mitochondrial function in rat isolated hearts. Different concentrations of the TZDs rosiglitazone and pioglitazone were administered in the presence or absence of the specific PPARγ antagonist GW9662, and their effects on mitochondrial redox state were measured by online NADH and FAD autofluorescence. Both TZDs resulted in dose‐dependent, reversible increases in mitochondrial oxidation that were not attenuated by GW9662. Taken together, these data suggest excessive mitochondrial uncoupling by a PPARγ‐independent mechanism. If translated clinically, this may explain in part how TZDs adversely enhance cardiac IR injury and adverse events in susceptible patients. Supported by Department of Veterans Affairs (CARA‐026‐10F), NIH and institutional funds.