gebhart/patrepeval huggingface dataset:
[2-(Alkylideneamino)benzoato]nickel(II) Complexes:  Active Catalysts for Ethylene Polymerization (2003)

The complexes [RR‘CNC6H4C(O)O-κ2N,O]Ni(η3-CH2CMeCH2) (R, R‘ = −(CH2)5−, 6; R = Et, R‘ = Et, 7; R = tBu, R‘ = H, 8) are prepared by reaction of the corresponding potassium salts with [(η3-CH2CMeCH2)NiCl]2 in CH3CN. Additions of 1 equiv of B(C6F5)3 afford the zwitterionic complexes [RR‘CNC6H4C{OB(C6F5)3}O-κ2N,O]Ni(η3-CH2CMeCH2) (R, R‘ = −(CH2)5−, 9; R = Et, R‘ = Et, 10; R = tBu, R‘ = H, 11), which give poly(ethylene) when ethylene gas is added. This result is interesting in that the corresponding 2-(diphenylphosphino)benzoato and 2-(diphenylamino)benzoato complexes give mainly butene. Reactions of the potassium salts with Ni(η3-CH2C6H5)Cl(PMe3) afford benzyl complexes, [RR‘CNC6H4C(O)O-κ2N,O]Ni(η1-CH2C6H5)(PMe3) (R, R‘ = −(CH2)5−, 12; R = Et, R‘ = Et, 13). Additions of 2 equiv of B(C6F5)3 to 12 and 13 afford the zwitterionic η3-benzyl complexes [RR‘CNC6H4C{OB(C6F5)3}O-κ2N,O]Ni(η3-CH2C6H5) (R, R‘ = −(CH2)5−, 14; R = Et, R‘ = Et, 15). Complex 14 is rather unstable, and a bis ligand complex, [(CH2)5CNC6H4C{OB(C6F5)3}O-κ2N,O]2Ni (16), is formed during recrystallization. Complexes 14 and 15 are highly active to ethylene polymerization, and activities reach 3000−4000 kg/((mol of Ni) h) at 75 psig pressure. Solid structures of 6, 9, 11, 15, and 16 were determined by X-ray crystallography.
MAESTROS: A Multiwavelength Time-Domain NIRS System to Monitor Changes in Oxygenation and Oxidation State of Cytochrome-C-Oxidase (2018)

We present a multiwavelength, multichannel, time-domain near-infrared spectroscopy system named MAESTROS. This instrument can measure absorption and scattering coefficients and can quantify the concentrations of oxy- and deoxy-haemoglobin ([HbO<sub>2</sub>], [HHb]), and oxidation state of cytochrome-c-oxidase ([oxCCO]). This system is composed of a supercontinuum laser source coupled with two acousto-optic tuneable filters. The light is collected by four photomultipliers tubes, connected to a router to redirect the signal to a single time-correlated single-photon counting card. The interface between the system and the tissue is based on optical fibres. This arrangement allows us to resolve up to 16 wavelengths, within the range of 650-900 nm, at a sampling rate compatible with the physiology (from 0.5 to 2 Hz). In this paper, we describe the system and assess its performance based on two specifically designed protocols for photon migration instruments, the basic instrument protocol and nEUROPt protocols, and on a well characterized liquid phantom based on Intralipid and water. Then, the ability to resolve [HbO<sub>2</sub> ], [HHb], and [oxCCO] is demonstrated on a homogeneous liquid phantom, based on blood for [HbO<sub>2</sub>], [HHb], and yeast for [oxCCO]. In the future, the system could be used to monitor brain tissue physiology.
Effects of Tunicamycin on the Cell‐Surface Binding, Internalization and Degradation of Low‐Density Lipoproteins in Human Fibroblasts (1981)

The effect of tunicamycin, an inhibitor of protein glycosylation via the dolichol pathway, on the binding, internalization and degradation of low‐density lippoproteins was studied in cultured human fibroblasts. Glycoprotein synthesis was inhibited 50% in tunicamycin‐treated cells, while protein and nucleic acid synthesis were minimally inhibited. The binding of 125 I‐labeled low‐ density lipoproteins (measured as dextran‐sulfate‐releasable 125 I‐lipoproteins) in the tunicamycin‐treated cells at 4°C was saturable, but the amount bound was only one‐half that found in control cells. When these cells were warmed to 37°C for 30 min, the amounts of lipoproteins that were internalized (dextran‐sulfate‐resistant 125 I‐labeled low‐density lipoproteins) and degraded wre proportional to the amounts bound in both the tunicamycin‐treated and control cells. Tunicamycin also had no effect on the rate of internaliztion of 125 I‐labeled low‐density lipoproteins that were displaced by increasing concentrations of unlabeled low‐density lipoproteins were the same in both tunicamycin and control cells, an effect that was accompanied by similar patterns of decrease in the internalization and degradation of 125 I‐labeled low density lipoproteins; high‐density lipoproteins and fettuin had no inhibitory effect on these processes. Tunicamycin did not inhibit the degradation of 125 I‐labeled low‐density lipoproteins in homogenates of fibroblasts at pH 4.0. The data suggest that tunicamycin affects the number rather than the functional capacity of receptors on the cell surfacce since the kinetics of binding of 125 I‐labeled low‐density lipoproteins to tunicamycin‐treated cells is normal and the bound lipoproteins are both internalized and degraded normally. The data further suggest a role of the dolichol‐saccharide pathway in the normal intracellular metabolism of the receptor for low‐density lipoproteins.
Prostate-Specific Antigen Kinetics as a Measure of the Biologic Effect of Granulocyte-Macrophage Colony-Stimulating Factor in Patients With Serologic Progression of Prostate Cancer (2002)

GM-CSF has a biologic effect in patients with serologic progression of prostate cancer after definitive local therapy, as measured by PSA declines and modulation of PSA kinetics.
Neurobiology of Sexual Response in Men and Women (2006)

Sexual desire, arousal, and orgasm are mediated by complex--and as yet not fully understood--interactions of the somatic and autonomic nervous systems, operating at cerebral, spinal, and peripheral levels. Furthermore, neural activity within these systems is modulated by the presence of steroid and peptide hormones, which affect male and female response differentially. At the central level, dopaminergic and serotonergic systems appear to play a significant role in various components of sexual response, although adrenergic, cholinergic, nitergic, gamma-aminobutyric acidergic, and other neuropeptide transmitter systems may contribute as well. At the peripheral level, adrenergic, cholinergic, and nitergic activation mechanisms control vascular changes that underlie vaginal lubrication and penile erection. In addition, these systems respond to descending brain and spinal influences that generate orgasmic response. Disruption of endocrine, neural, or vascular response--caused by aging, disease, surgery, or medication--has the potential to lead to sexual inadequacy. At the same time, psychological and relationship factors play an important role in healthy sexual response and may enhance or impair sexual functioning.
Inhibition of human leukocyte elastase by N-substituted peptides containing .alpha.,.alpha.-difluorostatone residues at P1 (1992)

A series of tripeptides which contain alpha,alpha-difluorostatone residues at P1-P1' and span the S3-S1' subsites have been shown to be potent inhibitors of human leukocyte elastase (HLE). The tripeptides described contain the nonproteinogenic achiral residue N-(2,3-dihydro-1H-inden-2-yl)glycine at the P2-position. This redidue has previously been shown in the case of HLE to be a good bioisosteric replacement for L-proline. Of the peptides prepared, those which contain the alpha,alpha-difluoromethylene keton derivative of L-valine (difluorostatone) are the preferred residue at the P1-primary specificity position. Substitution at P1 by the corresponding alpha,alpha-difluoromethylene ketones of L-leucine and L-phenylalanine gives inactive compounds. Of the tripeptides described the most potent in vitro compound is ethyl N-[N-CBZ-L-valyl-N-(2,3-dihydro-1H-inden-2-yl)glycyl]- 4(S)-amino-2,2-difluoro-3-oxo-5-methylhexanoate (17B) (IC50 = 0.635 microM). It is presumed that the inhibitor 17b interacts with the S3-S1' binding regions of HLE. Additionally extended binding inhibitors were prepared which interact with the S3-S3' binding subsites of HLE. In order to effect interaction with the S1'-S3' subsites of HLE, the leaving group side of cleaved peptides, spacers based upon Gly-Gly, and those linked via the N epsilon of L-lysine were utilized. One of the most potent extended compounds (P3-P3') in vitro is methyl N6-[4(S)-[[N-[N-CBZ-L-valyl-N- (2,3-dihydro-1H-inden-2-yl)glycyl]amino]-2,2-difluoro-3-oxo-5- methylhexanoyl]-2(S)-(acetylamino)-6-aminohexanoate (24b) (IC50 = 0.057 microM). The described in vitro active inhibitors were also evaluated in hamsters in an elastase-induced pulmonary hemorrhage (EPH) model. In this model, intratracheal (it.) administration of 22c, 5 min prior to HLE challenge (10 micrograms, it.) effectively inhibited hemorrhage (94.6%) in a dose-dependent manner. The described alpha,alpha-difluoromethylene ketone inhibitors are assumed to act as transition-state analogs. The inhibition process presumably acts via hemiketal formation with the active site Ser195 of HLE, and is facilitated by the strongly electron withdrawing effect of the alpha,alpha-difluoromethylene functionality.
Midlife Dietary Intake of Antioxidants and Risk of Late-Life Incident Dementia: The Honolulu-Asia Aging Study (2004)

Antioxidants have been hypothesized to protect against Alzheimer's disease, but studies conducted in late life have been inconsistent. Risk factors measured in midlife may better predict dementia in late life because they are less affected by the disease process. The authors examined the association of midlife dietary intake of antioxidants to late-life dementia and its subtypes. Data were obtained from the Honolulu-Asia Aging Study, a prospective community-based study of Japanese-American men who were aged 45-68 years in 1965-1968, when a 24-hour dietary recall was administered. The analysis included 2,459 men with complete dietary data who were dementia-free at the first assessment in 1991-1993 and were examined up to two times for dementia between 1991 and 1999. The sample included 235 incident cases of dementia (102 cases of Alzheimer's disease, 38 cases of Alzheimer's disease with contributing cerebrovascular disease, and 44 cases of vascular dementia). Relative risks by quartile of intake were calculated using Cox proportional hazards models with age as the time scale, after adjustment for sociodemographic and lifestyle factors, cardiovascular risk factors, other dietary constituents, and apolipoprotein E e4. Intakes of beta-carotene, flavonoids, and vitamins E and C were not associated with the risk of dementia or its subtypes. This analysis suggests that midlife dietary intake of antioxidants does not modify the risk of late-life dementia or its most prevalent subtypes.
Methylation-sensitive enrichment of minor DNA alleles using a double-strand DNA-specific nuclease (2016)

Aberrant methylation changes, often present in a minor allelic fraction in clinical samples such as plasma-circulating DNA (cfDNA), are potentially powerful prognostic and predictive biomarkers in human disease including cancer. We report on a novel, highly-multiplexed approach to facilitate analysis of clinically useful methylation changes in minor DNA populations. Methylation Specific Nuclease-assisted Minor-allele Enrichment (MS-NaME) employs a double-strand-specific DNA nuclease (DSN) to remove excess DNA with normal methylation patterns. The technique utilizes oligonucleotide-probes that direct DSN activity to multiple targets in bisulfite-treated DNA, simultaneously. Oligonucleotide probes targeting unmethylated sequences generate local double stranded regions resulting to digestion of unmethylated targets, and leaving methylated targets intact; and vice versa. Subsequent amplification of the targeted regions results in enrichment of the targeted methylated or unmethylated minority-epigenetic-alleles. We validate MS-NaME by demonstrating enrichment of RARb2, ATM, MGMT and GSTP1 promoters in multiplexed MS-NaME reactions (177-plex) using dilutions of methylated/unmethylated DNA and in DNA from clinical lung cancer samples and matched normal tissue. MS-NaME is a highly scalable single-step approach performed at the genomic DNA level in solution that combines with most downstream detection technologies including Sanger sequencing, methylation-sensitive-high-resolution melting (MS-HRM) and methylation-specific-Taqman-based-digital-PCR (digital Methylight) to boost detection of low-level aberrant methylation-changes.
Smoothing depth maps for improved steroscopic image quality (2004)

A technique to improve the image quality of stereoscopic pictures generated from depth maps (depth image based rendering or DIBR) is examined. In general, there are two fundamental problems with DIBR: a depth map could contain artifacts (e.g., noise or "blockiness") and there is no explicit information on how to render newly exposed regions ("holes") in the rendered image as a result of new virtual camera positions. We hypothesized that smoothing depth maps before rendering will not only minimize the effects of noise and distortions in the depth maps but will also reduce areas of newly exposed regions where potential artifacts can arise. A formal subjective assessment of four stereoscopic sequences of natural scenes was conducted with 23 viewers. The stereoscopic sequences consisted of source images for the left-eye view and rendered images for the right-eye view. The depth maps were smoothed with a Gaussian blur filter at different levels of strength before depth image based rendering. Results indicated that ratings of perceived image quality improved with increasing levels of smoothing of the depth maps. Even though the depth maps were smoothed, a negative effect on ratings of overall perceived depth quality was not found.
CD36 Mediates the In Vitro Inhibitory Effects of Thrombospondin-1 on Endothelial Cells (1997)

Thrombospondin-1 (TSP-1) is a naturally occurring inhibitor of angiogenesis that is able to make normal endothelial cells unresponsive to a wide variety of inducers. Here we use both native TSP-1 and small antiangiogenic peptides derived from it to show that this inhibition is mediated by CD36, a transmembrane glycoprotein found on microvascular endothelial cells. Both IgG antibodies against CD36 and glutathione-S-transferase-CD36 fusion proteins that contain the TSP-1 binding site blocked the ability of intact TSP-1 and its active peptides to inhibit the migration of cultured microvascular endothelial cells. In addition, antiangiogenic TSP-1 peptides inhibited the binding of native TSP-1 to solid phase CD36 and its fusion proteins, as well as to CD36-expressing cells. Additional molecules known to bind CD36, including the IgM anti-CD36 antibody SM, oxidized (but not unoxidized) low density lipoprotein, and human collagen 1, mimicked TSP-1 by inhibiting the migration of human microvascular endothelial cells. Transfection of CD36-deficient human umbilical vein endothelial cells with a CD36 expression plasmid caused them to become sensitive to TSP-1 inhibition of their migration and tube formation. This work demonstrates that endothelial CD36, previously thought to be involved only in adhesion and scavenging activities, may be essential for the inhibition of angiogenesis by thrombospondin-1.
Cooperation of Multiple CCR5 Coreceptors Is Required for Infections by Human Immunodeficiency Virus Type 1 (2000)

In addition to the primary cell surface receptor CD4, CCR5 or another coreceptor is necessary for infections by human immunodeficiency virus type 1 (HIV-1), yet the mechanisms of coreceptor function and their stoichiometries in the infection pathway remain substantially unknown. To address these issues, we studied the effects of CCR5 concentrations on HIV-1 infections using wild-type CCR5 and two attenuated mutant CCR5s, one with the mutation Y14N at a critical tyrosine sulfation site in the amino terminus and one with the mutation G163R in extracellular loop 2. The Y14N mutation converted a YYT sequence at positions 14 to 16 to an NYT consensus site for N-linked glycosylation, and the mutant protein was shown to be glycosylated at that position. The relationships between HIV-1 infectivity values and CCR5 concentrations took the form of sigmoidal (S-shaped) curves, which were dramatically altered in different ways by these mutations. Both mutations shifted the curves by factors of approximately 30- to 150-fold along the CCR5 concentration axis, consistent with evidence that they reduce affinities of virus for the coreceptor. In addition, the Y14N mutation specifically reduced the maximum efficiencies of infection that could be obtained at saturating CCR5 concentrations. The sigmoidal curves for all R5 HIV-1 isolates were quantitatively consistent with a simple mathematical model, implying that CCR5s reversibly associate with cell surface HIV-1 in a concentration-dependent manner, that approximately four to six CCR5s assemble around the virus to form a complex needed for infection, and that both mutations inhibit assembly of this complex but only the Y14N mutation also significantly reduces its ability to successfully mediate HIV-1 infections. Although several alternative models would be compatible with our data, a common feature of these alternatives is the cooperation of multiple CCR5s in the HIV-1 infection pathway. This cooperativity will need to be considered in future studies to address in detail the mechanism of CCR5-mediated HIV-1 membrane fusion.
Simultaneous Rapid Measurement of Whole Blood Myoglobin, Creatine Kinase MB, and Cardiac Troponin I by the Triage Cardiac Panel for Detection of Myocardial Infarction (1999)

This multicenter study evaluated the Biosite Triage(R) Cardiac Panel as a quantitative, multimarker, whole blood system for the detection of acute myocardial infarction (MI). Optimum cutoffs for the discrimination of acute MI (n = 192 patients, 59 with MI) as determined by ROC curve analyses were as follows: 0.4 microgram/L for cardiac troponin I (cTnI); 4.3 microgram/L for the creatine kinase MB isoenzyme (CK-MB); and 107 microgram/L for myoglobin. The Triage Panel showed the following concordances for detection or rule-out of MI compared with established devices: cTnI >89%; CK-MB >81%; myoglobin >69%. No significant differences were present between methods for the same marker. Diagnostic efficiencies demonstrated comparable sensitivities and specificities for the diagnosis of MI in patients presenting with symptoms compared with the Dade, Beckman, and Behring CK-MB, cTnI, and myoglobin assays; the ratio of sensitivity to specificity for each marker was as follows: cTnI, 98%:100%; CK-MB, 95%:91%; myoglobin, 81%:92%. The areas under the ROC curves for the Biosite myoglobin, CK-MB, and cTnI were 0.818, 0.905, and 0.970, respectively; the areas were significantly different, P <0.05. In patients with skeletal muscle injury and renal disease, the Triage cTnI showed 94% and 100% specificity, respectively. The Triage panel offers clinicians a whole blood, point-of-care analysis of multiple cardiac markers that provides excellent clinical sensitivity and specificity for the detection of acute MI.
The cyclization of calichemicin-esperamicin analogs: a predictive biradicaloid transition state (1989)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTThe cyclization of calichemicin-esperamicin analogs: a predictive biradicaloid transition stateJames P. SnyderCite this: J. Am. Chem. Soc. 1989, 111, 19, 7630–7632Publication Date (Print):September 1, 1989Publication History Published online1 May 2002Published inissue 1 September 1989https://doi.org/10.1021/ja00201a063RIGHTS & PERMISSIONSArticle Views176Altmetric-Citations61LEARN 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 InReddit PDF (419 KB) Get e-Alerts Get e-Alerts
Osteopontin prevents monocyte recirculation and apoptosis (2007)

Cells of the monocyte/macrophage lineage have been shown to be the principal targets for productive HIV-1 replication within the CNS. In addition, HIV-1-associated dementia (HAD) has been shown to correlate with macrophage abundance in the brain. Although increased entry of monocytes into the brain is thought to initiate this process, mechanisms that prevent macrophage egress from the brain and means that prevent macrophage death may also contribute to cell accumulation. We hypothesized that osteopontin (OPN) was involved in the accumulation of macrophages in the brain in neuroAIDS. Using in vitro model systems, we have demonstrated the role of OPN in two distinct aspects of macrophage accumulation: prevention from recirculation and protection from apoptosis. In these unique mechanisms, OPN would aid in macrophage survival and accumulation in the brain, the pathological substrate of HAD.
A System for Neural Recording and Closed-Loop Intracortical Microstimulation in Awake Rodents (2008)

There is growing interest in intracortical microstimulation as a means of providing sensory input in neuroprosthetic systems. We believe that precisely controlling the timing and parameters of stimulation in closed loop can significantly improve the efficacy of this technique. Here, we present a system for closed-loop microstimulation in awake rodents chronically implanted with multielectrode arrays. The system interfaces with existing commercial recording and stimulating hardware. Using custom-made hardware, we can stimulate and record from electrodes on the same implanted array and significantly reduce the stimulation artifact. Stimulation sequences can either be preprogrammed or triggered by neural or behavioral events. Specifically, this system can provide feedback stimulation in response to action potentials or features in the local field potential recorded on any of the electrodes within 15 ms. It can also trigger stimulation based on behavioral events, such as real-time tracking of rat whiskers captured with high-speed video. We believe that this system, which can be recreated easily, will help to significantly refine the technique of intracortical microstimulation and advance the field of neuroprostheses.
Mechanical control of tissue and organ development (2010)

Many genes and molecules that drive tissue patterning during organogenesis and tissue regeneration have been discovered. Yet, we still lack a full understanding of how these chemical cues induce the formation of living tissues with their unique shapes and material properties. Here, we review work based on the convergence of physics, engineering and biology that suggests that mechanical forces generated by living cells are as crucial as genes and chemical signals for the control of embryological development, morphogenesis and tissue patterning.