gebhart/patrepeval huggingface dataset:
A 3-year longitudinal study of sleep disordered breathing in the elderly (2012)

Limited and controversial data exist on the natural evolution of sleep disordered breathing (SDB) in untreated individuals. This study examines the evolution of SDB over a 3-yr period in a community-based sample of elderly subjects. From the initial cohort of 854 healthy subjects aged mean ± SD 68.4 ± 0.8 yrs, 519 untreated subjects accepted clinical and instrumental follow-up 3.6 ± 1.6 yrs later. SDB was defined as a respiratory disturbance index (RDI) >15 events · h(-1). At baseline, 202 (39%) subjects had an RDI ≤ 15 events · h(-1) and 317 (61%) had an RDI >15 events · h(-1). 3 yrs later, 280 (54%) subjects were non-SDB and 239 (46%) had SDB. Between evaluations, the RDI decreased from 22.3 ± 16.2 to 16.4 ± 13.0 events · h(-1), with a greater decrease in the number of cases with an RDI >30 events · h(-1) that in those with RDI ≥ 30 events · h(-1). In the non-SDB group, 81% had a stable RDI and 19% increased their RDI by a mean of 13.7 events · h(-1). In the SDB group, the RDI decreased to values ≤ 15 events · h(-1) in 36.6% of cases, 63.4% still having SDB. The RDI changes did not depend on weight changes. In healthy elderly subjects, the prevalence and severity of SDB did not show a tendency toward natural worsening, some cases having improvement or a remission independent of weight changes. These findings also suggest that in the elderly, natural SDB progression is still hypothetical.
Vagus Nerve Stimulation Improves Restless Legs Syndrome Associated With Major Depression (2007)

Article AbstractBecause this piece does not have an abstract, we have provided for your benefit the first 3 sentences of the full text.Sir: Vagus nerve stimulation (VNS) has shown effects in treatment-resistant epilepsy1 and major depressive episode.2 Epidemiologic studies have described restless legs syndrome (RLS) to exist in varying degrees of severity in 2.5% to 10% of the population.3 Treatment of first choice is dopamine agonists, but agents that enhance inhibitory mechanisms in the way that anticonvulsive drugs do are effective, too.†‹
Circulating HER-2/erbB-2/c-neu (HER-2) extracellular domain as a prognostic factor in patients with metastatic breast cancer: Cancer and Leukemia Group B Study 8662. (2001)

ECD/HER-2 levels are elevated in 35-40% of patients with metastatic breast cancer. Elevated ECD/HER-2 levels are associated with a poorer prognosis in these patients. However, no predictive role for ECD/HER-2 was identified, either for endocrine therapy or for anthracycline-based chemotherapy in the metastatic setting.
DEHYDROEPIANDROSTERONE AND ANDROSTERONE LEVELS IN HUMAN PLASMA. EFFECT OF AGE AND SEX; DAY-TO-DAY AND DIURNAL VARIATIONS* (1957)

METHODS have been described for the measurement of total 17-ketosteroids (17-KS) occurring in human plasma (1) and for their fractionation (2). Dehydroepiandrosterone (DHA) and androsterone have been isolated and found to be the principal 17-KS in the peripheral circulation of normal man (3, 4). The present study was carried out in order to obtain further information on the levels of DHA and androsterone in normal subjects and to ascertain the effect of age and sex on the concentrations of these steroids. It was also thought to be of interest to determine the diurnal variation as well as the day-to-day changes of the 17-KS levels in the same subjects. A 40-ml. sample of blood was drawn from each experimental subject between 8:30 and 9:30 a.m., except in the study of diurnal variations, when blood was obtained at various times of the day. The blood samples were heparinized. They were centrifuged within forty-five minutes following collection and the plasma was immediately separated from the red cells. When the determination was not carried out immediately, the plasma was kept in a freezer.
Bloodstream infections in patients with solid tumors (2016)

Little information is currently available regarding bloodstream infection (BSI) in patients with solid tumors who, for a variety of reasons, are particularly predisposed to develop this condition. In this review we focus on the incidence, epidemiology, clinical features, etiology, antimicrobial resistance, and outcomes of BSI of adult cancer patients with solid tumors. Most episodes of BSI occur in non-neutropenic patients, in whom the site of primary or metastatic tumor often serves as the portal of entry. The urinary tract and the abdomen are the most frequent sources of infection, and cholangitis is the most common recurrent source of BSI. Gram-negative bacilli are becoming the leading cause of BSI in patients with solid tumors, and the rate of multidrug resistance is increasingly being recognized. The case-fatality rate in patients with solid tumors and BSI is high, especially among those with comorbidities, advanced neoplasms, corticosteroid therapy, and shock at presentation.
MUTATIONS IN A SUBGROUP OF PATIENTS WITH MILD HAEMOPHILIA A AND A FAMILIAL DISCREPANCY BETWEEN THE ONE‐STAGE AND TWO‐STAGE FACTOR VIII:C METHODS (1996)

A subgroup of patients with haemophilia A who have a familial discrepancy between the one-stage and two-stage factor VIII:C results has previously been described. These patients show factor VIII:C levels by one-stage assay that are 2-7-fold higher than their two-stage results. We have studied 10 such families and identified six different mutations in the factor VIII gene in this group. The chemical cleavage method and DNA sequencing was used to identify mutations in factor VIII gene fragments generated by reverse transcription and PCR. All available family members were tested to confirm the presence of the mutation in affected individuals. These patients were found to have one of six single point substitutions causing a missense mutation and alteration to one codon in exons 7, 11, 14 or 18. The mutations comprise three that have not previously been described (Ala284Glu. Arg698Leu. Leu1932Phe) and three that have been previously described (Ser289Leu, Arg531His, Arg698Trp). Alterations to the amino acid composition of the A1, A2 and A3 domains of factor VIII are predicted by these molecular studies. In contrast, a control group of 23 mild haemophilia families with equivalent factor VIII:C results by one-stage and two-stage assays did not have any of the above mutations. Detailed studies in seven of these latter families identified four mutations affecting the A3, C1 and C2 domains of factor VIII. These findings suggest a genetic basis to the unusual factor VIII phenotype but do not explain the mechanism of the discrepant factor VIII activity.
Submicrometer gratings for solar energy applications (1995)

Diffractive optical structures for increasing the efficiency of crystalline silicon solar cells are discussed. As a consequence of the indirect band gap, light absorption becomes very ineffective near the band edge. This can be remedied by use of optimized diffraction gratings that lead to light trapping. We present blazed gratings that increase the optically effective cell thickness by approximately a factor of 5. In addition we present a wideband antireflection structure for glass that consists of a diffraction grating with a dielectric overcoat, which leads to an average reflection of less than 0.6% in the wavelength range between 300 and 2100 nm.
Nonmitogenic Anti-CD3 Monoclonal Antibodies Deliver a Partial T Cell Receptor Signal and Induce Clonal Anergy (1997)

Anti-CD3 monoclonal antibodies (mAbs) are potent immunosuppressive agents used in clinical transplantation. However, the activation-related adverse side effects associated with these mAbs have prompted the development of less toxic nonmitogenic anti-CD3 mAb therapies. At present, the functional and biochemical consequences of T cell exposure to nonmitogenic anti-CD3 is unclear. In this study, we have examined the early signaling events triggered by a nonmitogenic anti-CD3 mAb. Like the mitogenic anti-CD3 mAb, nonnmitogenic anti-CD3 triggered changes in the T cell receptor (TCR) complex, including zeta chain tyrosine phosphorylation and ZAP-70 association. However, unlike the mitogenic anti-CD3 stimulation, nonmitogenic anti-CD3 was ineffective at inducing the highly phosphorylated form of zeta (p23) and tyrosine phosphorylation of the associated ZAP-70 tyrosine kinase. This proximal signaling deficiency correlated with minimal phospholipase Cgamma-1 phosphorylation and failure to mobilize detectable Ca2+. Not only did biochemical signals delivered by nonmitogenic anti-CD3 resemble altered peptide ligand signaling, but exposure of Th1 clones to nonmitogenic anti-CD3 also resulted in functional anergy. Finally, a bispecific anti-CD3 X anti-CD4 F(ab)'2 reconstituted early signal transduction events and induced proliferation, suggesting that defective association of lck with the TCR complex may underlie the observed signaling differences between the mitogenic and nonmitogenic anti-CD3.
New Aqueous Inflow Inhibitors (1999)

Several new aqueous inflow inhibitors have been introduced over the past few years. These new agents include two alpha agonists, two topical carbonic anhydrase inhibitors, and a novel combination agent. All of these agent compare favorably with timolol in terms of aqueous suppression, though each has its own relative advantages and disadvantages.
Surface plasmon increase absorption in polymer photovoltaic cells (2007)

The authors demonstrate the triggering of surface plasmons at the interface of a metal grating and a photovoltaic bulk heterojunction blend of alternating polyfluorenes and a fullerene derivative. An increased absorption originating from surface plasmon resonances is confirmed by experimental reflection studies and theoretical modeling. Plasmonic resonances are further confirmed to influence the extracted photocurrent from devices. More current is generated at the wavelength position of the plasmon resonance peak. High conductivity polymer electrodes are used to build inverted sandwich structures with top anode and bottom metal grating, facilitating for triggering and characterization of the surface plasmon effects.
Monitoring solar activity on the far side of the sun from sky reflected Lyman α radiation (2000)

Solar active regions are known to be brighter in Lyman α radiation than the quiet sun. Accordingly, they illuminate more H atoms in interplanetary space through resonance scattering. As we show here, this excess of illumination related to active regions is clearly seen in full‐sky Lyman α maps recorded by the SWAN instrument on board SOHO, including those excesses resulting from active regions which are on the far side of the Sun. Since solar activity is most often connected to solar active regions, this technique could be used in the future to improve the quality of Space Weather forecast, by earlier detection of the birth of a new active region on the far side of the sun, before it comes into Earth's view at the East limb.
Time series community genomics analysis reveals rapid shifts in bacterial species, strains, and phage during infant gut colonization (2012)

The gastrointestinal microbiome undergoes shifts in species and strain abundances, yet dynamics involving closely related microorganisms remain largely unknown because most methods cannot resolve them. We developed new metagenomic methods and utilized them to track species and strain level variations in microbial communities in 11 fecal samples collected from a premature infant during the first month of life. Ninety six percent of the sequencing reads were assembled into scaffolds of >500 bp in length that could be assigned to organisms at the strain level. Six essentially complete (∼99%) and two near-complete genomes were assembled for bacteria that comprised as little as 1% of the community, as well as nine partial genomes of bacteria representing as little as 0.05%. In addition, three viral genomes were assembled and assigned to their hosts. The relative abundance of three Staphylococcus epidermidis strains, as well as three phages that infect them, changed dramatically over time. Genes possibly related to these shifts include those for resistance to antibiotics, heavy metals, and phage. At the species level, we observed the decline of an early-colonizing Propionibacterium acnes strain similar to SK137 and the proliferation of novel Propionibacterium and Peptoniphilus species late in colonization. The Propionibacterium species differed in their ability to metabolize carbon compounds such as inositol and sialic acid, indicating that shifts in species composition likely impact the metabolic potential of the community. These results highlight the benefit of reconstructing complete genomes from metagenomic data and demonstrate methods for achieving this goal.
Grignard Reagents:  Alkoxide-Directed Iodine−Magnesium Exchange at sp3 Centers (2007)

Sequential addition of i-PrMgCl and BuLi to sp3 hybridized iodoalcohols triggers a facile iodine-metal exchange. Intercepting the resulting cyclic Grignard reagents with a slight excess of an electrophile leads to a diverse range of substituted alcohols. The iodine-magnesium exchange strategy is effective with 3-carbon iodoalcohols bearing alkyl substitutents on the carbinol or adjacent carbons and with the chain-extended homolog 4-iodobutan-1-ol.
Mutational fingerprints of aging (2002)

Using a lacZ plasmid transgenic mouse model, spectra of spontaneous point mutations were determined in brain, heart, liver, spleen and small intestine in young and old mice. While similar at a young age, the mutation spectra among these organs were significantly different in old age. In brain and heart G:C-->A:T transitions at CpG sites were the predominant mutation, suggesting that oxidative damage is not a major mutagenic event in these tissues. Other base changes, especially those affecting A:T base pairs, positively correlated with increasing proliferative activity of the different tissues. A relatively high percentage of base changes at A:T base pairs and compound mutants were found in both spleen and spontaneous lymphoma, suggesting a possible role of the hypermutation process in splenocytes in carcinogenesis. The similar mutant spectra observed at a young age may reflect a common mutation mechanism for all tissues that could be driven by the rapid cell division that takes place during development. However, the spectra of the young tissues did not resemble that of the most proliferative aged tissue, implying that replicative history per se is not the underlying causal factor of age-related organ-specific differences in mutation spectra. Rather, differences in organ function, possibly in association with replicative history, may explain the divergence in mutation spectra during aging.
Activin and Inhibin Have Antagonistic Effects on Ligand-Dependent Heteromerization of the Type I and Type II Activin Receptors and Human Erythroid Differentiation (1997)

Activins and inhibins belong to the transforming growth factor beta (TGF-beta)-like superfamily and exert their effects on a broad range of cellular targets by modulating cell differentiation and proliferation. Members of this family interact with two structurally related classes of receptors (type I and type II), both containing a serine/threonine kinase domain. When expressed alone, the type II but not the type I activin receptor can bind activin. However, the presence of a type I receptor is required for signaling. For TGF-beta1, ligand binding to the type II receptor results in the recruitment and transphosphorylation of the type I receptor. Transient overexpression of the two types of activin receptor results in ligand-independent receptor heteromerization and activation. Nevertheless, activin addition to the transfected cells increased complex formation between the two receptors, suggesting a mechanism of action similar to that observed for the TGF-beta receptor. In the present study, we generated a stable cell line, overexpressing the two types of activin receptor upon induction, in the human erythroleukemia cell line K562. We demonstrate here that activin specifically induces heteromer formation between the type I and type II receptors in a time-dependent manner. Using this stable line, we analyzed the effects of activin and inhibin on human erythroid differentiation. Our results indicate that activin signal transduction mediated through its type I and type II receptors results in an increase in the hemoglobin content of the cells and limits their proliferation. Finally, using cell lines that can be induced to overexpress ActRII and ActRIB or ActRIB only, we show that the inhibin antagonistic effects on activin-induced biological responses are mediated through a competition for the type II activin receptor but also require the presence of an inhibin-specific binding component.
PI-Pful and PI-PfuII, intein-coded homing endonucleases from Pyrococcus furiosus. I. Purification and identification of the homing-type endonuclease activities (1999)

We screened for proteins with specific binding activity to Holliday junction DNA from the hyperthermophilic archaeon Pyrococcus furiosus and found a protein that has specific affinity for DNA with a branched structure, like a three-way or four-way junction. The protein was identified as one of the two inteins encoded in the gene for ribonucleotide reductase (RNR) by gene cloning. These two inteins were spliced out from the precursor protein as polypeptides with molecular weights of 53.078 and 43.976 kDa, respectively. The amino acid sequences of these inteins have two copies of the LAGLIDADG motif, which is found in the site-specific DNA endonucleases. The purified proteins actually cleaved double-stranded DNA with the sequence of the intein(-)allele, and, therefore, they were designated PI- Pfu I and PI- Pfu II. They generate a 4 bp 3'-OH overhang with a 5'-phosphate, like other known homing endonucleases originating from inteins. The optimal conditions of the DNA cleavage reaction, including temperature, pH, and concentrations of KCl and MgCl(2), have been determined. The high affinity for junction DNA of PI- Pfu I was confirmed using the purified protein.
Signaling through the sphingomyelin pathway. (1995)

Journal Article Signaling through the sphingomyelin pathway Get access Y Zhang, Y Zhang Search for other works by this author on: Oxford Academic Google Scholar R Kolesnick R Kolesnick Search for other works by this author on: Oxford Academic Google Scholar Endocrinology, Volume 136, Issue 10, 1 October 1995, Pages 4157–4160, https://doi.org/10.1210/endo.136.10.7664631 Published: 01 October 1995
Long-term fate and effects of exercise on sternal cartilage autografts used for repair of large osteochondral defects in horses (1994)

Bilateral osteochondral defects (10 mm2 x 3 mm deep) were created on the distal articular surface of the radial carpal bone of ten, 2- to 3-year-old horses. One defect of each horse was repaired, using a sternal cartilage autograft (treated), and the other was left untreated (control). The horses were exercised on a high-speed treadmill at incrementally increased speed and duration over the course of 12 months. Horses were evaluated arthroscopically at 6 to 7 weeks, and clinical examinations were conducted weekly at exercise. Twelve months after surgery, carpuses of each horse were radiographed and clinically examined prior to euthanasia. A gross pathologic evaluation of each joint was conducted, and samples were collected for histologic, histochemical, histomorphometric, and biochemical evaluation. Radiographically, the grafted joints had more extensive evidence of arthropathy, and clinically, 8 of the 10 horses were more lame in the grafted limb. On the basis of histomorphometry, the repair tissue of the grafted defects contained a greater median percentage of hyaline cartilage (45%) than that of control defects (4.5%), and the control defects contained a greater percentage of fibrocartilage (82%) than did grafted defects (28.5%). A greater median percentage of repair tissue stained with safranin-O in the grafted defects (24.5%) than in the control defects (3.5%). On gross pathologic and histologic evaluation, repair tissue of the control defects had better continuity and was more firmly attached to the subchondral bone than was repair tissue of the grafted defects. Repair tissue of the grafted defects had extensive fissure and flap formation. Histologically, subchondral bone reactivity and fibroplasia was extensive in grafted joints. Repair tissue of grafted defects had a greater percentage of type II collagen (mean +/- SEM, 83.5 +/- 2.95%) than did controls (mean, 79.4 +/- 3.87%) that was not statistically significant. Hexosamine content was significantly higher (P < 0.05) in repair tissue of the grafted defect (mean, 28.9 +/- 3.00 mg/g of dry weight) vs control (mean, 20.6 +/- 1.85 mg/g of dry weight). On the basis of this experimental model, sternal cartilage autografts cannot be recommended at this time for repair of osteochondral defects in athletic horses.
The Human Gene Map for Performance and Health-Related Fitness Phenotypes: The 2003 Update (2004)

This review presents the 2003 update of the human gene map for physical performance and health-related fitness phenotypes. It is based on peer-reviewed papers published by the end of 2003 and includes association studies with candidate genes, genome-wide scans with polymorphic markers, and single-gene defects causing exercise intolerance to variable degrees. The genes and markers with evidence of association or linkage with a performance or fitness phenotype in sedentary or active people, in adaptation to acute exercise, or for training-induced changes are positioned on the genetic map of all autosomes and the X chromosome. Negative studies are reviewed but a gene or locus must be supported by at least one positive study before being inserted on the map. By the end of 2000, 29 loci were depicted on the first edition of the map. In contrast, the 2003 human gene map for physical performance and health-related phenotypes includes 109 autosomal gene entries and QTL, plus two on the X chromosome. Moreover, there are 15 mitochondrial genes in which sequence variants have been shown to influence relevant fitness and performance phenotypes.
Rosuvastatin – A Highly Effective New 3-Hydroxy-3-Methylglutaryl Coenzyme A Reductase Inhibitor: Review of Clinical Trial Data at 10–40 mg Doses in Dyslipidemic Patients (2003)

Rosuvastatin (Crestor; licensed to AstraZeneca, Macclesfield, UK from Shionogi, Osaka, Japan) is a new statin with pharmacologic characteristics that translate into selectivity of effect in hepatic cells and enhanced potency in 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibition. It is approved for use at doses of 10-40 mg once daily to reduce low-density lipoprotein (LDL) cholesterol, increase high-density lipoprotein (HDL) cholesterol and improve other lipid measures in dyslipidemic patients. In a dose-ranging study in mild/moderate hypercholesterolemia, rosuvastatin reduced LDL cholesterol by 52-63% at 10-40 mg. Rosuvastatin 10 mg reduces LDL cholesterol significantly more than atorvastatin 10 mg, simvastatin 10-40 mg and pravastatin 10-40 mg, and enables significantly more patients to achieve National Cholesterol Education Program and Joint European Societies LDL cholesterol goals compared with each of these statins. Rosuvastatin also produces marked elevations in HDL cholesterol and maintains this effect across the dose range. Rosuvastatin favorably modifies triglycerides, LDL cholesterol and other lipid measures in patients with hypertriglyceridemia or mixed dyslipidemia, including diabetic patients, and may constitute a monotherapy option for many such patients. Rosuvastatin is well tolerated when used alone or in combination, exhibiting a safety profile similar to that of other available statins. Rosuvastatin offers considerable advantages for use in routine clinical practice.