gebhart/patrepeval huggingface dataset:
Indirect health effects of relative humidity in indoor environments. (1986)

A review of the health effects of relative humidity in indoor environments suggests that relative humidity can affect the incidence of respiratory infections and allergies. Experimental studies on airborne-transmitted infectious bacteria and viruses have shown that the survival or infectivity of these organisms is minimized by exposure to relative humidities between 40 and 70%. Nine epidemiological studies examined the relationship between the number of respiratory infections or absenteeism and the relative humidity of the office, residence, or school. The incidence of absenteeism or respiratory infections was found to be lower among people working or living in environments with mid-range versus low or high relative humidities. The indoor size of allergenic mite and fungal populations is directly dependent upon the relative humidity. Mite populations are minimized when the relative humidity is below 50% and reach a maximum size at 80% relative humidity. Most species of fungi cannot grow unless the relative humidity exceeds 60%. Relative humidity also affects the rate of offgassing of formaldehyde from indoor building materials, the rate of formation of acids and salts from sulfur and nitrogen dioxide, and the rate of formation of ozone. The influence of relative humidity on the abundance of allergens, pathogens, and noxious chemicals suggests that indoor relative humidity levels should be considered as a factor of indoor air quality. The majority of adverse health effects caused by relative humidity would be minimized by maintaining indoor levels between 40 and 60%. This would require humidification during winter in areas with cold winter climates. Humidification should preferably use evaporative or steam humidifiers, as cool mist humidifiers can disseminate aerosols contaminated with allergens.
Liver repopulation after cell transplantation in mice treated with retrorsine and carbon tetrachloride1 (2002)

This murine study demonstrates high levels of repopulation after liver cell transplantation into nongenetically modified livers, using a cell cycle inhibitor and chemical liver injury to provide transplanted cells a proliferative advantage. Liver repopulation was effected mostly by a small fraction of transplanted cells. Analogous nonsurgical liver cell transplantation strategies, but with clinically applicable drugs, could be devised for the treatment of liver-based metabolic diseases.
Fc receptor regulation of protective immunity against Chlamydia trachomatis (2002)

The prevailing paradigm for designing potentially efficacious vaccines against the obligate intracellular bacterium, Chlamydia trachomatis, advocates regimens capable of inducing a mucosal antigen-specific T helper type 1 (Th1) response. However, recent reports indicate that rapid and efficient clearance of a secondary infection also requires certain B-cell functions. We investigated the hypothesis that Fc receptor (FcR)-mediated antibody effector mechanisms are important B-cell-related functions involved in controlling a chlamydial genital reinfection. Microbiological analysis of genital chlamydial infection in FcR knockout (FcRKO) mice lacking the activatory FcgammaRI (CD64) and FcRgammaIII (CD16), as well as the inhibitory FcgammaRIIB1 (CD32), revealed a greater intensity of secondary infection (i.e. bacterial shedding) in FcRminus sign/minus sign as compared to FcR+/+ mice; however, the course of the primary infection was indistinguishable in both animals. Pathologically, FcRKO mice suffered greater ascending infection than immunocompetent wild-type (WT) mice after a secondary infection. Immunological evaluation indicated that the presence of specific anti-chlamydial antibodies enhanced chlamydial antigen presentation for induction of a Th1 response by FcR+/+, but not FcRminus sign/minus sign, antigen-presenting cells. In addition, specific anti-chlamydial antibodies augmented both macrophage killing of infected epithelial cells by antibody-dependent cellular cytotoxicity (ADCC) and macrophage inhibition of productive growth of chlamydiae in co-cultures. These results indicate that B cells participate in anti-chlamydial immunity via FcR-mediated effector functions of antibodies, which are operative during reinfections. Such effector functions include ADCC, and possibly enhanced uptake, processing and presentation of chlamydial antigens for rapid induction of a Th1 response, all facilitating the early clearance of an infection. These findings suggest that a future anti-chlamydial vaccine should elicit both humoral and T-cell-mediated immune responses for optimal memory response and vaccine efficacy.
Host-microbial symbiosis in the vertebrate gastrointestinal tract and the Lactobacillus reuteri paradigm (2010)

Vertebrates engage in symbiotic associations with vast and complex microbial communities that colonize their gastrointestinal tracts. Recent advances have provided mechanistic insight into the important contributions of the gut microbiome to vertebrate biology, but questions remain about the evolutionary processes that have shaped symbiotic interactions in the gut and the consequences that arise for both the microbes and the host. Here we discuss the biological principles that underlie microbial symbiosis in the vertebrate gut and the potential of the development of mutualism. We then review phylogenetic and experimental studies on the vertebrate symbiont Lactobacillus reuteri that have provided novel insight into the ecological and evolutionary strategy of a gut microbe and its relationship with the host. We argue that a mechanistic understanding of the microbial symbiosis in the vertebrate gut and its evolution will be important to determine how this relationship can go awry, and it may reveal possibilities by which the gut microbiome can be manipulated to support health.
Cross-presentation of tumor antigens by bone marrow–derived antigen-presenting cells is the dominant mechanism in the induction of T-cell tolerance during B-cell lymphoma progression (2001)

Tumor antigen-specific T-cell tolerance may limit the efficacy of therapeutic cancer vaccines. Direct presentation of antigens by tumor cells incapable of providing adequate costimulation to tumor-specific T cells has been suggested as the basis for this unresponsiveness. Using parent-into-F1 bone marrow (BM) chimeras, this study unambiguously demonstrates that the induction of this tolerant state requires T-cell recognition of tumor antigen presented by BM-derived antigen-presenting cells (APCs), not tumor cells themselves. In the absence of host APC presentation, tumor-specific T cells remained functional, even in the setting of antigen expressed by B-cell lymphomas residing in secondary lymphoid tissues. The intrinsic APC capacity of tumor cells has therefore little influence over T-cell priming versus tolerance, a decision that is regulated at the level of host APCs. (Blood. 2001;98:1070-1077)
Balloon Angioplasty and Stent Implantation Induce a Vascular Inflammatory Reaction (2002)

Purpose: To investigate whether peripheral balloon angioplasty with and without stent implantation independently causes an inflammatory vascular response measured by serum acute-phase reactants. Methods: This was a prospective cohort study enrolled 388 consecutive patients (218 men; median age 70 years, interquartile range 59–76) with peripheral artery disease undergoing balloon angioplasty (n = 187), stent implantation (n = 140), and diagnostic angiography (control group, n = 61). C-reactive protein (CRP) measured by standard and high-sensitivity assays, serum amyloid A (SAA), fibrinogen, and white blood cell (WBC) count were obtained at baseline and at 8, 24, and 48 hours postintervention. Polynomial logistic regression analysis was used to assess the independent association of acute-phase reactants and the interventional group. Results: CRP levels measured by both standard and the high-sensitivity assays significantly increased after balloon angioplasty (standard CRP, p = 0.02; high-sensitivity CRP, p = 0.02) and stent implantation (standard CRP, p = 0.004; high-sensitivity CRP, p = 0.008) compared to the control group adjusting for age, sex, duration of fluoroscopy, volume of contrast, and periprocedural complications. SAA values differed only between the stent group and controls (p = 0.05). Fibrinogen and WBCs were not different among the 3 interventional groups. Conclusions: Balloon injury and stent implantation induce a vascular inflammatory response at the dilated vessel segment measurable by serum acute-phase parameters. The standard CRP assay is adequate to quantify acute-phase response in these patients.
Global Transmission of Oseltamivir-Resistant Influenza (2009)

This winter, the circulating strain of seasonal influenza A virus (H1N1) is resistant to the neuraminidase inhibitor oseltamivir. Dr. Anne Moscona writes that the surprise element of the circulating resistant virus is its apparently spontaneous emergence since 2007.
Recentin vivoadvances in cell-penetrating peptide-assisted drug delivery (2015)

Despite recent advances in the field, confusions surrounding CPP internalization mechanisms and intracellular trafficking are hindering the development of new and more efficient vectors. Nevertheless, the recent increase in the number of publications containing in vivo CPP utilization looks promising that the number of clinical trials would also increase in the near future.
N-acetyltransferase 2 (NAT2) gene polymorphisms in Parkinson's disease (2006)

We found little evidence for differences in polymorphic acetylation genotypes in PD and control subjects. Results of the meta-analyses did not also provide conclusive evidence for an overall association of NAT2 slow acetylator genotypes to PD.
Molecular genetics of human inherited disease (1995)

Xp21 (Pseudohypertrophic) Muscular Dystrophy: Duchenne and Becker Muscular Dystrophy The Cystic Fibrosis Gene: Cloning and Characterization Huntington's Disease The Fragile X Mental Retardation Syndrome The Molecular Genetics of Myotonic Dystrophy Genetic and Molecular Analysis of the Human Y Chromosome Identification and Characterization of the Neurofibromatosis Type 1 Gene The Genetics of Psychiatric Disorders.
Frizzled homolog proteins, microRNAs and Wnt signaling in cancer (2012)

Wnt signaling pathways play important roles in tumorigenesis and are initiated by binding of Wnt to various receptors including frizzleds (FZDs). FZDs are one of several families of receptors comprised of FZD/LRP/ROR2/RYK in the Wnt signaling pathway. Expression of some FZD receptors are up regulated, thereby activating the Wnt signaling pathway and is correlated with cancer malignancy and patient outcomes (recurrence and survival) in many cancers. The FZD family contains ten genes in humans and their function has not been completely examined including the regulatory mechanisms of FZD genes in cancer. Knockdown of FZDs may suppress the Wnt signaling pathway resulting in decreased cell growth, invasion, motility and metastasis of cancer cells. Recently a number of microRNAs (miRNAs) have been identified and reported to be important in several cancers. MiRNAs regulate target gene expression at both the transcription and translation levels. The study of miRNA is a newly emerging field and promises to be helpful in understanding the pathogenesis of FZDs in cancer. In addition, miRNAs may be useful in regulating FZDs in cancer cells. Therefore, the aim of this review is to discuss current knowledge of the functional mechanisms of FZDs in cancer, including regulation by miRNAs and the potential for possible use of miRNAs and FZDs in future clinical applications.
Direct Charge Number and Molecular Weight Determination of Large Individual Ions by Electrospray Ionization Fourier Transform Ion Cyclotron Resonance Mass Spectrometry (1994)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTDirect Charge Number and Molecular Weight Determination of Large Individual Ions by Electrospray Ionization Fourier Transform Ion Cyclotron Resonance Mass SpectrometryRuidan. Chen, Qinyuan. Wu, Dale W. Mitchell, Steven A. Hofstadler, Alan L. Rockwood, and Richard D. SmithCite this: Anal. Chem. 1994, 66, 22, 3964–3969Publication Date (Print):November 15, 1994Publication History Published online1 May 2002Published inissue 15 November 1994https://pubs.acs.org/doi/10.1021/ac00094a018https://doi.org/10.1021/ac00094a018research-articleACS PublicationsRequest reuse permissionsArticle Views172Altmetric-Citations31LEARN 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-Alertsclose Get e-Alerts
Lactic acidosis in critical illness (1992)

The severity of lactic acidosis in critically ill patients correlates with overall oxygen debt and survival. Lactate determinations may be useful as an ongoing monitor of perfusion as resuscitation proceeds. Therapy of critically ill patients with lactic acidosis is designed to maximize oxygen delivery in order to reduce tissue hypoxia by increasing cardiac index, while maintaining hemoglobin concentration. Buffering agents have not been shown to materially affect outcome from lactic acidosis caused by shock. The benefits of other specific therapies designed to reduce the severity of lactic acidosis remain unproven.
IFN-γ and 1,25(OH)2D3 induce on THP-1 cells distinct patterns of cell surface antigen expression, cytokine production, and responsiveness to contact with activated T cells (1992)

Differentiation and maturation of monocytes are accompanied by the expression of specific surface glycoproteins, the secretion of cytokines, and the capacity to respond to ligands. These changes may be influenced by interactions with hormones, soluble lymphocytic products, or direct contact with lymphocytes. We have studied two distinct pathways in the differentiation of a human monocytic cell line, THP-1: one being induced by IFN-gamma and the other by 1 alpha,25-dihydroxyvitamin D3 (1,25(OH)2D3). In THP-1 cells, IFN-gamma induces cell surface expression of HLA-DR and CD54 and production of IL-1 beta, TNF-alpha, and IL-6. In contrast, 1,25(OH)2D3 increases cell surface expression of CD11b and CD14, but fails to stimulate cytokine production. Direct contact of THP-1 with stimulated fixed T cells markedly induces IL-1 beta, TNF-alpha, and IL-6 production by THP-1. Production is higher when THP-1 have been previously exposed to 1,25(OH)2D3 as compared to prior exposure to IFN-gamma. mAb raised against certain relevant cell surface glycoproteins on THP-1 were tested for their ability to block the response of THP-1 to T cells. Antibodies to CD11a, CD11b, and CD11c, alone or in combination, only partially blocked IL-1 beta production by THP-1, whereas antibodies to CD54 and CD14 did not. Thus other unknown structures on the THP-1 cells may be involved in the induction of THP-1 cytokine production by T cell contact.
Lifespan extension in C. elegans by a molecular chaperone dependent upon insulin‐like signals (2003)

Insulin-like signalling is a key determinate of lifespan in diverse species including mammals but the mechanism by which this pathway influences the rate of aging is unknown. In the roundworm Caenorhabditis elegans, mutations in the insulin-like signalling pathway extend adult lifespan and are associated with up-regulation of stress response genes including those for heat shock proteins (HSPs). We tested the hypothesis that the C. elegans insulin-like signalling pathway determines longevity through modulating HSP levels. We introduced extra copies of the gene encoding HSP-16 and this conferred stress resistance and longevity both in a wildtype and a long-lived mutant strain. The DAF-16 transcription factor is essential for maximal hsp-16 expression and for lifespan extension conferred by hsp-16. This demonstrates that lifespan is determined in part by insulin-like regulation of molecular chaperones.
Tumor necrosis factor/cachectin interacts with endothelial cell receptors to induce release of interleukin 1. (1986)

Tumor necrosis factor/cachectin (TNF) has been implicated as a mediator of the host response in sepsis and neoplasia. Recent work has shown that TNF can modulate endothelial cell hemostatic properties, suggesting that endothelium is a target tissue for TNF. This led us to examine whether endothelial cells have specific binding sites for TNF and augment the biological response to TNF by elaborating the inflammatory mediator, IL-1. Incubation of 125I-recombinant human TNF with confluent, cultured human umbilical vein endothelial cells resulted in time-dependent, reversible, and saturable binding. Binding was half-maximal at a TNF concentration of 105 +/- 40 pM, and at saturation 1,500 molecules were bound per cell. Heat-treated TNF, which is biologically inactive, did not bind to endothelium. In addition to surface binding, TNF induced the elaboration of IL-1 activity by endothelial cells in a time-dependent manner. Generation of IL-1 activity required protein synthesis and was half-maximal at a TNF concentration of 50 +/- 20 pM. IL-1 activity from TNF-treated endothelium could be adsorbed by an immobilized antibody to IL-1. Heat-treated TNF was ineffective in eliciting endothelial cell IL-1. These data indicate that TNF can bind specifically to endothelium and initiate a cascade of inflammatory and coagulant events on the vessel surface potentially central to the host response to neoplasia and sepsis.
Levonorgestrel-releasing intrauterine device versus hysteroscopic endometrial resection in the treatment of dysfunctional uterine bleeding (1997)

Somewhat less satisfactory results were obtained with a levonorgestrel-releasing intrauterine system compared with endometrial resection for dysfunctional uterine bleeding at 1 year of follow-up.
The Rate of Return on Universal Life Insurance (1987)

Universal life insurance is one of the newest products in the industry. It has been heavily promoted and has been acclaimed as an alternative to direct investment in the financial markets by policyholders. Because the policyholder purchases both term insurance protection and an investment stream, it is useful to compare the rate of return on this package to the alternative of buying term protection in the open market and investing in the financial markets on an individual basis. This article carries out the comparison by assessing internal rates of return on a large sample of universal life policies and comparing them to the current interest rates quoted by the companies. Under the assumptions made, the investor benefits from buying term insurance and investing premium residuals directly rather than purchasing a universal life policy. Further, this article examines the reasons underlying this result and concludes that in a vast majority of cases the annual loading and expense charges attendant to the universal life contract make it inferior to an open market insurance and investment strategy, assuming the open market strategy returns can, over time, approach the current interest rates quoted by the issuers of universal life insurance.
Cloning, expression, and nucleotide sequence of a lipase gene from Pseudomonas fluorescens B52 (1992)

In this study, we report the cloning and expression of lipase gene from Pseudomonas fluorescens B52, a psychrotrophic spoilage bacterium isolated from refrigerated raw milk. Sequence analysis revealed one major open reading frame of 1,428 nucleotides that was predicted to encode a protein with a molecular weight of 50,241. The predicted enzyme was found to contain an amino acid sequence highly homologous to the putative substrate-binding domain present within all lipases examined to date.
Nanometer-scale flow of molten polyethylene from a heated atomic force microscope tip (2012)

We investigate the nanometer-scale flow of molten polyethylene from a heated atomic force microscope (AFM) cantilever tip during thermal dip-pen nanolithography (tDPN). Polymer nanostructures were written for cantilever tip temperatures and substrate temperatures controlled over the range 100-260 °C and while the tip was either moving with speed 0.5-2.0 µm s(-1) or stationary and heated for 0.1-100 s. We find that polymer flow depends on surface capillary forces and not on shear between tip and substrate. The polymer mass flow rate is sensitive to the temperature-dependent polymer viscosity. The polymer flow is governed by thermal Marangoni forces and non-equilibrium wetting dynamics caused by a solidification front within the feature.
Risk Stratification for In-Hospital Mortality in Acutely Decompensated Heart Failure<SUBTITLE>Classification and Regression Tree Analysis</SUBTITLE> (2005)

These results suggest that ADHF patients at low, intermediate, and high risk for in-hospital mortality can be easily identified using vital sign and laboratory data obtained on hospital admission. The ADHERE risk tree provides clinicians with a validated, practical bedside tool for mortality risk stratification.
Proteolytic Activation of Alternative CCR1 Ligands in Inflammation (2005)

Although chemokines CCL3/MIP-1alpha and CCL5/RANTES are considered to be primary CCR1 ligands in inflammatory responses, alternative CCR1 ligands have also been described. Indeed, four such chemokines, CCL6/C10/MIP-related protein-1, CCL9/MIP-1gamma/MIP-related protein-2, CCL15/MIP-1delta/hemofiltrate CC chemokine-2/leukotactin-1, and CCL23/CKbeta8/myeloid progenitor inhibitory factor-1, are unique in possessing a separately encoded N-terminal domain of 16-20 residues and two additional precisely positioned cysteines that form a third disulfide bridge. In vitro, these four chemokines are weak CCR1 agonists, but potency can be increased up to 1000-fold by engineered or expression-associated N-terminal truncations. We examined the ability of proinflammatory proteases, human cell supernatants, or physiological fluids to perform N-terminal truncations of these chemokines and thereby activate their functions. Remarkably, most of the proteases and fluids removed the N-terminal domains from all four chemokines, but were relatively unable to cleave the truncated forms further. The truncated chemokines exhibited up to 1000-fold increases in CCR1-mediated signaling and chemotaxis assays in vitro. In addition, N-terminally truncated CCL15/MIP-1delta and CCL23/CKbeta8, but not CCL3/MIP-1alpha or CCL5/RANTES, were detected at relatively high levels in synovial fluids from rheumatoid arthritis patients. These data suggest that alternative CCR1 ligands are converted into potent chemoattractants by proteases released during inflammatory responses in vivo.
Pain on Injection of Lipid-Free Propofol and Propofol Emulsion Containing Medium-Chain Triglyceride: A Comparative Study (2005)

Pain on injection of two formulations of propofol was compared. A lipid-free formulation produced more pain on injection as compared with the emulsion containing medium-chain triglyceride.