tbuckley/cabot-search huggingface dataset:
Indoor air pollution and respiratory health in the elderly
Authors: M. Simoni, M.S. Jaakkola, L. Carrozzi, S. Baldacci, F. Di Pede, G. Viegi
Journal: European Respiratory Journal (2003)

People spend about ≥80–90% of their daily time indoors, elderly people especially at home. Thus, it is important to investigate possible health effects of indoor air pollutants and to consider their contributions to the total human exposure. This report summarises current knowledge on health effects of three common indoor air pollutants, respirable suspended particles, nitrogen dioxide and environmental tobacco smoke, with focus on the adults and the elderly. Preliminary findings on exposure distributions and health effects of these pollutants in older subjects of two panel studies carried out in Italian general populations will also be reported. The two indoor pollution studies were performed in the Po Delta area in North Italy (428 subjects and 140 houses investigated) and in Pisa in Central Italy (761 subjects and 282 houses investigated). Individuals aged ≥65 yrs spent a significantly larger number of hours at home than the other age groups both in winter and in summer. A trend of higher occurrence of acute respiratory symptoms in the presence of environmental tobacco smoke was shown in comparison to the unexposed elderly both in winter (31 versus 29%) and summer (33 versus 16%). The occurrence of acute respiratory symptoms was consistently higher in relation to the high respirable suspended particles-index exposure compared to low exposure (33 versus 27% in winter, 27 versus 21% in summer). Both the presence of environmental tobacco smoke at home and exposure to the high respirable suspended particles-index were associated with a decrease in the mean daily peak expiratory flow.
Impact of Providing Audiotapes of Primary Adjuvant Treatment Consultations to Women With Breast Cancer: A Multisite, Randomized, Controlled Trial
Authors: Thomas F. Hack, Tom Pickles, Barry D. Bultz, J. Dean Ruether, Lorna M. Weir, Lesley F. Degner, John R. Mackey
Journal: Journal of Clinical Oncology (2003)

Women with breast cancer were provided with an audiotape of their primary adjuvant treatment consultation, and the following patient outcomes were measured at 12 weeks postconsultation: perceived degree of information provision, audiotape satisfaction and use, communication satisfaction with oncologist, mood state, and cancer-specific quality of life.Participants included 628 women newly diagnosed with breast cancer and 40 oncologists from six cancer centers in Canada. The patients were block randomized to one of four consultation groups: standard care control, not audiotaped; audiotaped, no audiotape given; audiotaped, patient given audiotape; and audiotaped, patient offered choice of receiving audiotape or not.Patients receiving the consultation audiotape had significantly better recall of having discussed side effects of treatment than patients who did not receive the audiotape. Audiotape benefit was not significantly related to patient satisfaction with communication, mood state, or quality of life at 12 weeks postconsultation, and was not significantly affected by choice of receiving the audiotape. Patients rated the audiotape intervention positively, with an average score of 83.9 of 100.Audiotape provision benefits patients by facilitating their perception of being informed about treatment side effects, but does not significantly influence patient satisfaction with communication, mood state, or quality of life.
Hamster female protein, a sex-limited pentraxin, is a constituent of Syrian hamster amyloid.
Authors: J E Coe, M J Ross
Journal: Journal of Clinical Investigation (1985)

Female protein (FP) is a pentraxin of Syrian hamster which is a homologue of two human pentraxins, C-reaction protein (CRP) and amyloid P component (AP). Functionally, FP has been shown to be similar to CRP, although FP has more homology at the amino terminus with AP. The present work investigated amyloid in the Syrian hamster to determine whether FP was involved in a manner analogous to AP. FP was found to be a constituent of Syrian hamster amyloid. This conclusion was based on the following results: (a) FP was consistently detected in amyloid deposits by fluorescent microscopy with specific antisera; (b) The amount of FP extractable from hamster livers directly correlated with the presence of amyloid; and (c) 125I-FP injected intravenously into amyloidotic hamsters rapidly left the intravascular compartment and was found subsequently in amyloid deposits. This unusual alteration of plasma metabolism and amyloid localization of 125I-FP was a characteristic finding in amyloidotic hamsters and was specific for 125I-FP. Therefore, as an amyloid component, FP appears to be functionally similar to human AP. However, FP synthesis is under sex steroid control and the unique sex-limited expression of this pentraxin was associated with an equally novel propensity for deposition of amyloid in female hamsters under normal or experimental conditions. Thus, a high serum level of FP, as found in normal females or diethylstilbestrol-treated males, was associated with enhanced amyloidosis. Although speculative at present, a primary role for serum FP in hamster amyloid deposition may be experimentally approachable by hormonal manipulation of FP synthesis.
Safety and efficacy of tibolone in breast-cancer patients with vasomotor symptoms: a double-blind, randomised, non-inferiority trial
Authors: Peter Kenemans, Nigel J Bundred, Jean-Michel Foidart, Ernst Kubista, Bo von Schoultz, Piero Sismondi, Rena Vassilopoulou-Sellin, Cheng Har Yip, Jan Egberts, Mirjam Mol-Arts, Roel Mulder, Steve van Os, Matthias W Beckmann
Journal: The Lancet Oncology (2009)
Ligation of patent ductus arteriosus in very low birthweight premature neonates.
Authors: P K Ghosh, J Lubliner, M Mogilnar, V Yakirevich, B A Vidne
Journal: Thorax (1985)

The results of ligation of a patent ductus arteriosus in 30 premature neonates with a very low birth weight were analysed. The mean gestational age at birth was 27 weeks and the mean weight 811 g. Attempted closure of the ductus with indomethacin in 19 infants failed, though there was temporary closure in nine. Congestive heart failure was present in 29 and respiratory distress in 22 patients. Endotracheal intubation with assisted ventilation was necessary in all cases. The mean age at operation was 13.5 days and ductal ligation was performed in the intensive care unit under local anaesthesia supplemented with pancuronium and pethidine. There were no intraoperative deaths, but five infants died in hospital. There were seven late deaths. Eighteen survivors have been followed for a mean of 26.5 months. Early ligation of a patent ductus arteriosus in premature infants with a very low birth weight improved the cardiorespiratory state. Long term follow up showed good clinical progress in two thirds of the surviving group.
PD-1 Is Expressed by Tumor-Infiltrating Immune Cells and Is Associated with Poor Outcome for Patients with Renal Cell Carcinoma
Authors: R. Houston Thompson, Haidong Dong, Christine M. Lohse, Bradley C. Leibovich, Michael L. Blute, John C. Cheville, Eugene D. Kwon
Journal: Clinical Cancer Research (2007)

Abstract Purpose: B7-H1 is expressed by clinically aggressive forms of renal cell carcinoma (RCC) and predicts adverse outcome. B7-H1 is known to impair host immunity via interaction with the Programmed Death-1 (PD-1) receptor, which is expressed by activated T cells. Levels of immune cells expressing PD-1 (PD-1+) in clinical RCC tumors have not been evaluated. Thus, we tested whether immune cell PD-1 expression is observed within aggressive RCC tumors. Experimental Design: Between 2000 and 2003, 267 patients underwent nephrectomy at our institution for clear cell RCC and had fresh-frozen tissue available for review. These RCC specimens were immunostained using anti–PD-1 (clone MIH4) and outcome analyses were conducted. Results: Mononuclear immune cell infiltration was observed in 136 (50.9%) specimens. PD-1+ immune cells were present in 77 of these 136 (56.6%) tumors. In contrast, RCC tumor cells did not express PD-1. Patients with PD-1+ immune cells were significantly more likely to harbor B7-H1+ tumor cells (P &amp;lt; 0.001), larger tumors (P = 0.001), and tumors of higher nuclear grade (P = 0.001). Likewise, intratumoral PD-1+ immune cells were associated with advanced tumor-node-metastasis stage (P = 0.005), coagulative tumor necrosis (P = 0.027), and sarcomatoid differentiation (P = 0.008). With a median follow-up of 2.9 years, 52 patients died from RCC. Univariately, patients with PD-1+ immune cells were at significant risk of cancer-specific death compared with PD-1− patients (risk ratio, 2.24; P = 0.004). Conclusions: Levels of immune cells expressing PD-1 were increased in patients with high-risk RCC tumors. Interactions between immune cell PD-1 and B7-H1 may promote cancer progression by contributing to immune dysfunction in patients with RCC.
2'-deoxyguanosine toxicity for B and mature T lymphoid cell lines is mediated by guanine ribonucleotide accumulation.
Authors: Y Sidi, B S Mitchell
Journal: Journal of Clinical Investigation (1984)

Inherited deficiency of the enzyme purine nucleoside phosphorylase (PNP) results in selective and severe T lymphocyte depletion which is mediated by its substrate, 2'-deoxyguanosine. This observation provides a rationale for the use of PNP inhibitors as selective T cell immunosuppressive agents. We have studied the relative effects of the PNP inhibitor 8-aminoguanosine on the metabolism and growth of lymphoid cell lines of T and B cell origin. We have found that 2'-deoxyguanosine toxicity for T lymphoblasts is markedly potentiated by 8-aminoguanosine and is mediated by the accumulation of deoxyguanosine triphosphate. In contrast, the growth of T4+ mature T cell lines and B lymphoblast cell lines is inhibited by somewhat higher concentrations of 2'-deoxyguanosine (ID50 20 and 18 microM, respectively) in the presence of 8-aminoguanosine without an increase in deoxyguanosine triphosphate levels. Cytotoxicity correlates instead with a three- to fivefold increase in guanosine triphosphate (GTP) levels after 24 h. Accumulation of GTP and growth inhibition also result from exposure to guanosine, but not to guanine at equimolar concentrations. B lymphoblasts which are deficient in the purine salvage enzyme hypoxanthine guanine phosphoribosyltransferase are completely resistant to 2'-deoxyguanosine or guanosine concentrations up to 800 microM and do not demonstrate an increase in GTP levels. Growth inhibition and GTP accumulation are prevented by hypoxanthine or adenine, but not by 2'-deoxycytidine. 8-Aminoguanosine appears to effectively inhibit extracellular PNP activity; thus, it prolongs the extracellular half-life of 2'-deoxyguanosine and guanosine, but does not completely inhibit intracellular PNP activity in these lymphoid cells. As a result, 2'-deoxyguanosine and guanosine are phosphorolyzed and actively salvaged within the cell, accounting for the accumulation of GTP. Partial inhibition of PNP activity in vivo, therefore, may lead to nonselective cellular toxicity by a mechanism independent of dGTP accumulation.
Interferon and Murine Leukemia. VI. Effect of Interferon Preparations on the Lymphoid Leukemia of AKR Mice&lt;xref ref-type="fn" rid="FN2"&gt;2&lt;/xref&gt;
Authors: Ion Gresser, Jacques Coppey, Chantal Bourali
Journal: JNCI Journal of the National Cancer Institute (1969)

To determine the effect of prolonged interferon treatment on a spontaneous leukemia (and a spontaneous viral disease), litters of newborn AKR mice were inoculated with concentrated preparations of mouse brain interferon or control “normal” brain extract, or kept without treatment. In an initial experiment, interferon treatment (first 3 months of life) significantly increased the survival time of male mice and diminished the incidence of lymphoid leukemia. No difference was detected between treated and untreated female mice. In a second experiment, interferon treatment was continued for 1 year. The survival time of both male and female mice was prolonged and the incidence of leukemia reduced in both sexes. A similar interferon treatment also increased the survival time of male and female AKR mice inoculated at birth with an extract of leukemic tissue.
Absence of hyperactivity in lead-exposed developing rats.
Authors: D Krehbiel, G A Davis, L M LeRoy, R E Bowman
Journal: Environmental Health Perspectives (1976)

It has been reported that postnatal lead treatment produces hyperactivity in rodents. Using rats, we attempted to extend these findings. Locomotor activity of offspring of lead-intubated and pair-fed control mothers was measured at 24-27 days of age, and no significant differences in reactivity or basal activity were found. Observational scoring of the animals at 28-29 and 35-36 days of age indicated that active behaviors were slightly reduced in the lead-treated rats. The brain lead concentrations of experimental animals were slightly reduced in the lead-treated rats. The brain lead concentrations of experimental animals were significantly elevated over controls. Estimates of statistical power indicated that behavioral effects of the magnitude reported in the literature would likely have been detected. The present results indicate that low-level lead exposure may not reliably produce hyperactivity in rodents. A review of the literature suggests that other data provide little support for a recently proposed rodent model of hyperactivity in children.
Controlled clinical trial of L-dopa and nafoxidine in advanced breast cancer: an E.O.R.T.C. study.
Authors: E Engelsman, J C Heuson, J Blonk Van Der Wijst, A Drochmans, H Maass, F Cheix, L G Sobrinho, H Nowakowski
Journal: BMJ (1975)

L-Dopa lowers plasma prolactin levels, and there have been reports that patients with advanced breast cancer have been successfully treated with L-dopa. To test the potential value of L-dopa in this disease a randomized clinical trial of L-dopa and nafoxidine (as the reference compound) was conducted in postmenopausal women with advanced breast cancer. Objective remissions were obtained in sever out of 36 patients (19%) treated with nafoxidine but in none out of 40 patients treated with L-dopa. L-Dopa in the dose schedule used seems to be ineffective in advanced breast cancer.
Heterogeneous Nuclear Ribonucleoprotein K Is a Novel Regulator of Androgen Receptor Translation
Authors: Nishit K. Mukhopadhyay, Jayoung Kim, Bekir Cinar, Aruna Ramachandran, Martin H. Hager, Dolores Di Vizio, Rosalyn M. Adam, Mark A. Rubin, Pradip Raychaudhuri, Arrigo De Benedetti, Michael R. Freeman
Journal: Cancer Research (2009)

The regulation of androgen receptor (AR) expression in prostate cancer is still poorly understood. The activation of the epidermal growth factor receptor (EGFR) in prostate cancer cells was previously shown to lower AR expression by a rapamycin-sensitive, posttranscriptional mechanism involving the AR mRNA 5'-untranslated region (5'-UTR). In a search for an intermediate within the EGFR/phosphoinositide 3-kinase/Akt/mammalian target of rapamycin pathway that regulates AR at this site, we identified the nucleic acid-binding protein, heterogeneous nuclear ribonucleoprotein K (hnRNP-K), by mass spectrometric analysis of Akt immune complexes from lipid raft-enriched subcellular fractions. We show here that hnRNP-K is a novel inhibitor of AR mRNA translation that regulates androgen-responsive gene expression and prostate cancer cell proliferation. A functional hnRNP-K binding site involved in down-regulating AR protein levels was identified in the AR mRNA 5'-UTR. Further analysis revealed that hnRNP-K is also able to inhibit AR translation in the absence of the 5'-UTR, consistent with the presence of additional predicted hnRNP-K binding sites within the AR open reading frame and in the 3'-UTR. Immunohistochemical analysis of a human prostate cancer tissue microarray revealed an inverse correlation between hnRNP-K expression and AR protein levels in organ-confined prostate tumors and a substantial decline in cytoplasmic hnRNP-K in metastases, despite an overall increase in hnRNP-K levels in metastatic tumors. These data suggest that translational inhibition of AR by hnRNP-K may occur in organ-confined tumors but possibly at a reduced level in metastases. HnRNP-K is the first protein identified that directly interacts with and regulates the AR translational apparatus.
An Epigenetic Marker Panel for Detection of Lung Cancer Using Cell-Free Serum DNA
Authors: Shahnaz Begum, Mariana Brait, Santanu Dasgupta, Kimberly L. Ostrow, Marianna Zahurak, André L. Carvalho, Joseph A. Califano, Steven N. Goodman, William H. Westra, Mohammad Obaidul Hoque, David Sidransky
Journal: Clinical Cancer Research (2011)

Abstract Purpose: We investigated the feasibility of detecting aberrant DNA methylation of some novel and known genes in the serum of lung cancer patients. Experimental Design: To determine the analytic sensitivity, we examined the tumor and the matched serum DNA for aberrant methylation of 15 gene promoters from 10 patients with primary lung tumors by using quantitative methylation-specific PCR. We then tested this 15-gene set to identify the more useful DNA methylation changes in the serum of a limited number of lung cancer patients and controls. In an independent set, we tested the six most promising genes (APC, CDH1, MGMT, DCC, RASSF1A, and AIM1) for further elucidation of the diagnostic application of this panel of markers. Results: Promoter hypermethylation of at least one of the genes studied was detected in all 10 lung primary tumors. In majority of cases, aberrant methylation in serum DNA was accompanied by methylation in the matched tumor samples. In the independent set, using a single gene that had 100% specificity (DCC), 35.5% (95% CI: 25–47) of the 76 lung cancer patients were correctly identified. For patients without methylated DCC, addition of a logistic regression score that was based on the five remaining genes improved sensitivity from 35.5% to 75% (95% CI: 64–84) but decreased the specificity from 100% to 73% (95% CI: 54–88). Conclusion: This approach needs to be evaluated in a larger test set to determine the role of this gene set in early detection and surveillance of lung cancer. Clin Cancer Res; 17(13); 4494–503. ©2011 AACR.
From partner choice to equity – and beyond?
Authors: Felix Warneken
Journal: Behavioral and Brain Sciences (2013)

Abstract Baumard et al. provide an intriguing model where morality emerges from the dynamics of partner choice in mutualistic interactions. I discuss evidence from human and nonhuman primates that supports the overall approach, but highlights a gap in explaining the human specificity of moral cognition. I suggest that an essential characteristic of human fairness is to override concerns about merit in favor of promoting the welfare in others who are needy.
Environmental Signaling: What Embryos and Evolution Teach Us About Endocrine Disrupting Chemicals
Authors: John A. McLachlan
Journal: Endocrine Reviews (2001)

The term "endocrine disrupting chemicals" is commonly used to describe environmental agents that alter the endocrine system. Laboratories working in this emerging field—environmental endocrine research—have looked at chemicals that mimic or block endogenous vertebrate steroid hormones by interacting with the hormone's receptor. Environmental chemicals known to do this do so most often with receptors derived from the steroid/thyroid/retinoid gene family. They include ubiquitous and persistent organochlorines, as well as plasticizers, pharmaceuticals, and natural hormones. These chemicals function as estrogens, antiestrogens, and antiandrogens but have few, if any, structural similarities. Therefore, receptor-based or functional assays have the best chance of detecting putative biological activity of environmental chemicals. Three nuclear estrogen receptor forms—α, β, and γ—as well as multiple membrane forms and a possible mitochondrial form have been reported, suggesting a previously unknown diversity of signaling pathways available to estrogenic chemicals. Examples of environmental or ambient estrogenization occur in laboratory experiments, zoo animals, domestic animals, wildlife, and humans. Environmentally estrogenized phenotypes may differ depending upon the time of exposure—i.e., whether the exposure occurred at a developmental (organizational and irreversible) or postdevelopmental (activational and reversible) stage. The term "estrogen" must be defined in each case, since steroidal estrogens differ among themselves and from synthetic or plant-derived chemicals. An "estrogen-like function" seems to be an evolutionarily ancient signal that has been retained in a number of chemicals, some of which are vertebrate hormones. Signaling, required for symbiosis between plants and bacteria, may be viewed, therefore, as an early example of hormone cross-talk. Developmental feminization at the structural or functional level is an emerging theme in species exposed, during embryonic or fetal life, to estrogenic compounds. Human experience as well as studies in experimental animals with the potent estrogen diethylstilbestrol provide informative models. Advances in the molecular genetics of sex differentiation in vertebrates facilitate mechanistic understanding. Experiments addressing the concept of gene imprinting or induction of epigenetic memory by estrogen or other hormones suggest a link to persistent, heritable phenotypic changes seen after developmental estrogenization, independent of mutagenesis. Environmental endocrine science provides a new context in which to examine the informational content of ecosystem-wide communication networks. As common features come to light, this research may allow us to predict environmentally induced alterations in internal signaling systems of vertebrates and some invertebrates and eventually to explicate environmental contributions to human reproductive and developmental health.