121 research outputs found

    Effects on vital signs after twenty minutes of vaping compared to people exposed to second-hand vapor

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    Introduction: Very little is known about the immediate physiological implications of vaping or inhaling second-hand vapor. This study used a quantitative approach to understand the short-term physiological implications of vape use and exposure to sec-ond-hand vapor for people who do not vape. Material and methods: One hundred and forty-eight people participated in the study, 75 self-identified as non-vapers and 73 self-identified as people who vape. All participants were over the age of 18. Participants used or were exposed to non-flavored e-juice without nicotine in Sorin® vape devices. Heart rate, blood pressure, respiratory rate, blood oxygenation, blood glucose and pulmonary function tests were assessed. Physiological parameters were assessed prior to vape use or exposure to vapor and again after 20 minutes of vaping.Results: Findings indicated there were no significant changes in most health parameters except blood pressure which was reduced in both groups. Heart rate was also significantly reduced for vaping participants.Conclusion: Vaping without flavorings or nicotine do not appear to have an immediate negative health impact on vital signs. The physiological effects of long-term exposure and/or vape use requires additional investigation. Information was established regarding the physiological effects of non-flavored, non-nicotine vaping so future studies can compare the effects of vaping with assorted flavors and nicotine concentrations to the effects of vaping only the base ingredients (vegetable glycerin and propylene glycol). New knowledge was gleaned relating to exposure to vapor, a phenomenon not previously examined but common espe-cially among non-vaping people who attend social events where people are vaping

    The deubiquitinase (DUB) USP13 promotes Mcl-1 stabilisation in cervical cancer

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    Protein ubiquitination is a critical regulator of cellular homeostasis. Aberrations in the addition or removal of ubiquitin can result in the development of cancer and key components of the ubiquitination machinery serve as oncogenes or tumour suppressors. An emerging target in the development of cancer therapeutics are the deubiquitinase (DUB) enzymes that remove ubiquitin from protein substrates. Whether this class of enzyme plays a role in cervical cancer has not been fully explored. By interrogating the cervical cancer data from the TCGA consortium, we noted that the DUB USP13 is amplified in ~15% of cervical cancer cases. We confirmed that USP13 expression was increased in cervical cancer cell lines, cytology samples from patients with cervical disease and in cervical cancer tissue. Depletion of USP13 inhibited cervical cancer cell proliferation. Mechanistically, USP13 bound to, deubiquitinated and stabilised Mcl-1, a pivotal member of the anti-apoptotic BCL-2 family. Furthermore, reduced Mcl-1 expression partially contributed to the observed proliferative defect in USP13 depleted cells. Importantly, the expression of USP13 and Mcl-1 proteins correlated in cervical cancer tissue. Finally, we demonstrated that depletion of USP13 expression or inhibition of USP13 enzymatic activity increased the sensitivity of cervical cancer cells to the BH3 mimetic inhibitor ABT-263. Together, our data demonstrates that USP13 is a potential oncogene in cervical cancer that functions to stabilise the pro-survival protein Mcl-1, offering a potential therapeutic target for these cancers

    The biosocial genome? : Interdisciplinary perspectives on environmental epigenetics, health and society

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    In recent years, research on how the human environment and life-style influence gene expression has generated considerable scientific and public interest. Articles in prominent international newspapers with headlines such as “Why your DNA isn’t your destiny” (Time Magazine in 2010) or “Poverty leaves traces in children’s genome” (Süddeutsche Zeitung in 2016) have drawn public interest to the emerging field of environmental epigenetics. It is a sub-division of the much more heterogeneous research field of epigenetics, which aims to understand how interactions between the environment and the genome can lead to epigenetic modifications that affect gene expression. Environmental epigenetics is often heralded as providing a revolutionary perspective on disease etiology, particularly with regard to so-called ‘life-style diseases’ such as cardiovascular disease or diabetes. It is also often presented as a vital new framework for understanding differences in the susceptibility and resilience to mental illness and the long-term damaging effects of a wide variety of environmental factors. Environmental epigenetics engages with the social context of both individuals and populations. Studies investigate, for example, how socio-economic status, exercise habits, diet or experiences of trauma might influence biological processes at the molecular level. This has created great interest among social scientists and scholars in the humanities as it raises a number of questions at the intersection of the natural sciences, the social sciences and the humanities: for example, how to conceptualize the social environment in a laboratory context. To explore research areas at these intersections and assess the potential social and political implications of environmental epigenetics, international scholars from the life sciences, social sciences and humanities met in January 2017 in Munich, Germany. This article presents some of the main findings from these interdisciplinary discussions. We conclude that environmental epigenetics has great potential for elucidating how human society affects human biology, but we caution against over-simplified translations from social structures to biological processes and vice versa

    Seabird Trophic Position Across Three Ocean Regions Tracks Ecosystem Differences

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    We analyze recently collected feather tissues from two species of seabirds, the sooty tern (Onychoprion fuscatus) and brown noddy (Anous stolidus), in three ocean regions (North Atlantic, North Pacific, and South Pacific) with different human impacts. The species are similar morphologically and in the trophic levels from which they feed within each location. In contrast, we detect reliable differences in trophic position amongst the regions. Trophic position appears to decline as the intensity of commercial fishing increases, and is at its lowest in the Caribbean. The spatial gradient in trophic position we document in these regions exceeds those detected over specimens from the last 130 years in the Hawaiian Islands. Modeling suggests that climate velocity and human impacts on fish populations strongly align with these differences

    The Ninth Data Release of the Sloan Digital Sky Survey: First Spectroscopic Data from the SDSS-III Baryon Oscillation Spectroscopic Survey

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    The Sloan Digital Sky Survey III (SDSS-III) presents the first spectroscopic data from the Baryon Oscillation Spectroscopic Survey (BOSS). This ninth data release (DR9) of the SDSS project includes 535,995 new galaxy spectra (median z=0.52), 102,100 new quasar spectra (median z=2.32), and 90,897 new stellar spectra, along with the data presented in previous data releases. These spectra were obtained with the new BOSS spectrograph and were taken between 2009 December and 2011 July. In addition, the stellar parameters pipeline, which determines radial velocities, surface temperatures, surface gravities, and metallicities of stars, has been updated and refined with improvements in temperature estimates for stars with T_eff<5000 K and in metallicity estimates for stars with [Fe/H]>-0.5. DR9 includes new stellar parameters for all stars presented in DR8, including stars from SDSS-I and II, as well as those observed as part of the SDSS-III Sloan Extension for Galactic Understanding and Exploration-2 (SEGUE-2). The astrometry error introduced in the DR8 imaging catalogs has been corrected in the DR9 data products. The next data release for SDSS-III will be in Summer 2013, which will present the first data from the Apache Point Observatory Galactic Evolution Experiment (APOGEE) along with another year of data from BOSS, followed by the final SDSS-III data release in December 2014.Comment: 9 figures; 2 tables. Submitted to ApJS. DR9 is available at http://www.sdss3.org/dr

    The Oxford-Dartmouth Thirty Degree Survey I: Observations and Calibration of a Wide-Field Multi-Band Survey

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    The Oxford Dartmouth Thirty Degree Survey (ODTS) is a deep, wide, multi-band imaging survey designed to cover a total of 30 square degrees in BVRi'Z, with a subset of U and K band data, in four separate fields of 5-10 deg^2 centred at 00:18:24 +34:52, 09:09:45 +40:50, 13:40:00 +02:30 and 16:39:30 +45:24. Observations have been made using the Wide Field Camera on the 2.5-m Isaac Newton Telescope in La Palma to average limiting depths (5 sigma Vega, aperture magnitudes) of U=24.8, B=25.6, V=25.0, R=24.6, and i'=23.5, with observations taken in ideal conditions reaching the target depths of U=25.3, B=26.2, V=25.7, R=25.4, and i'=24.6. The INT Z band data was found to be severely effected by fringing and, consequently, is now being obtained at the MDM observatory in Arizona. A complementary K-band survey has also been carried out at MDM, reaching an average depth of K_{5\sigma}~18.5. At present, approximately 23 deg^2 of the ODTS have been observed, with 3.5 deg^2 of the K band survey completed. This paper details the survey goals, field selection, observation strategy and data reduction procedure, focusing on the photometric calibration and catalogue construction. Preliminary photometric redshifts have been obtained for a subsample of the objects with R <= 23. These results are presented alongside a brief description of the photometric redshift determination technique used. The median redshift of the survey is estimated to be z~0.7 from a combination of the ODTS photometric redshifts and comparison with the redshift distributions of other surveys. Finally, galaxy number counts for the ODTS are presented which are found to be in excellent agreement with previous studies.Comment: 18 pages, 21 figures, Accepted for publication in MNRA

    α7 Nicotinic Acetylcholine Receptor Signaling Modulates Ovine Fetal Brain Astrocytes Transcriptome in Response to Endotoxin

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    Neuroinflammation in utero may result in lifelong neurological disabilities. Astrocytes play a pivotal role in this process, but the mechanisms are poorly understood. No early postnatal treatment strategies exist to enhance neuroprotective potential of astrocytes. We hypothesized that agonism on α7 nicotinic acetylcholine receptor (α7nAChR) in fetal astrocytes will augment their neuroprotective transcriptome profile, while the inhibition of α7nAChR will achieve the opposite. Using an in vivo–in vitro model of developmental programming of neuroinflammation induced by lipopolysaccharide (LPS), we validated this hypothesis in primary fetal sheep astrocytes cultures re-exposed to LPS in the presence of a selective α7nAChR agonist or antagonist. Our RNAseq findings show that a pro-inflammatory astrocyte transcriptome phenotype acquired in vitro by LPS stimulation is reversed with α7nAChR agonistic stimulation. Conversely, α7nAChR inhibition potentiates the pro-inflammatory astrocytic transcriptome phenotype. Furthermore, we conducted a secondary transcriptome analysis against the identical α7nAChR experiments in fetal sheep primary microglia cultures. Similar to findings in fetal microglia, in fetal astrocytes we observed a memory effect of in vivo exposure to inflammation, expressed in a perturbation of the iron homeostasis signaling pathway (hemoxygenase 1, HMOX1), which persisted under pre-treatment with α7nAChR antagonist but was reversed with α7nAChR agonist. For both glia cell types, common pathways activated due to LPS included neuroinflammation signaling and NF-κB signaling in some, but not all comparisons. However, overall, the overlap on the level of signaling pathways was rather minimal. Astrocytes, not microglia—the primary immune cells of the brain, were characterized by unique inhibition patterns of STAT3 pathway due to agonistic stimulation of α7nAChR prior to LPS exposure. Lastly, we discuss the implications of our findings for fetal and postnatal brain development
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