Air quality monitoring for vulnerable groups in residential environments using a multiple hazard gas detector

© 2019 by the authors. Licensee MDPI, Basel, Switzerland. This paper presents a smart “e-nose” device to monitor indoor hazardous air. Indoor hazardous odor is a threat for seniors, infants, children, pregnant women, disabled residents, and patients. To overcome the limitations of using existing non-intelligent, slow-responding, deficient gas sensors, we propose a novel artificial-intelligent-based multiple hazard gas detector (MHGD) system that is mounted on a motor vehicle-based robot which can be remotely controlled. First, we optimized the sensor array for the classification of three hazardous gases, including cigarette smoke, inflammable ethanol, and off-flavor from spoiled food, using an e-nose with a mixing chamber. The mixing chamber can prevent the impact of environmental changes. We compared the classification results of all combinations of sensors, and selected the one with the highest accuracy (98.88%) as the optimal sensor array for the MHGD. The optimal sensor array was then mounted on the MHGD to detect and classify the target gases without a mixing chamber but in a controlled environment. Finally, we tested the MHGD under these conditions, and achieved an acceptable accuracy (70.00%)

Changes in triggering of ST-elevation myocardial infarction by particulate air pollution in Monroe County, New York over time: a case-crossover study

Background Previous studies have reported that fine particle (PM2.5) concentrations triggered ST elevation myocardial infarctions (STEMI). In Rochester, NY, multiple air quality policies and economic changes/influences from 2008 to 2013 led to decreased concentrations of PM2.5 and its major constituents (SO42−, NO3−, elemental and primary organic carbon). This study examined whether the rate of STEMI associated with increased ambient gaseous and PM component concentrations was different AFTER these air quality policies and economic changes (2014–2016), compared to DURING (2008–2013) and BEFORE these polices and changes (2005–2007). Methods Using 921 STEMIs treated at the University of Rochester Medical Center (2005–2016) and a case-crossover design, we examined whether the rate of STEMI associated with increased PM2.5, ultrafine particles (UFP, < 100 nm), accumulation mode particles (AMP, 100-500 nm), black carbon, SO2, CO, and O3 concentrations in the previous 1–72 h was modified by the time period related to these pollutant source changes (BEFORE, DURING, AFTER). Results Each interquartile range (3702 particles/cm3) increase in UFP concentration in the previous 1 h was associated with a 12% (95% CI = 3%, 22%) increase in the rate of STEMI. The effect size was larger in the AFTER period (26%) than the DURING (5%) or BEFORE periods (9%). There were similar patterns for black carbon and SO2. Conclusions An increased rate of STEMI associated with UFP and other pollutant concentrations was higher in the AFTER period compared to the BEFORE and DURING periods. This may be due to changes in PM composition (e.g. higher secondary organic carbon and particle bound reactive oxygen species) following these air quality policies and economic changes

First Results from Lattice Simulation of the PWMM

We present results of lattice simulations of the Plane Wave Matrix Model (PWMM). The PWMM is a theory of supersymmetric quantum mechanics that has a well-defined canonical ensemble. We simulate this theory by applying rational hybrid Monte Carlo techniques to a naive lattice action. We examine the strong coupling behaviour of the model focussing on the deconfinement transition.Comment: v3 20 pages, 8 figures, comment adde

Small inhibitor of Bcl-2, HA14-1, selectively enhanced the apoptotic effect of cisplatin by modulating Bcl-2 family members in MDA-MB-231 breast cancer cells

Inhibition or downregulation of Bcl-2 represents a new therapeutic approach to by-pass chemoresistance in cancer cells. Therefore, we explored the potential of this approach in breast cancer cells. Cisplatin and paclitaxel induced apoptosis in a dose-dependent manner in MCF-7 (drug-sensitive) and MDA-MB-231 (drug-insensitive) cells. Furthermore, when we transiently silenced Bcl-2, both cisplatin and paclitaxel induced apoptosis more than parental cells. Dose dependent induction of apoptosis by drugs was enhanced by the pre-treatment of these cells with HA14-1, a Bcl-2 inhibitor. Although the effect of cisplatin was significant on both cell lines, the effect of paclitaxel was much less potent only in MDA-MB-231 cells. To further understand the distinct role of drugs in MDA-MB-231 cells pretreated with HA14-1, caspases and Bcl-2 family proteins were studied. The apoptotic effect of cisplatin with or without HA14-1 pre-treatment is shown to be caspase-dependent. Among pro-apoptotic Bcl-2 proteins, Bax and Puma were found to be up-regulated whereas Bcl-2 and Bcl-x(L) were down-regulated when cells were pretreated with HA14-1 followed by paclitaxel or cisplatin. Enforced Bcl-2 expression in MDA-MB-231 cells abrogated the sensitizing effect of HA14-1 in cisplatin induced apoptosis. These results suggest that the potentiating effect of HA14-1 is drug and cell type specific and may not only depend on the inhibition of Bcl-2. Importantly, alteration of other pro-apoptotic or anti-apoptotic Bcl-2 family members may dictate the apoptotic response when HA14-1 is combined with chemotherapeutic drugs

Lovelock gravity from entropic force

In this paper, we first generalize the formulation of entropic gravity to (n+1)-dimensional spacetime. Then, we propose an entropic origin for Gauss-Bonnet gravity and more general Lovelock gravity in arbitrary dimensions. As a result, we are able to derive Newton's law of gravitation as well as the corresponding Friedmann equations in these gravity theories. This procedure naturally leads to a derivation of the higher dimensional gravitational coupling constant of Friedmann/Einstein equation which is in complete agreement with the results obtained by comparing the weak field limit of Einstein equation with Poisson equation in higher dimensions. Our study shows that the approach presented here is powerful enough to derive the gravitational field equations in any gravity theory. PACS: 04.20.Cv, 04.50.-h, 04.70.Dy.Comment: 10 pages, new versio

Identification of the genomic mutation in Epha4rb-2J/rb-2J mice

The EphA4 receptor tyrosine kinase is involved in numerous cell-signalling activities during embryonic development. EphA4 has the ability to bind to both types of ephrin ligands, the ephrinAs and ephrinBs. The C57BL/6J-Epha4rb-2J/GrsrJ strain, denoted Epha4rb-2J/rb-2J, is a spontaneous mouse mutant that arose at The Jackson Laboratory. These mutants exhibited a synchronous hind limb locomotion defect or “hopping gait” phenotype, which is also characteristic of EphA4 null mice. Genetic complementation experiments suggested that Epha4rb-2J corresponds to an allele of EphA4, but details of the genomic defect in this mouse mutant are currently unavailable. We found a single base-pair deletion in exon 9 resulting in a frame shift mutation that subsequently resulted in a premature stop codon. Analysis of the predicted structure of the truncated protein suggests that both the kinase and sterile α motif (SAM) domains are absent. Definitive determination of genotype is needed for experimental studies of mice carrying the Epha4rb-2J allele, and we have also developed a method to ease detection of the mutation through RFLP. Eph-ephrin family members are reportedly expressed as numerous isoforms. Hence, delineation of the specific mutation in EphA4 in this strain is important for further functional studies, such as protein–protein interactions, immunostaining and gene compensatory studies, investigating the mechanism underlying the effects of altered function of Eph family of receptor tyrosine kinases on phenotype

Clinical course, therapeutic responses and outcomes in relapsing MOG antibody-associated demyelination.

Abstract OBJECTIVE: We characterised the clinical course, treatment and outcomes in 59 patients with relapsing myelin oligodendrocyte glycoprotein (MOG) antibody-associated demyelination. METHODS: We evaluated clinical phenotypes, annualised relapse rates (ARR) prior and on immunotherapy and Expanded Disability Status Scale (EDSS), in 218 demyelinating episodes from 33 paediatric and 26 adult patients. RESULTS: The most common initial presentation in the cohort was optic neuritis (ON) in 54% (bilateral (BON) 32%, unilateral (UON) 22%), followed by acute disseminated encephalomyelitis (ADEM) (20%), which occurred exclusively in children. ON was the dominant phenotype (UON 35%, BON 19%) of all clinical episodes. 109/226 (48%) MRIs had no brain lesions. Patients were steroid responsive, but 70% of episodes treated with oral prednisone relapsed, particularly at doses <10\u2009mg daily or within 2 months of cessation. Immunotherapy, including maintenance prednisone (P=0.0004), intravenous immunoglobulin, rituximab and mycophenolate, all reduced median ARRs on-treatment. Treatment failure rates were lower in patients on maintenance steroids (5%) compared with non-steroidal maintenance immunotherapy (38%) (P=0.016). 58% of patients experienced residual disability (average follow-up 61 months, visual loss in 24%). Patients with ON were less likely to have sustained disability defined by a final EDSS of 652 (OR 0.15, P=0.032), while those who had any myelitis were more likely to have sustained residual deficits (OR 3.56, P=0.077). CONCLUSION: Relapsing MOG antibody-associated demyelination is strongly associated with ON across all age groups and ADEM in children. Patients are highly responsive to steroids, but vulnerable to relapse on steroid reduction and cessation

Identification of Pns6, a putative movement protein of RRSV, as a silencing suppressor

RNA silencing is a potent antiviral response in plants. As a counterdefense, most plant and some animal viruses encode RNA silencing suppressors. In this study, we showed that Pns6, a putative movement protein of Rice ragged stunt virus (RRSV), exhibited silencing suppressor activity in coinfiltration assays with the reporter green fluorescent protein (GFP) in transgenic Nicotiana benthamiana line 16c. Pns6 of RRSV suppressed local silencing induced by sense RNA but had no effect on that induced by dsRNA. Deletion of a region involved in RNA binding abolished the silencing suppressor activity of Pns6. Further, expression of Pns6 enhanced Potato virus × pathogenicity in N. benthamiana. Collectively, these results suggested that RRSV Pns6 functions as a virus suppressor of RNA silencing that targets an upstream step of the dsRNA formation in the RNA silencing pathway. This is the first silencing suppressor to be identified from the genus Oryzavirus

Human Tears Reveal Insights into Corneal Neovascularization

Corneal neovascularization results from the encroachment of blood vessels from the surrounding conjunctiva onto the normally avascular cornea. The aim of this study is to identify factors in human tears that are involved in development and/or maintenance of corneal neovascularization in humans. This could allow development of diagnostic tools for monitoring corneal neovascularization and combination monoclonal antibody therapies for its treatment. In an observational case-control study we enrolled a total of 12 patients with corneal neovascularization and 10 healthy volunteers. Basal tears along with reflex tears from the inferior fornix, superior fornix and using a corneal bath were collected along with blood serum samples. From all patients, ocular surface photographs were taken. Concentrations of the pro-angiogenic cytokines interleukin (IL)-6, IL-8, Vascular Endothelial Growth Factor (VEGF), Monocyte Chemoattractant Protein 1 (MCP-1) and Fas Ligand (FasL) were determined in blood and tear samples using a flow cytometric multiplex assay. Our results show that the concentration of pro-angiogenic cytokines in human tears are significantly higher compared to their concentrations in serum, with highest levels found in basal tears. Interestingly, we could detect a significantly higher concentration of IL- 6, IL-8 and VEGF in localized corneal tears of patients with neovascularized corneas when compared to the control group. This is the first study of its kind demonstrating a significant difference of defined factors in tears from patients with neovascularized corneas as compared to healthy controls. These results provide the basis for future research using animal models to further substantiate the role of these cytokines in the establishment and maintenance of corneal neovascularization