scholarly journals A Low-Cost, High-Throughput Digital Image Analysis of Stain Patterns on Smoked Cigarette Filter Butts to Estimate Mainstream Smoke Exposure

2021 ◽  
Vol 18 (19) ◽  
pp. 10546
Author(s):  
Clifford H. Watson ◽  
Jane Yan ◽  
Stephen Stanfill ◽  
Liza Valentin-Blasini ◽  
Roberto Bravo Cardenas ◽  
...  
Keyword(s):  
High Throughput ◽  
Low Cost ◽  
Smoking Behavior ◽  
Quantitative Information ◽  
Smoke Exposure ◽  
Design Parameters ◽  
Cigarette Smoke Exposure ◽  
Mainstream Smoke ◽  
Cigarette Filter ◽  
The Impact

Standard machine smoking protocols provide useful information for examining the impact of design parameters, such as filter ventilation, on mainstream smoke delivery. Unfortunately, their results do not accurately reflect human smoke exposure. Clinical research and topography devices in human studies yield insights into how products are used, but a clinical setting or smoking a cigarette attached to such a device may alter smoking behavior. To better understand smokers’ use of filtered cigarette products in a more natural environment, we developed a low-cost, high-throughput approach to estimate mainstream cigarette smoke exposure on a per-cigarette basis. This approach uses an inexpensive flatbed scanner to scan smoked cigarette filter butts and custom software to analyze tar-staining patterns. Total luminosity, or optical staining density, of the scanned images provides quantitative information proportional to mainstream smoke-constituent deliveries on a cigarette-by-cigarette basis. Duplicate sample analysis using this new approach and our laboratory’s gold-standard liquid chromatography/tandem mass spectrometry (LC/MS/MS) solanesol method yielded comparable results (+7% bias) from the analysis of 20 commercial cigarettes brands (menthol and nonmentholated). The brands varied in design parameters such as length, filter ventilation, and diameter. Plots correlating the luminosity to mainstream smoked-nicotine deliveries on a per-cigarette basis for these cigarette brands were linear (average R2 > 0.91 for nicotine and R2 > 0.83 for the tobacco-specific nitrosamine NNK), on a per-brand basis, with linearity ranging from 0.15 to 3.00 mg nicotine/cigarette. Analysis of spent cigarette filters allows exposures to be characterized on a per-cigarette basis or a “daily dose” via summing across results from all filter butts collected over a 24 h period. This scanner method has a 100-fold lower initial capital cost for equipment than the LC/MS/MS solanesol method and provides high-throughput results (~200 samples per day). Thus, this new method is useful for characterizing exposure related to filtered tobacco-product use.

scholarly journals Bacteria Getting into Shape: Genetic Determinants of E. coli Morphology

mBio ◽  
2017 ◽  
Vol 8 (2) ◽  
Author(s):  
Shawn French ◽  
Jean-Philippe Côté ◽  
Jonathan M. Stokes ◽  
Ray Truant ◽  
Eric D. Brown
Keyword(s):  
High Throughput ◽  
Genomic Library ◽  
Low Cost ◽  
Genetic Mutation ◽  
Cellular Functions ◽  
E Coli ◽  
Genetic Perturbations ◽  
Screening Platform ◽  
The Impact ◽  
Very High

ABSTRACT Perturbation of cellular processes is a prevailing approach to understanding biology. To better understand the complicated biology that defines bacterial shape, a sensitive, high-content platform was developed to detect multiple morphological defect phenotypes using microscopy. We examined morphological phenotypes across the Escherichia coli K-12 deletion (Keio) collection at the mid-exponential growth phase, revealing 111 deletions perturbing shape. Interestingly, 64% of these were uncharacterized mutants, illustrating the complex nature of shape maintenance and regulation in bacteria. To understand the roles these genes play in defining morphology, 53 mutants with knockouts resulting in abnormal cell shape were crossed with the Keio collection in high throughput, generating 1,373 synthetic lethal interactions across 1.7 million double deletion mutants. This analysis yielded a highly populated interaction network spanning and linking multiple phenotypes, with a preponderance of interactions involved in transport, oxidation-reduction, and metabolic processes. IMPORTANCE Genetic perturbations of cellular functions are a prevailing approach to understanding cell systems, which are increasingly being practiced in very high throughput. Here, we report a high-content microscopy platform tailored to bacteria, which probes the impact of genetic mutation on cell morphology. This has particular utility in revealing elusive and subtle morphological phenotypes associated with blocks in nonessential cellular functions. We report 111 nonessential mutations impacting E. coli morphology, with nearly half of those genes being poorly annotated or uncharacterized. Further, these genes appear to be tightly linked to transport or redox processes within the cell. The screening platform is simple and low cost and is broadly applicable to any bacterial genomic library or chemical collection. Indeed, this is a powerful tool in understanding the biology behind bacterial shape. IMPORTANCE Genetic perturbations of cellular functions are a prevailing approach to understanding cell systems, which are increasingly being practiced in very high throughput. Here, we report a high-content microscopy platform tailored to bacteria, which probes the impact of genetic mutation on cell morphology. This has particular utility in revealing elusive and subtle morphological phenotypes associated with blocks in nonessential cellular functions. We report 111 nonessential mutations impacting E. coli morphology, with nearly half of those genes being poorly annotated or uncharacterized. Further, these genes appear to be tightly linked to transport or redox processes within the cell. The screening platform is simple and low cost and is broadly applicable to any bacterial genomic library or chemical collection. Indeed, this is a powerful tool in understanding the biology behind bacterial shape.

scholarly journals The Impact of Maternal Cigarette Smoke Exposure in a Rodent Model on Renal Development in the Offspring

PLoS ONE ◽  
2014 ◽  
Vol 9 (7) ◽  
pp. e103443 ◽  
Author(s):  
Ibrahim Al-Odat ◽  
Hui Chen ◽  
Yik Lung Chan ◽  
Sawiris Amgad ◽  
Muh Geot Wong ◽  
...  
Keyword(s):  
Cigarette Smoke ◽  
Smoke Exposure ◽  
Rodent Model ◽  
Cigarette Smoke Exposure ◽  
Renal Development ◽  
The Impact

scholarly journals Streptococcus pneumoniae Colonization Is Required To Alter the Nasal Microbiota in Cigarette Smoke-Exposed Mice

2017 ◽  
Vol 85 (10) ◽  
Author(s):  
Pamela Shen ◽  
Fiona J. Whelan ◽  
L. Patrick Schenck ◽  
Joshua J. C. McGrath ◽  
Gilles Vanderstocken ◽  
...  
Keyword(s):  
Cigarette Smoke ◽  
Smoke Exposure ◽  
Cigarette Smoke Exposure ◽  
High Dose ◽  
Microbiota Composition ◽  
Content Type ◽  
Pneumococcal Colonization ◽  
Pathogen Colonization ◽  
The Impact ◽  
Nasal Microbiota

ABSTRACT Smokers have nasal microbiota dysbiosis, with an increased frequency of colonizing bacterial pathogens. It is possible that cigarette smoke increases pathogen acquisition by perturbing the microbiota and decreasing colonization resistance. However, it is difficult to disentangle microbiota dysbiosis due to cigarette smoke exposure from microbiota changes caused by increased pathogen acquisition in human smokers. Using an experimental mouse model, we investigated the impact of cigarette smoke on the nasal microbiota in the absence and presence of nasal pneumococcal colonization. We observed that cigarette smoke exposure alone did not alter the nasal microbiota composition. The microbiota composition was also unchanged at 12 h following low-dose nasal pneumococcal inoculation, suggesting that the ability of the microbiota to resist initial nasal pneumococcal acquisition was not impaired in smoke-exposed mice. However, nasal microbiota dysbiosis occurred as a consequence of established high-dose nasal pneumococcal colonization at day 3 in smoke-exposed mice. Similar to clinical reports on human smokers, an enrichment of potentially pathogenic bacterial genera such as Fusobacterium, Gemella, and Neisseria was observed. Our findings suggest that cigarette smoke exposure predisposes to pneumococcal colonization independent of changes to the nasal microbiota and that microbiota dysbiosis observed in smokers may occur as a consequence of established pathogen colonization.

Cigarette Smoke Exposure Inhibits Osteoclast Apoptosis via the mtROS Pathway

2021 ◽  
pp. 002203452110094
Author(s):  
Y. Qin ◽  
Y. Liu ◽  
Y. Jiang ◽  
S. Mei ◽  
Y. Liu ◽  
...  
Keyword(s):  
Bone Loss ◽  
Cigarette Smoke ◽  
Tooth Movement ◽  
Smoke Exposure ◽  
Mechanical Force ◽  
Cigarette Smoke Exposure ◽  
Control Group ◽  
The Impact ◽  
Osteoclast Apoptosis

It is widely known that smoking is a risk factor for bone loss and plays a key role in osteopenia. Despite this well-known association, the mechanisms by which smoking affects bone have not been definitively established. Since smoking increases bone loss and potentially affects bone resorption in response to mechanical force, we investigated the impact of cigarette smoke on osteoclast numbers and underlying mechanisms in a mouse model of orthodontic tooth movement (OTM). The experimental group was exposed to once-daily cigarette smoke while the control group was not, and tooth movement distance and osteoclast numbers were assessed. In addition, the effect of cigarette smoke extract (CSE) on osteoclast precursor proliferation and osteoclast apoptosis was assessed in vitro. We found that cigarette smoke exposure enhanced bone remodeling stimulated by mechanical force and increased osteoclast numbers in vivo. Also, CSE increased the number of osteoclasts by inhibiting osteoclast apoptosis via the mitochondrial reactive oxygen species/cytochrome C/caspase 3 pathway in vitro. Moreover, exposure of mice to cigarette smoke affected bone marrow cells, leading to increased formation of osteoclasts in vitro. This study identifies a previously unknown mechanism of how smoking has a detrimental impact on bone.

scholarly journals PRESEMO—a predictive model of codend selectivity—a tool for fishery managers

2007 ◽  
Vol 64 (8) ◽  
pp. 1558-1568 ◽  
Author(s):  
F. G. O'Neill ◽  
B. Herrmann
Keyword(s):  
Predictive Model ◽  
Selection Process ◽  
Simulated Data ◽  
Quantitative Information ◽  
Design Parameters ◽  
Gear Design ◽  
Management Context ◽  
The Impact ◽  
Potential Use ◽  
Targeted Approach

Abstract O'Neill, F. G., and Herrmann, B. 2007. PRESEMO—a predictive model of codend selectivity—a tool for fishery managers. – ICES Journal of Marine Science, 64: 1558–1568. The codend selectivity simulation model PRESEMO is a predictive model based on an understanding of the physical, biological, and behavioural mechanisms that underpin codend selection. In this paper, PRESEMO is used to predict the selectivity of a large range of codends of varying design. In particular, the selectivity of codends with mesh sizes in the range 80–160 mm, number of meshes around in the range 60–140, and netting twine thickness in the range 3–6 mm are predicted and, where possible, the predictions are validated with experimental data. Using the simulated data, the codend selectivity parameters are expressed in terms of the gear design parameters and in terms of both catch size and gear design parameters. The potential use of these results in a management context and for the development of more selective gears is highlighted by plotting iso-l50 and iso-sr curves used to identify gear design parameters that give equal estimates of the 50% retention length and the selection range, respectively. It is emphasized that this approach can be extended to consider the influence of other design parameters and, if sufficient relevant quantitative information exists, biological and behavioural parameters. As such, the model presented here will provide a better understanding of the selection process, permit a more targeted approach to codend selectivity experiments, and assist fishery managers to assess the impact of proposed technical measures that are introduced to reduce the catch of undersized fish and unwanted bycatch.

scholarly journals Cigarette Smoke or Cigarette Condensate Exposure Enhances Growth of FLT3-ITD AML Models and Alters DNA Methylation and Leukemic Gene Expression

Blood ◽  
2020 ◽  
Vol 136 (Supplement 1) ◽  
pp. 29-30
Author(s):  
Mary Figueroa ◽  
Maninder Khosla ◽  
Yue Lu ◽  
Marcos Estecio ◽  
Seyed Javad Moghaddam ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Cigarette Smoke ◽  
Research Funding ◽  
Smoke Exposure ◽  
Scid Mice ◽  
Cigarette Smoke Exposure ◽  
P Value ◽  
The Impact ◽  
Advisory Role

Current and former smoker AML patients have worse survival outcomes compared to never smokers. This worsened prognosis of smokers with AML can also be seen in patients who carry activating mutations of the Fms-like tyrosine kinase 3 (FLT3) and are treated with regimens that include newly approved kinase inhibitors. While the impact of genetic mutations on survival in AML have been studied, and some have been therapeutically targeted, the role of cigarette smoking or cigarette smoke exposure (which is potentially modifiable) on leukemia progression or treatment response is understudied. In order to elucidate molecular effects of cigarette smoke exposure (CSE) that contribute to the poor prognosis of AML patients, we developed a cigarette smoke exposure model for mice to mimic the current and former smoking habits of AML patients. NOD-SCID mice were exposed to CSE in a smoking robot for 2 hours, 5 days/week, for 2 weeks or to air alone as a control. Mice were then injected with luciferase-tagged human AML cell lines, and leukemic burden was monitored through non-invasive bioluminescent imaging. Control "non-smoking" mice were only subject to AML cell injection. Enhanced early leukemic-burden was observed two distinct FLT3-ITD AML models, MOLM13 and MOLM14, within one week post AML introduction (p-value <0.0001 and <0.001 respectively). Although the latter model showed slightly longer latency of disease with increased leukemic burden apparent 24 days post leukemic introduction (p-value <0.05). In order to address if the early increase in leukemic burden may have arisen from extrinsic factors in the tumor microenvironment, we utilized non-leukemia bearing immunocompetent mice exposed to CSE using the 2 week exposure scheme and saw enhanced myeloid progenitor growth, indicating evidence of microenvironment priming of myeloid cells by CSE. One month of CSE increased the MPP1 and MPP2 populations in the bone marrow of NOD-SCID mice. C57BL/6J mice had increased myeloid and hematopoietic stem cell populations after a month of CSE (p-value <0.05). We also modeled the effect of smoking cessation upon leukemia engraftment by halting smoke exposure compared to mice that continued smoking. Cessation significantly slowed leukemic growth in MOLM13 bearing mice (N=10, p-value<0.01). Cigarette smoke exposure globally alters DNA methylation in blood cells and these changes can persist for decades. Independent of mutations, DNA methylation patterns in AML patients have prognostic significance. To understand how CSE accelerated leukemic growth in vivo, DNA methylation was evaluated using reduced representative bisulfite sequencing. More than two hundred significant alterations in DNA methylation across the promoter region of genes were found AML cells from spleen samples of CSE MOLM13-bearing mice as compared to non-smoking mice. Among the genes with the most significantly altered DNA methylation were GATA-2, an important protein for hematopoietic differentiation, and aryl-hydrocarbon receptor repressor (AHRR), a gene whose hypomethylation is a hallmark of cigarette smoke exposure. To identify the impact of cigarette smoke exposure on the leukemia cells in the absence of the tumor microenvironment we treated AML cells directly using a cigarette smoke condensate (CSC) that contains the chemicals in cigarette smoke used in the previously described CSE model. MOLM13 cells either treated with DMSO or 10ug/ml CSC every passage for two weeks were injected into NOD-SCID mice. This model resulted in enhanced leukemic burden 3, 10, and 17 days after leukemic introduction (p-value <0.0001, <0.0001, and <0.001) indicating strong pro-leukemic effects of CSC. Evaluation of in vitro CSC treated AML cells was conducted to identify causes for the enhanced leukemic burden. While CSC treatment yielded no changes in proliferation or survival of the cells over the course of two months, within one week there was increased expression of DNMT1 in several cells lines. Increased basal and maximal oxygen consumption, and modulation of the antioxidant gene, HO-1, was also observed along with modulation of AHRR and GATA-2, reinforcing roles for methylation data gained from in vivo CSE experiments. Discovering the mechanisms promoting AML progression from cigarette smoke exposure will lead to improved, tailored treatment for AML patients with smoking histories and our further studies of these gene changes will aid in that endeavor. Disclosures Jabbour: Takeda: Other: Advisory role, Research Funding; AbbVie: Other: Advisory role, Research Funding; Amgen: Other: Advisory role, Research Funding; Pfizer: Other: Advisory role, Research Funding; Genentech: Other: Advisory role, Research Funding; BMS: Other: Advisory role, Research Funding; Adaptive Biotechnologies: Other: Advisory role, Research Funding. Konopleva:Genentech: Consultancy, Research Funding; Ascentage: Research Funding; Forty-Seven: Consultancy, Research Funding; Calithera: Research Funding; F. Hoffmann La-Roche: Consultancy, Research Funding; Reata Pharmaceutical Inc.;: Patents & Royalties: patents and royalties with patent US 7,795,305 B2 on CDDO-compounds and combination therapies, licensed to Reata Pharmaceutical; Ablynx: Research Funding; Agios: Research Funding; Amgen: Consultancy; AstraZeneca: Research Funding; Eli Lilly: Research Funding; Kisoji: Consultancy; Cellectis: Research Funding; Rafael Pharmaceutical: Research Funding; AbbVie: Consultancy, Research Funding; Stemline Therapeutics: Consultancy, Research Funding; Sanofi: Research Funding. DiNardo:Agios: Consultancy, Honoraria, Research Funding; Syros: Honoraria; AbbVie: Consultancy, Honoraria, Research Funding; Celgene: Consultancy, Honoraria, Research Funding; Takeda: Honoraria; Calithera: Research Funding; Daiichi Sankyo: Consultancy, Honoraria, Research Funding; Notable Labs: Membership on an entity's Board of Directors or advisory committees; Novartis: Consultancy; MedImmune: Honoraria; ImmuneOnc: Honoraria; Jazz: Honoraria.

scholarly journals Performance of an Electrothermal MEMS Cantilever Resonator with Fano-Resonance Annoyance under Cigarette Smoke Exposure

Sensors ◽  
2021 ◽  
Vol 21 (12) ◽  
pp. 4088
Author(s):  
Andi Setiono ◽  
Michael Fahrbach ◽  
Alexander Deutschinger ◽  
Ernest J. Fantner ◽  
Christian H. Schwalb ◽  
...  
Keyword(s):  
Cigarette Smoke ◽  
Simple Procedure ◽  
Low Cost ◽  
High Sensitivity ◽  
Smoke Exposure ◽  
Cigarette Smoke Exposure ◽  
Quick Response ◽  
Physical Chemical ◽  
Resonance Sensor ◽  
Good Agreement

An electrothermal piezoresistive cantilever (EPC) sensor is a low-cost MEMS resonance sensor that provides self-actuating and self-sensing capabilities. In the platform, which is of MEMS-cantilever shape, the EPC sensor offers several advantages in terms of physical, chemical, and biological sensing, e.g., high sensitivity, low cost, simple procedure, and quick response. However, a crosstalk effect is generated by the coupling of parasitic elements from the actuation part to the sensing part. This study presents a parasitic feedthrough subtraction (PFS) method to mitigate a crosstalk effect in an electrothermal piezoresistive cantilever (EPC) resonance sensor. The PFS method is employed to identify a resonance phase that is, furthermore, deployed to a phase-locked loop (PLL)-based system to track and lock the resonance frequency of the EPC sensor under cigarette smoke exposure. The performance of the EPC sensor is further evaluated and compared to an AFM-microcantilever sensor and a commercial particle counter (DC1100-PRO). The particle mass–concentration measurement result generated from cigarette-smoke puffs shows a good agreement between these three detectors.

Low-cost apparatus for cigarette smoke exposure in rats

2021 ◽  
pp. 109412
Author(s):  
Lucas dos Reis Izolan ◽  
Solange Bandiera ◽  
Rianne Remus Pulcinelli ◽  
Mauricio Schüler Nin ◽  
Felipe Borges Almeida ◽  
...  
Keyword(s):  
Cigarette Smoke ◽  
Low Cost ◽  
Smoke Exposure ◽  
Cigarette Smoke Exposure

Pengaruh Paparan Asap Rokok Tersier terhadap Kadar Kolesterol Total dan Trigliserida Mencit

2020 ◽  
Vol 2 (2) ◽  
Author(s):  
Putra Zam Zam Rachmatullah ◽  
Samsudin Surialaga ◽  
Annisa Rahmah Furqaani
Keyword(s):  
Treatment Group ◽  
Total Cholesterol ◽  
Smoke Exposure ◽  
Cigarette Smoke Exposure ◽  
Control Group ◽  
Thirdhand Smoke ◽  
Significant Difference ◽  
The Subject ◽  
The Impact

Jumlah perokok aktif saat ini semakin meningkat sehingga perokok pasif dan residu yang tersisa atau paparan asap tersier juga meningkat. Salah satu dampak buruk rokok dapat menyebabkan dislipidemia, di antaranya peningkatan kadar kolesterol total dan trigliserida. Tujuan penelitian adalah menganalisis pengaruh paparan asap rokok tersier terhadap kadar kolesterol total dan trigliserida. Penelitian ini merupakan eksperimental in vivo dengan subjek penelitian mencit yang dibagi menjadi dua kelompok, yaitu kelompok kontrol yang tidak diberikan perlakuan dan kelompok perlakuan yang diberikan paparan asap rokok tersier selama 29 hari. Hasil penelitian menunjukkan bahwa tidak terdapat perbedaan kadar kolesterol dan trigliserida antara kelompok kontrol dan kelompok perlakuan (p>0,05). Hasil ini mengindikasikan bahwa paparan asap rokok tersier belum memengaruhi kadar kolesterol total dan trigliserida. Durasi paparan asap rokok akut dengan intensitas ringan yang diberikan pada penelitian ini diduga belum memengaruhi metabolisme lipid. EFFECT OF THIRDHAND SMOKE EXPOSURE ON TOTAL CHOLESTEROL AND TRIGLYCERIDE LEVEL IN MICENowadays, an increase in the number of active smokers also indicates an increase in passive smokers and residual smoke or thirdhand smoke exposure. One of the impact of cigarette is dyslipidemia, characterized by elevation level of total cholesterol and triglycerides. The objective of the study was to analyze the effect of thirdhand smoke exposure on the level of total cholesterol and triglycerides. This study used an in vivo experimental design with one cigarette a day and 20 mice as the subject. The subjects divided into 2 groups, the control group received no treatment and the treatment group received thirdhand smoke exposure for 29 days. The result of the study showed there was no significant difference in the level of total cholesterol and triglycerides among the control group and the treatment group (p>0.05). The result indicated that thirdhand smoke exposure had no effect on the level of total cholesterol and triglycerides. The duration of acute cigarette smoke exposure with low intensity given in this study suspected to not affect the lipid metabolism.

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