Inhibition of canine parvovirus 2 (CPV-2) replication by TAT-scFv through targeting of the viral structural protein VP2 of CPV-2.

Canine parvovirus (CPV) causes severe infectious disease with a high mortality rate in dogs. CPV is still a major health issue of dogs in the clinic. Therefore, there is an urgent need to develop effective drugs to treat the disease. In this study, we fused the transactivating transcriptional activator peptide (TAT) with scFv. TAT-scFv was identified by Western blot. CCK8 kit was used to detect the toxicity of TAT-scFv to cells. The binding activity of TAT-scFv to CPV-2-VP2 was detected by DAS ELISA. The cell uptake rate of TAT-scFv was assessed by IFA. After infection with CPV-2, F81 cells were incubated by TAT-scFv. The replication of virus was measured to determine the neutralization effect of TAT-scFv on intracellular and extracellular viruses. Protein docking was used to predict the amino acid (AA) sites of VP2 binding to TAT-scFv. TAT-scFv was expressed in Escherichia coli and purified. The DAS ELISA showed that TAT-scFv could bind with CPV-2-VP2. We demonstrated that TAT-scFv entered cells in a dose-dependent and time-dependent manner and effectively inhibited the replication of CPV-2. Using protein docking, we determined the interaction pattern and found that the N-terminal region (AA 41-49) and the C-terminal region (AA 558) of VP2 interacted with the TAT-scFv. Taken together, these results suggest that, TAT-scFv may be a potential antiviral drug for inhibiting CPV-2 replication and controlling disease caused by CPV-2.

Concomitant Gastric Acid Suppressants on the Survival of Patients with Non-Small-Cell Lung Cancer Treated with Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitors: A Meta-Analysis.

Background: The influence of concomitant use of gastric acid suppressants (AS) on survival of patients with non-small-cell lung cancer (NSCLC) treated with epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) is inconsistent according to previous studies. We performed a meta-analysis to evaluate the effect of additional AS in patients with NSCLC taking TKIs. Methods: Relevant observational studies were identified by a search of Medline, Embase, and Web of Science databases. Only studies with multivariate analyses were included. A random-effect model was used to combine the results. Results: Thirteen retrospective studies with 12259 patients were included. Pooled results showed that concomitant use of AS was associated with worse progression-free survival (PFS, adjusted hazard ratio (HR): 1.57, 95% confidence interval (CI): 1.31 to 1.89, P < 0.001; I 2 = 65%) and overall survival (OS, adjusted HR: 1.38, 95% CI: 1.19 to 1.61, P < 0.001; I 2 = 70%) in NSCLC patients taking TKIs. Sensitivity analysis limited to studies including NSCLC with EGFR mutation showed consistent results (HR for PFS: 1.53, P=0.003; HR for OS: 1.43, P=0.001). Subgroup analyses indicated that the association between concomitant use of AS and poor survival was not significantly affected by the category of AS used (proton pump inhibitors or histamine type-2 receptor antagonists) or the country of the study (Asian or non-Asian, P for subgroup analysis all >0.05). Conclusions: Concomitant use of AS in patients with NSCLC taking TKIs may be associated with poor survival outcomes.

Artificial turf infill associated with systematic toxicity in an amniote vertebrate.

Artificial athletic turf containing crumb rubber (CR) from shredded tires is a growing environmental and public health concern. However, the associated health risk is unknown due to the lack of toxicity data for higher vertebrates. We evaluated the toxic effects of CR in a developing amniote vertebrate embryo. CR water leachate was administered to fertilized chicken eggs via different exposure routes, i.e., coating by dropping CR leachate on the eggshell; dipping the eggs into CR leachate; microinjecting CR leachate into the air cell or yolk. After 3 or 7 d of incubation, embryonic morphology, organ development, physiology, and molecular pathways were measured. The results showed that CR leachate injected into the yolk caused mild to severe developmental malformations, reduced growth, and specifically impaired the development of the brain and cardiovascular system, which were associated with gene dysregulation in aryl hydrocarbon receptor, stress-response, and thyroid hormone pathways. The observed systematic effects were probably due to a complex mixture of toxic chemicals leaching from CR, such as metals (e.g., Zn, Cr, Pb) and amines (e.g., benzothiazole). This study points to a need to closely examine the potential regulation of the use of CR on playgrounds and artificial fields.

Cellular vimentin promotes the nuclear transport of the HBoV1 structural protein VP1u.

Human bocavirus 1 (HBoV1) is an important pathogen causing lower respiratory tract infection. The VP1 unique region (VP1u), consisting of 129 amino acids at the N-terminus of the HBoV1 structural protein VP1, is an important component of virus infection. Bioinformatics analysis predicted that HBoV1 VP1u exhibits two bipartite nuclear localization signals (NLS) and contains four basic regions (BRs). The two potential bipartite NLSs consist of BR2 and 3 and BR3 and 4, respectively. In this study, we inserted the truncated vp1u sequences into a double EGFP fusion expression vector and confirmed the vimentin (VIM)-HBoV1 VP1u interaction by mass spectrometry and immunoprecipitation. The results of our IFA analysis showed that all four VP1u BRs displayed strong nuclear transport functions. We further demonstrated that VP1u interacted with VIM and that they colocalized in the cytoplasm. VP1u expression in the cells enhanced the VIM expression, and the VP1u expression also increased upon VIM overexpression, although it was not affected by VIM knockdown. Upon VIM overexpression, VP1u nucleation was significantly enhanced, but was inhibited by VIM downregulation. These results indicate that the VP1u-VIM interaction could be involved in the nuclear transport of VP1u. VP1u nucleation might further affect HBoV1 replication and infection. This study could potentially help clarify the function of VP1u by further revealing the HBoV1 nuclear transport mechanism and provide a new approach for elucidating the molecular mechanism of HBoV1 replication.

Lipopolysaccharide-Induced Acute Lung Injury Is Associated with Increased Ran-Binding Protein in Microtubule-Organizing Center (RanBPM) Molecule Expression and Mitochondria-Mediated Apoptosis Signaling Pathway in a Mouse Model.

BACKGROUND Acute lung injury (ALI) is a severe and life-threatening disorder treated in intensive care units. This study aimed to determine molecules or associated signaling pathways that are involved in lipopolysaccharide (LPS)-induced inflammation in an ALI model. MATERIAL AND METHODS An ALI mouse model was established by administering LPS (25 mg/kg via intratracheal instillation). Thirty-two ALI mice were divided into Model-4 h, Model-8 h, Model-12 h, and Model-24 h groups, while another 8 mice without LPS treatment were assigned as the Control group. Hematoxylin-eosin (HE) staining was used to evaluate inflammation of lung tissues. Wet weight/dry weight (W/D) ratio and myeloperoxidase (MPO) activity of lung tissue in ALI mice were evaluated. Expressions of Bcl-2, Bcl-XL, Bak, Bax, cleaved caspase-3 (C-caspase-3), and Ran-binding protein in microtubule-organizing center (RanBPM) were determined using Western blot analysis. RESULTS LPS administration caused obvious inflammatory cell infiltration of lung tissues in ALI mice. The W/D ratio of ALI mouse lung tissues was significantly higher in Model groups than in the Control group (p<0.05). MPO activity of ALI mice was remarkably higher in Model groups compared to the Control group (p<0.05). LPS-induced ALI model mice exhibited significantly higher levels of C-caspase 3 lung tissues compared to the Control group (p<0.05). LPS-induced ALI model mice had significantly lower Bcl-XL/Bcl-2 and remarkably higher Bak/Bax expression compared with the Control group (p<0.05). LPS-induced ALI model mice displayed obviously higher RanBPM expression than in the Control group (p<0.05). CONCLUSIONS Lipopolysaccharide-induced acute lung injury is associated with increased RanBPM molecule expression and with mitochondria-mediated apoptosis signaling pathway in a mouse model.

Danggui Sini decoction protects against oxaliplatin-induced peripheral neuropathy in rats.

The effects of Danggui Sini decoction on peripheral neuropathy in oxaliplatin-induced peripheral is established. The results indicated that Danggui Sini decoction treatment significantly reduced the current amplitude of dorsal root ganglia cells undergoing agonists stimuli compared to the model-dorsal root ganglia group (P < 0.05). Danggui Sini decoction treatment significantly inhibited the inflammatory response of dorsal root ganglia cells compared to the model-dorsal root ganglia group (P < 0.05). Danggui Sini decoction treatment significantly enhanced the amounts of Nissl bodies in dorsal root ganglia cells compared to the Model-dorsal root ganglia group (P < 0.05). Danggui Sini decoction treatment improved ultra-microstructures of dorsal root ganglia cells. In conclusion, Danggui Sini decoction protected against neurotoxicity of oxaliplatin-induced peripheral neuropathy in rats by suppressing inflammatory lesions, improving ultra-microstructures, and enhancing amounts of Nissl bodies.

Gastric Acid and Pepsin Work Together in Simulated Gastric Acid Inhalation Leading to Pulmonary Fibrosis in Rats.

BACKGROUND The clinical association between gastroesophageal reflux disease (GERD) and idiopathic pulmonary fibrosis (IPF) has been known for many years, but it is still unclear. The present study investigated the association between experimentally simulated aspiration and pulmonary fibrosis. MATERIAL AND METHODS A total of 120 male Sprague-Dawley rats were randomly divided into a negative control group, a bleomycin group, and 3 simulated aspiration groups. The bleomycin group was administered a one-time intratracheal injection of bleomycin, whereas the 3 simulated aspiration groups were treated either with an intratracheal instillation of gastric fluid combined with pepsin, with pepsin alone, or with hydrochloric acid, all twice a week, and the negative control group was administered normal saline twice a week. Lung tissues were collected to evaluate pathological changes and the mRNA expression levels of connective tissue growth factor (CTGF), type I collagen, and transforming growth factor. RESULTS The results demonstrated that the degree of fibrosis in the early stage was low in each of the 3 simulated aspiration groups, but gradually increased over time. The expression levels of the downstream factor of fibrosis, CTGF, and type I collagen also reflected this trend. CONCLUSIONS The study demonstrates that aspiration of gastric contents can cause pulmonary fibrosis, and mixed aspiration of pepsin and gastric fluid can accelerate this process. This study provides strong evidence in support of a potential association between human GERD and IPF.

Nonstructural Protein NP1 of Human Bocavirus 1 suppresses the growth of A549 cell by promoting autophagy.

Human bocavirus 1 (HBoV1) refers to a human parvovirus causing acute respiratory tract infection in children. Bocaviruses encode an NP1 protein, which has 47% amino acid homology with NP1 of Minute Virus of Canines (MVC) and Bovine Parvovirus (BPV), but not with any protein of other parvoviruses. NP1 was found to induce apoptosis in Hela cells, which does not depend on viral replication and other protein expression. However, whether NP1 induces pulmonary cell death is unclear. In the present study, we investigate the impacts of NP1 on the autophagy and viability of A549 cells by expressing NP1. The plasmid containing NP1 gene was transfected into A549 cells. The apoptosis of A549 was evaluated by apoptosis detection kit and expression of caspase3. Cell viability and cell migration were detected by CCK8 kit and cell scratch test, respectively. The autophagy-related proteins and HMGB1 were detected by Western blot after NP1 expression in transfected cells. The real-time PCR was employed to detect HMGB1 mRNA. The secretory HMGB1 in supernatant of cell culture was measured by ELISA kit. The transient expression of NP1 did not induce apoptosis in A549 cells, but inhibited cell viability and migration. The expression of Beclin1 and LC3 II increased significantly and that of autophagy substrate P62 decreased dramatically upon transfection of NP1. The expression of NP1 reduced both levels of mRNA and protein HMGB1. The NP1 induced A549 autophagy was activated by STAT3 signaling pathway. HBoV1 NP1 induced autophagy in A549 cells by activating phosphorylation of STAT3 signaling pathway and inhibited A549 cell viability. This study provides insight into further elucidating the replication mechanism of HBoV1.

Assessment of urinary metabolite excretion after rat acute exposure to perfluorooctanoic acid and other peroxisomal proliferators.

Perfluorooctanoic acid (PFOA) is a persistent environmental contaminant. Activation of the peroxisome proliferator activated receptor alpha (PPARα) resulting from exposure to PFOA has been extensively studied in rodents. However, marked differences in response to peroxisome proliferators prevent extrapolation of rodent PPARα activation to human health risks and additional molecular mechanisms may also be involved in the biological response to PFOA exposure. To further explore the potential involvement of such additional pathways, the effects of PFOA exposure on urinary metabolites were directly compared with those of other well-known PPARα agonists. Male rats were administered PFOA (10, 33, or 100 mg/kg/d), fenofibrate (100 mg/kg/d), or di(2-ethylhexyl) phthalate (100 mg/kg/d) by gavage for 3 consecutive days and allowed to recover for 4 days, and overnight urine was collected. Greater urinary output was observed exclusively in PFOA-treated rats as the total fraction of PFOA excreted in urine increased with the dose administered. Assessment of urinary metabolites (ascorbic acid, quinolinic acid, 8-hydroxy-2'-deoxyguanosine, and malondialdehyde) provided additional information on PFOA's effects on hepatic glucuronic acid and tryptophan-nicotinamide adenine dinucleotide (NAD) pathways and on oxidative stress, whereas increased liver weight and palmitoyl-CoA oxidase activity indicative of PPARα activation and peroxisomal proliferation persisted up to day five after the last exposure.

Measurements of selected brominated flame retardants in nursing women: implications for human exposure.

We have examined several emerging brominated flame retardants (BFRs) including 2-ethyl-1-hexyl-2,3,4,5-tetrabromobenzoate (TBB), bis(2-ethylhexyl) tetrabromophthalate (TBPH), 1,2-bis(2,4,6-tribromophenoxy) ethane (BTBPE), 4,5,6,7-tetrabromo-1,1,3-trimethyl-3-(2,3,4,5-tetrabromophenyl)-indane (OBIND), and decabromodiphenyl ethane (DBDPE) in paired human maternal serum (n = 102) and breast milk (n = 105) collected in 2008-2009 in the Sherbrooke region in Canada. Three legacy BFRs were also included in the study for comparison: decabromobiphenyl (BB-209), 2,2',4,4',5,5'-hexabromobiphenyl (BB-153), and 2,2',4,4',5,5'-hexabromodiphenyl ethers (BDE-153). TBB, BB-153, and BDE-153 had detection frequencies greater than 55% in both serum and milk samples. Their lipid weight (lw) adjusted median concentrations (ng g(-1) lw) in serum and milk were 1.6 and 0.41 for TBB, 0.48 and 0.31 for BB-153, and 1.5 and 4.4 for BDE-153, respectively. The detection frequencies for the other BFRs measured in serum and milk were 16.7% and 32.4% for TBPH, 3.9% and 0.0% for BTBPE, 2.0% and 0.0% for BB-209, 9.8% and 1.0% for OBIND, and 5.9% and 8.6% for DBDPE. The ratio of TBB over the sum of TBB and TBPH (fTBB) in serum (0.23) was lower than that in milk (0.46), indicating TBB has a larger tendency than TBPH to be redistributed from blood to milk. Overall, these data confirm the presence of non-PBDE BFRs in humans, and the need to better understand their sources, routes of exposure, and potential human health effects.

In vitro exposure to cigarette smoke induces oxidative stress in follicular cells of F1 hybrid mice.

This study assessed the influence of cigarette smoke condensate (CSC) and benzo(a)pyrene [B(a)P] on the levels of two oxidative stress biomarkers [8-isoprostane (8-IsoP) and 8-hydroxy-2-deoxy Guanosine (8-OH-dG)], in in-vitro spent media of follicle cells. Follicles (100-130 µm) isolated from ovaries of F1 hybrid (C57Bl/6j × CBA/Ca) mice were cultured for 13 days in media exposed to B(a)P [0 ng ml⁻¹ (control) to 45 ng ml⁻¹] or CSC [0 µg ml⁻¹ (control) to 130 µg ml⁻¹]. The concentrations of oxidative stress biomarkers in spent media were quantified by enzyme-linked immune sorbent assays (ELISA). CSC and B(a)P treatment induced a significant, dose-dependent increase in the concentrations of 8-IsoP and 8-OH-dG in the spent media. We conclude that CSC and B(a)P exposure can induce oxidative stress in ovarian follicles, an effect that may contribute to the previously documented decline in follicle development and premature ovarian failure in women who smoke.

Indoor environment, physiological factors, and diet as predictors of halogenated flame retardant levels in stool and plasma of children from a Canadian cohort.

Exposure to halogenated flame retardants (HFRs) has been associated with various adverse effects on human health. Human exposure to HFRs mainly occurs through diet, ingesting contaminated dust, and inhaling contaminated air. Understanding and characterizing the variables linked to these exposure pathways is essential for developing effective risk assessment and mitigation strategies. We investigated indoor environment quality, physiological factors, and diet as potential predictors of HFRs concentration in children's plasma and stool. A selected number of HFRs, including polybrominated diphenyl ethers (PBDEs), Dechlorane-like compounds, and emerging halogenated flame retardants, were measured in children from eastern Quebec (Canada). Information on indoor environment quality, physiological factors, and diet was obtained through self-report questionnaires. Our results show that lower brominated compounds, which are more volatile, were primarily correlated to indoor environment quality. Notably, the use of air purifiers was associated with lower BDE47 and BDE100 levels in blood and newer residential buildings were associated with higher concentrations of BDE47. A significant seasonal variation was found in stool samples, with higher levels of lower brominated PBDEs (BDE47 and BDE100) in samples collected during summer. No association between household income or maternal education degree and HFRs was found. Among emerging compounds, Dec602 and Dec603 were associated with the most variables, including the use of air dehumidifiers, air conditioning, and air purifiers, and the child's age and body fat percentage.

The 2009 pandemic (H1N1) viruses isolated from pigs show enhanced pathogenicity in mice.

Since the emergence of the 2009 pandemic (H1N1) virus (2009/H1N1) in April 2009, cases of transmission from humans to pigs have been reported frequently. In our previous studies, four 2009/H1N1 variants were isolated from pigs. To better understand the phenotypic differences of the pig isolates compared with the human isolate, in this study mice were inoculated intranasally with different 2009/H1N1 viruses, and monitored for morbidity, mortality, and viral replication, cytokine production and pathological changes in the lungs. The results show that all isolates show effective replication in lungs, but varying in their ability to cause morbidity. In particular, the strains of A/swine/Nanchang/3/2010 (H1N1) and A/swine/Nanchang/F9/2010 (H1N1) show the greatest virulence with a persisting replication in lungs and high lethality for mice, compared with the human isolate A/Liaoning /14/2009 (H1N1), which shows low virulence in mice. Furthermore, the lethal strains could induce more severe lung pathological changes and higher production of cytokines than that of other strains at an early stage. Amino acid sequence analysis illustrates prominent differences in viral surface glycoproteins and polymerase subunits between pig isolates and human strains that might correlate with their phenotypic differences. These studies demonstrate that the 2009/H1N1 pig isolates exhibit heterogeneous infectivity and pathogencity in mice, and some strains possess an enhanced pathogenicity compared with the human isolate.

Nationally representative levels of selected volatile organic compounds in Canadian residential indoor air: population-based survey.

A comprehensive, population-based national indoor air survey was conducted in 2009-2011 in Canada. A total of 84 volatile organic carbons (VOCs) from 3218 houses, 546 apartments, and 93 other dwelling types were measured using passive sampling followed by thermal desorption GC/MS. A total of 12 VOCs were measured in both this study and the 1992 Canadian national study. Arithmetic means of VOCs in this study were 2-5 times lower than those in the 1992 study with the exception of a higher styrene level (1.13 µg · m(-3)). Comparing the geometric means of the 24 VOCs showed that levels for the VOCs in this study were comparable to those reported in Europe. They were generally within a factor of 2; 1,4-dichlorobenzene (0.21 µg · m(-3)) and 1,2,4-trimethylbenzene (0.51 µg · m(-3)) were noticeably lower in this study than in the European studies. There were 47 VOCs detected in more than 50% of Canadian households; 33 of them were higher in houses than in apartments for all nonsmoking homes, while only 4 were lower in houses than in apartments. A total of 11 of 47 VOCs were higher in smoking homes compared to nonsmoking homes, while the rest had similar levels. Principal component analysis identified several groups of VOCs with possible common sources.

In vitro dermal absorption of di(2-ethylhexyl) adipate (DEHA) in a roll-on deodorant using human skin.

In vitro dermal absorption experiments were conducted using a roll-on deodorant that contains 1.56% di(2-ethylhexyl) adipate (DEHA), a plasticizer widely used in consumer products. Human skin specimens were fitted in Bronaugh flow-through Teflon diffusion cells. The diffusion cells were maintained at 32 °C to reflect the skin temperature. Two amounts (low dose: 5 mg of the product; high dose: 100 mg) were applied, in triplicate, each on four different human skins. DEHA was determined in the receiver solution at 6-h intervals, using headspace solid-phase microextraction gas chromatography-mass spectrometry (GC-MS). After 24 h, the experiment was terminated and masses of DEHA in the skin depot, skin wash, and upper and lower chambers of the diffusion cell were determined. A significant portion of applied DEHA, 28% in the low amount application and 34% in the high one, was found in the skin depot. In comparison, only 0.04% and 0.002% of applied DEHA were found in the receiver solutions for the low and high doses, respectively. Under our experimental conditions, an apparent steady-state flux of low DEHA mass penetrating from skin into the receiver solution was observed with a penetration rate of 2.2 ng/cm(2)/h for both the low and high doses. The average mass recovery was 81% for the low dose application and 56% for the high dose.

Implementation of the indoor air component of cycle 2 of the Canadian Health Measures Survey.

BACKGROUND: The presence of volatile organic compounds (VOCs) in indoor air may have negative health consequences, ranging from mild irritation to more severe illnesses. Indoor air data are required to assess Canadian population exposure to these VOCs. DATA AND METHODS: The 2009 to 2011 Canadian Health Measures Survey (CHMS) included an indoor air component. Respondents who went to the mobile examination centre to participate in the physical measures section of the survey were asked to deploy an indoor air sampler in their homes for 7 consecutive days. Data were collected for 84 VOCs. Control samples that were implemented included duplicates and blanks. RESULTS: Of the 4,686 indoor air samplers given to CHMS respondents, 4,581 were deployed and returned to the testing laboratory. Data from 3,857 samplers met the criteria for inclusion in the CHMS indoor air data files. Thirteen VOCs had a mean percentage difference between the duplicate pairs greater than 30%. The field and cleaning blank geometric means and medians were lower than 1 µg/m³ for 83 VOCs. INTERPRETATION: The high percentage of mobile examination centre participants who deployed samplers in their homes, the sampler return rate, and the quality of the data obtained demonstrate the feasibility of relying on respondents to handle indoor air samplers for large-scale collection of residential VOC data.

Predictors of indoor BTEX concentrations in Canadian residences.

BACKGROUND: Benzene, toluene, ethylbenzene and m-, p-xylenesand o-xylene (BTEX) are a group of volatile organic compounds that originate from similar sources. Given the potentially negative health implications of BTEX exposure and their prevalence in residential indoor air, it is important to understand typical residential concentrations and identify predictors. DATA AND METHODS: The 2009 to 2011 Canadian Health Measures Survey included an indoor air component. Questionnaires were administered, and respondents were asked to deploy an air sampler in their home for 7 consecutive days. This analysis is based on BTEX data from 5,191 respondents. Mean BTEX concentrations were examined overall, and by dwelling type and garage configuration. Stepwise regression models were used to examine potential sources of BTEX components. RESULTS: Means were 1.95 µg/m³ (benzene), 19.17 µg/m³ (toluene), 4.09 µg/m³ (ethylbenzene), 14.42 µg/m³ (m-, p-xylenes), and 4.16 µg/m³ (o-xylene). Significant predictors of the presence of BTEX included a garage on the property, regular smoking in the home, renovations in the past month, number of occupants, use of paint remover, and use of fragrance. INTERPRETATION: Results of this nationally representative study found that BTEX concentrations are relatively low among Canadian residences, and identified several different indoor sources.

Thermal reaction products and formation pathways of two monoterpenes under in situ thermal desorption conditions that mimic vaping coil temperatures.

Vaping has become more popular and different brands and types of vaping devices have rapidly emerged. However, little is known about the potential health risks of human inhalation exposures to the volatile chemicals in the vapour, which includes both directly vaporised components of vaping liquid and their reaction products formed during vaping processes. This study investigated reaction products of two monoterpenes (α-pinene and terpinolene) that are used as flavouring agents in vaping liquids with a focus on the identification of reaction products and their formation pathways. The thermal desorption was conducted under an in situ condition that is in the range of heating coil temperature in vaping by thermally desorbing the chemicals at a temperature range of 100-300 °C. Additional clean air was introduced during the thermal desorption. 36 and 29 reaction products were identified from α-pinene and terpinolene, respectively, at a relative concentration of 0.01% and greater in the desorbed mixture. 3-Carene was the dominant reaction product of α-pinene, while reaction products of terpinolene was dominated by p-isopropenyltoluene. Several reaction pathways including ring opening, allylic oxidation, cyclo-etherification, Wagner-Meerwein rearrangement, epoxidation, cleavage and removal of partial structure, and dehydration were involved in the formation of various reaction products. These pathways and resulting relative concentrations of residual parent compound and reaction products were influenced by both temperature and amount of air present during thermal desorption. The study results demonstrate possible existence of reaction products from thermally labile chemicals like monoterpenes in vaping aerosols and can help inform policies regulating vaping devices and products to protect public health.

Complementarity of plasma and stool for the characterization of children's exposure to halogenated flame retardants: Update on analytical methods and application to a Canadian cohort.

Sixteen halogenated flame retardants including Polybrominated diphenyl ethers (PBDEs), Dechlorane-like compounds, and emerging halogenated flame retardants were measured in stool and plasma samples from children aged 8.9-13.8 years old. Samples were obtained from a Canadian cohort investigating the effect of contaminants on children's neurodevelopment in the Estrie region, Québec, Canada. The method for stool analysis developed for this study showed good recovery for all targeted compounds (73%-93%) with associated relative standard deviation (RSD) in the range of 16.0%-30.7% for most compounds except for the thermosensitive BDE209, OBTMBI, and BTBPE, which showed slightly higher RSD, i.e., 49.3%, 37.2%, and 34.9% respectively. Complementarity investigation of stool and blood samples allowed us to better characterize human exposure to these halogenated flame retardants. Exposure patterns differed significantly between stool and blood, notably in the relative abundance of BDE47, BDE100, BDE99, and BDE153 and the detection frequencies of BDE209, syn-DP, anti-DP, and DBDPE. There was no correlation between the two matrices' PBDEs concentration levels except for BDE153 (rho = 0.44, p < 0.01). Our results indicate that future epidemiological studies may benefit from the use of stool as a complementary matrix to blood, especially investigations into chemical impacts on the gut microbiome. Results also revealed that children from the GESTE cohort, an Eastern Canadian semi-rural cohort, are exposed to both historical and emergent flame retardants.

The antigenic property of the H5N1 avian influenza viruses isolated in central China.

BACKGROUND: Three influenza pandemics outbroke in the last century accompanied the viral antigen shift and drift, resulting in the change of antigenic property and the low cross protective ability of the existed antibody to the newly emerged pandemic virus, and eventually the death of millions of people. The antigenic characterizations of the viruses isolated in central China in 2004 and 2006-2007 were investigated in the present study. RESULTS: Hemagglutinin inhibition assay and neutralization assay displayed differential antigenic characteristics of the viruses isolated in central China in two periods (2004 and 2006-2007). HA genes of the viruses mainly located in two branches in phylogeny analysis. 53 mutations of the deduced amino acids of the HA genes were divided into 4 patterns. Mutations in pattern 2 and 3 showed the main difference between viruses isolated in 2004 and 2006-2007. Meanwhile, most amino acids in pattern 2 and 3 located in the globular head of the HA protein, and some of the mutations evenly distributed at the epitope sites. CONCLUSIONS: The study demonstrated that a major antigenic drift had occurred in the viruses isolated in central China. And monitoring the antigenic property should be the priority in preventing the potential pandemic of H5N1 avian influenza virus.