The impact of conventional and nonconventional inhalants on children and adolescents

AimInhalant abuse in the adolescent population is a growing concern for care givers, communities, physicians, and medical providers. The aim of this article is to provide a review of the literature about this new challenge. In addition, it raises awareness about recent health policy rulings.MethodsReview of the literature was done.ResultsIn this review article, the prevalence of different modes of inhalant use and abuse in children and young adults and their potential health implications will be examined: Cigarettes, ENDS (E Cigarettes), Hookah, Marijuana, and Huffing. Additionally, marketing and advertising tactics will be reviewed to understand how they target this population. A review of current health policy recommendations from the FDA, American Thoracic Society, and the American Academy of Pediatrics will also be discussed.ConclusionThe rapid rise in e‐cigarette and hookah use in school aged children should trigger a call to action in the medical and public health communities. Health policy recommendations need to be made to reduce the level of adolescent substance abuse.Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/142898/1/ppul23836_am.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/142898/2/ppul23836.pd

Association of sub-acute changes in plasma amino acid levels with long-term brain pathologies in a rat model of moderate-severe traumatic brain injury.

INTRODUCTION Traumatic brain injury (TBI) induces a cascade of cellular alterations that are responsible for evolving secondary brain injuries. Changes in brain structure and function after TBI may occur in concert with dysbiosis and altered amino acid fermentation in the gut. Therefore, we hypothesized that subacute plasma amino acid levels could predict long-term microstructural outcomes as quantified using neurite orientation dispersion and density imaging (NODDI). METHODS Fourteen 8-10-week-old male rats were randomly assigned either to sham (n = 6) or a single moderate-severe TBI (n = 8) procedure targeting the primary somatosensory cortex. Venous blood samples were collected at days one, three, seven, and 60 post-procedure and NODDI imaging were carried out at day 60. Principal Component Regression analysis was used to identify time dependent plasma amino acid concentrations after in the subacute phase post-injury that predicted NODDI metric outcomes at day 60. RESULTS The TBI group had significantly increased plasma levels of glutamine, arginine, alanine, proline, tyrosine, valine, isoleucine, leucine, and phenylalanine at days three-seven post-injury. Higher levels of several neuroprotective amino acids, especially the branched-chain amino acids (valine, isoleucine, leucine) and phenylalanine, as well as serine, arginine, and asparagine at days three-seven post-injury were also associated with lower isotropic diffusion volume fraction measures in the ventricles and thus lesser ventricular dilation at day 60. DISCUSSION In the first such study, we examined the relationship between the long-term post-TBI microstructural outcomes across whole brain and the subacute changes in plasma amino acid concentrations. At days three to seven post-injury, we observed that increased plasma levels of several amino acids, particularly the branched-chain amino acids and phenylalanine, were associated with lesser degrees of ventriculomegaly and hydrocephalus TBI neuropathology at day 60 post-injury. The results imply that altered amino acid fermentation in the gut may mediate neuroprotection in the aftermath of TBI

Escalation of Tau Accumulation after a Traumatic Brain Injury: Findings from Positron Emission Tomography.

Traumatic brain injury (TBI) has come to be recognized as a risk factor for Alzheimer's disease (AD), with poorly understood underlying mechanisms. We hypothesized that a history of TBI would be associated with greater tau deposition in elders with high-risk for dementia. A Groups of 20 participants with self-reported history of TBI and 100 without any such history were scanned using [18F]-AV1451 positron emission tomography as part of the Alzheimer's Disease Neuroimaging Initiative (ADNI). Scans were stratified into four groups according to TBI history, and by clinical dementia rating scores into cognitively normal (CDR = 0) and those showing cognitive decline (CDR ≥ 0.5). We pursued voxel-based group comparison of [18F]-AV1451 uptake to identify the effect of TBI history on brain tau deposition, and for voxel-wise correlation analyses between [18F]-AV1451 uptake and different neuropsychological measures and cerebrospinal fluid (CSF) biomarkers. Compared to the TBI-/CDR ≥ 0.5 group, the TBI+/CDR ≥ 0.5 group showed increased tau deposition in the temporal pole, hippocampus, fusiform gyrus, and inferior and middle temporal gyri. Furthermore, the extent of tau deposition in the brain of those with TBI history positively correlated with the extent of cognitive decline, CSF-tau, and CSF-amyloid. This might suggest TBI to increase the risk for tauopathies and Alzheimer's disease later in life

Association of sub-acute changes in plasma amino acid levels with long-term brain pathologies in a rat model of moderate-severe traumatic brain injury

IntroductionTraumatic brain injury (TBI) induces a cascade of cellular alterations that are responsible for evolving secondary brain injuries. Changes in brain structure and function after TBI may occur in concert with dysbiosis and altered amino acid fermentation in the gut. Therefore, we hypothesized that subacute plasma amino acid levels could predict long-term microstructural outcomes as quantified using neurite orientation dispersion and density imaging (NODDI).MethodsFourteen 8–10-week-old male rats were randomly assigned either to sham (n = 6) or a single moderate-severe TBI (n = 8) procedure targeting the primary somatosensory cortex. Venous blood samples were collected at days one, three, seven, and 60 post-procedure and NODDI imaging were carried out at day 60. Principal Component Regression analysis was used to identify time dependent plasma amino acid concentrations after in the subacute phase post-injury that predicted NODDI metric outcomes at day 60.ResultsThe TBI group had significantly increased plasma levels of glutamine, arginine, alanine, proline, tyrosine, valine, isoleucine, leucine, and phenylalanine at days three-seven post-injury. Higher levels of several neuroprotective amino acids, especially the branched-chain amino acids (valine, isoleucine, leucine) and phenylalanine, as well as serine, arginine, and asparagine at days three-seven post-injury were also associated with lower isotropic diffusion volume fraction measures in the ventricles and thus lesser ventricular dilation at day 60.DiscussionIn the first such study, we examined the relationship between the long-term post-TBI microstructural outcomes across whole brain and the subacute changes in plasma amino acid concentrations. At days three to seven post-injury, we observed that increased plasma levels of several amino acids, particularly the branched-chain amino acids and phenylalanine, were associated with lesser degrees of ventriculomegaly and hydrocephalus TBI neuropathology at day 60 post-injury. The results imply that altered amino acid fermentation in the gut may mediate neuroprotection in the aftermath of TBI

Coupling ultrasound with enzyme-assisted extraction of essential oil from algerian artemisia herba-alba asso

The composition of the essential oil (EO) of Artemisia herba-alba Asso, extracted by Hydro-Distillation (HD) and by coupling Ultrasound with Enzyme-Assisted Extraction (UE-AE) prior to HD from the plant's aerial parts were analyzed by GC-MS. Antibacterial, antifungal and antioxidant activities of the obtained EOs were evaluated. The yield of EO extraction after pretreatment of the desert wormwood leaves by coupling ultrasound with enzymes was in the range of 1.56%±0.07 compared to 1.01% ±0.08 in HD process; also, the total time necessary to complete EO extraction is 180min for HD and 120min for UE-AE. GC-MS profiling of the EOs showed changes in chemo type obtained by HD from camphor/1,8-cineole/α-mujone/chrysanmenone to a new chemo type in the case of UE-AE: camphor/α-thujone/1,8-cineole/filifolone; Then, an increasing of filifolone, α-thujone, 3-octyne and cis-limonene oxide characterize the UE-EO. The antifungal activity of the EO has slightly increased when extracted by UE-AE, however, both antibacterial and antioxidant activities were interestingly increased

Tauopathy in veterans with long-term posttraumatic stress disorder and traumatic brain injury

PURPOSE: Traumatic brain injury (TBI) and posttraumatic stress disorder (PTSD) have emerged as independent risk factors for an earlier onset of Alzheimer's disease (AD), although the pathophysiology underlying this risk is unclear. Postmortem studies have revealed extensive cerebral accumulation of tau following multiple and single TBI incidents. We hypothesized that a history of TBI and/or PTSD may induce an AD-like pattern of tau accumulation in the brain of nondemented war veterans. METHODS: Vietnam War veterans (mean age 71.4 years) with a history of war-related TBI and/or PTSD underwent [18F]AV145 PET as part of the US Department of Defense Alzheimer's Disease Neuroimaging Initiative. Subjects were classified into the following four groups: healthy controls (n = 21), TBI (n = 10), PTSD (n = 32), and TBI+PTSD (n = 17). [18F]AV1451 reference tissue-normalized standardized uptake value (SUVr) maps, scaled to the cerebellar grey matter, were tested for differences in tau accumulation between groups using voxel-wise and region of interest approaches, and the SUVr results were correlated with neuropsychological test scores. RESULTS: Compared to healthy controls, all groups showed widespread tau accumulation in neocortical regions overlapping with typical and atypical patterns of AD-like tau distribution. The TBI group showed higher tau accumulation than the other clinical groups. The extent of tauopathy was positively correlated with the neuropsychological deficit scores in the TBI+PTSD and PTSD groups. CONCLUSION: A history of TBI and/or PTSD may manifest in neurocognitive deficits in association with increased tau deposition in the brain of nondemented war veterans decades after their trauma. Further investigation is required to establish the burden of increased risk of dementia imparted by earlier TBI and/or PTSD

Amyloid pathology fingerprint differentiates post-traumatic stress disorder and traumatic brain injury

INTRODUCTION: Traumatic brain injury (TBI) and post-traumatic stress disorder (PTSD) are risk factors for early onset of Alzheimer's disease (AD) and may accelerate the progression rate of AD pathology. As amyloid-beta (Aβ) plaques are a hallmark of AD pathology, we hypothesized that TBI and PTSD might increase Aβ accumulation in the brain. METHODS: We examined PET and neuropsychological data from Vietnam War veterans compiled by the US Department of Defense Alzheimer's Disease Neuroimaging Initiative, to examine the spatial distribution of Aβ in male veterans' who had experienced a TBI and/or developed PTSD. Subjects were classified into controls, TBI only, PTSD only, and TBI with PTSD (TBI_PTSD) groups and data were analyzed using both voxel-based and ROI-based approaches. RESULTS: Compared to controls, all three clinical groups showed a pattern of mainly increased referenced standard uptake values (SUVR) for the amyloid tracer [18F]-AV45 PET, with rank order PTSD > TBI_PTSD > TBI > Control, and same rank order was seen in the deficits of cognitive functions. SUVR increase was observed in widespread cortical regions of the PTSD group; in white matter of the TBI_PTSD group; and cerebellum and precuneus area of the TBI group, in contrast with controls. The [18F]-AV45 SUVR correlated negatively with cerebrospinal fluid (CSF) amyloid levels and positively with the CSF tau concentrations. CONCLUSION: These results suggest that both TBI and PTSD are substantial risk factors for cognition decline and increased Aβ deposition resembling that in AD. In addition, both PTSD and TBI_PTSD have a different pathways of Aβ accumulation

Using Zebrafish for Investigating the Molecular Mechanisms of Drug-Induced Cardiotoxicity

Over the last decade, the zebrafish (Danio rerio) has emerged as amodel organismfor cardiovascular research.Zebrafish have several advantages over mammalian models. For instance, the experimental cost of using zebrafish is comparatively low; the embryos are transparent, develop externally, and have high fecundity making them suitable for large-scale genetic screening. More recently, zebrafish embryos have been used for the screening of a variety of toxic agents, particularly for cardiotoxicity testing. Zebrafish has been shown to exhibit physiological responses that are similar to mammals after exposure to medicinal drugs including xenobiotics, hormones, cancer drugs, and also environmental pollutants, including pesticides and heavy metals. In this review, we provided a summary for recent studies that have used zebrafish to investigate themolecularmechanisms of drug-induced cardiotoxicity. More specifically, we focused on the techniques that were exploited by us and others for cardiovascular toxicity assessment and described several microscopic imaging and analysis protocols that are being used for the estimation of a variety of cardiac hemodynamic parameters.Huseyin C. Yalcin is supported by Qatar National Research Fund (QNRF), National Priority Research Program NPRP 10-0123-170222,and Qatar University internal funds,QUUGBRC-2017-3 and QUST-BRC-SPR\2017-1. The publication of this article was partially funded by the Qatar National Library

Expression and trans-specific polymorphism of self-incompatibility RNases in Coffea (Rubiaceae)

Self-incompatibility (SI) is widespread in the angiosperms, but identifying the biochemical components of SI mechanisms has proven to be difficult in most lineages. Coffea (coffee; Rubiaceae) is a genus of old-world tropical understory trees in which the vast majority of diploid species utilize a mechanism of gametophytic self-incompatibility (GSI). The S-RNase GSI system was one of the first SI mechanisms to be biochemically characterized, and likely represents the ancestral Eudicot condition as evidenced by its functional characterization in both asterid (Solanaceae, Plantaginaceae) and rosid (Rosaceae) lineages. The S-RNase GSI mechanism employs the activity of class III RNase T2 proteins to terminate the growth of "self" pollen tubes. Here, we investigate the mechanism of Coffea GSI and specifically examine the potential for homology to S-RNase GSI by sequencing class III RNase T2 genes in populations of 14 African and Madagascan Coffea species and the closely related self-compatible species Psilanthus ebracteolatus. Phylogenetic analyses of these sequences aligned to a diverse sample of plant RNase T2 genes show that the Coffea genome contains at least three class III RNase T2 genes. Patterns of tissue-specific gene expression identify one of these RNase T2 genes as the putative Coffea S-RNase gene. We show that populations of SI Coffea are remarkably polymorphic for putative S-RNase alleles, and exhibit a persistent pattern of trans-specific polymorphism characteristic of all S-RNase genes previously isolated from GSI Eudicot lineages. We thus conclude that Coffea GSI is most likely homologous to the classic Eudicot S-RNase system, which was retained since the divergence of the Rubiaceae lineage from an ancient SI Eudicot ancestor, nearly 90 million years ago.United States National Science Foundation [0849186]; Society of Systematic Biologists; American Society of Plant Taxonomists; Duke University Graduate Schoolinfo:eu-repo/semantics/publishedVersio