Cannabis use and anxiety: is stress the missing piece of the puzzle?

OBJECTIVE Comorbidity between anxiety and cannabis use is common yet the nature of the association between these conditions is not clear. Four theories were assessed, and a fifth hypothesis tested to determine if the misattribution of stress symptomology plays a role in the association between state-anxiety and cannabis. METHODS Three-hundred-sixteen participants ranging in age from 18 to 71 years completed a short online questionnaire asking about their history of cannabis use and symptoms of stress and anxiety. RESULTS Past and current cannabis users reported higher incidence of lifetime anxiety than participants who had never used cannabis; however, these groups did not differ in state-anxiety, stress, or age of onset of anxiety. State-anxiety and stress were not associated with frequency of cannabis use, but reported use to self-medicate for anxiety was positively associated with all three. Path analyses indicated two different associations between anxiety and cannabis use, pre-existing and high state-anxiety was associated with (i) higher average levels of intoxication and, in turn, acute anxiety responses to cannabis use; (ii) frequency of cannabis use via the mediating effects of stress and self-medication. CONCLUSION None of the theories was fully supported by the findings. However, as cannabis users reporting self-medication for anxiety were found to be self-medicating stress symptomology, there was some support for the stress-misattribution hypothesis. With reported self-medication for anxiety being the strongest predictor of frequency of use, it is suggested that researchers, clinicians, and cannabis users pay greater attention to the overlap between stress and anxiety symptomology and the possible misinterpretation of these related but distinct conditions

Introduction to the political economy of the sub-prime crisis in Britain : constructing and contesting competence

It is almost always inadvisable to try to second-guess the character of a General Election campaign before it begins in earnest. Yet, even in today’s shadow-boxing phase in advance of the British General Election due to be called in 2010, a number of important campaign contours are already in evidence. It is one of the unwritten laws of British electoral politics that governments unravel – particularly those of a certain longevity – as events appear ever more to have spiralled out of their control. The task for the Brown Government in the upcoming General Election campaign is to try to convince voters that there is still life left within Labour despite its current travails with the credit crunch and British banks’ self-imposed entrapment in the subprime crisis. Claim and counter-claim are likely to pass between the Government and the opposition parties as to where the blame lies for the current disarray of the banking sector, whose model of regulation is most responsible and who is best placed to ensure a successful clean-up operation. Whoever is perceived to have come out on top in this debate is likely to stand a very good chance of winning the election

Understanding High Recession Rates of Carbon Ablators Seen in Shear Tests in an Arc Jet

High rates of recession in arc jet shear tests of Phenolic Impregnated Carbon Ablator (PICA) inspired a series of tests and analysis on FiberForm (a carbon preform used in the fabrication of PICA). Arc jet tests were performed on FiberForm in both air and pure nitrogen for stagnation and shear configurations. The nitrogen tests showed little or no recession, while the air tests of FiberForm showed recession rates similar to that of PICA (when adjusted for the difference in density). While mechanical erosion can not be ruled out, this is the first step in doing so. Analysis using a carbon oxidation boundary condition within DPLR was used to predict the recession rate of FiberForm. The analysis indicates that much of the anomalous recession behavior seen in shear tests may simply be an artifact of the non-flight like test configuration (copper upstream of the test article) a result of dissimilar enthalpy and oxygen concentration profiles on the copper. Shape change effects were also investigated and shown to be relatively small

Internal colour gradients for E/S0 galaxies in Abell 2218

We determine colour gradients of $-0.15 \pm 0.08$ magnitudes per decade in radius in F450W$-$F606W and $-0.07 \pm 0.06$ magnitudes per decade in radius in F606W$-$F814W for a sample of 22 E/S0 galaxies in Abell 2218. These gradients are consistent with the existence of a mild ($\sim -0.3$ dex per decade in radius) gradient in metal abundance, (cf. previous work at lower and higher redshift for field and cluster galaxies). The size of the observed gradients is found to be independent of luminosity over a range spanning $M^*-1$ to $M^*+1.5$ and also to be independent of morphological type. These results suggest a fundamental similarity in the distributions of stellar populations in ellipticals and the bulges of lenticular galaxies. These results are not consistent with simple models of either monolithic collapse or hierarchical mergers.Comment: accepted by MNRA

An upper limit to the dry merger rate at <z> ~ 0.55

We measure the fraction of Luminous Red Galaxies (LRGs) in dynamically close pairs (with projected separation less than 20 $h^{-1}$ kpc and velocity difference less than 500 km s$^{-1}$) to estimate the dry merger rate for galaxies with $-23 < M(r)_{k+e,z=0.2} +5 \log h < -21.5$ and $0.45 < z < 0.65$ in the 2dF-SDSS LRG and QSO (2SLAQ) redshift survey. For galaxies with a luminosity ratio of $1:4$ or greater we determine a $5\sigma$ upper limit to the merger fraction of 1.0% and a merger rate of $< 0.8 \times 10^{-5}$ Mpc$^{-3}$ Gyr$^{-1}$ (assuming that all pairs merge on the shortest possible timescale set by dynamical friction). This is significantly smaller than predicted by theoretical models and suggests that major dry mergers do not contribute to the formation of the red sequence at $z < 0.7$.Comment: 8 pages emulateapj style, 3 figures, accepted by AJ (March 2010

Cannabis use and anxiety : Is stress the missing piece of the puzzle?

Objective: Comorbidity between anxiety and cannabis use is common yet the nature of the association between these conditions is not clear. Four theories were assessed, and a fifth hypothesis tested to determine if the misattribution of stress symptomology plays a role in the association between state-anxiety and cannabis. Methods: Three-hundred-sixteen participants ranging in age from 18 to 71 years completed a short online questionnaire asking about their history of cannabis use and symptoms of stress and anxiety. Results: Past and current cannabis users reported higher incidence of lifetime anxiety than participants who had never used cannabis; however, these groups did not differ in state-anxiety, stress, or age of onset of anxiety. State-anxiety and stress were not associated with frequency of cannabis use, but reported use to self-medicate for anxiety was positively associated with all three. Path analyses indicated two different associations between anxiety and cannabis use, pre-existing and high state-anxiety was associated with (i) higher average levels of intoxication and, in turn, acute anxiety responses to cannabis use; (ii) frequency of cannabis use via the mediating effects of stress and self-medication. Conclusion: None of the theories was fully supported by the findings. However, as cannabis users reporting self-medication for anxiety were found to be self-medicating stress symptomology, there was some support for the stress-misattribution hypothesis. With reported self-medication for anxiety being the strongest predictor of frequency of use, it is suggested that researchers, clinicians, and cannabis users pay greater attention to the overlap between stress and anxiety symptomology and the possible misinterpretation of these related but distinct conditions. © 2014 Temple, Driver and Brown

Rapid enhancement of touch from non-informative vision of the hand

Processing in one sensory modality may modulate processing in another. Here we investigate how simply viewing the hand can influence the sense of touch. Previous studies showed that non-informative vision of the hand enhances tactile acuity, relative to viewing an object at the same location. However, it remains unclear whether this Visual Enhancement of Touch (VET) involves a phasic enhancement of tactile processing circuits triggered by the visual event of seeing the hand, or more prolonged, tonic neuroplastic changes, such as recruitment of additional cortical areas for tactile processing. We recorded somatosensory evoked potentials (SEPs) evoked by electrical stimulation of the right middle finger, both before and shortly after viewing either the right hand, or a neutral object presented via a mirror. Crucially, and unlike prior studies, our visual exposures were unpredictable and brief, in addition to being non-informative about touch. Viewing the hand, as opposed to viewing an object, enhanced tactile spatial discrimination measured using grating orientation judgements, and also the P50 SEP component, which has been linked to early somatosensory cortical processing. This was a trial-specific, phasic effect, occurring within a few seconds of each visual onset, rather than an accumulating, tonic effect. Thus, somatosensory cortical modulation can be triggered even by a brief, non-informative glimpse of one’s hand. Such rapid multisensory modulation reveals novel aspects of the specialised brain systems for functionally representing the body

The effect of isocapnic hyperoxia on neurophysiology as measured with MRI and MEG

The physiological effect of hyperoxia has been poorly characterised, with studies reporting conflicting results on the role of hyperoxia as a vasoconstrictor. It is not clear whether hyperoxia is the primary contributor to vasoconstriction or whether induced changes in CO2 that commonly accompany hyperoxia are a factor. As calibrated BOLD fMRI based on hyperoxia becomes more widely used, it is essential to understand the effects of oxygen on resting cerebral physiology. This study used a RespirActTM system to deliver a repeatable isocapnic hyperoxia stimulus to investigate the independent effect of O2 on cerebral physiology, removing any potential confounds related to altered CO2. T1-independent Phase Contrast MRI was used to demonstrate that isocapnic hyperoxia has no significant effect on carotid blood flow (normoxia 201 ± 11 ml/min, -0.3 ± 0.8 % change during hyperoxia, p = 0.8), whilst Look Locker ASL was used to demonstrate that there is no significant change in arterial cerebral blood volume (normoxia 1.3 ± 0.4 %, -0.5 ± 5 % change during hyperoxia). These are in contrast to significant changes in blood flow observed for hypercapnia (6.8 ± 1.5 %/mmHg CO2). In addition, magnetoencephalography provided a method to monitor the effect of isocapnic hyperoxia on neuronal oscillatory power. In response to hyperoxia, a significant focal decrease in oscillatory power was observed across the alpha, beta and low gamma bands in the occipital lobe, compared to a more global significant decrease on hypercapnia. This work suggests that isocapnic hyperoxia provides a more reliable stimulus than hypercapnia for calibrated BOLD, and that previous reports of vasoconstriction during hyperoxia probably reflect the effects of hyperoxia-induced changes in CO2. However, hyperoxia does induce changes in oscillatory power consistent with an increase in vigilance, but these changes are smaller than those observed under hypercapnia. The effect of this change in neural activity on calibrated BOLD using hyperoxia or combined hyperoxia and hypercapnia needs further investigation

Targeting triple-negative breast cancer cells with the histone deacetylase inhibitor panobinostat

INTRODUCTION: Of the more than one million global cases of breast cancer diagnosed each year, approximately fifteen percent are characterized as triple-negative, lacking the estrogen, progesterone, and Her2/neu receptors. Lack of effective therapies, younger age at onset, and early metastatic spread have contributed to the poor prognoses and outcomes associated with these malignancies. Here, we investigate the ability of the histone deacetylase inhibitor panobinostat (LBH589) to selectively target triple-negative breast cancer (TNBC) cell proliferation and survival in vitro and tumorigenesis in vivo. METHODS: TNBC cell lines MDA-MB-157, MDA-MB-231, MDA-MB-468, and BT-549 were treated with nanomolar (nM) quantities of panobinostat. Relevant histone acetylation was verified by flow cytometry and immunofluorescent imaging. Assays for trypan blue viability, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) proliferation, and DNA fragmentation were used to evaluate overall cellular toxicity. Changes in cell cycle progression were assessed with propidium iodide flow cytometry. Additionally, qPCR arrays were used to probe MDA-MB-231 cells for panobinostat-induced changes in cancer biomarkers and signaling pathways. Orthotopic MDA-MB-231 and BT-549 mouse xenograft models were used to assess the effects of panobinostat on tumorigenesis. Lastly, flow cytometry, ELISA, and immunohistochemical staining were applied to detect changes in cadherin-1, E-cadherin (CDH1) protein expression and the results paired with confocal microscopy in order to examine changes in cell morphology. RESULTS: Panobinostat treatment increased histone acetylation, decreased cell proliferation and survival, and blocked cell cycle progression at G2/M with a concurrent decrease in S phase in all TNBC cell lines. Treatment also resulted in apoptosis induction at 24 hours in all lines except the MDA-MB-468 cell line. MDA-MB-231 and BT-549 tumor formation was significantly inhibited by panobinostat (10 mg/kg/day) in mice. Additionally, panobinostat up-regulated CDH1 protein in vitro and in vivo and induced cell morphology changes in MDA-MB-231 cells consistent with reversal of the mesenchymal phenotype. CONCLUSIONS: This study revealed that panobinostat is overtly toxic to TNBC cells in vitro and decreases tumorigenesis in vivo. Additionally, treatment up-regulated anti-proliferative, tumor suppressor, and epithelial marker genes in MDA-MB-231 cells and initiated a partial reversal of the epithelial-to-mesenchymal transition. Our results demonstrate a potential therapeutic role of panobinostat in targeting aggressive triple-negative breast cancer cell types