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This paper studies the dependence structure between the real estate and financial markets in the United States from roughly 1975 to 2010, including the stock, bond and foreign exchange markets. This analysis uses dynamic copulas, including the Gaussian, Gumbel and Clayton copula. The Gumbel and Clayton copulas are used to separately capture the tail dependence of data. The dependence between the property indices (HPI and NCREIF) and the three financial markets is analyzed using the parameters of the copula. The property indices are divided in two different ways: by different regions and by different types of real estate. Although we study the dependence between the real estate and the financial markets in the U.S., the main objective of this paper is to analyze the change in the dependence structure when financial disasters occur. This study indicates that the real estate and the stock markets were positively related during this time period, and this dependence drove extreme movement when financial crises occurred. This dependence differed depending on the type of financial crisis, such as the Internet bubble crisis or the financial crisis in 2008. The dependence between the real estate and bond markets was also positively related, and extreme movement also occurred during financial crises. As for the dependence between the real estate and foreign exchange markets, although the results shows that dependence decreased when financial crises occurred, this is because the value of U.S. dollars are opposite to those of the index, and the left tail dependence exists as previous result. When looking at different regions or types of property, the differences in dependence structure were not obvious, although they were positively related. Both right and left tail dependences existed for most regions and property types, although some regions or types showed either right or left tail dependences alone. Therefore, investors should focus on the relationship between different markets, not on the region or type of real estate.

Nicotine's rewarding effects are mediated through distinct subunits of nAChRs, encoded by different nicotinic cholinergic receptor (CHRN) genes and expressed in discrete regions in the brain. In the present study, we aimed to test the associations between rare variants at CHRN genes and nicotine dependence (ND), and alcohol dependence (AD). A total of 26,498 subjects with nine different neuropsychiatric disorders in 15 independent cohorts, which were genotyped on Illumina, Affymetrix, or PERLEGEN microarray platforms, were analyzed. Associations between rare variants (minor allele frequency (MAF) <0.05) at CHRN genes and nicotine dependence, and alcohol dependence were tested. The mRNA expression of all Chrn genes in whole mouse brain and 10 specific brain areas was investigated. All CHRN genes except the muscle-type CHRNB1, including eight genomic regions containing 11 neuronal CHRN genes and three genomic regions containing four muscle-type CHRN genes, were significantly associated with ND, and/or AD. All of these genes were expressed in the mouse brain. We conclude that CHRNs are associated with ND (mainly) and AD, supporting the hypothesis that the full catalog of ND/AD risk genes may contain most neuronal nAChRs-encoding genes.

Due to traumatic brain injury (TBI), numerous studies have focused on comprehensively determining the mechanical properties of the brain. This study examined the strain rate dependence of porcine brain under compression, and the microstructural damage was quantified using a confocal microscope and graphical user interface (GUI). The selected strain rates were 0.10 s-1, 0.025 s-1, and 0.00625 s-1 while the strain levels targeted for confocal imaging were 15%, 30%, and 40%. This study also characterized the stress-state dependence at a strain rate and strain level of 0.10 s-1 and 40%, respectively, under compression, tension, and shear. Strain rate dependency data exhibited viscoelastic behavior, and the analysis parameters correlated with increasing strain rate and strain level. Stress-state dependency data demonstrated distinct nonlinear behavior, and disparities were observed in the analysis parameters between different testing modes. Finite element procedures can implement this supplementary data for devising more realistic models.

The original publication is available at http://www.samj.org.za / Medical practitioners in South Africa are increasingly confronted with requests to treat patients with opioid use disorders. Many do not possess the required knowledge and skills to deal with these patients effectively. This overview of the medical treatment of opioid dependence was compiled by an elected working group of doctors working in the field of substance dependence. Recommendations are based on current best practice derived from scientific evidence and consensus of the working group, but should never replace individual clinical judgement. / Publishers' version

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Tobacco dependence dramatically increases health burdens and financial costs. Limitations of current smoking cessation therapies indicate the need for improved molecular targets. Nicotine, the main addictive component of tobacco, exerts its dependency effects via nicotinic acetylcholine receptors (nAChRs). The homomeric α7 nAChR is one of the most abundant receptors found in the brain and has unique features in comparison to other nAChR subtypes such as high calcium permeability, low probability of channel opening, and a rapid desensitization rate. α7 nAChR agonists reduce nicotine's rewarding properties in the conditioned place preference (CPP) test and i.v. self-administration. Recently, the peroxisome proliferator-activated receptor type-α (PPARα) has been implicated as a downstream signaling target of the α7 nAChR in ventral tegmental area dopamine cells. It is unknown whether the intrinsic characteristics of the α7 nAChR and PPARα are involved in its attenuation of nicotine reward. Therefore, this dissertation sought to investigate the role of α7 nAChRs in a mouse model of nicotine CPP and nicotine withdrawal by 1) investigating the impact of pharmacological modulation of α7 nAChR function in nicotine dependence and 2) evaluating a possible role for PPARα as a downstream mediator of α7 nAChRs in nicotine dependence. Positive allosteric modulators (PAMs) and a silent agonist were used to investigate the role of α7 nAChR conformations. The utilization of the α7 nAChR Type I PAM NS1738, Type II PAM PNU120596, and silent agonist NS6740 provided insight about the probability of channel opening (NS1738, PNU120596), desensitization (PNU120596, NS6740), and modulation of the endogenous acetylcholine/ choline tone (NS1738, PNU120596) as it relates to the α7 nAChR in nicotine CPP and withdrawal. In addition, this dissertation sought to elucidate the role of the α7 nAChR and PPARα in nicotine dependence using pharmacological interventions. The results suggest that the role of the α7 nAChR in nicotine dependence is conformation-dependent and PPARα-mediated. This dissertation is the first to report PPARα-mediation of the effects of α7 nAChR in nicotine reward and attenuation of nicotine withdrawal signs by PPARα activation. This data supports the development of α7 nAChR agonists and PPARα activators as possible smoking cessation aids.