ITunes is the world's easiest way to organize and add to your digital media collection. We are unable to find iTunes on your computer. To preview and buy music from Addicted to Bass Sub-Frequencies 2010 by Various Artists, download iTunes now.. Партнерская программа · Правила партнерской программы · Регистрация партнера · Личный кабинет партнера. звонок бесплатный. 8 800 250-07-08. Published online 2010 Oct 8. doi: 10.3390/ph3103101. encompassing the fields of addiction, endocrinology, immunology and neurology.. activator of the transient receptor potential, vanilloid sub-type, TRPV1 receptor [46,47]. elevated anandamide levels, as did drug-free schizophrenia patients.. 2007;28:83–92. ![]() Port of Call New Orleans Blu- ray (United Kingdom)Reviewed by Dr. Svet Atanasov, October 1. Winner of the Christopher D. Smithers Foundation Special Award at the Venice Film Festival, Werner Herzog's "Bad Lieutenant: Port of Call New Orleans" (2. Blu- ray courtesy of British distributors Lionsgate Films. The supplemental features on the disc include a making of featurette and a collection of interviews with director Werner Herzog, cinematographer Peter Zeitlinger, writer Billy Finkelstein, and actors Nicholas Cage, Eva Mendes, and Tom Bower. In English, with optional English SDH subtitles for the main feature. Region- B "locked". Though the title of Werner Herzog's latest film reminds about Abel Ferrara's 1. Bad Lieutenant, there are few similarities between the two films, if any at all. In Ferrara's film Harvey Keitel plays a cynical New York City cop whose life is slowly falling apart. He is an abusive father, drug addict, drunk, and sex addict whose heart and soul have literally been consumed by evil. Keitel's character realizes it, which is why he constantly punishes himself. In Herzog's film Nicolas Cage plays a bad cop with a good heart who lives among hopeless people who are slowly chipping away at his soul. The cop has also lost hope and started taking drugs. His girlfriend (Eva Mendez), a beautiful prostitute, is a drug addict as well. Herzog's film is set in New Orleans, a city with a rich history which has been devastated by Hurricane Katrina. This is a depressing place to live in - many businesses have left the area and homes have been abandoned. A few nightclubs have reopened but drug dealers have taken over the streets and started challenging each other. A family of Senegalese illegal immigrants is brutally murdered, and the cop is asked to solve the case. Before he even begins his investigation, however, he knows that drugs are to be blamed for the tragedy. There is a witness, an African- American kid (Denzel Whitaker) who has seen the killer, but he is afraid to talk. After a quick visit to the District Attorney's Office, the cop realizes that if he loses the kid the killer will never be brought to justice. Because he does not trust anyone, including his colleagues, he decides to take the kid with him - and loses him, while trying to help his girlfriend, who has been mistreated by a sadistic client. The cop then befriends one of the area's biggest drug dealers (Alvin 'Xzibit' Joiner), who may or may not have ordered the execution of the Senegalese family. The two are going to be partners - the cop will provide the drug dealer with valuable information and occasionally valuable product from the Police Department's evidence and property room, such as coke and heroine, while the drug dealer will help him solve some personal problems, such as outstanding debts and mafia goons looking to hurt the cop and have fun with his girlfriend. Even though the plot description suggests otherwise, Bad Lieutenant: Port of Call New Orleans is not a film about cops and drug dealers. In fact, the film's plot is very much irrelevant. What director Herzog has attempted to accomplish with Bad Lieutenant: Port of Call New Orleans is capture the pulse of a city which is trying to recover from an incredible catastrophe. Like the film's main protagonist, however, New Orleans is seriously hurt. Its residents are seen moving around, shopping, barbecuing, some even following their favorite football team again, but something does not feel right. Hurricane Katrina has changed everything, and the majority of the people who have returned to New Orleans have simply lost hope. Few of them are also clean - most either drink heavily or take drugs. Herzog has always been an incredibly difficult director to figure out, and Bad Lieutenant: Port of Call New Orleans certainly proves that he still sees what most people can't. Throughout the film his camera spends a great deal of time observing streets littered with garbage where dealers are selling whatever it is they have to sell, power brokers, corrupted cops, strangers who are on their way to take care of something. It isn't pretty, but this is life, which has reluctantly returned to New Orleans. Note: In 2. 00. 9, Bad Lieutenant: Port of Call New Orleans won the Christopher D. Smithers Foundation Special Award (Werner Herzog) at the Venice Film Festival. The film also received Toronto Film Critics Association Award for Best Actor (Nicolas Cage). There is only on audio track on this Blu- ray disc: English DTS- HD Master Audio 5. For the record, Lionsgate Films have provided optional English SDH subtitles for the main feature. The English DTS- HD Master Audio 5. Though not overly active the bass is potent, the rear channels intelligently used, and the high- frequencies not overdone. Generally speaking, there is a good range of dynamics that enhance the narrative rather well. The dialog is crisp, clean, stable, and easy to follow. There are no balance issues with Mark Isham's music score either. Lastly, while viewing the film I did not hear any annoying pops, cracks, hissings, or dropouts to report in this review. The English SDH subtitles, however, appear just a tad too big for my taste. Endocannabinoids and Schizophrenia. Abstract. The endocannabinoids anandamide and 2- arachydonoylglycerol (2- AG) are lipids naturally derived from membrane precursors which bind cannabinoid receptors (CB1, CB2). This endocannabinoid system is disturbed in schizophrenia. Indeed, there seems to be an association between schizophrenia and polymorphisms of the CB1 receptor gene. Moreover, CB1 receptors are found in higher density in the prefrontal cortex, hippocampus and basal ganglia of patients with schizophrenia. Similarly, anandamide levels are increased in the cerebrospinal fluid (CSF) and in the serum of schizophrenia patients, including during the prodromal state, suggesting that they may play a protective role in psychosis homeostasis. Future studies are needed to further explore the role of the endocannabinoid system in the pathophysiology of schizophrenia. Keywords: endocannabinoids, schizophrenia, cannabis, drug abuse, metabolism. Introduction. Schizophrenia is a complex psychiatric disorder with a lifetime prevalence of 0. Thus far, several etiological models have been proposed to explain the biological bases of the disorder, including neurodevelopmental, neurodegenerative or cortical- subcortical disconnection models. Admittedly, schizophrenia is associated with several comorbidities, encompassing the fields of addiction, endocrinology, immunology and neurology. It is of great interest to explain this aggregation of signs and symptoms from a neurobiological perspective. A disturbance of the cannabinoid system could contribute to the general understanding of the biological bases of schizophrenia and it may also be involved in its associated comorbidities. Here, we will review the literature about the endocannabinoid system, its biological roles and its interactions with neurotransmission systems, and we will subsequently evaluate its potential implication in the pathophysiology of schizophrenia and its associated comorbidities. Cannabis and Schizophrenia. Patients with schizophrenia are more prone to substance abuse than the general population [4]. Among them, 2. 5% have a lifetime prevalence of cannabis abuse/dependence, the most widely used illicit psychoactive substance [5]. Cannabis use disorder has a negative impact on response to antipsychotics, drug compliance and psychotic relapse. In regular users, cannabis induces euphoria, perceptual illusions, tachycardia, analgesia, memory and concentration alterations, and other cognitive deficits. Cannabinoid intoxication can provoke toxic psychoses or symptoms similar to the positive symptoms of schizophrenia and even the pathognomonic schneiderian psychotic symptoms (e. In a randomized, double- blind, placebo- controlled study, intra- venous Δ9- THC (the main psychoactive agent of cannabis) administered to human healthy controls produced positive (delusions and hallucinations) and negative symptoms (blunted affect and social withdrawal), as well as cognitive effects, suggesting that it can be used as a valid model of psychosis [6]. Similarly, inhaled Δ9- THC has been shown to impair verbal memory, selective and sustained attention in both healthy subjects and schizophrenia patients [7]. Chronically, cannabis seems to provoke an amotivational syndrome similar to the negative symptoms of schizophrenia [8]. Therefore, cannabis can be used as a psychosis model, because its effects are more representative of the full spectrum of schizophrenia symptoms than the amphetamine sensitization model. Importantly, the psychotomimetic effects Δ- 9- THC may not be solely mediated by dopamine- D2 receptor mechanisms in humans. Indeed, healthy subjects received haloperidol before receiving intra- venous Δ9- THC, but haloperidol pre- treatment failed to antagonize the psychotomimetic effects of Δ9- THC [9]. Further studies are therefore needed to better understand the link between cannabinoids and psychosis. Large longitudinal and cross- sectional studies have evidenced that cannabis smoking is a risk factor of psychosis [1. In addition, cannabis smoking can exacerbate psychosis in schizophrenia patients [1. Prospective studies revealed that cannabis consumption seems neither a sufficient nor a necessary cause for psychosis [1. Its influence appears more complex and it may interact with many other factors to produce psychosis. From a vulnerability- stress perspective, it has been shown that the risk of developing schizophrenia- spectrum disorders is more elevated in cannabis smokers carrying the Val- Val genotype of the catechol- O- methyltransferase (COMT) Val. Met gene polymorphism [1. COMT is an enzyme degrading catecholamines (dopamine and norepinephrine) in the frontal lobe, and the val- val genotype is associated with enhanced vulnerability for psychosis. Apart from these genetic influences, it seems that there is a dose- dependent relationship between the amount of cannabis used during adolescence and the subsequent risk of developing schizophrenia [1. Such findings have been viewed as evidence that cannabis would be an independent risk factor for the emergence of psychosis in individuals without a psychosis background [1. In this vein, it has been shown that a young age of commencement of substance abuse increases the risks of psychotic outcomes [1. Consistently with the neurodevelopmental model of schizophrenia, it is also possible that exogenous cannabis smoking influences the neurodevelopmental processes thought to lead to schizophrenia [1. These complex clinical, epidemiological and longitudinal relationships between schizophrenia and cannabis suggest that dysfunctions of the endogenous cannabinoid (ECB) system could be intrinsically involved in the pathophysiology of schizophrenia and some of its associated comorbidities. Endocannabinoid System. The term cannabinoid encompasses all substances structurally related to cannabis. The ECB system includes ECB ligands, which are substances synthesized from lipid precursors in the neuronal membrane, which are part of the ethanolamine family. There are two main ECBs, N- arachidonoyl ethanolamide (anandamide) and 2- arachidonoyglycerol (2- AG) and two main cannabinoid receptors, CB1 and CB2 [1. Receptors. The cannabinoid system includes two major receptors: CB1 and CB2. Cloned in 1. 99. 0 [1. CB1 receptors are the most abundant G protein- coupled receptors in the central nervous system (CNS). In fact, they have a density 1. ECBs have a high affinity for CB1 receptors, which are located in the pre- synaptic neurons. They are found mainly in the CNS in brain areas such as the globus pallidus, the hippocampus, the cerebral cortex, the hypothalamus, the cerebellum, the striatum, and the mesencephalic periaqueductal gray matter [1. Accordingly, ECBs are involved in brain functions such as pain, emotions, cognition and motivation [2. CB1 receptors are also found in the periphery in reproductive, metabolic, cardiovascular and gastro- intestinal systems. CB2 receptors were first identified on spleen macrophages [2. They are mostly located in the periphery, mainly in immune cells, and they can modulate immune cell migration and cytokine release in periphery and in the brain [2. They are notably highly expressed on B- cells and moderately found on monocytes and polymorphonuclear neutrophils, even though they are also found in the CNS on glial cells and brainstem and cerebellar neurons [2. The evolution of knowledge about cannabinoid receptors revealed that both of them control central and peripheral functions such as cellular functions, neuronal development, neurotransmission, inflammation, cardiovascular, respiratory, reproductive and hormonal functions, energy metabolism and antinociception [2. However, the exact role of neuronal CB2 receptors remains incompletely established. Ligands. Anandamide was the first discovered ECB [3. It is considered a full agonist of CB1 receptors [3. CB2 receptors [3. Anandamide has various roles in the CNS, including drug reward, memory and pain relief [1. AG is the second endogenous ligand of the cannabinoid system to be discovered [3. It seems to have a better intrinsic efficacy on CB receptors [3. Indeed, 2- AG is a CB1- selective agonist compared to anandamide, which is an agonist without CB receptor selectivity [2. As mentioned in the article, anandamide may affect neurophysiologic processes by interacting with other targets. In this perspective, 2- AG is increasingly considered the main ECB the recent literature. Elevation of anandamide by pharmacologic inhibition of its degradation enzyme, fatty acid amid hydrolase (FAAH), does not influence CB1 receptor activity [3. There is also an interaction between anandamide and 2- AG. In fact, anandamide inhibits 2- AG rather than competing with CB1 receptors [4. This finding raises the hypothesis that anandamide may affect neurophysiologic processes by interacting with other targets. More recently, new ECBs have been identified, namely: O- arachidonoylethanolamine (virodhamine), arachidonoyldopamine [4. Virodhamine is considered a partial agonist of CB1 receptors and has possibly agonist- antagonist effects on these receptors [4. As for palmithylethanolamide (PEA) and oleylethamolamide (OEA), these fatty acid ethanolamines involved in metabolism are considered endogenous ligands without bearing the cannabinoid denomination, because they have no effect on cannabinoid receptors (according to present knowledge) [4. Other Receptors. Among other ECB targets, there are surface non- cannabinoid receptors, ion channels receptors and nuclear receptors. Recently, GPR5. 5, a new orphan G protein- coupled receptor has been identified as a cannabinoid receptor [4. Moreover, it has also been discovered that anandamide is an endogenous activator of the transient receptor potential, vanilloid sub- type, TRPV1 receptor [4.
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