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During the initial stages of drug use, cocaine-induced neuroadaptations within the ventral tegmental area VTA are critical for drug-associated cue learning and drug reinforcement processes. These neuroadaptations occur, in part, from alterations to the transcriptome. Although cocaine-induced transcriptional mechanisms within the VTA have been examined, various regimens and paradigms have been employed to examine candidate target genes. In order to identify key genes and biological processes regulating cocaine-induced processes, we employed genome-wide RNA-sequencing to analyze transcriptional profiles within the VTA from male mice that underwent one of four commonly used paradigms: acute home cage injections of cocaine, chronic home cage injections of cocaine, cocaine-conditioning, or intravenous-self administration of cocaine. We found that cocaine alters distinct sets of VTA genes within each exposure paradigm. Using behavioral measures from cocaine self-administering mice, we also found several genes whose expression patterns corelate with cocaine intake. In addition to overall gene expression levels, we identified several predicted upstream regulators of cocaine-induced transcription shared across all paradigms. Although distinct gene sets were altered across cocaine exposure paradigms, we found, from Gene Ontology GO term analysis, that biological processes important for energy regulation and synaptic plasticity were affected across all cocaine paradigms. Coexpression analysis also identified gene networks that are altered by cocaine. These data indicate that cocaine alters networks enriched with glial cell markers of the VTA that are involved in gene regulation and synaptic processes. Our analyses demonstrate that transcriptional changes within the VTA depend on the route, dose and context of cocaine exposure, and highlight several biological processes affected by cocaine. Overall, these findings provide a unique resource of gene expression data for future studies examining novel cocaine gene targets that regulate drug-associated behaviors. Many UC-authored scholarly publications are freely available on this site because of the UC's open access policies. Let us know how this access is important for you. Skip to main content. Email Facebook. Cocaine induces paradigm-specific changes to the transcriptome within the ventral tegmental area. Abstract During the initial stages of drug use, cocaine-induced neuroadaptations within the ventral tegmental area VTA are critical for drug-associated cue learning and drug reinforcement processes. For improved accessibility of PDF content, download the file to your device. Thumbnails Document Outline Attachments. Highlight all Match case. Whole words. Toggle Sidebar. Zoom Out. More Information Less Information. Enter the password to open this PDF file:. Cancel OK. File name: -. File size: -. Title: -. Author: -. Subject: -. Keywords: -. Creation Date: -. Modification Date: -. Creator: -. PDF Producer: -. PDF Version: -. Page Count: -. Page Size: -. Fast Web View: -. Preparing document for printing….

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Konya where can I buy cocaine

Official websites use. Share sensitive information only on official, secure websites. Correspondence: Michele Mitaritonno, M. The term rhabdomyolysis describes a damage involving striated muscle cells or fibers, often complicated by acute kidney injury. This syndrome can have different causes, but it is generally divided into two main categories: traumatic and non-traumatic rhabdomyolysis. Among medical causes, drugs and abuse substances play a pivotal role, being opioids, alcohol, cocaine and other substances of abuse. Among drugs, the case of statins is certainly the best known. Here we describe a paradigmatic case of a man treated with success and good tolerance for years with rosuvastatin, who developed a severe rhabdomyolysis complicated by AKI needing hemodialysis, after the assumption of two substances of abuse cocaine and heroin. Emergency physicians need to be aware of this syndrome, since it must be clinically suspected in order to ask the Laboratory for appropriate tests. Keywords: rhabdomyolysis, cocaine, heroin, statin, acute kidney injury, creatine kinase. The term rhabdomyolysis describes the rapid breakdown of striated, or skeletal, muscle. As a consequence of the rupture and necrosis of muscle fibers, a release of cell products into the bloodstream and extracellular space takes place. The real incidence of rhabdomyolysis is unknown, mainly due to the fact that many mild i. Nevertheless, it has been reported that approximately Rhabdomyolysis occurs with a wide spectrum of signs and symptoms, ranging from a completely asymptomatic increase of plasma creatine kinase CK , through massive increases in blood levels of acute kidney injury AKI biomarkers, severe alterations of electrolyte balance and, in the most severe cases, disseminated intravascular coagulation DIC. This syndrome can have different causes, but it is generally divided into two main categories: traumatic and non-traumatic rhabdomyolysis 4. In trauma patients, it is important to distinguish among the terms rhabdomyolysis, crush injury, compartment syndrome and crush syndrome 3 , 5 - 7. Rhabdomyolysis describes a damage involving striated muscle cells or fibers; crush injury describes all those injuries that occur as a consequence of crushing of bodily parts usually a limb. Compartment syndrome describes the complications arising due to increased pressure inside one or more muscular compartments where rhabdomyolysis may, or may not, have occurred that can cause failure of regional circulation and onset of ischemic injury to nerves and muscles. Crush syndrome describes the complex pathophysiological consequences that may arise due to massive rhabdomyolysis involving kidneys and the coagulation system. Direct muscle injury remains the most common cause of severe rhabdomyolysis, although this syndrome includes a kaleidoscope of etiological categories, that are frequently overlapped: i hypoxic, ii physical, iii chemical, mainly represented by drugs or substances of abuse, iv biological 8. Among medical causes, drugs and abuse substances play a pivotal role, being opioids, alcohol, cocaine and other substances of abuse 9 the most frequently involved. Several cases of cocaine-induced rhabdomyolysis have been described in the past decades, and severity of muscle injury seemingly parallel the severity of cocaine intoxication. These patients may develop rhabdomyolysis in association with other causes, such as seizures, excessive muscle activity, hyperthermia, tissue hypoxia from limb compression following loss of consciousness, and hypovolemia 10 , Summarizing, these compounds directly trigger rhabdomyolysis, i. An increasing number of drugs is currently recognized as a possible, or even well established, cause of rhabdomyolysis, both as single therapy or in various associations. Among these, the case of statins is certainly the best known. The 3-hydroxymethylglutaryl coenzyme A reductase inhibitors i. Mechanisms of statin-induced muscle injury are not fully established and are probably multifactorial. Some studies described an association between some genetic polymorphisms and the risk of developing statin-induced rhabdomyolysis 13 - The clinical spectrum of statin-induced myopathy ranges from asymptomatic elevations of serum CK levels to muscle pain or weakness, up to rhabdomyolysis with muscle symptoms, elevated serum levels of CK and renal damage. Statin-associated rhabdomyolysis may be enhanced by use of fibrates 15 , 17 and may also be modulated by physical exercise Notably, cerivastatin was withdrawn from the market in , when its use was strongly associated with rhabdomyolysis, leading to 31 deaths, 12 of which involved the concomitant use of gemfibrozil. Although there is no established cut-off threshold, a concentration five to ten times the upper reference limit URL , i. CK levels increase in the first 12 h, peak on the second or third day and return to baseline days later. Recent evidence has emerged that peak values of myoglobin in serum or plasma could be better predictors of AKI than CK values 19 , Importantly, the traditional dipstick methods do not differentiate between hemoglobin, myoglobin or red blood cells. Hematuria is frequently detected in patients with rhabdomyolysis and it could be responsible of false positive results and leading to inappropriate therapeutic management. Here we describe a paradigmatic case of a man treated with success and good tolerance for years with rosuvastatin, who developed a severe rhabdomyolysis complicated by AKI after the assumption of two substances of abuse cocaine and heroin. A 45 years old man presented to our Emergency Department ED complaining for diffuse severe myalgia and weakness. No other significant findings on physical examination. There was no significant increase in troponin level. Clinical and laboratory features in rhabdomyolysis patient at baseline and after ED fluid infusion. He admitted to have abused in cocaine and heroin the day before ED admission. He also reported to be on rosuvastatin 10 mg daily since 3 years before due to familial hypercholesterolemia. No other significant features were found in his past medical history. Furthermore, 8. Due to severe renal failure, the patient was referred to the nephrologist, who decided to perform hemodialysis. The patient remained oliguric after first hemodialysis treatment, but parameters and clinical conditions improved, despite persistence of severe myalgia table 1. Serum CK markedly decreased, but remained significantly high. Ten days later, the patient was still under hemodialysis with renal function and urine output slowly improving table 1. The role of osmotic agents e. It should also be considered that sodium bicarbonate, targeting urine alkalinization around a pH of 6. Forced hydration should be continued until disappearance of myoglobinuria, which typically occurs in the third day. Hyperkalemia must be managed using the usual techniques, considering that treatment with glucose and insulin may be ineffective in this setting due to inability of damaged muscle tissues to catch potassium from the extracellular space, enhancing the importance of sodium bicarbonate infusion. It is often necessary to treat severe hyperkalemia with hemodialysis. This case is paradigmatic, displaying all the typical clinical features of non-traumatic rhabdomyolysis, thus demonstrating that even when a statin is well tolerated for years, an occasional interaction with other substances can trigger a dramatic cascade of events leading to severe rhabdomyolysis and AKI. Emergency physicians thus need to be aware of this syndrome, since it must be clinically suspected in order to ask the Laboratory for appropriate tests. Troponin concentrations, on the contrary, can be increased in case of severe rhabdomyolysis, possibly reflecting associated myocardial damage 22 , particularly when the syndrome is associated with cocaine abuse, due to the well-known detrimental cardiac effects of the substance Each author declares that he or she has no commercial associations e. As a library, NLM provides access to scientific literature. Acta Biomed. Find articles by Michele Mitaritonno. Find articles by Mariarosaria Lupo. Find articles by Ivana Greco. Find articles by Angela Mazza. Find articles by Gianfranco Cervellin. Received Sep 16; Accepted Sep 19; Issue date Open in a new tab. Similar articles. Add to Collections. Create a new collection. Add to an existing collection. Choose a collection Unable to load your collection due to an error Please try again. Add Cancel.

Konya where can I buy cocaine