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Nourisaeed, A. Clinical Psychology and Personality , 19 2 , Clinical Psychology and Personality , 19, 2, , Clinical Psychology and Personality , ; 19 2 : Toggle navigation. Introductoin: Acute myocardial infarction is one of the most common causes of admissions and referral in cardiovascular patients. In addition to physiological reasons, psychological factors play a key role in the onset and exacerbation of the disease. The purpose of this study was to evaluate the effectiveness of cognitive-behavioral therapy on perceived stress and coping skills in patients after myocardial infarction. Method: The present study was a clinical trial based on the experimental design pre-test, post-test with control, and follow-up group. The statistical population of the study was included 30 discharged patients with a diagnosis of myocardial infarction who referred to the Noor specialized Heart clinic in Rasht in The patients were divided into experimental 5 females and 10 males and control groups 8 females and 7 males with a simple random sampling method. Assessment tools included perceived stress and coping strategies questionnaires that were completed pre, post, and 3 months after the intervention. The experimental group was conducted to educate within eight 90min weekly sessions for two months. Data were analyzed using independent t-test, repeated measures analysis of variance, and Bonferroni test. Discussion and Conclusion: Cognitive-behavioral intervention is effective on perceived stress and coping skills in patients after myocardial infarction. European heart journal. Fourth Universal Definition of Myocardial Infarction Journal of the American College of Cardiology. Epidemiological features of risk factors occurrence and outcomes of myocardial infraction in patients admitted to hospitals in west azerbaijan province during the years and Urmia Medical Journal. Journal of Arak University of Medical Sciences. Lilly LS, Braunwald E. Braunwald's heart disease: a textbook of cardiovascular medicine: Elsevier Health Sciences; Coronary heart disease risk factors. Anxiety, depression, traumatic stress and quality of life in colorectal cancer after different treatments: a study with Portuguese patients and their partners. European Journal of Oncology Nursing. Coping style and stress hormone responses in genetically heterogeneous rats: comparison with the Roman rat strains. Behavioural brain research. Journal of advanced nursing. Stress profile, coping style, anxiety, depression, and gastric emptying as predictors of functional dyspepsia: a case-control study. Journal of psychosomatic research. Turning their pain to gain: Charismatic leader influence on follower stress appraisal and job performance. Academy of Management Journal. Relationships between coping strategies and burnout symptoms: A meta-analytic approach. Professional Psychology: Research and Practice. Effects of cognitive behavioural therapy for depression in heart failure patients: a systematic review and meta-analysis. Heart failure reviews. Internet-based cognitive behavioral therapy for symptoms of depression and anxiety among patients with a recent myocardial infarction: the U-CARE heart randomized controlled trial. Journal of medical Internet research. Sad and worried hearts: a psychological treatment for clinically significant depression, anxiety, and post-traumatic stress in patients with cardiac disease. Int J Clin Cardiol. A global measure of perceived stress. Journal of health and social behavior. Safaei M, Shokri O. Assessing stress in cancer patients: Factorial validity of the perceived stress scale in Iran. Lazarus RS, Folkman S. Stress, appraisal, and coping: Springer publishing company; Relationship between coping strategies and quality of life: Mediating role of cognitive emotion regulation skills. Scientific Journal Management System. Perceived stress in myocardial infarction: long-term mortality and health status outcomes. Relationship between stress and coping styles with coronary heart disease: Role of gender factor. Iranian Journal of Psychiatry and Clinical Psychology. Stress, anger, and hostility in coronary heart disease. A comparative study of stressful life events and stress coping strategies in coronary heart disease patients and non-patients. Avicenna Journal of Clinical Medicine. Psychosocial influences on the development and course of coronary heart disease: current status and implications for research and practice. Journal of consulting and clinical psychology. Self-efficacy for cocaine abstinence: Pretreatment correlates and relationship to outcomes. Addictive behaviors. Rajati F sG, sadeghi M. Comparison of three questionnaires on quality of life for heart Failure Patients in a cardic rehabilitation program. Journal of Health system. How to cite.
Unfamiliar names rendered phonetically or transliterated are enclosed in parentheses. Words or names preceded by a ques-.
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Tue, Oct 22, Remember me Create Account Reset Password. Full-Text: Views. Drug addiction is one of the main concerns of health care organizations. According to the literature, there are around Biological, social, environmental, and genetic factors can influence the vulnerability to addiction \[1, 2\]. Studies on families, twins, and adopted children have shown that the odds of inheriting drug abuse disorders is moderate to high 0. However, genetic or environmental factors alone do not increase the tendency to addiction \[4\]. In drug addiction, compulsive drug-seeking and drug-taking behavior persist despite serious negative consequences. Addictive substances induce adaptive changes in the central nervous system and lead to tolerance, physical dependence, sensitization, craving, and relapse \[5\]. Morphine is one of the opioids which is widely used as a painkiller and an addictive drug \[\]. Nicotine is the main ingredient of tobacco that causes addiction to smoke \[7, 8\]. Tobacco also is one of the leading causes of many diseases, mortality, and morbidity \[9, 10\]. Other opioids such as methadone and buprenorphine as an agonist of Mu-Opioid Receptor MOR are widely used for the treatment of dependence on other opioid drugs such as morphine \[8\]. Epigenetics refers to any change in the gene expression that does not alter the DNA sequence. DNA methylation and histone modification methylation, Acetylation, phosphorylation, ubiquitylation, and sumoylation are the most frequent epigenetic changes that regulate gene expression \[11, 12\]. Previous studies reported the involvement of DNA methylation and histone modifications in drug addiction \[\]. Based on the reports, cytosine methylation induces epigenetic changes and transcriptional regulation of the mammalian genome. There are approximately CpG islands in the human genome and in the rat genome \[18, 19\]. Generally, the DNA methylation in promoter sites is related to reduction of gene expression \[20, 21\]. Opioid receptors are G protein-linked receptors activated through the interaction of downstream signaling with heterotrimeric G-protein \[8\]. OPRM1 is a likely candidate gene for smoking and the main target in most drug therapies \[1, 23\]. Various studies have reported the higher level of DNA methylation in specific CpG sites in the Oprm1 promoter in addicted individuals to opioids compared to non-addicts \[13, 22, 24, 25\]. Hypermethylation of Oprm1 gene is followed by lower transcription of Oprm1 \[29, 30\]. Human studies on the OPRM1 gene of addicted people revealed more methylation rate of the promoter of this gene in the whole blood in addicted male compared with the control counterparts \[22\]. In Nielsen et al. Because addicted people usually use more than one drug, it is difficult to distinguish the exact effect of each drug on methylation in human, therefore this study was designed to evaluate the impact of four most commonly-used drugs nicotine, morphine, methadone, and buprenorphine on the methylation level of two CpG sites at the Oprm1 promoter in male Wistar rats separately. To the best of our knowledge, this is the first study to aim this critical goal. They were allowed to get habituated to the examiner and laboratory conditions hence were handled at least three days before the experiments. The studied animals were classified into 6 groups with 8 rats in each group: 1. The control intact group; 2. Their blood samples were taken from their venae cavae. Briefly, cells were lysed by optimized buffers and enzymes of this kit. Alcohol was added, and lysates loaded onto the QIAamp spin column. Wash buffers removed impurities, and pure, ready-to-use DNA was then eluted in water or low-salt buffer. The nucleotide sequence of the rat Oprm1 promoter region chr1: , Rat. It shows that the Oprm1 gene is located at position 1p11; the 18 CpG sites are located in position To apply the MSP method, DNA is treated with sodium bisulfite, in which process, all unmethylated cytosine is converted to uracil \[36, 37\]. During the sulfonation reaction, however, methylated cytosine cannot be converted \[38\]. Therefore, the differences created by the reaction between the methylated and unmethylated cytosine can be distinguished by MSP. In the MSP method, 2 sets of methylated and unmethylated cytosine-specific primers of targeted sequences are used, and the PCR reaction is separately carried out. The final product size of PCR was base pairs. Amplification was performed with 1. The place and status of PCR products in agarose gel were detected by staining with the fluorescent dye ethidium bromide under direct ultraviolet light. The results of electrophoresis in agarose gel were analyzed by observing the ultraviolet ray using gel documentation Figure 1. Figure 2 shows the results of the PCR process in which all samples have a positive response amplified by the unmethylated primer. The Chi-squared analysis is a suitable test for the investigation of frequency differences between studied groups. The frequency of unmethylated cases in groups was less than 4. Therefore, the data did not apply to this analysis. Table 2 presents the frequency of the methylation status of the groups. The results of the present study showed that nicotine, morphine, methadone, and buprenorphine in the doses used here led to the addiction of the male Wistar rats, demonstrating particular symptoms and behaviors, including ecstasy, solace, disquietude, seeking behaviors, standing, grooming, anxiety, and other abnormal signs such as constipation and diarrhea. These results are in agreement with the previous findings \[39\]. Surprisingly no change was observed in the methylation of Oprm1 gene promoter sites of blood lymphocytes. Our findings are contradictory to the previous studies carried out on the brain nucleus \[31\]. To the best of our knowledge, there is no study on methylation of Oprm1 gene promoter in lymphocytes of animals addicted to nicotine, morphine, methadone, or buprenorphine. However, human studies revealed the positive results of methylation of Oprm1 gene promoter in the blood sits 13, 22, 24, and In a recent study by Chorbov et al. They further reported a high level of DNA methylation only in 2 CpG sites in the DNA extracted from the sperm samples of the addicted individuals \[22\]. Then, the absence of methylation in our study could be accompanied with an inactive transcription of the gene \[40, 41\]. In addition, the study of DNA methylation on peripheral blood lymphocytes of heroin addicts under MMT of the Caucasian population showed that methylation is significantly associated with the two CpG sites 18 and 84 in the Oprm1 gene promoter \[13\]. These observations were later replicated by Nielsen et al. They reported that the level of DNA methylation in the Oprm1 gene promoter was higher in heroin addicts than in the control group in African-American and Hispanic populations. A comparison between these two populations revealed that the level of methylation in the Oprm1 gene promoter differs by geographical features \[24\]. Differences between human and animal studies might be related to the fact that addicted people often use a variety of drugs which can affect methylation rate cumulatively. The strong point of the present study relates to its capability to distinguish and specify the contribution of each drug to methylation. However, the limitation of our study was the evaluation of the methylation of other CpG regions or exons. Assessing all CpG sites in the promoter or exons might better explain the negative or positive epigenetic effect of nicotine, morphine, methadone, and buprenorphine. One possible explanation for negative results on methylation of the Oprm1 gene promoter in male Wistar rats following addiction drug usage might be the insufficiency of either the doses of drugs or duration of treatment. Also, these drugs might not have been capable of methylating Oprm1 gene promoter in rats and probably cannot be considered as epigenetic substances in this species. Thus, these animals may have an unknown protective mechanism against epigenetic changes to addiction. The current study shows that use of nicotine 0. The epigenetic mechanism is triggered by the environmental stimuli of the cells. Addiction is a multifactorial and polygenic condition; therefore, various factors and interactions must be considered in the study of epigenetics in addiction. For future studies, it is recommended to use a higher dose of drugs with different time courses to clarify the effect of addictive drugs on epigenetic changes. All study procedures complied with the ethical guidelines of the Declaration of Helsinki This research was part of the MSc. Design of the study: Parvaneh Keshavarz, Parvin Babaei; Collection of samples, and experimental procedure: Maedeh Mohammad Alizadeh; Interpretation of data, assembly, critical revision of the article for important intellectual content, and final approval of the study: Seyed Reza Kazemi Nezhad, Parvin Babaei, Parvaneh Keshavarz; Writing the article and its editing: Maedeh Mohammad Alizadeh, and Parvaneh Keshavarz. Opiate addiction and cocaine addiction: Underlying molecular neurobiology and genetics. J Clin Invest. Association of OPRD1 gene variants with opioid dependence in addicted male individuals undergoing methadone treatment in the north of Iran. J Psychoactive Drugs. Dick DM, Foroud T. Candidate genes for alcohol dependence: A review of genetic evidence from human studies. Alcohol Clin Exp Res. Exploring gene-environment interactions: Socioregional moderation of alcohol use. J Abnorm Psychol. Drug addiction. New Engl J of Med. Goodsell DS. The molecular perspective: Morphine. The oncologist. Pharmacogenetics of OPRM1. Pharmacol Biochem Behav. Graul AI, Prous J. Executive summary: Nicotine addiction. Drugs Today Barc. Society for research on nicotine and tobacco. Maze I, Nestler EJ. The epigenetic landscape of addiction. Ann N Y Acad Sci. Epigenetics of drug abuse: Predisposition or response. Maternal cocaine administration in mice alters DNA methylation and gene expression in hippocampal neurons of neonatal and prepubertal offspring. PlOS One. Mol Pharmacol. Feng J, Nestler EJ. Epigenetic mechanisms of drug addiction. Curr Opin Neurobiol. Jaenisch R, Bird A. Epigenetic regulation of gene expression: How the genome integrates intrinsic and environmental signals. Nat Genet. Gardiner-Garden M, Frommer M. CpG islands in vertebrate genomes. J Mol Biol. CpG island density and its correlations with genomic features in mammalian genomes. Genome Biol. DNA methylation and Sp1 binding determine the tissue-specific transcriptional activity of the mouse Abcc6 promoter. Biochem Biophys Res Commun. J Opioid Manag. Behav Brain Funct. Human Gene. J Hum Genet. Zhang N, Oppenheim JJ. Crosstalk between chemokines and neuronal receptors bridges immune and nervous systems. J leukoc biol. Bidlack JM. Detection and function of opioid receptors on cells from the immune system. Clin Diagn Lab Immunol. Expression of mu opioid receptor splice variants mRNA in human blood lymphocytes: A peripheral marker for opioid addiction studies. Int Immunopharmacol. Localization of promoter elements in the human mu-opioid receptor gene and regulation by DNA methylation. Mol brain res. J cell Mol Med. Litter gender composition and sex affect maternal behavior and DNA methylation levels of the oprm1 gene in rat offspring. Front Psychiatry. Eur J Neurosci. Effect of physical activity on symptoms of morphine addiction in rats, after and before of lesion of the mpfc area. Iran J Basic Med Sci. Flunitrazepam variably alters morphine, buprenorphine, and methadone lethality in the rat. Human and Exp Tox. Molecular, anatomical, physiological, and behavioral studies of rats treated with buprenorphine after spinal cord injury. J Neurotrauma. Oakeley EJ. DNA methylation analysis: a review of current methodologies. Pharmacol Ther. A genomic sequencing protocol that yields a positive display of 5-methylcytosine residues in individual DNA strands. Katzung BG. Basic and clinical pharmacology. Ehrlich M. Expression of various genes is controlled by DNA methylation during mammalian development. J Cell biochem. Doerfler W. On the biological significance of DNA methylation. Biochemistry Moscow. Add your comments about this article : Your username or Email:. Contact Information.
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