Discussion: Media v Peer Reviewed Research Comparison

Discussion: Media v Peer Reviewed Research Comparison ORDER NOW FOR CUSTOMIZED AND ORIGINAL ESSAY PAPERS ON Discussion: Media v Peer Reviewed Research Comparison I have chosen the two articles necessary to complete this assignment. one is a peerreviewed article (uploading it as a pdf) and the other is a CBS news media article: https://www.cbsnews.com/news/smoking-marijuana-whi… Discussion: Media v Peer Reviewed Research Comparison Summarize the popular-press article and support or discredit the popular media article with the peer- reviewed research article . Give evidence that will contradict or support the popular- press author’s claims. Include how the average parent could be influenced by the article. As a student of developmental psychology, would you recommend the article to a parent? please follow rubric for guidelines no plagiarism, no quotes •Your essay should be in APA format, with all sources correctly cited. oYour paper should include an APA-style title page oYour paper should include a reference page, listing your popular-press and peer-reviewed articles oYou do not need a abstract for this assignment the following questions need not all be addressed in your paper, but may help give your essay direction: •What is the author’s theoretical orientation? •Has the author evaluated the literature relevant to the issue? •Does the author include literature taking positions she or he does not agree with? •Does the author use appeals to emotion, one-sided examples, or rhetorically charged language and tone? •Is there an objective bias to the reasoning, or is the author merely “proving” what he or she already believes? •How does the author structure the argument? Can you “deconstruct” the flow of the argument to see whether or where it breaks down logically (e.g., in establishing cause-effect relationships)? •In what ways does the article contribute to our understanding and in what ways is it useful for practice? •What are the article’s strengths and limitations? Discussion: Media v Peer Reviewed Research Comparison paper_instructions.pdf peer_reviewed_article.pdf sourcecomparisonrubric.pdf Sources Comparison Paper Media vs. Peer-Reviewed Research Parents and caregivers are constantly bombarded with conflicting information from the media. For this assignment your job as a student of developmental psychology is to help them assess the accuracy of a particular media article. You will need to find an article that would be readily available to parents via popular media (internet, newspaper, magazine, or parenting book) and support or discredit the information with peerreviewed research. Give evidence that will contradict or support the popular- press author’s claims. Include how the average parent could be influenced by the article. As a student of developmental psychology, would you recommend the article to a parent? • Your popular media article should be geared towards parents and needs to address a development covered in class. Popular press sources include but are not limited to magazines, newspapers, etc. Further examples of articles are posted on Pinterest under various boards (http://pinterest.com/ DrKAtchison/). Students are encouraged to find their own article, but these may be used as well. • Summarize the popular-press article oAttach a copy of the article to your essay. • No quotes, unless previously approved by your instructor • Your essay should be in APA format, with all sources correctly cited. oYour paper should include an APA-style title page oYour paper should include a reference page, listing your popularpress and peer-reviewed articles oYou do not need a abstract for this assignment • Use at least 1 peer-reviewed resources to support or discredit the popular-press article. You may need more than 1 article to address the issues discussed in your popular-press article • You paper should be turned in to the iCollege dropbox in PDF form. I will not grade papers that aren’t the proper file type. The iCollege submission will also act as a plagiarism check. You will see the same report I see, so plan to submit it to iCollege early enough to make changes if needed, and then resubmit. (Please see schedule in syllabus for due date) • Proof of completely the plagiarism quiz must be submitted prior to grading the paper. I will not grade papers that are not accompanied by a plagiarism quiz. • A grading rubric will also be posted on iCollege and is attached. • You will turn in your articles ahead of time to make sure they are appropriate for the assignment. (Please see schedule in syllabus for due date) • Think Critically!! The following questions need not all be addressed in your paper, but may help give your essay direction. • What is the author’s theoretical orientation? • Has the author evaluated the literature relevant to the issue? K.K. Atchison Revised: September 9, 2019 • Does the author include literature taking positions she or he does not agree with? • Discussion: Media v Peer Reviewed Research Comparison Does the author use appeals to emotion, one-sided examples, or rhetorically charged language and tone? • Is there an objective bias to the reasoning, or is the author merely “proving” what he or she already believes? • How does the author structure the argument? Can you “deconstruct” the flow of the argument to see whether or where it breaks down logically (e.g., in establishing cause-effect relationships)? • In what ways does the article contribute to our understanding and in what ways is it useful for practice? • What are the article’s strengths and limitations? The questions above have been adapted from http://www.utoronto.ca/writing/litrev.html Note: Peer-reviewed articles can be located by searching the GSU library database. Examples of appropriate journals include Child Development, Infancy, Infant Behavior and Development, Developmental Science, Developmental Psychology, Journal of Experimental Child Psychology, and other similar journals. If you have a question about the appropriateness of a source, feel free to ask! For information on APA-style and references please visit: • APA style website: http://www.apastyle.org/ • Tips: http://www.apastyle.org/previoustips.html • FAQ’s: http://www.apastyle.org/faqs.html • Reference Examples: http://www.apastyle.org/faqs.html#8 • Additional APA help: https://owl.english.purdue.edu/owl/resource/560/01/ K.K. Atchison Revised: September 9, 2019 Neuropharmacology 149 (2019) 181–194 Contents lists available at ScienceDirect Neuropharmacology journal homepage: www.elsevier.com/locate/neuropharm Prenatal cannabinoid exposure and altered neurotransmission a a a Priyanka D. Pinky , Jenna Bloemer , Warren D. Smith , Timothy Moore Vishnu Suppiramaniama,b,??, Miranda N. Reeda,b,? a b c a,b c , Hao Hong , T Department of Drug Discovery and Development, Auburn University, Auburn, AL, USA Center for Neuroscience Initiative, Auburn University, Auburn, AL, USA Department of Pharmacology, China Pharmaceutical University, Nanjing, China HIGHLIGHTS cannabinoid use during pregnancy and its impact on fetal health is a major issue of concern. • Increased cannabinoid exposure has shown to modulate several neurotransmitter systems. • Prenatal cannabinoid exposure has shown to adversely affect several behavioral outcomes in preclinical studies. • Prenatal observed behavioral effects have often seemed to be sex dependent affecting the male population more. • The • Future studies should be focused on investigating the downstream signaling mechanism for the altered neurotransmissions. ARTICLE INFO ABSTRACT Keywords: Prenatal Cannabinoid Marijuana Neurotransmitter Developmental Endocannabinoid Marijuana is one of the most commonly used illicit drugs worldwide. In addition, use of synthetic cannabinoids is increasing, especially among adolescents and young adults. Although human studies have shown that the use of marijuana during pregnancy leads to adverse behavioral effects, such as deficiencies in attention and executive function in affected offspring, the rate of marijuana use among pregnant women is steadily increasing. Various aspects of human behavior including emotion, learning, and memory are dependent on complex interactions between multiple neurotransmitter systems that are especially vulnerable to alterations during the developmental period. Discussion: Media v Peer Reviewed Research Comparison Thus, exploration of neurotransmitter changes in response to prenatal cannabinoid exposure is crucial to develop an understanding of how homeostatic imbalance and various long-term neurobehavioral deficits manifest following the abuse of marijuana or other synthetic cannabinoids during pregnancy. Current literature confirms that vast alterations to neurotransmitter systems are present following prenatal cannabinoid exposure, and many of these alterations within the brain are region specific, time-dependent, and sexually dimorphic. In this review, we aim to provide a summary of observed changes to various neurotransmitter systems following cannabinoid exposure during pregnancy and to draw possible correlations to reported behavioral alterations in affected offspring. 1. Introduction Marijuana is the most commonly abused illicit drug by women (Azofeifa et al., 2016b; Fantasia, 2017; Metz and Stickrath, 2015), and marijuana use is associated with higher rates of cigarette smoking, alcohol intake, and use of other illicit drugs (Grant et al., 2018; Gunn et al., 2016; Noland et al., 2003; Schauer and Peters, 2018; SecadesVilla et al., 2015). The negative consequences of prenatal exposure to drugs, including nicotine and ethanol, have been extensively reported (Cross et al., 2017; Healy et al., 2016; Holbrook, 2016; Martin et al., 2016; Pennell, 2018). However, the rate of marijuana use by young, pregnant women has been steadily increasing in recent years (YoungWolff et al., 2017). While it is unclear why usage would increase despite the known ill-effects of fetal drug exposure, studies show 1 in 25 women report marijuana use during pregnancy and that 70% of pregnant women are of the opinion that there is little to no risk of harm ? Corresponding author. Department: Drug Discovery and Development, Auburn University, Harrison School of Pharmacy, 153 Pharmacy Research Building, 720 S. Donahue Drive, Auburn, AL, 36849, USA. ?? Corresponding author. Department: Drug Discovery and Development, Auburn University, Harrison School of Pharmacy, 151 Pharmacy Research Building, 720 S. Donahue Drive, Auburn, AL, 36849, USA. E-mail addresses: [email protected] (V. Suppiramaniam), [email protected] (M.N. Reed). https://doi.org/10.1016/j.neuropharm.2019.02.018 Received 28 September 2018; Received in revised form 18 January 2019; Accepted 12 February 2019 Available online 13 February 2019 0028-3908/ © 2019 Elsevier Ltd. All rights reserved. Neuropharmacology 149 (2019) 181–194 P.D. Pinky, et al. associated with once or twice weekly marijuana use (Ko et al., 2015). This disconnect between the known untoward, long-term effects of marijuana use and the opinions of those likely to use it during pregnancy may be due to factors such as decreased social stigmatization coupled to increased availability of marijuana in the marketplace, increased prescribing of medical marijuana by physicians, self-medication during pregnancy due to gestational-induced nausea and vomiting, and overall decriminalization of marijuana use in many states (Azofeifa et al., 2016a, 2016b; Grant et al., 2018). Furthermore, those who smoke marijuana during pregnancy are also more likely to be of lower socioeconomic status, have a lower level of education, and not seek out appropriate prenatal care (El-Mohandes et al., 2003; Ko et al., 2015). Advising women to abstain from psychoactive drug use during pregnancy is the standard of care and should be considered best practice for prevention of negative pregnancy outcomes and reduction of post-natal complications and disease development in the offspring.Discussion: Media v Peer Reviewed Research Comparison Furthermore, cannabis use by the mother can impair the mother’s attention and judgement while taking care of the baby, leading to unsafe conditions (Jansson et al., 2018). To date, clinical literature on the topic is dominated by data from two large longitudinal studies of prenatal cannabinoid exposure in humans, the Ottawa Prenatal Prospective Study (OPPS) and the Maternal Health Practices and Child Development Project (MHPCDP) (Campolongo et al., 2009; Fried, 2002b; Fried et al., 1998; Fried and Watkinson, 1990; Goldschmidt et al., 2012; Trezza et al., 2008). Additionally, recently published results from another large longitudinal study conducted in the Netherlands add more current insights to this body of literature from a different population (El Marroun et al., 2018). While attributing the findings of these studies specifically to prenatal marijuana exposure is complicated by concomitant cigarette and alcohol use, they nonetheless provide valuable insight on neurodevelopmental and behavioral disorders commonly observed in offspring of mothers who used marijuana during pregnancy. Findings from these studies indicate that prenatal cannabinoid exposure results in detectable neurobehavioral changes and executive functioning deficits in offspring that persist into later stages of brain development during childhood and adolescence. Additionally, affected offspring show variable, age-dependent deficits in attentiveness and cognition, as well as higher rates of hyperactivity and use of marijuana themselves during adolescence (Day et al., 2006; Goldschmidt et al., 2012). Although neurobehavioral effects of prenatal cannabinoid exposure has been noted, it is not clear whether prenatal exposure can also result in teratogenicity (Orsolini et al., 2017). Hence, there remains a dire need for further exploration of the neurobiological mechanisms underlying behavioral and cognitive deficits caused by cannabinoid exposure during fetal development. In this review, we provide a summary of literature reporting changes to various neurotransmitter systems following cannabinoid exposure during pregnancy and draw possible correlations as to how gestational alterations in neuroplasticity manifest as behavioral dysfunction in affected offspring. A comprehensive understanding of neurotransmitter changes in response to prenatal cannabinoid exposure also includes recognizing many of these alterations within the brain are region specific, time-dependent, and sexually dimorphic. clinical rodent and primate species (Asch and Smith, 1986; Bailey et al., 1987; Freudenthal et al., 1972; Vardaris et al., 1976). Also, THC is only one of over one-hundred chemical compounds found within cultivated cannabis plants, which complicates the isolation of effects attributable to a single component (Wilkinson et al., 2016). Combining aforementioned medical, legal, and psychosocial factors, a steady increase in THC content of cannabis family plants, and a reasonable assumption of human placental pharmacokinetics, it is safe to say that the risk of prenatal cannabinoid exposure is growing through a combination of complex biologic and sociologic elements. The endocannabinoid system, described in more detail below, remains the pharmacologic target for THC in both maternal and fetal nervous systems. However, due to variability in the function of this system in the mature versus developing brain, long-term implications of cannabinoid exposure to the fetus are presumably more impactful than long-term effects on the mother. Much of what is known regarding human-specific effects of prenatal cannabinoid exposure is limited to ex vivo studies comparing brain tissue from aborted fetuses with and without in utero cannabis exposure (Morris et al., 2011). Interestingly, the investigation of these samples elucidates an association between marijuana use in pregnancy and a quantifiable change in fetal neuronal physiology. Discussion: Media v Peer Reviewed Research Comparison For example, expression of dopamine receptor 2 (D2) mRNA in the amygdala and mesolimbic nucleus accumbens, but not the dorsal striatum, is inversely correlated with maternal marijuana use. This change is not attenuated after adjustment for simultaneous alcohol and nicotine exposure. Although it has been suggested that this change could be explained by a genetic predisposition for marijuana use in the mother, this finding has been replicated in a more controlled setting using prenatally exposed rat models (DiNieri et al., 2011; Wang et al., 2004). The clinical significance of these findings is multifactorial. Alterations in D2 expression are linked to increased substance abuse and addiction potential in humans, and this effect is strongly correlated with changes in dopaminergic signaling within the striatum (Gorwood et al., 2012; Jones and Comer, n.d.; Kenny et al., 2013; Trifilieff and Martinez, 2014). Additionally, genetic alterations in the D2 receptor and abnormalities in dopaminergic signaling are established risk factors for neurobehavioral pathologies such as attention deficit hyperactive disorder, tendencies toward antisocial behavior, pathological gambling, and sex addiction (Farré et al., 2015; Gold et al., 2014; Yau and Potenza, 2015). Prenatal alcohol and nicotine exposure also affect D2 receptor expression in the striatum, where the effects of marijuana use may be simultaneously masked and exacerbated by co-administration of these substances (Nutt et al., 2015). However, since exposure to nicotine and alcohol were controlled for within the various groups of fetal brain samples, it appears that marijuana exposure independently alters dopaminergic receptors in certain brain areas. Thus, the behavioral phenotypes observed in the OPPS and MHPCDP studies, which also controlled for co-utilization of nicotine and alcohol, may be in part due to alterations in dopaminergic neurotransmission (DiNieri et al., 2011; Wang et al., 2004). However, it is important to note that effects on the amygdala were significant only in male subjects, which is consistent with other trends of sexual dimorphism observed in various human and animal neurotransmitter systems and pathologies (Carroll and Smethells, 2015; Jutras-Aswad et al., 2009; Sanchis-Segura and Becker, 2016). For this reason, we try to consistently stress the sexual differences of experimental groups in our later summary of animal literature. Additionally, expression of dopamine receptor 1 (D1) in the striatum, a receptor strongly implicated in motor function, reward, and cognition (Nishi et al., 2011), remained unaltered in the tissue samples used for these studies. Regardless, it is anticipated that early-life, region-dependent modification of dopaminergic signaling will have longstanding impacts on these and other areas of the brain. Prenatal cannabinoid exposure has not only been linked to alterations in dopaminergic neurophysiology, but also to effects on the endogenous opioid system in human fetuses. Exposure results in increased 2. Human pharmacology and pathophysiology Delta-9-tetrahydrocannabinol (THC) is the primary psychoactive substance associated with marijuana abuse (Wilkinson et al., 2016), and this molecule has regularly served as a basis for the development of synthetic cannabinoids used in both clinical and recreational settings. Additionally, selective breeding and cultivation have led to a four-fold increase in the average THC content of confiscated cannabis-family specimens over the past twenty-five years (ElSohly et al., 2000, 2016; Potter et al., 2008). Though information regarding human placental penetration of THC is relatively scarce (Marchetti et al., 2017), this lipophilic psychoactive compound readily crosses the placenta in pre182 Neuropharmacology 149 (2019) 181–194 P.D. Pinky, et al. expression of mu opioid receptors in the amygdala and decreased expression of kappa opioid receptors in portions of the thalamus (Wang et al., 2006).Discussion: Media v Peer Reviewed Research Comparison In terms of the impact of opioid and dopaminergic systems on the propensity for substance abuse, habit formation, and addiction, the involvement of both systems indicates a significant risk additive to the more immediate neurobehavioral changes observed throughout human development. Because changes to these two systems could potentially increase an offspring’s risk for future drug abuse, the implications of prenatal cannabinoid exposure may introduce a generational effect where the offspring of mothers who smoke marijuana during pregnancy are more likely to expose themselves and their offspring to marijuana and other drugs of abuse during gestation. This is at least partially supported by the observation that prenatally exposed adolescents begin using marijuana earlier in life and with a higher frequency than their non-exposed counterparts (Day et al., 2006). There have been few studies in prenatally exposed human fetal brains to elucidate changes to other neurotransmitter systems. Although alterations in learning and memory are exhibited by offspring prenatally exposed to cannabinoids, the glutamatergic system has not been studied in human fetal brains to our knowledge. In addition, human studies assessing alterations in GABAergic, serotonergic, or cholinergic signaling following prenatal cannabinoid exposure have not been performed extensively, if at all. Although human-specific information is lacking, animal studies implicate alterations in these neurotransmitter systems following prenatal exposure, which will be the focus of the remainder of this review. 2001; Hillard et al., 1997). Both of the endocannabinoids are degraded via enzymatic hydrolysis (Bouaboula et al., 1995), and the enzymes responsible for endocannabinoid degradation are monoacylglycerol lipase (MAGL) and fatty acid amide hydrolase (FAAH), which hydrolyze 2-AG and AEA, respectively (Castillo et al., 2012). 3.2. Cannabinoid receptors Endocannabinoid signaling is involved in numerous physiologic processes including modulation of synaptic function in the central nervous system, analgesia, vasoregulation, thermoregulation, inflammation, and peripheral lipid and glucose h … Get a 10 % discount on an order above $ 100 Use the following coupon code : NURSING10

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