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User:Seppi333

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I'm a statistician with an academic background in mathematics, statistics, finance, and economics. I have a general interest in and deep knowledge of molecular neuropharmacology as well, particularly in relation to monoamine neurotransmission (e.g., signal transduction in monoamine neurons, neural pathways and systems, and the pharmacodynamics, pharmacokinetics, and pharmacogenomics of various monoaminergic drugs) and a handful of central nervous system disorders.
My primary goal as an editor is to improve the accuracy and overall quality of health information on Wikipedia. I typically only edit articles on topics related to neuroanatomy/neuroscience, pharmacology, molecular biology, medicine, psychology, statistics, or econometrics. I also spend a fair amount of time wikignoming and continually donate my 2¢ to WT:MED because I'm very generous with my pocket change. Face-smile.svg

Seppi333
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Unit roots

Four possible cases of stationarity and nonstationarity (with an I(1) unit root) for regressors and the error term (yt=α+βxtt). The time-series behavior of y is governed by the behavior of x and μ:

Table 4.2: Regression methods with nonstationary variables
Regressor Error Dependent variable Proper estimation method
X is I(0) μ is I(0) y will be I(0) Estimate with standard distributed-lag model.
X is I(0) μ is I(1) y will be I(1) Misspecified model. Cannot explain a nonstationary dependent variable with stationary regressors.
X is I(1) μ is I(1) y will be I(1) First-difference model to make all variables stationary, then use standard distributed-lag models
X is I(1) μ is I(0) y will be I(1) Variables x and y are cointegrated. Use error-correction model

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{{WPNEURO   |  class =  | importance =  }}
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{{Chemicals |  class =  | importance =  }}
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{{Reliable sources for medical articles}}

Molecular neuropharmacology textbook[edit]

Graduate level, 2nd edition (2009)[1]

<ref name="NHM-#">{{cite book | vauthors = Malenka RC, Nestler EJ, Hyman SE | title = Molecular Neuropharmacology: A Foundation for Clinical Neuroscience | year = 2009 | publisher = McGraw-Hill Medical | location = New York | isbn = 9780071481274 | pages = XX–YY | edition = 2nd | chapter = Chapter #:XYZ | quote= }}</ref>

Graduate level, 3rd edition (2015)[2]

<ref name="NHMH_3e-#">{{cite book | vauthors = Malenka RC, Nestler EJ, Hyman SE, Holtzman DM | title = Molecular Neuropharmacology: A Foundation for Clinical Neuroscience | year = 2015 | publisher = McGraw-Hill Medical | location = New York | isbn = 9780071827706 | edition = 3rd | chapter = Chapter #:XYZ | quote= }}</ref>

Econometrics textbooks[edit]

Undergraduate and master's level[3]

<ref name="Wooldridge Econometrics – X">{{cite book | author=Wooldridge, Jeffrey | title=Introductory Econometrics: A Modern Approach | date=2012 | publisher=South-Western Cengage Learning | isbn=9781111531041 | pages=XX–YY | edition=5th | chapter=Chapter #: XYZ }}</ref>

Graduate level[4]

<ref name="Greene Econometrics – X">{{cite book | author=Greene, William | title=Econometric Analysis | date=2012 | publisher=Pearson Education | isbn=9780273753568 | pages=XX–YY | edition=7th | chapter=Chapter #: XYZ}}</ref>

References

  1. ^ Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter #:XYZ". Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. pp. XX–YY. ISBN 9780071481274. 
  2. ^ Malenka RC, Nestler EJ, Hyman SE, Holtzman DM (2015). "Chapter #:XYZ". Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (3rd ed.). New York: McGraw-Hill Medical. ISBN 9780071827706. 
  3. ^ Wooldridge, Jeffrey (2012). "Chapter #: XYZ". Introductory Econometrics: A Modern Approach (5th ed.). South-Western Cengage Learning. pp. XX–YY. ISBN 9781111531041. 
  4. ^ Greene, William (2012). "Chapter #: XYZ". Econometric Analysis (7th ed.). Pearson Education. pp. XX–YY. ISBN 9780273753568. 

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reflist

References

  1. ^ De Luca LA, Menani JV, Johnson AK (2014). Neurobiology of Body Fluid Homeostasis: Transduction and Integration. Boca Raton: CRC Press/Taylor & Francis. ISBN 9781466506930. Retrieved 23 July 2016. 
  2. ^ Kennedy DO (January 2016). "B Vitamins and the Brain: Mechanisms, Dose and Efficacy-A Review". Nutrients. 8 (2). doi:10.3390/nu8020068. PMC 4772032Freely accessible. PMID 26828517. Furthermore, evidence from human research clearly shows both that a significant proportion of the populations of developed countries suffer from deficiencies or insufficiencies in one or more of this group of vitamins, and that, in the absence of an optimal diet, administration of the entire B-vitamin group, rather than a small sub-set, at doses greatly in excess of the current governmental recommendations, would be a rational approach for preserving brain health. ...
    RDAs are population statistics and they therefore represent rough estimates of the average requirement of individuals within a group/population, with an adjustment for the variations in the need for the nutrient among the individuals that make up the population. However, for most micronutrients some of the information that would be required to accurately calculate the daily requirement is either unknown or incomplete, and the recommendations are therefore made on the basis of a number of assumptions and considerations that could lead to large variations in the eventual RDA [81,82]. These figures have also changed little in the last four decades, despite emerging evidence of striking individual differences in the absorption and excretion of vitamins as a consequence of a wide range of factors, including specific genetic polymorphisms, gender, ethnicity, endocrine dysfunction, thyroid function, the habitual co-consumption of medicines, drugs, alcohol and other dietary factors, obesity, overall energy consumption, vigorous exercise, and age [9,21,45,83,84,85,86]. These gaps in our knowledge question the very existence of a “normal” population [87], and suggest that RDAs are, to some extent, arbitrary figures.
    Government figures also show that sizeable minorities of the populations of developed countries fail to consume even the minimum recommended quantity of any given micronutrient. As an example, Troesch et al. [88] presented data showing that a sizeable proportion of the populations of the US and several European countries consume less than the RDA for each of the five B vitamins that they assessed. They note that “a gap exists between vitamin intakes and requirements for a significant proportion of the population”. As a result, studies assessing the blood levels of vitamins show that small but significant proportions of the populations of developed countries have biochemical levels of each of the B vitamins that may well predispose them to deficiency related diseases. ... For instance, recent US government data [91] demonstrated that 10.5% of the entire US population were biochemically deficient in vitamin B6. A subsequent independent analysis that excluded the substantial minority taking supplements containing vitamin B6 demonstrated much higher deficiency rates of between 23% and 27% for adults, depending on age [16].
     
  3. ^ Bragg DA, Walling A (2015). "Metabolic Syndrome: Hyperlipidemia". FP Essent. 435: 17–23. PMID 26280341. When metabolic syndrome includes lipid abnormalities, management goals are weight loss and cardiovascular risk management through lifestyle modifications (eg, diet, exercise), and, when appropriate, lowering of lipid levels with pharmacotherapy. ... Lipid levels should be reevaluated 4 to 12 weeks after initiating therapy; lipid levels can be measured without fasting. A lack of improvement often indicates nonadherence. Bile acid sequestrants, fibric acids, and niacin can be used if other drugs are not tolerated. 
  4. ^ McCarty MF, DiNicolantonio JJ (2014). "The molecular biology and pathophysiology of vascular calcification". Postgrad Med. 126 (2): 54–64. doi:10.3810/pgm.2014.03.2740. PMID 24685968. Vascular calcification (VC), commonly encountered in renal failure, diabetes, and aging, is associated with a large increase in the risk for cardiovascular events and mortality. Calcification of the arterial media and of heart valves clearly plays a mediating role in this regard, whereas it is less clear how calcification of plaque influences atherogenesis and risk for plaque rupture. Vascular calcification is an active process in which vascular smooth muscle cells (VSMCs) adopt an osteoblastic phenotype and deposit hydroxyapatite crystals; apoptosis of VSMCs also promotes this deposition. Drivers of this phenotypic transition, which include elevated serum phosphate, advanced glycation end-products, bone morphogenetic proteins, inflammatory cytokines, and leptin, invariably induce oxidative stress in VSMCs ... Antioxidants that suppress reduced nicotinamide adenine dinucleotide phosphate oxidase activity may have the potential to block the osteoblastic transition of VSMCs. Minimizing the absorption of dietary phosphate may also be helpful in this regard, particularly in renal failure, and it can be achieved with plant-based dietary choices, avoidance of phosphate additives, and administration of pharmaceutical phosphate binders, supplemental magnesium, and niacin. 

Cognitive control deteriorates (poorer reasoning and problem solving, forgetting things, and impaired ability to exercise discipline and self-control)[1] as a result of:

  • excessive stress[1]
  • sadness/depression[1]
  • social isolation/loneliness[1]
  • poor health[1]
  • lack of physical exercise/fitness[1]

Impaired cognitive control can produce symptoms of ADHD in adults who did not have the disorder as a child.[1]

Cognitive control can be improved[1] through:

References

  1. ^ a b c d e f g h i j Diamond A (2013). "Executive functions". Annu Rev Psychol. 64: 135–168. doi:10.1146/annurev-psych-113011-143750. PMC 4084861Freely accessible. PMID 23020641. Core EFs are inhibition [response inhibition (self-control—resisting temptations and resisting acting impulsively) and interference control (selective attention and cognitive inhibition)], working memory, and cognitive flexibility (including creatively thinking “outside the box,” seeing anything from different perspectives, and quickly and flexibly adapting to changed circumstances). ... EFs and prefrontal cortex are the first to suffer, and suffer disproportionately, if something is not right in your life. They suffer first, and most, if you are stressed (Arnsten 1998, Liston et al. 2009, Oaten & Cheng 2005), sad (Hirt et al. 2008, von Hecker & Meiser 2005), lonely (Baumeister et al. 2002, Cacioppo & Patrick 2008, Campbell et al. 2006, Tun et al. 2012), sleep deprived (Barnes et al. 2012, Huang et al. 2007), or not physically fit (Best 2010, Chaddock et al. 2011, Hillman et al. 2008). Any of these can cause you to appear to have a disorder of EFs, such as ADHD, when you do not. You can see the deleterious effects of stress, sadness, loneliness, and lack of physical health or fitness at the physiological and neuroanatomical level in prefrontal cortex and at the behavioral level in worse EFs (poorer reasoning and problem solving, forgetting things, and impaired ability to exercise discipline and self-control). ...
    EFs can be improved (Diamond & Lee 2011, Klingberg 2010). ... At any age across the life cycle EFs can be improved, including in the elderly and in infants. There has been much work with excellent results on improving EFs in the elderly by improving physical fitness (Erickson & Kramer 2009, Voss et al. 2011) ... Inhibitory control (one of the core EFs) involves being able to control one’s attention, behavior, thoughts, and/or emotions to override a strong internal predisposition or external lure, and instead do what’s more appropriate or needed. Without inhibitory control we would be at the mercy of impulses, old habits of thought or action (conditioned responses), and/or stimuli in the environment that pull us this way or that. Thus, inhibitory control makes it possible for us to change and for us to choose how we react and how we behave rather than being unthinking creatures of habit. It doesn’t make it easy. Indeed, we usually are creatures of habit and our behavior is under the control of environmental stimuli far more than we usually realize, but having the ability to exercise inhibitory control creates the possibility of change and choice.
     
  2. ^ a b Ilieva IP, Hook CJ, Farah MJ (January 2015). "Prescription Stimulants' Effects on Healthy Inhibitory Control, Working Memory, and Episodic Memory: A Meta-analysis". J. Cogn. Neurosci.: 1–21. doi:10.1162/jocn_a_00776. PMID 25591060. Specifically, in a set of experiments limited to high-quality designs, we found significant enhancement of several cognitive abilities. ... The results of this meta-analysis ... do confirm the reality of cognitive enhancing effects for normal healthy adults in general, while also indicating that these effects are modest in size. 
  3. ^ a b Spencer RC, Devilbiss DM, Berridge CW (June 2015). "The Cognition-Enhancing Effects of Psychostimulants Involve Direct Action in the Prefrontal Cortex". Biol. Psychiatry. 77 (11): 940–950. doi:10.1016/j.biopsych.2014.09.013. PMID 25499957. Collectively, this evidence indicates that at low, clinically relevant doses, psychostimulants are devoid of the behavioral and neurochemical actions that define this class of drugs and instead act largely as cognitive enhancers (improving PFC-dependent function). This information has potentially important clinical implications as well as relevance for public health policy regarding the widespread clinical use of psychostimulants and for the development of novel pharmacologic treatments for attention-deficit/hyperactivity disorder and other conditions associated with PFC dysregulation. ... In particular, in both animals and humans, lower doses maximally improve performance in tests of working memory and response inhibition, whereas maximal suppression of overt behavior and facilitation of attentional processes occurs at higher doses. 
  4. ^ a b c Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter 13: Higher Cognitive Function and Behavioral Control". In Sydor A, Brown RY. Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York, USA: McGraw-Hill Medical. pp. 318, 321. ISBN 9780071481274. Therapeutic (relatively low) doses of psychostimulants, such as methylphenidate and amphetamine, improve performance on working memory tasks both in normal subjects and those with ADHD. ... stimulants act not only on working memory function, but also on general levels of arousal and, within the nucleus accumbens, improve the saliency of tasks. Thus, stimulants improve performance on effortful but tedious tasks ... through indirect stimulation of dopamine and norepinephrine receptors. ...
    Beyond these general permissive effects, dopamine (acting via D1 receptors) and norepinephrine (acting at several receptors) can, at optimal levels, enhance working memory and aspects of attention. Drugs used for this purpose include, as stated above, methylphenidate, amphetamines, atomoxetine, and desipramine.
     


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