Chemical Imbalances
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- The document traces the history of research into neurotransmitters in the brain from the 1930s to the 1960s, when key neurotransmitters like serotonin and GABA were discovered. By the 1960s, the theory of chemical transmission in the brain was widely accepted. - However, the theory that chemical imbalances in the brain cause psychiatric disorders like depression has not been proven. While correlations have been found, causation has not been established. Drug company marketing often presents chemical imbalances as the cause of disorders despite limited evidence. - Further research has found that factors like genetics and environment likely play a larger role than chemical levels alone in causing mental health conditions. The theory of a simple chemical imbalance remains an unsubstantiated
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Provide a 1-page description of a stressful event currently occurring in your life. Then, referring to information you learned throughout this course, address the following:
· What physiological changes occur in the brain due to the stress response?
· What emotional and cognitive effects might occur due to this stressful situation?
· Would the above changes (physiological, cognitive, or emotional) be any different if the same stress were being experienced by a person of the opposite sex or someone much older or younger than you?
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In addition to citing the online course and the text, you are also required to cite a minimum of two scholarly sources. Please see the Academic Resources section under Course Home to use the Argosy University online library to find appropriate scholarly sources. For reputable web sources, look for .gov or .edu sites as opposed to .com sites. Please do not use Wikipedia.
Your paper should be double-spaced, in 12-point Times New Roman font, and with normal 1-inch margins; written in APA style; and free of typographical and grammatical errors. It should include a title page with a running head, an abstract, and a reference page. The body of the paper should be at least 6 pages in length
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Selye proposed the concept of the general adaptation syndrome to account for the effect of stress on the body
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In the brain, the amygdala and the anterior cingulate cortex show structural and functional abnormalities in people with depression.
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Running Head: DEPRESSION 1
DEPRESSION 3
Lana Eliot
Depression
Psychology 630
Professor Benton
August 25, 2018
Many people throughout the world experience some type of depression in their lives and it is one of the most common mental disorders. The current statistic show that depression is linked to genetic, environmental, biological and is also psychological. Depression can ben found with any age person. A small child or an adult may have to deal with the depression that is affecting them. Chemical imbalances in the brain is the leading cause for a person dealing with the depressive order. The neurotransmitter is the what we call the communicator between the brain and the limbic system. Researchers study the limbic system in the brain as this is where depression starts; especially for anxiety and stress. The 3 major neurotransmitters; serotonin, norepinephrine, and dopamine all have direct relations with a persons’ depression and anxiety.
Serotonin plays a crucial role in our brain. It is associated with many physical actions that we may portray. The actions associated with serotonin are mood altering, sleeping patterns, eating disorders, and aggression. If a persons’ serotonin levels decrease, they may experience these depressive symptoms. This can also make persons have a feeling of self-worth and suicidal feelings.
Another transmitter in the brain which is associated with the depressive disorder is dopamine. This is the part of the brain that deals with our motivation and how we gain the feeling of self-worth and self-pleasure. Early studies suggested that an existence of neurotransmitter norepinephrine deficiency in some certain areas of the brain resulted in depression. One main cause of depression is the reduction in the concentration of certain neurotransmitters in the brain, such as serotonin and dopamine. The decrease in the concentration of these neurotransmitters leads to disturbed neuronal signal processing which leads to alterations in the structure of the neuronal networks. These basic changes are accepted to be one of the fundamental purposes behind sorrow. The emergence of neuroimaging techniques, magnetic resonance imaging (MRI), positron emission tomography (PET) and functional fMRI, established the importance of the ‘neurocircuit of emotion’ which has been expanded to include other important brain areas and the prefrontal cortex (PFC). These brain sites and their connections, which have been widely studied, are responsible for maintaining emotional stability and their malfunction is considered central to the pathophysiology of depression (Palazidou, E., 2012).
Recent follow up studies also shows that there is a group of individuals with a depression disorder who exhibit low levels of the chemical norepinephrine. In autopsy studies, it has been shown that in comparison,.
Psychology 4 10
Genetic factors, neurotransmitters, hormones, and circadian rhythms contribute to the biological view of depression according to studies. Family, twin, and adoption studies show depression may be inherited. Low levels of neurotransmitters like serotonin and norepinephrine are linked to depression. Cortisol and melatonin imbalances are also associated with depression. Seasonal affective disorder may be related to changes in melatonin levels and sunlight exposure. However, biological explanations of depression have limitations due to challenges directly measuring brain activity.
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CHAPTER SEVEN
Antipsychotic Medications
The Evolution of Treatment
Many readers may begin this chapter with some familiarity with antipsychotic medications. Others may think antipsychotic medications or the research related to them has not affected their lives. These latter readers may be wrong. Have you ever taken a prescription antihistamine such as Seldane or Allegra? Perhaps got over motion sickness with a compound that included promethazine? If so, your life has been affected by research into antipsychotics. As with so many other areas of research in psychotropic medication, antipsychotics and theories about their use have been developed through combined scientific effort, clinical research, market-driven agendas, and serendipity. Let's look at some history to introduce this topic. The primary source for the following is Healy (2002).
THE CURRENT IMPACT OF ANTIPSYCHOTICS
In a video designed for psychiatrists (Novartis Pharmaceuticals, 1998), a young man suffering from treatment-resistant schizophrenia is shown in an inpatient setting. Although his psychotic symptoms are temporarily under control, he is so incapacitated by medication side effects that he can barely walk across a small room. His movements are jerky contractions of muscle groups that he can hardly control. Anyone who has treated clients taking conventional antipsychotic medications knows that this young man is living a worst-case scenario in which the treatment is worse than the disorder being treated. The video progresses, showing the young man at monthly intervals as he is slowly weaned off the medications causing the side effects, and gradually titrated onto a new medication (clozapine). With each passing month, we see that the young man's psychotic symptoms remain under control but that he is gradually regaining control of his body. In the final video frame, we see the same young man enjoying a game of basketball and apparently having no problems with movement or symptoms of psychosis.
This was one of the first videos promoting what we describe later as an atypical antipsychotic, and at the time of their development most of us believed that clozapine and drugs modeled after its molecular structure launched another revolution in psychopharmacology. It was hoped that (as was hoped in the SSRI revolution in antidepressants) the new antipsychotics would change the way psychotic disorders are treated as well as the quality of life that patients can expect during treatment. As we will see, although newer agents do work better for some but not all people with schizophrenia, the newer agents have problematic side effects similar in impact (if different in quality) as the older agents. Also, the claims that newer medications worked better than the older ones now seem to be untrue ( Jones et al., 2006; Lieberman et al., 2005).
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The document discusses the biological causes of schizophrenia. It notes several lines of evidence including abnormal genes, brain structure differences, neurotransmitter abnormalities, and the effectiveness of medication. However, it also acknowledges that environmental factors like stress must play a role, as identical twins only have a 50% chance of both developing schizophrenia. The most widely accepted theory is the diathesis-stress model, where genetic vulnerabilities interact with stressors to trigger the onset of the disorder.
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Provide a 1-page description of a stressful event currently occurr.docx
Provide a 1-page description of a stressful event currently occurring in your life. Then, referring to information you learned throughout this course, address the following:
· What physiological changes occur in the brain due to the stress response?
· What emotional and cognitive effects might occur due to this stressful situation?
· Would the above changes (physiological, cognitive, or emotional) be any different if the same stress were being experienced by a person of the opposite sex or someone much older or younger than you?
· If the situation continues, how might your physical health be affected?
· What three behavioral strategies would you implement to reduce the effects of this stressor? Describe each strategy. Explain how each behavior could cause changes in brain physiology (e.g., exercise can raise serotonin levels).
· If you were encouraging an adult client to make the above changes, what ethical considerations would you have to keep in mind? How would you address those ethical considerations?
In addition to citing the online course and the text, you are also required to cite a minimum of two scholarly sources. Please see the Academic Resources section under Course Home to use the Argosy University online library to find appropriate scholarly sources. For reputable web sources, look for .gov or .edu sites as opposed to .com sites. Please do not use Wikipedia.
Your paper should be double-spaced, in 12-point Times New Roman font, and with normal 1-inch margins; written in APA style; and free of typographical and grammatical errors. It should include a title page with a running head, an abstract, and a reference page. The body of the paper should be at least 6 pages in length
Stress hormones increase blood pressure and have various other effects on the body that might not be adaptive over long periods.
Selye proposed the concept of the general adaptation syndrome to account for the effect of stress on the body
Currently, there are two primary systems for the classification of psychological disorders—The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) (American Psychiatric Association, 2013), and The International Statistical Classification of Diseases and Related Health Problems (ICD) (World Health Organization, 1992).
Major depressive disorder is characterized by a lowering of mood, energy, and activity that results in significant distress or impairment in life. There is much research focusing on imbalances in the monoamine neurotransmitters (dopamine, norepinephrine, and serotonin) in people suffering from depressive disorders
In the brain, the amygdala and the anterior cingulate cortex show structural and functional abnormalities in people with depression.
Bipolar disorder is characterized by an extremely elevated mood with increases in activity and energy (manic phase) followed by an equally low mood with decreases in activity and energy (depressive phase), resulting in significant distress or imp ...
Running Head DEPRESSION .docx
Running Head: DEPRESSION 1
DEPRESSION 3
Lana Eliot
Depression
Psychology 630
Professor Benton
August 25, 2018
Many people throughout the world experience some type of depression in their lives and it is one of the most common mental disorders. The current statistic show that depression is linked to genetic, environmental, biological and is also psychological. Depression can ben found with any age person. A small child or an adult may have to deal with the depression that is affecting them. Chemical imbalances in the brain is the leading cause for a person dealing with the depressive order. The neurotransmitter is the what we call the communicator between the brain and the limbic system. Researchers study the limbic system in the brain as this is where depression starts; especially for anxiety and stress. The 3 major neurotransmitters; serotonin, norepinephrine, and dopamine all have direct relations with a persons’ depression and anxiety.
Serotonin plays a crucial role in our brain. It is associated with many physical actions that we may portray. The actions associated with serotonin are mood altering, sleeping patterns, eating disorders, and aggression. If a persons’ serotonin levels decrease, they may experience these depressive symptoms. This can also make persons have a feeling of self-worth and suicidal feelings.
Another transmitter in the brain which is associated with the depressive disorder is dopamine. This is the part of the brain that deals with our motivation and how we gain the feeling of self-worth and self-pleasure. Early studies suggested that an existence of neurotransmitter norepinephrine deficiency in some certain areas of the brain resulted in depression. One main cause of depression is the reduction in the concentration of certain neurotransmitters in the brain, such as serotonin and dopamine. The decrease in the concentration of these neurotransmitters leads to disturbed neuronal signal processing which leads to alterations in the structure of the neuronal networks. These basic changes are accepted to be one of the fundamental purposes behind sorrow. The emergence of neuroimaging techniques, magnetic resonance imaging (MRI), positron emission tomography (PET) and functional fMRI, established the importance of the ‘neurocircuit of emotion’ which has been expanded to include other important brain areas and the prefrontal cortex (PFC). These brain sites and their connections, which have been widely studied, are responsible for maintaining emotional stability and their malfunction is considered central to the pathophysiology of depression (Palazidou, E., 2012).
Recent follow up studies also shows that there is a group of individuals with a depression disorder who exhibit low levels of the chemical norepinephrine. In autopsy studies, it has been shown that in comparison,.
Psychology 4 10
Genetic factors, neurotransmitters, hormones, and circadian rhythms contribute to the biological view of depression according to studies. Family, twin, and adoption studies show depression may be inherited. Low levels of neurotransmitters like serotonin and norepinephrine are linked to depression. Cortisol and melatonin imbalances are also associated with depression. Seasonal affective disorder may be related to changes in melatonin levels and sunlight exposure. However, biological explanations of depression have limitations due to challenges directly measuring brain activity.
CHAPTER SEVENAntipsychotic MedicationsThe Evolution of Treatme.docx
CHAPTER SEVEN
Antipsychotic Medications
The Evolution of Treatment
Many readers may begin this chapter with some familiarity with antipsychotic medications. Others may think antipsychotic medications or the research related to them has not affected their lives. These latter readers may be wrong. Have you ever taken a prescription antihistamine such as Seldane or Allegra? Perhaps got over motion sickness with a compound that included promethazine? If so, your life has been affected by research into antipsychotics. As with so many other areas of research in psychotropic medication, antipsychotics and theories about their use have been developed through combined scientific effort, clinical research, market-driven agendas, and serendipity. Let's look at some history to introduce this topic. The primary source for the following is Healy (2002).
THE CURRENT IMPACT OF ANTIPSYCHOTICS
In a video designed for psychiatrists (Novartis Pharmaceuticals, 1998), a young man suffering from treatment-resistant schizophrenia is shown in an inpatient setting. Although his psychotic symptoms are temporarily under control, he is so incapacitated by medication side effects that he can barely walk across a small room. His movements are jerky contractions of muscle groups that he can hardly control. Anyone who has treated clients taking conventional antipsychotic medications knows that this young man is living a worst-case scenario in which the treatment is worse than the disorder being treated. The video progresses, showing the young man at monthly intervals as he is slowly weaned off the medications causing the side effects, and gradually titrated onto a new medication (clozapine). With each passing month, we see that the young man's psychotic symptoms remain under control but that he is gradually regaining control of his body. In the final video frame, we see the same young man enjoying a game of basketball and apparently having no problems with movement or symptoms of psychosis.
This was one of the first videos promoting what we describe later as an atypical antipsychotic, and at the time of their development most of us believed that clozapine and drugs modeled after its molecular structure launched another revolution in psychopharmacology. It was hoped that (as was hoped in the SSRI revolution in antidepressants) the new antipsychotics would change the way psychotic disorders are treated as well as the quality of life that patients can expect during treatment. As we will see, although newer agents do work better for some but not all people with schizophrenia, the newer agents have problematic side effects similar in impact (if different in quality) as the older agents. Also, the claims that newer medications worked better than the older ones now seem to be untrue ( Jones et al., 2006; Lieberman et al., 2005).
This chapter is divided into seven sections. The first is an overview of schizophrenia and the spectrum of symptoms being treated. The second focuses on th.
Etiology of Schizophrenia
The document discusses the biological causes of schizophrenia. It notes several lines of evidence including abnormal genes, brain structure differences, neurotransmitter abnormalities, and the effectiveness of medication. However, it also acknowledges that environmental factors like stress must play a role, as identical twins only have a 50% chance of both developing schizophrenia. The most widely accepted theory is the diathesis-stress model, where genetic vulnerabilities interact with stressors to trigger the onset of the disorder.
Biological & sociological
The document summarizes several biological and sociological theories of schizophrenia. The biological theories discussed are the neurodevelopmental theory and the dopamine theory. The neurodevelopmental theory proposes that schizophrenia results from aberrations in early brain development. The dopamine theory attributes schizophrenia symptoms to disturbed dopamine signaling in the brain. The sociological theories discussed are stress theory, structural strain theory, and labeling theory. These theories suggest social and environmental factors can influence mental illness rates.
Neuroplasticity: The Brain That Changes Itself
The document discusses neuroplasticity and how the brain can change itself through experiences like stress, beliefs, environment, and activities. It provides examples of research that shows how thinking patterns can impact health conditions like heart disease, how environments and experiences can influence gene expression, and how cognitive behavioral therapy and mindfulness can help rewire the brain and reduce symptoms of obsessive compulsive disorder.
Running head PSYCHIATRIC DISORDER .docx
Running head: PSYCHIATRIC DISORDER 1
PSYCHIATRIC DISORDER 6
Psychiatric Disorder
Student’s Name
University Affiliation
Course Title
Date
Psychiatric disorder
Depression is one of the most common mental disorders found in the world. Current studies indicate that depression may result from genetic, biological, environmental, and psychological factors. People of all ages are susceptible to depression but the elderly are at a high risk than the young. In the brain, depression starts with simple chemical imbalances. Communication within the brain and to and fro the rest of the body is via the chemical transmitter, known as neurotransmitters. The brain limbic system has been a key interest for many researchers as it comes to anxiety, stress and depression. There exists relationship between depression and the functioning of three primary neurotransmitters; serotonin, norepinephrine, and dopamine.
Serotonin is a neurotransmitter that is associated with the control of many crucial bodily operations such as aggression, sleeping, sexual behavior, mood, and eating. The production of serotonin is in the serotonergic neurons. Some people are likely to suffer depression with a drop in the production of serotonin in the neurons. The resultant mood is one that is more particularly associated with individuals feeling suicidal.
Early studies suggested that an existence of neurotransmitter norepinephrine deficiency in some certain areas of the brain resulted in depression. Recent follow up studies also shows that there is a group of individuals with a depression disorder who exhibit low levels of the chemical norepinephrine. In autopsy studies, it has been shown that in comparison, people who lives have been marred with a recurrence of depressive episodes possess lesser norepinephrinergic neurons unlike those who have not had depressive history. Norepinephrine assist our bodies detect and respond to stressful instances. People who are susceptible to depression have a norepinephrinergic system which does not take care of the effects of stress very efficiently.
Dopamine is another chemical transmitter in the brain associated with depression. The neurotransmitter plays a critical part in controlling our motivation to seek out reward, also the ability to get a sense of pleasure. Low levels of dopamine may partly explain as to why some individuals suffering from depression do not get the same pleasure sense from people are activities that they used to before falling into depression.
Evidence is ever increasing to support the hypothesis that stress and the accompanying depression could involve structural variations in the brain. The resultant changes of depression are known as remodeling. An occurrence of remodeling due to stress can be prevented or even potentially tu ...
Is Drug Addiction a Disease?
The document discusses whether drug addiction should be considered a disease. It notes that some see it as a disease due to genetic factors, while others argue there is limited evidence for this. The concept of addiction as a disease emerged in the late 18th/early 19th century and became popularized by treatment centers in the 1920s-1930s. However, a disease must have predictable symptoms and progression, which addiction does not. The main reason it continues to be called a disease is to justify government funding for treatment.
Prozac and Depression Patients
This document discusses the hypothesis that the antidepressant effects of Prozac in depression patients may be due to its neurotrophic effects on neurons rather than its effects on serotonin reuptake. It proposes an experiment involving 20 depression patients, 10 receiving Prozac and 10 receiving a placebo, who would be evaluated psychologically and through fMRI brain scans before and after a week of treatment to analyze changes in neural activity. The expected results are that Prozac would show increased neural activity, supporting the hypothesis that its trophic factors rehabilitate neurons rather than its serotonin effects providing the antidepressant response.
The influence of the HPA axis in development of psychosis
This document discusses the influence of the hypothalamic-pituitary-adrenal (HPA) axis on the development of psychosis. It notes that psychosis sufferers often have elevated HPA axis activity and cortisol levels, especially during stressful periods and psychotic episodes. Long-term HPA axis dysregulation can lead to changes in the brain like reduced hippocampal volume and increased dopamine levels, contributing to psychosis symptoms. While cortisol levels may decrease in chronic cases, the HPA axis still plays a key role in the diathesis stress model of psychosis by mediating the effects of genetics and environment on mental illness onset and progression.
Heal your brain from depression
The document discusses how brain structure and function can change with depression and bipolar disorder. It describes how the hippocampus shrinks with these conditions, increasing risks for memory problems and dementia. Exercise and meditation are highlighted as ways to potentially reverse hippocampal shrinkage and improve brain plasticity and cognitive function. Drug therapies are noted to have risks of worsening symptoms or converting unipolar depression to bipolar disorder.
Stress And External Factors
This summary focuses on two articles that correlate stress and external factors. The first article by Theodore. B. Vanitallie, (2002) examines the pathology of stress while the research experiment by Bloch, M. (2007) investigates the effect of divorce on stress levels and physiological responses.
Presentation2
Brain chemistry involves the complex chemical messaging within the brain that allows it to perform functions like movement, thinking, and regulating bodily systems. Bipolar disorder may be partly caused by imbalances in brain circuits and neurotransmitters like noradrenaline, serotonin, and dopamine. In the 1950s, neurochemistry emerged as a scientific discipline focused on studying these brain chemicals and their roles in mental illnesses and neurological conditions. Imbalances in neurotransmitters like serotonin, dopamine, and GABA have been linked to depression, epilepsy, and other disorders.
Targets of Antidepressant Therapy
This document summarizes research on how antidepressants reverse the effects of depression in the hippocampus. It finds that depression causes changes in specific regions of the hippocampus like the dentate gyrus and CA1/CA3 regions. These changes include decreased volume, lower concentrations of proteins like BDNF, decreased dendritic spine density, and altered synaptic impulse speeds. Antidepressants target these deficiencies by increasing hippocampal volume, protein concentrations, dendritic spine density, and synaptic impulse speeds through neuroplasticity. However, one antidepressant may not be enough, so a new technique called polypharmacy uses two antidepressants to more precisely target the various causes of depression.
Brain based therapy
Brain Based Therapy summarizes a new model called BASE that incorporates neuroscience into psychotherapy. BASE stands for brain, attunement, systems of care, and evidence-based treatment. The model views the brain as shaped by relationships and experience, and sees the goal of therapy as helping clients manage stress to regulate their brain and enhance neuroplasticity through attunement and addressing lifestyle factors like sleep and exercise.
PSYA3 - The Biological Approach
The biological approach views mental disorders as medical conditions with physical causes, such as infections, biochemical imbalances, genetic factors, and neurological damage. Strengths include modern brain scanning technologies identifying biological abnormalities and some effective drug treatments. However, it is also reductionist by ignoring environmental influences, and drug treatments do not work for all disorders. The diathesis-stress model provides a more balanced view that both biological and environmental factors interact to cause psychopathology.
Schizophrenia- biological and neuropsychological approacesh
Here are the key points about the mesolimbic dopamine pathway and its relationship to positive symptoms of schizophrenia:
- The mesolimbic dopamine pathway projects from the ventral tegmental area in the brainstem to the nucleus accumbens in the ventral striatum.
- This pathway is important for motivation, pleasure, reward processing and emotional behaviors.
- Increased dopamine activity in this pathway, such as from stimulant drugs, can enhance or produce positive psychotic symptoms like delusions and hallucinations.
- Decreased dopamine activity, such as from antipsychotic drugs, can reduce positive symptoms.
- Antipsychotic drugs work by blocking D2 dopamine receptors, which are thought to mediate the
Joelle_Petrei_Finished_Grant_2016
1. The study examined mice with deficient NMDA glutamate receptors to investigate the role of glutamate in schizophrenia-like symptoms and potential treatments.
2. Experiments tested both symptoms in mice and various glutamate medications that could improve schizophrenia symptoms while furthering understanding of psychiatric disorders.
3. Tests measured cognitive abilities, genetic factors, and brain analysis post-mortem to compare untreated and treated mice and evaluate the effects of specific medications targeting neuronal synapses.
1179journal.publications.chestnet.org Th e Pathophys
1179journal.publications.chestnet.org
Th e Pathophysiology of Insomnia
Jessica C. Levenson , PhD ; Daniel B. Kay , PhD ; and Daniel J. Buysse , MD
Insomnia disorder is characterized by chronic dissatisfaction with sleep quantity or quality
that is associated with diffi culty falling asleep, frequent nighttime awakenings with diffi culty
returning to sleep, and/or awakening earlier in the morning than desired. Although progress
has been made in our understanding of the nature, etiology, and pathophysiology of insomnia,
there is still no universally accepted model. Greater understanding of the pathophysiology of
insomnia may provide important information regarding how, and under what conditions, the
disorder develops and is maintained as well as potential targets for prevention and treatment.
The aims of this report are (1) to summarize current knowledge on the pathophysiology of
insomnia and (2) to present a model of the pathophysiology of insomnia that considers evi-
dence from various domains of research. Working within several models of insomnia, evidence
for the pathophysiology of the disorder is presented across levels of analysis, from genetic to
molecular and cellular mechanisms, neural circuitry, physiologic mechanisms, sleep behavior, and
self-report. We discuss the role of hyperarousal as an overarching theme that guides our concep-
tualization of insomnia. Finally, we propose a model of the pathophysiology of insomnia that
integrates the various types of evidence presented. CHEST 2015; 147� ( 4 ): 1179 - 1192
ABBREVIATIONS: GABA 5 g -aminobutyric acid ; MnPO 5 median preoptic area ; NREM 5 non-rapid eye
movement ; PEP 5 pre-ejection period ; PSG 5 polysomnography ; REM 5 rapid eye movement ; SNP 5
single-nucleotide polymorphism ; TMN 5 tuberomammillary nucleus of the posterior hypothalamus ; VLPO 5
ventrolateral preoptic area
[ Contemporary Reviews in Sleep Medicine ]
Manuscript received July 3 , 2014 ; revision accepted October 28 , 2014 .
AFFILIATIONS: From the Department of Psychiatry, University of
Pittsburgh School of Medicine, Pittsburgh, PA.
FUNDING/SUPPORT: Dr Buysse is supported by the National Institutes
of Health [Grants MH024652, MH102412, AG020677, and HL125103].
Drs Levenson and Kay are supported by the National Institutes of
Health [Grant HL082610, T32, PI Buysse].
CORRESPONDENCE TO: Daniel J. Buysse, MD, University of Pittsburgh,
3811 O’Hara St, WPIC E-1127, Pittsburgh, PA 15213; e-mail: [email protected]
upmc.edu
© 2015 AMERICAN COLLEGE OF CHEST PHYSICIANS. Reproduction of
this article is prohibited without written permission from the American
College of Chest Physicians. See online for more details. ...
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Provide a 1-page description of a stressful event currently occurr.docx
Provide a 1-page description of a stressful event currently occurr.docx
CHAPTER SEVENAntipsychotic MedicationsThe Evolution of Treatme.docx
CHAPTER SEVENAntipsychotic MedicationsThe Evolution of Treatme.docx
The influence of the HPA axis in development of psychosis
The influence of the HPA axis in development of psychosis
Schizophrenia- biological and neuropsychological approacesh
Schizophrenia- biological and neuropsychological approacesh
1179journal.publications.chestnet.org Th e Pathophys
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Rasamanikya is a excellent preparation in the field of Rasashastra, it is used in various Kushtha Roga, Shwasa, Vicharchika, Bhagandara, Vatarakta, and Phiranga Roga. In this article Preparation& Comparative analytical profile for both Formulationon i.e Rasamanikya prepared by Kushmanda swarasa & Churnodhaka Shodita Haratala. The study aims to provide insights into the comparative efficacy and analytical aspects of these formulations for enhanced therapeutic outcomes.
Promoting Wellbeing - Applied Social Psychology - Psychology SuperNotes
A proprietary approach developed by bringing together the best of learning theories from Psychology, design principles from the world of visualization, and pedagogical methods from over a decade of training experience, that enables you to: Learn better, faster!
Top Effective Soaps for Fungal Skin Infections in India
Swisschem Dermacare has mentioned the List of The Best Antifungal Soap In India 2022. All of these soaps are trusted by various Dermatology Experts.
Top 10 Best Ayurvedic Kidney Stone Syrups in India
we have mentioned the best 10 ayurvedic Kidney Stone Syrups. You can check all these products and choose the best one for yourself.
The Electrocardiogram - Physiologic Principles
These lecture slides, by Dr Sidra Arshad, offer a quick overview of the physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Light House Retreats: Plant Medicine Retreat Europe
Our aim is to organise conscious gatherings and retreats for open and inquisitive minds and souls, with and without the assistance of sacred plants.
ABDOMINAL TRAUMA in pediatrics part one.
Abdominal trauma in pediatrics refers to injuries or damage to the abdominal organs in children. It can occur due to various causes such as falls, motor vehicle accidents, sports-related injuries, and physical abuse. Children are more vulnerable to abdominal trauma due to their unique anatomical and physiological characteristics. Signs and symptoms include abdominal pain, tenderness, distension, vomiting, and signs of shock. Diagnosis involves physical examination, imaging studies, and laboratory tests. Management depends on the severity and may involve conservative treatment or surgical intervention. Prevention is crucial in reducing the incidence of abdominal trauma in children.
How STIs Influence the Development of Pelvic Inflammatory Disease.pptx
STIs may cause PID. For the both disease, herbal medicine Fuyan Pill can be a solution.
8 Surprising Reasons To Meditate 40 Minutes A Day That Can Change Your Life.pptx
8 Surprising Reasons To Meditate 40 Minutes A Day That Can Change Your Life.pptxHolistified Wellness
We’re talking about Vedic Meditation, a form of meditation that has been around for at least 5,000 years. Back then, the people who lived in the Indus Valley, now known as India and Pakistan, practised meditation as a fundamental part of daily life. This knowledge that has given us yoga and Ayurveda, was known as Veda, hence the name Vedic. And though there are some written records, the practice has been passed down verbally from generation to generation.NVBDCP.pptx Nation vector borne disease control program
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
Role of Mukta Pishti in the Management of Hyperthyroidism
Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
Cell Therapy Expansion and Challenges in Autoimmune Disease
There is increasing confidence that cell therapies will soon play a role in the treatment of autoimmune disorders, but the extent of this impact remains to be seen. Early readouts on autologous CAR-Ts in lupus are encouraging, but manufacturing and cost limitations are likely to restrict access to highly refractory patients. Allogeneic CAR-Ts have the potential to broaden access to earlier lines of treatment due to their inherent cost benefits, however they will need to demonstrate comparable or improved efficacy to established modalities.
In addition to infrastructure and capacity constraints, CAR-Ts face a very different risk-benefit dynamic in autoimmune compared to oncology, highlighting the need for tolerable therapies with low adverse event risk. CAR-NK and Treg-based therapies are also being developed in certain autoimmune disorders and may demonstrate favorable safety profiles. Several novel non-cell therapies such as bispecific antibodies, nanobodies, and RNAi drugs, may also offer future alternative competitive solutions with variable value propositions.
Widespread adoption of cell therapies will not only require strong efficacy and safety data, but also adapted pricing and access strategies. At oncology-based price points, CAR-Ts are unlikely to achieve broad market access in autoimmune disorders, with eligible patient populations that are potentially orders of magnitude greater than the number of currently addressable cancer patients. Developers have made strides towards reducing cell therapy COGS while improving manufacturing efficiency, but payors will inevitably restrict access until more sustainable pricing is achieved.
Despite these headwinds, industry leaders and investors remain confident that cell therapies are poised to address significant unmet need in patients suffering from autoimmune disorders. However, the extent of this impact on the treatment landscape remains to be seen, as the industry rapidly approaches an inflection point.
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