This document summarizes research on animal models of bipolar disorder. It describes several approaches: the sleep deprivation model induces manic-like behaviors in rats; drug screening tests evaluate responses to medications; brain lesion models involve lesions early in development. The document also reviews animal models of depression, including chronic mild stress and forced swim tests. Finally, it discusses in vitro models using neural cells and Dictyostelium to screen for new treatments.
screening models for anxiolytics with detailed procedure and evaluation,
detailed classification about methods, pathophysiology of anxiety, components of anxiety, validity of anxiety,
difference bet pathological and physiological anxiety, different theories of anxiety, criteria of animal model, pharmacological manipulations, conditioned behavior, unconditioned behavior
screening models for anxiolytics with detailed procedure and evaluation,
detailed classification about methods, pathophysiology of anxiety, components of anxiety, validity of anxiety,
difference bet pathological and physiological anxiety, different theories of anxiety, criteria of animal model, pharmacological manipulations, conditioned behavior, unconditioned behavior
Preclinical Screening for Neurodegenerative Disease (Multiple Sclerosis)Drx Burade
This file includes introduction to multiple sclerosis (MS) , their sign and symptoms , types of multiple sclerosis, pathophysiology of MS , again this includes the medication that are used to treat MS , & the last point is the Preclinical Screening models or methods for multiple sclerosis . Preclinical Screening models includes in vivo and in vitro models
Screening methods of immunomodulators by shivam diwakerShivam Diwaker
Immune Modulators are the substances or drugs or chemical compounds that are used for the modification in the Immune system such as stimulate and suppress.
Metabolic depression in hibernation and major depression: an explanatory theo...Loki Stormbringer
Metabolic depression, an adaptive biological process for energy preservation, is responsible for torpor, hibernation and estivation. We propose that a form of metabolic depression, and not mitochondrial dysfunction, is the process underlying the observed hypometabolism, state-dependent neurobiological changes and vegetative symptoms of major depression in humans. The process of metabolic depression is reactivated via differential gene expression in response to perceived adverse stimuli in predisposed persons. Behavior inhibition by temperament, anxiety disorders, genetic vulnerabilities, and early traumatic experiences predispose persons to depression. The proposed theory is supported by similarities in the presentation and neurobiology of hibernation in bears and major depression and explains the yet unexplained neurobiological changes of depression. Although, gene expression is suppressed in other hibernators by deep hypothermia, bears were chosen because they hibernate with mild hypothermia. Pre-hibernation in bears and major depression with atypical features are both characterized by fat storage through overeating, oversleeping, and decreased mobility. Hibernation in bears and major depression with melancholic features are characterized by withdrawal from the environment, lack of energy, loss of weight from not eating and burning stored fat, changes in sleep pattern, and the following similar neurobiological findings: reversible subclinical hypothyroidism; increased concentration of serum cortisol; acute phase protein response; low respiratory quotient; oxidative stress response; decreased neurotransmitter levels; and changes in cyclic-adenosine monophosphate-binding activity. Signaling systems associated with protein phosphorylation, transcription factors, and gene expression are responsible for the metabolic depression process during pre-hibernation and hibernation. Antidepressants and mood stabilizers interfere with the hibernation process and produce their therapeutic effects by normalizing the fluctuation of activities in the different signaling systems, which are down-regulated during hibernation and depression and up-regulated during exodus from hibernation and the hypomanic or manic phase of mood disorders. The ways individuals cognitively perceive, understand, communicate, and react to the vegetative symptoms of depression, from downregulation in energy production, and in the absence of known medical causes, produce the other characteristics of depression including guilt, helplessness, hopelessness, suicidal phenomena, agitation, panic attacks, psychotic symptoms, and sudden switch to hypomanic or manic episodes. The presence of one or more of these characteristics depends on the person's neuropsychological function, its social status between the others, and the other's response to the person. Neurobiological changes associated with metabolic depression during entrance, maintenance, and exodus from hibernation in bears is suggested a
Preclinical Screening for Neurodegenerative Disease (Multiple Sclerosis)Drx Burade
This file includes introduction to multiple sclerosis (MS) , their sign and symptoms , types of multiple sclerosis, pathophysiology of MS , again this includes the medication that are used to treat MS , & the last point is the Preclinical Screening models or methods for multiple sclerosis . Preclinical Screening models includes in vivo and in vitro models
Screening methods of immunomodulators by shivam diwakerShivam Diwaker
Immune Modulators are the substances or drugs or chemical compounds that are used for the modification in the Immune system such as stimulate and suppress.
Metabolic depression in hibernation and major depression: an explanatory theo...Loki Stormbringer
Metabolic depression, an adaptive biological process for energy preservation, is responsible for torpor, hibernation and estivation. We propose that a form of metabolic depression, and not mitochondrial dysfunction, is the process underlying the observed hypometabolism, state-dependent neurobiological changes and vegetative symptoms of major depression in humans. The process of metabolic depression is reactivated via differential gene expression in response to perceived adverse stimuli in predisposed persons. Behavior inhibition by temperament, anxiety disorders, genetic vulnerabilities, and early traumatic experiences predispose persons to depression. The proposed theory is supported by similarities in the presentation and neurobiology of hibernation in bears and major depression and explains the yet unexplained neurobiological changes of depression. Although, gene expression is suppressed in other hibernators by deep hypothermia, bears were chosen because they hibernate with mild hypothermia. Pre-hibernation in bears and major depression with atypical features are both characterized by fat storage through overeating, oversleeping, and decreased mobility. Hibernation in bears and major depression with melancholic features are characterized by withdrawal from the environment, lack of energy, loss of weight from not eating and burning stored fat, changes in sleep pattern, and the following similar neurobiological findings: reversible subclinical hypothyroidism; increased concentration of serum cortisol; acute phase protein response; low respiratory quotient; oxidative stress response; decreased neurotransmitter levels; and changes in cyclic-adenosine monophosphate-binding activity. Signaling systems associated with protein phosphorylation, transcription factors, and gene expression are responsible for the metabolic depression process during pre-hibernation and hibernation. Antidepressants and mood stabilizers interfere with the hibernation process and produce their therapeutic effects by normalizing the fluctuation of activities in the different signaling systems, which are down-regulated during hibernation and depression and up-regulated during exodus from hibernation and the hypomanic or manic phase of mood disorders. The ways individuals cognitively perceive, understand, communicate, and react to the vegetative symptoms of depression, from downregulation in energy production, and in the absence of known medical causes, produce the other characteristics of depression including guilt, helplessness, hopelessness, suicidal phenomena, agitation, panic attacks, psychotic symptoms, and sudden switch to hypomanic or manic episodes. The presence of one or more of these characteristics depends on the person's neuropsychological function, its social status between the others, and the other's response to the person. Neurobiological changes associated with metabolic depression during entrance, maintenance, and exodus from hibernation in bears is suggested a
Factors modifying drug action such as
Body size
Age
Sex
Species and Race
Genetics
Route of administration
Environmental factors
Psychological factors
Pathological factors
Other drugs
Cumulative
Tolerance
Variation in drug response
Difference in PK handling of drug
Variation in number of receptors
Neurogenic, hormonal tone variation
Host, environmental factors
Guide appropriate drug, dose for a patient
Modify drug action quantitatively, qualitatively
this talks about the theories of personality. This tackles on how an individual develops their personality and can be utilized in studying personality disorders. These theories address whether personality is a biological trait or one that is developed through a person's interaction with their environment. Each personality type is defined by a set of stable characteristics: such as introversion or extroversion. Personality traits can be found within personality types: such as loyalty or generosity. Robert McCrae and Paul Costa: Introduced the big five theory, which identifies five key dimensions of personality: 1) extraversion, 2) neuroticism, 3) openness to experience, 4) conscientiousness, and 5) agreeableness. The trait theory of personality suggests that people have certain basic traits and it is the strength and intensity of those traits that account for personality differences. The trait approach to personality is one of the major theoretical areas in the study of personality. Learning about personality theories is important as it helps you reflect on your own personality from a different perspective. Understanding different personality theories can provide insight into your own strengths and weaknesses, as well as help you understand others better. Behaviorists do not believe personality characteristics are based on genetics or inborn predispositions. Instead, they view personality as shaped by the reinforcements and consequences outside of the organism. In other words, people behave in a consistent manner based on prior learning. B. F. Both psychological and physiological: Personality is a psychological construct, but research suggests that it is also influenced by biological processes and needs. Affects behaviors and actions: Personality not only influences how we move and respond in our environment, but it also causes us to act in certain ways. The psychoanalytic theory states that human personality development is the result of a person's unconscious conflicts between the id, ego, and superego; however, this theory has been difficult to prove or disprove. Psychoanalytic theory is based on the work of Sigmund Freud. Personality development plays an essential role not only in an individual's professional but also in personal life. It makes an individual disciplined, punctual, and an asset to his or her organization. In Students, It adds to one's self-confidence and self-esteem. Personality describes the unique patterns of thoughts, feelings, and behaviors that distinguish a person from others. A product of both biology and environment, it remains fairly consistent throughout life. Personality Characteristics Consistency: There is generally a recognizable order and regularity to behaviors. One of the most popular methods for understanding personality is to ask people to complete self-report questionnaires or surveys. These measures typically ask individuals to rate themselves on various personality traits or dimensions, such as extraversio
PARKINSONS DISEASE MEDICAL TREATMENT AND PHYSIOTHERAPY MANAGEMENT Srinitha Busam
This presentation contains brief description about parkinsons disease , its medical management and physiotherapy management ( aims of rehabilitation and exercise training for parkinsons disease patient)
47. Antiepileptic activity and toxicity of cyclic analogs of VPA 333mg: 6.5% resorption 0% alformation 538 171 NT 92 29 TMC-urea 660mg: 54% resorption 34%malformation 330mg: 27% malformation >500 NT NT >500 9 TMC-Thiadiazole(ip) 300mg: 8% resorption 1% malformation 381 85 >100;C 52 >250 TMCD 300mg: 15% resorption 1% alformation 163 41 40;h 45 82 MTMCD NT 333 150 NT 35 108 Methoxy-TMCD 600mg:8% resorption 41% alformation 784 269 80< 646 485 VPA Teratogenicity TD50mgkg Chung mg/kg Kindling mg/kg scMET mg/kg MES mg/kg Drug
48. NT >500 Inactive<160 NT >250 82 TMC-glycinamide NT >500 NT NT >250 41 N-Acetyl-tmc-urea Teratogenicity TD50- Chung mg/kg Kindling mg/kg scMET mg/kg MES mg/kg Drug
50. Antiepileptic activity and Toxicity of VPA-Derivatives 600mg: 10.4% resorbtion 0% malformation 63 NT NT 37 16 R-PID NT 500 NT NT 83 >250 Isovaleroylurea 600mg: 6.3%resorbtion 0%malformation 68 NT NT 37 31 PID (racemic) not teratogenic 87 NT NT 59 32 Valpromide not teratogenic >1000 226 161;C 300;h >750 73 Valrocemide (VGD) Teratogenicity TD50- Chung mg/kg Kindling mg/kg scMET mg/kg MES mg/kg Drug
51. Results of antiepileptic activity and toxicity of drugs given ip to mice 188 225 200 TMCA 279 240 269 Valnoctic acid 81 32 58 Valnoctamide 63 37 31 PID 57 41 87 DID 303 156 238 DIA TD50 scMET mg/kg MES mg/kg Drug
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