The document discusses the role of genetics and pharmacogenomics in personalized medicine and treatment of major depressive disorder. It outlines several genes and genetic variants that have been associated with variability in antidepressant drug response, including genes involved in drug metabolism (CYP2D6, CYP1A2, ABCB1), drug targets (SLC6A4, SLC6A3, HTR2A), and downstream signaling pathways (COMT, MAO-A, ADRB1, GNB3). Large clinical studies still need to determine how pharmacogenomic testing can improve clinical outcomes for depression.
Pharmacogenomics is a new trending branch which has created enormous hopes in improving diagnostic methods, treatment outcomes and preventing adverse events and therapeutic failures. In this ppt basics of pharmacogenomics and pharmacogenetics has been discussed in simplest possible way along with two case studies. Clinical applications of pharmacogenomics has also been discussed in brief.
Presentation on recent advances in Parkinsons disease. Tried to cover up new drugs as well as new devices like Duodopa set up. . i have tried to put a light on the established treatment of Parkinson's disease along with its mechanism of actions in circuit loops which will help to understand the topic in depth!
Pharmacogenomics is a new trending branch which has created enormous hopes in improving diagnostic methods, treatment outcomes and preventing adverse events and therapeutic failures. In this ppt basics of pharmacogenomics and pharmacogenetics has been discussed in simplest possible way along with two case studies. Clinical applications of pharmacogenomics has also been discussed in brief.
Presentation on recent advances in Parkinsons disease. Tried to cover up new drugs as well as new devices like Duodopa set up. . i have tried to put a light on the established treatment of Parkinson's disease along with its mechanism of actions in circuit loops which will help to understand the topic in depth!
1. WHAT IS GENE THERAPY
2. PRINCIPLE OF GENE THERAPY
3. TYPES OF GENE THERAPY
4. VECTORS IN GENE DELIVERY SYSTEM
5. ROLE OF GENE THERAPY IN CNS DISORDERS
6. GENE THERAPY FOR ALZHEIMERS DISEASE
7. GENE THERAPY FOR AMYOTROPIC LATERAL SCLEROSIS
8. GENE THERAPY FOR STROKE
9. CELL THERAPY FOR CNS DISORDERS
10. CELL THERAPY STRATEGIES
11. CELL THERAPY FOR PARKINSON
12. CELL THERAPY FOR HUNTINGTONS DISEASE
13. CRISPR/CAS9
Recent advances in the treatment of psychosesKarun Kumar
This presentation deals with atypical antipsychotics & new drugs in the pipeline (Clozapine, Risperidone, Olanzapine, Quetiapine, Ziprasidone, Aripiprazole, Second generation antipsychotics, atypical antipsychotics, Aspirin, Minocycline, Raloxifene, Estrogen, N-acetylcysteine). Introduction
Major psychiatric disorders Psychoses & affective disorders
Psychoses Disorders in which patients exhibit gross disturbances in their comprehension of reality as evidenced by false perception (hallucinations), false beliefs (delusions) and loss of contact with reality; schizophrenia most common form of psychosis (+ve n –ve symptoms)
Mostly concerned Abt –ve because poor prognosis , more difficult to treat, persist after positive symptoms have resolved
Mesolimbic Dopamine travels from the midbrain tegmental area to the nucleus accumbens. Increased activity in this pathway may cause delusions, hallucinations, and other so-called positive symptoms of schizophrenia.
Mesocortical pathways Decreased activity in the pathway that goes from the midbrain to the prefrontal lobe cortex can cause apathy, withdrawal, lack of motivation and pleasure, and other so-called negative symptoms of schizophrenia. Mesocortical dysfunction also disinhibits the mesolimbic pathway.
Nigrostriatal pathway from the substantia nigra to the striatum is involved in the coordination of body movements. Inhibition of this pathway causes the extrapyramidal side effects of antipsychotic drugs.
Tuberoinfundibular pathway from the hypothalamus to the pituitary inhibits the release of prolactin. Inhibition of this pathway leads to elevated serum prolactin levels.
2nd generation antipsychotics Clozapine, Risperidone, Olanazapine, Quetiapine, Ziprasidone, Aripiprazole (MOA, Dose, Brand name & A/E and receptor affinities)
Why do 1st gen. antipsychotics cause EPS & 2nd gen. do not? “Hit and run” hypothesis
Inflammation & schizophrenia
New drugs in pipeline Aspirin, Minocycline, Raloxifene, Estrogen, N-acetylcysteine (MOA and rationale of use)
Potential future targets of schizophrenia
Pharmacogenetics and pharmacogenomics is an upcoming branch in therapeutics. Various pharmacogenomic tests are currently available to aid in actual clinical practice. It has shown to have promising results in personalized medicine It is my attempt to compile the basic concepts from various books, articles, and online journals. Please feel free to comment.
Pharmacogenomics: A new age drug technologyMahek Sharan
the pharmacogenomics require the pharmacology and genomic together to improve the drug responses and the new age drug potential according to individual need
This slideshare is about what is autocoid,and differences between harmone and autocoid and had expalined about an example which is an autocoid and also an chemical messenger.and it is also known as happy harmone.
5HT widely distributed in:
GIT enterochromaffin cells (90%)
myenteric plexus where it serves as a prokinetic agent
As a neurotransmitter in CNS
platelets where it diffuses inside from plasma by active transport, and is released at the site of damage after platelet aggregation,
In lungs, bone marrow, pineal gland (as a precursor of melatonin)
5- HT is then stored in 5-HT containing cells such as enterochromaffin cells and neurons as co-transmitter together with various peptide hormones such as somatostatin, vasoactive intestinal peptide and substance P
5-HT is stored within storage vesicles, and its uptake at the vesicular membrane by vesicular monoamine transporter (VMAT-2) is inhibited by reserpine.
Degradation occurs through oxidative deamination by MAO, to 5-hydroxyindole acetaldehyde followed by its oxidation to 5-hydroxyindole acetic acid (5-HIAA)
5- HIAA is excreted in urine
Gaddum and Picarelli (1957) classified 5-HT receptors into musculotropic (D type) and neurotropic (M type) on the basis of their blockade by Dibenzyline (phenoxybenzamine) and Morphine.
5- HT Receptors: there are seven main types (5-HT1, to 5- HT7) of serotonin receptors. Of these, 5-HT1, and 5- HT2, are subdivided further. With a total of 14 (types plus subtypes) receptors.
5-HT Receptors Location:5-HT, receptors are located mainly in CNS. They function as inhibitory presynaptic receptors (auto receptor) and belong to the family of G-protein coupled receptors linked to adenylate cyclase
5-HT1 : Auto receptors; inhibit serotonergic neural activity in brain.
5-HT1A—present in raphe nuclei and hippocampus; buspirone (antianxiety) may act through these receptors.
5-HT1D/1B—Constricts cranial blood vessels and inhibits release of inflammatory neuropeptides in them; sumatriptan (antimigraine) acts through these receptors.
5-HT2A : Previously D type receptor; most important post junctional receptor mediating direct actions of 5-HT like vascular and visceral smooth muscle contraction, platelet aggregation, neuronal activation in brain; ketanserin blocks these receptors.
5-HT3 : Previously M type receptor; depolarizes neurones by gating cation channels; elicits reflex effects of 5-HT—emesis, gut peristalsis, bradycardia, transient hypotension, apnoea, pain, itch; ondansetron (antiemetic) acts by blocking these receptors.
5-HT4 : Mediate intestinal secretion, augmentation of peristalsis. Renzapride (prokinetic) is a selective 5-HT4 agonist.Central Nervous System :5-HT is an important neurotransmitter in CNS
5-HT is involved in the regulation of mood, behaviour, sleep, depression, pain perception, sexual activity, thermoregulation
in the hypothalamic control of the release of pituitary hormones.
a presentation on GABA including its synthesis, storage and degradation, types of receptors, and implications in various neuropsychiatric disorder, and finally a small chart on the drugs acting on GABA system.
Dr. Anjana Thadhani's presentation at Tata Learning Disability Forum (TDLF), 2013.
The Forum for Learning Disabilities centred on the theme ‘Learning Disabilities – a more inclusive perspective’. The forum this year included in its purview three additional Learning Disabilities (LD), namely Specific Learning Disability (SpLD), Attention Deficit Hyperactivity Disorder (ADHD) and Autism Spectrum Disorder (ASD).
In line with the TATA Group’s corporate sustainability endeavors, TIS initiated the Tata Learning Disability Forum (TLDF) in 2006 to ensure that students with special education needs receive the required attention as well as to spread awareness about LD which had been receiving scant attention in India. Since then, via the TLDF platform, TIS has been successful in generating an increased level of awareness and enabling progress in remediation activities for students with LD.
1. WHAT IS GENE THERAPY
2. PRINCIPLE OF GENE THERAPY
3. TYPES OF GENE THERAPY
4. VECTORS IN GENE DELIVERY SYSTEM
5. ROLE OF GENE THERAPY IN CNS DISORDERS
6. GENE THERAPY FOR ALZHEIMERS DISEASE
7. GENE THERAPY FOR AMYOTROPIC LATERAL SCLEROSIS
8. GENE THERAPY FOR STROKE
9. CELL THERAPY FOR CNS DISORDERS
10. CELL THERAPY STRATEGIES
11. CELL THERAPY FOR PARKINSON
12. CELL THERAPY FOR HUNTINGTONS DISEASE
13. CRISPR/CAS9
Recent advances in the treatment of psychosesKarun Kumar
This presentation deals with atypical antipsychotics & new drugs in the pipeline (Clozapine, Risperidone, Olanzapine, Quetiapine, Ziprasidone, Aripiprazole, Second generation antipsychotics, atypical antipsychotics, Aspirin, Minocycline, Raloxifene, Estrogen, N-acetylcysteine). Introduction
Major psychiatric disorders Psychoses & affective disorders
Psychoses Disorders in which patients exhibit gross disturbances in their comprehension of reality as evidenced by false perception (hallucinations), false beliefs (delusions) and loss of contact with reality; schizophrenia most common form of psychosis (+ve n –ve symptoms)
Mostly concerned Abt –ve because poor prognosis , more difficult to treat, persist after positive symptoms have resolved
Mesolimbic Dopamine travels from the midbrain tegmental area to the nucleus accumbens. Increased activity in this pathway may cause delusions, hallucinations, and other so-called positive symptoms of schizophrenia.
Mesocortical pathways Decreased activity in the pathway that goes from the midbrain to the prefrontal lobe cortex can cause apathy, withdrawal, lack of motivation and pleasure, and other so-called negative symptoms of schizophrenia. Mesocortical dysfunction also disinhibits the mesolimbic pathway.
Nigrostriatal pathway from the substantia nigra to the striatum is involved in the coordination of body movements. Inhibition of this pathway causes the extrapyramidal side effects of antipsychotic drugs.
Tuberoinfundibular pathway from the hypothalamus to the pituitary inhibits the release of prolactin. Inhibition of this pathway leads to elevated serum prolactin levels.
2nd generation antipsychotics Clozapine, Risperidone, Olanazapine, Quetiapine, Ziprasidone, Aripiprazole (MOA, Dose, Brand name & A/E and receptor affinities)
Why do 1st gen. antipsychotics cause EPS & 2nd gen. do not? “Hit and run” hypothesis
Inflammation & schizophrenia
New drugs in pipeline Aspirin, Minocycline, Raloxifene, Estrogen, N-acetylcysteine (MOA and rationale of use)
Potential future targets of schizophrenia
Pharmacogenetics and pharmacogenomics is an upcoming branch in therapeutics. Various pharmacogenomic tests are currently available to aid in actual clinical practice. It has shown to have promising results in personalized medicine It is my attempt to compile the basic concepts from various books, articles, and online journals. Please feel free to comment.
Pharmacogenomics: A new age drug technologyMahek Sharan
the pharmacogenomics require the pharmacology and genomic together to improve the drug responses and the new age drug potential according to individual need
This slideshare is about what is autocoid,and differences between harmone and autocoid and had expalined about an example which is an autocoid and also an chemical messenger.and it is also known as happy harmone.
5HT widely distributed in:
GIT enterochromaffin cells (90%)
myenteric plexus where it serves as a prokinetic agent
As a neurotransmitter in CNS
platelets where it diffuses inside from plasma by active transport, and is released at the site of damage after platelet aggregation,
In lungs, bone marrow, pineal gland (as a precursor of melatonin)
5- HT is then stored in 5-HT containing cells such as enterochromaffin cells and neurons as co-transmitter together with various peptide hormones such as somatostatin, vasoactive intestinal peptide and substance P
5-HT is stored within storage vesicles, and its uptake at the vesicular membrane by vesicular monoamine transporter (VMAT-2) is inhibited by reserpine.
Degradation occurs through oxidative deamination by MAO, to 5-hydroxyindole acetaldehyde followed by its oxidation to 5-hydroxyindole acetic acid (5-HIAA)
5- HIAA is excreted in urine
Gaddum and Picarelli (1957) classified 5-HT receptors into musculotropic (D type) and neurotropic (M type) on the basis of their blockade by Dibenzyline (phenoxybenzamine) and Morphine.
5- HT Receptors: there are seven main types (5-HT1, to 5- HT7) of serotonin receptors. Of these, 5-HT1, and 5- HT2, are subdivided further. With a total of 14 (types plus subtypes) receptors.
5-HT Receptors Location:5-HT, receptors are located mainly in CNS. They function as inhibitory presynaptic receptors (auto receptor) and belong to the family of G-protein coupled receptors linked to adenylate cyclase
5-HT1 : Auto receptors; inhibit serotonergic neural activity in brain.
5-HT1A—present in raphe nuclei and hippocampus; buspirone (antianxiety) may act through these receptors.
5-HT1D/1B—Constricts cranial blood vessels and inhibits release of inflammatory neuropeptides in them; sumatriptan (antimigraine) acts through these receptors.
5-HT2A : Previously D type receptor; most important post junctional receptor mediating direct actions of 5-HT like vascular and visceral smooth muscle contraction, platelet aggregation, neuronal activation in brain; ketanserin blocks these receptors.
5-HT3 : Previously M type receptor; depolarizes neurones by gating cation channels; elicits reflex effects of 5-HT—emesis, gut peristalsis, bradycardia, transient hypotension, apnoea, pain, itch; ondansetron (antiemetic) acts by blocking these receptors.
5-HT4 : Mediate intestinal secretion, augmentation of peristalsis. Renzapride (prokinetic) is a selective 5-HT4 agonist.Central Nervous System :5-HT is an important neurotransmitter in CNS
5-HT is involved in the regulation of mood, behaviour, sleep, depression, pain perception, sexual activity, thermoregulation
in the hypothalamic control of the release of pituitary hormones.
a presentation on GABA including its synthesis, storage and degradation, types of receptors, and implications in various neuropsychiatric disorder, and finally a small chart on the drugs acting on GABA system.
Dr. Anjana Thadhani's presentation at Tata Learning Disability Forum (TDLF), 2013.
The Forum for Learning Disabilities centred on the theme ‘Learning Disabilities – a more inclusive perspective’. The forum this year included in its purview three additional Learning Disabilities (LD), namely Specific Learning Disability (SpLD), Attention Deficit Hyperactivity Disorder (ADHD) and Autism Spectrum Disorder (ASD).
In line with the TATA Group’s corporate sustainability endeavors, TIS initiated the Tata Learning Disability Forum (TLDF) in 2006 to ensure that students with special education needs receive the required attention as well as to spread awareness about LD which had been receiving scant attention in India. Since then, via the TLDF platform, TIS has been successful in generating an increased level of awareness and enabling progress in remediation activities for students with LD.
هذا العرض هو عبارة عن ملخص لبحث عن انواع الصعوبات التعلمية , حيث فيه القيت الضوء انا ومجموعة من زملائي على صعوبة الديسليكسيا من كل النواحي,وذلك في احدى مقررات ماجستير التربية المختصة ,في كلية التربية الفصل الاول ,اضعه بين ايديكم على امل ان يقدم لكل من يهتم بالاطفال وبموضوع الصعوبات التعلمية الفائدة
This is a set of powerpoint slides with self-assessment questions interspersed throuought on drug metabolism and pharmacogenetics. The aim is to understand the mechanism of clinically significant drug interactions, recognize potentially clinically significant genetic influences on drug efficacy and toxicity, and genetic predispositions to disease due to altered drug metabolism or transport. This resource is appropriate for medical students or graduate healthcare professionals such as nursing students.
pharmacogenomics helps to improve healthcare sector by providing information about variability among genes for a particular class of drug hence reduces adverse drug reactions.
Personalized medicine involves the prescription of specific therapeutics best suited for an individual based on their genetic or proteomic profile. This talk discusses current approaches in drug discovery/development, the role of genetics in drug metabolism, and lawful/ethical issues surrounding the deployment of new health technology. I highlight some bioinformatic roles in the drug discovery process, and discuss the use of semantic web technologies for data integration and knowledge discovery..
INTRODUCTION
What is pharmacogenomics
History
Principle
So what’s new about pharmacogenomics?
single nucleotide polymorphism (SNP)?
Genes commonly involved in pharmacogenomic drug metabolism and response
The anticipated benefits of pharmacogenomics
Pharmacogenetics Research/Database Program
Some of the barriers to using pharmacogenomics
Conclusion
References
pharmacogenomics is a new drug discovry approach. It is the study of how genes affect a person's response to drugs, combining pharmacology and genomics
Similar to Pharmacogenetics of antipsychotic and antidepressent (20)
General psychiatry arabic 2020 كتاب الطب النفسي العام 2020ismail sadek
تم اعداد هذا الكتاب بمختصر للتدريس مادة الطب النفسي لطلبة الكليات منها كلية طب وكلية اداب قسم علم نفس وللاستعانة به وتم الاستعانة بالمزيد من المصادر العربية والاجنبية
دكتور اسماعيل صادق
Normal and abnormal behavioural sexual development in childhood & adolesc...ismail sadek
sexual behaviour in children has marked interest to both family and professional health care team what is normal, when to take care and when to need intervention
doctor patient relationship العلاقة العلاجية arabic & englishismail sadek
doctor patient relationship is a critical relation that need specific measure and qualities to proceed in treatment plan
العلاقة العلاجية من أهم العلاقات البشرية التي تعتبر من اخطرها حيث أن لها هدف هام وهو استمرار وتنفيذ الخطة العلاجية والتى تحتاجلقواعد وضوابط لتحكم هذه العلاقة فى اتجاهها السليم
كل انسان يفعل شيئ ما ولكن يبقي السؤال لمذا نفعل ذلك؟ بل ولماذا يختلف الناس فيما يفعلون؟ وعندما نقول اننا مجهدين ولا نستطيع العمل هل نحن مجهدين فعلا ام ليس لدينا دافع لفعل هذا العمل
Psychotherapy the biological dimensionismail sadek
is it real word can affect your brain?
many people say not and don't believe that the psychotherapy change not only our behavior but also it can change the brain structure
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
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Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
2. Determine the sequence of the 3 billion nucleotides that
make up human DNA
Characterize variability in the genome
Identify all the genes in human DNA
The Era of Genomic Medicine:
Improve prediction of drug efficacy or toxicity
Improve the diagnosis of disease
Earlier detection of genetic predisposition to disease
3. DNA
A, T, G, C
Codon
Gene
Chromosome
Genome
ENGLISH
Abcdefg….xyz
Word
Sentence
Chapter
Book
5. Age
Race/ethnicity
Weight
Gender
Concomitant Diseases
Concomitant Drugs
Social factors
GENETICS
PERSONALIZED
MEDICINE
6. Pharmacogenetics
Study of how genetic differences in a SINGLE
gene influence variability in drug response (i.e.,
efficacy and toxicity)
Pharmacogenomics
Study of how genetic (genome) differences in
MULTIPLE genes influence variability in drug
response (i.e., efficacy and toxicity)
7. Hypothesis
Variability in response, toxicity and adverse effects
following drug treatment is influenced by genetic
variation
Advantages
Genotyping can be done any time
Not influenced by current treatment
Can be measured very reliably
Genome fully sequenced
Easy to do – peripheral blood sample
9. Maximize drug efficacy
Minimize drug toxicity
Predict patients who will respond to intervention
Aid in new drug development
10. Mutation: difference in the DNA code that
occurs in less than 1% of population
Often associated with rare diseases
Cystic fibrosis, sickle cell anemia, Huntington’s
disease
Polymorphism: difference in the DNA code
that occurs in more than 1% of the population
A single polymorphism is less likely to be the
main cause of a disease
Polymorphisms often have no visible clinical
impact
11. Pronounced “snip”
Single base pair difference in the DNA sequence
Over 2 million SNPs in the human genome
Other polymorphisms:
Insertion/deletion polymorphisms
Gene duplications
Gene deletions
12. Alleles = different DNA
sequences at a locus
Codon 389 1-AR
Arg (0.75)
Gly (0.25)
Genotype = pair of alleles a
person has at a region of the
chromosome
Codon 389 1-AR
Arg389Arg
Arg389Gly
Gly389Gly
14. Evidence of an inherited basis for drug response
dates back in the literature to the 1950s
Succinylcholine: 1 in 3000 patients developed
prolonged muscle relaxation
Monogenic
Phenotype to genotype approach
15. CYP2D6 is responsible for the metabolism of a number of different
drugs
Antidepressants, antipsychotics, analgesics, cardiovascular drugs
Over 100 polymorphisms in CYP2D6 have been identified
Based on these polymorphisms, patients are phenotypically
classified as:
Ultrarapid metabolizers (UMs)
Extensive metabolizers (EMs)
Poor metabolizers (PMs)
16. Increased rate of adverse effects in poor metabolizers due to
increased plasma concentrations of drug:
Fluoxetine (Prozac) death in child attributed to CYP2D6 poor
metabolizer genotype
Side effects of antipsychotic drugs occur more frequently in
CYP2D6 poor metabolizers
CYP2D6 poor metabolizers with severe mental illness had more
adverse drug reactions, increased cost of care, and longer hospital
stays
17. Treatment of attention deficit hyperactivity disorder
CYP2D6 poor metabolizers have 10-fold higher
plasma concentrations to a given dose of
STRATTERA compared with extensive metabolizers
Approximately 7% of Caucasians are poor
metabolizers
Higher blood levels in poor metabolizers may lead to
a higher rate of some adverse effects of STRATTERA
18.
19. The Roche AmpliChip CYP450 Test is intended to identify a patient's
CYP2D6 and CYP2C19 genotype from genomic DNA extracted from a
whole blood sample.
Information about CYP2D6 and CYP2C19 genotype may be used
as an aid to clinicians in determining therapeutic strategy and treatment
dose for therapeutics that are metabolized by the CYP2D6 or CYP2C19
gene product.
20.
21. Direct protein target of drug
Receptor
Enzyme
Proteins involved in pharmacologic response
Signal transduction proteins or downstream proteins
Polymorphisms associated with
disease risk
“Disease-modifying” polymorphisms
“Treatment-modifying” polymorphisms
POLYGENIC
22.
23. Depression—Symptom rating scales
Indirect measure of drug response
Inter-rater reliability
Hypertension—Blood pressure
Minute to minute and diurnal variability
Influence of environmental factors (e.g. lack of rest before
measurement)
Diabetes—Blood glucose
Diurnal variation in blood glucose
Influence of environmental factors (e.g. diet/exercise)
24. It required a shift in clinician attitude and beliefs “not one
dose fits all”
Paucity of studies demonstrating improved clinical benefit from
use of pharmacogenomic data
Still much to be learned
Even some of the black block warnings currently on
drug labels may be overcalls of importance
Genome wide interrogation will likely be important to get the
entire picture
25. Larry Lesko, Director of the FDA Office of Clinical
Pharmacology and Biopharmaceutics
26.
27. Despite the enormous progress made in the understanding of
the neurobiology of MDD, treatment outcomes have improved
only slightly in the past few decades in spite of the broadening
of the target spectrum of antidepressants (ADs).
The recent Sequence Treatment Alternatives to Relieve
Depression (STAR*D) study indicate that even with systematic
measurement-based treatment, only approximately 50% of
patients show response to treatment after one treatment trial,
and only 30% of patients reach full remission.
28. There is a significant decrease in remission rate after two
failed trials, with only 60% reaching full remission after
four treatment trials
The long duration required to conclude treatment success
or failure (eight to twelve weeks) can prove to be a
difficult and frustrating experience for the patient and the
family and may even increase the risk of suicide,
29. Besides failure to reach remission, relapse rate is
also over 40%, especially in patients who did not
achieve full remission.
Treatment resistant depression (TRD) is an
extremely common problem, affecting a large
proportion of all patients suffering from major
depressive episodes
30. Since genetic factors contribute for about 50% of the
Adverse response, pharmacogenetic researchers have
assumed that in order to minimize disorder duration
and re-duce the occurrence of Adverse response it
would be useful to be able to predict the
pharmacological intervention likely to be effective and
tolerable for each patient according to the patient’s
specific genetic makeup.
31.
32. The cytochrome P450s (CYPs) are members of a
superfamily of oxidative enzymes, and act as the major
system for phase I oxidative metabolism of approximately
80% of the commonly used therapeu-tic substances
This important endogenous system has received the most
attention by pharmacogenetic researchers, leading to the
discovery of 58 different human CYP genes with various
polymorphisms that affect drug metabolism
33. The variations of DNA within the coding genes may
contribute to excessive metabolism as well as diminished
or absent metabolism of a drug, leading to the prolonged
presence of a toxic dose or failure to reach therapeutic
dose of the given medication.
The clinically most important isoenzymes of he-patic
CYPs, regarding AD metabolism, are CYP1A2, CYPC9/19,
CYP2D6, CYP3A4 and CYP2B6
34. The majority of ADs (fluoxetine; fluvoxamine; paroxetine;
venlafaxine; mirtazapine; amitriptyline; imipramine;
trimipramine; desipramine; nortriptyline) are metabolized
primarily by CYP2D6
35. CYP2D6 is the most researched gene in the field of
pharmacogenetics, and more than 100 different alleles
were identified which determine the level of activity of the
enzyme
According to the number of gene copies inherited,
individuals are classified as :
poor (PM),
intermediate (IM),
extensive (EM), or
ultrarapid metabolizers (UM).
36. A gene x environment effect has been shown
concerning the CYP1A2 izoenzyme, in which the
presence of an exogenous inducer, tobacco smoke
affects transcription and translation and may
contribute to an UM phenotype, resulting in an up to
50% reduction in plasma concentration of Ads
Some CYP1A2 polymorphisms (rs4646425;
rs2472304; rs2470890) may also influence treatment
response to paroxetine
37. P-glycoprotein (P-gp) is a member of the ATP-binding
cassette superfamily of membrane transport proteins
encoded by the ABCB1 gene also known as the multidrug
resistance protein 1 (MDR1) gene.
P-glyco-protein 1 is found in various human tissues,
including the endothelial cells of the blood-brain barrier
(BBB) and is responsible for the efflux of many exogenous
and endogenous substances against a concentration
gradient influencing antidepressant concentrations in the
brain as well.
38.
39. Monoamine transporters Serotonin
Transporter (SLC6A4) The human serotonin
transporter (5-HTT) gene is potentially
involved in mood regulation and the great
majority of currently used ADs influences the
activity of 5-HTT, making it an ideal
candidate for pharmacogenetic studies.
40. A 44-bp insertion/deletion poly-morphism with 2 allelic
forms within the serotonin transporter gene promoter region
(5-HTTLPR) that could affect SLC6A4 expression was shown
to have functional significance with the long allele (l)
associated with two times higher 5-HTT expression in the
basal state compared to the s allele according to in vitro
studies
Caucasian subjects report that presence of the s allele is
associated with lower response and remission
41. According to the results of a recent GWAS study
cer-tain genetic variations of the noradrenalin
transporter may be associated with the risk of
MDD. In addition, the noradrenalin transporter is
the principal site of action of some ADs
42. It is assumed that dopaminergic mechanisms play an
important role in AD drug action, since AD drugs, in particular
dopamine/norepinephrine reuptake inhibitor bupropion and
specific members of SSRIs (mainly sertraline) modulate
activity of the dopamine transporter.
A 40-base pair VNTR polymorphism in the SLC6A3 gene,
encoding for the dopamine transporter (DAT) has been
associated with expression levels of the transporter.
43. Tryptophan hydroxylase
The tryptophan hydroxylase (TPH) gene encoding
the rate-limiting enzyme in serotonin synthesis has
been studied intensively in psychiatric disorders,
yielding mixed results.
44. The COMT enzyme is responsible for the inactiva-
tion of various catecholamines including dopamine,
adrenalin and noradrenalin.
The COMT gene has several allelic variants,
including the most extensively studied rs4680
variant.
A functional G to A SNP at codon 158 leading to a
Val to Met substitution was identified contributing
to a high activity Val/Val, intermediate activity
Val/Met, low activity in Met/Met genotype
45. MAO-A is one of the enzymes responsible for the
degradation of monoamine neurotransmitters. One
polymorphism in the promoter region of the MAO-A gene
consisting of a repetitive sequence (VNTR) has been
linked to variations in the biological activity and
consequentially serotonin concentrations.
Variants with 3.5 or 4 copies of the repeat sequence
(“MAO-A High”) are expressed 2-10 times more efficiently
than those with 2, 3 or 5 copies of the repeat
46. Monoamine receptors are among the most
plausible candidates for modulation of AD
response, since most ADs act to increase
monoamine concentration in the synaptic
cleft.
47. About 50 known SNPs have been described regarding
the 5-HT1A autoreceptor. One of the most intensively
investigated functional polymorphism (rs6295; a.k.a.
1019C/G) is in the promoter region of the gene for 5-
HT1A receptor (Stahl, 1994). The majority of results
suggests an effect of the rs6295 on treatment outcome
with several classes of ADs,
48. Three important common SNPs of the 5HTR2A gene are
102T/C (rs6313), 1438A/G (rs6311) and 452His/Tyr (rs6314).
Overall, several studies have found that rs6313, rs6311 and
rs6314 SNPs are associated with response to AD treatment,
Another genetic variant of the 5HTR2A gene (rs7997012) is
also associated with success of AD treatment.
49. According to our current knowledge, among the
different adrenergic receptor subtypes, the β1 and
α2a receptors seem to play a role in response to AD
treatment
A recently identified functional polymorphism
G(1165)C (a.k.a. rs1801253) in the ADRβ1 gene
(encoding adrenergic β1 receptor), resulting in the
amino acid variation Gly389Arg, has been linked to
enhanced coupling to the stimulatory Gs protein and
increased adenylate cyclase activation. This SNP might
be responsible for faster response to AD treatment
50. G Protein β3 subunit
The β3 subunit of the G protein is present in all cells of the body
and has a key role in the downstream signaling cascade
following monoamine receptor activation.
The C825T (a.k.a. rs5443) functional polymorphism is the
most investigated variant within the GNβ3 gene in this field. It
was associated with AD treatment response; particularly the T
variant seems to predict better AD response.
51. CRH Receptors (CRHR1 and CRHR2)
Corticotropin releasing hormone (CRH) is a potent mediator
of endocrine, autonomic, behavioral, and immune
responses to stress.
An association between the rs242941 G/G geno-type and
homozygous GAG haplotype of the 3 SNPs (rs1876828,
rs242939, and rs242941) and therapeutic response to
fluoxetine
Another study did not find associations between some
other variants of CRHR1 gene (rs110402; rs242937) and
treatment response to citalopram
52. The GENDEP study identified three SNPs
(rs852977, rs10482633 and rs10052957) which
may predict response to both ADs used in the
study (nortriptyline and escitalopram)
53. Despite of expectations fuelled by the role of CREB in the
pathogenesis of depression, the role of CREB1 variants in
AD response was not verified .
Furthermore, two SNPs (rs4675690; rs7569963) were
found to have a role in treatment-emergent suicidal
ideation in patients with MDD during citalopram
treatment, but only in males, suggesting a significant
gene x sex interaction
54. Chronic stress leads to decreased levels of BDNF
in the brain, and serum/plasma BDNF levels of
patients with mood disorders are decreased.
55. Results of the GENDEP study have raised the possibility
that that there is an association between rs10835210
variation in the BDNF gene and response to escitalopram
and a strong association between rs962369 in the BDNF
gene and an increase in suicidal ideation during AD
treatment (the same study identified some other
suicidality related regions in the BDNF gene
56. According to results of the STAR*D study an SNP
(rs1954787) of the GRIK4 gene encoding kainate
receptor subunit 1 (KA1; a.k.a. GluK4) was
associated with treatment response to citalopram
57. Despite the impressive potential of pharmacogenetics and
the great progress in the understanding of the
pathomechanism of MDD and the genetic influence both
on emergence of depression and on response to AD
treatment, the use of pharmacogenetics in current clinical
practice is still very limited,
58. in part due to inconsistent results and failure to replicate
several associations.
Another problematic issue is the complexity and
ultifactorial nature of the genetics underlying psychiatric
disorders and medication response. Since the therapeutic
mechanism of ADs is not well understood, it is difficult for
pharmacogenetic researchers to select “candidate” genes.
59.
60. Since chlorpromazine was first introduced into
clinical psychiatry, various kinds of
antipsychotics have been developed and used
for schizophrenia.
Clinicians, however, still have considerable
difficulty in choosing an appropriate
antipsychotic for certain patients due to the
inter-individual diversities of drug response.
61. Most antipsychotics are extensively metabolized by
cytochrome (CYP) P450s that are members of a
super-family of oxidative enzymes and that
constitute a major system for the oxida-tive
metabolism of therapeutic substances.
62. The CYP2D6 has been most extensively
investigated in the field of psychiatry, since
this enzyme is involved in the metabolism
of many antipsychotics and has many
genetic polymorphisms that influence the
function of the enzyme.
63. There are more than 70 variant alleles at
the CYP2D6 gene locus, including the two
most common variants, CYP2D6*4 and
CYP2D6*45, encoding non-functional
products.1 Other variants that reduce
activity, alter substrate specificity or
increase activity have also been described
64. Compared with efficient metabolizers (EM), poor
metabolizers (PM) show no or reduced CYP2D6
activity bypolymorphisms resulting in potentially
increased concentrations of metabolized drugs.
65. On the other hand, ultra rapid metabolizers
(UM) that can be found in 1% of Caucasians
often do not reach therapeutic concentrations
and require an increased dose. Pronounced
ethnic differences in the prevalence of both PM
and UM have been reported; e.g., the frequency
of PM is 5 to 10% among Caucasians, about 2%
in Asians, and 7–8% in Africans.
66. PMs have higher plasma concentrations of and suffer more
adverse effects from antipsychotics. The incidence of the
acute side effects of these drugs, including postural hy-
potension, excess sedation, or extrapyramidal symptoms, is
disproportionately in PMs.
On the other hand, it is not clear whether the development
of chronic side effects such as tardive dyskinesia is
associated with a reduced metabolizing capacity of CYP2D6.
67.
68. All receptor and transporter genes for
neurotransmitters as well as genes located down-
stream of the intracellular signaling pathways
can be considered candidate genes for the
pharmacodynamics of antipsychotics.
It is difficult to select a good candidate gene,
since the true mechanism of therapeutic action of
antipsychotics has not been clarified yet.
69. genetic polymorphisms in serotonin (5-HT)
and dopamine (DA) systems have been
extensively investigated in the
pharmacodynamics of antipsychotics
70. The first candidate gene examined with regard to
clozapine response was the DA4 receptor gene
(DRD4) because in addition to its high affinity for
clozapine, the DA4 receptor is abundant in the
prefrontal cortex, (a brain region thought to be
related to the cognitive dysfunction of schizophrenia),
and the DRD4 gene itself is highly polymorphic.
71. Among polymorphisms in the DRD4, the 48 bp
variable number of tandem repeats (VNTR) has
been the most extensively investigated, since the
VNTR was shown an in vitro study to influence
the sodium chloride sensitivity of clozapine-
binding and inhibition of c-AMP synthesis.
72. The DA3 receptor, which shares homologies with both
the DA4 and DA2 receptors, has generated interest,
since the DA3 receptor gene (DRDA3) has a known
functional polymorphism,Ser9Gly, that influences
dopamine binding. However, the association between
the Ser9Gly and clozapine response remains
controversial.
73. The DA2 receptor is a major site of the action of conventional
antipsychotics such as chlorpromazine and haloperidol, and of
some atypical antipsychotics such as risperidone. One
functional polymorphism (-141 Ins/Del) in the promoter
region, as well as missense variants including Ser311Cer and
an intronic variant (Taq 1 A), have been identified in the DA2
receptor gene (DRD2).
74. The -141 Ins/Del polymorphism that influences
the expression of the DRD2 was reported to be
associated with anxiolytic and antidepressive
effects during treatment with two conventional
antipsychotics,
75. Although theSer311Cer was shown to influence c-
AMP synthesis, it has not been associated with
clozapine or with a typical antipsychotic response.
The Taq 1A that is located in the intron of DRD2
and has been reported to influence the density of
the receptor was shown to have an association
with the acute effects of a selective DA2 receptor
antagonist, nemonapride, and haloperidol.
76. The 5-HT receptor genes have been regarded as
good candidates for pharmacodynamic stud-ies of
antipsychotics, since 5-HT mediated mechanisms
seem crucial to atypical antipsychotic drug action,
including that of clozapine.
77. An association between the silent polymorphism
102T/C in the 5-HT2A receptor gene (HTR2A) and
clozapine has been reported.
Hys452Tyr12 was shown to influence the
intracellular signal transduction of the 5-HT2A
receptor, as measured by Ca2+ mobilization
induced by 5-HT stimulation.
78. In addition to the 5-HT2A receptor, other 5-HT receptors,
such as 5-HT 2C and 5-HT 6, have also been investigated in
psychopharmacognetic studies because atypical
antipsychotics also have high affinity for these receptors.
The Ser23 in the 5-HT2C receptor gene influences m-
chlorophenylpiperazine (m-CPP), a nonse-lective5-HT2C
agonist, binding, in comparison with Cys23. Therefore, the
Ser23 may be consti-tutively more active and tends to be
more desensitized.
79. Not just one gene but multiple genes play a role in
complex phenotypes, including the clini-cal response to
medication. Arranz et al. published the most
comprehensive study to date of a pharmacogenetics
screening strategy: a combination of 6 out of 19
candidate gene variants (in 5-HT2A, 2C, 5-HT transporter
and Histamin 2 receptor genes) predicted response to
clozapine with a prediction level of 76.9%
80. Interindividual Variability in Clozapine
Pharmacokinetics and Response: A Focus on
Cytochrome P450-1A2 (CYP1A2)-Mediated Enzyme
Metabolism
81.
82. Clinicians almost always initiate antipsychotic drugs in
schizophrenia “a priori” . However, this may lead to ineffective
treatment, to the use of an additional antipsychotic or multiple
antipsychotics, to different adverse effects, and result in
increased morbidity and mortality.
This represents a real concern and calls for accurate scientific
methods that could be used to predict a reasonable
therapeutic response and also drug-induced side effects.
83. Personalized prescription or “tailoring drugs to a patient’s
genetic makeup” would be more than beneficial (de Leon
2009b). In the context of personalized prescription,
clinicians need to consider environmental, personal and
genetic variables when prescribing any medication.
According to de Leon, personalized prescription in the
clinical practice may be described as personalized
selection of the drug and as personalized dosing
84. In personalized dosing the knowledge of
pharmacodynamic and pharmacokinetic dosing
properties should be applied.
85. At the present, in psychiatry there are five
pharmacogenomic tests that are currently
available on the market or are ready to be
introduced.
However, three of the five tests have not published
complete details concerning the genes used in
them
86. CYP 450 Test employs microarray technology for cytochrome
P450 (CYP) 2D6 and CYP 2C19 genotyping (de Leon et al.
2009c).
Genomic DNA is extracted from a whole-blood sample to
identify 27 alleles in CYP2D6 that are associated with four
CYP2D6 phenotypes, and to identify three alleles in CYP2C19
that are associated with two CYP2C19 phenotypes (de Leon
et al. 2009c).
The genotypes are then translated with software algorithms
into a predicted phenotype, which is indicative of the
CYP2D6 and CYP2C19 enzymatic activity.
87. One company offers a genetic test for the
determination of high (1,5%) or low (0,5%) risk of
drug-induced agranulocytosis.
The test can make a valuable prediction in the
treatment with clozapine, but does not obviate the
need for regular monitoring and has not a
significant impact on routine practice.
88. A new system, called PhyzioType System uses an
ensemble of DNA markers from several genes to
predict an individual’s risk of developing some
adverse drug reactions. The clinical applica-bility
of this array is still under investigation.
A recent study describes an array containing
probes to identify genetic variants for the risk of
hyperlipidemia.
89. PhyzioType System uses
Arranz et al. tried to combine genetic
information on the prediction of response to
clozapine. The prediction level in British
Caucasian patients on long-term treatment
was 76%, but the results were not replicated
in German cohort.