This presentation will:
- Review the concept of ‘fetal programming’
- Demonstrate that early life nutritional events may serve as molecular memory of individual in utero experiences
- Show how changes persist following multiple rounds of cell division
- Highlight extrinsic (recapitulation) & Intrinsic (genetic) mechanisms that strongly suggest Intergenerational transmission of traits via epigenetics in humans
- Look at how to best move forward as a scientific and clinical community
This presentation on Epigenetics is most advanced and evidence based one. Its Very helpful for Genetics students and research fellows, Reproductive Medicine specialist, Reproductive Biologist, Infertility practitioners
"Epigenetics refers to genetic factors that change an organism’s appearance or biological functions without changing the actual DNA sequence. In other words, gene expression changes but the genes themselves don’t. Epigenetics adds an additional level of complexity to the genetic code." - Public Health Cafe
Short intro epigenetics & nutrigenomics& the early impact of nutrition Norwich Research Park
Our “genes” are not fixed: “Plasticity” of the genotype by epigenetic mechanisms => important for the phenotypic impact of nutrition.
• Histone and DNA modifications have impact on gene transcription efficiency. Methylation (more stable) and acetylation (more flexible) have impact on chromatin
structures.
• Epigenetic modifications have impact on offspring, embryo development, ageing and disease development or prevention => example: Dutch Hunger Winter.
Health status of future parents are very important for the future health of children.
Early healthy nutrition & lifestyle essential for successful healthy life & “ageing”.
This presentation on Epigenetics is most advanced and evidence based one. Its Very helpful for Genetics students and research fellows, Reproductive Medicine specialist, Reproductive Biologist, Infertility practitioners
"Epigenetics refers to genetic factors that change an organism’s appearance or biological functions without changing the actual DNA sequence. In other words, gene expression changes but the genes themselves don’t. Epigenetics adds an additional level of complexity to the genetic code." - Public Health Cafe
Short intro epigenetics & nutrigenomics& the early impact of nutrition Norwich Research Park
Our “genes” are not fixed: “Plasticity” of the genotype by epigenetic mechanisms => important for the phenotypic impact of nutrition.
• Histone and DNA modifications have impact on gene transcription efficiency. Methylation (more stable) and acetylation (more flexible) have impact on chromatin
structures.
• Epigenetic modifications have impact on offspring, embryo development, ageing and disease development or prevention => example: Dutch Hunger Winter.
Health status of future parents are very important for the future health of children.
Early healthy nutrition & lifestyle essential for successful healthy life & “ageing”.
Overview of epigenetics and its role in diseaseGarry D. Lasaga
Epigenetics is the study of heritable changes in gene expression (active versus inactive genes) that do not involve changes to the underlying DNA sequence — a change in phenotype without a change in genotype — which in turn affects how cells read the genes.
A mitochondrion (singular of mitochondria) is part of every cell in the body that contains genetic material.
Mitochondria are responsible for processing oxygen and converting substances from the foods we eat into energy for essential cell functions.
The mitochondria of the zygote come from the oocyte, that is, from the mother and almost never from the sperm, form of transmission is called maternal inheritance
Which mitochondrial gene is mutated.
The extent of replicative segregation of the mutant mitochondrial genome during the early stages of embryonic development.
The abundance of the mutant mitochondrial gene in a particular tissue.
The threshold level of mutant mitochondrial DNA required in a tissue before an abnormality is evident clinically
Mitochondrial disease affects tissues most highly dependent on ATP production
*Nerves
*Muscles
Endocrine
Kidney
Low energy-requiring tissues are rarely directly affected, but may be secondarily
Lung
Connective tissue
Symptoms can be intermittent
Increased energy demand (illness, exercise)
Decreased energy supply (fasting)
Common feature
myoclonus epilepsy, deafness, blindness, anemia, diabetes, seizures and loss of cerebral blood supply (stroke).
Myoclonic epilepsy and ragged-red fiber disease (MERRF)
MERRF is a member of a group of disorders called mitochondrial encephalomyopathies that feature mitochondrial defects with altered brain and muscle functions.
The term “ragged red fibers” refers to large clumps of abnormal mitochondria that accumulate mostly in muscle cells and are stained red by a dye that is specific for complex II of the electron transport chain.
rare, maternally inherited, heteroplasmic, (point mutation in tRNA lysine gene)
Mutation is MTTK*MERRF8344G.
MT means mitochondrial gene is mutated
T means transfer RNA gene
K means the single-letter amino acid designation for lysine
MERRF means the clinical features
8344G means the mutant nucleotide is guanine (G) at nucleotide position 8344
If 90% of the mitochondria in nerve and muscle cells carry the MTTK*MERRF8344G mutation, then the defining symptoms of MERRF are present.
Maternally inherited mitochondrial disease
The MTTL1*MELAS3243G mutation accounts for more than 80% of the cases of MELAS.
This base substitution is in one of the two mitochondrial transfer RNALeu genes.
the A3243G mutation occurs in thetRNALeu(UUR) gene
When this mutation is present in ≥90% of the mitochondrial DNA of muscle tissue, there is an increased likelihood of recurrent strokes, dementia, epilepsy, and ataxia.
When heteroplasmy for the A3243G mutation
is ~40% to 50%, chronic progressive external ophthalmoplegia (CPEO), myopathy, and deafness are likely to occur.
Other MELAS mutations occur at sites 3252, 3271, and 3291 within the tRNALeu(UUR) gene and in the mitochondrial tRNAVal (MTTV) and COX III (MTCO3) genes.
Reduced activities in Complexes I and IV are established
“Inheritance” in images, from Darwin’s “tree of life” to DNA’s iconic crystallography to the epigenetic dynamicsHowever, the script needs to be interpreted and receives meaning only from the interplay with the environment
Epigenetics is the study, in the field of genetics, of cellular and physiological phenotypic trait variations that are caused by external or environmental factors that switch genes on and off and affect how cells read genes instead of being caused by changes in the DNA sequence. -Wikipedia
The epigenetic regulation of DNA-templated processes has been intensely studied over the last 15
years. DNA methylation, histone modification, nucleosome remodeling, and RNA-mediated targeting regulate many biological processes that are fundamental to the genesis of cancer. Here, we
present the basic principles behind these epigenetic pathways and highlight the evidence suggesting that their misregulation can culminate in cancer. This information, along with the promising clinical and preclinical results seen with epigenetic drugs against chromatin regulators, signifies that it
is time to embrace the central role of epigenetics in cancer.
Epigenetics definition, history of epigenetics, molecular basis of epigenetics, epigenetic modification, tools to study epigenetics, disease linked with epigenetics, DNA methylation demethylation and enzymes regulating DNA methylation
Genomics, Transcriptomics, Proteomics, Metabolomics - Basic concepts for clin...Prasenjit Mitra
This set of slides gives an overview regarding the various omics technologies available and how they can be used for improvement in clinical setting or research
Epigenomics: Emerging Opportunities in Biomarkers, Diagnostics and TherapeuticsReportLinker.com
THIS REPORT:Provides a comprehensive overview of the global market for epigenomicsDescribes the major epigenomics technologies impacting the market today and emerging opportunities in biomarkers, diagnostics and therapeuticsContains global market forecasts for epigenomics, with trends and forecasts for growth through 2014Offers a focus on particular applications of epigenomics, including research tools, diagnostics, drugs and cloning/tissue engineeringDiscusses industry structure including, mergers and acquisitions, distribution of products, government regulation and industry trendsProfiles the most competitive businesses in the industry.
Overview of epigenetics and its role in diseaseGarry D. Lasaga
Epigenetics is the study of heritable changes in gene expression (active versus inactive genes) that do not involve changes to the underlying DNA sequence — a change in phenotype without a change in genotype — which in turn affects how cells read the genes.
A mitochondrion (singular of mitochondria) is part of every cell in the body that contains genetic material.
Mitochondria are responsible for processing oxygen and converting substances from the foods we eat into energy for essential cell functions.
The mitochondria of the zygote come from the oocyte, that is, from the mother and almost never from the sperm, form of transmission is called maternal inheritance
Which mitochondrial gene is mutated.
The extent of replicative segregation of the mutant mitochondrial genome during the early stages of embryonic development.
The abundance of the mutant mitochondrial gene in a particular tissue.
The threshold level of mutant mitochondrial DNA required in a tissue before an abnormality is evident clinically
Mitochondrial disease affects tissues most highly dependent on ATP production
*Nerves
*Muscles
Endocrine
Kidney
Low energy-requiring tissues are rarely directly affected, but may be secondarily
Lung
Connective tissue
Symptoms can be intermittent
Increased energy demand (illness, exercise)
Decreased energy supply (fasting)
Common feature
myoclonus epilepsy, deafness, blindness, anemia, diabetes, seizures and loss of cerebral blood supply (stroke).
Myoclonic epilepsy and ragged-red fiber disease (MERRF)
MERRF is a member of a group of disorders called mitochondrial encephalomyopathies that feature mitochondrial defects with altered brain and muscle functions.
The term “ragged red fibers” refers to large clumps of abnormal mitochondria that accumulate mostly in muscle cells and are stained red by a dye that is specific for complex II of the electron transport chain.
rare, maternally inherited, heteroplasmic, (point mutation in tRNA lysine gene)
Mutation is MTTK*MERRF8344G.
MT means mitochondrial gene is mutated
T means transfer RNA gene
K means the single-letter amino acid designation for lysine
MERRF means the clinical features
8344G means the mutant nucleotide is guanine (G) at nucleotide position 8344
If 90% of the mitochondria in nerve and muscle cells carry the MTTK*MERRF8344G mutation, then the defining symptoms of MERRF are present.
Maternally inherited mitochondrial disease
The MTTL1*MELAS3243G mutation accounts for more than 80% of the cases of MELAS.
This base substitution is in one of the two mitochondrial transfer RNALeu genes.
the A3243G mutation occurs in thetRNALeu(UUR) gene
When this mutation is present in ≥90% of the mitochondrial DNA of muscle tissue, there is an increased likelihood of recurrent strokes, dementia, epilepsy, and ataxia.
When heteroplasmy for the A3243G mutation
is ~40% to 50%, chronic progressive external ophthalmoplegia (CPEO), myopathy, and deafness are likely to occur.
Other MELAS mutations occur at sites 3252, 3271, and 3291 within the tRNALeu(UUR) gene and in the mitochondrial tRNAVal (MTTV) and COX III (MTCO3) genes.
Reduced activities in Complexes I and IV are established
“Inheritance” in images, from Darwin’s “tree of life” to DNA’s iconic crystallography to the epigenetic dynamicsHowever, the script needs to be interpreted and receives meaning only from the interplay with the environment
Epigenetics is the study, in the field of genetics, of cellular and physiological phenotypic trait variations that are caused by external or environmental factors that switch genes on and off and affect how cells read genes instead of being caused by changes in the DNA sequence. -Wikipedia
The epigenetic regulation of DNA-templated processes has been intensely studied over the last 15
years. DNA methylation, histone modification, nucleosome remodeling, and RNA-mediated targeting regulate many biological processes that are fundamental to the genesis of cancer. Here, we
present the basic principles behind these epigenetic pathways and highlight the evidence suggesting that their misregulation can culminate in cancer. This information, along with the promising clinical and preclinical results seen with epigenetic drugs against chromatin regulators, signifies that it
is time to embrace the central role of epigenetics in cancer.
Epigenetics definition, history of epigenetics, molecular basis of epigenetics, epigenetic modification, tools to study epigenetics, disease linked with epigenetics, DNA methylation demethylation and enzymes regulating DNA methylation
Genomics, Transcriptomics, Proteomics, Metabolomics - Basic concepts for clin...Prasenjit Mitra
This set of slides gives an overview regarding the various omics technologies available and how they can be used for improvement in clinical setting or research
Epigenomics: Emerging Opportunities in Biomarkers, Diagnostics and TherapeuticsReportLinker.com
THIS REPORT:Provides a comprehensive overview of the global market for epigenomicsDescribes the major epigenomics technologies impacting the market today and emerging opportunities in biomarkers, diagnostics and therapeuticsContains global market forecasts for epigenomics, with trends and forecasts for growth through 2014Offers a focus on particular applications of epigenomics, including research tools, diagnostics, drugs and cloning/tissue engineeringDiscusses industry structure including, mergers and acquisitions, distribution of products, government regulation and industry trendsProfiles the most competitive businesses in the industry.
Train for a Fast Ironman in 12 Hours a WeekTrainingPeaks
You don't need to devote your entire life to training in order to achieve your Ironman goals. Based on the article "Minimalist Ironman Training" by Matt Fitzgerald, here's how to train for a fast Ironman in just 12 hours a week. For more training advice like this, visit TrainingPeaks.com/Blog.
September 7, 2016
Far too many people across the country are left dead, injured, or traumatized by community violence. Communities can be safer when neuroscience, public health strategies, and collective advocacy are aligned in practice and policy. This event convened experts to discuss the best next steps to fostering a broad science-informed advocacy movement to effectively address community violence.
Panelists
- Michelle Bosquet Enlow, PhD, Assistant Professor of Psychology, Harvard Medical School; Associate in Psychology, Boston Children's Hospital; Affiliated Faculty, Harvard University Center on the Developing Child
- Shannon Cosgrove, MPH, Director of Health Policy, Cure Violence
- Fatimah Loren Muhammad, Director, Trauma Advocacy Initiative, Equal Justice USA
- Charles Homer, MD, Deputy Assistant Secretary for Human Services Policy, Office of the Assistant Secretary for Planning and Evaluation, U. S. Department of Health and Human Services
- Moderator: Robert Kinscherff, PhD, JD, Senior Fellow in Law and Neuroscience, Center for Law, Brain & Behavior at Massachusetts General Hospital and Petrie-Flom Center; Associate Vice President for Community Engagement and Teaching Faculty in the Doctoral Clinical Psychology Program and for the Doctoral School Psychology Program, William James College; Faculty at the Center for Law, Brain and Behavior; and Senior Associate for the National Center for Mental Health and Juvenile Justice
Part of the Project on Law and Applied Neuroscience, a collaboration between the Center for Law, Brain & Behavior at Massachusetts General Hospital and the Petrie-Flom Center for Health Law Policy, Biotechnology, and Bioethics at Harvard Law School.
Learn more on the website: http://petrieflom.law.harvard.edu/events/details/battling-blood-in-the-streets.
What is the epidemiological evidence linking early life events and cancer risk and what are the potential critical windows for cancer prevention?
By Professor Ricardo Uauy, University of Chile, London School of Hygiene and Tropical Medicine
World Cancer Congress, Saturday 6 December 2014
Long-lasting alterations to DNA methylation and ncRNAs could underlie the eff...Ben Laufer
Fetal alcohol spectrum disorders (FASDs) are characterized by life-long changes in gene expression, neurodevelopment and behavior. What mechanisms initiate and maintain these changes are not known, but current research suggests a role for alcohol-induced epigenetic changes. We assessed alterations to adult mouse brain tissue by assaying DNA cytosine methylation and small noncoding RNA (ncRNA) expression, specifically the microRNA (miRNA) and small nucleolar RNA (snoRNA) subtypes. We found long-lasting alterations in DNA methylation as a result of fetal alcohol exposure, specifically in the imprinted regions of the genome harboring ncRNAs and sequences interacting with regulatory proteins. The findings of this study help to expand on the mechanisms behind the long-lasting changes in the brain transcriptome of FASD individuals.
Webinar Link: http://www.youtube.com/watch?v=fzdc0GIdCnA
A RESEARCH ON GENOMIC IMPRINTINGGenomic imprinting is the epig.docxransayo
A RESEARCH ON GENOMIC IMPRINTING
Genomic imprinting is the epigenetic phenomenon mostly occurring in gametogenesis. It has independently evolved in flowering plants and mammals. In both organisms, imprinting occurs in the embryo-nourishing tissues; the endosperm and the placenta respectively. Imprinting genes regulate the transfer of nutrients to developing progeny (Beery & Workman, 2011).The genomic imprinting usually occurs when both the maternal and the paternal alleles are present but one allele expresses itself while the other remains inactive ( Engel, N. 2015). Gene imprinting is believed to be important in regulation of growth in embryo and neonate
Experiments on androgenotes and gynogenotes , which are produced by nuclear transplantation, are used to create basis of genomic imprinting. The zygotes from androgenotes and gynogenotes were formed but neither type could undergo more development. From this situation, it is possible to suggest that the maternal and paternal effects are complimentary(Morgan, Li, & O’Neill, 2009). Each genome contains different viable and necessary properties. Another evidence that genomic imprinting has a major role in growth and development comes from a research by Li et al(1993).
Optimal method for gene imprinting is DNA methylation, which is carried out with enzyme DNA methyltransferase in mammals. DNA MTase acts on the DNA sequence 5’-6pG-3’. Primarily higher eukaryotes have CpG islands in their genomes. The islands are hardly methylated in the animal cells, this could be due to the bound transcription factors that block DNA MTase. Those sequences which are methylated are normally not active. Some research also show that methylated sequences can be active (Madek, 1974).
The importance of DNA methylation was demonstrated in the study of mammalian development(Li et al, 1993). They postulated that if mutation was introduced to the DNA MTase gene in embryonic stem cell of a mice, methylation of CpG would be abnormal and the gene expression would be affected (“DNA methylation and demethylation dynamics,” 2015). Gene mutation of DNA MTase was caused by homologous recombination and Southern blot analysis affirmed this (Wilkins, 2010). The genes used were insulin-like growth factors; H19, lgf2 and lgf2 receptor; lgf2r.
Normally H19 gene, whih is a maternal allele, is expressed while the paternal allele is inactive. Inactive paternal allele is methylated but the maternal allele is not; this should be noted carefully. RNase and Northern blot analysis essays procedures demonstrated the effects of decreased levels of DNA methylation on mutant mice. It was brought to light that typical DNA methylation is a requirement to keep for the paternal allele inactive for the H19 gene (Mightiness of science, 2016)
The lgf2 is opposite of the H19 gene in that it is expressed only in a methylated paternal allele. As a result, it is expressed in mice having deficient MTase activity. It is expected that the lgf2 gene wil.
Differences in the endometrial transcript profile during the receptive period between women who were refractory to implantation and those who achieved pregnancy.
By Luis Alberto Velásquez Cumplido
This presentation is an overview of our recent publication in the Appetite Journal. "Preclinical Evidence for the Addiction Potential of Highly Palatable Foods: Current Developments Related to Maternal Influence" by David Wiss, Kristin, Criscitelli, Mark Gold, and Nicole Avena.
Patologie digestive, extradigestive e MicrobiotaASMaD
Presentazione a cura del Professor Giovanni Barbara - M.A.S.T.E.R. ECM in Gastroenterologia: Focus on: Microbiota e dintorni - Fondazione Santa Lucia - Roma
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
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.
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.
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
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
These lecture slides, by Dr Sidra Arshad, offer a quick overview of 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 leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
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. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
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- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
Hemodialysis: Chapter 3, Dialysis Water Unit - Dr.Gawad
Developmental Origins of Obesity: The Role of Epigenetics
1. Zach Ferraro, PhD, CEP
CIHR Postdoctoral Fellow
Chronic Disease Program, Ottawa Hospital Research Institute (OHRI)
Clinical Research Associate, Division of Maternal-Fetal Medicine, The Ottawa Hospital
CON Obesity Summit 2015
Toronto, ON
April 29th, 2015
website: www.DrFerraro.ca
twitter: @DrFerraro
email: zach.ferraro@gmail.com
Developmental Origins of Obesity:
Inheritance or recapitulation?
2. Objectives
Review the concept of ‘fetal programming’
Early life nutritional events may serve as molecular memory of
individual in utero experiences
Following multiple rounds of cell division
Highlight extrinsic (recapitulation) & Intrinsic (genetic) mechanisms
Intergenerational epigenetics in humans
Moving forward
3. Birthweight & Metabolic Syndrome Risk
Dutch ‘hunger winter’ 1945
Pettitt DJ. Curr Diab Rep 2001; 1: 78–81; Von Hagens, 2005
Body Worlds; Ong KK. Horm Res 2006; 65: 65–69.
SGA & LGA neonates
Cardiometabolic Disease
5. Gluckman, PD et al. Nat. Rev. Endocrinol. 5, 401-408 (2009).
Environmental sensitivity of
epigenome throughout life
PA? PA? PA? PA?
Plasticity has high energetic cost & is limited to early development
Reengineering tissue/body after phenotype developed is costly
6. DEVELOPMENTAL PLASTICITY
AND CHRONIC DISEASE RISK
Gluckman et al. NEJM 2008 Jul 3;359(1):61-73.
M Desai et al. International Journal of Obesity (2015) 633 – 641
transmission
recapitulation
7. Epigenetics
“interactions of genes with their
environment which bring the phenotype
into being” - Conrad Waddington
Mitotic or meiotic heritable alterations in
gene expression potential that occur
without alterations in DNA sequence
Ozanne, S. E. Nat. Rev. Endocrinol. 11, 67–68 (2015)
Waddington, C. H. Organizers and Genes (Cambridge U Press, 1940)
M Desai et al. International Journal of Obesity (2015) 633 – 641
8. Regulatory mechanisms
DNA methylation: CH3-attached to CpG islands regulate gene activity. Renders
the DNA inaccessible and suppresses gene expression
Histone (covalent) modifications: methylation (Me) or acetylation (Ac) of
histones determines the activity of the DNA wrapped around them
microRNA (miRNA): noncoding (19-22 nucleotides) molecules that silence RNA
& post-transcriptional regulation of gene expression, bind to complementary
sequences in the 3′ end of mRNA and reduce the rate of protein synthesis
Gluckman et al. NEJM 2008 Jul 3;359(1):61-73.
9. DNA Methylation
Dynamic in embryogenesis
Pre-implantation, DNA hypo-Me, > DNA-Me over time
Differentiation & organogensis
Mediated by DNMT
Silenced expression
Role of in utero nutrition/CH3 donors
Clarke HJ. Biochem Cell Biol 1992; 70:
856–866; Weaver JR et al. Mamm
Genome 2009; 20: 532–543; Desai et al.
IJO (2015) 633-41; sciblogs.co.nz;
www.discoverymedicine.com
10. Transgenerational mechanisms
Inheritance
Transmitted through
genes that are
passed from parents
to children
The reception of
genetic qualities by
transmission from
parent to offspring
Recapitulation
The repetition of an evolutionary or
other process during development
Re-occurrence in an individual
organism's development (phenotype)
resembling the series of ancestral
types from which it descended so
offspring retraces the phylogeny of
its group
Largely environmental
Nutrition
Smoking/Alcohol/Drugs
Physical activity
Stress
Exposure to endocrine disruptors
Etc.
R. Waterland (personal communication); Waterland, Annu. Rev. Nutr. 2014;34:337–55;
http://ghr.nlm.nih.gov/glossary=geneticinheritance
11. Maternal Diet in Pregnancy
Classic example of CH3-dependent
Epigenetic Modification
BPA ↓ methylation of agouti gene
When mothers fed BPA their babies were
yellow & obese
When moms fed BPA + CH3-rich foods the
offspring were brown & healthy
Supplementation counteracted exposure
Demonstrates how environmental exposure in
utero can alter phenotypes in isogenetic pairs
Waterland, Annu. Rev. Nutr. 2014;34:337–55
http://learn.genetics.utah.edu/content/epigenetics/nutrition/
12. Inheritance: direct (epigenetics)
vs. indirect (recapitulation)
‘Soft’ inheritance or recapitulation operates indirectly,
via re-creation in each generation of the conditions,
which generate certain phenotypic effects in offspring
Extrinsic process
For instance, small mothers might generate small
offspring through:
↓ uterine size in each generation
Behaviours (e.g., smoking or food preference)
Factors that have familial component
13. Examples
Trangenerational Inheritance
Genetically driven
Intrinsic process
Recapitulation of Phenotype
Environmentally driven
Early acquisition of language
Extrinsic process
R. Waterland (personal communication); Waterland, Annu. Rev. Nutr. 2014;34:337–55 ; M Desai et al. International Journal of
Obesity (2015) 633 – 641; P. D. Gluckman et al., (2010). Journal of Developmental Origins of Health and Disease, 1, pp 618
14. Bariatric BPD surgery ↓ F1 Obesity
N= 49 moms who lost 36% body weight
sustained for 12yr & n=111 children (54
BMS and 57 AMS) aged 2.5–26
AMS children:
↓ birth weight
↓ macrosomia
↔ LBW
3x ↓ severe obesity at f/u
Extrinsic process
Epigenetic alteration in somatic tissues
with required repeat exposures each
generation
Altered maternal phenotype via nutrient
restriction
Smith, 2009. J Clin Endocrinol Metab, 94(11):4275–4283
15. Human evidence of transmission:
Famine & Overnutrition
In the Dutch Famine (1944–1945) cohort, 60 yo
adults prenatal exposure to famine showed hypo-
Me of whole blood IGF2 gene
Hyper-Me of 2 obesity-related non-imprinted genes
(IL-10, leptin) vs. unexposed, same-sex siblings
Hypo-He at IGF2 DMR associated
with paternal obesity
reprogramming of imprint marks during
spermatogenesis
16. Human evidence of transmission: GWG
(CpG) Dinucleotide site Me in newborn cord blood DNA from 88
participants Avon Longitudinal Study of Parents and Children
>GWG in T1 (0-18 wks) associated with ↑ DNA-Me in 4 CpG
sites at MMP7, KCNK4, TRPM5 and NFKB1 genes
Newborns of mom with excess GWG ↑ DNA-Me at MMP7 CpG
site vs. IOM-recommended GWG
17. A clean slate?
Following fertilisation, global DNA methyl tags are erased
By blastocyst stage (implantation), the genome is hypomethylated
After blastocyst hatching, DNA methylation levels are re-established in a lineage
specific manner
trophectoderm-derived cells remain hypo-Me vs. inner-cell mass-derived cells
Placenta is likely to show the > evidence of environmental ‘footprint’ or
‘memory’ of environmental insult during pregnancy
tissue most exposed to environmental factors during pregnancy
Placenta 33 (2012) 959-970
18. Persistent epigenetic marks
-CH3 marks not completely erased in early
development & gametogenesis
-CH3 sites preserved, replicated & DNA +
histones passed along during cell division
Effects stem cell fate & gene expression throughout life
Fan S et al. Biochem Biophys Res Commun 2009; 383: 421–425;
Flanagan JM et al. Am J Hum Genet 2006; 79: 67–84;Trasler JM. Mol
Cell Endocrinol 2009; 306: 33–36; Desai et al. IJO (2015) 633 – 641
19. Animal evidence of inheritance
Glucose intolerance & Obesity
Jimenez-Chillaron et al. Diabetes 58:460–468, 2009.
C & UN F1 females were mated at age 2 months with nonsibling F1-C or F1-UN males to
generate 4 experimental groups
Adverse neonatal exposure (UN) leads to F1, F2 & likely F3 obesity & IGT despite ad
libitum feeding during second pregnancy
Different aspects of these phenotypes transmitted via maternal lineage (obesity), the
paternal lineage (LBW), or both (glu intolerance)
6mo males 4mo males
20. Animal evidence of inheritance
Glucose intolerance & Obesity
Jimenez-Chillaron et al. Diabetes 58:460–468, 2009.
C & UN F1 females were mated at age 2 months with nonsibling F1-C or F1-UN males to generate 4
experimental groups
Adverse neonatal exposure (UN) leads to F1, F2 & likely F3 obesity & IGT despite ad libitum feeding
during second pregnancy
Different aspects of these phenotypes transmitted via maternal lineage (obesity), the paternal lineage
(LBW), or both (glu intolerance)
6mo males 4mo males
IGT in F1 & F2 generations is linked to impaired
beta-cell function partly explained by
dysregulation of Sur1 expression
21. Germline transmission
Suboptimal diet (UN) during fetal
development altered germ-cell DNA
methylome of male offspring when
nourished normally from weaning
Prenatal UN compromises male germline
epigenetic reprogramming & permanently
alters sperm DNA-Me in adult offspring
DNA-Me in late-gestation somatic tissues of
subsequent generation was not observed
Altered gene expression in F2
Gamete methylation may be ‘memory’ early
in utero & developmental exposures
Radford, E. J. et al. Science 345, 1255903 (2014);
Ozanne, S. E. Nat. Rev. Endocrinol. 11, 67–68 (2015)
22. Human evidence of inheritance
Dutch hunger winter
Offspring born during the famine were smaller than average and
risk of having smaller babies persisted 2 generations (F1 & F2)
Emanuel I, Filakti H, Alberman E, Evans SJ. Intergenerational studies of human
birthweight from the 1958 birth cohort. 1. Evidence for a multigenerational effect.
Br J Obstet Gynaecol 1992; 99: 67–74; Desai et al. IJO (2015) 633-41.
23. Human evidence of inheritance
Dutch hunger winter
Offspring born during the famine were smaller than average and
risk of having smaller babies persisted 2 generations (F1 & F2)
Emanuel I, Filakti H, Alberman E, Evans SJ. Intergenerational studies of human
birthweight from the 1958 birth cohort. 1. Evidence for a multigenerational effect.
Br J Obstet Gynaecol 1992; 99: 67–74; Desai et al. IJO (2015) 633-41.
Programmed obesity via alterations in
DNA methylation
Histone modifications & changes in chromatin
structure not demonstrated in humans
24. Conflicting evidence
Maternal diet during the F0
pregnancy affected the F2 BW,
independent of the F1 BW
Lumey LH. Paediatr Perinat Epidemiol 1992; 6: 240–253;
Stein & Lumey. Hum Biol 2000; 72: 641–654; Desai et al. IJO (2015) 633-641.
BW of women with T1 exposure ↑154 g & BW
of women T3 exp ↓ 251 g vs. BW of unexposed
Maternal prenatal famine exposure does not
affect the association between maternal and
offspring BW
VS.
25. Conflicts cont’d
Maternal Effect
Persists into F2?
F1 women exposed to famine
as fetuses had F2 babies with
↑ neonatal adiposity & poor
adult health
No Maternal, but
Paternal effect?
No transgenerational effects
if the grandmother had been
UN
↑ adiposity in offspring of
prenatally UN fathers
Painter et al. BJOG 2008; 115: 1243–1249;
Veenendaal et al. BJOG 2013; 120: 548–553; Desai et al. IJO (2015) 633–41.
26. Conflicting results
Different data collection methods
Early studies based on record
retrieval and relied on parents'
recall of their offspring's size at
birth and later health status
Phone surveys
Questionnaires
Interviews
Newer studies, the offspring
were directly contacted to assess
their body composition & health
Desai et al. IJO (2015) 633–641.
27. Human evidence lacking
“True transgenerational transmission [in humans] should be
demonstrable by effects [+/-] induced in F0 persisting to the
F3 generation, but such long-term studies are expensive and
not frequently performed”
Sir Peter Gluckman
Gluckman, PD et al. (2009). Nat. Rev. Endocrinol. 5, 401-408.
Gluckman, PD et al. (2010). J DOHD, 1, p 6-18.
PA? PA? PA? PA?
28. In utero milieu, fetal plasticity & chronic
disease risk
Gluckman et al. NEJM 2008 Jul 3;359(1):61-73.
M Desai et al. International Journal of Obesity (2015) 633 – 641
Role of nutrition
29. In utero milieu, fetal plasticity & chronic
disease risk
Gluckman et al. NEJM 2008 Jul 3;359(1):61-73.
M Desai et al. International Journal of Obesity (2015) 633 – 641
transmission
recapitulation
Maternal nutrition affects F1 gene
methylation
a. Immune response
b. Adipogenesis
c. Lipogenesis
= metabolic abnormalities
30. In utero milieu, fetal plasticity & chronic
disease risk
Gluckman et al. NEJM 2008 Jul 3;359(1):61-73.
M Desai et al. International Journal of Obesity (2015) 633 – 641
transmission
recapitulation
31. Predictive adaptive response
Human example
Thickened heel pads on the feet of infants at birth
prediction is reliable & assimilated into genomic determinants
No evolutionary explanation for these which does not
involve an anticipatory component
Classic example of a developmental process fixed in the
genome, yet it is a predictive response
Exact mechanisms remains to be establish
P. D. Gluckman, M. A. Hanson and T. Buklijas (2010). A conceptual framework for
the developmental origins of health and disease. Journal of Developmental
Origins of Health and Disease, 1, pp 618
32. Moving forward…
Quantify the influence of genotype, ENV, & intxn with human
epigenome
Most compare DNA methylation to phenotype independently of genotype
Genotype is an essential factor in these relationships
Assess the degree to which env influences are moderated by
genotype
Teh, 2014 Genome Research 24:1064–1074
33. Acute exercise remodels
promoter–Me in human muscle
Effects of chronic
exercise?
Muscle
Germ cells
Behavioural-induced
changes persistent
across generations?
Effect of postnatal
intervention on
offspring ‘exposed’ to
suboptimal env?
Barres et al., 2012. Cell Metabolism 15, 405–411.
34. Conclusions
Phenotype transmission demonstrated
Animals (DNA-Me & Histone Mods)
Humans (DNA-Me + familial components)
How does under- & over-nutrition produce similar phenotypes?
Predictive adaptive response?
How does an acute insult persist across generations?
Need to establish causal relationships between loci-specific epigenetic
marks in response to adverse ENV & metabolic adult disease phenotypes
Are epigenetic marks ‘erasable’ with intervention?
Can the beneficial effects be inherited?
Similar or different mechanisms?
Developmental origins of health and disease
35. Thank you.
Acknowledgements:
CIHR Allied care provider Fellowship, Human Development, Child & Youth Health
Dr. Erin Keely – The Ottawa Hospital Endocrinology/Metabolism
Dr. Kristi Adamo & Lab group – CHEO
Dr. Laura Gaudet – The Ottawa Hospital MFM
Dr. Mark Walker – The Ottawa Hospital MFM
Dr. Karen Fung Kee Fung – The Ottawa Hospital MFM
Dr. Felipe Moretti – The Ottawa Hospital MFM
The late Dr. Andree Gruslin – The Ottawa Hospital MFM/OHRI
Adamo Lab Staff & Students – CHEO
CON & CON-SNP staff, students, & volunteers
Everyone in attendance
For more discussion follow me on twitter: @DrFerraro