This document discusses fetal alcohol syndrome (FAS). It defines FAS as a congenital condition caused by a mother's alcohol consumption during pregnancy, characterized by stunted growth and facial abnormalities. Key points include:
- FAS affects 1-2 per 1,000 live births in the US. Alcohol crosses the placenta and impacts fetal development by disrupting cell growth and nutrient transport.
- Symptoms include growth retardation, distinctive facial features like smooth philtrum and small eyes, and central nervous system issues like microcephaly and developmental delays.
- Diagnosis requires growth problems, facial features, central nervous system abnormalities, and confirmed prenatal alcohol exposure. Treatment involves medical and behavioral interventions, while
FETAL ALCOHOL SYNDROME (FAS) is the leading known cause of mental retardation
and birth defects in the world. Fetal alcohol syndrome is a pattern of physical, behavioral and
cognitive abnormalities seen in individuals exposed to alcohol in uterus. Because alcohol is a
known teratogen and the damage done to a fetus by alcohol exposure is permanent, public
education about the dangers of prenatal alcohol exposure has been extensive. Many of the
features of the fetal alcohol syndrome are secondary to the effect of alcohol on brain
development. These include microcephaly, short palpebral fissures, the long smooth philtrum
and thin vermilion of the upper lip, joint anomalies, altered palmar crease pattern, and mental
retardation. Animal studies as well as a limited amount of human data also show that
maternal genotype is a key player : Advances in the development of novel antioxidant
therapies as an approach for fetal alcohol syndrome prevention. Peptides NAPVSIPQ (NAP)
and SALLRSIPA (SAL), related to activity-dependent neuroprotective protein (ADNP),
prevent alcohol-induced damage in a mouse model of FAS. In a recent study, the thyroxin
reversed the deficit both in the level of their genes and their social behaviour, research is
going on how the prenatal thyroid hormone supplementation reverses the behavioural deficits
in the fetal alcohol spectrum disorder model. Another study used a priori approach to assess
molecular phenotype in the cranial neural folds (head fold) of early mouse embryos soon
after maternal alcohol treatment. FAS can be modulated pharmacologically with PK11195, a
potent ligand with specific binding to the mitochondrial peripheral-type benzodiazepine
receptor recognition site. PK11195 has been shown to protect early mouse embryos from eye
and brain defects induced with diverse teratogens and to protect adult tissues from some
inflammatory lesions. Microarray transcript profiling of the embryonic head fold at 3.0 hr
after alcohol exposure or PK11195 counter-exposure enabled prioritization of candidate
pathways that integrate the genomic response with genetic susceptibility of the system. These
findings are consistent with the growing view that developmental exposure to alcohol alters
common signalling pathways linking receptor activation to cytoskeletal reorganization. The
programmatic shift in cell motility and metabolic capacity further implies cell signals and
responses that are integrated by the mitochondrial recognition site for PK11195.
CONCLUSIONS: Until the advent of effective prevention measures, it will remain
necessary to seek ways to treat the life-long neurobehavioral consequences of prenatal
alcohol exposure. Nevertheless, alcohol is a widely accepted and legal social drug, and many
pregnant mothers continue to drink it while pregnant. Whereas, FAS is totally preventable by
avoiding alco
What Is Fetal Alcohol Syndrome?
1) When a pregnant person drinks alcohol, some of that alcohol easily passes across the placenta to the fetus.
2) People with this condition may have problems with their vision, hearing, memory, attention span, and abilities to learn and communicate.
3) You can prevent fetal alcohol syndrome by avoiding alcohol during pregnancy.
FETAL ALCOHOL SYNDROME (FAS) is the leading known cause of mental retardation
and birth defects in the world. Fetal alcohol syndrome is a pattern of physical, behavioral and
cognitive abnormalities seen in individuals exposed to alcohol in uterus. Because alcohol is a
known teratogen and the damage done to a fetus by alcohol exposure is permanent, public
education about the dangers of prenatal alcohol exposure has been extensive. Many of the
features of the fetal alcohol syndrome are secondary to the effect of alcohol on brain
development. These include microcephaly, short palpebral fissures, the long smooth philtrum
and thin vermilion of the upper lip, joint anomalies, altered palmar crease pattern, and mental
retardation. Animal studies as well as a limited amount of human data also show that
maternal genotype is a key player : Advances in the development of novel antioxidant
therapies as an approach for fetal alcohol syndrome prevention. Peptides NAPVSIPQ (NAP)
and SALLRSIPA (SAL), related to activity-dependent neuroprotective protein (ADNP),
prevent alcohol-induced damage in a mouse model of FAS. In a recent study, the thyroxin
reversed the deficit both in the level of their genes and their social behaviour, research is
going on how the prenatal thyroid hormone supplementation reverses the behavioural deficits
in the fetal alcohol spectrum disorder model. Another study used a priori approach to assess
molecular phenotype in the cranial neural folds (head fold) of early mouse embryos soon
after maternal alcohol treatment. FAS can be modulated pharmacologically with PK11195, a
potent ligand with specific binding to the mitochondrial peripheral-type benzodiazepine
receptor recognition site. PK11195 has been shown to protect early mouse embryos from eye
and brain defects induced with diverse teratogens and to protect adult tissues from some
inflammatory lesions. Microarray transcript profiling of the embryonic head fold at 3.0 hr
after alcohol exposure or PK11195 counter-exposure enabled prioritization of candidate
pathways that integrate the genomic response with genetic susceptibility of the system. These
findings are consistent with the growing view that developmental exposure to alcohol alters
common signalling pathways linking receptor activation to cytoskeletal reorganization. The
programmatic shift in cell motility and metabolic capacity further implies cell signals and
responses that are integrated by the mitochondrial recognition site for PK11195.
CONCLUSIONS: Until the advent of effective prevention measures, it will remain
necessary to seek ways to treat the life-long neurobehavioral consequences of prenatal
alcohol exposure. Nevertheless, alcohol is a widely accepted and legal social drug, and many
pregnant mothers continue to drink it while pregnant. Whereas, FAS is totally preventable by
avoiding alco
What Is Fetal Alcohol Syndrome?
1) When a pregnant person drinks alcohol, some of that alcohol easily passes across the placenta to the fetus.
2) People with this condition may have problems with their vision, hearing, memory, attention span, and abilities to learn and communicate.
3) You can prevent fetal alcohol syndrome by avoiding alcohol during pregnancy.
Pediatrics. trisomy 21. Meiotic non-disjunction of chromosome 21. clinical features and associated abnormalities of down syndrome. screening test for down syndrome. counseling for parents in down syndrome.
Birth Defects: Introduction to birth defectsPiLNAfrica
Birth Defects was written for healthcare workers who look after individuals with birth defects, their families, and women who are at increased risk of giving birth to an infant with a birth defect. This book is being used in the Genetics Education Programme which trains healthcare workers in genetic counselling in South Africa. It covers: modes of inheritance, medical genetic counselling, birth defects due to chromosomal abnormalities, single gene defects, teratogens, multifactorial inheritance
PowerPoint presentation regarding many facets of Fetal Alcohol Spectrum Disorder. Feel free to share this with anyone who would benefit from this information. Some of the information is quite shocking. Included parenting and teaching strategies for those responsible for caring for a child with FASD.
Pediatrics. trisomy 21. Meiotic non-disjunction of chromosome 21. clinical features and associated abnormalities of down syndrome. screening test for down syndrome. counseling for parents in down syndrome.
Birth Defects: Introduction to birth defectsPiLNAfrica
Birth Defects was written for healthcare workers who look after individuals with birth defects, their families, and women who are at increased risk of giving birth to an infant with a birth defect. This book is being used in the Genetics Education Programme which trains healthcare workers in genetic counselling in South Africa. It covers: modes of inheritance, medical genetic counselling, birth defects due to chromosomal abnormalities, single gene defects, teratogens, multifactorial inheritance
PowerPoint presentation regarding many facets of Fetal Alcohol Spectrum Disorder. Feel free to share this with anyone who would benefit from this information. Some of the information is quite shocking. Included parenting and teaching strategies for those responsible for caring for a child with FASD.
Ironically, our life is an open book!
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presentation on fetal alcohol syndrome. thousands of infants are effected by this condition all around the world. its causes and effects. nutrition to deal with this condition.
The range of consequences from drinking alcohol during pregnancy are collectively called fetal alcohol spectrum disorders, as not all signs and symptoms are present in all children with the disorder. This range includes:
Alcohol-related neurodevelopmental disorder — intellectual disabilities or behavioral and learning problems caused by drinking alcohol during pregnancy
Alcohol-related birth defects — physical birth defects caused by drinking alcohol during pregnancy
Fetal alcohol syndrome — the severe end of the fetal alcohol spectrum disorders, which includes both neurodevelopmental disorder and birth defects caused by drinking alcohol during pregnancy
Partial fetal alcohol syndrome — presence of some signs and symptoms of fetal alcohol syndrome caused by drinking alcohol during pregnancy, but the criteria for the diagnosis are not met
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
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.
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
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.
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.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
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
- 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
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
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
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
2. INTRODUCTION
FAS can be defined as congenital disease, abnormality
or condition caused by consumption of alcohol by
mother during pregnancy, characterised by retardation
of mental development and of physical growth
particularly of skull and face of the infant.
Like any syndrome FAS is a group of signs and
symptoms that appear together to indicate the
condition.
No amount of alcohol consumption is safe during
pregnancy.
3. EPIDEMIOLOGY
Estimated 1-2 cases per 1000 live births in the United
States.
Ranges from 1 in 1000 to less than 1 in 10,000 live births
internationally.
Occurs in all race and ethnicity
4-5% of all children in the normal first grade in school
4. PATHOPHYSIOLOGY
Alcohol crosses the placenta and rapidly reaches the fetus
Fetus liver does not have significant alcoholdehydrogenase(ADH),
ALDH and other antioxidants like glutathion
Also amniotic acts as reservoir for alcohol, prolonging fetal
exposure
Acetaldehyde( metabolite of ethanol) disrupt cellular
differentiation and growth, disrupting DNA and protein synthesis
and inhibits cell migration
Acetaldehyde and ethanol modify metabolism of carbohydrate,
protein and fats
They both also decrease the transfer of amino acids, glucose, folic
acid, zinc and other nutrients across the placenta barrier which
affects fetal growth.
5. SYMPTOMS
Growth Retardation
Facial Features
Smooth philtrum
Thin upper lip (thin vermilion)
Small eyes
Short upturned nose
Flattened cheeks
Small jaw ( maxillae or mandible)
8. SYMPTOMS
Central nervous system features
Microcephaly
Mental retardation
Hyperactivity
Delayed development of gross motor skills like rolling
over, sitting up, crawling and walking
Impaired language development
Delayed in development of fine motor skills such as
grasping objects with the thumb and index fingers and
transfer objects from one hand to the other.
Seizures
9. OTHER SIGNS
Cardiac
• Heart murmur; usually disappears by one year of age
• VSD
• ASD
Skeletal: Joint abnormalities, altered palmer crease
pattern, small distal phalanges and small fifth
fingernail.
Renal: Horseshoe, aplastic, dysplastic or hypoplastic
kidney.
Ocular: Strabismus, optic nerve hypoplasia
10. DIAGNOSIS
The diagnostic criteria includes;
Growth deficiency
FAS facial features
Central nervous system damage
Prenatal alcohol exposure