This presentation provides an overview of Cell senescence, Aging, Theories of Aging,principle of senescence, Mechanism of action, Factors, Diseases caused due to this action, Senescence and cancer, Insulin signalling cascade, Telomere shortening.
This presentation provides an overview of Cell senescence, Aging, Theories of Aging,principle of senescence, Mechanism of action, Factors, Diseases caused due to this action, Senescence and cancer, Insulin signalling cascade, Telomere shortening.
Tumor, Tumor immunology, cancer, hallmarks of cancer, carcinoma, lymphoma, metastasis, malignant, benign, angiogenesis, oncogenes and cancer induction, kuby detailed study quick revision, proto-oncogenes, tumor antigens, antibody, experiments for tumor antigens, methods for characterization of TSTA, Immunoediting, Current research n new approaches, monoclonal antibody
Just regarded to those who trying to learn somethings.. . thanks to those who read this slide... Just pray for me , for my parents and for my teachers...
Cell death, particularly apoptosis, is probably one of the
most widely-studied subjects among cell biologists.
Understanding apoptosis in disease conditions is very
important as it not only gives insights into the pathogenesis
of a disease but may also leaves clues on how
the disease can be treated. In cancer, there is a loss of
balance between cell division and cell death and cells
that should have died did not receive the signals to do
so. The problem can arise in any one step along the way
of apoptosis.Apoptosis is an ordered and orchestrated cellular process that occurs in physiological and pathological conditions.
It is also one of the most studied topics among cell biologists. An understanding of the underlying mechanism of
apoptosis is important as it plays a pivotal role in the pathogenesis of many diseases. In some, the problem is due
to too much apoptosis, such as in the case of degenerative diseases while in others, too little apoptosis is the
culprit. Cancer is one of the scenarios where too little apoptosis occurs, resulting in malignant cells that will not
die. The mechanism of apoptosis is complex and involves many pathways. Defects can occur at any point along
these pathways, leading to malignant transformation of the affected cells, tumour metastasis and resistance to
anticancer drugs. Despite being the cause of problem, apoptosis plays an important role in the treatment of
cancer as it is a popular target of many treatment strategies. The abundance of literature suggests that targeting
apoptosis in cancer is feasible. However, many troubling questions arise with the use of new drugs or treatment
strategies that are designed to enhance apoptosis and critical tests must be passed before they can be used safely
in human subjects.. It is used,
in contrast to necrosis, to describe the situation in
which a cell actively pursues a course toward death
upon receiving certain stimule
Cancer is a group of diseases involving abnormal cell growth with the potential to invade or spread to other parts of the body. These contrast with benign tumors, which do not spread to other parts of the body.
## To understand how cancer develops and progresses, researchers first need to investigate the biological differences between normal cells and cancer cells. This work focuses on the mechanisms that underlie fundamental processes such as cell growth, the transformation of normal cells to cancer cells, and the spread, or metastasis, of cancer cells.
Cell within a tumor that possess the capacity to self-renew and to cause the heterogeneous lineages of cancer cells that comprise the tumor”.
“CSC can thus only be defined experimentally by their ability to recapitulate the generation of a continuously growing tumor”.
Oxidative Stress in Aging and Human Diseases - Exploring the MechanismsQIAGEN
Many modern diseases, including cancer, cardiovascular disease, diabetes, liver disease, arthritis and neurodegenerative disease are related to aging, and aging is closely linked to oxidative stress. Intensive research is being conducted to understand the antioxidant defense mechanism, the mechanisms of aging itself, as well as their roles in human diseases. This slidedeck provides an update on how oxidative stress is linked to aging and how inflammation leads to aging through DNA damage, telomere dysfunction, cellular senescence and oxidative stress. Recent progress on the health benefits of antioxidants and examination of their potential mechanisms in the prevention and treatment of chronic diseases are also covered. Various assay technologies to tackle the complex signaling pathways in this process will be introduced. Learn how you can apply these advanced tools to your research!
Aging is a natural phenomenon. it is the law of nature
this slide is about the various factors which independently or in combinations contribute to aging in humans
Tumor, Tumor immunology, cancer, hallmarks of cancer, carcinoma, lymphoma, metastasis, malignant, benign, angiogenesis, oncogenes and cancer induction, kuby detailed study quick revision, proto-oncogenes, tumor antigens, antibody, experiments for tumor antigens, methods for characterization of TSTA, Immunoediting, Current research n new approaches, monoclonal antibody
Just regarded to those who trying to learn somethings.. . thanks to those who read this slide... Just pray for me , for my parents and for my teachers...
Cell death, particularly apoptosis, is probably one of the
most widely-studied subjects among cell biologists.
Understanding apoptosis in disease conditions is very
important as it not only gives insights into the pathogenesis
of a disease but may also leaves clues on how
the disease can be treated. In cancer, there is a loss of
balance between cell division and cell death and cells
that should have died did not receive the signals to do
so. The problem can arise in any one step along the way
of apoptosis.Apoptosis is an ordered and orchestrated cellular process that occurs in physiological and pathological conditions.
It is also one of the most studied topics among cell biologists. An understanding of the underlying mechanism of
apoptosis is important as it plays a pivotal role in the pathogenesis of many diseases. In some, the problem is due
to too much apoptosis, such as in the case of degenerative diseases while in others, too little apoptosis is the
culprit. Cancer is one of the scenarios where too little apoptosis occurs, resulting in malignant cells that will not
die. The mechanism of apoptosis is complex and involves many pathways. Defects can occur at any point along
these pathways, leading to malignant transformation of the affected cells, tumour metastasis and resistance to
anticancer drugs. Despite being the cause of problem, apoptosis plays an important role in the treatment of
cancer as it is a popular target of many treatment strategies. The abundance of literature suggests that targeting
apoptosis in cancer is feasible. However, many troubling questions arise with the use of new drugs or treatment
strategies that are designed to enhance apoptosis and critical tests must be passed before they can be used safely
in human subjects.. It is used,
in contrast to necrosis, to describe the situation in
which a cell actively pursues a course toward death
upon receiving certain stimule
Cancer is a group of diseases involving abnormal cell growth with the potential to invade or spread to other parts of the body. These contrast with benign tumors, which do not spread to other parts of the body.
## To understand how cancer develops and progresses, researchers first need to investigate the biological differences between normal cells and cancer cells. This work focuses on the mechanisms that underlie fundamental processes such as cell growth, the transformation of normal cells to cancer cells, and the spread, or metastasis, of cancer cells.
Cell within a tumor that possess the capacity to self-renew and to cause the heterogeneous lineages of cancer cells that comprise the tumor”.
“CSC can thus only be defined experimentally by their ability to recapitulate the generation of a continuously growing tumor”.
Oxidative Stress in Aging and Human Diseases - Exploring the MechanismsQIAGEN
Many modern diseases, including cancer, cardiovascular disease, diabetes, liver disease, arthritis and neurodegenerative disease are related to aging, and aging is closely linked to oxidative stress. Intensive research is being conducted to understand the antioxidant defense mechanism, the mechanisms of aging itself, as well as their roles in human diseases. This slidedeck provides an update on how oxidative stress is linked to aging and how inflammation leads to aging through DNA damage, telomere dysfunction, cellular senescence and oxidative stress. Recent progress on the health benefits of antioxidants and examination of their potential mechanisms in the prevention and treatment of chronic diseases are also covered. Various assay technologies to tackle the complex signaling pathways in this process will be introduced. Learn how you can apply these advanced tools to your research!
Aging is a natural phenomenon. it is the law of nature
this slide is about the various factors which independently or in combinations contribute to aging in humans
The Root cause and Culprit behind Chronic Diseases, Cancer and Aging is well recognized now by many authorities. It includes: 1- A state of chronic low grade inflammation. 2- Mitochondrial dysfunction.
In order for our organs to function properly, they require energy, and that energy is produced by the mitochondria (the power engine). Mitochondrial function is at the very heart of everything that occurs in our body. Mitochondria our body’s lifeline are tiny organelles in our cell, thousands of them comprising 15 to 50% of the cell volume. Red blood cells and skin cells have very little to none, while germ cells have 100,000, but most cells have one to 2,000 of them. They're the primary source of energy for our body. They supply over 90% of our body’s energy. Converting the food we eat and the air we breathe into usable energy. It have enormous potential to influence our health, specifically cancer. Optimizing mitochondrial function and preventing mitochondrial dysfunction is extremely important for health and disease prevention and may be at the core of effective cancer treatment. Important nutrients and co-factors for mitochondrial function include: all B vitamins, magnesium, omega-3 fat, CoQ10, acetyl L- carnitine, D-ribose, and alpha-lipoic acid. Exercise is also important for mitochondrial health and function
Basic principles of Cell injury and AdaptationAkshayYadav176
Basic principles of Cell injury and Adaptation:
(As per new syllabus of PCI)
Introduction, definitions, Homeostasis, Components and Types of Feedback systems, Causes of cellular injury,Pathogenesis (Cell membrane damage, Mitochondrial damage, Ribosome damage, Nuclear damage),Morphology of cell injury – Adaptive changes (Atrophy, Hypertrophy, hyperplasia, Metaplasia, Dysplasia),Cell swelling, Intra cellular accumulation, Calcification, Enzyme leakage and Cell Death Acidosis & Alkalosis,Electrolyte imbalance.
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
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
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
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!
Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
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.
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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
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
263778731218 Abortion Clinic /Pills In Harare ,sisternakatoto
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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.
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
Novas diretrizes da OMS para os cuidados perinatais de mais qualidade
Ageing and its relationship with longevity genes
1.
2.
3.
4. In agreement with the last report of the UN on `Aging of the
World-wide Population”, published in 2009, the humanity has
improved its environmental conditions from the century last,
managing to increase the duration of the life in the developed
countries, of 15 years for the men and 22 years for the woman.
Nevertheless, the human beings we are limited to live an average
on 100 years, although exceptional cases of 150 years have been
registered. But some investigators think that we are not
programmed to die, which has impelled to the new science of
the biogerontología to give with the possible keys of the
rejuvenation.
The human being owns a genetic clock that seems to determine
the time of life, but the process does not happen in the same
way in all the individuals. These genetic variants associated with
the aging, would explain because some people seem to age more
express than others, according to the Nature magazine of
February of 2010.
5. The science of aging is among the most dynamic and
provocative in modern biology. Over the past two
decades we have seen a virtual explosion in research
investigating the molecular and behavioral systems
that control the aging process. But the more
researchers uncover about the science of aging, the
more questions emerge.
6. Aging is the progressive loss of physiological functions that
increases the probability of death…..
* The decline in function certainly occurs within cells. This is especially
true of cells that are no longer in the cell cycle
* Neurons in the brain
* Skeletal and cardiac muscle
* Kidney cells
Random mortality from
* Starvation
* Predation
* Infectious disease
* A harsh environment (e.g.. cold)
* Kills off most animals long before they begin to show signs of aging.
* Even for humans, aging has only become common in recent decades
7. Loss of structure and function in aging.
Figures represent percentage of a given function remaining in an average 75year-old man compared with that found in an average 30-year-old man, the
latter value taken as 100%.
Weight of brain
Blood supply to brain
Output of heart at rest
56%
80
70
Number of glomeruli in kidney
56
Glomerular filtration rate
69
Speed of return to normal pH of blood after
displacement
17
Number of taste buds
Vital capacity
Strength of hand grip
36
56
55
Maximum O2 uptake during exercise
40
Number of axons in spinal nerve
63
Velocity of nerve impulse
Body weight
90
88
8.
9.
10. LEADIND CAUSES OF DEATH IN MEN AND WOMEN
Men
01
02
03
04
05
06
07
08
09
10
Heart disease
Cancer
Accidents
Women
Heart disease
Cancer
Stroke
Chronic obstructive
Stroke
lung disease
Chronic obstructive lung disease
Diabetes
Diabetes
Alzheimer's disease
Pneumonia and influenze
Accidents
Pneumonia and
Suicide
influenze
Kidney disease
Kidney disease
Live disease
Blood infections
11. Programmed in our genes
* Single genes that increase life span in Drosophila,C.elegans, and
mice.
* Genes that suppress signaling by insulin and insulin-like growth
factor-1 (Igf-1) increase life span in these animals.
* Examples:
* Mice with one of their Igf-1 receptor genes “Knocked out" live
25% longer than normal mice.
* Antagonistic pleiotrophy. Genes that promote survival early in
life at the expense of maintaining the body will be selected.
* Some examples:
By forcing cells with damaged DNA to stop dividing and
become senescent or even to die by apoptosis, it protects the
organism from the threat of those cells becoming cancerous but
at the expense of reducing cell renewal
12. The increased life span of yeast
Calorie restriction requires a gene called SIR2 ("Silent
Information Regulator 2")encodes the Sir2 Deacetylase, an
enzyme
Removes acetyl groups from proteins.
Increasing the activity of Sir2 extends the life span
of yeast, C.elegans, and Drosophila.
But it turns out that mammals have 7 genes that encode
proteins — called sirtuins — similar to Sir2.
13. *Calorie restriction in mice causes
* A drop in
* The level
of circulating insulin and insulin-like growth
factor-1 (Igf-1)
* The
* The
level of glucose and triglycerides in the blood
level of NADH (produced by cellular respiration)
within cells
This leads to:
* The production of sirtuins to increase markedly
* Apoptosis of cells to be inhibited
* Formation of Adipose tissue to be suppressed
* Increased production of nitric oxide(NO) which is essential
for the benefits of CR to take effect
* Greatly increased physical activity and lower body weight
14.
15. * A major aspect of metabolism is the oxidation of foodstuffs by
the mitochondria
* Electron transport in the mitochondria generates reactive
oxygen species ("ROS") such as
* The superoxide anion (O2-), which generates
* Hydrogen peroxide (H2O2)
* Although cells contain enzymes catalase which breaks down
H2O2 they eventually and inevitably damage macromolecules in
the cell
* Proteins
* Lipids
16.
17. Food
Link to the
Genes
Specific Gene
Green Tea
Helps to inhibit
genes that fuel
breast cancer
HER-2
Broccoli
Boosts genes that
protect against
heart disease
Soybeans
Affect 123 genes
in- volved in
prostate cancer
Turmeric (a
curry
ingredient)
Suppresses genes
that bump up
inflammation
GST
p53
Cox-2
Function of
the Gene
Long-term
Effect
Triggers growth
Slow HER-2
signals in cells signaling in tumors
Produces the
body's master
antioxidant glutathione
The additional
glutathione helps
keep arteries
healthy
Increase activity of
the p53 gene to
Kill mutant cells
block tumor
formation
Makes
inflammatory
compounds
Help to ward off
heart disease, colon
cancer and
Alzheimer's
20. *Cells unless they retain the enzyme telomerase
*
Lose DNA from the tips of their chromosomes
with each cell division.
The telomeres in the cells of old animals-SHORTER
than in young cells.
*Cells genetically manipulated to express telomerase long
after they should have stopped- avoid replicative
senescence.
*If telomeres get too short (< 13 repeats in human cells),
chromosome abnormalities — a hallmark of CANCER —
NO Cancer if the cell ceases to divide. So telomere
shortening may protect against cancer at the price of cell
senescence.
22. Mice whose genes for telomerase have been "knocked out"
1: The number of Mitochondria in their cells decreases as does the
function of those that remain.
*
*
*
Oxygen consumption and ATP production declines.
The efficiency of the electron transport chain decreases.
This leads to an increased generation of reactive oxygen species(ROS)
2: The level of P53 activity increases.
*
*
*
mitosis declines
Apoptosis of cells increases
Replicative senescence increases
3: The anatomy and function of organs such as the liver and heart
show the degenerative changes of age.
25. Mice given ionizing radiation that damages DNA show early
aging.
Transgenic mice with a defect in the "proofreading" function of
the DNA polymerase responsible for copying mitochondrial DNA
accumulate many mutations in their mitochondrial genes;
show marked signs of premature aging.
26. Cells taken from old mice (and old humans) show slightly
elevated levels of somatic mutations and chromosome
abnormalities like translocations and aneuploidy.
Many of these changes also cause cancer so it is no
accident that the incidence of cancer rises with advancing
age (graph).
The hematopoietic stem cells of knockout mice deficient in
any one of these enzymes needed for genome maintenance
XPD for nucleotide excision repair (NER)
Ku80 for nonhomologous end joining (NHEJ)
TR (telomerase RNA) needed for telomere
maintenance lose their ability to supply the
various progenitor cells that produce the white blood
cells
27.
28. Interactions:
*Telomere shortening activates p53 which leads to
damaged mitochondria.
*The inefficient electron transport chain in damaged
mitochondria produces ROS.
*Abundant nutrients (e.g. amino acids) as well as
other growth stimulants activate TOR which
promotes anabolism (protein and lipid synthesis) with
attendant production of reactive oxygen species
(ROS) and aging.
*Calorie restriction, working through SIRT1 inhibits
TOR and its downstream effects.
*Inhibition of TOR relieves its inhibition
of autophagy allowing the cells to scavenge, for
example, damaged mitochondria.
29. * Gene expression declined in old age for many genes. Some
examples:
* Genes encoding proteins involved in synaptic activity in the
brain (e.g., learning, memory)
* NMDA, AMPA, GABA receptors
* calcium- calmodulin-dependent kinase II (CaMKII)
* Genes involved in mitochondrial functions, such as
* Production of ATP (needed for DNA repair)
* Production of damaging reactive oxygen species (ROS)
30. Clues from Premature Aging Syndromes
* Werner's syndrome-The hair of patients turns gray in their 20s
and most die in their late 40s with such signs of age
as osteoporosis, cataracts, and atherosclerosis.
* Cockayne syndrome (CS)-. While these people show only some
of the signs of aging, they do have a sharply-reduced life span.
31. Ataxia telangiectasia (AT)-These patients show signs of
premature aging. They lack a functioning gene (ATM)
product needed to detect DNA damage and initiate a repair
response.
Hutchinson-Gilford progeria syndrome-. Caused by
mutations in the gene (LMNA) for lamin the intermediate
filament protein that stabilizes the inner membrane of
the nuclear envelope.
32. SOME MODEL ORGANISNS USED IN LONGEVITY
RESEARCH
* Single mutants in Caenorhabditis elegans can reduce mortality
threefold and combinations of variants lead to as much as a sixfold
extension in lifespan, increasing to almost eightfold when combined with
dietary restriction.
* The first longevity mutant to be identified was the C. elegans gene age-
1 that encodes phosphatidylinositol 3-kinase (PI3K) , which has a key role in
a signalling pathway that is homologous to the mammalian insulin–IGF1
(insulin-like growth factor 1) pathway
33.
34. *The nematode affect mitochondrial function, the so-called
Mit mutants. Starting with the identification of clk-1, and
now involving about a hundred distinct loci, numerous Mit
mutations result in life extension, typically of 20–40% and
sometimes more. Many of these mutants interact with the
insulin–IGF1 pathway mutants to cause life extension
beyond that observed in single-gene mutants alone.
*Two key examples are sir-2 and Tor (Target of
rapamycin), which were identified in yeast and
35. Drosophila melanogaster, respectively. sir-2 encodes an
NAD-dependent protein deacetylase, which might mediate
the lifespan-extending effects of dietary restriction,
whereas Tor encodes a protein that is involved in sensing
amino-acid availability
36. * Many candidate genes have been investigated for putative
associations with human survival or longevity.
Cardiovascular genes
* APOE, which is the only gene with common variants that have
consistently been associated with longevity, has an important
role in regulating lipoproteins
* As three isoforms, APOE2, APOE3 and APOE4
* APOE4 has repeatedly been associated with a moderately
increased risk of both cardiovascular disease and Alzheimer
disease, whereas APOE2 is protective
37.
38.
39. *In
lipoprotein metabolism, microsomal triglyceride
transfer protein (MTTP), has also been implicated
in human longevity.
*Variants
in the gene encoding angiotensin Iconverting enzyme (ACE) are also biologically
plausible candidates for longevity
Metabolism-related genes
*Insulin–IGF1 signalling pathway. The presence
of at least one copy of a specific IGF1R allele
was shown to result in low levels of freeplasma IGF and to be more highly represented
among long-lived individuals. The same study
also reported that different combinations
ofIGF1R and PI3KCB alleles affect free-plasma
IGF1 levels and longevity.
40.
41. * Immune system genes
* The multifunctional cytokine interleukin 6 (IL6) is
central to this inflammation, and is overexpressed
in many of the stress-related conditions that are
characteristic features of ageing
45. Outlook: the future of human longevity genetics
* Although there are many biologically plausible
candidates for genes that influence human lifespan,
only one finding has so far been replicated
* Large-scale and carefully designed studies will be
essential for progress in genetic studies of human
longevity. Large international collaborations have
recently been established in the European Union
(the Genetics of Healthy Ageing project
GenomEUtwin) and the United States (the Long Life
Family Study) to identify genetic and non-genetic
factors of importance for exceptional longevity
46. These studies assess long-lived siblings and controls,
and some of these also include intermediate
phenotypes such as cardiovascular risk factors in
their offspring.
These studies are most promising when combined
with the use of high-throughput genotyping
techniques that make multi-locus analysis (of
haplotypes and gene–gene interactions) and genomewide association studies feasible. Genome-wide
association studies have the advantage that they do
not depend on biologically plausible candidate genes
or knowledge of specific variants.
Large-scale studies are logistically and financially
demanding
Understanding the genetic basis for longevity is an
extraordinarily difficult task, but it has the potential
to provide insights into central mechanisms of ageing
47. The record holder of maximum longevity belongs to France's Jeanne
Calment,who lived to be 122 years and 164 days old. Longevity ran in her
family. Calment's mother lived until she was 86 and her father until he was
94. Her personal outlook of life may also contribute; it is said that she was
immune to stress. She was once quoted: "If you can't do anything about
it,don’t worry about it”
48. *"Genes are not destiny!" ~ Bruce Lipton, Ph.D.
*The development of an understanding of the true factors
of longevity took place so that they may apply them in
their lives.
*The false belief constantly being expounded by media
sources as well as through word of mouth conversations,
is disappointing. Longevity genetics are in all of us just
waiting to be activated.
*It cannot be said that way as "I have longevity genes
because my mom lived past the age of 90, so I can eat
and do whatever I want." Here we have the entire field of
biology which is moving along and making
groundbreaking discoveries, yet because of the media's
misunderstandings and seemingly western culture's need
to avoid taking responsibility, people are not seeing the
truth that our health is guided by environmental factors.
49. However, we are beginning to see changes. The scientists and academics
are beginning to come out with this "new biology" in books and articles
geared towards the public.
Also with the advent of quantum physics, its applications to biology on a
microcosmic level are just becoming unveiled!
The need to bypass the media with information has become necessary since
they've developed ulterior motives and are generally focused on
communicating news from a place of fear and dis-empowerment. (For
example, the media constantly tries to report on the latest possible cancer
"cure" that's just around the corner feeds the public's craving for that onestop-magic-bullet-pill which is never going to exist and stops them from
truly taking control of their lifestyle.) The internet is making this very
possible. It is no coincidence that time and time again, true progress brings
us to a place of empowerment where we can liberate ourselves.
“The true secrets of longevity genetics is in your belief system!”
50. By:
Nazish Nehal,
M. Tech (Biotechnology),
University School of Biotechnology (USBT),
Guru Gobind Singh Indraprastha University,
New Delhi (INDIA)