Top British gerontologist, Chief Science Officer, SENS research foundation and fellow at the Institute for Ethics and Emerging Technologies speaks about his research work on regenerative medicine at Nigeria ICT Fest 2015.
Aubrey de grey why you're helpless now but not for longSelf Spark
This document discusses aging and age-related diseases. It notes that while infectious diseases have been prevented through sanitation, vaccines, antibiotics, and carrier control, age-related diseases have not. It describes aging as the lifelong accumulation of damage to tissues, cells, and molecules in the body from normal metabolic processes. This damage cannot be automatically reversed by the body and leads to disease and disability when too much damage accumulates. The document advocates for a maintenance approach to treating aging by repairing and preventing further damage as a way to significantly extend healthy lifespans. It provides examples of research into specific maintenance therapies and argues this approach could eliminate most age-related diseases.
Contents :
General features of pathology
Features of cell injury
Hypoxia
Ageing
Necrosis
General features of apoptosis
Apoptotic and anti apoptotic protein
Calcification
Atrophy and hypertrophy
Hyperplasia and metaplasia
Stem cells
Fixatives and stains
Pigment
Bactericidal system
Hydrogen peroxidase
Oxidative stress
Free radical
NADPH oxidase
Basement membrane
Inflammation
Inflammatory mediators
Hydrostatic and osmotic pressure
General features of inflammation
Systemic inflammatory response syndrome
Autoantigen and associated diseases
Acute inflammation
Chronic inflammation
Chronic granulomatous disease
Granuloma
Complement system
Opsonization
Phagocytosis
Chediak higashi syndrome
Chemotaxis
Neoplasia
Cell cycle
Causes of neoplasia
Features of neoplasia
Protooncogenes and tumor suppressor genes
Management of neoplasia
General features of tumor markers
CA-125
CEA
AFP
Features of tumors
For more details, visit www.medpgnotes.com
You can send your queries to medpgnotes@gmail.com
Multiple myeloma is a cancer of plasma cells that produce abnormal antibodies. It most commonly affects bones and causes symptoms like bone pain. Diagnosis involves blood and bone marrow tests to detect the abnormal plasma cells and antibodies. Treatment involves chemotherapy, steroids, immunomodulatory drugs, and stem cell transplantation to suppress the cancer. Outcomes have improved in recent years but still vary depending on individual risk factors.
Cell Injury in hindi
Cell injury is defined as the functional and morphologic effects of a variety of stresses on the cell from various etiologic agents which result in change in its internal and external environment.
The term cell injury is used to indicate a state in which the capacity for physiological adaptation is exceeded.
This may occur when the stimulus is excessive or when the cell is no longer capable to adapt without suffering some form of damage.
Cellular response to stress may vary depending upon following two factors:
Host Factors: Type of cell, Nutritional status of cell etc.
Factors pertaining to injurious agent: Its type, dose etc.
Etiology/Causes
Hypoxia and Ischaemia
Physical Agents
Chemicals and Drugs
Microbial Agents
Immunologic Causes
Nutritional Derangements
Ageing
Psychogenic Cause
Iatrogenic Cause
Idiopathic Disease
#rohitkumartrivedi
#cellinjury
#cellinjurypathology
The document discusses how the immune system changes with age. As people get older, their immune system responds more slowly, vaccines may be less effective, and healing is slowed. The ability to detect and repair cell damage declines as well. Aging leads to oxidative stress that damages proteins in dendritic cells, impairing their ability to activate the immune response. While aging of hematopoietic stem cells reduces lymphocyte production and shifts balance toward myeloid cells, the aging environment also contributes to declining immune function in elderly individuals. Various strategies to rejuvenate the thymus through hormones and growth factors have shown potential but require further evaluation.
The document discusses cell injury and cell death. It explains that cells have a normal steady state of homeostasis but stress can force cells to adapt or become injured if the stress exceeds their capacity. Cell injury can be reversible or irreversible and leads to cell death if irreversible. Key systems vulnerable to injury are membranes, respiration, protein synthesis and the genetic apparatus. Causes of injury include hypoxia, toxins, infections and more. Reversible injury disrupts mitochondria while irreversible injury causes mitochondrial and lysosomal damage leading to cell death.
This document discusses cellular injury. It defines cell injury as changes to a cell's internal and external environment caused by various stresses from etiological agents. Short term, mild stresses can lead to reversible cell injury through adaptations, while long term, severe stresses can cause irreversible injury and cell death. Reversible injury involves things like decreased ATP and protein synthesis, while irreversible injury includes nuclear damage, lysosomal enzyme release, and cell digestion. The document outlines various causes of cell injury and the morphological changes seen in reversible versus irreversible injury states.
This document provides an overview of cellular injury and cell death. It discusses the concepts of pathology, adaptation through hypertrophy, atrophy, hyperplasia and metaplasia. Cell injury occurs when stress exceeds a cell's adaptive capacity and can result from hypoxia, toxins, infections or genetic factors. Mitochondrial dysfunction reduces ATP and causes cell swelling. Reversible injuries include cloudy swelling and fatty change. Irreversible injuries include necrosis, which involves membrane rupture and organelle damage, and apoptosis, which is programmed single-cell death. Necrosis causes inflammation while apoptosis does not. The document also covers pathologic calcification and its dystrophic and metastatic forms.
Aubrey de grey why you're helpless now but not for longSelf Spark
This document discusses aging and age-related diseases. It notes that while infectious diseases have been prevented through sanitation, vaccines, antibiotics, and carrier control, age-related diseases have not. It describes aging as the lifelong accumulation of damage to tissues, cells, and molecules in the body from normal metabolic processes. This damage cannot be automatically reversed by the body and leads to disease and disability when too much damage accumulates. The document advocates for a maintenance approach to treating aging by repairing and preventing further damage as a way to significantly extend healthy lifespans. It provides examples of research into specific maintenance therapies and argues this approach could eliminate most age-related diseases.
Contents :
General features of pathology
Features of cell injury
Hypoxia
Ageing
Necrosis
General features of apoptosis
Apoptotic and anti apoptotic protein
Calcification
Atrophy and hypertrophy
Hyperplasia and metaplasia
Stem cells
Fixatives and stains
Pigment
Bactericidal system
Hydrogen peroxidase
Oxidative stress
Free radical
NADPH oxidase
Basement membrane
Inflammation
Inflammatory mediators
Hydrostatic and osmotic pressure
General features of inflammation
Systemic inflammatory response syndrome
Autoantigen and associated diseases
Acute inflammation
Chronic inflammation
Chronic granulomatous disease
Granuloma
Complement system
Opsonization
Phagocytosis
Chediak higashi syndrome
Chemotaxis
Neoplasia
Cell cycle
Causes of neoplasia
Features of neoplasia
Protooncogenes and tumor suppressor genes
Management of neoplasia
General features of tumor markers
CA-125
CEA
AFP
Features of tumors
For more details, visit www.medpgnotes.com
You can send your queries to medpgnotes@gmail.com
Multiple myeloma is a cancer of plasma cells that produce abnormal antibodies. It most commonly affects bones and causes symptoms like bone pain. Diagnosis involves blood and bone marrow tests to detect the abnormal plasma cells and antibodies. Treatment involves chemotherapy, steroids, immunomodulatory drugs, and stem cell transplantation to suppress the cancer. Outcomes have improved in recent years but still vary depending on individual risk factors.
Cell Injury in hindi
Cell injury is defined as the functional and morphologic effects of a variety of stresses on the cell from various etiologic agents which result in change in its internal and external environment.
The term cell injury is used to indicate a state in which the capacity for physiological adaptation is exceeded.
This may occur when the stimulus is excessive or when the cell is no longer capable to adapt without suffering some form of damage.
Cellular response to stress may vary depending upon following two factors:
Host Factors: Type of cell, Nutritional status of cell etc.
Factors pertaining to injurious agent: Its type, dose etc.
Etiology/Causes
Hypoxia and Ischaemia
Physical Agents
Chemicals and Drugs
Microbial Agents
Immunologic Causes
Nutritional Derangements
Ageing
Psychogenic Cause
Iatrogenic Cause
Idiopathic Disease
#rohitkumartrivedi
#cellinjury
#cellinjurypathology
The document discusses how the immune system changes with age. As people get older, their immune system responds more slowly, vaccines may be less effective, and healing is slowed. The ability to detect and repair cell damage declines as well. Aging leads to oxidative stress that damages proteins in dendritic cells, impairing their ability to activate the immune response. While aging of hematopoietic stem cells reduces lymphocyte production and shifts balance toward myeloid cells, the aging environment also contributes to declining immune function in elderly individuals. Various strategies to rejuvenate the thymus through hormones and growth factors have shown potential but require further evaluation.
The document discusses cell injury and cell death. It explains that cells have a normal steady state of homeostasis but stress can force cells to adapt or become injured if the stress exceeds their capacity. Cell injury can be reversible or irreversible and leads to cell death if irreversible. Key systems vulnerable to injury are membranes, respiration, protein synthesis and the genetic apparatus. Causes of injury include hypoxia, toxins, infections and more. Reversible injury disrupts mitochondria while irreversible injury causes mitochondrial and lysosomal damage leading to cell death.
This document discusses cellular injury. It defines cell injury as changes to a cell's internal and external environment caused by various stresses from etiological agents. Short term, mild stresses can lead to reversible cell injury through adaptations, while long term, severe stresses can cause irreversible injury and cell death. Reversible injury involves things like decreased ATP and protein synthesis, while irreversible injury includes nuclear damage, lysosomal enzyme release, and cell digestion. The document outlines various causes of cell injury and the morphological changes seen in reversible versus irreversible injury states.
This document provides an overview of cellular injury and cell death. It discusses the concepts of pathology, adaptation through hypertrophy, atrophy, hyperplasia and metaplasia. Cell injury occurs when stress exceeds a cell's adaptive capacity and can result from hypoxia, toxins, infections or genetic factors. Mitochondrial dysfunction reduces ATP and causes cell swelling. Reversible injuries include cloudy swelling and fatty change. Irreversible injuries include necrosis, which involves membrane rupture and organelle damage, and apoptosis, which is programmed single-cell death. Necrosis causes inflammation while apoptosis does not. The document also covers pathologic calcification and its dystrophic and metastatic forms.
MDS is a clonal hematopoietic stem cell disorder characterized by disordered cell proliferation and impaired differentiation, resulting in cytopenias and risk of progression to leukemia. It commonly affects elderly people over age 70 and has a slight male preponderance. Exposure to radiation, chemotherapy, benzene, and genetic disorders can increase the risk of developing MDS. Cytogenetic abnormalities are found in half of patients and certain mutations are associated with prognosis, such as spliceosome defects correlating with favorable outcomes and mutations in EZH2, TP53, RUNX1, and ASXL1 correlating with poor outcomes.
This document discusses cell injury and homeostasis. It defines cell injury as occurring when adaptive responses are exceeded or the cell is exposed to an injurious stimulus. There are two types of cell injury: reversible and irreversible. Free radicals can cause cell injury by reacting with lipids, DNA and proteins. Free radicals are generated through normal metabolic processes, radiation exposure, and chemical metabolism, and can be neutralized by antioxidants. Increased calcium levels and decreased ATP can also occur during cell injury.
1) Systemic lupus erythematosus (SLE) is a chronic autoimmune disorder that predominantly affects younger women. SLE can affect almost every system in the body.
2) Management of SLE is individualized depending on symptoms but may include medications like NSAIDs, antimalarials, steroids, immunosuppressants, and cytotoxic drugs. Nursing care focuses on monitoring for organ involvement, managing pain and fatigue, health promotion, and supporting the patient.
3) Key aspects of the nursing care plan include assessing for symptoms, monitoring organ systems affected, educating the patient
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.
This document discusses cellular injury and adaptation. It notes that cells exist in a state of homeostasis but can become injured by various stressors like hypoxia or toxins. Injuries can be reversible or irreversible. Initial injuries disrupt ATP production and increase intracellular calcium levels, activating damaging enzymes. This can lead to further damage of mitochondria and lysosomes as well as increased reactive oxygen species. Depending on the severity and duration of injury, cells may undergo apoptosis, necrosis, or adaptational changes in an attempt to survive.
SLE is an autoimmune disease resulting in butterfly rash and various other symtoms,a brief introduction and diagnosis and causes are mentioned in this ppt.
Mitochondrial myopathy is a group of neuromuscular diseases caused by damage to the mitochondria in nerve and muscle cells. Symptoms include muscle weakness, exercise intolerance, heart problems, movement disorders, and seizures. Most cases occur in people under 20 years old and begin with exercise intolerance or muscle weakness. While prognoses vary, these are progressive diseases that can lead to death. There is no cure, but physical therapy, vitamins, and supplements may provide relief from some symptoms.
The document summarizes the pathogenesis of systemic lupus erythematosus (SLE). SLE results from a failure of self-tolerance mechanisms, influenced by both genetic and environmental factors. Genetic factors that contribute include genes in the MHC region and those encoding early complement components. Environmental triggers involve ultraviolet light exposure and certain drugs. Immunological factors include defective B cell and T cell tolerance, activation of B cells by nucleic acids engaging toll-like receptors, and elevated type I interferons that stimulate dendritic cells and B cells. Together these genetic, environmental, and immunological abnormalities lead to production of autoantibodies against nuclear antigens.
Martin Borch Jensen - The Science of Aging 2019Impact.Tech
This document discusses the science of aging and challenges in aging research. It defines aging as the progressive decline in physiological function over time due to genetic and environmental factors. The document summarizes current understanding of aging mechanisms like DNA damage, protein misfolding, stem cell depletion, cellular senescence, and chronic inflammation. It also outlines the landscape of aging research including current funding levels and companies developing therapies. Major challenges discussed are the complexity of aging, difficulty capturing treatment value, and need for results in aged biological systems. The document advocates scaling therapeutic discovery through parallel in vivo testing in animal models of aging.
An early diagnosis kit is being developed that combines genetic and immunological tests to diagnose multiple sclerosis (MS) with high accuracy through a simple blood test. The kit leverages proven technologies from MS Genetics and Louphius that have shown accuracy rates of 83% and 91% respectively in differentiating MS from other conditions. By combining results from tests measuring gene expression, genetic risk alleles, and anti-glycan antibodies through conditional probability, the kit aims to outperform individual tests to enable early and differential diagnosis of MS with a high positive predictive value. A Horizon 2020 project is proposed to further optimize and validate the individual tests and their combined use in an integrated classification system to facilitate early treatment and reduce disability.
This document discusses MELAS (Mitochondrial Encephalomyopathy with Lactic Acidosis and Stroke-like Episodes), a mitochondrial disease. MELAS is most commonly caused by the A3243G mutation and is maternally inherited. It is characterized by stroke-like episodes typically beginning in the teenage years, as well as other symptoms like diabetes, deafness, and cognitive impairment. Brain imaging during episodes shows cortical lesions. Muscle biopsies may reveal abnormal mitochondria clustering in blood vessels. There is currently no cure, but certain treatments can help manage symptoms.
Biochemistry of Aging
Presented by Shanzay Annum Malik
Aging
Gradual change in an organism that leads to increased risk of weakness, disease, and death over the entire adult life span of any living thing.
There is a decline in biological functions and in ability to adapt to metabolic stress.
Changes in organs include
reduced immunity,
loss of muscle strength,
decline in memory and cognition,
loss of colour in the hair
elasticity in the skin.
Gerontology and Geriatrics
Gerontology is concerned with the changes that occur between maturity and death along with factors that influence these changes.
Geriatrics focuses on health care of elderly people and promote health by preventing and treating diseases and disabilities in older adults.
Factors of Aging
Mitochondria: main unit of chemical power supply
During the synthesis of macroergical bio-molecules(high energy releasing potentials e.g. ATP) free radicals are being produced as the by-product.
Free radicals released in large quantities cause intercellular oxidative stress (e.g. oxidative damage of mitochondria)
damaging mitochondria and cause early apoptosis
Free radical
A molecule that contains one or more unpaired electrons &is capable of independent existence.
Eg : Superoxide H2O2,
hydroperoxy radical (HOO+2 )
lipid peroxideradical (ROO)
Nitric oxide (NO)
Harmful effect of free radicals
Because of their reactive nature, free radical can provoke inflammation or altered cellular function through
Lipid peroxidation
Protein modification
DNA modification
Lipid peroxidation product:
React with amino acid mainly CYS, HIS,LYS to modify protein structure & function.
Can crosslink lipid in cell membrane interrupting structure & fluidity.
Protein modification
DNA modification :
Free radical induced DNA damage includes
strand break.
DNA protein crosslink.
large range of base & sugar modification.
Telomeres
Repetitive DNA sequences at the ends of all human chromosomes
aging cells have shorter telomeres
length differs between species
in humans 8-14kb long
Telomeres are thought to be the "clock" that regulates how many times an individual cell can divide.
Telomeric sequences shorten each time the DNA replicates.
Once the telomere shrinks to a certain level, the cell can no longer divide. Its metabolism slows down, it ages, and dies
Apoptosis and Necrosis
There are two ways that a cell can die:
Necrosis occurs when a cell is damaged by an external force, such as poison, a bodily injury, an infection or getting cut off from the blood supply (which might occur during a heart attack or stroke). When cells die from necrosis, it's a rather messy affair. The death causes inflammation that can cause further distress or injury within the body.
Apoptosis or programmed cell death
When a cell is compelled to commit suicide proteins called caspases go into action.
They break down the cellular components needed for surviva
Cellular adaptation
Adjustments which the cells make in response to stresses.
Adjustments may be for physiologic need or response to non-lethal pathogenic injury (Pathologic adaptation).
Adaptive responses are reversible on withdrawal of stimulus.
If the irritant stimulus persists for longer duration or is more lethal, the cell may not be able to survive.
“Survival of the Adaptable”
TYPES OF CELLULAR ADAPTATION:
Atrophy
Hypertrophy
Hyperplasia
Metaplasia
Dysplasia
Mitochondrial myopathies are a group of disorders caused by abnormalities in mitochondrial DNA. They can cause a variety of symptoms depending on the specific syndrome, including Kearns-Sayre syndrome, MERRF (myoclonic epilepsy with ragged red fibers), and MELAS (mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes). MERRF is characterized by myoclonus, epilepsy, and ragged red fibers seen on muscle biopsy. It is generally diagnosed in childhood or adolescence. While there is no cure, treatment focuses on managing symptoms in affected body systems like the brain, eyes, and heart.
This document summarizes a student's course research work on degenerative brain disorders in aging people. It provides an overview of several common neurodegenerative diseases including Alzheimer's disease, Pick's disease, Parkinson's disease, Huntington's disease, and amyotrophic lateral sclerosis. For each disease, it discusses classification, clinical features, pathological findings, and prognosis. It also includes statistics on disease rates according to age and country. The research was conducted for a pathological anatomy course at Kursk State Medical University under the supervision of an associated professor.
Leukemia is caused by an overproduction of blood cells that do not die off normally, taking up space needed for healthy blood cells. It is not a communicable disease and anyone can develop leukemia. Symptoms of leukemia can include fever, fatigue, bruising, and bone or joint pain. A blood test and sometimes tissue test can confirm a diagnosis of leukemia, which can be either acute or chronic. Treatment involves chemotherapy, radiation, and sometimes bone marrow transplants, though regular exercise may help reduce cancer risks. Leukemia remains a serious disease.
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.
Dr Aubrey de Grey, né le 20 avril 1963, à Londres, est un scientifique anglais, ancien informaticien à l’université de Cambridge et autodidacte en biogérontologie. Il vit actuellement à San Francisco. Lors de la conférence FUTUR DE LA SANTÉ tenue le 10 octobre 2017, il a présenté les avancées de la technologie combinées à la génomique permettant de développer un moyen de régénérer les tissus cellulaires pour rajeunir et allonger l’espérance de vie humaine.
MDS is a clonal hematopoietic stem cell disorder characterized by disordered cell proliferation and impaired differentiation, resulting in cytopenias and risk of progression to leukemia. It commonly affects elderly people over age 70 and has a slight male preponderance. Exposure to radiation, chemotherapy, benzene, and genetic disorders can increase the risk of developing MDS. Cytogenetic abnormalities are found in half of patients and certain mutations are associated with prognosis, such as spliceosome defects correlating with favorable outcomes and mutations in EZH2, TP53, RUNX1, and ASXL1 correlating with poor outcomes.
This document discusses cell injury and homeostasis. It defines cell injury as occurring when adaptive responses are exceeded or the cell is exposed to an injurious stimulus. There are two types of cell injury: reversible and irreversible. Free radicals can cause cell injury by reacting with lipids, DNA and proteins. Free radicals are generated through normal metabolic processes, radiation exposure, and chemical metabolism, and can be neutralized by antioxidants. Increased calcium levels and decreased ATP can also occur during cell injury.
1) Systemic lupus erythematosus (SLE) is a chronic autoimmune disorder that predominantly affects younger women. SLE can affect almost every system in the body.
2) Management of SLE is individualized depending on symptoms but may include medications like NSAIDs, antimalarials, steroids, immunosuppressants, and cytotoxic drugs. Nursing care focuses on monitoring for organ involvement, managing pain and fatigue, health promotion, and supporting the patient.
3) Key aspects of the nursing care plan include assessing for symptoms, monitoring organ systems affected, educating the patient
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.
This document discusses cellular injury and adaptation. It notes that cells exist in a state of homeostasis but can become injured by various stressors like hypoxia or toxins. Injuries can be reversible or irreversible. Initial injuries disrupt ATP production and increase intracellular calcium levels, activating damaging enzymes. This can lead to further damage of mitochondria and lysosomes as well as increased reactive oxygen species. Depending on the severity and duration of injury, cells may undergo apoptosis, necrosis, or adaptational changes in an attempt to survive.
SLE is an autoimmune disease resulting in butterfly rash and various other symtoms,a brief introduction and diagnosis and causes are mentioned in this ppt.
Mitochondrial myopathy is a group of neuromuscular diseases caused by damage to the mitochondria in nerve and muscle cells. Symptoms include muscle weakness, exercise intolerance, heart problems, movement disorders, and seizures. Most cases occur in people under 20 years old and begin with exercise intolerance or muscle weakness. While prognoses vary, these are progressive diseases that can lead to death. There is no cure, but physical therapy, vitamins, and supplements may provide relief from some symptoms.
The document summarizes the pathogenesis of systemic lupus erythematosus (SLE). SLE results from a failure of self-tolerance mechanisms, influenced by both genetic and environmental factors. Genetic factors that contribute include genes in the MHC region and those encoding early complement components. Environmental triggers involve ultraviolet light exposure and certain drugs. Immunological factors include defective B cell and T cell tolerance, activation of B cells by nucleic acids engaging toll-like receptors, and elevated type I interferons that stimulate dendritic cells and B cells. Together these genetic, environmental, and immunological abnormalities lead to production of autoantibodies against nuclear antigens.
Martin Borch Jensen - The Science of Aging 2019Impact.Tech
This document discusses the science of aging and challenges in aging research. It defines aging as the progressive decline in physiological function over time due to genetic and environmental factors. The document summarizes current understanding of aging mechanisms like DNA damage, protein misfolding, stem cell depletion, cellular senescence, and chronic inflammation. It also outlines the landscape of aging research including current funding levels and companies developing therapies. Major challenges discussed are the complexity of aging, difficulty capturing treatment value, and need for results in aged biological systems. The document advocates scaling therapeutic discovery through parallel in vivo testing in animal models of aging.
An early diagnosis kit is being developed that combines genetic and immunological tests to diagnose multiple sclerosis (MS) with high accuracy through a simple blood test. The kit leverages proven technologies from MS Genetics and Louphius that have shown accuracy rates of 83% and 91% respectively in differentiating MS from other conditions. By combining results from tests measuring gene expression, genetic risk alleles, and anti-glycan antibodies through conditional probability, the kit aims to outperform individual tests to enable early and differential diagnosis of MS with a high positive predictive value. A Horizon 2020 project is proposed to further optimize and validate the individual tests and their combined use in an integrated classification system to facilitate early treatment and reduce disability.
This document discusses MELAS (Mitochondrial Encephalomyopathy with Lactic Acidosis and Stroke-like Episodes), a mitochondrial disease. MELAS is most commonly caused by the A3243G mutation and is maternally inherited. It is characterized by stroke-like episodes typically beginning in the teenage years, as well as other symptoms like diabetes, deafness, and cognitive impairment. Brain imaging during episodes shows cortical lesions. Muscle biopsies may reveal abnormal mitochondria clustering in blood vessels. There is currently no cure, but certain treatments can help manage symptoms.
Biochemistry of Aging
Presented by Shanzay Annum Malik
Aging
Gradual change in an organism that leads to increased risk of weakness, disease, and death over the entire adult life span of any living thing.
There is a decline in biological functions and in ability to adapt to metabolic stress.
Changes in organs include
reduced immunity,
loss of muscle strength,
decline in memory and cognition,
loss of colour in the hair
elasticity in the skin.
Gerontology and Geriatrics
Gerontology is concerned with the changes that occur between maturity and death along with factors that influence these changes.
Geriatrics focuses on health care of elderly people and promote health by preventing and treating diseases and disabilities in older adults.
Factors of Aging
Mitochondria: main unit of chemical power supply
During the synthesis of macroergical bio-molecules(high energy releasing potentials e.g. ATP) free radicals are being produced as the by-product.
Free radicals released in large quantities cause intercellular oxidative stress (e.g. oxidative damage of mitochondria)
damaging mitochondria and cause early apoptosis
Free radical
A molecule that contains one or more unpaired electrons &is capable of independent existence.
Eg : Superoxide H2O2,
hydroperoxy radical (HOO+2 )
lipid peroxideradical (ROO)
Nitric oxide (NO)
Harmful effect of free radicals
Because of their reactive nature, free radical can provoke inflammation or altered cellular function through
Lipid peroxidation
Protein modification
DNA modification
Lipid peroxidation product:
React with amino acid mainly CYS, HIS,LYS to modify protein structure & function.
Can crosslink lipid in cell membrane interrupting structure & fluidity.
Protein modification
DNA modification :
Free radical induced DNA damage includes
strand break.
DNA protein crosslink.
large range of base & sugar modification.
Telomeres
Repetitive DNA sequences at the ends of all human chromosomes
aging cells have shorter telomeres
length differs between species
in humans 8-14kb long
Telomeres are thought to be the "clock" that regulates how many times an individual cell can divide.
Telomeric sequences shorten each time the DNA replicates.
Once the telomere shrinks to a certain level, the cell can no longer divide. Its metabolism slows down, it ages, and dies
Apoptosis and Necrosis
There are two ways that a cell can die:
Necrosis occurs when a cell is damaged by an external force, such as poison, a bodily injury, an infection or getting cut off from the blood supply (which might occur during a heart attack or stroke). When cells die from necrosis, it's a rather messy affair. The death causes inflammation that can cause further distress or injury within the body.
Apoptosis or programmed cell death
When a cell is compelled to commit suicide proteins called caspases go into action.
They break down the cellular components needed for surviva
Cellular adaptation
Adjustments which the cells make in response to stresses.
Adjustments may be for physiologic need or response to non-lethal pathogenic injury (Pathologic adaptation).
Adaptive responses are reversible on withdrawal of stimulus.
If the irritant stimulus persists for longer duration or is more lethal, the cell may not be able to survive.
“Survival of the Adaptable”
TYPES OF CELLULAR ADAPTATION:
Atrophy
Hypertrophy
Hyperplasia
Metaplasia
Dysplasia
Mitochondrial myopathies are a group of disorders caused by abnormalities in mitochondrial DNA. They can cause a variety of symptoms depending on the specific syndrome, including Kearns-Sayre syndrome, MERRF (myoclonic epilepsy with ragged red fibers), and MELAS (mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes). MERRF is characterized by myoclonus, epilepsy, and ragged red fibers seen on muscle biopsy. It is generally diagnosed in childhood or adolescence. While there is no cure, treatment focuses on managing symptoms in affected body systems like the brain, eyes, and heart.
This document summarizes a student's course research work on degenerative brain disorders in aging people. It provides an overview of several common neurodegenerative diseases including Alzheimer's disease, Pick's disease, Parkinson's disease, Huntington's disease, and amyotrophic lateral sclerosis. For each disease, it discusses classification, clinical features, pathological findings, and prognosis. It also includes statistics on disease rates according to age and country. The research was conducted for a pathological anatomy course at Kursk State Medical University under the supervision of an associated professor.
Leukemia is caused by an overproduction of blood cells that do not die off normally, taking up space needed for healthy blood cells. It is not a communicable disease and anyone can develop leukemia. Symptoms of leukemia can include fever, fatigue, bruising, and bone or joint pain. A blood test and sometimes tissue test can confirm a diagnosis of leukemia, which can be either acute or chronic. Treatment involves chemotherapy, radiation, and sometimes bone marrow transplants, though regular exercise may help reduce cancer risks. Leukemia remains a serious disease.
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.
Dr Aubrey de Grey, né le 20 avril 1963, à Londres, est un scientifique anglais, ancien informaticien à l’université de Cambridge et autodidacte en biogérontologie. Il vit actuellement à San Francisco. Lors de la conférence FUTUR DE LA SANTÉ tenue le 10 octobre 2017, il a présenté les avancées de la technologie combinées à la génomique permettant de développer un moyen de régénérer les tissus cellulaires pour rajeunir et allonger l’espérance de vie humaine.
Theories of Aging - Part 1 in medicine and health sciencesJackTan88
This document provides an overview of theories of aging. It discusses both biological/physiological and psychological perspectives on aging. From a biological standpoint, it describes programmed aging theories like the telomere theory, which proposes that cells can only divide a finite number of times due to shortening telomeres. It also discusses error theories of aging, like the free radical theory, which suggests aging results from cellular damage over time. The document aims to explain the aging process and major theories about what causes aging.
Cellular ageing is the progressive decline in cellular function and viability caused by genetic abnormalities and the accumulation of damage over time. There are several theories that attempt to explain the aging process, including evolutionary, molecular, cellular, and systemic theories. At the cellular level, ageing is caused by DNA damage from both endogenous and exogenous sources, as well as telomere shortening after each cell division. Other factors that contribute to cellular ageing include defective protein homeostasis, disrupted nutrient sensing pathways, and the accumulation of damaged or mutated proteins and organelles within the cell over time. Premature ageing disorders provide insights into how defects in certain genes involved in DNA repair and maintenance can accelerate the normal ageing process.
Cellular ageing is the progressive decline in cellular function and viability caused by genetic abnormalities and the accumulation of damage over time. There are several theories that attempt to explain the aging process, including evolutionary, molecular, cellular, and systemic theories. At the cellular level, ageing is caused by DNA damage from both endogenous and exogenous sources, as well as telomere shortening after each cell division. Other factors that contribute to cellular ageing include defective protein homeostasis, disrupted nutrient sensing pathways, and a decline in cellular repair mechanisms. Premature ageing disorders provide insights into how disrupting certain ageing processes can accelerate ageing. While cellular senescence limits cell proliferation and acts as a tumor suppressor, it is
This document discusses several theories of aging at the cellular, molecular, evolutionary, and systems levels. The main cellular theories discussed are telomere shortening and free radical damage accumulation over time. Evolutionary theories proposed include mutation accumulation, antagonistic pleiotropy, and the declining force of natural selection with age. Lifestyle and future biomedical interventions are mentioned as potential ways to promote healthy aging or extend lifespan.
Cellular adaptations and injury can occur through various mechanisms:
(1) When cells are exposed to stressors, they may undergo reversible changes like atrophy, hypertrophy, hyperplasia, metaplasia, or dysplasia to adapt. (2) If the stressors are severe or persistent, irreversible cell injury and death through necrosis or apoptosis can result. (3) Cellular injury can be caused by free radicals, hypoxia, physical trauma, chemicals, radiation, or biological agents and can lead to tissue dysfunction or infection if necrosis occurs.
The document discusses cellular responses and adaptations to stress and injury. It provides an overview of how normal cells require specific environmental conditions to function properly and will try to adapt to changes through processes like hypertrophy, hyperplasia, atrophy and metaplasia. If cells cannot adapt to stress, either reversible or irreversible injury can occur, potentially leading to cell death through necrosis or apoptosis. The mechanisms of cellular injury include oxidative stress, depletion of ATP, calcium dysregulation, and damage to organelles like mitochondria and lysosomes.
This document discusses necrosis and apoptosis. It defines necrosis as the premature death of cells in living tissue due to irreversible injury. Necrosis can be caused by ischemia, physical agents, chemicals, or immunological injury. There are several types of necrosis including coagulative, liquefactive, caseous, and gangrenous necrosis. Treatment involves debridement and excision of dead tissue. Apoptosis is programmed cell death that occurs as part of normal development and tissue homeostasis. It is mediated by caspases and involves cell shrinkage, chromatin condensation, and fragmentation into apoptotic bodies that are phagocytosed. Dysregulation of apoptosis can contribute to diseases.
Here I show to you very interesting research news and medical utility. We can see the future of the epigenetics and molecular medicine.
Universidad Pontificia Bolivariana
Medicina School
The document discusses normal aging and provides definitions and theories related to the aging process. It addresses topics like the mechanisms of aging, theories of aging, hallmarks of aging, and changes that occur in the brain with aging. It also discusses mental health and personality in older adults, coping strategies, and factors involved in successful aging. The document provides an overview of many aspects of the normal aging process from a biological, psychological, and social perspective.
Nursing class lecture cell injury 2nd class.pptxvandana thakur
This document summarizes different types of cellular adaptation:
1. Atrophy and hypertrophy refer to decreases or increases in cell size, respectively. Pathologic atrophy can result from starvation, ischemia, disuse, neuropathy, or endocrine imbalances.
2. Hyperplasia is an increase in cell number, either physiologically like during pregnancy or pathologically like in wound healing.
3. Metaplasia is a reversible change from one adult cell type to another, which can progress to cancer if prolonged. Epithelial and mesenchymal metaplasia are described.
4. Dysplasia involves disordered cell development seen as increased layers, mitosis, and pleomorphism.
Cell injury can be reversible or irreversible, leading to cell death. Reversible injury causes pathological changes that can be reversed when the stressor is removed, while irreversible injury causes permanent changes and cell death. Cell injury is caused by various stressors like hypoxia, physical/chemical agents, microbiological agents, genetic defects, and nutritional imbalances. The key targets of injury are the mitochondria, cell membrane, proteins, cytoskeleton, and DNA. Injury disrupts cellular energy production and increases reactive oxygen species, calcium influx, and damage to membranes and DNA/proteins. This can lead to either reversible injury or the irreversible processes of necrosis or apoptosis.
Cellular Adaptation: Pathophysiology discusses various types of cellular changes that can occur in response to stimuli or injury. It describes adaptive changes like atrophy, hypertrophy, hyperplasia, and metaplasia that allow cells to adjust their size or function. It also discusses dysplastic changes and how they can potentially progress to cancer. The document outlines various causes of cellular injury including chemical, biological, physical, hypoxic, and nutritional factors. It details different types of cell death processes and conditions that can result like gangrene. The key cellular changes, causes of injury, and types of cell death are summarized.
Cellular adaptation allows cells to change their structure and function in response to stimuli to promote survival. Adaptations include atrophy (shrinking), hypertrophy (enlargement), hyperplasia (increased cell number), metaplasia (one cell type replaces another), dysplasia (abnormal cell growth), and neoplasia (uncontrolled cell growth). Cells can accumulate substances like lipids, fluid, or carbon. Injury occurs via mechanical, chemical, biological, radiation, or hypoxic/ischemic means and may cause reversible or irreversible damage depending on severity.
Cell death can occur through two main processes: necrosis and apoptosis. Necrosis is unregulated cell death caused by external factors like trauma or toxins. It involves the premature death of cells and tissue damage. Apoptosis is a tightly regulated form of programmed cell death that eliminates unnecessary or potentially dangerous cells. It involves changes to the cell like nuclear fragmentation, blebbing of the cell membrane, and formation of apoptotic bodies that are then cleared by phagocytes without inducing inflammation. Apoptosis plays an important role in development, homeostasis, and eliminating infected or damaged cells.
This document discusses cellular injury and cell death. It begins by introducing the hierarchical structure of the human body from cells to organs to systems. It then describes the different types of tissues and cellular adaptations and injuries. The main types of cellular injury discussed are reversible and irreversible injuries. Reversible injuries include changes like swelling while irreversible injuries involve cell death through necrosis or apoptosis. The document closes by defining different patterns of necrosis like coagulation, liquefactive, and caseous necrosis.
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1. Apoptosis and necrosis are two main types of cell death. Apoptosis is programmed cell death that plays an important role in development and maintaining tissue homeostasis, while necrosis is unregulated cell death caused by external factors like injury.
2. Cancer develops due to mutations in genes that regulate cell growth, allowing cells to proliferate uncontrollably. Cancer cells evade apoptosis and are able to metastasize, or spread to other parts of the body. Abnormalities in apoptosis may contribute to diseases like cancer, neurodegeneration, and autoimmune disorders.
This document discusses several key physiological traits associated with aging:
Genomic instability causes accumulation of genetic damage to DNA over a lifetime from various sources. Telomere attrition refers to shortening of telomeres each time a cell divides, ultimately limiting it to around 50 divisions. Epigenetic alterations change gene expression through factors like histone modifications and chromatin structure. Loss of proteostasis reduces the cell's ability to regulate protein production, allowing damaged proteins to accumulate. Additional traits discussed include mitochondrial dysfunction, deregulated nutrient sensing, altered intercellular communication, and cellular senescence.
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Aubrey de Grey's Slide - Nigeria ICT Fest 2015
1. Aubrey D.N.J. de Grey, Ph.D.
Chief Science Officer
SENS Research Foundation
aubrey@sens.org
http://www.sens.org/
2. Most infectious diseases have been easily
prevented
Sanitation
Vaccines
Antibiotics
Carrier control
Age-related diseases have not. Why not?
3. reduced light adaptation
reduced ethanol metabolism
altered drug pharmacokinetics
somatopause
loss of cardiac adaptability
incontinence
impaired wound healing
idiopathic axonal polyneuropathy
autonomic neuropathy
arrhythmia
chronic obstructive pulmonary disorder
benign prostatic hypertrophy
menopause
leukoaraiosis
stroke
vascular dementia
frontotemporal dementia
immunosenescence
anosmia
cachexia
anorexia of aging
systolic hypertension
ageusia
erectile dysfunction
orthostatic hypotension
impaired adaptive beta-cell proliferation
fibroblast collapse
anergic T-cell clones
cellular senescence
vascular calcification
impaired transdermal absorption
impaired thermoregulation
reduced tactile acuity
impaired vasoconstriction
loss of neuromuscular junctions
delayed withdrawal reflex
impaired pH maintenance
reduced chemical clearance
altered dermal immune cell residence and function
aberrant allergic and irritant reactions
loss of skin elasticity
impaired vitamin D synthesis
reduced renal reserve
renal cortex atrophy
gut dysbiosis
loss of jejunal villus height
impaired response to vaccination
impaired thirst
lentigo senilis
thinning hair
impaired proprioception
impaired balance
reduced vital capacity
reduced cardiorespiratory endurance
impaired sweat response
impaired blood distribution
nutrient malabsorption
diverticular disease
presbyphagia
increased reflux
alveolar loss
neuronal loss
senile emphysema
degenerative disc disease
joint calcification
pineal calcification
aberrant differentiation
gait instability
frontal demyelination
axonal atrophy
impaired functional connectivity
impaired working memory
presbycusis
osteoporosis
osteoarthritis
autoimmunity
greying hair
presbyopia
cataract
glaucoma
temporal arteritis
polymyalgia rheumatica
wrinkling
Alzheimer's disease
Pick's disease
corticobasal degeneration
progressive supranuclear palsy
Parkinson's disease
multiple system atrophy
dementia with Lewy bodies
sarcopenia
glomerulonephritis
senile cardiac amyloidosis
atherosclerosis
arteriosclerosis
age-related macular degeneration
cardiomyopathy
diastolic heart failure
cancer
systemic inflammation
oxidative stress
reduced coronary blood flow
loss of cardiac reserve
andropause
thymic involution
reduced plasma renin activity
reduced aldosterone
reduced melatonin diurnal rhythm
4. Aging is:
The life-long accumulation of “damage” to
the body that occurs as an intrinsic side-
effect of the body’s normal operation.
The body can tolerate some damage, but
too much of it causes disease and disability.
12. Cell loss, cell atrophy
Division-obsessed cells
Death-resistant cells
Mitochondrial mutations
Intracellular junk
Extracellular junk
Extracellular matrix stiffening
No new type of
damage
confirmed
since 1982
And, I’ve said
so without
challenge
since 2002
Damage type
13. Why? That was easy
How? That’s where we have a new plan
What? That’s where we show you it’s a
good plan (can be done, is being done)
15. Total synthesis of glucosepane, allowing identification
of antibodies and degraders (Science, 2015)
Modified bacterial enzyme protects cells from
atherogenic oxysterols (Biotech Bioeng, 2012)
Catalytic antibodies cleave cardiotoxic amyloid (J Biol
Chem, 2014)
Much more ongoing in our research centre and
funded labs
16. See their names, their awesome
credentials and their hard-hitting
endorsement of our research
approach at
www.sens.org/about/leadership/resea
22. Available at Amazon and all good book stores.
Paperback is cheaper, and has an extra chapter!
Visit us on the web at
http://www.sens.org/
Read the (semi-technical) book.
Drop us a line at
foundation@sens.org
Learn more