The document discusses apoptosis, or programmed cell death. It defines apoptosis as a tightly regulated suicidal program in cells that activates enzymes to degrade the cell's own DNA and proteins. Apoptosis is important for normal development and tissue homeostasis by removing unwanted cells. The mechanisms of apoptosis involve both intrinsic pathways related to mitochondrial damage and extrinsic pathways activated by death receptors. Key regulators and effectors of apoptosis like caspases, Bcl-2 family proteins, and cytochrome c are discussed. Disorders related to too much or too little apoptosis can lead to conditions like neurodegeneration or cancer.
Apoptosis is an orderly process in which the cell's contents are packaged into small packets of membrane for “garbage collection” by immune cells. Apoptosis removes cells during development, eliminates potentially cancerous and virus-infected cells, and maintains balance in the body.
Apoptosis is a process of programmed cell death that occurs in multicellular organisms. Biochemical events lead to characteristic cell changes (morphology) and death.
Apoptosis also known as cell suicide. Difference between necrosis and apoptosis. Changes in apoptosis. Mechanism of apoptosis. Functional significance of apoptosis. Applied aspects of apoptosis
g protein coupled receptors, ion channels, types of receptors, wnt signalling, cell signalling, tranduction pathway, disorders regarding the signalling
Introduction
Definition
History
Evolution and origin of apoptosis
Significance
Purpose of apoptosis
Steps /process
Morphological and biochemical changes
Mechanism of apoptosis
Caspases
Regulation of apoptosis
Disorders of apoptosis
Application
Conclusion
Referances
Apoptosis is an orderly process in which the cell's contents are packaged into small packets of membrane for “garbage collection” by immune cells. Apoptosis removes cells during development, eliminates potentially cancerous and virus-infected cells, and maintains balance in the body.
Apoptosis is a process of programmed cell death that occurs in multicellular organisms. Biochemical events lead to characteristic cell changes (morphology) and death.
Apoptosis also known as cell suicide. Difference between necrosis and apoptosis. Changes in apoptosis. Mechanism of apoptosis. Functional significance of apoptosis. Applied aspects of apoptosis
g protein coupled receptors, ion channels, types of receptors, wnt signalling, cell signalling, tranduction pathway, disorders regarding the signalling
Introduction
Definition
History
Evolution and origin of apoptosis
Significance
Purpose of apoptosis
Steps /process
Morphological and biochemical changes
Mechanism of apoptosis
Caspases
Regulation of apoptosis
Disorders of apoptosis
Application
Conclusion
Referances
Apoptosis is a
-pathway of cell death that is
-induced by an internally regulated program
-in which cells destined to die activate intrinsic enzymes that --degrade the cells’ own nuclear DNA and also nuclear and cytoplasmic proteins
-With minimal host reaction.
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
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
- Video recording of this lecture in Arabic language: https://youtu.be/SINlygW1Mpc
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
263778731218 Abortion Clinic /Pills In Harare ,sisternakatoto
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ABDOMINAL TRAUMA in pediatrics part one.drhasanrajab
Abdominal trauma in pediatrics refers to injuries or damage to the abdominal organs in children. It can occur due to various causes such as falls, motor vehicle accidents, sports-related injuries, and physical abuse. Children are more vulnerable to abdominal trauma due to their unique anatomical and physiological characteristics. Signs and symptoms include abdominal pain, tenderness, distension, vomiting, and signs of shock. Diagnosis involves physical examination, imaging studies, and laboratory tests. Management depends on the severity and may involve conservative treatment or surgical intervention. Prevention is crucial in reducing the incidence of abdominal trauma in children.
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
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of the 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 lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
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. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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
4. Apoptosis - Definition
• A pathway of cell death induced by a tightly
regulated suicidal program, in which the
cells destined to die activate enzymes that
degrade cells own nuclear DNA and nuclear,
cytoplasmic proteins.
sclero dinesh
5. Kerr Wyllie and Currie paper, British Journal of Cancer, 1972
Aug;26(4):239-57
"We are most grateful to Professor James Cormack of
the Department of Greek, University of Aberdeen, for
suggesting this term. The word "apoptosis" ( πόπτωσισ)ἁ
is used in Greek to describe the "dropping off" or "falling
off" of petals from flowers, or leaves from trees. To show
the derivation clearly, we propose that the stress should
be on the penultimate syllable, the second half of the
word being pronounced like "ptosis" (with the "p" silent),
which comes from the same root "to fall", and is already
used to describe the drooping of the upper eyelid
sclero dinesh
11. APOPTOSIS NECROSIS
NATURAL YES NO
EFFECTS BENEFICIAL DETRIMENTAL
Physiological or
pathological
Always pathological
Single cells Sheets of cells
Energy dependent Energy independent
Cell shrinkage Cell swelling
Membrane integrity
maintained
Membrane integrity lost
sclero dinesh
12. APOPTOSIS NECROSIS
Role for mitochondria and cytochrome C No role for mitochondria
No leak of lysosomal enzymes Leak of lysosomal enzymes
Characteristic nuclear changes Nuclei lost
Apoptotic bodies form Do not form
DNA cleavage No DNA cleavage
Activation of specific proteases No activation
Regulatable process Not regulated
Evolutionarily conserved Not conserved
Dead cells ingested by neighboring cells Dead cells ingested by neutrophils and
macrophages
sclero dinesh
13. Significance of apoptosis
• During development many cells are produced in excess which eventually
undergo programmed cell death and thereby contribute to sculpturing many
organs and tissues [Meier, 2000]
• In human body about one lakh cells are produced every second by mitosis
and a similar number die by apoptosis (Vaux and Korsmayer ,1999, cell)
• Between 50 and 70 billion cells die each day due to apoptosis in the
average human adult. For an average child between the ages of 8 and 14,
approximately 20 billion to 30 billion cells die a day. ( Karam, Jose A. (2009).
Apoptosis in Carcinogenesis and Chemotherapy. Netherlands: Springer. ISBN
978-1-4020-9597-9)
sclero dinesh
15. Why should a cell commit suicide?
• 1. Programmed cell death is as needed for proper normal
development as mitosis is.
Examples:
o The resorption of the tadpole tail in frog .
o The formation of the fingers and toes of the fetus requires the
removal, by apoptosis.
o The sloughing off of the endometrium at the start of menstruation.
o The formation of the proper connections (synapses) between
neurons in the brain.
sclero dinesh
16. • 2. Programmed cell death is needed to destroy cells that
represent a threat to the integrity of the organism.
• Examples:
o Cells infected with viruses
o Cells of the immune system
o Cells with DNA damage
o Cancer cells (Uncontrolled proliferated cells)
sclero dinesh
17. Apoptosis in physiologic situations
o Programmed destruction during embryogenesis
o Involution of hormone dependent tissues
o Cell loss in proliferating cell populations
o Elimination of harmful self- reactive lymphocytes
o Death of host cells
sclero dinesh
18. Apoptosis in bud
formation during
which many
interdigital cells
die. They are stained
black by a TUNEL
method
Incomplete differentiation
in two toes due to lack of
apoptosis
sclero dinesh
23. Apoptosis in pathological conditions
- DNA damage
- Accumulation of misfolded proteins
- Cell death in certain infections
- Pathological atrophy in parenchymal organs
sclero dinesh
24. Cells of the immune system
• CTLs induce apoptosis in each other and even in
themselves.
• Defects in the apoptotic machinery is associated with
autoimmune diseases such as lupus erythematosus and
rheumatoid arthritis.
sclero dinesh
25. Cells infected with viruses
• One of the methods by which cytotoxic T lymphocytes
(CTLs) kill virus-infected cells is by inducing apoptosis
sclero dinesh
26. Cells with DNA damage
• Damage to its genome
can cause a cell
» to disrupt
proper
embryonic
development
leading to birth
defects
» to become
cancerous.
• Cells respond to DNA
damage by increasing
their production of p53.
p53 is a potent inducer
of apoptosis.
sclero dinesh
27. – Cancer cells
• Radiation and chemicals used in cancer therapy induce apoptosis
in some types of cancer cells.
Fig. 1: SC-1 induced apoptosis in stomach carcinoma cells
Left: Before induction
Middle: 24h after induction
Right: 48h after induction sclero dinesh
35. Caspases
• Caspase are Cysteine- Aspartic acid specific proteases that mediates
the events that are associated with programmed cell death.
• Their catalytical activity depends on a critical cysteine-residue within a
highly conserved active-site pentapeptide QACRG,
• Caspases specifically cleave their substrates after Asp residues.
• Caspase- 8, Caspase- 9
• acts as an initiator of the caspase activation cascade.
• Caspase-3
• key effector in the apoptosis pathway, amplifying the signal from
initiator caspases and signifying full commitment to cellular
disassembly.
sclero dinesh
36. Initiation
• Absence of stimuli - hormones, growth factors
• Activation of receptors – TNF family
• Heat ,radiation, chemicals
• Genetically programmed events
sclero dinesh
37. STAGES OF CLASSIC APOPTOSIS
Healthy cell
DEATH SIGNAL / STIMULI (extrinsic or intrinsic)
Commitment to die (reversible)
EXECUTION (irreversible)
Dead cell (condensed, crosslinked)
ENGULFMENT (macrophages, neighboring cells)
DEGRADATION
sclero dinesh
39. Apoptosis triggered by external signals: the extrinsic or
death receptor pathway
sclero dinesh
40. Regulation of apoptosis
• Regulatory proteins – BCL -2, equivalent to
CED -9
• Apoptosis depends on binding of BCL -2 with
pro apoptotic and anti apoptotic proteins.
• Situated in the outer mitochondrial
membrane.
• Apaf -1 equivalent to CED -4.
• Tp 53, caspases, BAX, viruses such as adeno,
papilloma , hepatitis B.
sclero dinesh
41. Intrinsic pathway (damage):
Mitochondria
Cytochrome c release
Pro-caspase 9 cleavage
Pro-execution caspase (3) cleavage
Caspase (3) cleavage of cellular proteins,
nuclease activation,
etc.
Death
BAX
BAK
BOK
BCL-Xs
BAD
BID
B IK
BIM
NIP3
BNIP3
BCL-2
BCL-XL
BCL-W
MCL1
BFL1
DIVA
NR-13
Several
viral
proteins
sclero dinesh
44. Intracellular signals
Oxidative damage from free radicals, Radiation, Virus infection, Nutrient
deprivation, Pro-apoptotic Factors
Damage to the mitochondrial membrane increasing permeability
Entry of Cytochrome C into the
cytoplasm
Cytochrome C binds to Apaf-1 forming an
apoptosome
Apoptosome activates procaspase-9 to
caspase-9
Caspase-9 cleaves and activates caspase-3 and
caspase-7.
This executioner caspases activate a cascade of proteolytic activity that leads
to: Chromatin condensation, DNA fragmentation, Protein cleavage,
Membrane permeability
sclero dinesh
49. Apoptosis: Role in Disease
TOO MUCH: Tissue atrophy
TOO LITTLE: Hyperplasia
Neurodegeneration
Thin skin
etc
Cancer
Athersclerosis
etc
sclero dinesh
50. Apoptosis: Role in Disease
Neurodegeneration
oNeurons are post-mitotic (cannot replace themselves; neuronal stem cell
replacement is inefficient)
oNeuronal death caused by loss of proper connections, loss of proper growth
factors (e.g. NGF), and/or damage (especially oxidative damage).
oNeuronal dysfunction or damage results in loss of synapses or loss of cell
bodies (synaptosis, can be reversible; apopsosis, irreversible)
oPARKINSON'S DISEASE
oALZHEIMER'S DISEASE
oHUNTINGTON'S DISEASE etc.
sclero dinesh
51. Apoptosis: Role in Disease
Cancer
oApoptosis eliminates damaged cells (damage => mutations =>
cancer
oTumor suppressor p53 controls senescence and apoptosis
responses to damage.
oMost cancer cells are defective in apoptotic response(damaged,
mutant cells survive)
oHigh levels of anti-apoptotic proteins
or
oLow levels of pro-apoptotic proteins ===> CANCER
sclero dinesh
52. Apoptosis: Role in Disease
Cancer
Virus associated cancer
• Several human papilloma viruses (HPV) have been
implicated in causing cervical cancer. One of them
produces a protein (E6) that binds and inactivates the
apoptosis promoter p53.
• Epstein-Barr Virus (EBV), the cause of mononucleosis
and associated with some lymphomas
– produces a protein similar to Bcl-2
– produces another protein that causes the cell to
increase its own production of Bcl-2. Both these
actions make the cell more resistant to apoptosis
(thus enabling a cancer cell to continue to proliferate).
sclero dinesh
53. • Some B-cell leukemia and lymphomas express high
levels of Bcl-2, thus blocking apoptotic signals they may
receive. The high levels result from a translocation of the
BCL-2 gene into an enhancer region for antibody
production.
• Melanoma (the most dangerous type of skin cancer)
cells avoid apoptosis by inhibiting the expression of the
gene encoding Apaf-1.
Apoptosis: Role in Disease
Cancer
sclero dinesh
54. •Other cancer cells express high levels of FasL, and can
kill any cytotoxic T cells (CTL) that try to kill them
because CTL also express Fas (but are protected from
their own FasL).
•Some cancer cells, especially lung and colon cancer
cells, secrete elevated levels of a soluble "decoy"
molecule that binds to FasL, plugging it up so it cannot
bind Fas. Thus, cytotoxic T cells (CTL) cannot kill the
cancer cells
Apoptosis: Role in Disease
Cancer
sclero dinesh
55. Apoptosis: Role in Disease
Aging
Aging --> both too much and too little apoptosis
(evidence for both)
Too much (accumulated oxidative damage?)
---> tissue degeneration
Too little (defective sensors, signals?
---> dysfunctional cells accumulate
hyperplasia (precancerous lesions)
sclero dinesh
56. Apoptosis: Role in Disease
• Apoptosis and AIDS
Hallmark- the decline in the number of the
patient's CD4+ T cells (normally about 1000
per microliter (µl) of blood).
sclero dinesh
57. In Immune system
o Very rarely humans are encountered with
genetic defects in apoptosis.
o The most common one is a mutation in the
gene for Fas
o mutations in the gene for FasL or even one of
the caspases are occasionally seen.
Autoimmune lymphoproliferative syndrome
or ALPS.
sclero dinesh
59. Cells are balanced between life and death
DAMAGE Physiological death signals
DEATH SIGNAL
PROAPOPTOTIC
PROTEINS
(dozens!)
ANTIAPOPTOTIC
PROTEINS
(dozens!)
DEATHsclero dinesh