This document provides information on autoimmune disorders like rheumatoid arthritis and systemic lupus erythematosus. It explains that autoimmunity occurs when the immune system attacks the body's own cells, causing diseases. Rheumatoid arthritis specifically causes joint inflammation and damage through autoantibodies attacking joint linings. Systemic lupus erythematosus more broadly attacks tissues, producing symptoms like rashes, fever, and kidney issues. Both have no cure but can be treated to reduce immune response and manage symptoms.
Autoimmune DIseases : Types, Mechanism, Diagnosis, TreatmentDr Mehul Dave
This is a presentation useful to learners of immunology as well as acadeicians. Useful in undergraduate as well as postgraduate courses. NEET students/Teachers can also get advantage of it.
Autoimmune DIseases : Types, Mechanism, Diagnosis, TreatmentDr Mehul Dave
This is a presentation useful to learners of immunology as well as acadeicians. Useful in undergraduate as well as postgraduate courses. NEET students/Teachers can also get advantage of it.
Autoimmunity is the system of immune responses of an organism against its own healthy cells and tissues. Any disease that results from such an aberrant immune response is termed an "autoimmune disease".
Secondary Immunodeficiency
By Dr. Usama Ragab Youssif
Reference: Included in Slides
Include causes of secondary immunodeficiency including AIDS and other viral infections
Type II Hypersensitivity-Antibody mediated cytotoxic HypersensitivityAnup Bajracharya
Type II Hypersensitivity is antibody-mediated immune reaction in which antibodies (IgG or IgM) are directed against cellular or extracellular matrix antigens with the resultant cellular destruction, functional loss, or damage to tissues.
antibodies are a large proteins. based on electrophorosis and centrifugation anti bodies are mainly five types .these are protects on human body from various microorganisms.
Autoimmunity is the system of immune responses of an organism against its own healthy cells and tissues. Any disease that results from such an aberrant immune response is termed an "autoimmune disease".
Secondary Immunodeficiency
By Dr. Usama Ragab Youssif
Reference: Included in Slides
Include causes of secondary immunodeficiency including AIDS and other viral infections
Type II Hypersensitivity-Antibody mediated cytotoxic HypersensitivityAnup Bajracharya
Type II Hypersensitivity is antibody-mediated immune reaction in which antibodies (IgG or IgM) are directed against cellular or extracellular matrix antigens with the resultant cellular destruction, functional loss, or damage to tissues.
antibodies are a large proteins. based on electrophorosis and centrifugation anti bodies are mainly five types .these are protects on human body from various microorganisms.
Introduction Autoimmune Disease by Dr. Kelly CobbNouriche Medspa
The immune system represents an interface between a constant ever-changing external environment and an internal system that is striving to maintain homeostasis and defend its boundaries from harmful foreign invaders.
AUTOIMMUNITY AND AUTO IMMUNE DISEASES.pdfnithyatulasi1
The immune system could go awry and, instead of reacting against foreign antigens, could focus its attack on self-antigens. Paul Ehrlich termed this condition “horror autotoxicus.”
Mechanisms of self-tolerance normally protect an individual from potentially self-reactive lymphocytes, there are failures. They result in an inappropriate response of the immune system against self-components termed autoimmunity.
AUTOIMMUNITY AND ITS ASSOCIATED DISEASES.pdfnithyatulasi1
The immune system could go awry and, instead of reacting against foreign antigens, could focus its attack on self-antigens. Paul Ehrlich termed this condition “horror autotoxicus.”
Mechanisms of self-tolerance normally protect an individual from potentially self-reactive lymphocytes, there are failures. They result in an inappropriate response of the immune system against self-components termed autoimmunity.
The immune system provides protection against infectious organisms and repairs tissue damage induced by infections or physical damage. Under normal conditions, an immune response cannot be triggered against the cells of one's own body. In certain cases, however, immune cells make a mistake and attack the very cells that they are meant to protect.
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https://www.etran.rs/2024/en/home-english/
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I Introduction
II Subalternation and Theology
III Theology and Dogmatic Declarations
IV The Mixed Principles of Theology
V Virtual Revelation: The Unity of Theology
VI Theology as a Natural Science
VII Theology’s Certitude
VIII Conclusion
Notes
Bibliography
All the contents are fully attributable to the author, Doctor Victor Salas. Should you wish to get this text republished, get in touch with the author or the editorial committee of the Studia Poinsotiana. Insofar as possible, we will be happy to broker your contact.
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Slide 1: Title Slide
Extrachromosomal Inheritance
Slide 2: Introduction to Extrachromosomal Inheritance
Definition: Extrachromosomal inheritance refers to the transmission of genetic material that is not found within the nucleus.
Key Components: Involves genes located in mitochondria, chloroplasts, and plasmids.
Slide 3: Mitochondrial Inheritance
Mitochondria: Organelles responsible for energy production.
Mitochondrial DNA (mtDNA): Circular DNA molecule found in mitochondria.
Inheritance Pattern: Maternally inherited, meaning it is passed from mothers to all their offspring.
Diseases: Examples include Leber’s hereditary optic neuropathy (LHON) and mitochondrial myopathy.
Slide 4: Chloroplast Inheritance
Chloroplasts: Organelles responsible for photosynthesis in plants.
Chloroplast DNA (cpDNA): Circular DNA molecule found in chloroplasts.
Inheritance Pattern: Often maternally inherited in most plants, but can vary in some species.
Examples: Variegation in plants, where leaf color patterns are determined by chloroplast DNA.
Slide 5: Plasmid Inheritance
Plasmids: Small, circular DNA molecules found in bacteria and some eukaryotes.
Features: Can carry antibiotic resistance genes and can be transferred between cells through processes like conjugation.
Significance: Important in biotechnology for gene cloning and genetic engineering.
Slide 6: Mechanisms of Extrachromosomal Inheritance
Non-Mendelian Patterns: Do not follow Mendel’s laws of inheritance.
Cytoplasmic Segregation: During cell division, organelles like mitochondria and chloroplasts are randomly distributed to daughter cells.
Heteroplasmy: Presence of more than one type of organellar genome within a cell, leading to variation in expression.
Slide 7: Examples of Extrachromosomal Inheritance
Four O’clock Plant (Mirabilis jalapa): Shows variegated leaves due to different cpDNA in leaf cells.
Petite Mutants in Yeast: Result from mutations in mitochondrial DNA affecting respiration.
Slide 8: Importance of Extrachromosomal Inheritance
Evolution: Provides insight into the evolution of eukaryotic cells.
Medicine: Understanding mitochondrial inheritance helps in diagnosing and treating mitochondrial diseases.
Agriculture: Chloroplast inheritance can be used in plant breeding and genetic modification.
Slide 9: Recent Research and Advances
Gene Editing: Techniques like CRISPR-Cas9 are being used to edit mitochondrial and chloroplast DNA.
Therapies: Development of mitochondrial replacement therapy (MRT) for preventing mitochondrial diseases.
Slide 10: Conclusion
Summary: Extrachromosomal inheritance involves the transmission of genetic material outside the nucleus and plays a crucial role in genetics, medicine, and biotechnology.
Future Directions: Continued research and technological advancements hold promise for new treatments and applications.
Slide 11: Questions and Discussion
Invite Audience: Open the floor for any questions or further discussion on the topic.
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2. Autoimmunity
Autoimmunity is the system of immune responses of an
organism against its own cells and tissues.
Any disease that results from such an aberrant immune
response is termed an autoimmune disease.
3. History
In the 1960s, it was believed that all self-reactive lymphocytes
were eliminated during their development in the bone marrow
and thymus and that a failure to eliminate these lymphocytes led
to autoimmune consequences.
In 1970s ,experimental reveal that not all self-reactive
lymphocytes are deleted during T-cell and B-cell maturation.
normal healthy individuals have been shown to possess mature, ,
self-reactive lymphocytes. their activity must be regulated in
normal individuals through clonal anergy .A breakdown in this
regulation can lead to activation of self-reactive clones of T or B
cells, generating humoral or cell-mediated responses against
selfantigens. which can cause serious damage to cells and organs.
.
4. (AARDA)
According to the American Autommunity Related Disease
Association (AARDA) an autoimmune disease develops when
our immune system, which defends our body against disease
decide our healthy cells are forigen ,as a result immune
system attacks healthy cells.
5. Autoimmunity
• Diseases often run in families.
• 75% are women are effected.
• 4th largest disease class in females.
• African Americans, Native Americans also have
an increased risk of developing an autoimmune disease.
6. Classification of autoimmune
disease:
• 1: Organ specific
• 2: Systemic diseases.
Organ specific
The organ-specific diseases involve an autoimmune response
directed primarily against a single organ or gland.
The normal function of the organ is blocked.
eg. Autoimmune Hemolytic Anemia, Pernicious Anemia etc
7. Systemic diseases:
The systemic diseases are directed against a broad spectrum
of tissues and have manifestations in a variety of organs
resulting from cell-mediated responses and cellular damage
caused by auto-antibodies.(an antibody produced by an
organism in response to a constituent of its own tissues)
eg. Systemic Lupus Erythematous, Arthritis
8. rheumatoid arthritis
• A chronic progressive disease causing inflammation in the
joints and resulting in painful deformity and immobility,
especially in the fingers, wrists, feet, and ankles
9. • Rheumatoid arthritis is a common autoimmune disorder, most
often affecting women from 40 to 60 years old.
• The major symptoms:
• chronic inflammation of the joints
• although the hematologic, cardiovascular, and respiratory
systems are also frequently affected
10. overview
• Many individuals with rheumatoid arthritis produce a group
of auto-antibodies called rheumatoid factors that are reactive
with determinants in the Fc region of IgG. The classic
rheumatoid factor is an IgM antibody with that reactivity.Such
auto-antibodies bind to normal circulating IgG,forming IgM-
IgG complexes that are deposited in the joints. These immune
complexes can activate hypersensitive reaction,which leads to
chronic inflammation of the joints.
11. • The immune system produces antibodies that attach to the
linings of joints. Immune system cells then attack the joints,
causing inflammation, swelling, and pain.
• If untreated, rheumatoid arthritis causes gradually causes
permanent joint damage.
• Treatments for rheumatoid arthritis can include various oral or
injectable medications that reduce immune system over
activity.
12. What Causes Rheumatoid
Arthritis?
• rheumatoid arthritis
• happens when your immune system targets your joint linings.
It’s a long-term condition that also affects other tissue, but the
joints are usually the most severely affected.
• It may be a combination of genes and other things.
• Some researchers think an infection with a bacteria or virus
can trigger the disease in some people.
13. • As rheumatoid arthritis develops, some of the body's immune
cells start to attack healthy tissue, mistaking it for an invader.
This triggers a chain reaction that leads to more inflammation
and damage.
• The main target of RA's inflammation is the synovium, the thin
layer of tissue that lines the joints. The inflammation also
spreads to other areas in the body, which can cause ongoing
pain, fatigue, and other problems.
14. What Are the Symptoms of
Rheumatoid Arthritis?
• When It’s in Your Joints
• RA always affects the joints. It makes them inflamed. The
classic signs are:
• Stiffness. The joint is harder to use and doesn't move as well
as it should. It’s especially common in the morning
15. • Swelling. Fluid enters the joint and makes it puffy.
• Pain . Inflammation inside a joint makes it sensitive and
tender. Over time, it causes damage and pain.
• Redness and warmth. The joints may be warmer and more
pink or red than skin around it.
16. Rheumatoid Arthritis That
Affect the Entire Body
• Rheumatoid Arthritis can go beyond your joints. You may feel:
• Fatigue
• Sickness
• Less appetite than normal, which can lead to weight loss
• Muscle aches
• Some people with RA also get rheumatoid nodules, which are
bumps under the skin that most often appear on the elbows.
Sometimes they are painful.
17. Treatment
• Drugs:
• (NSAID). nonsteroidal anti-inflammatory drug. These
medications reduce pain and inflammation but do not slow
down RA.
• “DMARDs” stands for disease-modifying anti rheumatic drugs.
They help slow or stop RA from getting worse
• Surgery for Rheumatoid Arthritis
• Physical and Occupational Therapy
18. Systematic lupus erthymatosus
• It typically appears in women between 20 and 40 years of age.
• In this the human immune system becomes hyperactive and
attacks normal, healthy tissues.
• Although “lupus” actually includes a number of different
diseases, SLE is the most common type of lupus.
19. SYMPTOMS OF LUPUS
• SLE is characterized by
• fever.
• weakness.
• Arthritis.
• skin rashes.
• pleurisy.( an inflammation of the pleura, which is the moist
double-layered membrane that surrounds the lungs)
• and kidney dysfunction
20. CAUSES OF LUPUS
• Is is not linked to a certain gene.
• Ultraviolet rays.
• Certain medications.
• A virus, physical or emotional stress, and trauma.
21. MECHANISM
• Affected individuals may produce autoantibodies to a vast
array of tissue antigens, such as DNA
• When immune complexes of auto-antibodies
• are deposited along the walls of small blood vessels.
• hypersensitive reaction develops.
• The complexes activate the complement system
22. • And damage the wall of the blood vessel.
• Excessive complement activation in patients with severe SLE
produces elevated serum levels of the complement split
products C3a and C5a.
• This lead to tissue damage
24. TREATMENT
• Treatment for SLE is not curative. But Treatments may include:
• anti-inflammatory medications for joint pain.
• steroid creams for rashes
• corticosteroids of varying doses to minimize the immune
response