Cell adaptation involves changes cells undergo in response to stimuli. Cells can adapt by changing size (atrophy and hypertrophy), number (hyperplasia and atrophy), or form (metaplasia). Atrophy is a decrease in cell size due to decreased protein synthesis. Hypertrophy is an increase in cell size due to increased protein synthesis. Hyperplasia is an increase in cell number. Metaplasia is the replacement of one cell type with another. Adaptations can be physiological or pathological responses. Dysplasia and anaplasia represent abnormal cellular changes that can precede cancer.
Cellular adaptations and growth disturbancesZaid Wani
cellular adaptations and growth disturbances and their mechanisms. please refer the books given in reference section of this presentation for further understandings and examples of subtypes.
Information about how cell get injured from different stimuli. Mechanism of cellular injury. Different types of cellular injury. Different examples of cellular injury with images which makes it easy to understand.
Cellular adaptations and growth disturbancesZaid Wani
cellular adaptations and growth disturbances and their mechanisms. please refer the books given in reference section of this presentation for further understandings and examples of subtypes.
Information about how cell get injured from different stimuli. Mechanism of cellular injury. Different types of cellular injury. Different examples of cellular injury with images which makes it easy to understand.
Multi-source connectivity as the driver of solar wind variability in the heli...Sérgio Sacani
The ambient solar wind that flls the heliosphere originates from multiple
sources in the solar corona and is highly structured. It is often described
as high-speed, relatively homogeneous, plasma streams from coronal
holes and slow-speed, highly variable, streams whose source regions are
under debate. A key goal of ESA/NASA’s Solar Orbiter mission is to identify
solar wind sources and understand what drives the complexity seen in the
heliosphere. By combining magnetic feld modelling and spectroscopic
techniques with high-resolution observations and measurements, we show
that the solar wind variability detected in situ by Solar Orbiter in March
2022 is driven by spatio-temporal changes in the magnetic connectivity to
multiple sources in the solar atmosphere. The magnetic feld footpoints
connected to the spacecraft moved from the boundaries of a coronal hole
to one active region (12961) and then across to another region (12957). This
is refected in the in situ measurements, which show the transition from fast
to highly Alfvénic then to slow solar wind that is disrupted by the arrival of
a coronal mass ejection. Our results describe solar wind variability at 0.5 au
but are applicable to near-Earth observatories.
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.
THE IMPORTANCE OF MARTIAN ATMOSPHERE SAMPLE RETURN.Sérgio Sacani
The return of a sample of near-surface atmosphere from Mars would facilitate answers to several first-order science questions surrounding the formation and evolution of the planet. One of the important aspects of terrestrial planet formation in general is the role that primary atmospheres played in influencing the chemistry and structure of the planets and their antecedents. Studies of the martian atmosphere can be used to investigate the role of a primary atmosphere in its history. Atmosphere samples would also inform our understanding of the near-surface chemistry of the planet, and ultimately the prospects for life. High-precision isotopic analyses of constituent gases are needed to address these questions, requiring that the analyses are made on returned samples rather than in situ.
Deep Behavioral Phenotyping in Systems Neuroscience for Functional Atlasing a...Ana Luísa Pinho
Functional Magnetic Resonance Imaging (fMRI) provides means to characterize brain activations in response to behavior. However, cognitive neuroscience has been limited to group-level effects referring to the performance of specific tasks. To obtain the functional profile of elementary cognitive mechanisms, the combination of brain responses to many tasks is required. Yet, to date, both structural atlases and parcellation-based activations do not fully account for cognitive function and still present several limitations. Further, they do not adapt overall to individual characteristics. In this talk, I will give an account of deep-behavioral phenotyping strategies, namely data-driven methods in large task-fMRI datasets, to optimize functional brain-data collection and improve inference of effects-of-interest related to mental processes. Key to this approach is the employment of fast multi-functional paradigms rich on features that can be well parametrized and, consequently, facilitate the creation of psycho-physiological constructs to be modelled with imaging data. Particular emphasis will be given to music stimuli when studying high-order cognitive mechanisms, due to their ecological nature and quality to enable complex behavior compounded by discrete entities. I will also discuss how deep-behavioral phenotyping and individualized models applied to neuroimaging data can better account for the subject-specific organization of domain-general cognitive systems in the human brain. Finally, the accumulation of functional brain signatures brings the possibility to clarify relationships among tasks and create a univocal link between brain systems and mental functions through: (1) the development of ontologies proposing an organization of cognitive processes; and (2) brain-network taxonomies describing functional specialization. To this end, tools to improve commensurability in cognitive science are necessary, such as public repositories, ontology-based platforms and automated meta-analysis tools. I will thus discuss some brain-atlasing resources currently under development, and their applicability in cognitive as well as clinical neuroscience.
Comparing Evolved Extractive Text Summary Scores of Bidirectional Encoder Rep...University of Maribor
Slides from:
11th International Conference on Electrical, Electronics and Computer Engineering (IcETRAN), Niš, 3-6 June 2024
Track: Artificial Intelligence
https://www.etran.rs/2024/en/home-english/
Cancer cell metabolism: special Reference to Lactate PathwayAADYARAJPANDEY1
Normal Cell Metabolism:
Cellular respiration describes the series of steps that cells use to break down sugar and other chemicals to get the energy we need to function.
Energy is stored in the bonds of glucose and when glucose is broken down, much of that energy is released.
Cell utilize energy in the form of ATP.
The first step of respiration is called glycolysis. In a series of steps, glycolysis breaks glucose into two smaller molecules - a chemical called pyruvate. A small amount of ATP is formed during this process.
Most healthy cells continue the breakdown in a second process, called the Kreb's cycle. The Kreb's cycle allows cells to “burn” the pyruvates made in glycolysis to get more ATP.
The last step in the breakdown of glucose is called oxidative phosphorylation (Ox-Phos).
It takes place in specialized cell structures called mitochondria. This process produces a large amount of ATP. Importantly, cells need oxygen to complete oxidative phosphorylation.
If a cell completes only glycolysis, only 2 molecules of ATP are made per glucose. However, if the cell completes the entire respiration process (glycolysis - Kreb's - oxidative phosphorylation), about 36 molecules of ATP are created, giving it much more energy to use.
IN CANCER CELL:
Unlike healthy cells that "burn" the entire molecule of sugar to capture a large amount of energy as ATP, cancer cells are wasteful.
Cancer cells only partially break down sugar molecules. They overuse the first step of respiration, glycolysis. They frequently do not complete the second step, oxidative phosphorylation.
This results in only 2 molecules of ATP per each glucose molecule instead of the 36 or so ATPs healthy cells gain. As a result, cancer cells need to use a lot more sugar molecules to get enough energy to survive.
Unlike healthy cells that "burn" the entire molecule of sugar to capture a large amount of energy as ATP, cancer cells are wasteful.
Cancer cells only partially break down sugar molecules. They overuse the first step of respiration, glycolysis. They frequently do not complete the second step, oxidative phosphorylation.
This results in only 2 molecules of ATP per each glucose molecule instead of the 36 or so ATPs healthy cells gain. As a result, cancer cells need to use a lot more sugar molecules to get enough energy to survive.
introduction to WARBERG PHENOMENA:
WARBURG EFFECT Usually, cancer cells are highly glycolytic (glucose addiction) and take up more glucose than do normal cells from outside.
Otto Heinrich Warburg (; 8 October 1883 – 1 August 1970) In 1931 was awarded the Nobel Prize in Physiology for his "discovery of the nature and mode of action of the respiratory enzyme.
WARNBURG EFFECT : cancer cells under aerobic (well-oxygenated) conditions to metabolize glucose to lactate (aerobic glycolysis) is known as the Warburg effect. Warburg made the observation that tumor slices consume glucose and secrete lactate at a higher rate than normal tissues.
Observation of Io’s Resurfacing via Plume Deposition Using Ground-based Adapt...Sérgio Sacani
Since volcanic activity was first discovered on Io from Voyager images in 1979, changes
on Io’s surface have been monitored from both spacecraft and ground-based telescopes.
Here, we present the highest spatial resolution images of Io ever obtained from a groundbased telescope. These images, acquired by the SHARK-VIS instrument on the Large
Binocular Telescope, show evidence of a major resurfacing event on Io’s trailing hemisphere. When compared to the most recent spacecraft images, the SHARK-VIS images
show that a plume deposit from a powerful eruption at Pillan Patera has covered part
of the long-lived Pele plume deposit. Although this type of resurfacing event may be common on Io, few have been detected due to the rarity of spacecraft visits and the previously low spatial resolution available from Earth-based telescopes. The SHARK-VIS instrument ushers in a new era of high resolution imaging of Io’s surface using adaptive
optics at visible wavelengths.
2. Definition
• These are changes a cell goes through in response to an appropriate stimulus and ceases once the need for adaptation has ceased.
• Stimulus can include:
• Physiological
• Hormonal
• Cells adapt by changing their:
• size (atrophy and hypertrophy),
• Number (hyperplasia and atrophy)
• Form (metaplasia).
3.
4. ATROPHY
• Decrease in size of a cell .
• Decrease in protein synthesis.
• Decreased size results in decreased oxygen consumption and
metabolic needs of the cells and may increase the overall efficiency of
cell function.
• Atrophy is generally a reversible process, except for atrophy caused by
loss of nervous innervation to a tissue.
• Causes of atrophy include:
1. Physiological
2. pathologic
5. PHYSIOLOGICAL PATHOLOGICAL(LOCAL OR GEENERALISED)
Some embryonic structures during fetal development
e.g notochord, thyroglossal duct
Disuse (paralysis)
Uterus after pregnancy Denervation
Ischemia ( decrease in blood supply)
Aging
Loss of endocrine stimulation
NUTRITION
6. Kidney: atrophy via renal artery stenosis. NB: decrease in cortex (most metabolically active cells)
7. MECHANISM
• Reduction in structural componentse.g mitochondria, myofilaments,
ER via proteolysis (lysosomal protease, Increase in number of
autophagic vacuoles, Residual bodies (i.e. lipofuscin brown
atrophy)
• NB: diminished function but not dead
8. Pathologic atrophy
• Pathologic atrophy: Shrinkage of our brains as we age
• Disuse atrophy: Essentially when an organ is underused/not used, it
undergoes atrophy.
• Another example of this is an immobilized limb, which undergoes
muscle wasting upon casting.
• Local atrophy: Most often the result of decreased blood flow to that
area
9. HYPERTROPHY
• Increase in cell size .
• There is increased protein synthesis.
• Occurs when a cell or tissue is exposed to an increased workload.
• Occurs in tissues that cannot undergo mitosis eg cardiac cells,skeletal cells
and nerve cells as an adaptive response.
N.B. THERE IS A LIMIT TO THE AMOUNT OF A TISSUE CAN ENLARGE
• The three basic types of hypertrophy are
1. Physiologic- a response to disease.
2. Compensatory- when cell size increases to take over for non-functioning
cells.
3. Pathologic- is a response to disease.
10. PATHOLOGICAL PHYSIOLOGICAL COMPENSATORY
Myocardial hypertrophy due to
hypertension
Increased muscle size following
weigh training/ physical labor
e.g. one kidney will undergo
hypertrophy when the other is not
functioning or is removed.
uterus and breast enlarge in
pregnancy
One limb will undergo hypertrophy
when the other is lame
11. Mechanism
• Increased synthesis of structural proteins via
1. Transcription factors (i. e. c-fos and c-jun)
2. Growth factors (TGF-b, IGF-1, FGF)
3. Vasoactive agents (endothelien-1, AII)
12. Hypertrophy of uterus
Physiologic Hypertrophy: A: rt = normal uterus, left = gravid uterus; B: left: small, spindle-shaped smooth
muscle cells; rt: larger, more rounded cells of gravid uterus
13. HYPERPLASIA
• Hyperplasia is an increase in the
number of cells caused by increased
workload, hormonal stimulation, or
decreased tissue density.
• Hyperplasia is important in wound
healing
• Increase in the number of cells in an
organ or tissue, usually resulting in
increased volume of the organ or
tissue hence increased protein
synthesis.
• Like hypertrophy, hyperplasia may
be physiologic, compensatory, or
pathologic.
14. Physiologic hyperplasia
Physiologic hyperplasia can be divided into:
• Hormonal hyperplasia, which increases the functional capacity of a tissue when
needed,
1. Proliferation of the glandular epithelium of the female breast at puberty and during
pregnancy
2. Occurs in the pregnant uterus.
• Compensatory hyperplasia, which increases tissue mass after damage or partial
resection.
1. Partial hepatectomy --- proliferation of residual liver cells and regeneration of the
liver.
2. After unilateral nephrectomy--- when remaining tissue grows to make up for partial
tissue loss
15. PATHOLOGIC HYPERPLASIA
• Caused by excessive hormonal stimulation or growth factors acting on target
cells.
• Endometrial hyperplasia: Increase in the amount of oestrogen.
• Benign prostatic hyperplasia: Induced by responses to hormones
(androgens).
• Genital watts.
• Gigantism
16. METAPLASIA
• Metaplasia is the replacement of one cell type with another cell type.
• A common cause of metaplasia is constant irritation or injury that initiates an
inflammatory response.
• Almost exclusively occurs in epithelial cells.
May predispose to cancer
Involves reprogramming of undifferentiated stem cells
Allows to cells to better survive in a hostile environment
It is reversible
• Metaplasia may be
1. physiologic
2. pathologic.
17.
18. PATHOLOGIC METAPLASIA
• Pathologic metaplasia is a response to an extrinsic toxin or stressor
and is generally irreversible.
• For example,
1. after years of exposure to cigarette smoke, stratified squamous
epithelial cells replace the normal ciliated columnar epithelial
cells of the bronchi.
• Although the new cells can better withstand smoke, they don't
secrete mucus nor do they have cilia to protect the airway.
• If exposure to cigarette smoke continues, the squamous cells can
become cancerous.
19. 2. Acid reflux where columnar epithelial cells change into squamous
metaplasia (Barrett esophagus)
3. Connective tissue metaplasia where there is formation of bone,
cartilage, or adipose tissue in tissues that normally don’t contain them
20. PHYSIOLOGIC METAPLASIA
• Physiologic metaplasia is a normal response to changing conditions
and is generally transient. For example, in the body's normal response
to inflammation, monocytes that migrate to inflamed tissues
transform into macrophages. It is reversible.
21. Dysplasia
• A derangement of cell growth that leads to tissues with cells of varying size, shape
and appearance.
• Abnormal change in size, shape and organisation of cells within the tissue.
• Generally occurs in response to chronic irritation and inflammation.
• Common examples include dysplasia of epithelial cells of the cervix or the
respiratory tract.
• Dysplasia is considered A STRONG PRECURSOR OF CANCER!!! E.g. Cervical dysplasia
• However, dysplasia is an adaptive process – may or may not lead to cancer