The document discusses apoptosis or programmed cell death. It provides background on the history of apoptosis, definitions, key morphological changes, major players involved like caspases and Bcl-2 proteins, and the two main pathways of apoptosis - the intrinsic mitochondrial pathway and extrinsic death receptor pathway. Detection methods for apoptotic cells are also covered, including electron microscopy, DNA fragmentation analysis, TUNEL assay, and flow cytometry. Therapeutic implications for targeting apoptosis in diseases like cancer, neurodegeneration and myocardial infarction are also mentioned.
Cell death, particularly apoptosis, is probably one of the
most widely-studied subjects among cell biologists.
Understanding apoptosis in disease conditions is very
important as it not only gives insights into the pathogenesis
of a disease but may also leaves clues on how
the disease can be treated. In cancer, there is a loss of
balance between cell division and cell death and cells
that should have died did not receive the signals to do
so. The problem can arise in any one step along the way
of apoptosis.Apoptosis is an ordered and orchestrated cellular process that occurs in physiological and pathological conditions.
It is also one of the most studied topics among cell biologists. An understanding of the underlying mechanism of
apoptosis is important as it plays a pivotal role in the pathogenesis of many diseases. In some, the problem is due
to too much apoptosis, such as in the case of degenerative diseases while in others, too little apoptosis is the
culprit. Cancer is one of the scenarios where too little apoptosis occurs, resulting in malignant cells that will not
die. The mechanism of apoptosis is complex and involves many pathways. Defects can occur at any point along
these pathways, leading to malignant transformation of the affected cells, tumour metastasis and resistance to
anticancer drugs. Despite being the cause of problem, apoptosis plays an important role in the treatment of
cancer as it is a popular target of many treatment strategies. The abundance of literature suggests that targeting
apoptosis in cancer is feasible. However, many troubling questions arise with the use of new drugs or treatment
strategies that are designed to enhance apoptosis and critical tests must be passed before they can be used safely
in human subjects.. It is used,
in contrast to necrosis, to describe the situation in
which a cell actively pursues a course toward death
upon receiving certain stimule
Cell death, particularly apoptosis, is probably one of the
most widely-studied subjects among cell biologists.
Understanding apoptosis in disease conditions is very
important as it not only gives insights into the pathogenesis
of a disease but may also leaves clues on how
the disease can be treated. In cancer, there is a loss of
balance between cell division and cell death and cells
that should have died did not receive the signals to do
so. The problem can arise in any one step along the way
of apoptosis.Apoptosis is an ordered and orchestrated cellular process that occurs in physiological and pathological conditions.
It is also one of the most studied topics among cell biologists. An understanding of the underlying mechanism of
apoptosis is important as it plays a pivotal role in the pathogenesis of many diseases. In some, the problem is due
to too much apoptosis, such as in the case of degenerative diseases while in others, too little apoptosis is the
culprit. Cancer is one of the scenarios where too little apoptosis occurs, resulting in malignant cells that will not
die. The mechanism of apoptosis is complex and involves many pathways. Defects can occur at any point along
these pathways, leading to malignant transformation of the affected cells, tumour metastasis and resistance to
anticancer drugs. Despite being the cause of problem, apoptosis plays an important role in the treatment of
cancer as it is a popular target of many treatment strategies. The abundance of literature suggests that targeting
apoptosis in cancer is feasible. However, many troubling questions arise with the use of new drugs or treatment
strategies that are designed to enhance apoptosis and critical tests must be passed before they can be used safely
in human subjects.. It is used,
in contrast to necrosis, to describe the situation in
which a cell actively pursues a course toward death
upon receiving certain stimule
Apoptosis is a process of programmed cell death that occurs in multicellular organisms. Biochemical events lead to characteristic cell changes (morphology) and death.
Content-
1. Background
2. Introduction
3. Difference between apoptosis and necrosis
4. Apoptosis in biologic processes
5. Apoptosis in pathologic processes
6. Morphologic features
7. Techniques to identify and count apoptotic cells
8. Biochemical changes
9. Molecular mechanism of apoptosis
10. Recent advancement and emerging trends in apoptosis
11. References
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
Apoptosis is a process of programmed cell death that occurs in multicellular organisms. Biochemical events lead to characteristic cell changes (morphology) and death.
Content-
1. Background
2. Introduction
3. Difference between apoptosis and necrosis
4. Apoptosis in biologic processes
5. Apoptosis in pathologic processes
6. Morphologic features
7. Techniques to identify and count apoptotic cells
8. Biochemical changes
9. Molecular mechanism of apoptosis
10. Recent advancement and emerging trends in apoptosis
11. References
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
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.
Cancer pathways: Communication and documentation. Presented by Janfrey Doak, Southern Cancer Network and Phyllis Meier, Central Cancer Network, at HINZ 2014, 12 November 2014, 11.15am, Plenary Room 2
Seminar led by Prof. Thomas Kaufmann. Institute of Pharmacology, University of Bern, Switzerland, at VHIR (15 November 2012).
Content: We are interested to investigate the molecular mechanisms by which pro- and anti-apoptotic members of the BCL-2 family regulate the intrinsic (mitochondrial) apoptotic pathway. The pathway is initiated by members of the BH3-only protein subgroup, which act as sensors in response to a variety of intracellular stress stimuli. Some BH3-only proteins, including Bid and Bim, can be activated downstream of death receptors (e.g. Fas/CD95, TNF-R1) and thus mediate a crosstalk from the extrinsic to the mitochondrial apoptotic pathway. We investigate these processes in mouse liver (and more recently also in mouse granulocytes), as hepatocytes strongly rely on this crosstalk for death receptor-induced apoptosis to be effective. We are further interested in the role of 'X-linked inhibitor of apoptosis protein' (XIAP) in these same cell death pathways.
Evaluating the ability of anti-cancer drugs Etoposide and Staurosporine to in...Davient Bala
Cervical cancer is considered one of the most prevalent cancers affecting Singaporean women.
Although many novel chemotherapeutics have been developed recently, little has been done to
determine the efficiency of current anti-cancer agents working in combination. Here, we aimed to
evaluate the apoptosis induction efficiency of Etoposide and Staurosporine in HeLa cells. Cell cultures
were subjected to either 50 μM Etoposide, 10 nM Staurosporine or both for 24 hours prior visualization
under a fluorescence microscope. We found that Etoposide alone had an efficiency of 16.1% while
Staurosporine alone had 18.3%. However, the polytherapy achieved an efficiency of up to 33.6%,
which indicates an additive effect of both drugs to induce apoptosis. Our results demonstrate that
Etoposide and Staurosporine are both capable of inducing apoptosis in HeLa cells. Furthermore, it
reveals the potential of Etoposide-Staurosporine polytherapy to be a potent combinative treatment
option for cervical cancer patients resistant or sensitive to conventional anti-cancer agents.
Apoptosis or programmed cell death, is carefully coordinated collapse of cell, protein degradation , DNA fragmentation followed by rapid engulfment of corpses by neighbouring cells.
Apoptosis is a form of cell death that permits the removal of damaged, senescent or unwanted cells in multicellular organisms, without damage to the cellular microenvironment, but it is also involved in a wide range of pathological processes, including cancer. An understanding of the underlying mechanism of apoptosis is important as it plays a pivotal role in the pathogenesis of many diseases. Defective apoptosis represents a major causative factor in the development and progression of cancer. The majority of chemotherapeutic agents, as well as radiation, utilize the apoptotic pathway to induce cancer cell death. Recent knowledge on apoptosis has provided the basis for novel targeted therapies that exploit apoptosis to treat cancer by acting in the extrinsic/intrinsic pathway. Defects can occur at any point along these pathways, leading to malignant transformation of the affected cells, tumour metastasis and resistance to anticancer drugs. In particular, this review provides references concerning the apoptotic molecules, their interactions, the mechanisms involved in apoptosis resistance, and also the modulation of apoptosis for the treatment of cancer. Despite being the cause of problem, apoptosis plays an important role in the treatment of cancer as it is a popular target of many treatment strategies.
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.
Salas, V. (2024) "John of St. Thomas (Poinsot) on the Science of Sacred Theol...Studia Poinsotiana
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.
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.
The ability to recreate computational results with minimal effort and actionable metrics provides a solid foundation for scientific research and software development. When people can replicate an analysis at the touch of a button using open-source software, open data, and methods to assess and compare proposals, it significantly eases verification of results, engagement with a diverse range of contributors, and progress. However, we have yet to fully achieve this; there are still many sociotechnical frictions.
Inspired by David Donoho's vision, this talk aims to revisit the three crucial pillars of frictionless reproducibility (data sharing, code sharing, and competitive challenges) with the perspective of deep software variability.
Our observation is that multiple layers — hardware, operating systems, third-party libraries, software versions, input data, compile-time options, and parameters — are subject to variability that exacerbates frictions but is also essential for achieving robust, generalizable results and fostering innovation. I will first review the literature, providing evidence of how the complex variability interactions across these layers affect qualitative and quantitative software properties, thereby complicating the reproduction and replication of scientific studies in various fields.
I will then present some software engineering and AI techniques that can support the strategic exploration of variability spaces. These include the use of abstractions and models (e.g., feature models), sampling strategies (e.g., uniform, random), cost-effective measurements (e.g., incremental build of software configurations), and dimensionality reduction methods (e.g., transfer learning, feature selection, software debloating).
I will finally argue that deep variability is both the problem and solution of frictionless reproducibility, calling the software science community to develop new methods and tools to manage variability and foster reproducibility in software systems.
Exposé invité Journées Nationales du GDR GPL 2024
Richard's aventures in two entangled wonderlandsRichard Gill
Since the loophole-free Bell experiments of 2020 and the Nobel prizes in physics of 2022, critics of Bell's work have retreated to the fortress of super-determinism. Now, super-determinism is a derogatory word - it just means "determinism". Palmer, Hance and Hossenfelder argue that quantum mechanics and determinism are not incompatible, using a sophisticated mathematical construction based on a subtle thinning of allowed states and measurements in quantum mechanics, such that what is left appears to make Bell's argument fail, without altering the empirical predictions of quantum mechanics. I think however that it is a smoke screen, and the slogan "lost in math" comes to my mind. I will discuss some other recent disproofs of Bell's theorem using the language of causality based on causal graphs. Causal thinking is also central to law and justice. I will mention surprising connections to my work on serial killer nurse cases, in particular the Dutch case of Lucia de Berk and the current UK case of Lucy Letby.
Earliest Galaxies in the JADES Origins Field: Luminosity Function and Cosmic ...Sérgio Sacani
We characterize the earliest galaxy population in the JADES Origins Field (JOF), the deepest
imaging field observed with JWST. We make use of the ancillary Hubble optical images (5 filters
spanning 0.4−0.9µm) and novel JWST images with 14 filters spanning 0.8−5µm, including 7 mediumband filters, and reaching total exposure times of up to 46 hours per filter. We combine all our data
at > 2.3µm to construct an ultradeep image, reaching as deep as ≈ 31.4 AB mag in the stack and
30.3-31.0 AB mag (5σ, r = 0.1” circular aperture) in individual filters. We measure photometric
redshifts and use robust selection criteria to identify a sample of eight galaxy candidates at redshifts
z = 11.5 − 15. These objects show compact half-light radii of R1/2 ∼ 50 − 200pc, stellar masses of
M⋆ ∼ 107−108M⊙, and star-formation rates of SFR ∼ 0.1−1 M⊙ yr−1
. Our search finds no candidates
at 15 < z < 20, placing upper limits at these redshifts. We develop a forward modeling approach to
infer the properties of the evolving luminosity function without binning in redshift or luminosity that
marginalizes over the photometric redshift uncertainty of our candidate galaxies and incorporates the
impact of non-detections. We find a z = 12 luminosity function in good agreement with prior results,
and that the luminosity function normalization and UV luminosity density decline by a factor of ∼ 2.5
from z = 12 to z = 14. We discuss the possible implications of our results in the context of theoretical
models for evolution of the dark matter halo mass function.
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.
Professional air quality monitoring systems provide immediate, on-site data for analysis, compliance, and decision-making.
Monitor common gases, weather parameters, particulates.
2. The history of Apoptosis
What Apoptosis means
Significance of Apoptosis.
Morphological changes
Major players in apoptosis.
Pathways to apoptosis
Therapeutic implications.
Pathological implication
Detection of apoptotic cells
2
3. The History of Apoptosis
John Kerr:
a Brisbane pathologist in 1972
introduced a concept ‘Apoptosis’.
(Richardson, et al., 2000)
3
4. Synonyms: - Antonym: -
Programmed cell death. Necrosis
Programmed cellcell death are of two types: -are of two types: -
Apoptosis : -(Type I)
Autophagic : -(Cytoplasmic, or Type II)
The formation of large vacuoles that eat away organelles
before the nucleus is destroyed.
(Offermanns & Rosenthal , 2004)
4
5. Greek origin word known ‘Falling off or Dropping off.’
Self destruction programmed genetically sequenced in
biomedical events.
It’s a kind of counterbalance by elimination of similar
number of cells.
Death by design.
Apoptosis: -
(Rang & Dale, 2008)
5
6. Significance of Apoptosis
Deletion of dangerous & damage cells.
Development of organs
Without apoptosis human
gut can grow 19 km,whole
epithelial lining changes every
23 days.
Regulation of immune system(T-cells)
Incomplete differentiation
due to lack of apoptosis
Cancer & Neurodegenerative diseases.
(Gewies, 2003)
6
7. Apoptosis Necrosis
• Energy dependent PCD • Cell dies due to damage
• One cell • Group of cells
• No inflammation • Acute inflammation
• Role of mitochondria • No role of mitochondria
• Dead cells eaten by
macrophages
• Dead cells removed by
macrophages.
• Cell shrinkage • Cell swelling
(Haiat, 2006)
7
10. Major players in Apoptosis
Apoptosis Initiating factor(AIF):-
Release from mitochondria enter in
nucleus & trigger cell suicide.
Caspases
Bcl-2 Proteins
Apoptosome
p53 gene and p53 protein
(Rang & Dale, 2008)
10
11. • It is family of cystein protease.
• present in cell in inactive form.
• Cleave protein bearing a amino acid
sequence located at the terminal.
(cystein aspartic acid specific protease)
(Hill,et al., 2003)
11
18. The Bcl-2 Family
Regulator Protein of Mitochondria.
Isolated from gene involve in B-cell lymphoma.(Bcl-2)
All have BH3 domain (Bcl-2 Homology)
BH3:-It is Proapoptotic domain expose on activation.
(Dash, et al., 2001)
18
20. Functions:-
Regulate the balance between Pro-Apoptotic &
anti-apoptotic.
Involved in Intrinsic pathway.
Induction of Bcl-2 is by death signals.
20
21. Apoptosome
Multisubunit protease activation complex.
Form after induction of death signal in mitochondrial
pathway.
Discovery of Apoptosome by ‘prof. Wang’.
Wheel-like structure connected to seven radial spokes
(Adrain, 2001; Dash, 2003)
21
24. p53 gene & p53 protein
p53 is a tumor suppressor gene.
Prevent completion of cell cycle.
If DNA damage occurs activation of gene p53 response to
cell death.
Curable damage can be repaired
In curable damage of DNA leads to cell death
(Dlamini et al.,2005)
24
25. Pathways to Apoptosis
1) Death receptor pathways /(Extrinsic Pathway)
2) Mitochondrial pathways /(Intrinsic Pathway)
25
26. Death receptor pathways /(Extrinsic Pathway)
Induction is mediated through cell surface receptors
know to be ‘Death receptors’.
Death ligands are activating these receptors.
Further activation of Caspases leads to cell death
(Rang & Dale, 2008)
26
27. Death Receptors
TNFR - Super family
TNFR-Tumor necrosis factor Receptor, CD: -Cluster differentiation
TRAIL- Tumor necrosis factor –α related apoptosis inducing ligand
Fas:- Apoptosis stimulating fragment.
Death receptorDeath receptor Death ligandsDeath ligands
TNFR-1
CD95 (Apo-1) (Fas) (TNFR-2)
TRAIL-R1 (DR-4)
TRAIL-R2 (DR-5)
TNF-α
CD95L (FasL)
TRAIL-R1
TRAIL-R2
(Ashkenazi, 2002)
27
28. TNF Receptor signaling
Binding of Ligand
to Death receptor
Binding of Ligand
to Death receptor
Binding of adapter
protein with
Activation of
Another protein
TRAF-2
Binding of adapter
protein with
Activation of
Another protein
TRAF-2
TRAF-2: -TNF associated factor -2,
TRADD:- TNF associated death domain,
28
29. Fas:- Apoptosis stimulating fragment ., FADD:- Fas Associated death domain
Adapter Protein
Fas signaling pathway
29
30. Death receptors signal transductionDeath receptors signal transduction
Effectors domain
30
31. The Extrinsic Apoptosis Pathway
FADD, Fas-associated death domain, DR:- Death receptors.
Pro-apoptotic ligands
Caspase 3, 6, 7
Apoptosis
FADD
DR5
DR4
Procaspase 8, 10
Caspase 8, 10
Plasma
membrane
(Ashkenazi A. Nat Rev Cancer 2002;2:420–430.)
31
33. Mitochondrial pathways /(Intrinsic Pathway)
Release of protein from mitochondrial inner membrane
into cytosol.
DNA damage induce apoptosis.
Cellular stress, heat shock, oxidative stress, cellular
damage, that are also induced apoptosis.
(Martin, et al., 2003)
33
38. Pathological Implications
Growth of tissue & organs in embryo.
Replenishment of time-expire cells like gut-epithelium.
Repair & healing after injury or inflammation.
Regeneration of tissue.
Hyperplasia.
(Barton, et al., 2004)
38
40. Neurodegenerative disease: -Neurodegenerative disease: -
Alzheimer’s disease show excessive Apoptosis.
Neuronal growth factor & brain derived
neurotrophic factors.
Secrets protein that maintain the balance Pro-
Apoptotic & Anti-Apoptotic.
Blocking of these factor are new area of interest for
Target drug delivery.
Alzheimer’s disease show excessive Apoptosis.
Neuronal growth factor & brain derived
neurotrophic factors.
Secrets protein that maintain the balance Pro-
Apoptotic & Anti-Apoptotic.
Blocking of these factor are new area of interest for
Target drug delivery.
(Gerald, 2002)
40
42. Myocardial Infraction: -Myocardial Infraction: -
Occur due to blockage of coronary artery by
thrombus.
Decrease in oxygen supply leads to (M.I.) by necrosis
or Apoptosis
Two pathways of cell death
1) Necrosis 2) Apoptosis
(Rang & Dale, 2008)
42
43. Current approach are finding to
inhibit these pathway which are
beneficial in clinical
43
ICE:-interleukin -1 converting enzyme.
PARP:- (poly-ADP-ribose-polymerase .
44. Targets for Anti-cancer drugs: -Targets for Anti-cancer drugs: -
Bcl-2 family as a target for new drug.
Bcl-2 is Anti-apoptotic & increase resistance to
cancer chemotherapy.
Death receptor & there respective ligands are useful
in targeting the Anti-cancer drug.
(Fischer, et al., 2005)
44
46. Detection of apoptic cells
Electron Microscopy
Fluorescence Microscopy
Staining with Eosin
Detection of PCD Based on Morphology
Detection of DNA Fragmentation
Agarose Gel Electrophoresis
DNA Fragments by Cell Fractionation
Detection of DNA Fragmentation by Filtration Assay.
(Kaufmann, 2000)
46
48. Detection Based on Morphology: -Detection Based on Morphology: -
Shrinkage of the cell.
Detachment from its neighbors.
Fragmentation of nucleus.
Packaging of the cell into multiple plasma
membrane.
Phagocytosis of these fragments.
48
52. Detection of DNA fragmentation by Gel
Electrophoresis.
Detection of DNA fragmentation by Gel
Electrophoresis.
Agarose gel with suitable separation properties.
Application of total cellular DNA to an Agarose.
The fragments are spared throughout agarose gel.
Fragments will be detected by Ethidium bromide.
(Anders, 2002)
52
53. 1. DNA from apoptotic cells.
2. DNA isolated from necrotic
cells
3. No samples
4. DNA from normal cell
5. DNA from normal cell
6. No sample
Gel Electrophoresis
53
54. Flow CytometryFlow Cytometry
Well known as a ‘Flow Microfluriometer.
To study Normal & Malignant Lymphocytes.
Measures amount of fluorescence associated with cell.
Photomultiplier tube is a detector.
Analyzing the population of cell.
Around 20,000 cells can be analyzed in few min.
(Kaufmann, 2000)
54
57. Adrain, C. Martin, S.J. 2001 The mitochondrial apoptosome: A killer
unleashed by the cytochrome seas. Trends Biochem. Sci. 26, 390–397.
Ashkenazi, A.Dixit, V. M., 1999. Apoptosis control by death and decoy
receptors. Current Opinion in Cell Biology 11, 255-60.
Dash, P., 2001. Apoptosis Basic Medical Sciences
St.George’s, University of London
Fischer, U.OsthofF, K. S., 2005. New Approaches and Therapeutics
Targeting Apoptosis in Disease: Pharmacological reviews, 57 (2), p.187-
215.
Hill, M.M. Adrain, C. Martin S.J., 2003.Molecular Cell Biology
Laboratory, Department of Genetics Smurfit Institute, 3 (1) p.19-24.
57
58. Gewies, A., 2003. Introduction to Apoptosis :Apo Review p.1-26
Hill, M. M.Adrain, C., 2003. Portrait of the killer the mitochondrial
Apoptosome emerges from the shawdo:molecular intervention. 3
(1)p.19-24.
Kaufmann, S.2001. Apoptosis:Phaarmacological implication and
therapeutic opportunites.New York: Academic Press
Li, L.Y., Luo, X. Wang, X., 2001 Endonuclease G is an apoptotic
DNase when released from mitochondria. Nature 412, 95–99.
Margaret, K.T. Cohen, J., 2001. Standard Quantitative Assays for
Apoptosis: Molecular Biotechnology, 19 p.305-315
58
59. Offermanns, S. Rosentha, W., 2004. Encyclopedic Reference of
Molecular Pharmacology,Springer
Rang, H. P. Dale, M. M., 2008.Cell proliferation and Apoptosis:
Pharmacology.6th
ed.Churchill Livingstone Elsevier.p.72-88.
http://www.researchapoptosis.com
http://www.apoptosisinfo.org
http:// www.bitessizebio.com
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