Dr Zahid Azeem, working as Assistant Professor of Biochemistry at Azad Jammu and Kashmir Medical College, Muzaffarabad since 2012.
email; paym_zahid@live.com
CELL CYCLE
CELL CYCLE CHECK POINT
PHASES IN CELL CYCLE CHECK POINT
ROLE OF CYLINE AND CDKS
MUTURATIONAL PROMOTING FACTOR
FUNCTION OF MPR
CONCLUSION
REFRENCE
CELL CYCLE
CELL CYCLE CHECK POINT
PHASES IN CELL CYCLE CHECK POINT
ROLE OF CYLINE AND CDKS
MUTURATIONAL PROMOTING FACTOR
FUNCTION OF MPR
CONCLUSION
REFRENCE
this presentation has detailed information on cell cycle. it includes steps as well as how the proteins take part in cell cycle.
i have also added information on some experiments that were carried out.
happy studying :)
here in this presentation you will be studying about cell cycle , cell checkpoints , cell cycle regulators etc .
very informative slides by anshika singh
Describes the plasma membrane in detail, explains the each major component with its functions.
Transport mechanism across the cell is covered with detailed explanation with examples.
by Dr. N.Sivaranjani, MD
a deeply explained process of cell division, for understanding it thoroughly. i tried to put in all the information i knew and collected. i hope it is helpful or you.
Cytoskeleton - microtubules ,microfilaments and intermediate filamentsBIOTECH SIMPLIFIED
The cytoskeleton is a structure that helps cells maintain their shape and internal organization, and it also provides mechanical support that enables cells to carry out essential functions like division and movement. There is no single cytoskeletal component. Rather, several different components work together to form the cytoskeleton.
This is a clear to understand presentation about the cell cycle and the process of mitosis. After reading this, you will get a deeper sense of the importance of cell cycle and mitosis that is going on inside every living thing.
this presentation has detailed information on cell cycle. it includes steps as well as how the proteins take part in cell cycle.
i have also added information on some experiments that were carried out.
happy studying :)
here in this presentation you will be studying about cell cycle , cell checkpoints , cell cycle regulators etc .
very informative slides by anshika singh
Describes the plasma membrane in detail, explains the each major component with its functions.
Transport mechanism across the cell is covered with detailed explanation with examples.
by Dr. N.Sivaranjani, MD
a deeply explained process of cell division, for understanding it thoroughly. i tried to put in all the information i knew and collected. i hope it is helpful or you.
Cytoskeleton - microtubules ,microfilaments and intermediate filamentsBIOTECH SIMPLIFIED
The cytoskeleton is a structure that helps cells maintain their shape and internal organization, and it also provides mechanical support that enables cells to carry out essential functions like division and movement. There is no single cytoskeletal component. Rather, several different components work together to form the cytoskeleton.
This is a clear to understand presentation about the cell cycle and the process of mitosis. After reading this, you will get a deeper sense of the importance of cell cycle and mitosis that is going on inside every living thing.
Cell cycle regulation presentation by me and my colleagues. Not the Best work but still it will give a general idea about DNA damage checkpoints, roles of Cdk-Cyclin complexes, Rb proteins, ATM&ATR kinases, p51, etc.
Reference : Nature reviews & The Cell a molecular approach. (cooper)
WHAT IS CELL?
WHAT IS CELL DIVISION OR CELL CYCLE?
WHY DO CELL DIVIDE?
HISTORY
CELL CYCLE
INTERPHASE
M-PHASE
MOLECULAR EVENT DURING CELL CYCLE AND CELL REGULATION
TYPES OF CELL DIVISION
IMPORTANCE OF CELL DIVISION
ABNORMALTIES OF CELL CYCLE
REFRENCES
A cell cycle is a series of events that a cell passes through from the time until it reproduces its replica.
Howard and Pelc (1953) first time described it.
It is the growth and division of single cell into daughter cells and duplication (replication).
In prokaryotic cells, the cell cycle occurs via a process termed binary fission.
In eukaryotic cells, the cell cycle can be divided in two periods-
a) interphase
b) mitosis
Cell cycle and cell division are fundamental processes governing the growth, development, and reproduction of all living organisms. Understanding these processes is crucial in the field of biology as they play a pivotal role in shaping life at both the cellular and organismal levels.
For more information, visit-www.vavaclasses.com
Eukayotic_cell_cycle-diff_phases_mol_events
Different Phases and Molecular Events
-Control mechanisms: Role of
(A) Cyclins and cyclin-dependent kinases
(B) Retinoblastoma and E2F proteins
-Cytokinesis and cell plate formation
The cell cycle, or cell-division cycle, is the series of events that take place in a cell that cause it to divide into two daughter cells. These events include the duplication of its DNA (DNA replication) and some of its organelles, and subsequently the partitioning of its cytoplasm and other components into two daughter cells in a process called cell division.
here u will find every detail of cell cycle.
for more details ,visit @biOlOgy BINGE-insight learning
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
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These lecture slides, by Dr Sidra Arshad, offer a quick overview of 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 leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
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. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
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
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New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
Ocular injury ppt Upendra pal optometrist upums saifai etawah
Cell cycle. sgd[1]
1. Dr Zahid Azeem
Assistant Professor
Biochemistry
AJK Medical College
MBBS-Batch 2019 --- CMB Module
2. Define Cell Cycle
Cell reproduces by performing orderly sequence of
events in which it duplicates its contents and then
divides in two. This type of duplication and division is
called Cell Cycle.
3. Major Questions
To explain how cells reproduce, we therefore have to
consider three major questions:
(1) How do cells duplicate their contents?
(2) How do they partition the duplicated contents and
split in two?
(3) How do they coordinate/regulate all the machinery
that is required for these two processes?
4. 1- How do cells duplicate their contents?
Five Phases of the Cell CycleFive Phases of the Cell Cycle
1-1- GG11 - primary growth phase- primary growth phase
2- S – synthesis; DNA replicated2- S – synthesis; DNA replicated
3- G3- G22 - secondary growth phase- secondary growth phase
4- M – mitosis4- M – mitosis
5- C - cytokinesis5- C - cytokinesis
M-phase
Interphase
6. Interphase
During all of interphase, a cell generally continues to
transcribe genes,
synthesize proteins, and grow in mass.
Together, G1 and G2 phases provide additional time
for the cell to grow and duplicate its cytoplasmic
organelles
if interphase lasted only long enough for DNA
replication, the cell would not have time to double its
mass before it divided and would consequently shrink
with each division.
7. In some animal embryos, for example, the first
cell divisions after fertilization (called cleavage
divisions) serve to subdivide a giant egg cell into
many smaller cells as quickly as possible.
In these embryonic cell cycles, the G1 and G2
phases are drastically shortened, and the cells do
not grow before they divide.
8. Timelines for Cell Cycle Phases
G1-phase 10-12 hours
S- phase 8-10 hours
G-2 phase 4-6 hour
M-Phase 1-2 hours
Total 24 hour
This time calculation and frequency is true for majority
of cells. Cell cycle can be very short as in embryonic
cells.
9. Frequency of cell division
Frequency of cell division varies by cell type
1- embryo
cell cycle < 30 minute
2- skin cells
divide frequently throughout life
12-24 hours cycle
3- liver cells
retain ability to divide, but keep it in reserve
divide once every year or two
4- mature nerve cells
do not divide at all after maturity
permanently in G0
10. Interphase - GInterphase - G11
11stst
growth stage after cell divisiongrowth stage after cell division
Cells mature by making more cytoplasm &Cells mature by making more cytoplasm &
organellesorganelles
Cell carries on its normal metabolic activitiesCell carries on its normal metabolic activities
11. Interphase – S StageInterphase – S Stage
1- Synthesis stage1- Synthesis stage
2- DNA is copied or replicated2- DNA is copied or replicated
TwoTwo
identicalidentical
copies ofcopies of
DNADNA
Original DNAOriginal DNA
12. Interphase – GInterphase – G22 StageStage
22ndnd
Growth StageGrowth Stage
Occurs after DNA has been copiedOccurs after DNA has been copied
All cell structures needed for division are madeAll cell structures needed for division are made
(e.g. centrioles)(e.g. centrioles)
Both organelles & proteins are synthesizedBoth organelles & proteins are synthesized
13. What the cell looks likeWhat the cell looks like
Animal Cell
17. What the cell looks likeWhat the cell looks like
What’s happeningWhat’s happening
18. CytokinesisCytokinesis
Means division of the cytoplasmMeans division of the cytoplasm
Division of cell into two, identical halves called daughterDivision of cell into two, identical halves called daughter
cellscells
In plant cells, cell plate forms at the equator to divide cellIn plant cells, cell plate forms at the equator to divide cell
In animal cells, cleavage furrow forms to split cellIn animal cells, cleavage furrow forms to split cell
20. G1
G1 checkpoint
G1
G0
If a cell receives a go-ahead
signal at the G1 checkpoint,
the cell continues on in the
cell cycle.
If a cell does not receive a
go-ahead signal at the G1
checkpoint, the cell exits the
cell cycle and goes into G0, a
nondividing state.
21. Question -3
How do they coordinate/regulate all the machinery that
is required for these two processes?
22. How is progress through
cell cycle regulated?
“Cell-cycle control system”
The ‘Checkpoint’ model
How are they controlled?
-- intracellular and extracellular signals
What are the effectors
-- lots of kinases & phosphatases
23. How is cell division and
growth regulated?
Growth factors
-- stimulate cell growth
Mitogens
-- trigger cell division
-- e.g., EGF, phytoestrogens
Survival signals
-- disable apoptotic mechanisms
24. What did study of frog embryos reveal about the control
system?
Be sure to read
How we know
Frog egg cytoplasmic
transfer experiments
Something in the cytosol
triggers mitosis
-- called MPF
Activity of MPF oscillates
during the cell cycle
What is MPF?
25. What do we know about
MPF & cyclin?
MPF is a cyclin bound to a Cdk
‘cyclin-dependent protein kinase’
= M-Cdk
Several Cyclins and Cdks
-- regulate different cell cycle events
Table 18–2 The Major Cyclins and Cdks
of Vertebrates
Cyclin–Cdk Complex Cyclin Cdk partner
G1-Cdk cyclin D Cdk4, Cdk6
G1/S-Cdk cyclin E Cdk2
S-Cdk cyclin A Cdk2
M-Cdk cyclin B Cdk1
26. How is cyclin-CDK
activity regulated?
Two processes
1. Synthesis &
destruction of cyclin
-- ubiquination
-- proteasomes
2. Inactivation & activation
-- Activating/inhibitory
Kinases/phosphatase
-- Pos feedback rapid activation
27. How do cyclin-cdk’s trigger
cellular events?
S-Cdk triggers DNA replication
-- activates replication origins
-- blocks reactivation
What does activated M-CDK do?
1) Phosphorylates H1 histone
(triggering C’some condensation)
2) Disassembly of nuclear lamina
3) Changes behavior of microtubules
-- phosphorylates MAPs
28. How is cyclin-Cdk coupled
to checkpoint control?
Tumor suppressor genes
-- inactivation can dispose cell
toward tumor formation
-- P53, P21 and Rb are all TSGs
-- loss of both alleles necessary
Why?
P53 can also trigger apoptosis
Figures 18-14 + 18-15
33. Cell Growth and Cancer
How can growth factors inhibit cell division?
Alterations in what kinds of genes lead to
development of cancer?
How do oncogenes cause cancer?
34. Cell Growth and Cancer
How does the p53
tumor suppressor gene
work?