DNA replication is the process by which DNA makes a copy of itself during cell division.The separation of the two single strands of DNA creates a 'Y' shape called a replication 'fork'. The two separated strands will act as templates for making the new strands of DNA.
DNA replication is the process by which DNA makes a copy of itself during cell division.The separation of the two single strands of DNA creates a 'Y' shape called a replication 'fork'. The two separated strands will act as templates for making the new strands of DNA.
DNA replication is fundamental process occurring in all living organism to copy their DNA. The process is called replication in sense that each strand of dsDNA serve as template for reproduction of complementary strand.
DNA replication is fundamental process occurring in all living organism to copy their DNA. The process is called replication in sense that each strand of dsDNA serve as template for reproduction of complementary strand.
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
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
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
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.
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
2. Lectures Objectives
Describe the flow of genetic information
Define Replication
List basic rules of replication
Explain how the problems after denaturation are
overcome
List steps of DNA replication
List the proteins involved in replications and outline
their functions
Compare leading and lagging strands
Describe Proofreading
List difference of eukaryotic replication vs prokaryote
5. DNA Replication = DNA DNA
Process of duplication of the
entire DNA prior to cell division.
So each daughter cell gets a complete copy
DNA Replication
6. Basic rules of replication
A. Semi-conservative
B. Starts at the ‘origin’
C. Bidirectional
D. Synthesis always in the 5-3 direction
E. Semi-discontinuous
F. RNA primers required
7. • DNA Synthesis
The DNA bases on each
strand act as a template to
synthesize a complementary
strand
• Recall that Adenine (A)
pairs with thymine (T)
and guanine (G) pairs
with cytosine (C)
The process is
semiconservative because
each new double-stranded
DNA contains one old
strand (template) and one
newly-synthesized
complementary strand
DNA Replication
A
G
C
T
G
T
C
G
A
C
A
G
C
T
G
T
C
G
A
C
A
G
C
T
G
T
C
G
A
C
A
G
C
T
G
T
C
G
A
C
T
C
G
A
C
A
G
C
T
G
10. The mechanism of DNA replication
Arthur Kornberg, a Nobel prize winner and
other biochemists deduced steps of
replication
11. The mechanism of DNA replication
– Initiation
• Proteins bind to DNA and open up double
helix
• Prepare DNA for complementary base
pairing
– Elongation
• Proteins connect the correct sequences
of nucleotides into a continuous new
strand of DNA
– Termination
• Proteins release the replication complex
14. Replication: 1st step
• Unwind DNA
• Helicase Cleaves the hydrogen bonds between the
two DNA strands and require energy provided by
ATP
• Stabilized by Single stranded binding protein
replication fork
single-stranded binding proteins
helicase
17. DNA supercoiling
• As the 2 strands are separated from each
other, this creates coils infront of the
separated part (supercoils) which prevents
further separation of the helix.
18. • Toposiomerases are enzymes that are
responsible for the elimination of
supercoils.
Toposiomerases
20. DNA Replication
• DNA Polymerase
Enzyme that catalyzes the covalent bond between the phosphate of one
nucleotide and the deoxyribose (sugar) of the previous nucleotide
DNA Polymerization
21. 3 end has a free deoxyribose
5 end has a free phosphate
DNA polymerase:
can only build the new strand in
the 5 to 3 direction
Thus scans the template strand in
3 to 5 direction
DNA Replication
22. DNA polymerase can not initiate DNA synthesis
DNA Replication
DNA polymerase
23. DNA polymerase can not initiate DNA synthesis
• Primase (a type of RNA polymerase) builds an RNA primer
(5-10 ribonucleotides long)
• DNA polymerase attaches onto the 3 end of the RNA primer
DNA Replication
DNA polymerase
25. Elongation
• DNA polymerase uses each strand as a template in the 3 to 5 direction
to build a complementary strand in the 5 to 3 direction
results in a leading strand and a lagging strand
DNA Replication
26. Limits of DNA polymerase III
Unidirectional ,synthesizes DNA
from 5 to 3 direction only
Leading & Lagging strands
5
5
5
5
3
3
3
5
3
5
3 3
Leading strand
Lagging strand
continuous synthesis
DNA polymerase III
3
5
growing
replication fork
27. DNA polymerase III
______________________
built by ________________
serves as starter sequence for
DNA polymerase III
Limits of DNA polymerase III
can not initiate DNA synthesis
Starting DNA synthesis: RNA primers
5
5
5
3
3
3
5
3
5
3 5 3
growing
replication fork primase
RNA
29. 5’
5’
3’ 3’
5’
3’
5’ 3’
5’
3’
3’
5’
Excision of RNA primers
and their replacement by DNA
It localizes the 5’end of the
RNA primer and then
cleaves the phosphodiester
bonds of RNA primer one
by one from 5’→3’
RNA primer of each
Okazaki fragment is
removed by DNA
polymerase I enzyme by its
5’→3’ exonuclease activity.
30. As it removes the RNA, DNA pol I replaces it with
deoxynucleotides, synthesizing DNA in 5’→3’ direction till
the RNA is totally degraded and the gap is filled with DNA
3’
5’
3’
5’ 3’
5’
3’
3’
5’
31. 3’
5’
3’
5’ 3’
5’
3’
3’
5’
DNA Ligase
Then by DNA ligase enzyme, the DNA fragments will be
joined together. The enzyme requires energy, which in
eukaryotes is provided by the cleavage of ATP to (AMP +
PPi). Ligase seals the nick in the sugar-phosphate
backbone
32. Proof Reading
• Proof Reading of the newly synthesized DNA
(Replication fidelity):
DNA polymerase, is
self-correcting: it has
a proofreading activity
33. Steps of Proofreading of newly
synthesized DNA
3- A correct base is added by 5’to 3’polymerase activity.A correct
base is then base paired to the template.
2- Incorrect base which had been added by 5’ to 3’ activity is
removed by Pol 3’ to 5’ exonuclease activity
1- Incorrect base had been added by 5’ to 3’ polymerase
(Pol.)activity. Incorrect as it is not complementary to the template,
so not base paired to the template.
34. Comparison of Prokaryotic DNA
polymerases
Feature Pol I Pol II Pol III
53 exonuclease activity + --- ---
35 exonuclease activity + + +
Synthesis rate (nucleotide/min) 600 30 30000
Replication + --- +
Repair + + +
