The glucuronic acid pathway is a quantitatively minor route of glucose metabolism. Like the pentose phosphate pathway, it provides biosynthetic precursors and inter-converts some less common sugars to ones that can be metabolized.
Glycogen is the storage form of Glucose which maintain the blood glucose level under various condition. Glycogen Metabolism is the important pathway of carbohydrate metabolism which gives the information about the glycogen synthesis (Glycogenesis), Glycogen breakdown (Glucogenolysis). Glycogen metabolism also gives the information how this pathway is regulated. Their are various diseases which are associated with this metabolism, commonly known as Glycogen storage diseases.
Gluconeogenesis: Defined as biosynthesis of glucose from non-carbohydrate precursors
-Gluconeogenesis: an intro
-Thermodynamic Barriers (Each barrier detail explanation)
- Energetics of gluconeogenesis
-Substrates of gluconeogenesis (each substrate and pathway explained)
-Regulation of Gluconeogenesis, hormonal and transcriptional regulation
It is an metabolic pathway of synthesis of glucose from non carbohydrate precursors like pyruvate, lactate, amino acid, glycerol etc. Main sites are liver and kidney. It uses enzymes from both cytosol and mitochondria.
This powerpoint gives detailed description and clear view about Glycogenesis and glycogenolysis . these two metabolic actions are very important for regulating blood glucose levels. it also explains about the glycogen storage
The glucuronic acid pathway is a quantitatively minor route of glucose metabolism. Like the pentose phosphate pathway, it provides biosynthetic precursors and inter-converts some less common sugars to ones that can be metabolized.
Glycogen is the storage form of Glucose which maintain the blood glucose level under various condition. Glycogen Metabolism is the important pathway of carbohydrate metabolism which gives the information about the glycogen synthesis (Glycogenesis), Glycogen breakdown (Glucogenolysis). Glycogen metabolism also gives the information how this pathway is regulated. Their are various diseases which are associated with this metabolism, commonly known as Glycogen storage diseases.
Gluconeogenesis: Defined as biosynthesis of glucose from non-carbohydrate precursors
-Gluconeogenesis: an intro
-Thermodynamic Barriers (Each barrier detail explanation)
- Energetics of gluconeogenesis
-Substrates of gluconeogenesis (each substrate and pathway explained)
-Regulation of Gluconeogenesis, hormonal and transcriptional regulation
It is an metabolic pathway of synthesis of glucose from non carbohydrate precursors like pyruvate, lactate, amino acid, glycerol etc. Main sites are liver and kidney. It uses enzymes from both cytosol and mitochondria.
This powerpoint gives detailed description and clear view about Glycogenesis and glycogenolysis . these two metabolic actions are very important for regulating blood glucose levels. it also explains about the glycogen storage
Metabolism (/məˈtæbəlɪzəm/, from Greek: μεταβολή metabolē, "change") is the set of life-sustaining chemical reactions in organisms. The three main purposes of metabolism are: the conversion of food to energy to run cellular processes; the conversion of food/fuel to building blocks for proteins, lipids, nucleic acids, and some carbohydrates; and the elimination of nitrogenous wastes. These enzyme-catalyzed reactions allow organisms to grow and reproduce, maintain their structures, and respond to their environments. (The word metabolism can also refer to the sum of all chemical reactions that occur in living organisms, including digestion and the transport of substances into and between different cells, in which case the above described set of reactions within the cells is called intermediary metabolism or intermediate metabolism).
Metabolic reactions may be categorized as catabolic - the breaking down of compounds (for example, the breaking down of glucose to pyruvate by cellular respiration); or anabolic - the building up (synthesis) of compounds (such as proteins, carbohydrates, lipids, and nucleic acids). Usually, catabolism releases energy, and anabolism consumes energy.
This PPT contains content of Gluconeogenesis, Steps involved in Gluconeogenesis, (Gluconeogenesis from Pyruvate, Gluconeogenesis from lactate, Gluconeogenesis from amino acids, Gluconeogenesis from glycerol, Gluconeogenesis from Propionate), Regulation and significance of Gluconeogenesis
Glycogenolysis pathway and its regulation a detailed study.AnjaliKR3
glycogenolysis detailed study. Glycogen breakdown pathway explained each step in detail. regulation of glycogenolysis pathway. allosteric regulation, hormonal regulation and calcium ion regulation.
Glycogenolysis, process by which glycogen, the primary carbohydrate stored in the liver and muscle cells of animals, is broken down into glucose to provide immediate energy and to maintain blood glucose levels during fasting. These slides will provide you detail explanation of Glycogenolysis.
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
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
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
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
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.
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.
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
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.
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
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.
3. • Glycogen is a chain of glucose subunits held
together by( α 1,4 glycosidic bonds),
glycogen is a branched structure. At the
branch points, subunits are joined by ( α1g6
glycosidic bonds).
• Branches occur every 8-10 residues.
4.
5.
6. Glycogenesis is the process of
Glycogen synthesis
• Glycogen is synthesized when blood
glucose levels are high .
• Glucose is converted into glucose-6phosphate by the action of :
Hexokinase catalyses this reaction in most
tissues.
In the liver and pancreas there is an extra
enzyme; Glucokinase exhibiting different
kinetic properties.
8. • This state is reflected inside liver cells by
the presence of high levels of glucose-6phosphate. G6P is converted to G1P by
phosphoglucomutase.
• This reaction is analogous to the reaction
catalyzed by phosphoglycerate mutase in of
glycolysis, and proceeds by a similar
mechanism, with a bisphosphate
intermediate.
9.
10. • Conversion of G1P into glycogen is
energetically unfavorable, so another source
of energy input is required.
• This comes in the form of hydrolysis of
UTP (uridine triphosphate). The highenergy phosphoanhydride bonds in UTP are
equivalent to those in ATP. First, UTP is
combined with G1P by UDP-glucose
pyrophosphorylase.
11.
12.
13. :::Next, glycogen synthase catalyzes the addition of this
activated glucose subunit to the C4-hydroxyl group at the
end of a glycogen chain (the non-reducing end).
14. • After the chain is more than four residues long, glycogen
synthase takes over. Glycogenin remains bound to the
reducing end of glycogen (the C1 hydroxyl group at the
right side of the pictures). Glycogen synthase works
efficiently only when it is bound to glycogenin.
• Thus the number of glycogen granules in a cell is
determined by the number of glycogenin molecules
available, and the size of the granules is limited by the
need for physical association between glycogenin and
glycogen synthase. When the granule grows too large, the
synthase stops working.
15. • Formation of branches is catalyzed by
"branching enzyme",( amylo (α-1,4ـــα1,6)
transglycosylase).
• This enzyme breaks off a chain of about 5 to 8
glucose residues from the growing end of
glycogen by hydrolyzing an( α 1,4 glycosidic
linkage), and transfers the short chain to another
residue in the same glycogen molecule that is at
least four residues away from the cleavage point,
forming an( α 1,6 glycosidic linkage)
16. After the transfer, both the old C4 end and the newly exposed C4 end
can be elongated by glycogen synthase.
As soon as the new ends are long enough, they can again be
branched. A mature glycogen granule may have seven layers of
branches.
17. • Branching gives glycogen two advantages
over starch as a storage form of glucose.
• First, it is more soluble than its unbranched
cousin.
• Second, the exposure of more C4
(nonreducing) ends means that glycogen
can be both sythesized and degraded more
quickly than a single starch chain with the
same number of residues.
18. Control and regulations
Epinephrine (Adrenaline)
• Glycogen phosphorylase is activated by phosphorylation, whereas
glycogen synthase is inhibited.
• Glycogen phosphorylase is converted from its less active "b" form to
an active "a" form by the enzyme phosphorylase kinase. This latter
enzyme is itself activated by protein kinase A and deactivated by
phosphoprotein phosphatase-1. Protein kinase A itself is activated by the
hormone adrenaline.
• Epinephrine binds to a receptor protein that activates adenylate
cyclase. The latter enzyme causes the formation of cyclic adenosine
monophosphate AMP from Adenosine triphosphate (ATP); two
molecules of cyclic AMP bind to the regulatory subunit of protein
kinase A, which activates it allowing the catalytic subunit of protein
kinase A to dissociate from the assembly and to phosphorylate other
proteins.
19. • Returning to glycogen phosphorylase, the less active
"b" form can itself be activated without the
conformational change. AMP acts as an allosteric
activator, whereas ATP is an inhibitor, as already
seen with phosphofructokinase control, helping to
change the rate of flux in response to energy demand.
• Epinephrine not only activates glycogen
phosphorylase but also inhibits glycogen synthase.
This amplifies the effect of activating glycogen
phosphorylase. This inhibition is achieved by a
similar mechanism, as protein kinase A acts to
phosphorylate the enzyme, which lowers activity.
This is known as co-ordinate reciprocal control.
20. Insulin
• Insulin has an antagonistic effect to adrenaline.
• When insulin binds on the G protein-coupled receptor,
the alpha subunit of Guanosine diphosphate GDP in the
G protein changes to Guanosine-triphosphate GTP and
dissociates from the inhibitory beta and gamma subunits.
• The alpha subunit binds on adenylyl cyclase to inhibit its
activity.
• As a result, less cyclic AMP then less protein kinase A
will be produced. Thus, glycogen synthase, one of the
targets of protein kinase A, will be in nonphosphorylated form, which is the active form of
glycogen synthase.
21. Calcium ions
• Calcium ions or cyclic AMP (cAMP) act as
secondary messengers.
• This is an example of negative control. The
calcium ions activate phosphorylase kinase. This
activates glycogen phosphorylase and inhibits
glycogen synthase.
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24. Regulation
• Glycogenolysis is regulated hormonally in
response to blood sugar levels by glucagon
and insulin, and stimulated by epinephrine
during the fight-or-flight response.
• In myocytes, glycogen degradation may
also be stimulated by neural signals.