1. Beta-oxidation is the major pathway for fatty acid oxidation that occurs in the mitochondria. It involves activation of fatty acids to acyl-CoA derivatives, transport into the mitochondria, and four steps of beta-oxidation to sequentially cleave two-carbon acetyl-CoA units, producing ATP.
2. Minor pathways include alpha-oxidation of phytanic acid in peroxisomes, omega-oxidation of fatty acids in the ER, and peroxisomal beta-oxidation of very long chain fatty acids.
3. Defects in these pathways can cause diseases like Refsum's disease and Zellweger syndrome. Medium chain acyl-CoA
Pentose phosphate pathway is also called Hexose monophosphate pathway/ HMP shunt/ Phosphogluconate pathway.
It is an alternative route for the metabolism of glucose.
It is more complex pathway than glycolysis.
It is more anabolic in nature.
It takesplace in cytosol.
The tissues such as liver, adipose tissue, adrenal gland, erythrocytes,testes and lactating mammary gland are highly active in HMP shunt.
It concern with the biosynthesis of NADPH and pentoses.
Substrate level phosphorylation and it's mechanism || Biochemistry || B Pharmacy || Project || slideshare || biology || chemistry
*images use in this ppt is only for educational purpose
In this presentation, i tell about substrate level phosphorylation
Phosphorylation involves the transfer of phosphate
group from one compound to other.
➢ Substrate level phosphorylation is a direct
phosphorylation of ADP with a phosphatase group by
using the energy obtain from a coupled reaction.
➢ Occurs in cytoplasm ( glycolysis – due to aerobic and
anaerobic condition) and in mitochondrial matrix ( krebs
cycle – anaerobic condition)
Pentose phosphate pathway is also called Hexose monophosphate pathway/ HMP shunt/ Phosphogluconate pathway.
It is an alternative route for the metabolism of glucose.
It is more complex pathway than glycolysis.
It is more anabolic in nature.
It takesplace in cytosol.
The tissues such as liver, adipose tissue, adrenal gland, erythrocytes,testes and lactating mammary gland are highly active in HMP shunt.
It concern with the biosynthesis of NADPH and pentoses.
Substrate level phosphorylation and it's mechanism || Biochemistry || B Pharmacy || Project || slideshare || biology || chemistry
*images use in this ppt is only for educational purpose
In this presentation, i tell about substrate level phosphorylation
Phosphorylation involves the transfer of phosphate
group from one compound to other.
➢ Substrate level phosphorylation is a direct
phosphorylation of ADP with a phosphatase group by
using the energy obtain from a coupled reaction.
➢ Occurs in cytoplasm ( glycolysis – due to aerobic and
anaerobic condition) and in mitochondrial matrix ( krebs
cycle – anaerobic condition)
it is bypass cycle of citric acid cycle.
it give the brief description of glyoxylate cycle.
it is the summary of glyoxylate cycle for m.sc, bsc, science students.
it is very important topic for entrance exam of biology stream.
ATP synthase—also called FoF1 ATPase is the universal protein that terminates oxidative phosphorylation by synthesizing ATP from ADP and phosphate.
ATP Synthase is one of the most important enzymes found in the mitochondria of cells
it is bypass cycle of citric acid cycle.
it give the brief description of glyoxylate cycle.
it is the summary of glyoxylate cycle for m.sc, bsc, science students.
it is very important topic for entrance exam of biology stream.
ATP synthase—also called FoF1 ATPase is the universal protein that terminates oxidative phosphorylation by synthesizing ATP from ADP and phosphate.
ATP Synthase is one of the most important enzymes found in the mitochondria of cells
explains the palmitate synthesis- which is most common FA stored in Adipose tissue , elongation system and Desaturation system, compares oxidation with synthesis.
Lipid metabolism is the synthesis and degradation of lipids in cells, involving the breakdown and storage of fats for energy and the synthesis of structural and functional lipids, such as those involved in the construction of cell membranes. In animals, these fats are obtained from food and are synthesized by the liver. Lipogenesis is the process of synthesizing these fats. The majority of lipids found in the human body from ingesting food are triglycerides and cholesterol.[4] Other types of lipids found in the body are fatty acids and membrane lipids. Lipid metabolism is often considered as the digestion and absorption process of dietary fat; however, there are two sources of fats that organisms can use to obtain energy: from consumed dietary fats and from stored fat.[5] Vertebrates (including humans) use both sources of fat to produce energy for organs such as the heart to function. Since lipids are hydrophobic molecules, they need to be solubilized before their metabolism can begin. Lipid metabolism often begins with hydrolysis, which occurs with the help of various enzymes in the digestive system.Lipid metabolism also occurs in plants, though the processes differ in some ways when compared to animals.[8] The second step after the hydrolysis is the absorption of the fatty acids into the epithelial cells of the intestinal wall.[6] In the epithelial cells, fatty acids are packaged and transported to the rest of the body.[9]
Metabolic processes include lipid digestion, lipid absorption, lipid transportation, lipid storage, lipid catabolism, and lipid biosynthesis. Lipid catabolism is accomplished by a process known as beta oxidation which takes place in the mitochondria and peroxisome cell organelles.
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
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
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
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.
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
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
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.
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
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.
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
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
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
2. Major and minor fatty acid
oxidation
Major oxidation:
Mitochondrial beta oxidation
• Minor Oxidation:
Alpha oxidation
Omega oxidation
Peroxisomal Beta oxidation
3. Beta- Oxidation
Beta –oxidation is defined as the oxidation and
splitting of two carbon units at beta carbon atom.
This results in sequential removal of 2 carbon
fragments as acetyl CoA until the complete oxidation
of fatty acids.
Beta oxidation occurs almost in all tissues except,
erythrocytes and adrenal medulla.
4. Stages of beta-oxidation
Three major steps involved :
1. Preparative stage (Activation of fatty acid) occurs
in cytosol.
2. Transport of fatty acyl CoA through carnitine
shuttle, present in mitocondrial membrate
3. Beta – oxidation proper in mitochondrial matrix.
5. Activation of fatty acid
Activation occurs in Cytosol
Acyl CoA synthetase / Thokinase
Fatty acid Fatty acyl CoA
ATP AMP + ppi
LCFA requires carnitine shuttle for transport into
mitochondrial menbrane
SCFA/MCFA do not require carnitine suttle
6. Transport of Fatty acyl CoA
Acyl CoA
Acyl
carnitine
Acyl
carnitine
Acyl CoA
8. Steps of Beta–oxidation proper
Fatty acyl CoA
FAD
FADH2 ETC 2 ATP
Trans enoyl CoA
H2O
B- hydroxyacyl CoA
NAD
NADH ETC 3ATP
B –ketoacyl CoA
CoA
AcylCoA +Acetyl CoA
Acyl CoA
dehydrogenase
Hydratase
β- hydroxyacyl
CoA
dehydrogenase
Thiolase
Inner Mitochondrial Membrane
10. FORMULA FOR CALCULATING ENERGETICS
FOR EVEN CHAIN FATTY ACID
n= Number of carbon atoms present in fatty acid
Number of acetyl CoA produced = n/2
Number of cycles for fatty acids= (n/2 -1)
Number of reduced coenzyme = (n/2-1) (FADH2 +NADH)
For example if 16C (palmitic acid) undergoes beta oxidation
No. of acetyl CoA produced= 8 {1 Acetyl CoA = 12 ATP in TCA}
8×12= 96 ATPs
No.of cycles for palmitic acid= 7
No.of reduced coenzymes produced= 7( FADH2 + NADH)
7(2+3)= 35 ATPs
Total no. of ATPs produced= 96+35= 131 ATPs
No. of ATPs utilized during activation= 2 ATPs
Net gain= 131-2= 129 (ATPs According to old energeitcs concept)
11. FORMULA FOR CALCULATING ENERGETICS FOR
ODD CHAIN FATTY ACID
• No. of acetyl coA produced= (n-3)/2
No. of Cycles =(n-3)/2
No. of reduced coenzymes= (n-3)/2[ FADH2+NADH]
Remaining 3C is propionyl CoA
For example if 17c fatty acid undergoes beta oxidation
No. of acetyl CoA = 7 { 1 acetylCoA= 12 ATPin TCA}
7×12=84 ATPs
No.of Cycles= 7
No. of reduced coenzymes= 7( FADH2+ NADH)
7(2+3)= 35ATPs
Total no. of ATPs produced= 84+35= 119ATPs
No. of ATPs utilized for activation=2 ATPs
Net gain= 119-2= 117 ATPs
Remaining 3C compound is propionyl CoA which converts to
succinyl CoA and ebters TCA cycel
12. β- Oxidation for odd chain fatty acid
Beta oxidation for odd chain fatty acid occurs in the
same way as for even chain fatty acid except the
cleavage step yields propionyl CoA and Acetyl CoA
ATP ADP+Pi
Fig: -Fate of Propionyl CoA
Biotin
13. Regulation of beta-oxidation
Increased availability of FFA increases the rate of beta
oxidation
Glucagon increases FFA and Insulin decreases FFA
CAT-I is inhibited by Malonyl CoA( substrate for fatty
acid synthesis). Thus during denovo synthesis of fatty
acid beta oxidation is inhibited
15. Alpha - oxidation
Defined as the oxidation of fatty acid (methyl group
at beta carbon) with the removal of one carbon unit
adjacent to the α carbon from the carboxylic end in
the form of CO2
Alpha oxidation occurs in those fatty acids that have
a methyl group(CH3) at the beta-carbon, which blocks
beta oxidation.
Substrate:-Phytanic acid, which is present in milk or
derived from phytol present in chlorophyll and animal
fat
peroxisomes is the cellular site.
No production of ATP
16. Steps of alpha oxidation
1. Activation of phytanic acid
2. Hydroxylation
3. Removal of formyl CoA( CO2)
4. Oxidation of Pristanal
5. Beta-oxidation of pristanic acid
17. Alpha Oxidation
Phytanic acid
ATP
AMP+ ppi
Phytanoyl CoA
α KG + O2
Succinate +CO2
2-hydroxy phytanoyl CoA
Formyl CoA CO2
Pristanal
NADP
NADPH
Pristanic acid
Phytanoyl CoA
synthetase
Phytanoyl CoA
Hydroxylase
Lyase
Aldehyde
dehydrogenase
19. Significance of alpha oxidation
Oxidation of methylated fatty acid
Production of cerebronic acid which synthesizes
cerebroside and sulfatides
Production of odd chain fatty acids
20. Adult Refsum’s Disease
Biochemical defect
Defect in enzyme phytanoyl CoA hydroxylase(
Phytanic acid oxidase)
Autosomal reccesive
Phytanic acid is acumulated in brain and other
tissue
lab Findings
Plasma Level of phytanic acid > 200µmol/L
Normal< 3oµmol/L
21. Infantile Refsum’s Disease
Biochemical defect
It is a disorder observed in zellweger syndrome.
Congenital peroxisomal biogenesis disorder
Lab findings
1. Phytanic acid in the serum is More than 30µmol/L
and less than 200µmol/L
2. VLCFA and LCFA in serum is increased
22. Molecular Toxicology of Refsum’s Disease
PA is directly toxic to ciliary ganglion cells and induces
calcium –driven apoptosis in purkinji cells
Recent studies has found that PA has a Rotenone like
action in inhibiting complex –I and producing reactive
oxygen species
This is the reason why neuronal cells and retina rich in
mitochondria are prime tissue affected in Refsum’s
disease
23. Refsum’s Disease
Clinical manifestations
Severe neurological symptoms such as
Polyneuropathy,
retinitis pigmentosa,
Nerve deafness
Cerebellar ataxia
Patients should avoid intake of diet such as green
vegetables and milk.
24. Omega(ω) Oxidation
Cellular site: Endoplasmic reticulum
oxidation occurs at (ω-omega) carbon—the carbon
most distant from the carboxyl group.
Substrates : Medium and long chain fatty acid
Importance: It is a minor pathway but becomes active
when beta oxidation is defective.
The product formed are di-carboxylic acid
25.
26. Peroxisomal Beta Oxidation
Beta oxidation occurs in modified form in
peroxisomes.
Very Long chain fatty acids (>C22) are often oxidized
in peroxisomes.
FADH2 produced by the action of Acycl CoA
dehydrogenases pass electrons directly to oxygen.
This results in formation of H2O2.
H2O2 is again cleaved by peroxisomal catalase.
Subsequent steps are identical with their
mitochondrial counterparts.
They are carried out by different isoform of the
enzymes.
27. Initial step of Peroxisomal beta oxidation
O2 H2O2 H2O+ 1/2O2
Acyl CoA dehydrogenase Acyl CoA dehydrogenase
(ox, FAD) (red, FADH2)
Fatty acyl CoA Tans enoyl CoA
Catalase
28. Zellweger syndrome
Biochemical defect
Defect in the gene for peroxisome biogenesis
reduction or absence of Peroxisomes in the cells
of the liver, kidneys, and brain.
VLCFA and LCFA are not oxidized and accumulates in
tissue , particularly in brain ,liver and kidney.
Lab findings:
Increased level of VLCFA in serum
Increased level of phytanic acid in serum
29. Medium chain acylCoA dehydrogenase deficiency
(MCAD deficiency)
Most common inborn error of fatty acid oxidation.
Being found in 1:14,000 births worldwide.
Decreased ability to oxidize fatty acids with six to ten
carbons.
MCFA accumulates in tissue and also excreted in
urine.
Symptoms:
Hypoglycemia
Sleepiness
Vomiting
Fat accumulation in liver
30. Deficiencies of Carnitine or carnitine transferase
or carnitine translocase
Causes:
• Deficiency of carnitine
Inherited CPT-I deficiency affects only the liver.
CPT-II deficiency affects primarily skeletal muscle
and, when severe, the liver.
Symptoms:
muscle cramps are precipitated by fasting, exercise
and high fat diet.
Hypoglycemia
31. Jamaican vomiting sickness
Caused by eating unripe ackee fruit which contains
unusal toxic amino acids hypoglycin A and B
It inhibits enzyme acyl CoA dehydrogenase .
Beta-oxidation is blocked leading to serious
complications.
Symptoms :
Severe hypoglycemia
vomiting
Convulsions
Coma
Ackee fruit