Introduction to Targeted Therapies in OncologyMohamed Abdulla
Describes the molecular background which represents the core for developing targeted therapies against specific biological events in malignant cellular clones.
Introduction to Targeted Therapies in OncologyMohamed Abdulla
Describes the molecular background which represents the core for developing targeted therapies against specific biological events in malignant cellular clones.
We studied the review article about How I investigate eosinophilia, which was published in the International Journal of Laboratory Hematology in August 2018. This paper has clearly and simply introduced how clinicians investigate eosinophilia. Hopefully, it can be helpful to everyone who interested in this field.
Leukemia, were surviving is regarded as a victory, a disease that still acts as a risk factor among the folks of Hiroshima and Nagasaki, stays as one of the fields to be looked forward for the further research. The above presentation includes the topics to be covered during a presentation on Leukemia. Apt for the students of Pharmacology.
drug induced liver disease
DILD is caused by many different drugs of mostly painkillers and fever reducers which contain acetaminophen drug this is hepatotoxic because drugs are absorbed by liver on high dose of this drug lead damage of liver known as liver injury. Rarely absorbed in children. actually people who drink alcohol has high prone to drug injury, but in children in happened because of antiepileptic and antiniotics.the antibiotics most often implicated with liver injury are amoxicillin/clavulanic acid, flucloxacillin and erythromycin .Nonalcoholic Fatty Liver Disease (NAFLD) is the most common forms of chronic liver disease in children and adolescents. It is an inherited disorder that affects the metabolism – the way the body breaks food down into energy.Drug-induced liver injury in children (cDILI) accounts for about 1% of all reported adverse drug reactions throughout all age groups, less than 10% of all clinical DILI cases, and around 20% of all acute liver failure cases in children. The overall DILI susceptibility in children has been assumed to be lower than in adults. Nevertheless, controversial evidence is emerging about children's sensitivity to DILI, with children's relative susceptibility to DILI appearing to be highly drug-specific. The culprit drugs in cDILI are similar but not identical to DILI in adults (aDILI). This is demonstrated by recent findings that a drug frequently associated with aDILI (amoxicillin/clavulanate) was rarely associated with cDILI and that the drug basiliximab caused only cDILI but not aDILI. The fatality in reported cDILI studies ranged from 4% to 31%. According to the US Food and Drug Administration-approved drugs labels, valproic acid, dactinomycin, and ampicillin appear more likely to cause cDILI. In contrast, deferasirox, isoniazid, dantrolene, and levofloxacin appear more likely to cause aDILI. Animal models have been explored to mimic children's increased susceptibility to valproic acid hepatotoxicity or decreased susceptibility to acetaminophen or halothane hepatotoxicity. However, for most drugs, animal models are not readily available, and the underlying mechanisms for the differential reactions to DILI between children and adults remain highly hypothetical. Diagnosis tools for cDILI are not yet available. A critical need exists to fill the knowledge gaps in cDILI. This review article provides an overview of cDILI and specific drugs associated with cDILI.
Out of 298 patients enrolled 273 (92%) resolved ⩽1 year from DILI recognition and 25 patients (8%) were chronic. Independent risk factors for chronicity were older age [OR:1.06, p=0.011], dyslipidemia [OR:4.26, p=0.04] and severe DILI [OR:14.22, p=0.005]. Alanine aminotransferase (ALT), alkaline phosphatase (ALP) and total bilirubin (TB) median values were higher in the chronic group during follow-up. Values of ALP and TB >1.1 xULN and 2.8 xULN respectively, in the second month from DILI onset, were found to predict chronic DILI (p<0.001)
this is mainly about about roe v wade (abortion case) and the ethical view of it
at the end i added a quick brief about the most legal abortion methods especially the medical one
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- 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
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
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
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.
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
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.
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.
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 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
3. Protein Kinase
• Is kinase enzyme that modifies other proteins by chemically
adding phosphate groups to them (phosphorylation)
• The phosphate is often taken from ATP
• Phosphorylation of proteins by kinases is an
important mechanism in communicating
signals within a cell (signal transduction)
and regulating cellular activity, such as
cell division.
3
4. Categories of Protein Kinases
1. Kinases that specifically phosphorylate
tyrosine residues.
2. Kinases that phosphorylate serine and
threonine residues.
4
5. Tyrosine Kinase
• Is an enzyme that can transfer a phosphate group
from ATP to a protein in a cell.
• It functions as an "on" or "off" switch
in many cellular functions.
• The phosphate group is attached to the
amino acid tyrosine on the protein.
5
10. Oncogenic Activation of Receptor Tyrosine Kinases
• Normally the level of cellular tyrosine kinase
phosphorylation is tightly controlled by the
antagonizing effect of tyrosine kinase
and tyrosine phosphatases.
• Some Common mechanisms
of oncogenic activation:
1. Activation by mutation
2. BCR-ABL and human leukemia
10
11. Targeted Therapy
• is a type of medication that blocks the growth of cancer
cells by interfering with specific targeted molecules needed
for carcinogenesis and tumor growth.
• rather than by simply interfering with all rapidly dividing
cells (e.g. with traditional chemotherapy).
11
17. Dasatinib
Toxicity:
• Cardiovascular: Fluid retention (21% to 35%)
• Central nervous system: Headache (12% to 33%), fatigue (8% to
24%), fever (5% to 18%)
• Dermatologic: Rash (11% to 21)
• Endocrine & metabolic: Hypophosphatemia (5% to 18%)
• Gastrointestinal: Diarrhea (18% to 31%), nausea (9% to 24%),
vomiting (5% to 16%), abdominal pain (3% to 12%)
• Hematologic: Thrombocytopenia (19% to 85%), neutropenia (22%
to 79%), anemia (11% to 74%), neutropenic fever (1% to 12%)
• Neuromuscular & skeletal: Musculoskeletal pain (≤19%)
• Respiratory: Pleural effusion (12% to 24%)
• Miscellaneous: Infection (9% to 12%)
17
18. Gefitinib
• MOA:
Gefitinib is a tyrosine kinase inhibitor (TKI) which inhibits
numerous tyrosine kinases associated with transmembrane cell
surface receptors found on both normal and cancer cells, including
the tyrosine kinase associated with the epidermal growth factor
receptor, EGFR.
• Indications:
Non-small Cell Lung Cancer (NSCLC)
Monotherapy for continued treatment of locally advanced or
metastatic NSCLC after failure of both platinum-based and
Docetaxel regimens
• website
http://www.iressa.com
18
19. Gefitinib
Toxicity
• Dermatologic: Rash (43% to 54%), acne (25% to 33%), dry
skin (13% to 26%), paronychia (14%)
• Gastrointestinal: Diarrhea (48% to 67%), nausea (13% to
18%), vomiting (9% to 12%)
19
20. Lapatinib
• MOA:
Tyrosine kinase (dual kinase) inhibitor; inhibits EGFR (ErbB1) and
HER2 (ErbB2). Combination therapy with lapatinib and endocrine
therapy may overcome endocrine resistance occurring in HER2+
and hormone receptor positive disease.
• Indications:
Metastatic Breast Cancer in combination with Capecitabine in
patients whose tumors overexpress HER2 and who have received
prior therapy including an Anthracycline, a Taxane, and
Trastuzumab.
website
http://www.tykerb.com/
20
21. Lapatinib
Toxicity
• Central nervous system: Fatigue (10% to 20%), headache (≤14%)
• Dermatologic: (hand-and-foot syndrome) (with capecitabine: 53%),
rash (28% to 44%), alopecia (≤13%)
• Gastrointestinal: Diarrhea (64% to 65%), nausea (31% to 44%),
vomiting (17% to 26%),
• Hematologic: Anemia (with capecitabine: 56%), neutropenia (with
capecitabine: 22%)
• Hepatic: total bilirubin increased (22% to 45%)
• Neuromuscular & skeletal: weakness (≤12%), back pain (≤11%)
• Respiratory:Dyspnea (≤12%)
21
22. Sorafinib
• MOA:
Multikinase inhibitor; inhibits tumor growth and angiogenesis by
inhibiting intracellular Raf kinases, and cell surface kinase receptors
(VEGFR-1, VEGFR-2, VEGFR-3, PDGFR-beta, cKIT, FLT-3, and
RET).
• Indications:
Treatment of advanced renal cell cancer (RCC); treatment of
unresectable hepatocellular cancer (HCC)
website
http://www.nexavar-us.com/scripts/pages/en/patient/index.php
22
23. Sorafinib
Toxicity
• Cardiovascular: Hypertension (9% to 17%)
• Central nervous system: Fatigue (37% to 46%),
• Dermatologic: Rash (19% to 40%), hand-foot syndrome (21% to
30%), alopecia (14% to 27%)
• Endocrine & metabolic: Hypoalbuminemia (≤59%),
• Gastrointestinal: Diarrhea (43% to 55%), weight loss (10% to
30%),, nausea (23% to 24%), vomiting (15% to 16%), constipation
(14% to 15%)
• Hematologic: Lymphopenia (23% to 47%),
• Hepatic: Liver dysfunction (≤11%)
• Neuromuscular & skeletal: Muscle pain, weakness
• Respiratory: Dyspnea (≤14%), cough (≤13%)
23