This is about glomerulonephritis and all that you need to know. It contains different images illustrating this subject matter, well defined outline, different aspect of glomerulonephritis, which include acute and chronic glomerulonephritis, nephritic and nephrotic syndrome, investigations, how to diagnose glomerulonephritis, treatment and important discussions on Glomerulonephritidis. It is a presentation you need to check out.
This is about glomerulonephritis and all that you need to know. It contains different images illustrating this subject matter, well defined outline, different aspect of glomerulonephritis, which include acute and chronic glomerulonephritis, nephritic and nephrotic syndrome, investigations, how to diagnose glomerulonephritis, treatment and important discussions on Glomerulonephritidis. It is a presentation you need to check out.
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
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.
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.
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
- 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
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
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.
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
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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.
2. • Epidemiology and Classification
• Pathogenesis
• Clinical feature
• Laboratory studies
• Kidney biopsy
• Differential Diagnosis of GN
3. Introduction
• Glomerulonephritis (GN) is serious disorder that can lead to
end-stage renal disease (ESRD), other serious morbidity, or
death.
• GN is particular topic in nephrology with many clinical
variants
• Could be asymptomatic or full blown
• Patients may come with abnormal urinalysis as the only
presentation.
• Little is know about the epidemiology of GN, since no large-
scale examination of GN incidence and prevalence is
available.
7. Classification of Glomerular Disease
Glomerular Disease
Defect in glomerular filtration barrier causing one or more of the
following: glomerular proteinuria, glomerular hematuria or decrease
in GFR.
Primary Glomerulopathy
Begins in the glomerulus
and causing damage only
to the glomerulus- Primary
FSGS
Secondary
Glomerulopathy
Glomerular disease due to
systemic disease
2nd degree FSGS
Glomerular disease due to
severe nephron loss. The
remaining nephron will be
hyperperfused and having focal
segmental sclerosis.
Am J Nephrol 2013
Minimal change disease
Post-streptococcal acute GN
Idiopathic membranous
nephropathy
Anti-GBM disease
IgA nephritis
Primary FSGS
Diabetic nephropathy
Lupus Nephritis
Amyloidosis
ANCA-related vasculitis
Type 1, 2, 3 cryoglobulinemia
infection-related GN
Nonglomerular CKD causing
severe nephron loss
.
8.
9.
10. Importance of the site of glomerular injury
• The major determinant of whether the patient presents with GN and
an active urine sediment (nephritic syndrome) or with proteinuria
(nephrotic syndrome) and hematuria, the site of glomerular injury—
particularly, which glomerular cells are targeted.
• There are three major types of resident glomerular cells: epithelial
cells (visceral and parietal), endothelial cells, and mesangial cells.
11. Pathogenesis
• Most forms of GN are thought to be immune-mediated.
• The immunopathogenesis of GN is often complex and may
be the result of of genetics and unfavorable environmental
conditions. Genetic factors clearly predispose certain
individuals to develop immune responses that can lead to
GN.
• Glomerular injury is usually mediated by the actions of
multiple elements of both the innate and the adaptive
immune systems, resulting in diverse clinical and pathologic
manifestations.
Am J Nephrol 2013
13. Mechanism of Immune Injury: Inflammatory
and Non-Inflammatory
• Inflammatory injury GN is characterized by glomerular infiltration by
hematopoietic cells such as neutrophils and macrophages and/or
proliferation of resident glomerular cells.
Am J Nephrol 2013
14. • Noninflammatory GN resulting from immune injury usually target the
glomerular podocyte.
•
• associated with major functional changes in the glomerulus that result in an
increase in glomerular permeability to albumin and other proteins
• The major clinical features of noninflammatory glomerular lesions are
proteinuria and the nephrotic syndrome, with little or no hematuria and no
red blood cell casts.
• Common causes of immune-mediated nephrotic syndrome without
inflammatory changes are minimal change disease (MCD) and membranous
nephropathy (MN).
Mechanism of Immune Injury
Bonegio RGB UTD 2019
16. Systemic findings
• Constitutional – fevers, chills, weight loss, night sweats, fatigue
• Eye – retinitis or uveitis
• Ear, nose, and throat – epistaxis, sinusitis, oral ulcers
• Cardiovascular – murmurs, pain (pericarditis), or heart failure
• Lungs – hemoptysis, infiltrates, or nodules
• Abdomen – enteritis, colitis, or pancreatitis
• Nervous system – seizures or peripheral neuropathy
• Extremities – digital ischemia or infarction
• Skin – purpura or rash
• Musculoskeletal – arthritis, arthralgias, myalgias
• Infections – particularly evidence of Staphylococcus, Streptococcus, hepatitis
virus, or human immunodeficiency virus (HIV), syphilis
•
17. History Taking
•Patients may come with symptoms or asymptomatic
•Oedema, hypertension, history of infection may be
present
•Systemic illness: SLE, diabetes, hypertension,
amyloidosis, vasculitis
•Family history: Alport syndrome, genetic-related
FSGS, familial IgA disease
Clin J Am Soc Nephrol 2017
26. Nephritic Syndrome
•Decrease in GFR, non-nephrotic proteinuria,
oedema, hypertension, hematuria
•Classical form: paediatric post streptococcal
glomerulonephritis
•Nephritic syndrome can be overlapped with
nephrotic syndrome
31. Rapidly Progressive
Glomerulonephritis (RPGN)
•Abrupt decrease in renal function (days-weeks)
•Pts may come to ER with uremic syndrome
•Hallmark: crescentic appearance in kidney
biopsy
•Biopsy: to differentiate with ATN, hypertensive
crises, sepsis
Clin J Am Soc Nephrol 2017
34. Minimal Change Disease
•Most common cause of idiopathic nephrotic
syndrome in children
•Adults: 10%-15% of idiopathic nephrotic
syndrome
•Massive proteinuria
•Oedema
•Good prognosiscomplete remission
•Biopsy: Podocyte swelling and foot processes
effacement
Clin J Am Soc Nephrol 2017
36. Focal Segmental Glomerulosclerosis (FSGS)
•Most common cause of
ESRD in patients with
glomerular disease
•Nephrotic or sub-
nephrotic proteinuria
•Segmental sclerosis in
glomerulus
•Six forms: see picture
Clin J Am Soc Nephrol 2017
40. Membranoproliferative
Glomerulonephritis
•Refers to type I membranoproliferative
glomerulonephritis
•Immune deposition in mesangium and
subendothelial space
•In cryoglobulinemic glomerulonephritis caused by
hepatitis C virus and lupus nephritis
Clin J Am Soc Nephrol 2017
41. Ig-A Nephropathy
•Most prevalent glomerulonephritis globally
•Lead to CKD and ESRD
•In developing countries: falsely low prevalence
because lack of kidney biopsy data
•Pathogenesis involving genetic and environmental
factors multi hit process
•Aberrant glycocylated IgA
•Patients may come with microscopic hematuria to
severe kidney impairment
Clin J Am Soc Nephrol 2017
43. Post Streptococcal Glomerulonephritis
• After group A streptococcal infection, especially
nephritogenic strain
• Onset 7-10 days after infection
• Inflammation with endothelial and mesangial
proliferation
• Patients may come with classic nephritic syndrome
• Biopsy: subepithelial space “humps”immune complex
translocation through glomerular basal membrane
Comprehensive Clinical Nephrology 2015
44.
45. Goodpasture Disease
•Also known as anti-glomerular basal membrane
disease
•Autoantibody against alpha-3 chain in type-IV
collagen in glomerular basal membrane
•Small vessel vasculitis affecting capillaries in lungs
and kidneys
•>80% pts come with RPGN
•50% present with pulmonary haemorrhage
Comprehensive Clinical Nephrology 2015
Clin J Am Soc Nephrol 2017
46. ANCA-related Vasculitis
•Very severe form of glomerular damage
•Common findings: pauci-immune necrotizing
glomerulonephritis and crescent type
•Usually in adults >50 years
•2012 Chapel Hill Consensus:
• Microscopic polyangiitisp-ANCA
• Granulomatosis with polyangiitis (Wegener)c-ANCA
• Eosinophilic granulomatosis with polyangiitis (Churg-
Strauss)c-ANCA
