Comprehensive description of various primary dyslipidemias, cholesterol transport and molecular mechanisms involved.
View in slideshow after downloading for better experience.
Prepared in Dec 2013.
D dimer test and sample collection procedure anjalatchi
Normally D-dimer levels are undetectable or detectable at very low levels, but they rise sharply when the body breaks down clots. D-dimer tests help in ruling out pulmonary embolisms in hospitalised Covid-19 patients
A lysosomal storage disease caused by acid sphingomyelinase deficiency (ASMD), which catalyzes the hydrolysis of sphingomyelin (SM) to ceramide and phosphocholine.
Comprehensive description of various primary dyslipidemias, cholesterol transport and molecular mechanisms involved.
View in slideshow after downloading for better experience.
Prepared in Dec 2013.
D dimer test and sample collection procedure anjalatchi
Normally D-dimer levels are undetectable or detectable at very low levels, but they rise sharply when the body breaks down clots. D-dimer tests help in ruling out pulmonary embolisms in hospitalised Covid-19 patients
A lysosomal storage disease caused by acid sphingomyelinase deficiency (ASMD), which catalyzes the hydrolysis of sphingomyelin (SM) to ceramide and phosphocholine.
This presentation will show the diagnosttic criteria of metabolic syndrome and life style modification to cope up with this common disease .
also shows some quiz for medical students
obesity diseases--is a medical condition in which excess body fat has accumulated to the extent that it may have a negative effect on health.
Its hazards
Treatment of Obesity
This was a lecture in the course "Significant Medical Conditions in Seniors" presented at Peer Learning in Chapel Hill, NC, USA in 2016 by Michael C. Joseph, MD, MPH.
Adv. biopharm. APPLICATION OF PHARMACOKINETICS : TARGETED DRUG DELIVERY SYSTEMSAkankshaAshtankar
MIP 201T & MPH 202T
ADVANCED BIOPHARMACEUTICS & PHARMACOKINETICS : UNIT 5
APPLICATION OF PHARMACOKINETICS : TARGETED DRUG DELIVERY SYSTEMS By - AKANKSHA ASHTANKAR
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.
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
Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
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.
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
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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
4. • Type 1 ( familial hyperchylomicronemia)
• Type 2A (familial hypercholesterolemia)
• Type 2B ( familial combined(mixed)
hyperlipidemia)
• Type 3 (familial dysbetalipoproteinemia)
• Type 4 (familial hypertriglyceridemia)
• Type 5 ( familial mixed hypertriglyceridemia)
Types of disorder metabolism :
5. Familial hyperchylomicronemia defined as :
A rare inherited inborn error of metabolism
involving the absence of the enzyme called
lipoprotein lipase which results in increased
blood triglyeride and chylomicron levels. More
detailed information about
the symptoms,causes, and treatments of
Familial hyperchylomicronemia is available
below
6.
7. • Massive fasting hyperchylomicronemia, even
following normal fat dietry intake, resulting in
greater elevated serum TG levels.
• Deficiency of lipoprotein lipase or deficiency of
normal apolipoprotein Cll (rare).
• It is not associated with an increase in coronary
heart diseases
• Treatment is uptake of low fat diet. No drug
therapy is effective
. Type 1 : ( Familial
Hyperchylomicronemia )
8. Chylomicron syndrome
Familial chylomicronemia syndrome (FCS) —
also referred to as familial LPL deficiency
(LPLD), or hyperlipoproteinemia Type 1 — is
a very rare hereditary condition. Individuals
with FCS lack a properly functioning enzyme
called lipoprotein lipase (LPL), that is
involved with lipid metabolism. The
disruption of the enzyme activity leads to a
build-up of triglycerides and chylomicrons
(chylomicronemia).
9. Chylomicron syndrome
Under normal conditions, triglycerides are
packaged into chylomicrons in the intestine and
transported to fat and muscle cells. In
individuals with FCS, lack of functioning LPL
results in their triglycerides not being degraded,
which leads to very high concentrations of
triglycerides and chylomicrons.
10. Chylomicron syndrome
The high concentration of chylomicrons can trigger
a host of problems, including the development of
skin lesions known as eruptive xanthoma, a creamy
appearance of the retinal blood vessels (lipaemia
retinalis), abdominal pain, acute recurrent
inflammation of the pancreas (pancreatitis), and/or
abnormal enlargement of the liver and/or spleen
(hepatosplenomegaly)
11. Chylomicron syndrome
This very rare disease may go undetected, or may be
improperly diagnosed as hypertriglyceridemia during
childhood. In many cases, patients are not properly
diagnosed until they are young adults and experience
severe abdominal pain due to pancreatitis.
FCS is not yet well understood. More natural history
studies and clinical trials are needed to better understand
this very rare condition. Natural history studies provide
information on how the disease progresses over time and
its impact on patients’ daily lives. Clinical trials provide
data on the safety and efficacy of treatment options
12. Clinical Signs and
Symptoms
Individuals with FCS often present with abdominal pain, repetitive
colicky pains, and repetitive episodes of pancreatitis. Failure to
thrive also has been reported.
Other common symptoms and/or signs of FCS include the
development of skin lesions known as eruptive xanthoma, a creamy
appearance of the retinal blood vessels
(lipaemia retinalis), and/or abnormal enlargement of the liver and/or
spleen (hepatosplenomegaly). A routine blood sample may often
reveal the condition since it is often been described as ‘creamy’ due
to the high chylomicron levels.
Most persons with FCS are diagnosed by age 10, but some may not
be diagnosed until young adulthood since lipid levels are routinely
not measured in children
14. Diagnosis :
FCS typically presents early in childhood with
severe hypertriglyceridemia, recurrent episodes of
severe abdominal pain, a lower tolerance to dietary
fat, and failure to thrive (infancy). Presentation in
the absence of secondary causes – such as
diabetes, alcohol consumption, hormone intake,
paraproteinemia, and treatment with
antihypertensive agents – profoundly increases the
likelihood of FCS as a diagnosis.6
16. Treatment :
There is currently no pharmacotherapy approved in the United
States to treat patients with FCS.
Though there is anecdotal evidence that some patients MAY benefit
from approved triglyceride lowering medications [fibrates, niacin
(nicotinic acid) or statins (HMG-CoA reductase inhibitors)], FCS
experts believe that strict adherence to a low fat diet is the only
effective way to manage FCS.
Plasmapheresis (removal, cleaning, and reinsertion of patient’s
blood/plasma) may be necessary for some patients.
The possibility of gene therapy for FCS is currently being explored.
17. Type 2A ( Familial Hypercholesterolemia )
• Elevated LDL, with normal VLDL levels
due to a block in LDL degradation.
Increased serum cholesterol but normal
TG levels.
• Caused by defects in synthesis of LDL
receptors.
• Ischemic heart disease accelerated.
• Treatment: diet and drugs
18. Familial Hypercholesterolemia
FH is short for Familial Hypercholesterolemia. It is
an inherited disorder that leads to aggressive and
premature cardiovascular disease. This includes
problems like heart attacks, strokes, and even
narrowing of our heart valves. For individuals with
FH, although diet and lifestyle are important, they
are not the cause of high LDL. In FH patients,
genetic mutations make the liver incapable of
metabolizing (or removing) excess LDL. The result
is very high LDL levels which can lead to premature
cardiovascular disease (CVD).
19. Familial Hypercholesterolemia
High cholesterol often has no symptoms. Cholesterol is a
silent killer, so the damage may be done long before you
notice anything is wrong. Some of the signs and
symptoms are:
• angina from heart disease
• xanthomas (fatty skin deposits) on the elbows, buttocks,
knees, and tendons
• cholesterol deposits around the eyelids, also known as
xanthelasmas
• cholesterol deposits around the corneas, also known as
corneal arcus
Blood tests will reveal that your cholesterol levels—both
total and LDL—are higher than normal.
20.
21.
22. Drug Therapy :
If lifestyle modifications do not work, you may
need medications to reduce your cholesterol.
Statins are the most common drugs used to
reduce LDL cholesterol. Examples of statins
include simvastatin (Zocor), lovastatin
(Mevacor), atorvastatin (Lipitor) and
rosuvastatin (Crestor).
Other drugs that lower cholesterol include bile
acid-sequestering resins, ezetimibe, nicotinic
acid and fibrates.
23. Type 2B ( Familial Mixed
Hyperlipidemia)
• Similar to type 2A except VLDL also
increased, resulting in elevated
serum TG and cholesterol levels.
• Caused by overproduction of VLDL
by liver.
• Treatment : diet and drug therapy
24. Type 2B ( Familial Mixed Hyperlipidemia)
Familial combined
hyperlipidemia is a disorder of
high cholesterol and high blood
triglycerides that is inherited,
which means it is passed down
through families.
25. Symptoms :
Chest pain (angina) may occur. However, there
may not be any physical symptoms.
Persons with this condition develop high
cholesterol or triglyceride levels during the
teenage years. The levels remain high
throughout life. They have an increased risk of
early coronary artery disease and heart attacks.
Those with familial combined hyperlipidemia
have a higher rate of obesity and glucose
intolerance.
26.
27.
28.
29.
30. Treatment :
The goal of treatment is to reduce the risk
of atherosclerotic heart disease.
31. Treatment :
LIFESTYLE CHANGES
The first step is to change what you eat. Most of the time, this
is tried for several months before your doctor recommends
medicines, too. Diet changes include lowering the amount of
fat in your diet so it is less than 30% of your total calories.
Here are some ways to eat less saturated fat:
• Eat less beef, chicken, pork, and lamb
• Substitute low-fat dairy products for full-fat ones
• Eliminate palm oil
You can reduce your the amount of cholesterol you eat by
eliminating egg yolks and organ meats.
Counseling is often recommended to help people make
changes to their eating habits. Weight loss and regular
exercise may also help lower your cholesterol levels.
See also: Heart disease and diet