1. Autoimmune reactions against heat shock proteins (HSPs), particularly HSP60, may play an important role in the early development of atherosclerosis.
2. HSPs released from necrotic cells in advanced atherosclerotic plaques can stimulate the innate immune response and promote inflammation, attracting more inflammatory cells. This may link HSPs to complications like plaque rupture and thrombosis.
3. Both humoral and cellular immune reactions against HSP60 work together with classical cardiovascular risk factors to promote atherosclerosis and its complications.
RHEUMATOID ARTHRITIS BY DR BASHIR AHMED DAR ASSOCIATE PROFESSOR MEDICINE SOPO...Prof Dr Bashir Ahmed Dar
Dr Bashir ahmed dar associate professor medicine chinkipora sopore kashmir presently working in medical college malaysia describes rheumatoid arthritis which is a autoimmune disorder in which Immune system identifies the synovial membrane as "foreign" and begins attacking it.
TREATMENT OF RHEUMATOID ARTHRITIS BY DR BASHIR AHMED DAR ASSOCIATE PROFESSOR ...Prof Dr Bashir Ahmed Dar
Dr Bashir ahmed dar associate professor medicine chinkipora sopore kashmir presently working in medical college malaysia describes rheumatoid arthritis which is a autoimmune disorder in which Immune system identifies the synovial membrane as "foreign" and begins attacking it.
RHEUMATOID ARTHRITIS BY DR BASHIR AHMED DAR ASSOCIATE PROFESSOR MEDICINE SOPO...Prof Dr Bashir Ahmed Dar
Dr Bashir ahmed dar associate professor medicine chinkipora sopore kashmir presently working in medical college malaysia describes rheumatoid arthritis which is a autoimmune disorder in which Immune system identifies the synovial membrane as "foreign" and begins attacking it.
Monocytosis and Angiotensin II-Induced HypertensionKimberly Williams
A Christian’s relationship with God is vital to a Christian walk but other relationships and friendships require a reflection on the Christians personal walk with the superior being.
Summary on biblical friendships
Relationships gain more strength through proximity. The physical presence of friends is a source of joy and strength to a Christian. Distance makes friendship more difficult. For example, according to II John 12, John knew that he would be happier if he went to his own people and speak to them face to face (Dietrich B. 19).
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
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
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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!
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.
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
- 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
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Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
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.
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
1. Atherosclerosis, an Autoimmune Disease?
What could be the culprit antigen(s)? A brief appraisal of the role
of heat shock proteins.
Mohammad Madjid, MD
Center for Vulnerable Plaque Research
University of Texas-Houston Health Science Center and
Texas Heart Institute
2. In1856 Virchow described atherosclerosis as
“endarteritis”. A century later Russel Ross named
atherosclerosis “an inflammatory disease”. Ross
likened atherosclerosis to other chronic inflammatory
diseases such as rheumatoid arthritis and
glomerulonephritis. 1
The central role of immune system in atherosclerosis
and its clinical complications is now widely accepted.
Many investigators are searching to find out what
antigens attract immune cells into the arterial wall and
possibly later on into atherosclerotic plaques. 2,3,4
Autoantibodies against oxidized low-density lipoprotein
(oxLDL), cardiolipin, beta2-glycoprotein-I and heat-
shock protein 60/65 have been suggested. 2
3. Georg Wick, Qingbo Xu, and colleagues have
hypothesized that an autoimmune reaction
against heat shock protein 60s, expressed by
endothelial cells in areas that are subject to
increased hemodynamic stress, is the initiating
event in atherogenesis.5,6
The hypothesis indicates that because a high
degree of antigenic homology exists between
microbial (bacterial and parasitic) and human
HSP60, the 'cost' of immunity to microbes
might be the danger of cross-reactivity with
human HSP60 expressed by the endothelial
cells of stressed arteries subjected to classical
risk factors.7
4. Two major families of HSPs (60s and 70s) have
been related to atherosclerosis. Unlike HSP60s,
HSP70s are not reported as strong triggers of
autoimmune reactions, however, Bond, Johnson
and colleagues have suggested certain role for
HSP70s in atherosclerosis. 8,9
Chen et al described autologous hsp60 as a danger
signal to the innate immune system.10
Xu et al. showed induction of arteriosclerosis in
normocholesterolemic rabbits by immunization with
heat shock protein 65. 5
George, Afek, and colleagues reported induction of
arteriosclerosis in normocholesterolemic rabbits by
immunization with heat shock protein 65. 11,12
5. A number of other experimental and observational
studies have shown a significant relationship between
heat shock proteins and atherosclerosis. 9,11,13,14
In humans, expression of HSP60 is correlated
positively with atherosclerotic severity, with the highest
levels of expression seen in the shoulder regions and
around the necrotic core of atherosclerotic plaques. 15
6. In addition to its antigenic properties, bacterial HSP60
product may stimulate macrophages by production of
cytokines such as TNF-α and also MMPs. It may as
well interfere with innate immunity by binding to CD14
and activating monocytes and/or macrophages and
endothelial cells. 8, 21, 22
Bocharov et al reported that HSP60 is a high-affinity
high-density lipoprotein binding protein suggesting a
potential mechanism to explain the known association
between immunity developed against HSP60 and the
development of atherosclerosis. 16
7. Comparing the similarities between atherosclerosis
and other autoimmune disorders such as
rheumatoid arthritis (as indicated by Ross in the
following slide) can also give some hints about the
potential role of autoimmune mechanisms in
atherosclerosis and it’s complications. 1
Interestingly, recent studies have uncovered an
important role for heat shock proteins in
pathogenesis of rheumatoid arthritis. 17,18
Like in rheumatoid arthritis, the suggested role of
HSPs in atherosclerosis may also in part explain
the missing link between infectious agents and
atherosclerosis where a high degree of antigenic
homology between human and microbial HSPs can
cause cross-reaction. 17,7
8. DiseaseDisease Monocytes &Monocytes &
MacrophageMacrophage
LymphocyteLymphocyte GranulocyteGranulocyte Connective-Connective-
Tissue CellsTissue Cells
ExtracellularExtracellular
MatrixMatrix
Pathogenetic MechanismsPathogenetic Mechanisms
AtherosclerosisAtherosclerosis
++ ++ -- SMCsSMCs Collagen typeCollagen type
I, III, IV,I, III, IV,
elastin,elastin,
fibronectin,fibronectin,
proteoglycanproteoglycan
Endothelial-cell injury andEndothelial-cell injury and
dysfunction; fibrous cap;dysfunction; fibrous cap;
new matrix formation &new matrix formation &
degeneration; necrotic coredegeneration; necrotic core
CirrhosisCirrhosis
++ ++ -- FibroblastsFibroblasts Collagen typeCollagen type
I, IIII, III
Parenchymal cell injury, newParenchymal cell injury, new
matrix and scarringmatrix and scarring
replacing necroticreplacing necrotic
parenchymaparenchyma
RheumatoidRheumatoid
arthritisarthritis ++ ++ +/-+/- SynovialSynovial
fibroblastsfibroblasts
Collagen typeCollagen type
I, III,I, III,
fibronectin,fibronectin,
proteoglycanproteoglycan
Synovial-cell injury; erosionSynovial-cell injury; erosion
of cartilage; new matrixof cartilage; new matrix
scarring (pannus)scarring (pannus)
Glomeruloscle-Glomeruloscle-
rosisrosis ++ ++ -- MesangialMesangial
cellscells
Collagen typeCollagen type
I, IV,I, IV,
fibronectinfibronectin
Epithelial- and endothelial-Epithelial- and endothelial-
cell injury and dysfunction;cell injury and dysfunction;
decrease in glomerulardecrease in glomerular
filtration; new matrixfiltration; new matrix
formation;formation;
PulmonaryPulmonary
fibrosisfibrosis ++ ++ +/-+/- SMCs,SMCs,
FibroblastsFibroblasts
Collagen typeCollagen type
III, IV,III, IV,
fibronectinfibronectin
Inflammatory exudate inInflammatory exudate in
alveoli & bronchi; organizedalveoli & bronchi; organized
by extensive matrixby extensive matrix
deposition and scarringdeposition and scarring
ChronicChronic
pancreatitispancreatitis ++ ++ -- FibroblastsFibroblasts Collagen,Collagen,
fibronectin,fibronectin,
proteoglycanproteoglycan
Epithelial injury; periductalEpithelial injury; periductal
inflammation; interstitial fatinflammation; interstitial fat
necrosis; new matrixnecrosis; new matrix
formationformation
Ross R. Atherosclerosis--an inflammatory disease. N Engl J Med. 1999 Jan 14;340(2):115-26
9. Kanwar, Krissansen, et al. found that
expression of HSP60 and HSP70 was strongly
upregulated very early at lesion-prone sites in
the aortas of young apoE-/- knockout mice and
then dramatically down-regulated in the chronic
lesions of aged mice. 20
They showed that HSP60 and HSP70 were
detectable in the aortas of 3-week-old apoE-/-
mice and were highly expressed in the aortas
of 8-week-old mice. 20
10. Kanwar et al. indicated that in 8-week-old
apoE-/- mice, HSP60 and 70 were strongly
expressed at valve commissures of the aortic
sinus, extending to the free aortic wall and
including expression by endothelial and intimal
cells. 20
They concluded that HSP60 and HSP70 were
heterogeneously expressed in lesions of 20-
week-old mice. HSP60 and HSP70 were
strongly expressed in advanced plaques of the
abdominal aorta of 20-week-old mice, whereas
medial layers lack expression. 20
11. In 69-week-old mice, there was complete loss
of HSP60 and HSP70 in advanced
complicated collagen-rich plaques of the
aortic sinus. (down-regulated in aged mice) 20
As a result of this study, lesion-prone sites
displayed strong endothelial HSP60
expression, whereas non–lesion-prone sites
of the distal abdominal aorta lacked hsp
expression. 20
Monocytes/macrophages expressing HSP70
and hsp60 (data not shown) were the most
prominent cell type in lesions. 20
12. Summary:Summary:
1- Autoimmune reactions (cellular and humoral) against
HSPs particularly HSP60s may play an important role
in early stage development of atherosclerosis.
2- HSP60s and HSP70s released from necrotic cells in
the core area of advanced plaques may stimulate the
innate immune response to promote inflammation and
attract new inflammatory cells thereby may link to
complications of plaque such as rupture and or
thrombosis.
3- Humoral and cellular reactions against HSP60 work in
conjunction with classical proven CVD risk factors.
13. Debates:Debates:
I. According to our current body of knowledge, the
development of atherosclerosis seems to have two
major preceding components, metabolic disorder
(lipid abnormality etc.) and inflammatory disorder
(enhanced immune or autoimmune response). The
question is which one comes first?
II. Since the complication of atherosclerosis (vulnerable
plaque) is more important than it’s development
(stable plaque), the question is which one of the two
(1-metabolic, 2-Immune) components of
atherosclerosis plays a more important role?
14. Debates:Debates:
III. How feasible is the idea of vaccination against HSPs
or oxidized-LDL or other suggested antigens? Can
we induce tolerance against HSPs without damaging
the innate immune system?
IV. Which one is more feasible? Eradication of
atherosclerosis by vaccination against triggers of
plaque development, or, eradication of vulnerable
plaque by vaccination against triggers of plaque
vulnerability?
15. 1. Ross R. Atherosclerosis--an inflammatory disease.
N Engl J Med. 1999 Jan 14;340(2):115-26. Review
2. Shoenfeld Y, Sherer Y, George J, Harats D. ;Autoantibodies associated with
atherosclerosis. Ann Med. 2000 Dec;32 Suppl 1:37-40. Review.
3. Hansson, G.; Immunological markers of atherosclerosis.
Lancet. 1993 Jan 30;341(8840):278.
4. Witztum JL, Palinski W. ; Are immunological mechanisms relevant for the
development of atherosclerosis? Clin Immunol. 1999 Feb;90(2):153-6. Review.
5. Xu Q, Dietrich H, Steiner HJ, Gown AM, Schoel B, Mikuz G, Kaufmann SH, Wick
G. ; Induction of arteriosclerosis in normocholesterolemic rabbits by
immunization with heat shock protein 65. Arterioscler Thromb. 1992
Jul;12(7):789-99.
6. Wick G, Schett G, Amberger A, Kleindienst R, Xu Q.; Is atherosclerosis an
immunologically mediated disease?; Immunol Today. 1995 Jan;16(1):27-33.
Review.
References
16. 7. Wick G, Perschinka H, Millonig G. ; Atherosclerosis as an autoimmune disease:
an update.; Trends Immunol. 2001 Dec 1;22(12):665-669.
8. Johnson AD, Berberian PA, Tytell M, Bond MG. ; Differential distribution of 70-
kD heat shock protein in atherosclerosis. Its potential role in arterial SMC
survival.; Arterioscler Thromb Vasc Biol. 1995 Jan;15(1):27-36.
9. Berberian PA, Myers W, Tytell M, Challa V, Bond MG.; Immunohistochemical
localization of heat shock protein-70 in normal-appearing and atherosclerotic
specimens of human arteries.; Am J Pathol. 1990 Jan;136(1):71-80.
10. Chen W, Syldath U, Bellmann K, Burkart V, Kolb H.; Human 60-kDa heat-shock
protein: a danger signal to the innate immune system.; J Immunol. 1999 Mar
15;162(6):3212-9.
11. George J, Shoenfeld Y, Afek A, Gilburd B, Keren P, Shaish A, Kopolovic J, Wick
G, Harats D.; Enhanced fatty streak formation in C57BL/6J mice by
immunization with heat shock protein-65. Arterioscler Thromb Vasc Biol. 1999
Mar;19(3):505-10.
References
17. 12. Afek A, George J, Gilburd B, Rauova L, Goldberg I, Kopolovic J, Harats D,
Shoenfeld Y.; Immunization of low-density lipoprotein receptor deficient (LDL-
RD) mice with heat shock protein 65 (HSP-65) promotes early atherosclerosis.;
J Autoimmun. 2000 Mar;14(2):115-21.
13. Hansen PR, Chew M, Zhou J, Daugherty A, Heegaard N, Jensen P, Mouritsen
S, Falk E.; Freunds adjuvant alone is antiatherogenic in apoE-deficient mice and
specific immunization against TNFalpha confers no additional benefit.
Atherosclerosis. 2001 Sep;158(1):87-94.
14. George J, Afek A, Gilburd B, Shoenfeld Y, Harats D.; Cellular and humoral
immune responses to heat shock protein 65 are both involved in promoting fatty-
streak formation in LDL-receptor deficient mice.
J Am Coll Cardiol. 2001 Sep;38(3):900-5.
15. Kleindienst R, Xu Q, Willeit J, Waldenberger FR, Weimann S, Wick G.
Immunology of atherosclerosis. Demonstration of heat shock protein 60
expression and T lymphocytes bearing alpha/beta or gamma/delta receptor in
human atherosclerotic lesions.; Am J Pathol. 1993 Jun;142(6):1927-37.
References
18. 16. Bocharov AV, Vishnyakova TG, Baranova IN, Remaley AT, Patterson AP,
Eggerman TL.; Heat shock protein 60 is a high-affinity high-density lipoprotein
binding protein.; Biochem Biophys Res Commun. 2000 Oct 14;277(1):228-35.
17. Gaston, JS.; Heat shock proteins and arthritis--new readers start here.
Autoimmunity. 1997;26(1):33-42. Review.
18. Schett G, Tohidast-Akrad M, Steiner G, Smolen J.; The stressed synovium.;
Arthritis Res. 2001;3(2):80-6. Review.
19. Gaston, JS. ; Heat shock proteins and arthritis--new readers start here.;
Autoimmunity. 1997;26(1):33-42. Review.
20. Rupinder K. Kanwar, Jagat R. Kanwar, Dongmao Wang, Douglas J. Ormrod,
and Geoffrey W. Krissansen Temporal Expression of Heat Shock Proteins 60
and 70 at Lesion-Prone Sites During Atherogenesis in ApoE-Deficient Mice
Arterioscler Thromb Vasc Biol 2001 21: 1991-1997.
References
19. 21.21. Kol A, Sukhova GK, Lichtman AH, Libby P.Kol A, Sukhova GK, Lichtman AH, Libby P. Chlamydial heat shock protein 60Chlamydial heat shock protein 60
localizes in human atheroma and regulates macrophage tumor necrosis factor-localizes in human atheroma and regulates macrophage tumor necrosis factor-
alpha and matrix metalloproteinase expression. Circulation. 1998 Jul 28;98(4):300-alpha and matrix metalloproteinase expression. Circulation. 1998 Jul 28;98(4):300-
7.7.
22.22. Kol A, Lichtman AH, Finberg RW, Libby P, Kurt-Jones EA.Kol A, Lichtman AH, Finberg RW, Libby P, Kurt-Jones EA. Cutting edge: heatCutting edge: heat
shock protein (HSP) 60 activates the innate immune response: CD14 is anshock protein (HSP) 60 activates the innate immune response: CD14 is an
essential receptor for HSP60 activation of mononuclear cells. J Immunol. 2000 Janessential receptor for HSP60 activation of mononuclear cells. J Immunol. 2000 Jan
1;164(1):13-7.1;164(1):13-7.
References