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Ubiquitin Ligases as Key Elements for the Modulation of the
Immune Response: An Insight in the Pathogenesis of Autoimmunity.
Jorge Alcocer-Varela, Diana Gómez-Martín,
Mariana Díaz Zamudio, Jorge Romo-Tena
[Abstract] [FULL-TEXT
INQUIRY] [BSP/CRR/E-Pub/0011]
A review of the English and Russian language literature
on the osteoarticular manifestations of Brucellosis infection.
Tamar Akhvlediani, Michael W Ellis, Robert Rivard, Otar
Zenaishvili, Daniel J. Battafarano, Matthew J Hepburn
[Abstract] [FULL-TEXT
INQUIRY] [BSP/CRR/E-Pub/0012]
Ankylosing spondylitis, HLA-B27, Klebsiella and “Popper
sequences”
Alan Ebringer, Taha Rashid, Mark Fielder, Clyde Wilson
[Abstract] [FULL-TEXT
INQUIRY] [BSP/CRR/E-Pub/0013]
Cardiovascular Risk, Inflammation and Physical Activity
in Rheumatoid Arthritis
Marie Tierney, Alexander Fraser, Norelee Kennedy
[Abstract] [FULL-TEXT
INQUIRY] [BSP/CRR/E-Pub/0014]
Abstracts
Ubiquitin Ligases as Key Elements for the Modulation of the
Immune Response: An Insight in the Pathogenesis of Autoimmunity.
Jorge Alcocer-Varela, Diana Gómez-Martín,
Mariana Díaz Zamudio, Jorge Romo-Tena
[FULL-TEXT
INQUIRY] [BSP/CRR/E-Pub/0011]
Ubiquitin ligases are the substrate specific elements
of the ubiquitination system, which comprises a post-translational
mechanism by which the immune response can be modulated, setting
the tune for the TCR activation. Proteolysis dependent and
independent mechanisms have been implicated. Ubiquitin ligases
have been proven as key modulators of central and peripheral
tolerance, involving the regulation of anergy and regulatory
T cells. These enzymes involve a complex regulatory network
designed to maintain an active surveillance system. Cbl-b,
GRAIL and Itch are the main E3 ligases, considered as negative
regulators of the immune response as part of the anergy induced
genetic program. Recently, other ubiquitin ligases have been
related to autoimmune pathologies such as Roquin and Ro52.
Other key signalling pathways for the immune response, such
as the NF-κ
and TGF-β
signalling are prone to be modulated by these ubiquitin ligases.
Diverse processes have been implicated in the broad mechanisms
of modulation of the immune response by these ubiquitin ligases,
among them, the setting for TCR responsiveness, T cell differentiation,
regulation of activation and costimulatory molecules as well
as of inflammatory pathways are the best well characterized.
The defective expression of some of these ubiquitin ligases
has been related to the development of autoimmune disease,
in experimental murine and human models. Most of the evidence
points towards the physiopathogenic role of ubiquitin ligases,
primarily Cbl-b in systemic [1] and organ-specific (type 1
Diabetes Mellitus and multiple sclerosis) autoimmune diseases.
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A review of the English and Russian language
literature on the osteoarticular manifestations of Brucellosis
infection.
Tamar Akhvlediani, Michael W Ellis, Robert Rivard, Otar
Zenaishvili, Daniel J. Battafarano, Matthew J Hepburn
[FULL-TEXT
INQUIRY] [BSP/CRR/E-Pub/0012]
Brucellosis continues to adversely affect human health
throughout the world. Acute and chronic osteoarticular manifestations
of brucellosis include sacroiliitis, spondylitis, peripheral
arthritis, osteomyelitis, and bursitis. Substantial clinical
experience with the presentation, clinical course, and treatment
of brucellosis exists in countries of the former Soviet Union,
including the Republic of Georgia. The present article reviews
the unique Georgian and Russian medical literature in addition
to the English-language medical literature on the topic of
osteoarticular complications of brucellosis. Special emphasis
is placed on current diagnostic approaches for osteoarticular
brucellosis, including imaging techniques and laboratory tests
(bacteriology, serology, PCR).
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Ankylosing spondylitis, HLA-B27, Klebsiella and “Popper
sequences”
Alan Ebringer, Taha Rashid, Mark Fielder, Clyde Wilson
[FULL-TEXT
INQUIRY] [BSP/CRR/E-Pub/0013]
The cause of ankylosing spondylitis (AS) was investigated
through 13 Karl Popper sequences. “Popper sequences”
provide a powerful method of investigating a scientific problem.
A “Popper sequence” consists of a “problem”,
“tentative theory”, “error elimination”
which then leads to a “new fact”. The 13 “Popper
sequences” establish that: (1) HLA-B27 lymphocytes injected
into a rabbit evoke antibodies against Klebsiella,
(2) anti-HLA-B27 tissue typing sera bind to Klebsiella
antigens, (3) total serum IgA is elevated in AS patients,
(4) antibodies to Klebsiella are present in AS patients
from 16 different countries, (5) antibodies to Klebsiella
in AS patients are disease specific, (6) Klebsiella
bacteria can be grown from fecal cultures, (7) only Klebsiella
bacteria evoke statistically significant (p<0.001) titres
of antibodies in AS patients, (8) the sequence QTDRED found
in HLA-B27 resembles a sequence DRDE found in pullulanase-D
enzyme of Klebsiella, (9) Klebsiella pullulanase-A
contains a sequence IRRET which resembles type I, II, and
IV collagens, (10) sera from AS patients have cytopathic properties
against sheep red cells coated with the cross-reacting peptides
found in Klebsiella and HLA-B27 sequences, (11) Klebsiella
bacteria grow preferentially on carbohydrate substrates, (12)
methods used to decrease bowel bacteria lead to a reduction
of inflammatory parameters, (13) post-pubertal hormonally-induced
muscle mass leads to increased starch consumption and onset
of AS. The use of “Popper Sequences” suggests
that Klebsiella microbes are the probable causative
agents of AS.
[Back to top]
Cardiovascular Risk, Inflammation and Physical Activity
in Rheumatoid Arthritis
Marie Tierney, Alexander Fraser, Norelee Kennedy
[FULL-TEXT
INQUIRY] [BSP/CRR/E-Pub/0014]
Individuals with Rheumatoid Arthritis (RA) have increased
mortality when compared to the general population. Much of
this increased mortality can be attributed to cardiovascular
causes. It is not fully understood why this is the case. However,
factors including traditional cardiovascular risk factors,
the effects of anti-rheumatic drug treatment and non-traditional
cardiovascular risk factors specific to the RA population
(in particular inflammation) have been highlighted in the
literature.
Inflammatory markers are specific markers in the bloodstream
which may be raised or decreased in response to inflammation.
Inflammation plays a central role in all phases of atherosclerosis.
Therefore, assessment of inflammatory markers may help identify
those at high risk of future cardiovascular events.
Physical Activity is ‘any bodily movement produced by
skeletal muscles that results in energy expenditure’
[1, p.126] and is associated with improvements in cardiovascular
health in many populations. With specific regard to inflammatory
markers, the general consensus from the literature conducted
to date on the effect of physical activity on these markers
is that high physical activity levels are inversely related
with inflammatory marker counts. Although the literature is
scarce regarding the Rheumatoid Arthritis population, it appears
the same may be true for these individuals.
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