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1.
Mean platelet volume (MPV), an indicator of platelet activation, is a newly emerging risk factor for atherothrombosis. There
is evidence of platelet activation in psoriasis and psoriatic arthritis (PsA). The association between psoriasis, PsA, and
atherosclerosis is well documented, yet, the underlying mechanisms remain unclear. The aim of this study was to investigate
the differences of MPV values in patients with psoriasis, PsA, and healthy subjects and the correlation between MPV and the
clinical disease activity. A total of 106 patients with psoriasis were included in this study. The study population grouped
as 48 patients with PsA (group 1) and 58 patients without PsA (group 2) and 95 healthy controls (group 3). MPV was measured
in psoriasis and PsA patients. MPV values were collected from standard complete blood count samples. Clinical features and
PASI scores in group 1 and 2 were also recorded. MPV in patients with psoriasis 8.7 ± 0.9 fL was significantly higher than
that of control subjects 7.3 ± 0.8 fL (p < 0.001). There was also statistical difference between MPV levels of patients with (9.5 ± 0.8) and without (8.0 ± 0.7) arthritis
(p < 0.001). MPV levels were positively correlated with psoriasis area and severity index score (p = 0.000, r = +0.735). MPV levels showed positive correlation with disease duration (p = 0.01, r = 0.518). MPV levels are increased in patients with psoriasis and PsA. MPV may be a marker for the severity of psoriasis.
This study may confirm previous observation indicating increased platelet activation in psoriasis. Increased platelet activity
could contribute to increasing the atherosclerotic risk in patients with psoriasis and PsA. 相似文献
2.
We examined the effects of polyarticular juvenile idiopathic arthritis (pJIA) serum on proliferation, differentiation, mineralization,
and apoptosis of human osteoblast cells (hOb) in culture. The hOb were cultured with 10% serum from active pJIA and healthy
controls (CT) and were tested for DNA synthesis, alkaline phosphatase (AP) activity, osteocalcin (OC) secretion, calcium levels,
caspase 3 activity, and DNA fragmentation. None of the patients had used glucocorticoids for at least 1 month before the study,
or any other drug that can affect bone mineral metabolism. Human inflammatory cytokine levels (IL-6, IL-8, IL-10, IL-1β, TNF-α,
and IL-12p70) were measured in pJIA and CT sera. Low levels of AP activity was observed in pJIA cultures compared with CT
cultures (67.16 ± 53.35 vs 100.11 ± 50.64 μmol p-nitrophenol/h−1 mg−1 protein, P = 0.008). There was also a significant decrease in OC secretion (9.23 ± 5.63 vs 12.82 ± 7.02 ng/mg protein, P = 0.012) and calcium levels (0.475 ± 0.197 vs 0.717 ± 0.366 mmol/l, P = 0.05) in pJIA hOb cultures. No difference was observed in cell proliferation (323.56 ± 108.23 vs 328.91 ± 88.03 dpm/mg
protein, P = 0.788). Osteoblasts cultured with JIA sera showed lower levels of DNA and increased fragmentation than osteoblasts cultured
with CT sera. pJIA sera showed higher IL-6 values than CT (21.44 ± 9.31 vs 3.58 ± 2.38 pg/ml, P < 0.001), but no difference was observed related to IL-8, IL-10, IL-1β, TNF-α, and IL-12p70 between pJIA and controls. This
study suggests that serum from children with pJIA inhibits differentiation, mineralization and may increase apoptosis of hOb
cultures, and inflammatory cytokines such as IL-6 might be a mechanism in this find. These results may represent an alternative
therapeutic target for prevention and treatment of bone loss in JIA. 相似文献
3.
The objective of our study was to elucidate serum levels of atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP),
and C-type natriuretic peptide (CNP) in Behcet’s disease (BD) patients with active and inactive period. The multicenter study
included 53 patients with active (n = 28) and inactive (n = 25) BD (mean age, 34.3 ± 9 years; 15 men and 38 women) satisfying the International Study Group criteria and 26 healthy
controls (mean age, 34.4 ± 6.1 years; seven men and 19 women) matched for age and gender from a similar ethnic background.
Serum natriuretic peptides levels were determined by enzyme immunoassay kit. Mean serum ANP concentrations in the active patients
(4.01 ± 1.21 ng/ml) were significantly lower than in the healthy controls (5.76 ± 1.99 ng/ml, p = 0.004). Mean serum BNP levels were found to be significantly higher in both the active (6.19 ± 2.97 ng/ml) and inactive
(6.49 ± 2.88 ng/ml) BD groups compared with the control group (3.82 ± 1.1 ng/ml, p = 0.004 and p = 0.001, respectively). Mean serum CNP concentrations in the active patients (0.49 ± 0.12 ng/ml) were significantly lower
than in the inactive patients (0.65 ± 0.2 ng/ml, p = 0.017) and the healthy controls (0.8 ± 0.27 ng/ml, p < 0.001). Our results suggest that changes in natriuretic peptide levels may be associated with vasculitis that play role
in the etiopathogenesis of the BD. 相似文献
4.
Levels of vascular endothelial growth factor and hepatocyte growth factor in sera of patients with rheumatic diseases 总被引:2,自引:0,他引:2
Naoaki Hashimoto Tsuyoshi Iwasaki Masayasu Kitano Atsushi Ogata Teruaki Hamano 《Modern rheumatology / the Japan Rheumatism Association》2003,13(2):129-134
Angiogenesis plays an important role in the progression of rheumatic disease. We measured the levels of vascular endothelial
growth factor (VEGF) and hepatocyte growth factor (HGF) in sera from patients with rheumatic diseases and investigated whether
these angiogenic factors would be useful in the evaluation of rheumatic diseases. Serum VEGF and HGF levels were determined
using ELISA in 128 patients with rheumatic diseases and in 11 healthy controls. Serum VEGF and HGF levels were significantly
higher in patients with rheumatic diseases compared to healthy controls [VEGF, 312 ± 20 pg/ml versus 61 ± 8 pg/ml (mean ±
SE), P < 0.001; HGF, 935 ± 36 pg/ml versus 413 ± 49 pg/ml, P < 0.01]. Serum VEGF and HGF levels were significantly elevated in patients with adult Still's disease (VEGF, 1021 ± 258 pg/ml;
HGF, 1500 ± 295 pg/ml) and were relatively increased in patients with active rheumatoid arthritis (RA) (VEGF, 359 ± 94 pg/ml)
and systemic sclerosis (SSc) (VEGF, 356 ± 43 pg/ml; HGF, 1294 ± 224 pg/ml). HGF levels correlated with the clinical course
and disease severity in rheumatic disease patients. VEGF levels correlated with the presence of Raynaud's phenomenon (P < 0.05), interstitial lung disease (ILD) (P < 0.05), and serum KL-6 levels (P < 0.01), whereas HGF levels correlated with cryoglobulinemia (P < 0.05), ILD (P < 0.05), serum C-reactive protein (CRP) (P < 0.05), thrombomodulin (P < 0.05), and KL-6 levels (P < 0.05) in rheumatic disease patients. VEGF levels correlated with the skin scores and KL-6 levels in SSc patients and also
correlated with the disease activity of RA patients. These data suggest that serum VEGF and HGF levels are related to rheumatic
disease activity and the presence of complications. Analysis of VEGF and HGF may be useful in the clinical evaluation of rheumatic
disease patients.
Received: February 19, 2002 / Accepted: August 13, 2002
Acknowledgment We are grateful to Ms. Aki Nomura for assistance with the ELISA of VEGF and HGF. 相似文献
5.
Bystander immune suppression has been demonstrated in experimental models of oral immune tolerance induction. This phenomenon
is associated with expression of transforming growth factor (TGF)-β1 and T-helper cell (Th) 2 cytokines. We have studied serum
levels of Th cytokines and B- and T-lymphocyte subsets in chronic idiopathic thrombocytopenic purpura (ITP), a disorder in
which the production of platelet autoantibodies might be caused by a cytokine network dysregulation. Forty-six patients with
ITP were separated into three groups depending on the platelet count (pltc): (1) <50×109/l, (2) 50–150×109/l and (3) >150×109/l. We found significantly elevated plasma levels of the Th3 cytokine TGF-β1 in patients with pltc >150×109/l (23.5±2.8 ng/ml), compared with patients with pltc <50×109/l (2.3±0.6 ng/ml;P<0.0001), patients with pltc 50–150×109/l (7.2±1.7 ng/ml;P<0.0001) and healthy volunteers (9.8±1.3 ng/ml;P<0.01). The serum levels of the Th1 cytokines interleukin (IL)-2 and interferon (IFN)-γ were below the detection limits of
the assays. Likewise, the Th2 cytokine IL-4 was not detectable or was very low both in patients and controls. The serum levels
of IL-10, a Th2 cytokine, were within the assay range and patients with pltc <50×109/l had significantly lower levels (0.6±0.1 pg/ml) than both patients with pltc 50–150×109/l (1.8±0.1 pg/ml;P<0.005) and healthy volunteers (1.4±0.1 pg/ml;P<0.005). Furthermore, patients with pltc <50×109/l and splenectomised patients had significantly higher levels of CD4+CD25+ activated T cells [26.2±14.8% (P<0.05) and 26.7±11.9% (P<0.005), respectively] than healthy controls (16.5±4.0%). Also, the number of natural killer (NK) cells among patients with
pltc >150×109/l were significantly elevated (26.6±16.0%;P<0.05) compared with controls (17.4±7.6%). In conclusion, our data corroborate previous findings of elevated numbers of activated
T cells in chronic ITP patients with active disease, but neither a clear-cut Th1 nor a Th2 serum cytokine profile could be
established. However, ITP in remission was associated with elevated TGF-β1, which might be a part of a bystander immune suppression.
We propose that the effect of possible expression of TGF-β1 by oral immune tolerance induction deserves to be explored in
ITP patients with an active disease.
Received: 29 September 1999 / Accepted: 25 January 2000 相似文献
6.
Paola Caramaschi Alessandra Dalla Gassa Orazio Ruzzenente Alessandro Volpe Viviana Ravagnani Ilaria Tinazzi Giovanni Barausse Lisa M. Bambara Domenico Biasi 《Clinical rheumatology》2010,29(12):1419-1425
Vitamin D displays many extraosseous immunomodulatory effects. The aim of the study was to evaluate the level of vitamin D
in patients with systemic sclerosis (SSc) and to analyze the associations between the concentration of the vitamin and clinical
manifestations. In March-April 2009, 65 consecutive SSc patients underwent evaluation of vitamin D concentrations by the LIAISON
immunoassay (normal 30-100 ng/ml). Serum levels between 10 and 30 ng/ml were classified as vitamin D insufficiency, while
concentrations <10 ng/ml as vitamin D deficiency. None of the patients were receiving vitamin D supplementation at the time
of or during the year prior to study entry. The mean level of vitamin D was 15.8 ± 9.1 ng/ml. Only three cases showed normal
values; vitamin D insufficiency and deficiency were found in 43 and 19 cases, respectively. Patients with vitamin D deficiency
showed longer disease duration (13.1 ± 6.8 versus 9.4 ± 5.5 years, P = 0.026), lower diffusing lung capacity for carbon monoxide (63.7 ± 12.4 versus 76.4 ± 20.2, P = 0.014), higher estimated pulmonary artery pressure (28.9 ± 9.9 versus 22.8 ± 10.4, P = 0.037) and higher values of ESR (40 ± 25 versus 23 ± 13 mm/h, P = 0.001) and of CRP (7 ± 7 and 4 ± 2 mg/l, P = 0.004) in comparison with patients with vitamin D insufficiency; moreover, late nailfold videocapillaroscopic pattern was
more frequently found (52.6% versus 18.6%, P = 0.013). None of the patients showed evidence of overt mal-absorption. Low levels of vitamin D are very frequent in patients
with SSc. Intestinal involvement is not likely the cause of vitamin D deficit; other factors such as skin hyperpigmentation
and reduced sun exposition for psychological and social reasons may be implicated. Patients with vitamin D deficiency showed
more severe disease in comparison with patients with vitamin D insufficiency, above all concerning lung involvement. Further
trials are awaited to determine whether vitamin D could represent a modifiable factor able to interfere with SSc evolution. 相似文献
7.
Chen-Liang Chou Min-Jung Wu Chia-Li Yu Ming-Chi Lu Song-Chou Hsieh Tsai-Hung Wu Chung-Tei Chou Chang-Youh Tsai 《Clinical rheumatology》2010,29(8):875-881
Anti-agalactosyl IgG antibody (anti-Gal(0) IgG) has been regarded as a useful serological marker for rheumatoid arthritis
(RA). It is unknown whether it is also elevated in serum and implicated in the pathogenesis of joint inflammation in seronegative
spondyloarthropathy (SpA) such as ankylosing spondylitis (AS) and psoriatic arthritis (PsA). Sera were collected from 43 patients
with AS or PsA with axial joint involvement, 22 patients with RA, and 25 healthy normal individuals for the detection of anti-Gal(0)
IgG with a cup-type lectin enzyme immunoassay (Eitest CA.RF). The disease activity of the AS/PsA was evaluated by Bath Ankylosing Spondylitis Disease Activity Score (BASDAI), the
serum C-reactive protein (CRP) and IgA were measured by nephelometry, and erythrocyte sedimentation rate (ESR) was measured
by Westergren’s method. The median titers of anti-Gal(0) IgG were significantly elevated in patients with RA (167.85, 15.73∼797.58 AU/mL)
and AS/PsA (186.15, 34.71∼651.19 AU/mL), compared to those of the normal controls (13.04, 12.00∼202.43 AU/mL). The titers
of the anti-Gal(0) IgG in patients with AS/PsA were correlated to the BASDAI scores (r
2 = 0.422, SEE = 1.443, p < 0.001) and serum CRP (r
2 = 0.345, SEE = 2.434, p < 0.001) but not to IgA (r
2 = 0.0259, SEE = 126.30, p < 0.001) or ESR (r
2 = 0.171, SEE = 31.053, p = 0.0059). Collectively, the anti-Gal(0) IgG is elevated and vaguely correlated with the disease activity of AS/PsA although
its titers in these patients were erratic. The result of the present investigation has suggested that anti-Gal(0) IgG may
be more ubiquitously present in inflammatory arthritides including RA or SpA. 相似文献
8.
We evaluated the significance of platelet activation in patients with rheumatoid arthritis (RA). The expression of CD62P and
CD63 by platelets was determined using flow cytometry in 18 active RA patients, 10 remission RA and 15 normal controls. Meanwhile,
the erythrocyte sedimentation rate (ESR) and C-reactive protein was also determined in all groups. The expression of CD62P
in active RA patients (11.88 ± 2.47%) was significantly higher than that in remission RA group (2.85 ± 1.60%; P < 0.01) and control group (2.78 ± 1.04%; P < 0.01). The expression of CD63 in active RA patients (9.90 ± 3.02%) was significantly higher than that in remission RA group
(4.11 ± 2.00%; P < 0.01) and control group (4.13 ± 1.85%; P < 0.01). The level of CRP (54.33 ± 23.35 mg/l) and ESR (86.06 ± 33.67 mm/h) in active RA patients was higher than that in
remission RA group (2.55 ± 1.01 mg/l, 14.70 ± 4.57 mm/h; P < 0.01 for both) and normal control group (3.21 ± 2.18 mg/l, 12.25 ± 5.05 mm/h; P < 0.01 for both). There was a positive correlation between CD62P and ESR (r = 0.5224, P < 0.01) and also a positive correlation between CD62P and CRP (r = 0.7048, P < 0.01) as well as between CD63 and ESR (r = 0.4476, P < 0.05) but no correlation between CD63 and CRP. Platelet activation may be a sign of RA exacerbation. 相似文献
9.
Costa L Caso F D'Elia L Atteno M Peluso R Del Puente A Strazzullo P Scarpa R 《Clinical rheumatology》2012,31(4):711-715
The objective of the study was the evaluation of arterial stiffness, a cardiovascular risk factor, in patients with psoriatic
arthritis (PsA). Twenty PsA patients classified on the basis of the CASPAR criteria (M/W, 14/6; mean age, 38.6 years; range,
22–53), attending our out-patient clinic, and 20 healthy control subjects (M/W, 14/6; mean age, 38.7 years; range, 22–53)
matched for age, weight, height and with similar cardiometabolic profile entered the study. An exclusion criterion was the
presence of known cardiovascular risk factors. Central hemodynamic parameters and aortic pulse wave velocity (aPWV) were assessed
non-invasively by a SphygmoCor device. A significantly higher aPWV was recorded in PsA patients when compared to controls.
The difference remained statistically significant after adjustment for age, weight, height, heart rate (HR) and central mean
pressure (mean±SE; PsA, 8.3 ± 0.2 versus control, 6.8 ± 0.2 m/s; p < 0.0001). Among PsA patients, aPWV was related to known duration of disease (r = 0.63; p = 0.003). This result was confirmed after adjustment for the main confounders (β = 0.011; p = 0.013). These results support the concept of psoriatic disease as a systemic condition involving not only the skin, joints
and gastrointestinal tract but also arterial vessels. The involvement of the vascular system indicates the presence of pathogenetic
mechanisms that could accelerate the atherosclerotic process in this condition. 相似文献
10.
Previous studies have shown that sleep complaints are common in adult patients with cystic fibrosis (CF). However, there is
very little data on sleep in children and adolescents with CF and the association with severity of lung disease. A prospective
study was conducted in CF children and age-matched controls. All patients completed sleep questionnaire and underwent an overnight
polysomnographic study. Thirty-eight children and adolescents met the criteria for entry into the analysis, 24 children and
adolescents with CF (S) and 14 controls (C). Sleep complaints were common in children and adolescents with CF; 43.5% reported
sleep onset problem, 39.1% reported sleep maintenance problem, 30.4% were noted to snore at night, and 73.9% reported daytime
sleepiness. Children and adolescents with CF had a significant decrease in sleep efficiency [SE; 75.2 ± 2.5% (S) vs 85.6 ± 1.7%(C);
P < 0.01], prolonged rapid eye movement (REM) latency [150.5 ± 16.6 min (S) vs 85.6 ± 11.0 min (C); P < 0.05], and reduction in percentage of REM sleep [12.7 ± 1.5% (S) vs 18.3 ± 1.3% (C); P < 0.05]. The degree of sleep disruption as indicated by SE was correlated with forced expiratory volume in one second (FEV1; r = 0.52, P < 0.05). However, there was no significant correlation between SE and minimum oxygen saturation [r = 0.30, P=not significant (NS)] or SE and maximal end-tidal pCO2 (r = 0.11, P=NS). It is concluded that children and adolescents with CF have frequent sleep complaints and significant alteration in the
sleep architecture. The magnitude of sleep disruption is associated with severity of lung disease, but is not directly correlated
with the degree of nocturnal hypoxemia or hypoventilation. It is speculated that sleep disruption in children and adolescents
with CF may have an impact on quality of life and clinical outcomes in this population. 相似文献
11.
Our study was designed in an attempt to determine the dynamics of changes in serum tumor necrosis factor (TNF)-α, soluble
forms of its receptors (sTNFR 1, sTNFR 2), and adhesion molecules (sE-selectin, sP-selectin, sVCAM-1, sICAM-1) over a 2-year
follow-up of patients with coronary artery disease (CAD). The study involved 70 patients with stable CAD (stable angina class
II/III according to the Canadian Cardiovascular Society) and 20 apparently healthy subjects. Over the follow-up period a marked
attenuation of angina (P < 0.001) was observed. Interventional treatment (percutaneous coronary intervention, coronary artery bypass grafting) was
used in 53 CAD patients. Laboratory analysis revealed a significant decrease of serum TNF-α and sTNFR1 at 2 years (TNF-α:
12.1 ± 0.7 pg/ml; sTNFR 1: 1306 ± 46 pg/ml) as compared to baseline levels (16.5 ± 0.7 pg/ml, P = 0.030; 1551 ± 82 pg/ml, P = 0.048, respectively). The levels of sP-selectin (159 ± 7 vs 201 ± 14 ng/ml, P < 0.01) and sICAM-1 (133 ± 4 vs 153 ± 6 ng/ml, P < 0.05) were found to be significantly increased as compared to the baseline. Interventional procedures resulted in suppression
of both cytokine (TNF-α, sTNFR 2) and adhesion molecule (sE-selectin, sP-selectin) activation in the CAD group. The baseline
and post-follow-up TNF-α and sTNFR 1 levels showed persistent elevation in CAD patients as compared to the controls (9.0,
956.3 pg/ml, respectively; P < 0.01). There were no differences between baseline and final cytokines and adhesion molecules in healthy subjects. The course
of CAD as modified by a clinically effective therapy is characterized by changes of immune markers activation. Revascularization
seems to be an important factor suppressing both cytokine and adhesion molecule activation in CAD patients. 相似文献
12.
We studied the levels of miR-146a and miR-155 in the urine sediment of SLE patients. The levels of miR-146a and miR-155 in
the urine sediment of 40 SLE patients who were receiving calcitriol treatment and 13 healthy controls were determined with
real-time quantitative polymerase chain reaction. The levels of urinary miR-146a and miR-155 in patients with SLE were significantly
higher than that in healthy controls. Calcitriol treatment reduced the levels of urinary miR-155 in patients with SLE. The
level of urinary miR-146a significantly correlated with estimated glomerular filtration rate (r = 0.242, P = 0.008). The level of urinary miR-155 significantly correlated with proteinuria (r = 0.407, P < 0.001) and systemic lupus erythematosus disease activity index (r = 0.278, P = 0.002). The level of urinary miR-146a reversely correlated with the urinary expression of TNF-α (r = −0.247, P = 0.012). Our results suggested that miR-146a and miR-155 might play important roles in the pathophysiology of SLE and the
levels of urinary miR-146a and miR-155 could be used as potential markers for diagnosis, disease activity, and therapeutic
response. 相似文献
13.
Sun LY Zhou KX Feng XB Zhang HY Ding XQ Jin O Lu LW Lau CS Hou YY Fan LM 《Clinical rheumatology》2007,26(12):2073-2079
Defects of hematopoietic stem cells (HSCs) have been suggested to contribute to the development of systemic lupus erythematosus
(SLE). The aim of this study was to investigate the phenotypic characteristics of bone marrow (BM) CD34+ cells in patients with SLE and its relationship with SLE disease activity. Ten SLE patients and 10 healthy subjects were
recruited and their BM CD34+ cells were analyzed by flow cytometric analysis with CD45/SSC gating for the expression of CD90, CD95, CD117, CD123, CD164,
CD166, FAS-L, and HLA-DR. The percentage of BM CD34+ cells was significantly decreased in active SLE patients (1.48 ± 0.41%, n = 7) compared to the healthy controls (2.31 ± 0.75%, n = 10, p < 0.01), but no significant difference was found between the inactive patients (2.04 ± 0.44%, n = 3) and the controls. The expression of CD95, CD123, and CD166 on BM CD34+ cells were significantly increased in SLE patients (48.31 ± 10.59%, 44.9 ± 21.5%, 30.9 ± 19.54%, respectively, n = 10) when compared with the control subjects (24.33 ± 11.1%, 19.5 ± 4.4%, 10.7 ± 5.5%, respectively, n = 10, p < 0.05). The increased CD123 expression was negatively correlated with the number of peripheral white blood cells (r = −0.700, p < 0.05, n = 10). The percentage of CD166 expression was found significantly correlated with the index of SLE disease activity (r = 0.472, p < 0.05, n = 10) and 24 h proteinuria (r = 0.558, p < 0.05, n = 10), but negatively correlated with serum C3 level (r = −0.712, p < 0.01, n = 10). Our study found that the surface marker expression of CD95, CD123, and CD166 on BM CD34+ cells were significantly increased in patients. This supports the hypothesis that there are abnormalities of the HSC in SLE.
Since CD166 and CD123 correlated with the overall lupus activity, their role as a biomarker of inflammatory disease activity
also requires further study. 相似文献
14.
We and others have previously shown that IL-17 is elevated in the synovial fluid of patients with reactive arthritis (ReA)/undifferentiated
spondyloarthropathy (uSpA) having acute synovitis. Major source for IL-17 is Th17 cells, which differentiate from Th0 cells
under the influence of TGF-β and IL-6, IL1-β and are maintained by IL-21 and 23. There is a paucity of data on these cytokines
in ReA/uSpA. Thus, we measured the levels of Th-17 differentiating and maintaining cytokines in synovial fluid of patients
with ReA and uSpA. Fifty patients with ReA/uSpA (ReA 24, uSpA 26), 19 patients with rheumatoid arthritis (RA) and 11 patients
with osteoarthritis (OA) were included in the study. Synovial fluid (SF) were collected from knee joint and stored at −80°C
until analysis. Cytokines were assayed using ELISA in SF specimens. The median IL-17A levels were significantly elevated in
ReA (48.3 pg/ml) and uSpA (32.5 pg/ml) as compared to non-inflammatory OA controls (<7.8 pg/ml; p < 0.0001), while comparable to RA (57.9 pg/ml). Further, IL-6 median values were higher in ReA (25.2 ng/ml) and uSpA (13.6 ng/ml)
as compared to OA (0.76 ng/ml; p < 0.0001), and comparable to RA (15.8 ng/ml). The median levels of IL-1β, IL-21 levels were elevated in ReA, uSpA and RA
as compared to OA but were not statistically significant. TGF-β levels in ReA and uSpA were similar to OA but lower than in
RA (4340 pg/ml; p < 0.05). IL-23 was not detectable in any synovial fluid sample. However, levels of these cytokines did not correlate with
disease activity parameters. Significant positive correlation was observed between IL-17 and IL-1β (r = 0.38, p < 0.005), IL-17 and IL-6 (r = 0.659, p < 0.0001), and IL-1β and IL-6 (r = 0.391, p < 0.0001) in ReA and uSpA group. Inflammatory synovitis in ReA/uSpA is mediated by pro-inflammatory cytokines like IL-17,
IL-6, IL-1β, and IL-21. However, IL-23 was not detectable in SF. Good correlation between IL-17, IL-6, and IL 1β suggest that
either they are co-regulated or they regulate each other. 相似文献
15.
Tong J Utzschneider KM Carr DB Zraika S Udayasankar J Gerchman F Knopp RH Kahn SE 《Diabetologia》2007,50(2):439-442
Aims/hypothesis Pancreatic polypeptide (PP) is produced by the F-cells of the pancreas, and its plasma concentration has been used as a marker
of parasympathetic activity. Recent work in rodents suggests that there is both sympathetic and parasympathetic innervation
of white adipose tissue and that parasympathetic activity is anabolic resulting in lipid accumulation. We have examined whether
in humans increased PP levels are associated with increased intra-abdominal fat (IAF), and thereby insulin resistance.
Materials and methods We measured PP levels in 177 non-diabetic subjects (75 male/102 female; age 32–75 years) 3 min after an i.v. glucose bolus
during a frequently sampled intravenous glucose tolerance test. IAF and s.c. fat (SCF) areas were measured by CT scan. The
insulin sensitivity index (S
I) was quantified using Bergman’s minimal model.
Results PP levels were higher in men than in women (96.2 ± 72.2 vs 76.1 ± 55.0 pg/ml, mean ± SD, p = 0.037), as was IAF area (124.7 ± 67.4 vs 83.0 ± 57.7 cm2, p < 0.001). While PP levels were significantly associated with IAF (r = 0.16, p = 0.031), WHR (r = 0.30, p < 0.001) and age (r = 0.37, p < 0.01), they were not associated with SCF (r = 0.02, p = 0.829). The association between PP and IAF was not independent of age and/or sex. S
I was negatively associated with PP levels (r = −0.17, p = 0.026) and IAF area (r = −0.65, p < 0.001). The association between S
I and PP disappeared after adjusting for IAF area, indicating that S
I was not a major determinant of PP levels.
Conclusions/interpretation In humans, age and sex may modulate the association between plasma PP level and IAF area, suggesting that they may be determinants
of parasympathetic activity and thus IAF accumulation. 相似文献
16.
Increased angiogenin expression in gastric cancer correlated with cancer progression 总被引:12,自引:0,他引:12
Purpose: The purpose of this study is to elucidate the expression of angiogenin and its previously undemonstrated clinical significance
in gastric cancer (GC). Methods: Angiogenin expression was examined immunohistochemically in 21 GC tissues and 21 corresponding normal gastric tissues. The
serum concentration was determined by enzyme-linked immunosorbent assay (ELISA) in GC patients preoperatively (n=48) and postoperatively (n=41), in nonneoplastic patients preoperatively (n=23) and postoperatively (n=19), and in 32 healthy volunteers. The amount of angiogenin in the tissue of 21 GC patients was also determined by ELISA.
Results: Angiogenin expression was observed in GC cells as well as in some fundic glandular cells and some inflammatory cells. The
mean serum concentration in GC patients (407.8 ± 105.2 ng/ml) was significantly higher than that in the nonneoplastic patients
(345.7 ± 58.3 ng/ml; P < 0.003) and in the healthy volunteers (333.0 ± 59.3 ng/ml; P < 0.0002). The mean serum angiogenin concentrations were progressively higher in the order T1+T2 (P < 0.04) < T3+T4 (P < 0.0001) < recurrent GC (P < 0.05) subgroups, in the order node-negative (P < 0.05) < node-positive (P < 0.0002) subgroups, and in the order stage I+II (P < 0.02) < stage III and over (P < 0.0005) subgroups as compared with those in the healthy volunteers. These elevated serum angiogenin concentrations in each
subgroup were significantly (P < 0.0003) reduced after cancer resection. The amounts of angiogenin in GC tissues correlated significantly with the serum
angiogenin concentration (P < 0.01). Conclusions: These results suggest that angiogenin expression is increased in GC and that the increased serum concentration in GC patients
correlates with cancer progression.
Received: 15 December 1999 / Accepted: 14 February 2000 相似文献
17.
Di Mario F Cavallaro LG Moussa AM Caruana P Merli R Maini A Bertolini S Dal Bó N Rugge M Cavestro GM Aragona G Plebani M Franzé A Nervi G 《Digestive diseases and sciences》2006,51(10):1791-1795
We sought to study the relationship between serum pepsinogens and different histopathologic features of Helicobacter pylori-related chronic gastritis. One hundred forty-nine consecutive dyspeptic patients underwent endoscopy with biopsies; serum
pepsinogens I and II were measured by immunoassay. Serum levels of pepsinogens (sPG) were significantly correlated with H. pylori density both of the corpus (sPGI: r = 0.32, P < .001; sPGII: r = 0.56, P < .001) and antrum (sPGI: r = 0.41, P < .001; sPGII: r = 0.43, P < .001) as well as with chronic inflammation (sPGI: r = 0.26, P < .001; sPGII: r = 0.49, P < .001) and activity (sPGI: r = 0.38, P < .001; sPGII: r = 0.50, P < .001) in the antrum. Only sPGII was correlated with chronic inflammation (r = 0.44, P < .001) and activity (r = 0.40, P < .001) in the corpus. SPGI was inversely correlated with atrophy (r = –0.33, P < .001) and intestinal metaplasia (r = –0.37, P < .001) in the corpus. sPGII levels could be considered as markers of gastric inflammation all over in the stomach. sPGI
levels are inversely related to atrophic body gastritis. 相似文献
18.
Rosa Weiss Telles Gilda Aparecida Ferreira Neusa Pereira da Silva Emilia Inoue Sato 《Rheumatology international》2010,30(6):779-784
The objective of the study was to quantify plasma myeloperoxidase (MPO) levels in systemic lupus erythematosus (SLE) patients
and to evaluate a correlation between MPO levels and disease activity. 71 female SLE patients and 70 controls were studied.
Patients were divided into two groups: Group I (n = 48) with SLEDAI-2K score 0–5 and Group II (n = 23) with SLEDAI-2K score ≥6. Mann–Whitney test and Spearman rank correlation were used. Two-sided P values <0.05 were considered significant and P values ≥0.05 and <0.08 were considered as a tendency. The median age of patients and controls were comparable and the mean
disease duration was 99.2 ± 61.7 months. MPO levels were higher in patients than controls [5.99 (4.38–8.64) vs. 5.00 (3.33–7.08) ng/ml,
P = 0.02]. We did not find correlation between MPO levels and SLEDAI-2k (r = 0.07, P = 0.58). MPO levels were not affected by treatment with prednisone, cyclophosphamide or azathioprine, however, a tendency
of lower levels was observed among patients under antimalarial drugs. There was no significant difference in MPO plasma levels
between Group I and Group II (5.83 vs. 6.02 ng/ml, P = 0.99). MPO levels were higher in patients with arthritis than in those without arthritis (8.15 vs. 5.56 ng/ml, P = 0.010). No difference was observed among patients with and without other organs/systems involvement. SLE patients presented
increased MPO plasma levels than healthy controls. Despite the lack of correlation between MPO plasma levels and disease activity,
the higher MPO levels in patients with articular involvement suggests MPO may play a different role in the inflammatory process
of some SLE manifestations. 相似文献
19.
Fujiwara T Matsunaga T Kameda K Abe N Ono H Higuma T Yokoyama J Hanada H Osanai T Okumura K 《Heart and vessels》2007,22(5):303-309
Nicorandil, a hybrid KATP channel opener and nicotinamide nitrate, reduces no-reflow phenomenon and improves cardiac function in patients with acute
myocardial infarction (AMI). We repoted that nicorandil suppresses radical formation in patients with AMI undergoing primary
percutaneous coronary intervention (PCI). In the present study, we tested the hypothesis that nicorandil treatment suppresses
MMP activities and predicts ventricular remodeling in AMI. Sixty-two patients with AMI were randomized into nicorandil pretreatment
(n = 31) and control (n = 31) groups after admission and underwent primary PCI. Nicorandil was administered as a bolus injection (4 mg) followed
by constant infusion (8 mg/h) for 24 h just after admission. On days 1, 2, and 14 after the onset of AMI, the plasma levels
of matrix metalloproteinase (MMP)-2 and MMP-9 were measured by enzyme-linked immunosorbent assay and the activities by gelatin
zymography. There were no differences in the baseline clinical characteristics between the two groups. On day 1, there were
no differences in both MMP-2 and MMP-9 levels and their activities between the two groups. However, both MMP-2 and MMP-9 levels
and their activities were significantly lower in nicorandil than in control group on day 2 (MMP-2 level, 1 014 ± 39 vs 1 174
± 44 ng/ml; MMP-9 level, 17 ± 1 vs 23 ± 2 ng/ml; both P < 005) and on day l4 (MMP-2 level, 970 ± 38 vs 1 221 ± 44 ng/ml; MMP-9 level, 17 ± 1 vs 23 ± 1 ng/ml; both P < 0.05). Left ventricular end-diastolic volume index (LVEDVI) at acute phase was not different between the two groups. At
6 months after AMI, LVEDVI was significantly smaller in nicorandil than in the control group (83 ± 4 vs 96 ± 4 ml/m2, P < 0.05). The change in LVEDVI from acute phase to 6 months was positively correlated with MMP-2 and MMP-9 levels and activities.
Nicorandil suppresses the increases in MMP levels and activities and prevents the development of ventricular remodeling in
AMI. 相似文献