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Systemic JIA (SJIA) is one subtype of juvenile idiopathic
arthritis (JIA) that is a leading cause of short-term and
long-term disability in children [1]. Although SJIA repre
sents only 10%–20% of all cases of JIA, it accounts for
more than two-thirds of the mortality associated with this
condition [2]. The etiology and pathogenesis of SJIA
remain unknown. Further understanding of SJIA pathogen
esis may facilitate new therapeutic approaches.
Interleukin-18 (IL-18) was originally identified as an
interferon gamma (IFN)-γ-inducing factor, and IL-18 can
induce INF-g production by splenocytes, hepatic lympho
cytes, and type 1T helper (Th1) cell clones [3]. IL-18 levels
have been shown to be abnormal in some inflammatory dis
eases and in autoimmune diseases. IL-18 expression has
been reported to be up-regulated in lupus nephritis (LN),
type 1 diabetes, and other autoimmune diseases [4]. IL-18
binding protein (IL-18BP) is a circulating decoy receptor
that binds to IL-18 with high affinity. IL-18BP can effi
ciently antagonize the biological activities of IL-18 [5].
Experiments have shown that IL-18BP could prevent or at
tenuate the development of some autoimmune diseases [6].
Currently, the balance between IL18 and IL-18BP in
SJIA patients remains unknown. The hypothesis that an im
balance between IL-18 and IL-18BP may play an important
role in SJIA was demonstrated in the present study by com
paring the plasma levels and mRNA expression of IL-18
and IL-18BP in peripheral blood mononuclear cells from
active patients, remission patients, and healthy children.
Forty-five acute-phase SJIA patients (20 males and 25
obtained from the Medical Ethics Committee of the Qilu
Hospital and Second Hospital of Shandong University.
We measured the IL-18 levels with a commercial enzyme
linked immunosorbent assay (ELISA) (USCNLIFTM; Wuhan
EIAab Science Co., Wuhan, China). The lower detection limit
of the assay was 15.6 pg/ml. An ELISA (Human IL-18BPa
DuoSet; R&D Systems, Minneapolis, USA) was used to
detect IL-18BP. Multiplex real-time PCR was performed for
IL-18, IL-18BP, and the endogenous control (b-actin) on an
ABI PRISMw7500 Sequence Detection System (Applied
Biosystems, Foster City, USA) using SYBRw Green (Toyobo,
Japan) as a double-strand DNA-specific binding dye.
It was found that plasma IL-18 and IL-18BP levels were
higher in patients with acute SJIA (n ¼ 45) than those in
healthy children (n ¼ 20) or in the remission group (n ¼
23). The patients in remission had similar plasma levels of
IL-18 and IL-18BP compared with healthy children. The
expression levels of IL-18 mRNA in the patients with
active SJIA were 4.8-fold higher than those in the healthy
control group (P , 0.05), and the levels of IL-18 mRNA in
the remission group were 2.8-fold higher than those in the
healthy control group [P , 0.05; Fig. 1(A)]. The expression
levels of IL-18BP mRNA in the active SJIA group were
2.2-fold higher than those in healthy controls (P , 0.05),
and the expression levels in the remission group were
1.9-fold higher than those in healthy controls [P , 0.05;
Fig. 1(B)]. The ratio of IL-18/IL-18BP levels and of IL-18/
IL-18BP mRNA expression in the plasma was higher in the
SJIA patients than in the remission group or in the healthy


Posted by on 2017-02-13 18:24:55

Method: Baseline serum AFABP levels were measured in 1136
Chinese type 2 diabetic subjects recruited from the Hong
Kong West Diabetes Registry. Chronic kidney disease (CKD)
progression was defined as a drop in estimated glomerular
filtration rate (eGFR) category accompanied by a 25% or greater
drop in eGFR from baseline. The role of AFABP in predicting
CKD progression over a median follow-up of 4 years was
analyzed using Cox regression analysis.
Result: At baseline, serum AFABP levels increased progressively with CKD staging (p for trend <0.001). Amongst 1071
subjects with baseline CKD stage 3 or less, 171 subjects (16.0%)
had CKD progression after a median follow up of 4 years.
Subjects with CKD progression were older (p < 0.001), with
longer duration of diabetes (p = 0.001) and higher baseline
HbA1c levels (p = 0.008), more of them being hypertensive
(p < 0.001) and on anti-hypertensive medications including
ACEI or ARB (p < 0.001), lower baseline eGFR (p < 0.001), higher
C-reactive protein (p < 0.001) and higher serum triglyceride
levels (p < 0.001) than those without CKD progression. Serum
AFABP levels were significantly higher in those with CKD
progression during follow-up than those without progression
(p < 0.001). Baseline sex-adjusted serum AFABP levels were
higher in subjects with CKD progression (10.9 mg/L [IQR 6.76–
17.2] vs 7.00 mg/L [IQR 4.41–11.6] in male and 17.2 mg/L [IQR
11.1–28.0] vs 12.4 mg/L [IQR 7.94–21.9] in female; p < 0.001]).
On multivariable Cox regression analysis including also other
biologically relevant variables, baseline serum AFABP level
was independently associated with CKD progression (Hazard
ratio 1.52; 95% CI = 1.18–1.96; p < 0.001), together with sex,
age, body mass index, smoking status, duration of diabetes,
HbA1c, systolic blood pressure, the use of ACEI/ARB and
C-reactive protein level at baseline.
Conclusion: Elevated baseline serum AFABP level appears
to be a useful biomarker for predicting kidney diseas


Hypoxia-inducible factor-1α (HIF-1α) is one of the most potent angiogenic growth factors. It regulates genes involved in angiogenesis, but is inactivated rapidly by normoxia. Ad-HIF-1α-Trip was constructed by transforming Pro402, Pro564, and Asn803 in HIF-1α to alanine in order to delay degradation and create a constitutive transcriptional activator. In this study, we investigated whether Ad-HIF-1α-Trip could induce functional mature angiogenesis and the possible mechanisms involved. We found that Ad-HIF-1α-Trip increased the expression of multiple angiogenic genes in cultured HMVEC-Ls, including VEGF, PLGF, PAI-1, and PDGF. In a rabbit model of acute hind limb ischemia, Ad-HIF-1α-Trip improved tissue perfusion and collateral vessels, as measured by contrast-enhanced ultrasound (CEU), CT angiography, and vascular casting. Ad-HIF-1α-Trip also produced more histologically identifiable capillaries, which were verified by immunostaining, compared with controls. Interestingly, inhibition of CBP/p300 by curcumin prevented HIF-1α from inducing the expression of several angiogenic genes. The present study suggests that Ad-HIF-1α-Trip can induce mature angiogenesis and improve tissue perfusion in ischemic rabbit skeletal muscle. CBP/p300, which interacts with the transactivation domains of HIF-1α, is important for HIF-1α-induced transcription of angiogenic genes.


Diagnostic Outcomes of Soluble Major Histocompatibility Complex Class I Related Chain Molecule A and Des-γ Carboxy Prothrombin versus AlphaFetoProtein for Hepatitis C Virus-Induced Hepatocellular Carcinoma in Egyptian Patients

Objectives: Hepatitis C virus (HCV) infection is a major threat for developing hepatocellular carcinoma (HCC) in Egypt which represents an increased cause of mortality. HCC usually presents at a very late stage thus many patients miss the best opportunity for treatment because of lack of early symptoms and early reliable diagnostic marker for malignant transformation. This study aimed to perform a head-to-head comparison of the diagnostic performance of soluble major histocompatibility complex class I related chain molecule A (sMICA), Des-γ Carboxy Prothrombin (DCP) and Alpha-Feto Protein (AFP) in HCC patients.

Subjects and methods: The study included 250 subjects. They were including 50 chronic hepatitis patients, 50 cirrhotic patients, 100 patients with HCC on top of cirrhosis and 50 apparently healthy control subjects. HCC group was subdivided into two subgroups, 61 patients with tumor size from 2 to 5 cm and 39 patients with tumor size >5cm. Serum levels of sMICA, DCP as well as AFP were measured in the sera of all subjects by Enzyme Immune Assay (EIA).

Results: AFP, DCP and sMICA showed statistical significant increased levels in HCC group when compared to other groups (p<0.05). However, there was a highly significant increase in AFP levels in other patients groups when compared to control group (p ≤ 0.001). There was no significant difference in DCP level between chronic hepatitis and liver cirrhosis groups and as well when both were compared to the control group. sMICA levels were mostly increased in HCC patients in comparison to healthy or disease controls (p ≤ 0.001). The area under the receiver operating characteristic (ROC) curve (AUC) was used to evaluate the diagnostic efficacies of sMICA, DCP and AFP. When employing the ROC curve, the superiority of sMICA [AUC: 0.928] to both AFP [AUC: 0.886] and DCP [AUC: 0.656] was evident in the diagnosis of HCC, in discriminating HCC from LC and CH patients [AUC: 0.908] as well as in discriminating HCC with small focal lesions (tumor size from 2-5cm) from both cirrhotic and CH patients [AUC: 0.917 & sensitivity: 88.5%]. The sensitivity of sMICA was the highest (88.5%) versus (62%) for AFP and (54%) for DCP.

Conclusion: sMICA levels showed a stepwise increase from CH to LC and up to the most in HCC. However, AFP levels were increased in HCC and other chronic liver diseases while DCP levels were increased only in HCC. As well, sMICA has superior diagnostic performance for HCV-induced HCC on both AFP and DCP with even better performance for distinguishing HCC with small focal lesions. Consequently, measurement of sMICA as a single marker or beside AFP and/or DCP may be valuable in the screening for early malignant transformation of chronic liver diseases to HCC.




To develop a preclinical large animal model of autoimmune diabetes to facilitate the translational research of autoimmune diabetes in human.

Materials and methods

Nine young rhesus monkeys received multiple-low-dose (MLD) intravenous injections of streptozotocin for five consecutive days, followed by two additional boosting injections of STZ given 1 week apart. The induction of autoimmune diabetes was evaluated by regular metabolic testing, serological assessment of islet-reactive autoantibodies and histological examination of pancreatic tissues.


Seven of nine treated animals became diabetic with moderate hyperglycemia initially and more severe hyperglycemia thereafter. All diabetic animals exhibited severely impaired glucose tolerance, limited islet function, and required insulin therapy to maintain relatively normal glucose metabolism and healthy status. Serological tests showed that all diabetic monkeys developed autoantibodies specifically against insulin and islet antigens. Furthermore, histological examination of the pancreata from diabetic animals revealed evidence of specific destruction of islet β cells and islets infiltrated with T lymphocytes. Overt and persistent diabetes can be induced in young rhesus monkeys by the injection of MLD-STZ, and autoimmune responses to pancreatic islet cells seem to be involved in the development of glucose intolerance and diabetes.


These data indicate for the first time that autoimmune diabetes can be induced in primates; this may serve as a valuable preclinical model for studying the pathogenesis of and potential therapies for autoimmune diabetes in humans.

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