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Reduced levels of free and total insulin-like growth factor 1 (IGF-I) have been observed in type-1 diabetes (T1D) patients. The bioavailability of IGF-I from the circulation to the target cells is controlled by multifunctional IGF-binding proteins (IGFBPs). The aim of this study was to profile serum IGFBPs in T1D and its complications.', 'We measured the IGFBP levels in 3662 patient serum samples from our ongoing Phenome and Genome of Diabetes Autoimmunity (PAGODA) study. IGFBP levels of four different groups of T1D patients (with 0, 1, 2, and 3 complications) were compared with healthy controls.', 'Three serum IGFBPs (IGFBP-1, -2, and -6) are significantly higher in T1D patients, and these alterations are greater in the presence of diabetic complications. IGFBP-3 is lower in patients with diabetic complications. Analyses using quintiles revealed that risk of T1D complications increases with increasing concentrations of IGFBP-2 (fifth quintile ORs: 18-60, p<10(-26)), IGFBP-1 (fifth quintile ORs: 8-20, p<10(-15)), and IGFBP-6 (fifth quintile ORs: 3-148, p<10(-3)). IGFBP-3 has a negative association with T1D complications (fifth quintile ORs: 0.12-0.25, p<10(-5)).
Do iGF-Binding Proteins in Type-1 Diabetes Are More Severely Altered in the Presence of Complications?

Dengue is a mosquito-borne viral disease caused by the four dengue viruses (DENV-1 to 4) that can also be transmitted by blood transfusion and organ transplantation. The distribution of DENV in the components of blood from infected donors is poorly understood.', 'We used an in-house TaqMan qRT-PCR assay to test residual samples of plasma, cellular components of whole blood (CCWB), serum and clot specimens from the same collection from blood donors who were DENV-RNA-reactive in a parallel blood safety study. To assess whether DENV RNA detected by TaqMan was associated with infectious virus, DENV infectivity in available samples was determined by culture in mosquito cells.', 'DENV RNA was detected by TaqMan in all tested blood components, albeit more consistently in the cellular components; 78.8% of CCWB, 73.3% of clots, 86.7% of sera and 41.8% of plasma samples. DENV-1 was detected in 48 plasma and 97 CCWB samples while DENV-4 was detected in 21 plasma and 31 CCWB samples. In mosquito cell cultures, 29/111 (26.1%) plasma and 32/97 (32.7%) CCWB samples were infectious. A subset of samples from 29 donors was separately analyzed to compare DENV viral loads in the available blood components. DENV viral loads did not differ significantly between components and ranged from 3-8 log10 PCR-detectable units/ml.
Does distribution of Dengue Virus type 1 and 4 in Blood Components from Infected Blood Donors from Puerto Rico?

Chronic hypoxia causes redistribution of fetal cardiac output by mechanisms poorly understood. We tested the hypothesis that chronic hypoxia alters vascular reactivity of arteries from near-term fetal guinea pigs.', 'Pregnant guinea pigs (50 days, term = 65 days) were exposed to either normoxia (room air) or hypoxia (12% O2) for 14 days. Carotid artery ring segments from anesthetized fetuses were mounted onto myographs for measurement of force. Contractile responses to cumulative addition of prostaglandin F2alpha (PGF2alpha, 10(-9) M to 10(-5) M), U46619, a thromboxane mimetic (10(-12) M to 12(-6) M), and KCl (10 to 120 mM) were measured in the presence and absence of INDO (INDO, 10(-5) M) alone and INDO plus nitro-L-arginine (LNA, 10(-4) M), or INDO plus N6-iminoethyl-L-lysine (LNIL, 5 x 10(-5) M, a selective iNOS inhibitor), and measured in endothelium-intact and denuded arteries. Nitric oxide synthase (NOS) activity was measured in isolated arteries by 14C-L-arginine to 14C-L-citrulline conversion.', 'Hypoxia decreased contractile responses to both PGF2alpha and U46619 under control conditions. Maximal contraction to both agonists was increased in hypoxemic arteries after INDO alone and INDO + LNA compared to normoxic controls. Endothelium-denudation abolished the differences between the groups. KCl contraction was unaffected by hypoxia. LNIL potentiated maximal PGF(2alpha) contraction but was similar between groups. Hypoxia increased (P < .05) total and Ca(2+)-dependent NOS activities by 1.7- and 2.1-fold, respectively, but had no effect on Ca(2+)-independent activity.
Does chronic hypoxia inhibit contraction of fetal arteries by increased endothelium-derived nitric oxide and prostaglandin synthesis?