Evaluation of Serum Interleukin-21 and HLA-C1 Polymorphism in Pediatrician Hematopoietic Stem Cell Transplantation for Early Diagnosis of Acute Graft-Versus-Host Disease

Background: Allogenic hematopoietic stem cell transplantation (HSCT) is a strategy used for treatment of different malignant diseases. However, success of allo-HSCT can be hampered by graft-versus-host-disease (GVHD). Natural killer (NK) cells may play an important role in activating antigen presenting cells and subsequent activation of T cells. The main purpose of this study was the evaluation of IL-21, as a blood biomarker, for early detection of acute GVHD (aGVHD) in children after HSCT and also the study of human leukocytes antigen (HLA)-C1 polymorphism, as a targeting ligand for NK cells in these patients. Methods: Fifty one children receiving HSCT were studied. Blood samples were collected at -8, 7, and 14 days of transplantation. The -8-day samples were analyzed for HLA-C1 polymorphism by PCR-sequence-specific primer technique and pre-transplantation IL-21 assay. To study the serum levels of IL-21, two blood samples were collected on days +7 and +14 and analyzed by ELISA technique. Results: The results indicated that the incidence of aGVHD in pediatric is associated with a polymorphism of HLA-C1, as alleles HLA-C01:12 (P<0.001), HLA-C01:22 (P<0.004), and HLA-C01:67 (P<0.009). On the other hand, the serum levels of IL-21 in children with aGVHD were decreased after transplantation compared to before transplantation. The serum levels of the IL-21 at 14 days after transplantation had a significant correlation with the occurrence of aGVHD (P=0.05). Conclusion: Based on the findings of this study, there is a significant correlation between HLA-C1 polymorphisms and the serum levels of IL-21 with the incidence of aGVHD.

Removal of C.I. Basic Yellow 2 from aqueous solution by low-cost adsorbent: hardened paste of Portland cement.

The adsorption of C.I. Basic Yellow 2 (BY2) from aqueous solutions on to hardened paste of Portland cement (HPPC) as a low-cost adsorbent and its adsorption kinetics at different conditions were studied. The adsorption process was followed by an online spectrophotometric analysis system, which consisted of a UV-Vis spectrophotometer, a designed spectrophotometric cell, a peristaltic pump and a glass reactor. The effect of experimental parameters, including initial dye concentration, mass of HPPC, initial pH and temperature, on adsorption was studied over a 30 miin adsorption period. For the kinetic study, the obtained data were treated according to various kinetic models. The results revealed that the experimental data were better fitted to the first-order kinetics model than to the second-order and intraparticle diffusion models. Equilibrium isotherms for the adsorption of BY2 on HPPC were analysed by Freundlich and Langmuir isotherms equations using the linear correlation coefficient. The Freundlich isotherm gave the best correlation of adsorption.

Metabolic recovery following human traumatic brain injury based on FDG-PET: time course and relationship to neurological disability.

OBJECTIVE: Utilizing [(18)F]fluorodeoxyglucose positron emission tomography (FDG-PET), we assessed the temporal pattern and the correlation of functional and metabolic recovery following human traumatic brain injury. DESIGN AND SUBJECTS: Fifty-four patients with injury severity ranging from mild to severe were studied. Thirteen of these patients underwent both an acute and delayed FDG-PET study. RESULTS: Analysis of the pooled global cerebral metabolic rate of glucose (CMRglc) values revealed that the intermediate metabolic reduction phase begins to resolve approximately one month following injury, regardless of injury severity. The correlation, in the 13 patients studied twice, between the extent of change in neurologic disability, assessed by the Disability Rating Scale (DRS), and the change in CMRglc from the early to late period was modest (r = -0.42). Potential explanations for this rather poor correlation are discussed. A review of the pertinent literature regarding the use of PET and related imaging modalities, including single photon emission tomography (SPECT) for the assessment of patients following traumatic brain injury is given. CONCLUSION: The dynamic profile of CMRglc that changes following traumatic brain injury is seemingly stereotypic across a broad range and severity of injury types. Quantitative FDG-PET cannot be used as a surrogate technique for estimating degree of global functional recovery following traumatic brain injury.

Exposure of astrocytes to thrombin reduces levels of the metabotropic glutamate receptor mGluR5.

Thrombin is one of the first regulatory molecules present at sites of CNS trauma or injury. Exposure of neuronal and glial cells to thrombin produces potent morphological as well as cytoprotective and cytotoxic effects, but little is known about how this important modulator affects neurotransmitter signaling. In astrocyte cultures that have been morphologically differentiated by exposure to transforming growth factor-alpha, addition of thrombin induced a retraction of astrocytic processes and suppressed the stimulation of phosphoinositide hydrolysis by the selective metabotropic glutamate receptor (mGluR) agonist 1-aminocyclopentane-1S,3R-dicarboxylic acid. In addition to the suppression of phosphoinositide hydrolysis, thrombin treatment produced a corresponding reduction in level of mGluR5 mRNA as demonstrated with ribonuclease protection assay and reduced content of mGluR5 receptor protein as seen with western blotting. In contrast, thrombin exposure up-regulated astrocyte beta-actin mRNA levels. A synthetic hexapeptide with a sequence corresponding to the amino-terminus of the thrombin receptor's tethered ligand also mimicked the ability of thrombin to suppress mGluR5 levels and to increase beta-actin mRNA content, suggesting that these effects of thrombin are mediated by proteolytically activated cell surface thrombin receptors. Thrombin's suppressive effect on mGluR5 was resistant to pretreatment with pertussis toxin or various protein kinase and protein phosphatase inhibitors. However, the serine/threonine protein kinase inhibitor H-7 did prevent thrombin-induced reversal of astrocyte stellation and induction of beta-actin mRNA levels, indicating that these effects of thrombin involve a signaling pathway distinct from the one that mediates the suppressive effects of thrombin on mGluR5.