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Background: M. pneumoniae infection in children is usual and diagnosis of its neurologic complications for rapid treatment is very important. To compare the CSFM. pneumoniae antibody level between febrile children with acute neurologic signs (Menigoencephalitis, Guillan Barre Syndrome (GBS), Transverse myelitis, Ataxia and so on) with unaffected ones. Methods: A cross sectional/ case control study in pediatric wards of Rasoul-e-Akram & Mofid hospitals (2007-2009) was done. The amount of Specific M. pneumoniae IgG (ELISA) antibody level determined in CSF of 55 cases and in 10 controls. Chi square values (CI 95%, p< 0.05) calculated for all categorical variables. Sensitivity; specificity; Positive Predictive Value (PPV); Negative Predictive Value (NPV) of CSF antibody level determined by using the Area under the ROC Curve. Results: Cases (n= 55) aged between five month to 13 years with mean age of 3.84±3.43 years. Area Under Curve (AUC) in ROC was 0.876 (%95 CI, 0.78- 0.96; p< 0.0001). Cut off level for antibody was 0.0025 with 73% sensitivity; 90% specificity; 100% PPV; 28.8% NPV. CSF antibody level had significant difference between cases and controls [0.08± 0.26 Versus 0.001± 0.001; p: 0.02]; It had poor agreement between cases and controls (Kappa= 0.27). Lowest amount seen in cases with aseptic meningitis; highest amount observed in cases with GBS and cases with focal neurologic signs. Conclusion: The presence of very low amount (0.0025) of M. pneumoniae antibody in CSF of febrile children with acute neurologic signs had 70% sensitivity and 90% specificity; 100% PPV; but had low (28.8%) NPV. M. pneumoniae would be a rare cause in cases with aseptic meningitis. Finding the M. pneumoniae-DNAs in CSF are not so frequent (2%) but in high suspicious cases adding this test to determining the CSF antibody level might be helpful. [ABSTRACT FROM AUTHOR]

Background: Chronic Rhinosinusitis (CRS) is a persistent inflammatory disease affecting paranasal sinuses. CRS is categorized into two distinct subgroups defined as CRS with nasal polyps (CRSwNP) and CRS without nasal polyps (CRSsNP). Although several immune cells are involved in the CRS pathogenesis, the role of T cells is not fully understood. The objective of the present study was to evaluate the frequency of CD4+ and CD8+ T cells and macrophages in the sinonasal mucosa of CRS patients, as well as to investigate the specific transcription factors for Th1, Th2, Th17, and Treg cells. Methods: In this study, 15 healthy controls, 12 CRSsNP, and 23 CRSwNP patients participated. CD4+, CD8+, and CD68+ cells were investigated in the sinonasal tissues using immunohistochemistry. The expression of transcription factors related to Th subsets (T-bet, GATA3, Ror-γt, and FoxP3) was evaluated using real-time PCR. Furthermore, CRSwNP patients were defined as eosinophilic when eosinophils consisted of more than 10% of total inflammatory cells. The Kruskal–Wallis, Mann–Whitney, and Spearman tests were used in statistical analyses. Results: The median (range) age of the studied groups was: 32 (14–67) for CRSwNP, 28 (10–43) for CRSsNP, and 27 (17–44) for controls. The number of eosinophils in CRSwNP patients was higher than two other groups, whereas neutrophils were elevated in both CRSwNP and CRSsNP groups in comparison to controls. The frequency of CD4+ and CD8+ T cells, macrophages, and total inflammatory cells were significantly increased in CRSwNP and CRSsNP patients compared with controls. The mRNA expression of GATA3 was increased in CRSwNP patients while mRNA expression of Ror-γt was elevated in CRSsNP patients. No significant difference was observed in T-bet mRNA expression among three groups. Both CRSwNP and CRSsNP patients showed decreased FoxP3 mRNA expression in comparison to controls. Conclusion: The frequency of CD4+ and CD8+ T cells was elevated in CRS patients. In addition, we demonstrated Th2 dominance in CRSwNP patients and Th17 dominance in CRSsNP patients, implicating different mechanisms may underlie the disease. Better CRS classification and targeted therapeutic strategies may be achievable by determining the pattern of infiltrating inflammatory cells. Therefore, further experimental investigations on T cells are needed. [ABSTRACT FROM AUTHOR]

Presents an abstract of the article "Amniotic Fluid Alpha Feto Protein Levels in Down Syndrome Pregnancies and Other Chromosomal Abnormalities," by Ahmad Rajaee, Ariana Kariminejad, Maryam Mirzazadeh, Hanieh Jafarieh, Valeh Hadavi, Mehdi Shekarabi, Mohammad Hasan Kariminejad, Hossein Najmabadi, Raymond Dalgleish.

Background: Both genetic and environmental factors are important in pathogenesis of diabetes. Non HLA (Human Leukocyte Antigen) genes such as INS-VNTR and CTLA-4 in addition of HLA genes have influence on genetic susceptibility for diabetes mellitus. In this study the association of +49 A/G CTLA-4 and -23 A/T INS-VNTR polymorphisms with diabetes and their association with islet autoantibodies were investigated. Methods: Thirty four autoantibody positive adult persons with diabetes mellitus and 39 persons with Type 1diabetes mellitus (T1DM), 40 autoantibody negative Type 2 diabetes mellitus (T2DM) patients and 40 healthy controls were studied using Polymerase Chain Reaction-Restriction Fragment Length Polymorphism (PCR-RFLP) technique. Results: The frequencies of -23 A/T INS-VNTR genotypes were not significantly different among study groups. It was shown that the distribution of the +49A/G CTLA-4 allele and genotype frequencies did not differ between T1DM patients, autoantibody positive adult patients and controls. With increasing CTLA-4 G allele and GG/AG genotypes, the frequency of Glutamic Acid Decarboxylase Autoantibody (GADA), Islet Cell Autoantibody (ICA) and Islet Antigen 2 Antibody (IA2A) positive patients were increased. Conclusion: Our results suggest that susceptibility allele A of -23A/T INS-VNTR does not have any role in the pathogenesis of diabetes in our patients and susceptibility allele G of +49 A/G CTLA-4 if not, has a small role in pathogenesis of diabetes in T1DM and autoantibody positive adult patients and in spite of significant increase in autoantibody negative T2DM group it does not have any role in disease pathogenesis.