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Objective Through the detection of MIP-1α and VEGF levels in serum and CSF of ALS patients, we evaluated the clinical value of MIP-1 and VEGF levels in ALS patients. Methods A total of 80 patients with ALS were collected from Kuangwu Hospital of Tongchuanin from Jan, 2012 to Jun, 2015, and 67 patients with non-inflammation neurological diseases were chosen as control group. We obtained CSF and serum samples,and the MIP-1α and VEGF levels were measured by ELISA method. Results The MIP-1α levels in serum and CSF of ALS patients were statistically and significantly higher than those in the control group (P＜0.05) . The VEGF levels in serum of ALS patients were statistically and significantly higher than those in the control group (P＜0.05).The VEGF levels in CSF of ALS patients were not higher than those in the control group,statistically insignificant (P＞0.05).MIP-1 alpha and VEGF levels was positively correlated with ALS course. The MIP-1αand VEGF levels of the long duration group were greater than the short duration group (P＜0.05) . Conclusion The rising of MIP-1α and VEGF may indicate an activation of compensatory responses in ALS which suggested that MIP-1 alpha and VEGF are involved in the pathophysiology of amyotrophic lateral sclerosis. We propose that MIP-1α and VEGF may be a useful biomarker witha prognostic and evaluating potential for ALS.
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<p><b>OBJECTIVE</b>To investigate the changes in the proportion and function of peripheral CD4(+)LAP(+)regulatory T cells (CD4(+)LAP(+)Treg cells) in children with asthma, as well as the role of CD4(+)LAP(+)Treg cells in the pathogenesis of asthma.</p><p><b>METHODS</b>A total of 75 children who were diagnosed with asthma from March 2014 to September 2015 were enrolled as study subjects, and according to their conditions, they were divided into acute-stage asthma group (40 children) and remission-stage asthma group (35 patients). Another 30 children who underwent physical examination were enrolled as the healthy control group. Flow cytometry was used to determine the percentage of peripheral CD4(+)LAP(+)Treg cells, and [(3)H]-thymidine incorporation assay was performed to analyze the immunosuppression of CD4(+)LAP(+)Treg cells in each group.</p><p><b>RESULTS</b>The acute-stage asthma group showed significant reductions in the proportion of CD4(+)LAP(+)Treg cells compared with the remission-stage asthma group and the healthy control group (2.0%±1.0% vs 4.1%±2.4%/4.6%±3.0%; P<0.05). The acute-stage asthma group also showed a significant reduction in the immunosuppression rate of CD4(+)LAP(+)Treg cells compared with the remission-stage asthma group and the healthy control group (21%±4% vs 55%±9%/62%±11%; P<0.05).</p><p><b>CONCLUSIONS</b>In children with asthma, the reduction in the number and inhibitory function of peripheral CD4(+)LAP(+)Treg cells may be involved in the pathogenesis of asthma.</p>
Subject(s)
Child , Child, Preschool , Female , Humans , Male , Asthma , Allergy and Immunology , T-Lymphocytes, Regulatory , Allergy and ImmunologyABSTRACT
<p><b>OBJECTIVE</b>To study the relationship between insertion/deletion (I/D) polymorphism of 287 bp in the 16th intron of angiotensin converting enzyme (ACE) and essential hypertension in children.</p><p><b>METHODS</b>I/D polymorphism of 287 bp in the 16th intron of ACE was detected using PCR in 105 children with essential hypertension and 105 normal children as control group.</p><p><b>RESULTS</b>There was an I/D polymorphism in the 16th intron of ACE in the hypertension and the control groups: type II, type ID and type DD. The genotype frequencies of type DD, type ID and type II in the hypertension group were 30.5%, 47.6% and 21.9%, respectively. The genotype frequencies of type DD, type ID and type II in the control group were 14.3%, 46.7% and 39.1%, respectively. There were significant differences in the genotype frequencies of types DD and II between the two groups (P<0.01). The allele frequency of type D (54.3% vs 37.6%) was significantly higher in the hypertension group; in contrast, the allele frequency of type I (45.7% vs 62.4%) was significantly lower than in the control group (P<0.01).</p><p><b>CONCLUSIONS</b>Polymorphism of type II, type ID and type DD exits in ACE. The deletion of 287 bp in the 16th intron of ACE might be associated with the occurrence of essential hypertension in children.</p>
Subject(s)
Adolescent , Child , Female , Humans , Male , Gene Frequency , Genotype , Hypertension , Genetics , Peptidyl-Dipeptidase A , Genetics , Polymorphism, GeneticABSTRACT
Objective To explore the diagnostic value of detecting respiratory syncytial virus(RSV)-IgM for viral pneumonia in children.Methods Seventy-six cases with interstitisl pneumonia,32 cases with bronchiolitis among 108 cases children with viral pneumonia and 40 healthy children as control group were included,RSV-IgM was detected by indirect immunofluorescence in 108 children with viral pneumonia and healthy control group.Results The positive rates of RSV-IgM in 76 cases with interstitisl pneumonia and 32 cases with bronchiolitis were 48.68% and 25.0%,respectively,there was significant difference between 2 groups(?2=5.20 P
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<p><b>OBJECTIVE</b>To identify an interaction between the interleukin-1 receptor antagonist gene polymorphism and risk of Alzheimer's disease.</p><p><b>METHODS</b>The study included 117 healthy controls, 85 patients with Alzheimer's disease in a Northeastern Chinese population of Han nationality. Genotypes were determined by a polymerase chain reaction amplification of the intron 2 fragment, harbouring a variable number of short tandem nucleotide sequences. Amplification products were separated on a 2% agarose gel.</p><p><b>RESULTS</b>The allele 2 frequency was 27% in healthy controls, and 21% in patients with Alzheimer's disease. Thus for allele 2 as well as for all other alleles, genotypes, or carriage rates, no significant differences compared with controls.</p><p><b>CONCLUSIONS</b>No association of interleukin-1 receptor antagonist gene polymorphism with Alzheimer's disease was identified in this population. It is also possible that the increased risk and disease modifying effects are caused by linkage disequilibrium with other genomic variants in other nearby genes.</p>