Objective To look for susceptible and resistant HLA gene of Atopic Dermatitis(AD), analyze single strand conformation polymorphism of the susceptible gene and observe whether the base sequence was different from healthy Method Polymerase chain reaction sequence specific primer(PCR SSP)was used to classify the HLA DRB allele of 122 patients and 80 controls PCR single strand conformation polymorphism(SSCP) was used to analyse the susceptible gene Results The DR 3 frequency of extrinic type of “pure” AD(EAD)group and complicated group was higher than that of the control group ( RR =5 27 and 3 59 respectively P 0 05). Conclusion HLA DR 3 was the susceptible gene of AD, while HLA DR 6 was the resistant gene of AD It indicated that people with HLA DR 3 were reliable to AD, while people with HLA DR 6 were not But there was no base difference between these people and the healthy in HLA DR 3

Objective To investigate the effect of caveolin-1 scaffolding domain (CSD) peptides on heme oxygenase-1 (HO-1) activity increasing and M1/M2 phenotype polarization in rat alveolar macrophages (AMs) induced by lipopolysaccharide (LPS).Methods Bioinformatics was used to analyze the binding of full-length wild-type CSD polypeptide and 101 amino acid deleted truncated mutant CSD polypeptide (Δ101CSD) to HO-1. Primary AMs were isolated from rats, when cell fusion reached 80％, they were synchronized with serum-free medium and divided into five groups: no treatment was given to the blank control group; LPS group was treated with 100μg/L LPS for 16 hours;LPS+ hemin group was treated with 100μg/L LPS and 20μmol/L hemin for 16 hours; wild-type CSD polypeptide+ LPS+hemin group was pretreated with 10μmol/L wild-type CSD polypeptide 6 hours before LPS treatment; Δ101CSD+ LPS+hemin group was pretreated with 10μmol/L Δ101CSD polypeptide 6 hours before LPS treatment. After treatment for 16 hours, the co-localization between caveolin-1 (Cav-1) and HO-1 was displayed by confocal microscope; the mRNA expressions of inflammatory cytokines interleukin-1β (IL-1β) and monocyte chemoattractant protein-1 (MCP-1) and M1/M2 polarization cytokines tumor necrosis factor-α (TNF-α), inducible nitric oxide synthase (iNOS), leukocyte differentiation antigen 206 (CD206) and IL-10 were determined by real-time fluorescent quantitative reverse transcription-polymerase chain reaction (RT-qPCR); the HO-1 activity and nitric oxide (NO) production were determined by spectrophotometry.Results Bioinformatics analysis showed: both wild-type CSD and Δ101CSD peptides could bind to HO-1, and there was no significant difference in the binding ability between the two peptides, but the deletion of 101 Arg resulted in the disappearance of part of the binding region between Δ101CSD and HO-1. The results of laser confocal microscopy showed: the expressions of Cav-1 and HO-1 were lowed in the blank control group, and Cav-1 was bound to HO-1 in LPS group and LPS+ hemin group. Both wild-type CSD and Δ101CSD peptides pretreatment could significantly reduce the binding of HO-1 to Cav-1 induced by LPS. HO-1 activity analysis showed: after LPS stimulation, the activity of HO-1 was significantly higher than that of the blank control group; the activity of HO-1 induced by LPS was increased by hemin; after pretreatment with two kinds of CSD peptides, the activity of HO-1 was further increased, and the effect of wild-type CSD peptide was more significant, which showed a statistically significant difference as compared with that of LPS+ hemin group (pmol·mg-1·h-1: 3683±266 vs. 2408±132,P < 0.05). RT-qPCR results showed: LPS could induce elevation of cytokines and M1 markers and decrease of M2 markers, while hemin could inhibit LPS-induced inflammatory response and M1/M2 phenotypic polarization. Compared with LPS+ hemin group, after pretreatment with wild-type CSD peptide, the levels of inflammatory factors in AMs were decreased, and the mRNA expression levels of TNF-α and iNOS, M1 markers, were decreased [TNF-α mRNA (2-??Ct): 6.82±0.05 vs. 8.70±0.24, iNOS mRNA (2-??Ct): 331.50±32.05 vs. 506.70±0.10, bothP < 0.05], and IL-10 mRNA expression level was increased (2-??Ct: 269.09±6.54 vs. 119.05±3.30,P < 0.05). The deletion of 101 site partially weakened the inhibitory effect of CSD peptides on inflammatory factors and only reduced the expression of iNOS mRNA (2-??Ct: 429.11±8.92 vs. 506.70±0.10,P < 0.05), indicating that its ability to transform AMs from M1 phenotype to M2 phenotype was poor. The two peptides had no effect on the expression of CD206.Conclusion Wild-type CSD had beneficial effects of anti-inflammation by reducing Cav-1 binding to HO-1 induced by LPS, restoring the HO-1 activity and driving M2 phenotype in alveolar macrophages.

Objective: To analyze the Oxford classification (MESTC) and the International Study of Kidney Disease in Children (ISKDC) classification for evaluating the clinical manifestations, histological lesion and short-term prognosis of children with Henoch-Schönlein purpura nephritis (HSPN). Methods: According to the Oxford classification and ISKDC classification, the histological lesions of children with HSPN diagnosed by renal biopsy from Beijing Children's Hospital affiliated to Capital Medical University from January 2018 to December 2018 were re-evaluated. The renal biopsy specimens of the selected subjects were scored according to the Oxford classification and the ISKDC classification. According to whether the first symptom was combined with renal performance, MESTC score and ISKDC classification, children were grouped. The differences in clinicopathological manifestations between the groups were compared. Correlation between MESTC and ISKDC grades was analyzed by nonparametric test rank correlation. Kaplan-Meier survival curve and Log-rank test were used to compare the difference of proteinuria remission rate between the two groups. Univariate and multivariate Cox regression equations were used to analyze the influencing factors of the proteinuria remission rate. Results: A total of 78 children with HSPN were enrolled. There were 37 male patients (47.4%) with age of (10.4±2.9) years. When the patients were divided according to MESTC scores and ISKDC classification, the results showed that the proportion of children with nephrotic-range proteinuria in the group of endocapillary hypercellularity (E1, P=0.008), segmental glomerulosclerosis (S1, P=0.015) and ISKDCⅢ(P=0.041) was higher than that of E0, S0 and ISKDCⅡ groups. The proportion of children with E1 (P=0.015), crescents (C1&C2, P=0.025) or ISKDCⅢ(P=0.017) that had been treated with high-dose methylprednisolone was higher. The result of Kaplan-Meier survival curve showed more difficult for proteinuria remission in children with C2 are than C0&C1 group (P=0.026), while no difference were found when children were grouped by M, E, S, T and ISKDC. Multivariate Cox regression analysis showed that the C2 (HR=0.143, 95%CI 0.020-1.046, P=0.055) might be a risk factor for proteinuria remission, while the P value was close to 0.05. Conclusions Children with HSPN scored as ISKDCⅢ, E1 and S1 are more likely to show nephrotic-range proteinuria. C2 may indicate that patients are more difficult to achieve proteinuria remission.

Lycophytes and seed plants constitute the typical vascular plants. Lycophytes have been thought to have no paleo-polyploidization although the event is known to be critical for the fast expansion of seed plants. Here, genomic analyses including the homologous gene dot plot analysis detected multiple paleo-polyploidization events, with one occurring approximately 13-15 million years ago (MYA) and another about 125-142 MYA, during the evolution of the genome of Selaginella moellendorffii, a model lycophyte. In addition, comparative analysis of reconstructed ancestral genomes of lycophytes and angiosperms suggested that lycophytes were affected by more paleo-polyploidization events than seed plants. Results from the present genomic analyses indicate that paleo-polyploidization has contributed to the successful establishment of both lineages-lycophytes and seed plants-of vascular plants.
Evolution, Molecular ; Genome, Plant ; Genomics ; Phylogeny ; Polyploidy ; Selaginellaceae/genetics*