Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 3 de 3
Filtrar
Adicionar filtros








Intervalo de ano
1.
Chinese Journal of Immunology ; (12): 882-886,891, 2018.
Artigo em Chinês | WPRIM | ID: wpr-702836

RESUMO

Objective:To obtain recombinant D227A mutation Staphylococcal enterotoxin A protein(rSEAD227A) with low toxicity but still retain its immunological activity and high purity. Methods: The SEA gene containing D227A mutation was cloned by PCR. By constructing pET44a-SEAD227Avector and transfecting the expression strain Rosetta, inclusion bodies were solubilized with guanidium hydrochloride and refolded by gradient dialysis;proteins were purified using StrepⅡ affinity chromatography,and identified by Western blot and high performance liquid chromatography-mass spectrometry(LC-MS/MS). Results: The D227A mutation of SEA was cloned and the expression system of Rosetta-rSEAD227Awas constructed. The purified rSEAD227Aprotein was obtained by refolding with gradient dialysis and affinity purification. LC-MS/MS analysis confirmed that the tryptic digested rSEAD227A peptide sequences matched the sequences of SEA in the database. Conclusion: The rSEAD227A protein in high purity was obtained,which provided the ex-perimental basis for further basic research and clinical application of SEA.

2.
Chinese Medical Journal ; (24): 1867-1871, 2009.
Artigo em Inglês | WPRIM | ID: wpr-240780

RESUMO

<p><b>BACKGROUND</b>ADULT syndrome (acro-dermato-ungual-lacrimal-tooth syndrome) is a rare ectodermal dysplasia disorder known as autosomal dominant inheritance. Recent studies have linked p63 gene mutation to the development of this disease. However, the genetic characteristics of ADULT syndrome were still not well understood.</p><p><b>METHODS</b>Mutation analysis of p63 gene in the first Chinese ADULT syndrome family was performed using direct DNA sequencing.</p><p><b>RESULTS</b>The sequence analysis of exon 8 of p63 gene disclosed a heterozygous G>A substitution at nucleotide 893 (R298Q) in the proband. In addition, a single nucleotide polymorphism (SNP) rs16864880 in the downstream flanking region (DFR) of p63 exon 8 was also identified in this family. The proband and the paternal side including her father exhibited the C/G genotype at this position. The C/G variant frequency in the paternal was significantly higher as compared with the maternal (6/10 vs 0/6, P = 0.034).</p><p><b>CONCLUSIONS</b>ADULT syndrome may be caused by the p63 gene mutation, and it might have closer genetic association with the paternal side in this family.</p>


Assuntos
Adulto , Feminino , Humanos , Masculino , Povo Asiático , Genética , Análise Mutacional de DNA , Displasia Ectodérmica , Genética , Predisposição Genética para Doença , Modelos Moleculares , Mutação , Genética , Linhagem , Estrutura Terciária de Proteína , Transativadores , Química , Genética , Fatores de Transcrição , Proteínas Supressoras de Tumor , Química , Genética
3.
Chinese Journal of Otorhinolaryngology Head and Neck Surgery ; (12): 830-834, 2008.
Artigo em Chinês | WPRIM | ID: wpr-339258

RESUMO

<p><b>OBJECTIVE</b>To explore the establishment of the mimetic aging effect in guinea pigs induced by D-galactose, and to detect the biological indicatrix associated with hearing loss and provide a new tool for molecular pathogenesis of hearing loss.</p><p><b>METHODS</b>Total of 51 guinea pigs were randomly divided into three groups: group A (model aging group, n = 25), which were injected with D-galactose (200 mgxkg(-1)xd(-1)) by intra peritoneum for 6 weeks, group B (model control group, n = 18), which were given the same amount of saline only, and group C (vacant group, n = 15) were not treated. Then, The guinea pigs in group A and B were exposed in noise for 8 days, 8 hours once a day. Auditory brainstem response (ABR) was used to test the hearing threshold of guinea pigs thrice, first before the drug administered, then after 6 weeks the drug used, third after noise exposure. And colorimetry was used to analyze the activity of superoxide dismutase (SOD) and malon dialdehyde (MDA) in brain and liver tissue. The DNA of inner ear tissue was harvested and amplified fragment length polymorphism (AFLP) was used to detect the differential polymorphic markers.</p><p><b>RESULTS</b>After injection, there was no significant difference in elevation of ABR threshold between the group A and group B (t = 1.14, P > 0.05). However, exposure of noise later, elevation in ABR threshold of (22.97 +/- 10.56) dB peSPL was observed in group A, and (14.16 +/- 7.36) dB peSPL in group B. The was significant difference in variation of hearing threshold between group A and group B (t = 2.78, P < 0.05). The activity of SOD in brain and liver tissue in group A was lower than that in group B. the level of MDA was opposite between group A and group B. The difference between group A and group B was significant (P < 0.01). A differential polymorphic marker was observed by AFLP.</p><p><b>CONCLUSIONS</b>The mimetic aging effect of the guinea pigs can be induced by D-galactose, and this model can not directly induce the hearing loss. The differential polymorphic marker possibly act as a predisposing factor which can greatly enhance the sensitivity of the ear to the noise.</p>


Assuntos
Animais , Feminino , Masculino , Envelhecimento , Análise do Polimorfismo de Comprimento de Fragmentos Amplificados , Limiar Auditivo , Modelos Animais de Doenças , Potenciais Evocados Auditivos do Tronco Encefálico , Galactose , Farmacologia , Cobaias , Presbiacusia
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA