ABSTRACT
To report a case of imported furuncular cutaneous myiasis,and to analyze the sequence of the mitochondrial cytochrome C oxidase subunit Ⅰ (CO Ⅰ) gene of the pathogenic Cordylobia anthropophaga.A 33-year-old female patient had a travel history to Ghana and Cameroon in Africa 1 month prior to the presentation.No anti-mosquito measures were taken during her stay,and she hung up the laundries outside to dry for several times.Skin examination showed furuncular protuberances with diameters of 1-2 cm on the inner side of the left upper arm as well as on the outer side of the left chest,which were bright red and hard on palpation with irregular borders and a small hole on their central surface.Morphological identification revealed that the larva squeezed from the lesion was suspected as myiasis.After PCR amplification of the CO Ⅰ gene of the larva,an about 650-bp PCR product was acquired.Sequencing and BLAST analysis showed that this product was most closely related to the CO Ⅰ gene (GenBank accession number:FR719158.1) of Cordylobia anthropophaga isolated in Cameroon in 2010 with the sequence similarity being 99.84％,and they were grouped together on the phylogenetic tree.According to the clinical features and travel history of the patient and the sequencing results of the pathogenic Cordylobia anthropophaga,this case was confirmed as imported furuncular cutaneous myiasis caused by Cordylobia anthropophaga.
ABSTRACT
Objective To investigate the neuroprotective effect of miR-181c on hypoxia-preconditioned ischemia in rats and its mechanism.Methods Thirty-nine male SD rats were randomly divided into 5 groups of control group,sham-operated group,middle cerebral artery occlusion (MCAO)group,hypoxia-preconditioned group,hypoxia-preconditioned and MCAO group.Infarct volume and behavioral deficits were quantified.Real-time PCR was applied to detect the expression levels of miR-181c and Western blotting was used to verify the target protein of mt-cox1.Results Under the treatment of hypoxia-preconditioned,the neurological impairment was alleviated and the infarct volume was reduced significantly from 22.50％ ±2.96％ to 16.40％ ±3.13 ％ (t =5.26,P ＜0.01).The expression of miR-181c was decreased significantly in hypoxia-preconditioned and MCAO group than that in MCAO group (1.89 ± 0.14 vs 3.05 ± 0.26,t =6.10,P ＜ 0.01),and the expression of mt-cox1 protein was also significantly decreased (0.54 ± 0.07 vs 0.93 ± 0.04,t =8.01,P ＜ 0.01).Conclusion Hypoxia-preconditioned may attenuate the ischemic injury in SD rats,which may be related to the down-regulation of the expression of miR-181c,therefore increasing the expression of its targeted protein mt-cox1.
ABSTRACT
Objective To construct Cox7a2 fluorescent vector and study its effect on cytochrome C oxidase (COX) activity in mouse Sertoli cell line TM4. Methods The coding region of Cox7a2 was amplified from mouse Sertoli cell line TM4 by RT-PCR. The PCR product was inserted into pEYFP-C1 vector with BamH I and EcoR I restriction site, and confirmed by DNA sequencing. The recombinant fusion protein vector was amplified by transforming into DH5a and transfected into TM4 cells. The protein expression was identified by Western blot. COX activity was measured by spectrophotometer 6, 12, 24 and 48 h after the transfection of recombinant vector into the TM4 cell line. Results The entire coding sequence of Cox7a2 was cloned with 252 bp length. Plasmid pEYFP-C1-Cox7a2 vector was constructed and the positive clones were verified by restriction enzymes digestion and DNA sequencing. The transfection efficiency of the TM4 cell line was about 70% and 37000 D fusion protein was obtained. The COX activities were (0.642±0.051), (0.542±0.049), (0.311±0.021) and (0.216±0.010) U/mg 6, 12, 24 and 48 h after the transfection of recombinant vector in the TM4 cell line. Meanwhile, the COX activities were (0.714±0.064) and (0.653±0.031) U/mg in non-tranfected and naked vector group respectively. Compared with the non-tranfected group, COX activity decreased significantly 12, 24 and 48 h after the transfection. Conclusions The recombint plasmid vector was successfully constructed. Cox7a2 gene has an inhibiting effect on COX activity and may play an important role in the regulation of COX activity in mouse Sertoli cell line TM4.