RESUMO
The complete mitochondrial genome (mitogenome) of Bullanga florida (Neuroptera: Myrmeleontidae) was determined. The entire sequence is 15,937 bp in length which contains 13 protein-coding genes (PCGs), 22 tRNAs, two rRNAs and one non-coding AT-rich region. The overall A + T content of mitogenome is 73.3%. The gene order and arrangement are similar to other Neuroptera mitogenomes. Thirteen PCGs start with standard ATN initiation codons and stop with termination codons TAA or T. All tRNA genes have a typical clover-leaf secondary structure except for tRNASer (AGN), whose dihydrouridine (DHU) arm do not form a stable stem-loop structure. Two rRNA genes (rrnL and rrnS) are 1325 bp and 776 bp in size, respectively. The phylogenetic analysis is based on the amino acid sequences of 13 PCGs indicates that B. florida is a sister group to Epacanthaclisis banks, and Myrmeleontiformia is the monophyletic group.
RESUMO
The complete mitochondrial genome of Pycnarmon lactiferalis (Walker, 1859) has been determined. The entire sequence is 15,219 bp in length which contains 13 protein-coding genes (PCGs), 22 transfer RNA genes, two ribosomal RNA genes, and an A + T-rich region. All PCGs start with the typical ATN codon except for COI with CGA. TAA is used for all the PCGs, while the COI, COII and ND5 possess incomplete termination codons T or TA. The secondary structure of 22 tRNAs have the typical clover-leaf pattern except for tRNASer(AGN) lacking the dihydrouridine (DHU) stem. The A + T-rich region, located between the srRNA and tRNAMet , do not contain the motif "ATAGA" that is conserved across other lepidopteran species mitogenomes. A phylogenetic relationship of Pyraloidea has been reconstructed based on 13 PCGs data using Bayesian inference (BI) method.
RESUMO
OBJECTIVE: To understand how aquaporin4 (AQP4) and dystroglycan (DG) polarized distribution change and their roles in brain edema formation after traumatic brain injury (TBI). METHODS: Brain water content, Evans blue detection, real-time PCR, western blot, and immunofluorescence were used. RESULTS: At an early stage of TBI, AQP4 and DG maintained vessel-like pattern in perivascular endfeet; M1, M23, and M1/M23 were increased in the core lesion. At a later stage of TBI, DG expression was lost in perivascular area, accompanied with similar but delayed change of AQP4 expression; expression of M1, M23, and DG and the ratio of M1/M2 were increased. CONCLUSION: At an early stage, AQP4 and DG maintained the polarized distribution. Upregulated M1 and M23 could retard the cytotoxic edema formation. At a later stage AQP4 and DG polarized expression were lost from perivascular endfeet and induced the worst cytotoxic brain edema. The alteration of DG expression could regulate that of AQP4 expression after TBI.
