We review the cicada genus Auritibicen Lee, 2015 based on the description of ten new species: A. aethus sp. n., A. daoxianensis sp. n., A. pallidus sp. n., A. rotundus sp. n., A. curvatus sp. n., A. purus sp. n., A. parvus sp. n., A. gracilis sp. n., A. septatus sp. n. and A. lijiangensis sp. n. Auritibicen shikokuanus (Kato, 1959) is confirmed to be a synonym of Auritibicen kyushyuensis (Kato, 1926). Diagnoses and descriptions, along with illustrations of the structure of male genitalia, are provided for all Auritibicen species. The systematics of Auritibicen is elucidated using both morphological and molecular characterization. Thirty-five morphological characters of the 24 species of Auritibicen and one outgroup taxon, Chremistica ochracea (Walker, 1850), were scored. Morphological phylogenetic analyses reveal the relationships among related species of Auritibicen, which are supported by a number of morphological characters. The mitochondrial gene fragments of Cytochrome Oxidase I (COI) of 11 species of Auritibicen and two outgroup Lyristes species were analyzed and yielded identical robust phylogenetic trees. The phylogram based on a Bayesian analysis of both morphological and molecular data is similar to the ML/BI topologies based only on the molecular data. The molecular phylogenetic analysis indicates that species of Auritibicen are structured phylogeographically, with related species clustered into three lineages. The divergence time estimated based on molecular data indicates that the divergence of Auritibicen from Lyristes occurred during the Miocene, and the most recent common ancestor (tMRCA) of Auritibicen evolved during the Pliocene. However, the time when the main divergence events of species of Auritibicen occurred was the Pleistocene. From the combination of the phylogeny and updated geographical distributions, we infer that the center of distribution of Auritibicen could be Southwest China (e.g., Sichuan and Yunnan Provinces), from where species of this genus spreaded northeastwards to Shaanxi, Hubei and other provinces along the Qinling and Daba Mountains, then further northeastwards to Hebei Province in China and also to Far East Russia, the Korean Penisula, and Japan.
Ulinastatin [or called as urinary trypsin inhibitor (UTI)] plays a role in regulating neurological deficits evoked by transient cerebral ischemia. However, the underlying mechanisms still need to be determined. The present study was to examine the effects of UTI on autophagy, Nrf2-ARE and apoptosis signal pathway in the hippocampus in the process of neurological functions after cerebral ischemia using a rat model of cardiac arrest (CA). CA was induced by asphyxia followed by cardiopulmonary resuscitation (CPR) in rats. Western blot analysis was employed to determine the expression of representative autophagy (namely, Atg5, LC3, Beclin 1), p62 protein (a maker of autophagic flux), and Nrf2-ARE pathways. Neuronal apoptosis was assessed by determining expression levels of Caspase-3 and Caspase-9, and by examining terminal deoxynucleotide transferase-mediated dUTP nick-end labeling (TUNEL). The modified neurological severity score (mNSS) and spatial working memory performance were used to assess neurological deficiencies in CA rats. Our results show that CA amplified autophagy and apoptotic Caspase-3/Caspase-9, and downregulated Nrf2-ARE pathway in the hippocampus CA1 region. Systemic administration of UTI attenuated autophagy and apoptosis, and largely restored Nrf2-ARE signal pathway following cerebral ischemia and thereby alleviated neurological deficits with increasing survival of CA rats. Our data suggest that UTI improves the worsened protein expression of autophagy and apoptosis, and restores Nrf2-ARE signals in the hippocampus and this is linked to inhibition of neurological deficiencies in transient cerebral ischemia. UTI plays a beneficial role in modulating neurological deficits induced by transient cerebral ischemia via central autophagy, apoptosis and Nrf2-ARE mechanisms., Xiao-Ming Jiang, Jing-Hai Hu, Lu-Lu Wang, Chi Ma, Xu Wang, Xiao-Liang Liu., and Obsahuje bibliografii