DNA Barcode Identification of Fish Products from Guiyang Markets in Southwestern People's Republic of China.

ABSTRACT: Global fish consumption is increasing in tandem with population growth, resulting in the dilemma of overfishing. Overfished high-value fish are often replaced with other fish in markets. Therefore, the accurate identification of fish products in the market is important. In this study, full-DNA and mini-DNA barcoding were used to detect fish product fraud in Guiyang, Guizhou Province, People's Republic of China. The molecular results revealed that 39 (20.42%) of the 191 samples were inconsistent with the labels. The percentages of mislabeling of fresh, frozen, cooked, and canned fish products were 11.70, 20.00, 34.09, and 50.00%, respectively. The average Kimura two-parameter distances of mini-DNA barcoding within species and within genera were 0.56 and 6.42%, respectively, and those of full-DNA barcoding were 0.53 and 7.25%, respectively. Commercial fraud was evident in this study; most high-priced fish were replaced with low-priced fish with similar features. Our findings indicate that DNA barcoding is an effective tool for identifying fish products and could be used to enhance transparency and fair trade in domestic fisheries.

Down-regulation of microRNA-216a confers protection against yttrium aluminium garnet laser-induced retinal injury via the GDNF-mediated GDNF/GFRα1/RET signalling pathway.

Retinal injury plays a leading role in the onset of visual impairment. Current forms of treatment are not able to ameliorate scarring, cell death and tissue and axon regeneration. Recently, microRNA-216a (miR-216a) has been reported to regulate snx5, a novel notch signalling pathway component during retinal development. This study aims to elucidate the role of miR-216a in yttrium aluminium garnet (YAG) laser-induced retinal injury by targeting glial cell line-derived neurotrophic factor (GDNF) via GDNF/GDNF family neurotrophic factor receptor α1 (GFRα1)/rearranged during transfection (RET) signalling pathway. Wistar male rats were first randomly assigned into control and model groups. Immunohistochemistry was performed to detect the GDNF positive expression rate and terminal deoxynucleotidyl transferase-mediated dUTP nick end labelling (TUNEL) staining for apoptotic index (AI) of retinal tissue. Retinal neurons were divided into normal, blank, negative control (NC), miR-216a mimic, miR-216a inhibitor, siRNA-GDNF and miR-216a inhibitor?siRNA-GDNF groups. Dual luciferase reporter assay was conducted in order to identify the targeting relationship between GDNF and miR-216a. Reverse transcription quantitative polymerase chain reaction (RT-qPCR) and western blot were used for the analysis of mRNA and protein levels of miR-216a and related genes. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay was used to determine cell proliferation and flow cytometry was used to observe cell cycle and apoptosis. Results show that the model group had an increased GDNF positive rate, AI of retinal tissue and mRNA and protein levels of cellular oncogene fos (c-fos), vascular endothelial growth factor (VEGF), brain-derived neurotrophic factor (BDNF), GDNF, GFRα1 and bcl-2-associated X protein (bax), declined miR-216a level and mRNA and protein levels of RET and bcl-2 compared with the control group. GDNF was verified as the target gene for miR-216a. Compared with the blank and NC groups, the miR-216a mimic and siRNA-GDNF groups had higher mRNA and protein levels of c-fos, VEGF and bax, cell number in the G1 phase and increased cell apoptosis but reduced BDNF, GDNF, GFRα1, RET and bcl-2 expression, cell proliferation and cell numbers in the S phase, while the opposite trend was observed in the miR-216a inhibitor group. Taken together, our findings demonstrate that elevated GDNF levels can reduce the retinal injury, whereby down-regulated miR-216a aggravates the YAG laser-induced retinal injury by targeting the GDNF level through the GDNF/ GFRα1/RET signalling pathway.

Calcitonin gene-related peptide protects rats from cerebral ischemia/reperfusion injury via a mechanism of action in the MAPK pathway.

The aim of the present study was to investigate the protective function and underlying mechanism of calcitonin gene-related peptide (CGRP) on cerebral ischemia/reperfusion damage in rats. Adult male Wistar rats were selected for the establishment of an ischemia/reperfusion injury model through the application of a middle cerebral artery occlusion. Animals were randomly divided into 6 groups of 24 animals. Drugs were administered according to the design of each group; animals were administered CGRP, CGRP8-37, PD98059 and SB20358. The neurobehavioral scores of the rat cerebral ischemia model in each group were calculated. The infarction range of the rat brain tissues was observed by 2,3,5-triphenyltetrazolium chloride staining. The expression levels of three proteins, phosphorylated c-Jun N-terminal kinase (JNK)/JNK, phosphorylated extracellular signal-regulated protein kinase (ERK)/ERK and p-p38/p38, in the mitogen-activated protein kinase (MAPK) pathway in the brain tissues was detected by western blotting. The results showed that CGRP could improve the neurobehavioral function of the ischemic rats and reduce the infarction range. Western blotting results confirmed that the function of the CGRP was mediated mainly through the reduction of the JNK and p38 phosphorylation and the promotion of ERK phosphorylation. Therefore, the present study confirmed that an increase in the exogenous CRGP could effectively improve ischemia/reperfusion injury of the brain tissue. The mechanisms of action were achieved through a reduction in JNK and p38 phosphorylation and an increase in ERL phosphorylation in the MAPK pathway. These mechanisms were interdependent.

Trigeminal neuralgia caused by brain arteriovenous malformations: A case report and literature review.

Few cases of trigeminal neuralgia (TGN) induced by brain arteriovenous malformations (bAVMs) have previously been reported. The present case report described one case of TGN caused by bAVMs in a 32-year-old male patient who suffered from recurrent pain in his right cheek for a period of two years, for whom the seizure frequency and duration of pain increased for 6 months. Magnetic resonance imaging was performed, which demonstrated flow-void signals in the abnormal vessels in the right cerebellopontine angle. Subsequent digital subtraction angiography confirmed the diagnosis of bAVMs, and showed the nidus was fed by the right superior cerebellar and the right anterior inferior cerebellar, and drained into the adjacent venous sinuses on the same side. The patient underwent an interventional embolization treatment. TGN was completely relieved following embolization of the majority of the bAVMs. Pain relief may be associated with blocking of the pulsatile compression of the feeding arteries of the bAVMs, the arterialized draining veins or the malformed niduses following embolization, which is similar to the effects induced by microvascular decompression surgery of the trigeminal nerve. In the present case study and review, the underlying mechanism and treatment strategy of TGN caused by bAVMs were discussed in the context of present case, and a literature review was carried out.

Experimental study of temperature-sensitive chitosan/ß-glycerophosphate embolic material in embolizing the basicranial rete mirabile in swines.

The aim of the present study was to evaluate the feasibility of the non-adhesive temperature-sensitive liquid embolic material, chitosan/ß-glycerophosphate (C/GP), in embolizing the basicranial rete mirabile (REM) in a swine model of cerebral arteriovenous malformation (cAVM). A total of 24 domestic swines were used as the experimental animals, among which 12 pigs underwent direct embolization of one side of the REM, while the other 12 pigs underwent embolization of the bilateral REM following anastomosis of the carotid artery and jugular vein. A super-selective microcatheter was introduced into the REM during the embolization procedure, and the C/GP hydrogel was injected until an image of the REM disappeared in the angiography examination. Further angiography examinations were performed after 2 and 6 weeks, and histological examination of the REM was performed after 6 weeks. Of the 24 domestic swines, 23 cases underwent successful thrombosis. Convulsions occurred in one case and that pig died during the embolization procedure. Following embolization, the angiography observations revealed that the embolized REM was no longer able to be developed, and adhesion of the microcatheter tip with the embolic agent did not occur. In addition, no apparent revascularization was observed in the angiography examinations performed at weeks 2 and 6. Therefore, the current preliminary study indicated that use of the non-adhesive temperature-sensitive embolic material was feasible for the embolization of cAVM; thus, C/GP may be used as an ideal embolic material for the treatment of cAVM.