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Tris (1,3-dichloro-2-propyl) phosphate (TDCIPP), widely applied as flame retardant into a variety of products, can be physically leached out to the aquatic environment. Measurable values of TDCIPP have been found in the environment and within biota. Many toxicological assessments have shown that TDCIPP could cause developmental toxicity and oxidative stress in fish. In this study, we focused on the effects of TDCIPP on the growth and oxidative stress of an important commercial fish species in China, silver carp (Hypophthalmichthys molitrix). Fish larvae was exposed to environmentally relevant concentrations (0.05, 0.5, 5 and 50 μg/L) of TDCIPP for 7, 14 and 28 days. Simultaneously, the transcription levels of genes associated with the growth hormone/insulin-like growth factor (GH/IGF) axis and the antioxidative enzymes were examined. The body length and body mass of silver carp larvae decreased significantly only under exposure to 5 and 50 μg/L of TDCIPP at 14 days compared with the control group, while differences on those paraments were observed at 0.05, 0.5, 5 and 50 μg/L when larvae were exposed for 28 days. The observation evidenced the time- and dose- dependent growth inhibitions caused by TDCIPP on silver carp larvae. Exposure to TDCIPP also decreased the contents of GH and IGF1 in fish attended by significant down-regulation of gh and igf1. Moreover, TDCIPP up-regulated the expression of cat, sod1 and gstt followed by an increase of the activities of catalase (CAT) and superoxide dismutase (SOD) and the levels of malondialdehyde (MDA) and glutathione (GSH), but the activities of glutathione peroxidase (GPX) were decreased. These results suggested that growth inhibition and oxidative stress co-occurred in silver carp larvae after exposure to environmentally relevant concentrations of TDCIPP accompanied by the abnormal expression of genes which associated with the GH/IGF axis and antioxidative enzymes.

N-isopropyl-N-phenyl-1,4-phenylenediamine (IPPD) is used as a ubiquitous antioxidant worldwide, it is an additive in tire rubber easily discharged into the surrounding environment. At present, there is no study concerning the subacute toxicity of IPPD on fish. We used zebrafish embryos (2 h post-fertilization) exposed to IPPD for 5 days at concentrations of 0, 0.0012, 0.0120 and 0.1200 mg/L to investigate its toxic effects of embryonic development, disruption of growth hormone/insulin-like growth factor (GH/IGF) and hypothalamic-pituitary-thyroid (HPT) axis. The results showed that IPPD exposure decreased hatchability, weakened movement ability, reduced body length, and caused multiple types of deformities in zebrafish embryos. The expression of genes involved to GH/IGF and HPT axis were altered after exposure to IPPD in zebrafish larvae. Meanwhile, exposure to IPPD significantly decreased thyroxine (T4) and 3,5,3'-triiodothyronine (T3) contents in larvae, which indicated that HPT axis was in a disturbed state. Moreover, treatment of IPPD decreased the enzymatic activities of superoxide dismutase (SOD) and catalase (CAT) as well as levels of glutathione (GSH). While the contents of malondialdehyde (MDA) were elevated after exposure to IPPD. The present study thus demonstrated that IPPD induced oxidative stress, caused developmental toxicity and disrupted the GH/IGF and HPT axis of zebrafish, which could be responsible for developmental impairment and growth inhibition.

Mercury (Hg) is a global environmental contaminant, and excessive mercury levels in water can adversely affect the growth of fish. Silver carp (Hypophthalmichthys molitrix) is one of the important freshwater aquaculture fish in China, and its natural resources have been critically declining. However, the effects of Hg

Blood‐brain barrier (BBB) disruption and neuronal apoptosis are important pathophysiological processes after traumatic brain injury (TBI). In clinical stroke, Dl‐3n‐butylphthalide (Dl‐NBP) has a neuroprotective effect with anti‐inflammatory, anti‐oxidative, anti‐apoptotic and mitochondrion‐protective functions. However, the effect and molecular mechanism of Dl‐NBP for TBI need to be further investigated. Here, we had used an animal model of TBI and SH‐SY5Y/human brain microvascular endothelial cells to explore it. We found that Dl‐NBP administration exerts a neuroprotective effect in TBI/OGD and BBB disorder, which up‐regulates the expression of tight junction proteins and promotes neuronal survival via inhibiting mitochondrial apoptosis. The expressions of autophagy‐related proteins, including ATG7, Beclin1 and LC3II, were significantly increased after TBI/OGD, and which were reversed by Dl‐NBP treatment both in vivo and in vitro. Moreover, rapamycin treatment had abolished the effect of Dl‐NBP for TBI recovery. Collectively, our current studies indicate that Dl‐NBP treatment improved locomotor functional recovery after TBI by inhibiting the activation of autophagy and consequently blocking the junction protein loss and neuronal apoptosis. Dl‐NBP, as an anti‐inflammatory and anti‐oxidative drug, may act as an effective strategy for TBI recovery.

Lead (Pb) widely exists in the water environment and has severe toxic effects on aquatic organisms. The yellow catfish (Pelteobagrus fulvidraco) is one of the most important commercial species in China, and moreover, its natural populations are declining with the degradation of environmental water quality. However, little is known about the toxic effects of Pb on its immune organs. This study was performed to determine waterborne Pb exposure on bioaccumulation, histomorphology, antioxidant status, apoptotic and immune response in the head kidney and spleen of yellow catfish. Experimental fish were randomly allocated into twelve tanks (3 tanks per group), and the Pb concentrations of the four groups were 0, 5, 50, and 500 μg/L, respectively. The results reflected that the Pb bioaccumulation of the head kidney and spleen increased with increasing Pb exposure dose and time. Severe histological alterations in the head kidney and spleen were observed at concentration 500 ug/L. With increasing Pb exposure concentrations, the plasma activity of superoxide dismutase (SOD) and catalase (CAT) significantly increased after exposure 7 days and 14 days, and the levels significantly decreased after exposure 28 days. The change trend of glutathione (GSH) levels was opposite to that of SOD and CAT at corresponding exposure time. The plasma malondialdehyde (MDA) levels together with the activities of plasma alkaline phosphatase (AKP) and acid phosphatase (ACP) increased significantly with the increasing Pb concentrations. In contrast, the levels of lysozyme (LYZ), complement 3 (C3) and immunoglobulin M (IgM) decreased significantly with increasing Pb concentrations. Moreover, Pb exposure induced transcriptional upregulation of heat shock protein 70 (hsp70), metallothionein (mt), sod, cat, interleukin-10 (il-10), transforming growth factor-β (tgf-β), and tumor necrosis factor-α (tnf-α), bcl-2-associated X protein (bax), and cysteinyl aspartate specific proteinase -9 (caspase-9), genes in the head kidney and spleen tissues, while downregulating the levels of the lyz, c3, igm and B-cell lymphoma-2 (bcl-2) genes. Our data provide evidence that Pb impaired immune function and tissue integrity in yellow catfish through oxidative stress, inflammatory and apoptosis, and the results can serve as reference data to better protect water environments from Pb eco-toxicants.

Perfluorooctane sulfonate (PFOS) is a persistent organic pollutant that has been widely detected in the environment and has caused growing international concern. The liver is the main target organ of PFOS exposure. Animal experiments have shown that PFOS exposure can increase the risk of liver tumorigenesis. However, whether PFOS can accelerate liver tumor progression is still unclear. In this study, transgenic zebrafish Tg(fabp10:rtTA2s-M2; TRE2:EGFP-KRAS

Traumatic brain injury (TBI) caused by an external mechanical force acting on the brain is a serious neurological condition. Inflammation plays an important role in prolonging secondary tissue injury after TBI, leading to neuronal cell death and dysfunction. Isoliquiritigenin (ILG) is a flavonoid monomer with anti-inflammatory characteristic. Thus, we had investigated the potential protective effects of ILG on TBI-induced injuries and identified the mechanisms underlying it. Here, we have demonstrated that ILG preserves blood brain barrier (BBB) integrity in vivo, suppresses the activation of microglia and inflammatory responses in mice after TBI, consequently leading to neurofunctional deficits, brain oedema, structural damage, and macrophage infiltration. In vitro, ILG exerts anti-inflammatory effect, and upregulates tight junction proteins 120‑β‑catenin and occludin in SH‑SY5Y cells under oxygen glucose deprivation/reoxygenation (OGD/D) condition. Additionally, we found that PI3K/AKT/GSK‑3β signalling pathway is involved in ILG treatment for TBI. To further confirm it, we had used SC79 (ethyl 2‑amino‑6‑chloro‑4‑(1‑cyano‑2‑ethoxy‑2‑oxoethyl)‑4H‑chromene‑3‑carboxylate), an Akt specific activator, to activate Akt, we found that SC79 partially reduces the protective effect of ILG for TBI. Overall, our current study reveals the neuroprotective role of ILG on TBI-induced BBB damage, downregulated tight junction proteins via PI3K/AKT/GSK‑3β signalling pathway. Furthermore, ILG suppresses the secretion of pro-inflammatory cytokines after TBI through inhibiting the PI3K/AKT/GSK‑3β/NF‑κB signalling pathway. Our findings suggest that GSK‑3β is a key regulatory factor during TBI-induced secretion of inflammatory cytokines, neuronal apoptosis and destruction of BBB.

Traumatic brain injury (TBI) is one of the most serious public health problems in the world. TBI causes neurological deficits by triggering secondary injuries. Hydrogen sulfide (H2S), a gaseous mediator, has been reported to exert neuroprotective effects in central nervous system diseases, such as TBI. However, the molecular mechanisms involved in this effect are still unclear. The present study was designed to explore the ability of NaHS, a H2S donor, to provide neuroprotection in a mouse model of TBI and to discover the associated molecular mechanisms of these protective effects. Here, we found that administration of NaHS not only maintained the integrity of the blood brain barrier (BBB), protected neurons from apoptosis, and promoted remyelination and axonal reparation but also protected mitochondrial function. In addition, we found that autophagy was inhibited after treatment with NaHS following TBI, an effect that was induced by activation of the PI3K/AKT/mTOR signalling pathway. Our study indicated that H2S treatment is beneficial for TBI, pointing to H2S as a potential therapeutic target for treating TBI.

Background/Aims: Basic fibroblast growth factor (bFGF) and nerve growth factor (NGF) are essential for proper development, survival, growth, and maintenance of neurons in the central and peripheral nervous systems. However, because bFGF and NGF have short half-life and rapid diffusion rate, they have limited clinical efficacy. Thus, there is an urgent need to develop an effective delivery system to protect bFGF and NGF from proteolysis while maintaining their normal bioactivities. Methods: To more efficiently deliver bFGF and NGF, we used a coacervate (synthesized with heparin and a biodegradable polycation at mass ratio of 500: 100). The maximal package loads of GFs in coacervate were determined by Western Blotting; release efficiency of bFGF and NGF was measured by ELISA. Additionally, we evaluated the effect of bFGF and NGF on the viability, survival, and proliferation of neurons by MTT assay, BrdU cell proliferation, and calcein staining. Results: Our coacervate incorporated bFGF and NGF and continuously released them for at least three weeks. This enhanced the growth and proliferation of PC12 cells and SH-SY5Y cells. Moreover, co-delivery of bFGF and NGF using coacervate was more neuroprotective than free application of both factors or coacervate delivery of each GF separately. Conclusions: Dual delivery of bFGF and NGF binding coacervate was neuroprotective via stimulating the growth and proliferation of neurons.

In recent years, the adverse effects of cadmium (Cd

The adverse effects of triphenyltin (TPT) on aquatic systems have attracted much attention because TPT is widely used and prevalent in aquatic environments. Here, zebrafish embryos/larvae were exposed to TPT (0, 0.039, 0.39, and 3.9 nM; 0, 15, 150 and 1500 ng/L) for 7 or 14 days to determine its toxic effects on the hypothalamic–pituitary–thyroid (HPT) axis. The results showed that whole-body total T4 and T3 levels were significantly decreased, which was accompanied by the significant upregulation of the expression of the dio1, dio2 and ugt1ab genes after exposure to TPT for 7 and 14 days. Genes related to thyroid hormone synthesis (crh, tshβ, nis, tpo and tg) were upregulated at both 7 and 14 days after TPT exposure. This might have been due to the positive feedback regulation of the HPT axis, which is caused by a decrease in thyroid hormone in the whole body in zebrafish. In addition, the survival rates and body lengths were reduced after treatment with TPT for 7 and 14 days. This indicated that TPT caused adverse effect on the development of zebrafish embryos/larvae. In summary, the results suggested that TPT caused thyroid disruption and developmental toxicity in zebrafish larvae.

In recent years, many studies have focused on autophagy, an evolutionarily conserved mechanism that relies on lysosomes to achieve cellular metabolic requirements and organelle turnover, and revealed its important role in animal models of traumatic injury. Autophagy is a double-edged sword. Appropriate levels of autophagy can promote the removal of abnormal proteins or damaged organelles, while hyperactivated autophagy can induce autophagic apoptosis. However, recent studies suggest that autophagic flux seems to be blocked after traumatic brain injury (TBI), which contributes to the apoptosis of brain cells. In this study, valproic acid (VPA), which was clinically used for epilepsy treatment, was used to treat TBI. The Morris water maze test, hematoxylin & eosin staining and Nissl staining were first conducted to confirm that VPA treatment had a therapeutic effect on mice after TBI. Western blotting, enzyme-linked immunosorbent assay and immunofluorescence staining were then performed to reveal that VPA treatment reversed TBI-induced blockade of autophagic flux, which was accompanied by a reduced inflammatory response. In addition, the variations in activation and phenotypic polarization of microglia were observed after VPA treatment. Nevertheless, the use of the autophagy inhibitor 3-methyladenine partially abolished VPA-induced neuroprotection and the regulation of microglial function after TBI, resulting in the deterioration of the central nervous system microenvironment and neurological function. Collectively, VPA treatment reversed the TBI-induced blockade of autophagic flux in the mouse brain cortex, subsequently inhibiting brain cell apoptosis and affecting microglial function to achieve the promotion of functional recovery in mice after TBI. Cover Image for this issue: doi: 10.1111/jnc.14755.

The South China tiger (Panthera tigris amoyensis) is endemic to China and also the most critically endangered subspecies of living tigers. It is considered extinct in the wild and only about 150 individuals survive in captivity to date, whose genetic heritage, however, is ambiguous and controversial. Here, we conducted an explicit genetic assessment of 92 studbook-registered South China tigers from 14 captive facilities using a subspecies-diagnostic system in the context of comparison with other voucher specimens to evaluate the genetic ancestry and level of distinctiveness of the last surviving P. t. amoyensis. Three mtDNA haplotypes were identified from South China tigers sampled in this study, including a unique P. t. amoyensis AMO1 haplotype not found in other subspecies, a COR1 haplotype that is widespread in Indochinese tigers (P. t. corbetti), and an ALT haplotype that is characteristic of Amur tigers (P. t. altaica). Bayesian STRUCTURE analysis and parentage verification confirmed the verified subspecies ancestry (VSA) as the South China tiger in 74 individuals. Genetic introgression from other tigers was detected in 18 tigers, and subsequent exclusion of these and their offspring from the breeding program is recommended. Both STRUCTURE clustering and microsatellite-based phylogenetic analyses demonstrated a close genetic association of the VSA South China tigers to Indochinese tigers, an issue that could only be elucidated by analysis of historical South China tiger specimens with wild origin. Our results also indicated a moderate level of genetic diversity in the captive South China tiger population, suggesting a potential for genetic restoration.

Spinal cord injury (SCI) induces the disruption of the blood-spinal cord barrier (BSCB) which leads to infiltration of blood cells, an inflammatory response, and neuronal cell death, resulting spinal cord secondary damage. Retinoic acid (RA) has a neuroprotective effect in both ischemic brain injury and SCI, however the relationship between BSCB disruption and RA in SCI is still unclear. In this study, we demonstrated that autophagy and ER stress are involved in the protective effect of RA on the BSCB. RA attenuated BSCB permeability and decreased the loss of tight junction (TJ) molecules such as P120, β-catenin, Occludin and Claudin5 after injury in vivo as well as in Brain Microvascular Endothelial Cells (BMECs). Moreover, RA administration improved functional recovery in the rat model of SCI. RA inhibited the expression of CHOP and caspase-12 by induction of autophagic flux. However, RA had no significant effect on protein expression of GRP78 and PDI. Furthermore, combining RA with the autophagy inhibitor chloroquine (CQ) partially abolished its protective effect on the BSCB via exacerbated ER stress and subsequent loss of tight junctions. Taken together, the neuroprotective role of RA in recovery from SCI is related to prevention of of BSCB disruption via the activation of autophagic flux and the inhibition of ER stress-induced cell apoptosis. These findings lay the groundwork for future translational studies of RA for CNS diseases, especially those related to BSCB disruption.

Objective:To investigate the expression pattern of resistin (RSTN) in skeletal muscle tissue and its influence on glycometabolism in rats with traumatic brain injury (TBI). Methods:Seventy-eight SD rats were randomly divided into traumatic group (n=36), RSTN group (n=36) and sham operation group (n=6). Fluid percussion TBI model was developed in traumatic and RSTN groups and the latter received additional 1 mg RSTN antibody treatment for each rat. At respectively 12 h, 24 h, 72 h, 1 w, 2 w, and 4 w after operation, venous blood was collected and the right hind leg skeletal muscle tissue was sampled. We used real-time PCR to determine mRNA expression of RSTN in skeletal muscles, western blot to determine RSTN protein expression and ELISA to assess serum insulin as well as fasting blood glucose (FBG) levels. Calculation of the quantitative insulin sensitivity check index (Q value) was also conducted. The above mentioned indicators and their correction were statistically analyzed. Results:Compared with sham operation group, the RSTN expression in the skeletal muscle as well as serum insulin and FBG levels revealed significant elevation (P

The blood-spinal cord barrier (BSCB) plays important roles in the recovery of spinal cord injury (SCI), and caveolin-1 is essential for the integrity and permeability of barriers. Basic fibroblast growth factor (bFGF) is an important neuroprotective protein and contributes to the survival of neuronal cells. This study was designed to investigate whether bFGF is beneficial for the maintenance of junction proteins and the integrity of the BSCB to identify the relations with caveolin-1 regulation. We examined the integrity of the BSCB with Evans blue dye and fluorescein isothiocyanate-dextran extravasation, measured the junction proteins and matrix metalloproteinases, and evaluated the locomotor function recovery. Our data indicated that bFGF treatment improved the recovery of BSCB and functional locomotion in contusive SCI model rats, reduced the expression and activation of matrix metalloproteinase-9, and increased the expressions of caveolin-1 and junction proteins, including occludin, claudin-5, p120-catenin, and β-catenin. In the brain, in microvascular endothelial cells, bFGF treatment increased the levels of junction proteins, caveolin-1 small interfering RNA abolished the protective effect of bFGF under oxygen-glucose deprivation conditions, and the expression of fibroblast growth factor receptor 1 and co-localization with caveolin-1 decreased significantly, which could not be reversed by bFGF treatment. These findings provide a novel mechanism underlying the beneficial effects of bFGF on the BSCB and recovery of SCI, especially the regulation of caveolin-1.

In order to investigate the mitochondrial genome of Panthera tigris amoyensis, two South China tigers (P25 and P27) were analyzed following 15 cymt-specific primer sets. The entire mtDNA sequence was found to be 16,957 bp and 17,001 bp long for P25 and P27 respectively, and this difference in length between P25 and P27 occurred in the number of tandem repeats in the RS-3 segment of the control region. The structural characteristics of complete P. t. amoyensis mitochondrial genomes were also highly similar to those of P. uncia. Additionally, the rate of point mutation was only 0.3% and a total of 59 variable sites between P25 and P27 were found. Out of the 59 variable sites, 6 were located in 6 different tRNA genes, 6 in the 2 rRNA genes, 7 in non-coding regions (one located between tRNA-Asn and tRNA-Tyr and six in the D-loop), and 40 in 10 protein-coding genes. COI held the largest amount of variable sites (9 sites) and Cytb contained the highest variable rate (0.7%) in the complete sequences. Moreover, out of the 40 variable sites located in 10 protein-coding genes, 12 sites were nonsynonymous.

Decellularization processes may variably distort or degrade extracellular matrix (ECM) structure. In this study, two perfusion routes (PR) were tested on SD rat lung samples. One decellularization protocol, PR1, was perfused through the pulmonary artery. The other decellularization protocol, PR2, was perfused through the trachea. Both decellularization protocols were used by the same detergent-based (sodium dodecyl sulphate and Triton X-100) with different flow continuous perfusion. There was no visible difference in vessel architecture between PR1- and PR2-decellularized scaffold. However, the airway structure and alveoli architecture of pulmonary decellularized scaffolds generated through PR2 at a flow rate of 8 mL/min were destroyed partly when compared to that in native lung and PR1-decellularized scaffold. Ultramicroscopic assessment of scaffolds was similar in both protocols and showed filamentous ECM with preserved fiber disposition and structure. Histological analysis and immunostaining showed no detectable cells remaining in the pulmonary scaffolds compare with native lung. The DNA concentration was significantly reduced in the decellularized scaffolds compared to the native lungs. A549 cells reseeded onto decellularized pulmonary scaffolds were no significant difference between PR1 and PR2 in cell viability, p0.05. We conclude that under the same high flow velocity status, perfusion decellularization through the pulmonary artery may be an optimal pathway to obtain decellularized scaffolds for pulmonary regeneration. This article is protected by copyright. All rights reserved. © 2016 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 104A: 2567-2575, 2016.

After spinal cord injury (SCI), disruption of blood–spinal cord barrier (BSCB) elicits blood cell infiltration such as neutrophils and macrophages, contributing to permanent neurological disability. Previous studies show that epidermal growth factor (EGF) produces potent neuroprotective effects in SCI models. However, little is known that whether EGF contributes to the integrity of BSCB. The present study is performed to explore the mechanism of BSCB permeability changes which are induced by EGF treatment after SCI in rats. In this study, we demonstrate that EGF administration inhibits the disruption of BSCB permeability and improves the locomotor activity in SCI model rats. Inhibition of the PI3K/Akt pathways by a specific inhibitor, LY294002, suppresses EGF‐induced Rac1 activation as well as tight junction (TJ) and adherens junction (AJ) expression. Furthermore, the protective effect of EGF on BSCB is related to the activation of Rac1 both in vivo and in vitro. Blockade of Rac1 activation with Rac1 siRNA downregulates EGF‐induced TJ and AJ proteins expression in endothelial cells. Taken together, our results indicate that EGF treatment preserves BSCB integrity and improves functional recovery after SCI via PI3K‐Akt‐Rac1 signalling pathway.

Many traumatic brain injury (TBI) survivors sustain neurological disability and cognitive impairments due to the lack of defined therapies to reduce TBI-induced blood-brain barrier (BBB) breakdown. Exogenous basic fibroblast growth factor (bFGF) has been shown to have neuroprotective function in brain injury. The present study therefore investigates the beneficial effects of bFGF on the BBB after TBI and the underlying mechanisms. In this study, we demonstrate that bFGF reduces neurofunctional deficits and preserves BBB integrity in a mouse model of TBI. bFGF suppresses RhoA and upregulates tight junction proteins, thereby mitigating BBB breakdown. In vitro, bFGF exerts a protective effect on BBB by upregulating tight junction proteins claudin-5, occludin, zonula occludens-1, p120-catenin, and β-catenin under oxygen glucose deprivation/reoxygenation (OGD) in human brain microvascular endothelial cells (HBMECs). Both the in vivo and in vitro effects are related to the activation of the downstream signaling pathway, PI3K/Akt/Rac-1. Inhibition of the PI3K/Akt or Rac-1 by specific inhibitors LY294002 or si-Rac-1, respectively, partially reduces the protective effect of bFGF on BBB integrity. Overall, our results indicate that the protective role of bFGF on BBB involves the regulation of tight junction proteins and RhoA in the TBI model and OGD-induced HBMECs injury, and that activation of the PI3K/Akt /Rac-1 signaling pathway underlies these effects.

Liobagrus kingi is endemic to southwest China and listed as endangered species (IUCN 2012). Genetic diversity is necessary for conservation issue. In studying this, the complete mitochondrial genome sequence of L. kingi has been obtained with PCR, which contains 13 protein-coding genes, 22 tRNA genes, 2 rRNA genes, and a non-coding control region with the total length of 16,483 bp. The gene arrangement and composition are similar to that of other vertebrates. Most of the genes are encoded on heavy strand, except for eight tRNA and ND6 genes. Just like most other vertebrates, the against bias of G has a universality in different statistical results. The complete mitochondrial genome sequence of L. kingi would contribute to better understand population genetics and protect its genetic diversity.

In the present study, the complete mitogenome sequence of Pseudolaubuca sinensis was determined using PCR amplificationand DNA sequencing, which contains 13 protein-coding genes, 22 tRNA genes, 2 rRNA genes, and a non-coding control region with the total length of 16,617 bp. Except for eight tRNA and ND6 genes, all other mitochondrial genes are encoded on the heavy strand. The codon usage followed the typical vertebrate mitochondrial pattern (ATG or GTG for start codon and TAA or TAG for stop codon). There are 6 regions of gene share totaling 22 bp and 14 intergenic spacer regions totaling 66 bp. The complete mitochondrial genome sequence is useful for phylogenetic analysis and studies of population genetics of Pseudolaubuca sinensis.

In this study, the complete mitochondrial genome of Sinobdella sinensis was reported. The circular genome is 16,540 bp in length and consists of 13 protein-coding genes, 22 tRNA genes, 2 ribosomal RNA genes, and 1 control region. The overall nucleotide composition was 30.0% A, 26.5% T, 28.7% C, and 14.8% G, with an A + T bias of 56.5%. The gene composition and the structural arrangement of the S. sinensis complete mtDNA were identical to most other vertebrates. The molecular data here we presented could play a useful role to study the evolutionary relationships and population genetics of Mastacembelidae fish.

In the present study, the complete mitogenome sequence of Gnathopogon imberbis is determined using PCR amplification and DNA sequencing, which contains 13 protein-coding genes, 22 tRNA genes, 2 rRNA genes and a non-coding control region with the total length of 16,598 bp. Except for eight tRNA and ND6 genes, all other mitochondrial genes are encoded on the H-strand. The codon usage followed the typical vertebrate mitochondrial pattern (ATG or GTG for start codon and TAA or TAG for stop codon). The overall nucleotide composition was 30.0% A, 27.0% T, 25.8% C and 17.2% G, with an A + T bias of 57.0%. The complete mitochondrial genome sequence will be useful for phylogenetic analysis and studies of population genetics of G. imberbis.

The complete mitogenome of an endemic fish in China flat-lip gudgeon, Platysmacheilus exiguous, was determined using the polymerase chain reaction and directly sequenced with the primer walking method. The whole mitogenome was 16,604 bp in length, consisting of 13 protein-coding genes, 22 transfer RNA (tRNA) genes, 2 ribosomal RNA (rRNA) genes and 1 control region. It had the typical circular molecule structure of vertebrate's mitogenome. The whole base composition was estimated to be 30.77%A, 26.06%T, 26.64%C and 16.53%G with AT bias of 56.83%. The complete mitogenome of P. exiguus provides the fundamental data for conservation genetics study on this species.

In this paper, we first determined the complete mitochondrial genome sequence of Squalidus argentatus, which was 16,607 bp in size and the whole base composition was estimated to be 30.48% A, 25.45% T, 27.36% C, 16.72% G with AT bias of 55.93%. The complete mitogenome comprised 13 protein-coding genes, 22 transfer RNA (tRNA) genes, 2 ribosomal RNA (rRNA) genes and 1 control region, with the gene order and content identical to other vertebrate mitogenomes. The complete mitogenome of S. argentatus provides the valuable information for population genetics and phylogeography studies on this species.

The study assessed the effects of surgically implanted dummy ultrasonic transmitters on physiological response of bighead carp Hypophthalmichthys nobilis in April 2011. Before the surgery, 15 blood samples were extracted randomly from 195 bighead carp samples, and then the rest of the fish were divided into three groups: (1) control group, handing but no tagging, (2) sham group, surgical procedure without implantation of transmitter and (3) surgery group, surgical implantation of transmitters. In 3 h, 24 h, 7 days and 14 days after surgery, 15 fish were extracted randomly from the three groups, respectively, for sampling. Then the plasma samples were analyzed, and physiological measures of stress response (cortisol, glucose), tissue damage [alanine aminotransferase (ALT) and aspartate aminotransferase (AST)] and nutritional status [total protein, globulin, albumin, triglyceride, cholesterol, and alkaline phosphatase (ALP)] were compared. The result showed that there was no significant difference between sham and surgery groups in 3 h, 24 h, 7 days and 14 days after surgery. When compared to the control group, there were significant increases in concentrations of plasma cortisol, glucose, ALT, AST, total protein and globulin of sham and surgery groups in 3 h after surgery. After 24 h, the levels of plasma cortisol, ALT, AST, total protein, globulin and ALP were elevated in both sham and surgery groups, whereas the levels of plasma glucose had declined to normal level and plasma albumin, cholesterol and triglyceride were significantly decreased in both sham and surgery groups. After 7 days, the levels of plasma glucose, albumin and cholesterol continued to decline, while the level of plasma ALT, globulin and ALP had declined but still remained higher for sham and surgery groups than control group; however, the plasma total protein level had returned to normal. After 14 days, there was no significant difference between the three groups. The above results showed that surgical implantation of ultrasonic transmitters had indeed caused significantly negative effects on the physiological response of bighead carp. However, all the negative influences on stress response, tissue damage and nutritional status had disappeared in 14 days after surgery, and the presence of transmitters had no significant negative impact. Therefore, the bighead carp should be temporary cultured at least 14 days for the recovery of physiological response and then released into the free water for the ultrasonic telemetry research.

Liobagrus nigricauda is endemic to the Yangtze River system (Ding 1994, The fishes of Sichuan province. pp. 470-78) and listed as an endangered species (IUCN 2012, Red list of threatened species. http://www.iucnredlist.org ). In this study, the complete mitochondrial genome sequence of L. nigricauda has been obtained with polymerase chain reaction (PCR), which contains 13 protein-coding genes, 22 tRNA genes, 2 rRNA genes, and a noncoding control region with the total length of 16,512 bp. The gene arrangement and composition are similar to that of other vertebrates. Most of the genes are encoded on heavy strand, except for eight tRNA and ND6 genes. Just like most other vertebrates, the bias against G has a universality in different statistics results. The mitogenome sequence of L. nigricauda would contribute to better understand population genetics and to protect its genetic diversity.

The past decade has seen increased international recognition of the importance of the services provided by natural ecosystems. It is unclear however whether such international awareness will lead to improved environmental management in many regions. We explore this issue by examining the specific case of fish migration and dams on the Mekong river. We determine that dams on the Mekong mainstem and major tributaries will have a major impact on the basin’s fisheries and the people who depend upon them for food and income. We find no evidence that current moves towards dam construction will stop, and consider two scenarios for the future of the fisheries and other ecosystems of the basin. We conclude that major investment is required in innovative technology to reduce the loss of ecosystem services, and alternative livelihood strategies to cope with the losses that do occur.

Astrocytes have critical roles in immune defense, homeostasis, metabolism, and synaptic remodeling and function in the central nervous system (CNS); however, excessive activation of astrocytes with increased intermediate filaments following neuronal trauma, infection, ischemia, stroke, and neurodegenerative diseases results in a pro-inflammatory environment and promotes neuronal death. As an important neurotrophic factor, the secretion of endogenous basic fibroblast growth factor (bFGF) contributes to the protective effect of neuronal cells, but the mechanism of bFGF in reactive astrogliosis is still unclear. In this study, we demonstrated that exogenous bFGF attenuated astrocyte activation by reducing the expression of glial fibrillary acidic protein (GFAP) and other markers, including neurocan and vimentin, but not nestin and decreased the levels of pro-inflammatory cytokines, such as interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α), via the regulation of the upstream toll-like receptor 4/nuclear factor κB (TLR4/NFκB) signaling pathway. Our study suggests that the function of bFGF is not only related to the neuroprotective and neurotrophic effect but also involved in the inhibition of excessive astrogliosis and glial scarring after neuronal injury.

In this study, the complete mitochondrial genome sequence of the Leptobotia rubrilaris has been obtained. The genome includes 13 protein-coding genes, 22 tRNA genes, 2 rRNA genes and a non-coding control region with the total length of 16,585 bp. The gene arrangement and composition were identical to other vertebrate. Most of the genes are encoded on heavy strand, except for eight tRNA and ND6 genes. The complete mitochondrial genome sequence of L. rubrilaris would contribute to better understand population genetics and protect its genetic diversity.

The smallscale yellowfin, Plagiognathops microlepis is the only one species in the genus Plagiognathops. In this study, we sequenced the complete mitochondrial genome of the P. microlepis. The complete mitogenome was 16,623 bp in size, consisting of 13 protein-coding genes, 22 transfer RNA (tRNA) genes, 2 ribosomal RNA (rRNA) genes, and 1 control region. It has the typical circular molecule structure of vertebrate’s mitochondrial genome. The whole base composition was estimated to be 30.60% A, 25.19% T, 27.32% C and 16.89% G with AT bias of 55.79%. The complete mitogenome of P. microlepis provides the basis for preservation of genetic resources and genetic breeding studies on this species.

The Leptobotia microphthalma belongs to family Cobitidae, which is endemic to the upper reaches of the Yangtze River in China. In this studying, the complete mitochondrial genome sequence of L. microphthalma has been obtained with PCR, which contains 13 protein-coding genes, 22 tRNA genes, 2 rRNA genes and a non-coding control region with the total length of 16,512 bp. The gene arrangement and composition are similar to that of other vertebrates. Most of the genes are encoded on heavy strand, except for eight tRNA and ND6 genes. The complete mitochondrial genome sequence of L. microphthalma would contribute to better understand population genetics and protect its genetic diversity.