3DPhenoFish: Application for two- and three-dimensional fish morphological phenotype extraction from point cloud analysis.

Fish morphological phenotypes are important resources in artificial breeding, functional gene mapping, and population-based studies in aquaculture and ecology. Traditional morphological measurement of phenotypes is rather expensive in terms of time and labor. More importantly, manual measurement is highly dependent on operational experience, which can lead to subjective phenotyping results. Here, we developed 3DPhenoFish software to extract fish morphological phenotypes from three-dimensional (3D) point cloud data. Algorithms for background elimination, coordinate normalization, image segmentation, key point recognition, and phenotype extraction were developed and integrated into an intuitive user interface. Furthermore, 18 key points and traditional 2D morphological traits, along with 3D phenotypes, including area and volume, can be automatically obtained in a visualized manner. Intuitive fine-tuning of key points and customized definitions of phenotypes are also allowed in the software. Using 3DPhenoFish, we performed high-throughput phenotyping for four endemic Schizothoracinae species, including Schizopygopsis younghusbandi, Oxygymnocypris stewartii, Ptychobarbus dipogon, and Schizothorax oconnori. Results indicated that the morphological phenotypes from 3DPhenoFish exhibited high linear correlation (>0.94) with manual measurements and offered informative traits to discriminate samples of different species and even for different populations of the same species. In summary, we developed an efficient, accurate, and customizable tool, 3DPhenoFish, to extract morphological phenotypes from point cloud data, which should help overcome traditional challenges in manual measurements. 3DPhenoFish can be used for research on morphological phenotypes in fish, including functional gene mapping, artificial selection, and conservation studies. 3DPhenoFish is an open-source software and can be downloaded for free at https://github.com/lyh24k/3DPhenoFish/tree/master.

Serum lncRNA LOXL1-AS1 is a diagnostic and prognostic marker for epithelial ovarian cancer.

BACKGROUND: The present study aimed to examine the levels of circulating LOXL1-AS1 in epithelial ovarian cancer (EOC) patients and to analyze its diagnostic and prognostic value. METHODS: The levels of LOXL1-AS1 in 185 EOC patients and 43 healthy volunteers were evaluated by a quantitative reverse transcriptase-polymerase chain reaction. The potential of LOXL1-AS1 as a biomarker for EOC diagnosis was determined by receiver-operating characteristic (ROC) curve assays. The associations between clinicopathological parameters and LOXL1-AS1 expression were analyzed using a chi-squared test. The influence of LOXL1-AS1 on overall survival was analyzed by the use of Kaplan-Meier. A Cox proportional hazards assays were conducted for the determination of the prognostic value of LOXL1-AS1. RESULTS: The expression of LOXL1-AS1 was dramatically higher in EOC patients compared to healthy controls (p < 0.01). LOXL1-AS1 yielded an area under the ROC curve of 0.843 with 65.3% sensitivity and 68.2% specificity in discriminating high-grade EOC from healthy controls. It was also shown that LOXL1-AS1 expression was associated with advanced FIGO stage (p = 0.004) and positively distant metastasis (p = 0.013). Kaplan-Meier assays revealed that patients with high LOXL1-AS1 expression had a shorter overall survival than those with low expression (p = 0.0006). By performing multivariate assays, LOXL1-AS1 was confirmed to be an independent prognostic factor for predicting the prognosis of EOC patients. CONCLUSIONS: We provide evidence indicating that LOXL1-AS1 expression is correlated with a poor clinical outcome in EOC patients and may act as an independent prognostic indicator, as well as a new diagnostic biomarker.

Sandwich-Type Polyoxotungstate Consisting of Two Different Trilacunary Keggin-Type Units.

A unique mixed W/Sb/Mn/Ag sandwich-type metal-O cluster was isolated, in which the six-membered {Ag4O3[Mn(OH2)]2}2+ cationic belt is sandwiched between two different anionic slices: the trilacunary B-ß-[SbW9O33]9- and the central-atom-lost A-α-{[Mn(OH2)]2W7O32}18-.

Protective effects of BAY 73-6691, a selective inhibitor of phosphodiesterase 9, on amyloid-ß peptides-induced oxidative stress in in-vivo and in-vitro models of Alzheimer's disease.

Alzheimer's disease (AD) is accompanied by enhanced oxidative stress and excess free radicals. Phosphodiesterase 9 inhibitors (PDE-9Is) showed memory improving effects in many pharmacological deficit models. However, whether BAY 73-6691 (a selective PDE-9I) may attenuate the oxidative stress during the development of AD is still unclear. For this purpose, primary cultures of SH-SY5Y cells were incubated with 20µM beta-amyloid25-35 (Aß25-35), followed by exposure to different concentrations (50, 100, 150 and 200µg/ml) of BAY 73-6691. Furthermore, the antioxidant effect of BAY 73-6691 was evaluated in mice subjected to intracerebroventricular injection of Aß25-35 (day 0) and treatment with BAY 73-6691 by intraperitoneal injection once daily (days 1-10). Our results elucidated that treatment with BAY 73-6691 attenuated the Aß25-35-induced cytotoxicity and oxidative stress in SH-SY5Y cells. In vivo, BAY 73-6691 protected Aß25-35-induced oxidative damage in hippocampus, associated with the attenuation of impairments in hippocampal neurons. Administration of BAY 73-6691 improved learning and memory in the Morris water maze test, and restored several hippocampal memory-associated proteins. Our study identified a neuroprotective role for BAY 73-6691 against Aß25-35-induced oxidative stress in vivo and in vitro, harboring therapeutic potential for the treatment of AD by alleviating the impairments in spatial memory and hippocampal neurons.

In vivo protective effects of urocortin on ischemia-reperfusion injury in rat heart via free radical mechanisms.

The aim of this study was to investigate the effects of urocortin (UCN) on oxidative stress and the mechanisms of urocortin on ischemia-reperfusion injury in vivo in the rat model. Thirty-six Sprague-Dawley rats were divided into 6 groups, including sham, control (normal saline solution), UCN1, UCN2, UCN3, and verapamil groups. The left anterior descending coronary artery of all rats except those in the sham group was treated with a 30-min occlusion followed by a 60-min reperfusion. Just before the occlusion, normal saline solution, UCN (5, 10, and 20 microg/kg body mass), or verapamil (1 mg/kg body mass) was administered. Heart rates, beating rhythm, and S-T segments were constantly monitored using an ECG. At the completion of the drug administration, blood samples were taken to measure the activity of superoxide dismutase (SOD), malonaldehyde (MDA), glutathione peroxidase (GSH-PX), and nitric oxide (NO) to evaluate the effects of UCN on oxidative stress. Finally, the size of infarction was measured. Arrhythmia rates were significantly lower, and the infarction size was significantly smaller (p < 0.01), in the UCN groups vs. the control group. Verapamil also significantly reduced arrhythmia rates and infarction size. The MDA activities were remarkably diminished, whereas the SOD, GSH-PX, and NO activities were significantly higher in the UCN and VER groups (p < 0.01). MDA, SOD, and NO activities were strongly correlated with UCN doses. These results suggest that UCN may play a protective role in ischemia-reperfusion injury in rat hearts against the oxidative stress by inhibiting free radicals' activities.

Effects of SNP, GLU and GABA on the neuronal activity of striatum nucleus in rats.

This study investigated the activity of nitric oxide (NO) in the striatum (STR) for a further comprehension of the pathogenesis of Parkinson's disease (PD). Microiontophoresis was used to observe the effects of sodium nitroprusside (SNP), L-glutamic acid (GLU) and gamma-aminobutyric acid (GABA) on STR neurons' firing rates. It was observed that 77.27% (51/66) of the tested STR neurons were excited by SNP. This excitatory effect could be antagonized by the NO synthase (NOS) inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME). During the microiontophoresis of GLU, the excitatory firing of STR neurons was also attenuated by addition of L-NAME while SNP application could enhance the excitation of the neurons. On the other hand, in the presence of GABA, SNP still excited the tested STR neurons. These results demonstrated that NOergic, GLUergic and GABAergic co-existed in the same STR neurons. NOergic and GLUergic were excitatory whereas GABAergic was inhibitory on the firing activity in STR neurons.

Effect of urocortin on L-type calcium currents in adult rat ventricular myocytes.

The newly isolated peptide, urocortin (UCN) has been found to have potent cardioprotective effects. In order to investigate the effect of UCN on L-type calcium currents (I(Ca,L)), exploring the mechanisms of UCN's cardioprotective effects, we directly measured the I(Ca,L) in the adult rat cardiac myocytes exposed to UCN using standard whole-cell patch-clamp recording technique. Our results showed that UCN exerted decreasing effects on the I(Ca,L) of the single adult rat cardiac myocytes. The current density was inhibited by about 35% after exposure of the cells to UCN (0.1 micromol L(-1)) for 10 min, from the control value of 7.19 +/- 1.44 pA/pF to 4.74 +/- 0.75 pA/pF (n = 5, P < 0.05). This I(Ca,L)-inhibiting action of UCN was concentration dependent. Moreover, no frequency dependence of UCN effects on I(Ca,L) was observed. In combination with previous reports, our results suggest that there might be a close relationship between the cardioprotective effects of UCN and L-type calcium channels.