SR-POD : sample rotation based on principal-axis orientation distribution for data augmentation in deep object detection

Convolutional neural networks (CNNs) have outperformed most state-of-the-art methods in object detection. However, CNNs suffer the difficulty of detecting objects with rotation, because the dataset used to train the CCNs often does not contain sufficient samples with various angles of orientation. In this paper, we propose a novel data-augmentation approach to handle samples with rotation, which utilizes the distribution of the object's orientation without the time-consuming process of rotating the sample images. Firstly, we present an orientation descriptor, named as "principal-axis orientation" to describe the orientation of the object's principal axis in an image and estimate the distribution of objects’ principal-axis orientations (PODs) of the whole dataset. Secondly, we define a similarity metric to calculate the POD similarity between the training set and an additional dataset, which is built by randomly selecting images from the benchmark ImageNet ILSVRC2012 dataset. Finally, we optimize a cost function to obtain an optimal rotation angle, which indicates the highest POD similarity between the two aforementioned data sets. In order to evaluate our data augmentation method for object detection, experiments, conducted on the benchmark PASCAL VOC2007 dataset, show that with the training set augmented using our method, the average precision (AP) of the Faster RCNN in the TV-monitor is improved by 7.5%. In addition, our experimental results also demonstrate that new samples generated by random rotation are more likely to result in poor performance of object detection

Osmotic Demyelination Syndrome: Clinical, Neuroimaging Characteristics, and Outcomes in a Series of 18 Cases

Objective. To investigate the etiology, clinical as well as neuroimaging characteristics, and outcomes after proper treatment in a series of 18 patients with osmotic demyelination syndrome. Methods. Medical records, including video records, of 18 patients with osmotic demyelination syndrome were retrospectively examined. Demographic and clinical information, imaging results, plans of management, and outcomes during the follow-up period were collected and analyzed. Results. Eighteen patients, including 10 males and 8 females, were included in the present study. The mean age at diagnosis of CNS insult was 47.4±13.3 years (ranged from 30 to 78 years). Etiologies included rapidly corrected hyponatremia (50%), alcoholism (27.8%), and others. Neurological manifestations included encephalopathy (61.1%), dysphonia (50%), extrapyramidal symptoms (38.9%), and seizures (22.2%). Neuroimaging results showed that 6 patients (33.3%) had central pontine myelinolysis, 5 (27.8%) had extrapontine myelinolysis, and 7 (38.9%) had both. After treatment, 12 patients showed improvement and the other 6 did not. Among these patients, those who showed symptoms of encephalopathy had a favorable outcome. The majority of those who presented with mental retardation, seizures, and no other symptoms recovered better than their counterparts who had other symptoms. Nine out of 11 patients with pseudobulbar paralysis and/or extrapyramidal symptoms showed improvement, but the other 2 did not show improvement. Five patients who did not improve after treatment during admission were followed up for 1-3 months with rehabilitation training recommended, and it was found that 3 showed significant improvement after training, and the other 2 did not respond to this training. Conclusions. Osmotic demyelination syndrome is a complex disease entity due to a variety of etiologies, manifesting with symptoms involving diverse systems of the brain. Early identification and removal/correction of conditions leading to osmotic demyelination syndrome are the key to prevent and/or manage this disease

Nickel-Catalyzed Enantioselective Hydrogenation of β‑(Acylamino)acrylates: Synthesis of Chiral β‑Amino Acid Derivatives

The nickel-catalyzed asymmetric hydrogenation of β-(acylamino)­acrylates has been developed, affording chiral β-amino acid derivatives with excellent yields (95–99% yield) and enantioselectivities (97–99% ee). With the Ni–Binapine system, high enantioselectivities (98–99% ee) have also been obtained in the hydrogenation of <i>Z</i>/<i>E</i> isomeric mixtures of β-alkyl and β-aryl β-(acylamino)­acrylates. The synthesis of chiral β-amino acid derivatives on a gram scale has also been achieved with 0.2 mol % catalyst loading

Efficient Expression of Glutathione Peroxidase with Chimeric tRNA in Amber-less <i>Escherichia coli</i>

The active center of selenium-containing glutathione peroxidase (GPx) is selenocysteine (Sec), which is is biosynthesized on its tRNA in organisms. The decoding of Sec depends on a specific elongation factor and a Sec Insertion Sequence (SECIS) to suppress the UGA codon. The expression of mammalian GPx is extremely difficult with traditional recombinant DNA technology. Recently, a chimeric tRNA (tRNA^UTu) that is compatible with elongation factor Tu (EF-Tu) has made selenoprotein expression easier. In this study, human glutathione peroxidase (hGPx) was expressed in amber-less <i>Escherichia coli</i> C321.ΔA.exp using tRNA^UTu and seven chimeric tRNAs that were constructed on the basis of tRNA^UTu. We found that chimeric tRNA^UTu2, which substitutes the acceptor stem and T-stem of tRNA^UTu with those from tRNA^Sec, enabled the expression of reactive hGPx with high yields. We also found that chimeric tRNA^UTuT6, which has a single base change (A59C) compared to tRNA^UTu, mediated the highest reactive expression of hGPx1. The hGPx1 expressed exists as a tetramer and reacts with positive cooperativity. The SDS-PAGE analysis of hGPx2 produced by tRNA^UTuT6 with or without sodium selenite supplementation showed that the incorporation of Sec is nearly 90%. Our approach enables efficient selenoprotein expression in amber-less <i>Escherichia coli</i> and should enable further characterization of selenoproteins <i>in vitro</i>

Yohimbine promotes cardiac NE release and prevents LPS-induced cardiac dysfunction via blockade of presynaptic α2A-adrenergic receptor.

Myocardial depression is an important contributor to mortality in sepsis. We have recently demonstrated that α2-adrenoceptor (AR) antagonist, yohimbine (YHB), attenuates lipopolysaccharide (LPS)-induced myocardial depression. However, the mechanisms for this action of YHB are unclear. Here, we demonstrated that YHB decreased nitric oxide (NO) and tumor necrosis factor-alpha (TNF-α) levels in the myocardium and plasma, attenuated cardiac and hepatic dysfunction, but not kidney and lung injuries in endotoxemic mice. Immunohistochemical analysis revealed that cardiac α2A-AR was mostly located in sympathetic nerve presynaptic membrane; YHB decreased cardiac α2A-AR level and promoted cardiac norepinephrine (NE) release in endotoxemic mice. Reserpine that exhausted cardiac NE without markedly decreasing plasma NE level abrogated the inhibitory effects of YHB on cardiac TNF-α and iNOS expression as well as cardiac dysfunction, but not the suppressive effects of YHB on plasma TNF-α and NO elevation in LPS-challenged mice. Furthermore, both reserpine and YHB significantly inhibited LPS-induced myocardial apoptosis. α1-AR, β2-AR, but not β1-AR antagonists reversed the inhibitory effect of YHB on LPS-stimulated myocardial apoptosis. However, β1-AR antagonist attenuated LPS-caused cardiomyocyte apoptosis, partly abolished the protective effect of YHB on the left ventricular ejection fraction in endotoxemic mice. Altogether, these findings indicate that YHB attenuates LPS-induced cardiac dysfunction, at least in part, through blocking presynaptic α2A-AR and thus increasing cardiac NE release. YHB-elevated cardiac NE improves cardiac function via suppressing cardiac iNOS and TNF-α expression, activating β1-AR and inhibiting cardiomyocyte apoptosis through α1- and β2-AR in endotoxemic mice. However, cardiac β1-AR activation promotes LPS-induced cardiomyocyte apoptosis

Self-supported porous copper oxide nanosheet arrays for efficient and selective electrochemical conversion of nitrate ions to nitrogen gas

Electrochemical techniques have shown advantages for the removal of low-concentration nitrate. Here, copper oxide nanosheets were grown on self-supporting nickel foam (NF) to prepare electrodes (CuO/NF), which realized the rapid and highly selective conversion of nitrate pollutants in sewage into nontoxic and harmless N2. The CuO/NF afforded 100% NO3– removal within 100 min and 99.53% selectivity for N2 at –50 mA without producing a lot of by-products (NO2–, NH4+, and N2H4). Furthermore, 81.8% of NO3– was removed under the given conditions after six experimental repetitions. These results suggest that the catalyst has excellent electrochemical stability. The performance of CuO/NF for the electrocatalytic removal of NO3– in simulated wastewater (which contained Cl– and SO42–) was almost unaffected. Because of the high efficiency, high stability, and low cost of CuO/NF, this catalyst is practical for the removal of nitrate for wastewater purification

Berberine inhibits doxorubicin-triggered cardiomyocyte apoptosis via attenuating mitochondrial dysfunction and increasing Bcl-2 expression.

Cardiomyocyte apoptosis is an important event in doxorubicin (DOX)-induced cardiac injury. The aim of the present study was to investigate the protection of berberine (Ber) against DOX- triggered cardiomyocyte apoptosis in neonatal rat cardiomyocytes and rats. In neonatal rat cardiomyocytes, Ber attenuated DOX-induced cellular injury and apoptosis in a dose-dependent manner. However, Ber has no significant effect on viability of MCF-7 breast cancer cells treated with DOX. Ber reduced caspase-3 and caspase-9, but not caspase-8 activity in DOX-treated cardiomyocytes. Furthermore, Ber decreased adenosine monophosphate-activated protein kinase α (AMPKα) and p53 phosphorylation at 2 h, cytosolic cytochrome c and mitochondrial Bax levels and increased Bcl-2 level at 6 h in DOX-stimulated cardiomyocytes. Pretreatment with compound C, an AMPK inhibitor, also suppressed p53 phosphorylation and apoptosis in DOX-treated cardiomyocytes. DOX stimulation for 30 min led to a loss of mitochondrial membrane potential and a rise in the AMP/ATP ratio. Ber markedly reduced DOX-induced mitochondrial membrane potential loss and an increase in the AMP/ATP ratio at 1 h and 2 h post DOX exposure. In in vivo experiments, Ber significantly improved survival, increased stroke volume and attenuated myocardial injury in DOX-challenged rats. TUNEL and Western blot assays showed that Ber not only decreased myocardial apoptosis, caspase-3 activation, AMPKα and p53 phosphorylation, but also increased Bcl-2 expression in myocardium of rats exposed to DOX for 84 h. These findings indicate that Ber attenuates DOX-induced cardiomyocyte apoptosis via protecting mitochondria, inhibiting an increase in the AMP/ATP ratio and AMPKα phosphorylation as well as elevating Bcl-2 expression, which offer a novel mechanism responsible for protection of Ber against DOX-induced cardiomyopathy

Berberine Alleviates Doxorubicin-Induced Myocardial Injury and Fibrosis by Eliminating Oxidative Stress and Mitochondrial Damage via Promoting Nrf-2 Pathway Activation

Doxorubicin (DOX)-related cardiotoxicity has been recognized as a serious complication of cancer chemotherapy. Effective targeted strategies for myocardial protection in addition to DOX treatment are urgently needed. The purpose of this paper was to determine the therapeutic effect of berberine (Ber) on DOX-triggered cardiomyopathy and explore the underlying mechanism. Our data showed that Ber markedly prevented cardiac diastolic dysfunction and fibrosis, reduced cardiac malondialdehyde (MDA) level and increased antioxidant superoxide dismutase (SOD) activity in DOX-treated rats. Moreover, Ber effectively rescued the DOX-induced production of reactive oxygen species (ROS) and MDA, mitochondrial morphological damage and membrane potential loss in neonatal rat cardiac myocytes and fibroblasts. This effect was mediated by increases in the nuclear accumulation of nuclear erythroid factor 2-related factor 2 (Nrf2) and levels of heme oxygenase-1 (HO-1) and mitochondrial transcription factor A (TFAM). We also found that Ber suppressed the differentiation of cardiac fibroblasts (CFs) into myofibroblasts, as indicated by decreased expression of &alpha;-smooth muscle actin (&alpha;-SMA), collagen I and collagen III in DOX-treated CFs. Pretreatment with Ber inhibited ROS and MDA production and increased SOD activity and the mitochondrial membrane potential in DOX-challenged CFs. Further investigation indicated that the Nrf2 inhibitor trigonelline reversed the protective effect of Ber on both cardiomyocytes and CFs after DOX stimulation. Taken together, these findings demonstrated that Ber effectively alleviated DOX-induced oxidative stress and mitochondrial damage by activating the Nrf2-mediated pathway, thereby leading to the prevention of myocardial injury and fibrosis. The current study suggests that Ber is a potential therapeutic agent for DOX-induced cardiotoxicity that exerts its effects by activating Nrf2

Berberine Alleviates Doxorubicin-Induced Myocardial Injury and Fibrosis by Eliminating Oxidative Stress and Mitochondrial Damage via Promoting Nrf-2 Pathway Activation

Doxorubicin (DOX)-related cardiotoxicity has been recognized as a serious complication of cancer chemotherapy. Effective targeted strategies for myocardial protection in addition to DOX treatment are urgently needed. The purpose of this paper was to determine the therapeutic effect of berberine (Ber) on DOX-triggered cardiomyopathy and explore the underlying mechanism. Our data showed that Ber markedly prevented cardiac diastolic dysfunction and fibrosis, reduced cardiac malondialdehyde (MDA) level and increased antioxidant superoxide dismutase (SOD) activity in DOX-treated rats. Moreover, Ber effectively rescued the DOX-induced production of reactive oxygen species (ROS) and MDA, mitochondrial morphological damage and membrane potential loss in neonatal rat cardiac myocytes and fibroblasts. This effect was mediated by increases in the nuclear accumulation of nuclear erythroid factor 2-related factor 2 (Nrf2) and levels of heme oxygenase-1 (HO-1) and mitochondrial transcription factor A (TFAM). We also found that Ber suppressed the differentiation of cardiac fibroblasts (CFs) into myofibroblasts, as indicated by decreased expression of α-smooth muscle actin (α-SMA), collagen I and collagen III in DOX-treated CFs. Pretreatment with Ber inhibited ROS and MDA production and increased SOD activity and the mitochondrial membrane potential in DOX-challenged CFs. Further investigation indicated that the Nrf2 inhibitor trigonelline reversed the protective effect of Ber on both cardiomyocytes and CFs after DOX stimulation. Taken together, these findings demonstrated that Ber effectively alleviated DOX-induced oxidative stress and mitochondrial damage by activating the Nrf2-mediated pathway, thereby leading to the prevention of myocardial injury and fibrosis. The current study suggests that Ber is a potential therapeutic agent for DOX-induced cardiotoxicity that exerts its effects by activating Nrf2