StructNeRF: Neural Radiance Fields for Indoor Scenes With Structural Hints.

Neural Radiance Fields (NeRF) achieve photo-realistic view synthesis with densely captured input images. However, the geometry of NeRF is extremely under-constrained given sparse views, resulting in significant degradation of novel view synthesis quality. Inspired by self-supervised depth estimation methods, we propose StructNeRF, a solution to novel view synthesis for indoor scenes with sparse inputs. StructNeRF leverages the structural hints naturally embedded in multi-view inputs to handle the unconstrained geometry issue in NeRF. Specifically, it tackles the texture and non-texture regions respectively: a patch-based multi-view consistent photometric loss is proposed to constrain the geometry of textured regions; for non-textured ones, we explicitly restrict them to be 3D consistent planes. Through the dense self-supervised depth constraints, our method improves both the geometry and the view synthesis performance of NeRF without any additional training on external data. Extensive experiments on several real-world datasets demonstrate that StructNeRF shows superior or comparable performance compared to state-of-the-art methods (e.g. NeRF, DSNeRF, RegNeRF, Dense Depth Priors, MonoSDF, etc.) for indoor scenes with sparse inputs both quantitatively and qualitatively.

Learning Implicit Glyph Shape Representation.

Automatic generation of fonts can greatly facilitate the font design process, and provide prototypes where designers can draw inspiration from. Existing generation methods are mainly built upon rasterized glyph images to utilize the successful convolutional architecture, but ignore the vector nature of glyph shapes. We present an implicit representation, modeling each glyph as shape primitives enclosed by several quadratic curves. This structured implicit representation is shown to be better suited for glyph modeling, and enables rendering glyph images at arbitrary high resolutions. Our representation gives high-quality glyph reconstruction and interpolation results, and performs well on the challenging one-shot font style transfer task comparing to other alternatives both qualitatively and quantitatively.

Effect of maternal BDE-209 exposure on sexual development in male offspring rats / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To investigate the effect of maternal decabromodiphenyl ether (BDE-209) exposure on the sexual development in male offspring rats.</p><p><b>METHODS</b>Twenty-four pregnant Sprague-Dawley rats were randomly divided into three BDE-209 exposure groups and one control group. The three BDE-209 exposure groups were given BDE-209 (100, 300, and 900 mg/kg) by gavage on gestational days 12∼18, and the control group was given corn oil. The body weight and body length of each newborn male rat was measured at postnatal days 4, 10, 16, and 21. Twelve newborn male rats were randomly selected from each group; anogenital distance was measured at postnatal day 21, serum testosterone was measured, and the organ coefficient of testis was calculated.</p><p><b>RESULTS</b>The newborn male rats in all exposure groups showed declining trends in body weight and body length compared with those in the control group, and the 900 mg/kg BDE-209 exposure group had significantly lower body weight and body length than the control group at postnatal days 4, 10,16, and 21 (P < 0.01). At postnatal day 21, the 100, 300, and 900 mg/kg BDE-209 exposure groups had anogenital distances of 17.82±2.35 mm, 16.32±1.66 mm, and 15.80±1.34 mm, respectively, demonstrating a significant decrease with increased exposure dose (P < 0.05), but no significant difference was found when comparing these values with that of the control group (16.64±2.38 mm) (P > 0.05). There were no significant differences in serum testosterone and organ coefficients of testis and epididymis between the control group and BDE-209 exposure groups (P > 0.05).</p><p><b>CONCLUSION</b>Maternal exposure to BDE-209 has adverse effect on the growth of male offspring rats, but it leads to no significant changes in sexual development.</p>

Effect of carbon disulfide on mitochondrial respiratory chain in spermatogenic cells in male rats / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To investigate the effect of carbon disulfide (CS(2)) on the mitochondrial respiratory chain in testicular spermatogenic cells in male rats and to explore the possible mechanism of reproductive system damage caused by CS(2) in male rats.</p><p><b>METHODS</b>Twenty-four male Sprague-Dawley rats (clean grade) were randomly divided into four groups: three CS(2) exposure groups (CS(2) concentrations: 50, 250, and 1250 mg/m(3)) and a control group. The rats in CS(2) exposure groups were exposed to CS(2) by static inhalation for 10 weeks (2 h/d, 5 d/w), while the rats in control group were exposed to air. Then, all rats were sacrificed by decapitation; testicular tissues were collected, and mitochondrial protein in spermatogenic cells were extracted; the levels of mitochondrial respiratory chain enzyme complex I∼V were measured by enzyme-linked immunosorbent assay.</p><p><b>RESULTS</b>Compared with the control group, all CS(2) exposure groups had significantly increased levels of mitochondrial respiratory chain enzyme complex I∼V in spermatogenic cells (P < 0.05). There were no significant differences in the levels of respiratory chain enzyme complex I∼IV between the CS(2) exposure groups (P < 0.05), but the level of respiratory chain enzyme complex V rose significantly as the concentration of CS(2) increased (P<0.05).</p><p><b>CONCLUSION</b>Various levels of CS(2) exposure may increase the levels of mitochondrial respiratory chain enzyme complex in testicular spermatogenic cells among male rats, thus affecting the normal oxidative phosphorylation in mitochondria.</p>

Effect of carbon disulfide on mitochondrial apoptosis-related proteins in cytoplasm of testicular tissue among male rats / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To investigate the role of mitochondrial pathway in the apoptosis of spermatogenic cells induced by inhalation of carbon disulfide in male rats.</p><p><b>METHODS</b>Twenty-four male Sprague-Dawley rats (clean grade) were divided into four groups according to their body weights: three CS(2) exposure groups (CS(2) concentrations: 50, 250, and 1250 mg/m(3)) and a control group. The rats in CS(2) exposure groups were exposed to CS(2) by static inhalation for 10 weeks (2 h/d, 5 d/w), while the rats in control group were exposed to air. Then, all rats were sacrificed by decapitation; testicular tissues were collected, and cytoplasmic proteins were extracted; the levels of apoptosis-inducing factor (AIF), cytochrome c (cyto c), Bcl-2, Bax, procaspase-9, and procaspase-3 were measured by Western blot, and the activities of caspase-9 and caspase-3 were measured using a test kit.</p><p><b>RESULTS</b>Compared with the control group, all CS(2) exposure groups had significantly increased levels of cyto c in the cytoplasm of testicular tissue (P<0.05); in the 250 mg/m(3) CS(2) exposure group, the Bax/Bcl-2 ratio and activities of caspase-9 and caspase-3 increased significantly (P<0.05), and the content of procaspase-9 and procaspase-3 decreased significantly (P<0.05); in the 1250 mg/m(3) CS(2) exposure group, the relative expression levels of Bax and AIF in cytoplasm increased significantly (P<0.05), and the expression level of Bcl-2 decreased significantly (P<0.05).</p><p><b>CONCLUSION</b>Mitochondrial pathway plays an important role in the CS(2)-induced apoptosis of spermatogenic cells in testicular tissue among male rats.</p>

Effects of carbon disulfide on the expression and activity of nitric oxide synthase in rat hippocampus / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Carbon disulfide (CS(2)) is a commonly used organic solvent. Many epidemiological investigations and animal experiments have indicated that learning and memory ability can be affected to different degrees after long-term exposure to CS(2), but the mechanisms are still unclear. The aim of this study was to explore the possible mechanisms of CS(2)-related impairment of the learning and memory ability of rats, by investigating the effects of CS(2) on nitric oxide synthase (NOS) activity and NOS mRNA expression in rat hippocampus.</p><p><b>METHODS</b>Rat models of toxicity were generated by inhalation of various doses of CS(2). After two months of inhaling intoxication, the activities of constitutive NOS (cNOS) and induced NOS (iNOS) in the hippocampus were measured. The levels of neuronal NOS (nNOS) mRNA and iNOS mRNA were measured by semi-quantitative reverse transcription polymerase chain reaction (RT-PCR).</p><p><b>RESULTS</b>cNOS activity was significantly decreased compared with controls, while iNOS activity was changed only slightly. CS(2) treatment significantly decreased nNOS mRNA levels. iNOS mRNA levels were significantly increased only at higher doses of CS(2).</p><p><b>CONCLUSION</b>The effect of CS2 on learning and memory ability in rats is related to the activity of NOS and the expression of nNOS in the hippocampus.</p>

Apoptosis and gene FasL expression induced by carbon disulfide in rat sertoli cells / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To study apoptosis and gene FasL expression induced by carbon disulfide in sertoli cells of male rats.</p><p><b>METHODS</b>Sertoli cells were exposed to different concentrations of CS(2) (0, 0.36, 0.72, 1.44 micromol/ml) for 24 hours. Survival rate, apoptosis rate, expression level of gene FasL were measured using MTT, FCM, and RT-PCR methods respectively.</p><p><b>RESULTS</b>Sertoli cell survival rate decreased as the concentration of CS(2) increased. The survival rate (73.34% +/- 1.39%) was significantly lower than the control group (99.98% +/- 5.48%) when the concentration of CS(2) > or = 1.44 micromol/ml (P < 0.05). Apoptosis rate increased as the CS(2) concentration increased. Apoptosis rate (7.93% +/- 0.43%) was significantly higher when the concentration of CS(2) > or = 1.44 micromol/ml (P < 0.05). Expression level of the FasL significantly increased as the concentrations of CS(2) (P < 0.05).</p><p><b>CONCLUSION</b>CS(2) is cytotoxic to sertoli cells. It could cause apoptosis of sertoli cells.</p>