GlowGAN: Unsupervised Learning of HDR Images from LDR Images in the Wild

Most in-the-wild images are stored in Low Dynamic Range (LDR) form, serving as a partial observation of the High Dynamic Range (HDR) visual world. Despite limited dynamic range, these LDR images are often captured with different exposures, implicitly containing information about the underlying HDR image distribution. Inspired by this intuition, in this work we present, to the best of our knowledge, the first method for learning a generative model of HDR images from in-the-wild LDR image collections in a fully unsupervised manner. The key idea is to train a generative adversarial network (GAN) to generate HDR images which, when projected to LDR under various exposures, are indistinguishable from real LDR images. The projection from HDR to LDR is achieved via a camera model that captures the stochasticity in exposure and camera response function. Experiments show that our method GlowGAN can synthesize photorealistic HDR images in many challenging cases such as landscapes, lightning, or windows, where previous supervised generative models produce overexposed images. We further demonstrate the new application of unsupervised inverse tone mapping (ITM) enabled by GlowGAN. Our ITM method does not need HDR images or paired multi-exposure images for training, yet it reconstructs more plausible information for overexposed regions than state-of-the-art supervised learning models trained on such data

An Implicit Neural Representation for the Image Stack: Depth, All in Focus, and High Dynamic Range

In everyday photography, physical limitations of camera sensors and lenses frequently lead to a variety of degradations in captured images such as saturation or defocus blur. A common approach to overcome these limitations is to resort to image stack fusion, which involves capturing multiple images with different focal distances or exposures. For instance, to obtain an all-in-focus image, a set of multi-focus images is captured. Similarly, capturing multiple exposures allows for the reconstruction of high dynamic range. In this paper, we present a novel approach that combines neural fields with an expressive camera model to achieve a unified reconstruction of an all-in-focus high-dynamic-range image from an image stack. Our approach is composed of a set of specialized implicit neural representations tailored to address specific sub-problems along our pipeline: We use neural implicits to predict flow to overcome misalignments arising from lens breathing, depth, and all-in-focus images to account for depth of field, as well as tonemapping to deal with sensor responses and saturation - all trained using a physically inspired supervision structure with a differentiable thin lens model at its core. An important benefit of our approach is its ability to handle these tasks simultaneously or independently, providing flexible post-editing capabilities such as refocusing and exposure adjustment. By sampling the three primary factors in photography within our framework (focal distance, aperture, and exposure time), we conduct a thorough exploration to gain valuable insights into their significance and impact on overall reconstruction quality. Through extensive validation, we demonstrate that our method outperforms existing approaches in both depth-from-defocus and all-in-focus image reconstruction tasks. Moreover, our approach exhibits promising results in each of these three dimensions, showcasing its potential to enhance captured image quality and provide greater control in post-processing

Polo-like kinase 1 regulates mitotic arrest after UV irradiation through dephosphorylation of p53 and inducing p53 degradation

AbstractUltraviolet (UV) irradiation can result in cell cycle arrest. The reactivation of Polo-like kinase 1 (Plk1) is necessary for cell cycle reentry. But the mechanism of how Plk1 regulates p53 in UV-induced mitotic arrest cells remained elusive. Here we find that UV treatment leads HEK293 cells to inverse changes of Plk1 and p53. Over-expression of Plk1 rescue UV-induced mitotic arrest cells by inhibiting p53 activation. Plk1 could also inhibit p53 phosphorylation at Ser15, thus facilitates its nuclear export and degradation. Further examination shows that Plk1, p53 and Cdc25C can form a large complex. Plk1 could bind to the sequence-specific DNA-binding domain of p53 and active Cdc25C by hyperphosphorylation. These results hypothesize that Plk1 and Cdc25C participate in recovery the mitotic arrest through binding to the different domain of p53. Cdc25C may first be actived by Plk1, and then its phosphatase activity makes p53 dephosphorylated at Ser15

Abnormal expression of an ADAR2 alternative splicing variant in gliomas downregulates adenosine-to-inosine RNA editing

BACKGROUND: RNA editing is catalyzed by adenosine deaminases acting on RNA (ADARs). ADAR2 is the main enzyme responsible for recoding editing in humans. Adenosine-to-inosine (A-to-I) editing at the Q/R site is reported to be decreased in gliomas; however, the expression of ADAR2 mRNA was not greatly affected. METHODS: We determined ADAR2 mRNA expression in human glioblastoma cell lines and in normal human glial cells by real-time RT-PCR. We also determined ADAR2 mRNA expression in 44 glioma tissues and normal white matter. After identifying an alternative splicing variant (ASV) of ADAR2 in gliomas, we performed sequencing. We then classified glioblastomas based on the presence (+) or absence (–) of the ASV to determine the correlations between ASV + and malignant features of glioblastomas, such as invasion, peritumoral brain edema, and survival time. RESULTS: There were no significant differences in ADAR2 mRNA expression among human glioblastoma cell lines or in gliomas compared with normal white matter (all p > 0.05). The ASV, which contained a 47-nucleotide insertion in the ADAR2 mRNA transcript, was detected in the U251 and BT325 cell lines, and in some glioma tissues. The expression rate of ASV differed among gliomas of different grades. ASV + glioblastomas were more malignant than ASV – glioblastomas. CONCLUSIONS: ADAR2 is a family of enzymes in which ASVs result in differences in enzymatic activity. The ADAR2 ASV may be correlated with the invasiveness of gliomas. Identification of the mechanistic characterization of ADAR2 ASV may have future potential for individualized molecular targeted-therapy for glioma

A superior preparing method for daidzein-hydroxypropyl-β-cyclodextrin complexes with improved solubility and dissolution: supercritical fluid process

Advantages of the supercritical fluid (SCF) process compared to the conventional solution stirring method (CSSM) in the preparation of daidzein-hydroxypropyl-β-cyclodextrin (HPβCD) complexes were investigated. Formation of daidzein/HPβCD inclusion complexes was confirmed by Fourier transformed-infrared spectroscopy (FTIR), differential scanning calorimetry (DSC), X-ray diffraction (XRD) and scanning electron microscopy (SEM). Particle size, inclusion yield, drug solubility and dissolution of daidzein/HPβCD complexes were evaluated. Compared to CSSM, the SCF process resulted in higher inclusion yield and higher solubility. Also, extended dissolution of daidzein from the SCF processed HPβCD inclusion complexes was observed, with only 22.94 % released in 45 min, compared to its rapid release from those prepared by CSSM, with 98.25 % drug release in 15 min. This extended release of daidzein from SCF prepared inclusion complexes was necessary to avoid drug precipitation and improve drug solubilisation in the gastrointestinal tract. The results showed that the SCF process is a superior preparation method for daidzein-hydroxypropyl-β-cyclodextrin complexes

Arbitrary spectral synthesis and waveform generation with HiBi fiber loop mirrors

An arbitrary spectral synthesis scheme with parallel-connecting high-birefringence fiber loop mirrors (HiBi-FLMs) based on Fourier synthesis theory has been proposed and demonstrated. Three typical spectra of triangle, rectangle and sawtooth shape have been synthesized by implementing only four HiBi-FLMs. The experimental results are in good agreement with theoretical simulations with a goodness of fit of 0.9565. Furthermore, higher precise optical spectrum with narrower bandwidth can be obtained by adopting longer polarization- maintaining fiber and more sections of HiBi-FLMs. Besides, a typical application of arbitrary waveform generation has been implemented. By incorporating with frequency-to- time mapping, triangle- and sawtooth-shaped electrical pulses with repetition rate of 1 GHz and pulse width of ~860 ps have been generate

Aurora-A down-regulates IkappaBα via Akt activation and interacts with insulin-like growth factor-1 induced phosphatidylinositol 3-kinase pathway for cancer cell survival

<p>Abstract</p> <p>Background</p> <p>The mitotic Aurora-A kinase exerts crucial functions in maintaining mitotic fidelity. As a bona fide oncoprotein, Aurora-A aberrant overexpression leads to oncogenic transformation. Yet, the mechanisms by which Aurora-A enhances cancer cell survival remain to be elucidated.</p> <p>Results</p> <p>Here, we found that Aurora-A overexpression was closely correlated with clinic stage and lymph node metastasis in tongue carcinoma. Aurora-A inhibitory VX-680 suppressed proliferation, induced apoptosis and markedly reduced migration in cancer cells. We further showed that insulin-like growth factor-1, a PI3K physiological activator, reversed VX-680-decreased cell survival and motility. Conversely, wortmannin, a PI3K inhibitor, combined with VX-680 showed a synergistic effect on inducing apoptosis and suppressing migration. In addition, Aurora-A inhibition suppressed Akt activation, and VX-680-induced apoptosis was attenuated by Myr-Akt overexpression, revealing a cross-talk between Aurora-A and PI3K pathway interacting at Akt activation. Significantly, we showed that suppression of Aurora-A decreased phosphorylated Akt and was associated with increased IkappaBα expression. By contrast, Aurora-A overexpression upregulated Akt activity and downregulated IkappaBα, these changes were accompanied by nuclear translocation of nuclear factor-κB and increased expression of its target gene Bcl-xL. Lastly, Aurora-A overexpression induced IkappaBα reduction was abrogated by suppression of Akt either chemically or genetically.</p> <p>Conclusion</p> <p>Taken together, our data established that Aurora-A, via activating Akt, stimulated nuclear factor-κB signaling pathway to promote cancer cell survival, and promised a novel combined chemotherapy targeting both Aurora-A and PI3K in cancer treatment.</p