Image denoising with multi-layer perceptrons, part 1: comparison with existing algorithms and with bounds

Image denoising can be described as the problem of mapping from a noisy image to a noise-free image. The best currently available denoising methods approximate this mapping with cleverly engineered algorithms. In this work we attempt to learn this mapping directly with plain multi layer perceptrons (MLP) applied to image patches. We will show that by training on large image databases we are able to outperform the current state-of-the-art image denoising methods. In addition, our method achieves results that are superior to one type of theoretical bound and goes a large way toward closing the gap with a second type of theoretical bound. Our approach is easily adapted to less extensively studied types of noise, such as mixed Poisson-Gaussian noise, JPEG artifacts, salt-and-pepper noise and noise resembling stripes, for which we achieve excellent results as well. We will show that combining a block-matching procedure with MLPs can further improve the results on certain images. In a second paper, we detail the training trade-offs and the inner mechanisms of our MLPs

Soft Contributions to Hard Pion Photoproduction

Hard, or high transverse momentum, pion photoproduction can be a tool for probing the parton structure of the beam and target. We estimate the soft contributions to this process, with an eye toward delineating the region where perturbatively calculable processes dominate. Our soft process estimate is based on vector meson dominance and data based parameterizations of semiexclusive hadronic cross sections. We find that soft processes dominate in single pion photoproduction somewhat past 2 GeV transverse momentum at a few times 10 GeV incoming energy. The recent polarization asymmetry data is consistent with the perturbative asymmetry being diluted by polarization insensitive soft processes. Determining the polarized gluon distribution using hard pion photoproduction appears feasible with a few hundred GeV incoming energy (in the target rest frame).Comment: 6 pages, 5 figure

Absence of Evidence of Rift Valley Fever Infection in Eulemur fulvus (Brown Lemur) in Mayotte During an Interepidemic Period.

The potential role of Eulemur fulvus (brown lemur) in the epidemiology of Rift Valley fever (RVF) in Mayotte, during an interepidemic period, was explored. In February and March 2016, 72 animals were blood sampled and tested for RVF. No evidence of RVF genome or antibodies was found in the samples. The role of other wild mammals on the island should, however, be further investigated

Prospective longitudinal study of immune checkpoint molecule (ICM) expression in immune cell subsets during curative conventional therapy of head and neck squamous cell carcinoma (HNSCC)

Programmed-death-1 (PD1) antibodies are approved for recurrent and metastatic head and neck squamous cell carcinoma. Multiple drugs targeting costimulatory and coinhibitory immune checkpoint molecules (ICM) have been discovered. However, it remains unknown how these ICM are affected by curative conventional therapy on different immune cell subsets during the course of treatment. In the prospective noninterventional clinical study titled “Immune Response Evaluation to Curative conventional Therapy” (NCT03053661), 22 patients were prospectively enrolled. Blood samples were drawn at defined time points throughout curative conventional treatment and follow-up. Immune cells (IC) from the different time points were assessed by multicolor flow cytometry. The following ICM were measured by flow cytometry: PD1, CTLA4, BTLA, CD137, CD27, GITR, OX40, LAG3 and TIM3. Dynamics of ICM expression were assessed using nonparametric paired samples tests. Significant changes were noted for PD1, BTLA and CD27 on multiple IC types during or after radiotherapy. Nonsignificant trends for increased expression of OX40 and GITR from baseline until the end of RT were observed on CD4 T cells and CD4+ CD39+ T cells. In patients with samples at recurrence of disease, a nonsignificant increase of TIM3 and LAG3 positive CD4+ CD39+ T cells was evident, accompanied by an increase of double positive cells for TIM3/LAG3. Potential future targets to be combined with RT in the conventional treatment and anti-PD1/PD-L could be BTLA agonists, or agonistic antibodies to costimulatory ICM like CD137, OX40 or GITR. The combination of cetuximab with CD27 agonistic antibodies enhancing ADCC or the targeting of TIM3/LAG3 may be another promising strategy

Increasing mean age of head and neck cancer patients at a German tertiary referral center

Background: The impact of demographic change on the age at diagnosis in German head and neck cancer (HNC) patients is unclear. Here we present an evaluation of aging trends in HNC at a tertiary referral center. Methods: Retrospective cohort study on aging trends at the initial diagnosis of newly diagnosed patients with HNC between 2004 and 2018 at the head and neck cancer center Ulm in relation to demographic data of the catchment area. Results: The study population consisted of 2450 individuals diagnosed with HNC with a mean age of 62.84 (±11.67) years. We observed a significant increase in annual incidence rates and mean age over time. Mean age among HNC patients increased significantly more than among the population in the catchment area. Whereas the incidence rate of patients <50 years did not change, the incidence of HNC patients aged ≥70 years increased the most. The mean patient age in the main tumor sites increased significantly. Surprisingly, HPV-positive patients were not younger than HPV-negative patients, but showed a non-significant trend towards a higher mean age (63.0 vs. 60.7 years). Conclusions: Increasing incidence rates in older patients pose a challenge for health care systems. A nationwide study is needed to assess the dynamics and impact of aging on the incidence of HNC

BTK isoforms p80 and p65 are expressed in head and neck squamous cell carcinoma (HNSCC) and involved in tumor progression

Here, we describe the expression of Bruton’s Tyrosine Kinase (BTK) in head and neck squamous cell carcinoma (HNSCC) cell lines as well as in primary HNSCC samples. BTK is a kinase initially thought to be expressed exclusively in cells of hematopoietic origin. Apart from the 77 kDa BTK isoform expressed in immune cells, particularly in B cells, we identified the 80 kDa and 65 kDa BTK isoforms in HNSCC, recently described as oncogenic. Importantly, we revealed that both isoforms are products of the same mRNA. By investigating the mechanism regulating oncogenic BTK-p80/p65 expression in HNSSC versus healthy or benign tissues, our data suggests that the epigenetic process of methylation might be responsible for the initiation of BTK-p80/p65 expression in HNSCC. Our findings demonstrate that chemical or genetic abrogation of BTK activity leads to inhibition of tumor progression in terms of proliferation and vascularization in vitro and in vivo. These observations were associated with cell cycle arrest and increased apoptosis and autophagy. Together, these data indicate BTK-p80 and BTK-p65 as novel HNSCC-associated oncogenes. Owing to the fact that abundant BTK expression is a characteristic feature of primary and metastatic HNSCC, targeting BTK activity appears as a promising therapeutic option for HNSCC patients

Measuring Polarized Gluon and Quark Distributions with Meson Photoproduction

We calculate polarization asymmetries in photoproduction of high transverse momentum mesons, focusing on charged pions, considering the direct, fragmentation, and resolved photon processes. The results at very high meson momentum measure the polarized quark distributions and are sensitive to differences among the existing models. The results at moderate meson momentum are sensitive to the polarized gluon distribution and can provide a good way to measure it. Suitable data may come as a by-product of deep inelastic experiments to measure $g_1$ or from dedicated experiments.Comment: RevTeX, 11 pages, 13 postscript figures; changes made in response to the referee's comment

Beyond Repair Foci: DNA Double-Strand Break Repair in Euchromatic and Heterochromatic Compartments Analyzed by Transmission Electron Microscopy

DNA double-strand breaks (DSBs) generated by ionizing radiation pose a serious threat to the preservation of genetic and epigenetic information. The known importance of local chromatin configuration in DSB repair raises the question of whether breaks in different chromatin environments are recognized and repaired by the same repair machinery and with similar efficiency. An essential step in DSB processing by non-homologous end joining is the high-affinity binding of Ku70-Ku80 and DNA-PKcs to double-stranded DNA ends that holds the ends in physical proximity for subsequent repair.Using transmission electron microscopy to localize gold-labeled pKu70 and pDNA-PKcs within nuclear ultrastructure, we monitored the formation and repair of actual DSBs within euchromatin (electron-lucent) and heterochromatin (electron-dense) in cortical neurons of irradiated mouse brain.While DNA lesions in euchromatin (characterized by two pKu70-gold beads, reflecting the Ku70-Ku80 heterodimer) are promptly sensed and rejoined, DNA packaging in heterochromatin appears to retard DSB processing, due to the time needed to unravel higher-order chromatin structures. Complex pKu70-clusters formed in heterochromatin (consisting of 4 or ≥ 6 gold beads) may represent multiple breaks in close proximity caused by ionizing radiation of highly-compacted DNA. All pKu70-clusters disappeared within 72 hours post-irradiation, indicating efficient DSB rejoining. However, persistent 53BP1 clusters in heterochromatin (comprising ≥ 10 gold beads), occasionally co-localizing with γH2AX, but not pKu70 or pDNA-PKcs, may reflect incomplete or incorrect restoration of chromatin structure rather than persistently unrepaired DNA damage.Higher-order organization of chromatin determines the accessibility of DNA lesions to repair complexes, defining how readily DSBs are detected and processed. DNA lesions in heterochromatin appear to be more complex, with multiple breaks in spatial vicinity inducing severe chromatin disruptions. Imperfect restoration of chromatin configurations may leave DSB-induced epigenetic memory of damage with potentially pathological repercussions