Ultrasonic Image's Annotation Removal: A Self-supervised Noise2Noise Approach

Accurately annotated ultrasonic images are vital components of a high-quality medical report. Hospitals often have strict guidelines on the types of annotations that should appear on imaging results. However, manually inspecting these images can be a cumbersome task. While a neural network could potentially automate the process, training such a model typically requires a dataset of paired input and target images, which in turn involves significant human labour. This study introduces an automated approach for detecting annotations in images. This is achieved by treating the annotations as noise, creating a self-supervised pretext task and using a model trained under the Noise2Noise scheme to restore the image to a clean state. We tested a variety of model structures on the denoising task against different types of annotation, including body marker annotation, radial line annotation, etc. Our results demonstrate that most models trained under the Noise2Noise scheme outperformed their counterparts trained with noisy-clean data pairs. The costumed U-Net yielded the most optimal outcome on the body marker annotation dataset, with high scores on segmentation precision and reconstruction similarity. We released our code at https://github.com/GrandArth/UltrasonicImage-N2N-Approach.Comment: 10 pages, 7 figure

Dynamic Nonlinear Effect on Lasing in a Random Medium

We have studied both experimentally and numerically the dynamic effect of nonlinearity on lasing in disordered medium. The third-order nonlinearity not only changes the frequency and size of lasing modes, but also modifies the laser emission intensity and laser pulse width. When the nonlinear response time is longer than the lifetime of the lasing mode, the nonlinearity changes the laser output through modifying the size of the lasing mode. When the nonlinear response is faster than the buildup of the lasing mode, positive nonlinearity always extracts more laser emission from the random medium due to the enhancement of single particle scattering

A higher-order numerical scheme for system of two-dimensional nonlinear fractional Volterra integral equations with uniform accuracy

We give a modified block-by-block method for the nonlinear fractional order Volterra integral equation system by using quadratic Lagrangian interpolation based on the classical block-by-block method. The core of the method is that we divide its domain into a series of subdomains, that is, block it, and use piecewise quadratic Lagrangian interpolation on each subdomain to approximate $\mathit{\boldsymbol{\kappa}}(x, y, s, r, u(s, r))$. Our proposed method has uniform accuracy and its convergence order is $O(h_x^{4-\alpha}+h_y^{4-\beta})$. We give a strict proof for the error analysis of the method, and give several numerical examples to verify the correctness of the theoretical analysis

Isolation Housing Exacerbates Alzheimer\u27s Disease-Like Pathophysiology in Aged APP/PS1 Mice

BACKGROUND: Alzheimer\u27s disease is a neurodegenerative disease characterized by gradual declines in social, cognitive, and emotional functions, leading to a loss of expected social behavior. Social isolation has been shown to have adverse effects on individual development and growth as well as health and aging. Previous experiments have shown that social isolation causes an early onset of Alzheimer\u27s disease-like phenotypes in young APP695/PS1-dE9 transgenic mice. However, the interactions between social isolation and Alzheimer\u27s disease still remain unknown. METHODS: Seventeen-month-old male APP695/PS1-dE9 transgenic mice were either singly housed or continued group housing for 3 months. Then, Alzheimer\u27s disease-like pathophysiological changes were evaluated by using behavioral, biochemical, and pathological analyses. RESULTS: Isolation housing further promoted cognitive dysfunction and Aβ plaque accumulation in the hippocampus of aged APP695/PS1-dE9 transgenic mice, associated with increased γ-secretase and decreased neprilysin expression. Furthermore, exacerbated hippocampal atrophy, synapse and myelin associated protein loss, and glial neuroinflammatory reactions were observed in the hippocampus of isolated aged APP695/PS1-dE9 transgenic mice. CONCLUSIONS: The results demonstrate that social isolation exacerbates Alzheimer\u27s disease-like pathophysiology in aged APP695/PS1-dE9 transgenic mice, highlighting the potential role of group life for delaying or counteracting the Alzheimer\u27s disease process

Recurrent renal secondary hyperparathyroidism caused by supernumerary mediastinal parathyroid gland and parathyromatosis: A case report

BackgroundSurgical parathyroidectomy (PTX) is necessary for patients with severe and progressive secondary hyperparathyroidism (SHPT) refractory to medical treatment. Recurrence of SHPT after PTX is a serious clinical problem. Both supernumerary mediastinal parathyroid gland and parathyromatosis are the rare causes of recurrent renal SHPT. We report a rare case of recurrent renal SHPT due to supernumerary mediastinal parathyroid gland and parathyromatosis.Case presentationA 53-year-old man underwent total parathyroidectomy with autotransplantation due to the drug-refractory SHPT 17 years ago. In the last 11 months, the patient experienced symptoms including bone pain and skin itch, and the serum intact parathyroid hormone (iPTH) level elevated to 1,587 pg/ml. Ultrasound detected two hypoechoic lesions located at the dorsal area of right lobe of the thyroid gland, and both lesions presented as characteristics of hyperparathyroidism in contrast-enhanced ultrasound. 99mTc-MIBI/SPECT detected a nodule in the mediastinum. A reoperation involved a cervicotomy for excising parathyromatosis lesions and the surrounding tissue and a thoracoscopic surgery for resecting a mediastinal parathyroid gland. According to a histological examination, two lesions behind the right thyroid lobe and one lesion in the central region had been defined as parathyromatosis. A nodule in the mediastinum was consistent with hyperplastic parathyroid. The patient remained well for 10 months with alleviated symptoms and stabilized iPTH levels in the range of 123–201 pg/ml.ConclusionAlthough rare, recurrent SHPT may be caused by a coexistence of both supernumerary parathyroid glands and parathyromatosis, which should receive more attention. The combination of imaging modalities is important for reoperative locations of parathyroid lesions. To successfully treat parathyromatosis, all the lesions and the surrounding tissue must be excised. Thoracoscopic surgery is a reliable and safe approach for the resection of ectopic mediastinal parathyroid glands

Asian Female Facial Beauty Prediction Using Deep Neural Networks via Transfer Learning and Multi-Channel Feature Fusion

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Correlation analysis of field-aligned currents measured by Swarm

The orientation of field-aligned current sheets (FACs) can be inferred from dual-spacecraft correlations of the FAC signatures between two Swarm spacecraft (A and C), using the maximum correlations obtained from sliding data segments. Statistical analysis of both the correlations and the inferred orientations shows clear trends in magnetic local time (MLT) which reveal behaviour of both large and small scale currents. The maximum correlation coefficients show distinct behaviour in terms of either the time shift, or the shift in longitude between Swarm A and C for various filtering levels. The low-latitude FACs show the strongest correlations for a broad range of MLT centred on dawn and dusk, with a higher correlation coefficient on the dusk-side and lower correlations near noon and midnight. The current sheet orientations are shown to broadly follow the mean shape of the auroral boundary for the lower latitudes corresponding to Region 2 FACs and that these are most well-ordered on the dusk side. Together with these correlation trends, individual events have also been sampled by higher altitude spacecraft in conjunction with Swarm (mapping both to region 1 and 2), showing that two different domains of FACs are apparent: small-scale (some tens of km) which are time variable and large-scale (>100 km) which are rather stationary. We investigate further how these FAC regimes are dependent on geomagnetic activity, focusing on high activity events. The trends found here for different activities are compared to effects seen in the ground magnetometer signals (dH/dt)

Bmi-1 Absence Causes Premature Brain Degeneration

Bmi-1, a polycomb transcriptional repressor, is implicated in cell cycle regulation and cell senescence. Its absence results in generalized astrogliosis and epilepsy during the postnatal development, but the underlying mechanisms are poorly understood. Here, we demonstrate the occurrence of oxidative stress in the brain of four-week-old Bmi-1 null mice. The mice showed various hallmarks of neurodegeneration including synaptic loss, axonal demyelination, reactive gliosis and brain mitochondrial damage. Moreover, astroglial glutamate transporters and glutamine synthetase decreased in the Bmi-1 null hippocampus, which might contribute to the sporadic epileptic-like seizures in these mice. These results indicate that Bmi-1 is required for maintaining endogenous antioxidant defenses in the brain, and its absence subsequently causes premature brain degeneration

Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes. For example, a key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process versus those that measure fl ux through the autophagy pathway (i.e., the complete process including the amount and rate of cargo sequestered and degraded). In particular, a block in macroautophagy that results in autophagosome accumulation must be differentiated from stimuli that increase autophagic activity, defi ned as increased autophagy induction coupled with increased delivery to, and degradation within, lysosomes (inmost higher eukaryotes and some protists such as Dictyostelium ) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the fi eld understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in many cases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. It is worth emphasizing here that lysosomal digestion is a stage of autophagy and evaluating its competence is a crucial part of the evaluation of autophagic flux, or complete autophagy. Here, we present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes. These guidelines are not meant to be a formulaic set of rules, because the appropriate assays depend in part on the question being asked and the system being used. In addition, we emphasize that no individual assay is guaranteed to be the most appropriate one in every situation, and we strongly recommend the use of multiple assays to monitor autophagy. Along these lines, because of the potential for pleiotropic effects due to blocking autophagy through genetic manipulation it is imperative to delete or knock down more than one autophagy-related gene. In addition, some individual Atg proteins, or groups of proteins, are involved in other cellular pathways so not all Atg proteins can be used as a specific marker for an autophagic process. In these guidelines, we consider these various methods of assessing autophagy and what information can, or cannot, be obtained from them. Finally, by discussing the merits and limits of particular autophagy assays, we hope to encourage technical innovation in the field