Compensation of Frequency-Dependent Attenuation for Tissue Harmonic Pulse Compression Imaging

Tissue harmonic imaging (THI) is highly effective for correct diagnosis. On the other hand, pulse compression is often used in a radar system and an ultrasound imaging system to perform high SNR measurement. Therefore, the performance of pulse compression of tissue harmonic imaging is required to be improved. The frequency-dependent attenuation (FDA) is a crucial problem in medical tissue imaging. In the pulse compression imaging, the deterioration of echoes by the FDA lowers the performance of a matched filtering using an ideal transmitted pulse as a template signal. Since, especially in the harmonic imaging, higher-frequency components are used for imaging than the fundamental imaging, the compensation of the FDA is strongly important for high-definition imaging. In this study, we examine a method to reduce the influence of the FDA on harmonics

Resolution of the curse of dimensionality in single-cell RNA sequencing data analysis

1細胞データ解析の精度が飛躍的に向上する前処理法の開発. 京都大学プレスリリース. 2022-08-09.Clearing the mist hiding the genome. 京都大学プレスリリース. 2022-08-09.Single-cell RNA sequencing (scRNA-seq) can determine gene expression in numerous individual cells simultaneously, promoting progress in the biomedical sciences. However, scRNA-seq data are high-dimensional with substantial technical noise, including dropouts. During analysis of scRNA-seq data, such noise engenders a statistical problem known as the curse of dimensionality (COD). Based on high-dimensional statistics, we herein formulate a noise reduction method, RECODE (resolution of the curse of dimensionality), for high-dimensional data with random sampling noise. We show that RECODE consistently resolves COD in relevant scRNA-seq data with unique molecular identifiers. RECODE does not involve dimension reduction and recovers expression values for all genes, including lowly expressed genes, realizing precise delineation of cell fate transitions and identification of rare cells with all gene information. Compared with representative imputation methods, RECODE employs different principles and exhibits superior overall performance in cell-clustering, expression value recovery, and single-cell–level analysis. The RECODE algorithm is parameter-free, data-driven, deterministic, and high-speed, and its applicability can be predicted based on the variance normalization performance. We propose RECODE as a powerful strategy for preprocessing noisy high-dimensional data

Inhibition of c-Jun NH2-terminal kinase activity improves ischemia/reperfusion injury in rat lungs

Although c-Jun NH 2 -terminal kinase (JNK) has been implicated in the pathogenesis of transplantation-induced ischemia/reperfusion (I/R) injury in various organs, its significance in lung transplantation has not been conclusively elucidated. We therefore attempted to measure the transitional changes in JNK and AP-1 activities in I/R-injured lungs. Subsequently, we assessed the effects of JNK inhibition by the three agents including SP600125 on the degree of lung injury assessed by means of various biological markers in bronchoalveolar lavage fluid and histological examination including detection of apoptosis. In addition, we evaluated the changes in p38, extracellular signal-regulated kinase, and NF-B-DNA binding activity. I/R injury was established in the isolated rat lung preserved in modified Euro-Collins solution at 4°C for 4 h followed by reperfusion at 37°C for 3 h. We found that AP-1 was transiently activated during ischemia but showed sustained activation during reperfusion, leading to significant lung injury and apoptosis. The change in AP-1 was generally in parallel with that of JNK, which was activated in epithelial cells (bronchial and alveolar), alveolar macrophages, and smooth muscle cells (bronchial and vascular) on immunohistochemical examination. The change in NF-B qualitatively differed from that of AP-1. Protein leakage, release of lactate dehydrogenase and TNF-␣ into bronchoalveolar lavage fluid, and lung injury were improved, and apoptosis was suppressed by JNK inhibition. In conclusion, JNK plays a pivotal role in mediating lung injury caused by I/R. Therefore, inhibition of JNK activity has potential as an effective therapeutic strategy for preventing I/R injury during lung transplantation