Application of Transfer Matrix Method with Signal Flow-Chart to Analyze Optical Multi-Path Ring-Resonator

A multi-path ring-resonator (MPRR) was proposed to extend FSR of ring resonator. However, it is complicated to analyze the MPRR by using well-known analysis techniques such as scattering matrix or other numerical methods. This paper describes procedure for deriving transfer matrix by means of signal flow-chart to analyze the MPRR. We do not need complicated calculation for steady state analysis because transfer matrix elements are formulated clearly. As a result, The calcultaion time in this method can be reduced 1/3 to 1/20 times compared with using scattering matirx method. Furthermore, a transmittance characteristics of the MPRR at FSR extension-factor of 10 will also be shown. This suggests that analysis of other types of the MPRR by using this method can be performed simply and take a shorter time

Application of Transfer Matrix Method with Signal Flow-Chart to Analyze Optical Multi-Path Ring-Resonator

A multi-path ring-resonator (MPRR) was proposed to extend FSR of ring resonator. However, it is complicated to analyze the MPRR by using well-known analysis techniques such as scattering matrix or other numerical methods. This paper describes procedure for deriving transfer matrix by means of signal flow-chart to analyze the MPRR. We do not need complicated calculation for steady state analysis because transfer matrix elements are formulated clearly. As a result, The calcultaion time in this method can be reduced 1/3 to 1/20 times compared with using scattering matirx method. Furthermore, a transmittance characteristics of the MPRR at FSR extension-factor of 10 will also be shown. This suggests that analysis of other types of the MPRR by using this method can be performed simply and take a shorter time

Complete paternal uniparental isodisomy for chromosome 1 revealed by mutation analyses of the TRKA (NTRK1) gene encoding a receptor tyrosine kinase for nerve growth factor in a patient with congenital insensitivity to pain with anhidrosis

Uniparental disomy (UPD) is defined as the presence of a chromosome pair that derives from only one parent in a diploid individual. The human TRKA gene on chromosome 1q21-q22 encodes a receptor tyrosine kinase for nerve growth factor and is responsible for an autosomal recessive genetic disorder: congenital insensitivity to pain with anhidrosis (CIPA). We report here the second case of paternal UPD for chromosome 1 in a male patient with CIPA who developed normally at term and did not show overt dysmorphisms or malformations. He had only the usual features of CIPA with a homozygous mutation at the TRKA locus and a normal karyotype with no visible deletions or evidence of monosomy 1. Haplotype analysis of the TRKA locus and allelotype analyses of whole chromosome 1 revealed that the chromosome pair was exclusively derived from his father. Non-maternity was excluded by analyses of autosomes other than chromosome 1. Thus, we have identified a complete paternal isodisomy for chromosome 1 as the cause of reduction to homozygosity of the TRKA gene mutation, leading to CIPA. Our findings further support the idea that there are no paternally imprinted genes on chromosome 1 with a major effect on phenotype. UPD must be considered as a rare but possible cause of autosomal recessive disorders when conducting genetic testing

Design, implementation, and evaluation of the computer-aided clinical decision support system based on learning-to-rank: collaboration between physicians and machine learning in the differential diagnosis process

Abstract Background We are researching, developing, and publishing the clinical decision support system based on learning-to-rank. The main objectives are (1) To support for differential diagnoses performed by internists and general practitioners and (2) To prevent diagnostic errors made by physicians. The main features are that “A physician inputs a patient's symptoms, findings, and test results to the system, and the system outputs a ranking list of possible diseases”. Method The software libraries for machine learning and artificial intelligence are TensorFlow and TensorFlow Ranking. The prediction algorithm is Learning-to-Rank with the listwise approach. The ranking metric is normalized discounted cumulative gain (NDCG). The loss functions are Approximate NDCG (A-NDCG). We evaluated the machine learning performance on k-fold cross-validation. We evaluated the differential diagnosis performance with validated cases. Results The machine learning performance of our system was much higher than that of the conventional system. The differential diagnosis performance of our system was much higher than that of the conventional system. We have shown that the clinical decision support system prevents physicians' diagnostic errors due to confirmation bias. Conclusions We have demonstrated that the clinical decision support system is useful for supporting differential diagnoses and preventing diagnostic errors. We propose that differential diagnosis by physicians and learning-to-rank by machine has a high affinity. We found that information retrieval and clinical decision support systems have much in common (Target data, learning-to-rank, etc.). We propose that Clinical Decision Support Systems have the potential to support: (1) recall of rare diseases, (2) differential diagnoses for difficult-to-diagnoses cases, and (3) prevention of diagnostic errors. Our system can potentially evolve into an explainable clinical decision support system

Does the routine handling affect the phenotype of disease model mice?

The three different mouse handling methods, picking up by tails, tunnels, and open hands were performed using the ICGN glomerulonephritis mouse and the severity of symptoms was evaluated. The handling groups exhibited a tendency of more severe symptoms than the non-handling control group. Female mice handled by their tails showed significantly more severe symptoms than the control group. In addition, we subjected the normal laboratory mice, C57BL/6 and BALB/c mice to tail and tunnel handling to assess the stress conditions. The plasma corticosterone level in the tail-handled mice was higher than that in control mice. These results indicate that handling causes stress and may affect the phenotype of disease model mice

Does the routine handling affect the phenotype of disease model mice?

The three different mouse handling methods, picking up by tails, tunnels, and open hands were performed using the ICGN glomerulonephritis mouse and the severity of symptoms was evaluated. The handling groups exhibited a tendency of more severe symptoms than the non-handling control group. Female mice handled by their tails showed significantly more severe symptoms than the control group. In addition, we subjected the normal laboratory mice, C57BL/6 and BALB/c mice to tail and tunnel handling to assess the stress conditions. The plasma corticosterone level in the tail-handled mice was higher than that in control mice. These results indicate that handling causes stress and may affect the phenotype of disease model mice

Severe cytokine release syndrome resulting in purpura fulminans despite successful response to nivolumab therapy in a patient with pleomorphic carcinoma of the lung: a case report

Abstract Background Immune checkpoint inhibitors (ICIs) have provided more options in the treatment of lung cancer. However, ICIs can cause several unfavorable reactions generally referred to as immune-related adverse effects. Case presentation In this report, we present the case of a 52-year-old woman with successful regression of pleomorphic carcinoma of the lung following nivolumab therapy. She developed purpura fulminans (PF) ultimately resulting in amputation of both lower extremities. Blood tests revealed thrombocytopenia with increased serum soluble IL-2 receptor, ferritin, and triglyceride levels suggesting hemophagocytic lymphohistiocytosis (HLH). In addition, serum A disintegrin-like and metalloproteinase with thrombospondin type 1 motifs 13 activity was decreased, suggesting thrombotic thrombocytopenic purpura (TTP). Further detailed analysis revealed severe hypercytokinemia including increased levels of IL-1β, IL-6, IL-10, TNFα, IFNγ, and G-CSF. Conclusion The severe systemic inflammatory reaction and impaired peripheral circulation in this patient was attributed to excessive immunological effect induced by nivolumab resulting in cytokine release syndrome (CRS). This is the first report of a patient with multiple pathological conditions including HLH, TTP-like condition, and PF presumably arising from ICI-induced CRS. Further accumulating thoroughly investigated cases would lead to better understanding of the disease and development of reliable cancer immunotherapy

Evaluation of peripheral bronchiole visualization using model-based iterative reconstruction in quarter-detector computed tomography.

This study aimed to evaluate the visualization of peripheral bronchioles in normal lungs via quarter-detector computed tomography (QDCT). Visualization of bronchioles within 10 mm from the pleura is considered a sign of bronchiectasis. However, it is not known peripheral bronchioles how close to the pleura in normal lungs can be tracked using QDCT. This study included 228 parts in 76 lungs from 38 consecutive patients who underwent QDCT. Reconstruction was performed with different thicknesses, increments, and matrix sizes: 0.5-mm thickness and increment with 512 and 1024 matrixes (Group5 and Group10, respectively) and 0.25-mm thickness and increment with 1024 matrix (Group10Thin). The distance between the most peripheral bronchiole visible and the pleura was determined in the three groups. The distance between the peripheral bronchial duct ends and the nearest pleural surface were significantly shorter in the order of Group10Thin, Group10, and Group5, and the mean distances from the pleura in Group10Thin and Group10 were shorter than 10 mm. These findings suggest the visualization of peripheral bronchioles in QDCT was better with a 1024 axial matrix than with a 512 matrix, and with a 0.25-mm slice thickness/increment than with a 0.5-mm slice thickness/increment. Our study also indicates bronchioles within 10 mm of the pleura do not necessarily indicate pathology

Analysis for genetic loci controlling protoscolex development in the Echinococcus multilocularis infection using congenic mice

The resistance/susceptibility to Echinococcus multilocularis infection in mice is genetically controlled. However, genetic factors responsible for these differences remain unknown. Our previous study in genetic linkage analysis has revealed that there is a significant quantitative trait locus (QTL) for the establishment of cyst (Emcysl), and a highly significant QTL for the development of protoscolex of E. multilocularis larvae (Empscl), on mouse chromosomes 6 and 1, respectively. The current study aimed to confirm these QTLs and narrow down the critical genetic region that controls resistance/susceptibility to E. multilocularis infection by establishing congenic and subcongenic lines from C57BL/6 (B6) and DBA/2 (D2) mice. For protoscolex development phenotype, two congenic lines, B6.D2-Empscl and D2.B6-Empscl were developed, where responsible QTL, Empsc1 was introgressed from D2 into B6 background and vice versa. For cyst establishment phenotype, two congenic lines, B6.D2-Emcys1 and D2.B6-Emcys1 were developed, where responsible QTL, Emcys1 was introgressed from D2 into B6 background and vice versa. Because there was no significant difference in cyst establishment between B6.D2Emcysl and D2.B6-Emcys1 mice after challenge with E. multilocularis, it is suggested that the Emcysl does not solely control the cyst establishment in mouse liver. However, infection experiments with B6.D2-Empscl and D2.B6-Empsc1 mice showed a significant difference in protoscolex development in the cyst. It confirms that the Empsc1 controls phenotype of the protoscolex development in the cyst. Subsequently, two subcongenic lines, B6.D2-Empsc1.1 and B6.D2-Empsc1.2 from B6.D2-Emcysl and one subcongenic line, D2.B6-Empsc1.1 from D2.B6-Empscl were developed to narrow down the critical region responsible for protoscolex development. From the results of infection experiments with E. multilocularis in these subcongenic mice, it is concluded that a gene responsible for protoscolex development is located between D1Mit290 (68.1 cM) and D1Mit511 (97.3 cM)