581 research outputs found
Cardiac Innervation and Sudden Cardiac Death
The heart is extensively innervated and its performance is tightly controlled by the nervous system. Cardiac innervation density varies in diseased hearts leading to unbalanced neural activation and lethal arrhythmia. Diabetic sensory neuropathy causes silent myocardial ischemia, characterized by loss of pain perception during myocardial ischemia, which is a major cause of sudden cardiac death in diabetes mellitus (DM). Despite its clinical importance, the mechanisms underlying the control and regulation of cardiac innervation remain poorly understood
Phylogenetic analyses of Japanese golden chanterelles and a new species description, Cantharellus anzutake sp nov.
ArticleMycoscience. 59(2): 153-165. (2018)journal articl
PALF: Pre-Annotation and Camera-LiDAR Late Fusion for the Easy Annotation of Point Clouds
3D object detection has become indispensable in the field of autonomous
driving. To date, gratifying breakthroughs have been recorded in 3D object
detection research, attributed to deep learning. However, deep learning
algorithms are data-driven and require large amounts of annotated point cloud
data for training and evaluation. Unlike 2D image labels, annotating point
cloud data is difficult due to the limitations of sparsity, irregularity, and
low resolution, which requires more manual work, and the annotation efficiency
is much lower than 2D image.Therefore, we propose an annotation algorithm for
point cloud data, which is pre-annotation and camera-LiDAR late fusion
algorithm to easily and accurately annotate. The contributions of this study
are as follows. We propose (1) a pre-annotation algorithm that employs 3D
object detection and auto fitting for the easy annotation of point clouds, (2)
a camera-LiDAR late fusion algorithm using 2D and 3D results for easily error
checking, which helps annotators easily identify missing objects, and (3) a
point cloud annotation evaluation pipeline to evaluate our experiments. The
experimental results show that the proposed algorithm improves the annotating
speed by 6.5 times and the annotation quality in terms of the 3D Intersection
over Union and precision by 8.2 points and 5.6 points, respectively;
additionally, the miss rate is reduced by 31.9 points
Critical role of TNF-alpha-TNFR1 signaling in intracranial aneurysm formation
BACKGROUND: Intracranial aneurysm (IA) is a socially important disease due to its high incidence in the general public and the severity of resultant subarachnoid hemorrhage that follows rupture. Despite the social importance of IA as a cause of subarachnoid hemorrhage, there is no medical treatment to prevent rupture, except for surgical procedures, because the mechanisms regulating IA formation are poorly understood. Therefore, these mechanisms should be elucidated to identify a therapeutic target for IA treatment. In human IAs, the presence of inflammatory responses, such as an increase of tumor necrosis factor (TNF)-alpha, have been observed, suggesting a role for inflammation in IA formation. Recent investigations using rodent models of IAs have revealed the crucial role of inflammatory responses in IA formation, supporting the results of human studies. Thus, we identified nuclear factor (NF)-kappaB as a critical mediator of inflammation regulating IA formation, by inducing downstream pro-inflammatory genes such as MCP-1, a chemoattractant for macrophages, and COX-2. In this study, we focused on TNF-alpha signaling as a potential cascade that regulates NF-kappaB-mediated IA formation. RESULTS: We first confirmed an increase in TNF-alpha content in IA walls during IA formation, as expected based on human studies. Consistently, the activity of TNF-alpha converting enzyme (TACE), an enzyme responsible for TNF-alpha release, was induced in the arterial walls after aneurysm induction in a rat model. Next, we subjected tumor necrosis factor receptor superfamily member 1a (TNFR1)-deficient mice to the IA model to clarify the contribution of TNF-alpha-TNFR1 signaling to pathogenesis, and confirmed significant suppression of IA formation in TNFR1-deficient mice. Furthermore, in the IA walls of TNFR1-deficient mice, inflammatory responses, including NF-kappaB activation, subsequent expression of MCP-1 and COX-2, and infiltration of macrophages into the IA lesion, were greatly suppressed compared with those in wild-type mice. CONCLUSIONS: In this study, using rodent models of IAs, we clarified the crucial role of TNF-alpha-TNFR1 signaling in the pathogenesis of IAs by inducing inflammatory responses, and propose this signaling as a potential therapeutic target for IA treatment
In vitro ectomycorrhization of Tricholoma matsutake strains is differentially affected by soil type.
ArticleMycoscience. 59(1): 89-97. (2018)journal articl
Efficient establishment of pure cultures of yellow chanterelle Cantharellus anzutake from ectomycorrhizal root tips, and morphological characteristics of ectomycorrhizae and cultured mycelium
ArticleMycoscience. 60(1): 45-53. (2019)journal articl
Endothelin-3 like immunoreactivity in plasma of patients with cirrhosis of the liver
A highly specific and sensitive radioimmunoassay (RIA) has been established for determination of endothelin-3 like immunoreactivity in human plasma to investigate its possible role in hemodynamic alterations due to liver disease. Crossreactivity with other endothelin isoforms was always below 4 %, the lower detection limit following extraction on Sep-Pak C18 cartridges was 0.5 pg/ml. The concentration of endothelin-3 (mean ± SEM) was 4.16 ± 0.56 pg/ml (n = 13) in plasma of patients with cirrhosis of the liver, three fold higher than in age matched controls (1.35 ± 0.27 pg/ml, n = 12, p < 0.01). Plasma immunoreactivity was confirmed to be endothelin-3 related by reverse-phase HPLC. These data could suggest a role of plasma endothelin-3 in circulatory changes, as they occur in cirrhosis of the liver
Physiological variation among Tricholoma matsutake isolates generated from basidiospores obtained from one basidioma
ArticleMycoscience. 60(2): 102-109. (2019)journal articl
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