Catalogue of the spiders (Arachnida: Araneae) of Tottori Prefecture, western Honshu, Japan

文献記録と新たに採集された標本にもとづき, 鳥取県産として44科438種の真正クモ類(クモガタ綱クモ目)の記録をまとめた。次の26種は鳥取県内初記録となる：イトグモ, テナガマシラグモ, ナルトミダニグモ, コガネヒメグモ, マダラヒメグモ, クロササヒメグモ, クロテナガグモ, シバサラグモ, タイリクコサラグモ, ズブトヌカグモ, チュウガタシロカネグモ, チクニドヨウグモ, キタドヨウグモ, キヌアシナガグモ, オオクマヤミイロオニグモ, シロゴミグモ, クマダギンナガゴミグモ,Lathysdihamata Paik 1979,ムナキワシグモ, ヤマヨリメケムリグモ, モリメキリグモ, アシダカグモ, トライコアシダカグモ, チクニエビスグモ, ヤガタハエトリ, ナカヒラハエトリ。|On the basis of literature records and specimens newly obtained, a total of 438 species belonging to 44 familes of spiders (Arachnida, Araneae) from Tottori Prefecture, western Honshu, Japan are catalogued. Following 26 species are recorded as new to spider fauna of Tottori Prefecture: Loxosceles rufescens (Duf'our, 1820), Masirana longimana Yaginuma, 1970, Ischnothyreus narutomii (Nakatsudi, 1942), Chrysso scintillans (Thorell,1895), Steatoda triangulosa (Walckenaer, 1802) , Thymoites okumae (Yoshida, 1988), Bathyphantes robustus Oi, 1960, Neriene herbosa (Oi, 1960), Parasisis amurensis Eskov, 1984, Saitonia orientalis (Oi, 1960), Leucauge blanda (L. Koch, 1878) , Metleucauge chikunii Tanikawa, 1992, Metleucauge yaginumai Tanikawa, 1992; Tetragnatha lauta Yaginuma, 1959; Araneus acusisetus Zhu & Song, 1994, Cyclosa alba Tanikawa, 1992, Cyclosa kumadai Tanikawa,1992, Lathys dihamata Paik, 1979, Cladothela unciinsignita (Bösenberg & Strand, 1906), Drassyllus sasakawai Kamura, 1987, Gnaphosa potanini Simon, 1895,Heteropoda venatoria (Linnaeus, 1763), Sinopoda koreana (Paik, 1968), Synaema chikunii Ono, 1983, Pseudeuophrys erratica (Walckenaer, 1825), Sibianor kochiensis (Bohdanowicz & Proszynski, 1987)

An evolutionary ‘intermediate state’ of mitochondrial translation systems found in Trichinella species of parasitic nematodes: co-evolution of tRNA and EF-Tu

EF-Tu delivers aminoacyl-tRNAs to ribosomes in the translation system. However, unusual truncations found in some animal mitochondrial tRNAs seem to prevent recognition by a canonical EF-Tu. We showed previously that the chromadorean nematode has two distinct EF-Tus, one of which (EF-Tu1) binds only to T-armless aminoacyl-tRNAs and the other (EF-Tu2) binds to D-armless Ser-tRNAs. Neither of the EF-Tus can bind to canonical cloverleaf tRNAs. In this study, by analyzing the translation system of enoplean nematode Trichinella species, we address how EF-Tus and tRNAs have evolved from the canonical structures toward those of the chromadorean translation system. Trichinella mitochondria possess three types of tRNAs: cloverleaf tRNAs, which do not exist in chromadorean nematode mitochondria; T-armless tRNAs; and D-armless tRNAs. We found two mitochondrial EF-Tu species, EF-Tu1 and EF-Tu2, in Trichinella britovi. T.britovi EF-Tu2 could bind to only D-armless Ser-tRNA, as Caenorhabditis elegans EF-Tu2 does. In contrast to the case of C.elegans EF-Tu1, however, T.britovi EF-Tu1 bound to all three types of tRNA present in Trichinella mitochondria. These results suggest that Trichinella mitochondrial translation system, and particularly the tRNA-binding specificity of EF-Tu1, could be an intermediate state between the canonical system and the chromadorean nematode mitochondrial system

Bisoprolol Transdermal Patch Is Effective for the Treatment of AF Tachycardia

Atrial fibrillation (AF) is an irregular and often rapid heart rate that can increase the risk of stroke, heart failure, and other heart-related complications. Its incidence increases with age and the presence of concomitant heart disease. We present the cases of a 93-year-old woman, an 82-year-old man, and an 87-year-old woman who developed AF tachycardia. This report highlights the use of a bisoprolol transdermal patch to treat AF tachycardia in 3 adult elderly patients. In this paper, we report an initial treatment strategy using a bisoprolol transdermal patch and show heart rate trends for 24 hours

Long COVID presenting with intermittent fever after COVID-19 pneumonia

A 72-year-old man presented to our hospital with a fever. Chest computed tomography showed typical coronavirus disease 2019 (COVID-19) pneumonia. The fever normalized after a few days, and the pneumonia was alleviated. However, the intermittent fever subsequently re-occurred and persisted for over a month. Various tests, including blood tests, culture tests, and image evaluations, were performed. However, the conclusion was that long COVID was the cause of the intermittent fever as an exclusion diagnosis. Many patients suffer from persistent symptoms of COVID-19, but the symptoms and their durations vary. Here we report a case of prolonged fever after COVID-19 pneumonia

Adaptor proteins NUMB and NUMBL promote cell cycle withdrawal by targeting ERBB2 for degradation

Failure of trabecular myocytes to undergo appropriate cell cycle withdrawal leads to ventricular noncompaction and heart failure. Signaling of growth factor receptor ERBB2 is critical for myocyte proliferation and trabeculation. However, the mechanisms underlying appropriate downregulation of trabecular ERBB2 signaling are little understood. Here, we have found that the endocytic adaptor proteins NUMB and NUMBL were required for downregulation of ERBB2 signaling in maturing trabeculae. Loss of NUMB and NUMBL resulted in a partial block of late endosome formation, resulting in sustained ERBB2 signaling and STAT5 activation. Unexpectedly, activated STAT5 overrode Hippo-mediated inhibition and drove YAP1 to the nucleus. Consequent aberrant cardiomyocyte proliferation resulted in ventricular noncompaction that was markedly rescued by heterozygous loss of function of either ERBB2 or YAP1. Further investigations revealed that NUMB and NUMBL interacted with small GTPase Rab7 to transition ERBB2 from early to late endosome for degradation. Our studies provide insight into mechanisms by which NUMB and NUMBL promote cardiomyocyte cell cycle withdrawal and highlight previously unsuspected connections between pathways that are important for cardiomyocyte cell cycle reentry, with relevance to ventricular noncompaction cardiomyopathy and regenerative medicine

Impact of Progressive Site-Directed Therapy in Oligometastatic Castration-Resistant Prostate Cancer on Subsequent Treatment Response

The purpose of this study was to evaluate the impact of progressive site-directed therapy (PSDT) for oligometastatic castration-resistant prostate cancer (OM-CRPC) on the efficacy of subsequent androgen receptor axis-targeted (ARAT) drugs, and to demonstrate the possibility of prolonging overall survival (OS). We performed a retrospective analysis of 15 OM-CRPC patients who underwent PSDT and subsequently received first-line ARAT drugs (PSDT group) and 13 OM-CRPC patients who were treated with first-line ARAT drugs without PSDT (non-PSDT group). PSDT was performed with the intention of treating all progressing sites detected by whole-body diffusion-weighted MRI with radiotherapy. Thirteen patients (86.7%) treated with PSDT had a decrease in PSA levels, which was at least 50% in 10 (66.7%) patients. The median PSA progression-free survival (PFS) for PSDT was 7.4 months. The median PSA-PFS for ARAT was 27.2 months in patients in the PSDT group and 11.7 months in the non-PSDT group, with a significant difference between the two groups (hazard ratio [HR], 0.28; p = 0.010). The median OS was not reached in the PSDT group and was significantly longer than 44.5 months in the non-PSDT group (HR, 0.11; p = 0.014). In OM-CRPC, PSDT may improve the efficacy of subsequent ARAT and OS

Apparent Diffusion Coefficient Map-Based Texture Analysis for the Differentiation of Chromophobe Renal Cell Carcinoma from Renal Oncocytoma

Preoperative imaging differentiation between ChRCC and RO is difficult with conventional subjective evaluation, and the development of quantitative analysis is a clinical challenge. Forty-nine patients underwent partial or radical nephrectomy preceded by MRI and followed by pathological diagnosis with ChRCC or RO (ChRCC: n = 41, RO: n = 8). The whole-lesion volume of interest was set on apparent diffusion coefficient (ADC) maps of 1.5T-MRI. The importance of selected texture features (TFs) was evaluated, and diagnostic models were created using random forest (RF) analysis. The Mean Decrease Gini as calculated through RF analysis was the highest for mean_ADC_value. ChRCC had a significantly lower mean_ADC_value than RO (1.26 vs. 1.79 × 10−3 mm2/s, p < 0.0001). Feature selection by the Boruta method identified the first-quartile ADC value and GLZLM_HGZE as important features. ROC curve analysis showed that there was no significant difference in the classification performances between the mean_ADC_value-only model and the Boruta model (AUC: 0.954 vs. 0.969, p = 0.236). The mean ADC value had good predictive ability for the distinction between ChRCC and RO, comparable to that of the combination of TFs optimized for the evaluated cohort. The mean ADC value may be useful in distinguishing between ChRCC and RO

Perm1 promotes cardiomyocyte mitochondrial biogenesis and protects against hypoxia/reoxygenation-induced damage in mice.

Normal contractile function of the heart depends on a constant and reliable production of ATP by cardiomyocytes. Dysregulation of cardiac energy metabolism can result in immature heart development and disrupt the ability of the adult myocardium to adapt to stress, potentially leading to heart failure. Further, restoration of abnormal mitochondrial function can have beneficial effects on cardiac dysfunction. Previously, we identified a novel protein termed Perm1 (PGC-1 and estrogen-related receptor (ERR)-induced regulator, muscle 1) that is enriched in skeletal and cardiac-muscle mitochondria and transcriptionally regulated by PGC-1 (peroxisome proliferator-activated receptor gamma coactivator 1) and ERR. The role of Perm1 in the heart is poorly understood and is studied here. We utilized cell culture, mouse models, and human tissue, to study its expression and transcriptional control, as well as its role in transcription of other factors. Critically, we tested Perm1's role in cardiomyocyte mitochondrial function and its ability to protect myocytes from stress-induced damage. Our studies show that Perm1 expression increases throughout mouse cardiogenesis, demonstrate that Perm1 interacts with PGC-1α and enhances activation of PGC-1 and ERR, increases mitochondrial DNA copy number, and augments oxidative capacity in cultured neonatal mouse cardiomyocytes. Moreover, we found that Perm1 reduced cellular damage produced as a result of hypoxia and reoxygenation-induced stress and mitigated cell death of cardiomyocytes. Taken together, our results show that Perm1 promotes mitochondrial biogenesis in mouse cardiomyocytes. Future studies can assess the potential of Perm1 to be used as a novel therapeutic to restore cardiac dysfunction induced by ischemic injury