Current classification and diversity of Fusarium species complex, the causal pathogen of Fusarium wilt disease of banana in Malaysia

The re-emergence of the Fusarium wilt caused by Fusarium odoratissimum (F. odoratissimum) causes global banana production loss. Thirty-eight isolates of Fusarium species (Fusarium spp.) were examined for morphological characteristics on different media, showing the typical Fusarium spp. The phylogenetic trees of Fusarium isolates were generated using the sequences of histone gene (H3) and translation elongation factor gene (TEF-1α). Specific primers were used to confirm the presence of F. odoratissimum. The phylogenetic trees showed the rich diversity of the genus Fusarium related to Fusarium wilt, which consists of F. odoratissimum, Fusarium grosmichelii, Fusarium sacchari, and an unknown species of the Fusarium oxysporum species complex. By using Foc-TR4 specific primers, 27 isolates were confirmed as F. odoratissimum. A pathogenicity test was conducted for 30 days on five different local cultivars including, Musa acuminata (AAA, AA) and Musa paradisiaca (AAB, ABB). Although foliar symptoms showed different severity of those disease progression, vascular symptoms of the inoculated plantlet showed that infection was uniformly severe. Therefore, it can be concluded that the Fusarium oxysporum species complex related to Fusarium wilt of banana in Malaysia is rich in diversity, and F. odoratissimum has pathogenicity to local banana cultivars in Malaysia regardless of the genotype of the banana plants

Finishing the euchromatic sequence of the human genome

The sequence of the human genome encodes the genetic instructions for human physiology, as well as rich information about human evolution. In 2001, the International Human Genome Sequencing Consortium reported a draft sequence of the euchromatic portion of the human genome. Since then, the international collaboration has worked to convert this draft into a genome sequence with high accuracy and nearly complete coverage. Here, we report the result of this finishing process. The current genome sequence (Build 35) contains 2.85 billion nucleotides interrupted by only 341 gaps. It covers ∼99% of the euchromatic genome and is accurate to an error rate of ∼1 event per 100,000 bases. Many of the remaining euchromatic gaps are associated with segmental duplications and will require focused work with new methods. The near-complete sequence, the first for a vertebrate, greatly improves the precision of biological analyses of the human genome including studies of gene number, birth and death. Notably, the human enome seems to encode only 20,000-25,000 protein-coding genes. The genome sequence reported here should serve as a firm foundation for biomedical research in the decades ahead

Psychological stress in aged female mice causes acute hypophagia independent of central serotonin 2C receptor activation

Sex differences exist in the activation of the hypothalamic-pituitary-adrenal axis following exposure to stress, and the stress response is further affected by aging. This study was conducted to elucidate the mechanism of hypophagia in aged female mice exposed to stress. Immediately after a stress load, aged female mice exhibited acute hypophagia and a rise in plasma corticosterone levels. The administration of a serotonin 2C receptor (5-T2CR) antagonist suppressed plasma corticosterone but did not affect the reduction in food intake. In contrast, an endogenous ghrelin enhancer, rikkunshito (RKT), significantly inhibited the reduction in food intake. An increase in peripheral acylated ghrelin levels during fasting, which occurs in young mice, was not observed in aged female mice. Moreover, in these mice, significantly increased levels of ghrelin and gastric preproghrelin mRNA expression were observed in the fed status. Moreover, plasma ghrelin levels were elevated by RKT and not by the 5-HT2CR antagonist. In female mice, the hypothalamic non-edited (INI) and partially edited mRNA 5-HT2CR isoforms (VNV, VNI, VSV or VSI) decreased with age, while in male mice, the editing isoform was unchanged by aging or stress. Estrogen receptor alpha (ER alpha)-positive cell counts in the arcuate nucleus of young male mice exposed to stress and control aged male mice were increased compared with those in young control mice. In aged male mice exposed to stress, the number of ER alpha-expressing cells in the paraventricular nucleus were significantly increased compared with those in aged control mice; in female mice, there was no increase in the number of ER alpha-positive cells. Hypophagia in aged female mice exposed to stress may be independent of 5-HT2CR activation. It seems likely that the mechanisms may be caused by sex dependent, differential regulation in 5-HT2CR mRNA expression, peripheral acylated ghrelin secretion and/or hypothalamic ER alpha expression

CRF receptor 1 antagonism and brain distribution of active components contribute to the ameliorative effect of rikkunshito on stress-induced anorexia

Rikkunshito (RKT), a Kampo medicine, has been reported to show an ameliorative effect on sustained hypophagia after novelty stress exposure in aged mice through serotonin 2C receptor (5-HT2CR) antagonism. We aimed to determine (1) whether the activation of anorexigenic neurons, corticotropin-releasing factor (CRF), and pro-opiomelanocortin (POMC) neurons, is involved in the initiation of hypophagia induced by novelty stress in aged mice; (2) whether the ameliorative effect of RKT is associated with CRF and POMC neurons and downstream signal transduction; and (3) the plasma and brain distribution of the active components of RKT. The administration of RKT or 5-HT2CR, CRF receptor 1 (CRFR1), and melanocortin-4 receptor antagonists significantly restored the decreased food intake observed in aged male C57BL/6 mice in the early stage after novelty stress exposure. Seven components of RKT exhibited antagonistic activity against CRFR1. Hesperetin and isoliquiritigenin, which showed antagonistic effects against both CRFR1 and 5-HT2CR, were distributed in the plasma and brain of male Sprague-Dawley rats after a single oral administration of RKT. In conclusion, the ameliorative effect of RKT in this model is assumed to be at least partly due to brain-distributed active components possessing 5-HT2CR and CRFR1 antagonistic activities

TJN-259 Improves Mesangial Lesions in Experimental Immunoglobulin A Nephropathy in ddY Mice

TJN-259 is a chemical substance based on the structural features of the botanically derived ingredient acteoside. This study was performed in order to elucidate the antinephritic effects of TJN-259 in experimental immunoglobulin A (IgA) nephropathy. In this study, 28-week-old ddY mice were used as a spontaneous model of IgA nephropathy. With regard to spontaneous IgA nephropathy, we investigated the effects of TJN-259 administered from 28 to 40 weeks. In addition, an accelerated model of IgA nephropathy was experimentally induced in ddY mice by oral administration of bovine serum albumin, followed by reticuloendothelial blocking by colloidal carbon injection and heminephrectomy. At 10 weeks after the 3rd carbon injection, we also examined the effects of TJN-259 on accelerated IgA nephropathy. To investigate the effects of TJN-259 on transforming growth factor (TGF)-β1 production in accelerated IgA nephropathy, kidneys were isolated and measured TGF-β1 by the enzyme-linked immunosorbent assay (ELISA) method. The administration of TJN-259 to mice with spontaneous IgA nephropathy decreased the incidence of mesangial expansion as well as the number of nuclei per glomerular cross-section in comparison with that of non-treated mice. In addition, TJN-259 treatment prevented the increase in the incidence of mesangial expansion, crescent formation, and segmental sclerosis in glomeruli in accelerated IgA nephropathy. TJN-259 also inhibited the increased immunostaining score of collagen type IV and TGF-β1 in glomeruli of accelerated IgA nephropathy. Treatment with TJN-259 inhibited the increases in renal total and mature TGF-β1 protein levels in accelerated type IgA nephropathy. TJN-259 failed to inhibit the increase in serum IgA levels in both models. These results suggest that TJN-259 was an effective treatment against IgA nephropathy in ddY mice, acting via the suppression of TGF-β1 production in glomeruli

本来性と自他への信頼感が過剰適応に与える影響

過剰適応とは，外的適応が過度で内的適応と外的適応のバランスが崩れた状態とされる。一方で，適応方略や防衛機制としての側面も指摘されている。過剰適応的な適応スタイルは青年期以前に身につけられるが，問題として顕在化するのは青年期以降であると考えられる。そのため，過剰適応の支援を考える上では青年期以降にも介入可能な要因について過剰適応との関連を検討する必要がある。本研究では外的影響を受けにくい本来性と，青年期以降も変容，発達する信頼感をとりあげ過剰適応との関連を検討した。本来性，適応行動の高低により群分けしSEMによるパス解析を行った。群間に異質性が認められ，本来性の高低によって過剰適応行動をとるプロセスは異なり， 2つの過剰適応タイプがあるという重要な示唆を得た。外的適応行動の得点が高い者のうち，本来性低群は自己が希薄な代わりに他者の期待に応えることで外的適応を保っていると考えられた。一方，本来性高群では自己信頼や他者信頼，他者影響感が外的適応行動に影響を与えていることが示され，他者との関係を維持するために積極的に自己抑制することが考えられた。Over-adaptation is a maladjusted state of adaptation where external adaptation is excessive and the balance between internal and external adaptation is lost, while the aspects for adaptation strategies or defense mechanism are also pointed. It is necessary to clarify the factors that influence over-adaptation that can change even after adolescence because the problem of over-adaptation don’t become apparent until adolescence. This study examined the relationship between the authenticity that is hard to change, the sense of trust that can change and develop, and the adaptive behavior. A questionnaire survey was conducted and 263 responses were obtained. Date was divided into four groups according to the level of authenticity and adaptive behavior. Path analysis and consequent refinement of the model resulted in final models that differed from the level of authenticity. It suggested there were two types of over-adaptation. Among those with high adaptive behavior, the group of low authenticity maintained external adaptation by responding to the expectations from others instead of having a weak self-consciousness, and in the high authenticity group it was considered that they positively restrain themselves to maintain the relationship with others

A Case of Eosinophilic Chronic Rhinosinusitis Associated with Choroidal Folds and Ocular Motility Disorder

We report a case of eosinophilic chronic rhinosinusitis (ECRS) associated with choroidal folds and ocular motility disorder. A 50-year-old male with rhinosinusitis and bronchial asthma presented with anorthopia of the lower visual field and ocular motility disorder of the left eye. Dilated fundus examination and optical coherence tomography (OCT) revealed wavy choroidal folds in the upper retina. An emergent computed tomography (CT) showed sinusitis, a partial defect of the superior wall of the orbit on the left side, and deformation of the left eye. Based on the clinical findings, the patient was diagnosed with sinusitis complicated by ocular motility disorder. Endoscopic sinus surgery (ESS) was performed. A histopathological examination of the excised polyps showed extensive eosinophil invasion. According to the clinical findings of the nasal polyps, CT images, and peripheral blood tests, he was diagnosed as ECRS. One month after ESS, both ocular movement and anorthopia were improved. The choroidal folds observed using OCT disappeared 2 months after ESS. Although ECRS is rarely associated with ocular complications, bone involvement in sinusitis may result in deformation of the eyeball leading to choroidal folds and ocular motility disorder

TJN-419 Improves Dextran Sulfate Sodium-Induced Colitis via Inhibition of Interleukin-12 Release

We investigated the association of interleukin-12 (IL-12) with development of dextran sulfate sodium (DSS)-induced colitis in mice, and examined the effects of TJN-419, a synthetic compound derived from acteoside, on this process. Enhanced IL-12 production in lipopolysaccharide (LPS)-stimulated macrophages was dose-dependently inhibited by addition of TJN-419 to culture medium, and this effect was abolished by pretreatment with PD98059, an inhibitor of extracellular-regulated kinase. We then assessed the effect of TJN-419 or a neutralizing antibody against murine IL-12 in a DSS-induced colitis model in C57 BL/6 mice. Colitis was induced by 5% DSS solution given as drinking water. Treatment with the anti-IL-12 antibody was performed intravenously and TJN-419 was administered orally. We also investigated the effect of TJN-419 on erosion in the rectum in a DSS-induced colitis model in rat. The IL-12 level in the rectum was significantly enhanced and the IL-10 level was significantly decreased in animals with DSS-induced colitis compared with untreated controls. Intravenous injection of the anti-IL-12 antibody and oral administration of TJN-419 inhibited clinical symptoms in DSS-induced colitis. TJN-419 also inhibited the increase in IL-12 and suppressed the area of erosion in the rectum in DSS-induced colitis in rats. These results indicate that IL-12 has a possible role in development of DSS-induced colitis and that TJN-419 is effective for treatment of this disease model via inhibition of IL-12 production