27 research outputs found

    Studies on the Gametogenesis in Polyploid Ginbuna Carassius auratus langsdorfii

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    The structural changes of the chromosomes during meiosis of gynogenetic triploid female ginbuna Carassius auratus langsdorfii, and naturally produced or sex-reversed male ginbuna were studied cytologically. In triploid female ginbuna, at zygotene stage two homologue-like chromosomes out of three were sometimes adjacent each other in the neighbourhood. At pachytene stage almost all of the chromosomes were univalents, and at diplotene stage almost all of lampbrush chromosomes were also univalents. From these results it seems probable that the two homologue-like chromosomes undergo synapsis at zygotene stage, but they might be separated to univalents on and after pachytene stage. Thereafter, each univalent chromosome might be split to two chromatids and result in separation of one chromatids to one direction and the other to the opposite one. In this way, the egg may maintain the maternal chromosome number and karyotype throughout the oogenesis. On the other hand, in some specimens at diplotene stage at most two to three bivalent lampbrush chromosomes, connected with one chiasma, were observed. These facts seem to explain the hypervariabilities among the gynogenetic triploid ginbuna. On the other hand, male individuals were almost similar to the processes in meiosis, though in some chromosomes it observed a few bivalents and rod-shaped bi-, tri-, and multivalent chromosomes at metaphase.Article信州大学理学部紀要 19(1): 37-52(1984)departmental bulletin pape

    Young athlete with sudden cardiac arrest treated with therapeutic hypothermia

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    Reported herein is a coronary anomaly that occurred in a young adolescent athlete who presented with cardiopulmonary arrest. The patient was resuscitated and treated with therapeutic hypothermia. The patient had no associated neurological complications at follow up. Enhanced computed tomography of the heart indicated an anomalous left main coronary artery originating from the right coronary sinus and coursing between the aorta and the pulmonary artery. The patient underwent surgical intervention with coronary artery bypass grafting to prevent symptom recurrence.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/100297/1/ped12144.pd

    Quantum critical behavior of the hyperkagome magnet Mn3CoSi

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    β-Mn-type family alloys Mn3TX (T = Co, Rh, and Ir; X = Si and Ge) have a three-dimensional antiferromagnetic (AF) corner-shared triangular network, i.e., the hyperkagome lattice. The antiferromagnet Mn3RhSi shows magnetic short-range order over a wide temperature range of approximately 500 K above the Néel temperature TN of 190 K. In this family of compounds, as the lattice parameter decreases, the long-range magnetic ordering temperature decreases. Mn3CoSi has the smallest lattice parameter and the lowest TN in the family. The quantum critical point (QCP) from AF to the quantum paramagnetic state is expected near a cubic lattice parameter of 6.15 Å. Although the Néel temperature of Mn3CoSi is only 140 K, the emergence of the quantum critical behavior in Mn3CoSi is discussed. We study how the magnetic short-range order appears in Mn3CoSi by using neutron scattering, μSR, and bulk characterization such as specific heat capacity. According to the results, the neutron scattering intensity of the magnetic short-range order in Mn3CoSi does not change much at low temperatures from that of Mn3RhSi, although the μSR short-range order temperature of Mn3CoSi is largely suppressed to 240 K from that of Mn3RhSi. Correspondingly, the volume fraction of the magnetic short-range order regions, as shown by the initial asymmetry drop ratio of μSR above TN, also becomes small. Instead, the electronic-specific heat coefficient γ of Mn3CoSi is the largest in this Mn3T Si system, possibly due to the low-energy spin fluctuation near the quantum critical point

    Inhibitory effect of neopterin on NADPH-dependent superoxide-generating oxidase of rat peritoneal macrophages

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    AbstractThe effect of the oxidized form of neopterin (NP) on the NADPH-dependent superoxide-generating oxidase (NADPH-oxidase) was investigated in both whole-cell and cell-free activation systems by using peritoneal macrophages of rats which had received an intraperitoneal injection of mineral oil. In the whole-cell system, NP remarkably inhibited the generation of Superoxides in macrophages stimulated with phorbol myristate acetate (PMA). NP also showed an significant suppression of the activation of superoxide-generating NADPH-oxidase in the cell-free system using solubilized membranes and sodium dodecyl sulfate (SDS) as a stimulant. The 50%-inhibitory concentration (IC50) of NP was about 1 μM in both assay systems. In a kinetic study, competitive inhibition of the NADPH-oxidase by NP was observed in the cell-free system with a calculated inhibition constant (Ki) of 6.50 μM. These findings suggest that NP may play an important role in the suppression of Superoxide generation via the inhibition of the NADPH-oxidase in phagocytes

    Eosinophilic Cystitis Presented as a Manifestation of Hypereosinophilic Syndrome: A Case Report and Review of the Literature

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    Background: Hypereosinophilic syndrome (HES) is a group of disorders marked by the sustained overproduction of eosinophils, in which eosinophilic infiltration and inflammatory substance release cause damage to multiple organs. Eosinophilic cystitis (EC) is an inflammatory disorder caused by eosinophilic infiltration of the bladder wall. Although EC is often associated with eosinophilia, it has been rarely reported as a manifestation of HES. We report a case of EC as a primary manifestation of HES. The patient was a 27-year-old male with a history of complete intracardiac repair of tetralogy of Fallot who presented with an acute onset of dysuria accompanied by eosinophilia (7.5 × 103/µl, 60% of white blood cells). Ultrasonography and MRI of the bladder showed a bladder mass, a biopsy of which revealed eosinophilic infiltration and degranulation. Methods: We performed a literature search in PubMed from 2001 to 2012 to find patients with EC who may have had HES. Results: There were 4 patients with HES who had EC including the present case. Of 14 patients reported as EC in whom the eosinophil count was described, 5 had eosinophils of ≥1,500/µl. None of the 5 patients had secondary causes for eosinophilia. Of the 9 patients with definite or probable HES, 7 patients (78%) were male and 5 patients (56%) showed a concomitant eosinophilic gastrointestinal disorder. Conclusion: HES may not be uncommon as the cause of EC. Thorough evaluation and close monitoring are warranted in EC patients with elevated eosinophils

    Clec4A4 is a regulatory receptor for dendritic cells that impairs inflammation and T-cell immunity

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    International audienceDendritic cells (DCs) comprise several subsets that are critically involved in the initiation and regulation of immunity. Clec4A4/DC immunoreceptor 2 (DCIR2) is a C-type lectin receptor (CLR) exclusively expressed on CD8 alpha(-) conventional DCs (cDCs). However, how Clec4A4 controls immune responses through regulation of the function of CD8 alpha(-) cDCs remains unclear. Here we show that Clec4A4 is a regulatory receptor for the activation of CD8 alpha(-) cDCs that impairs inflammation and T-cell immunity. Clec4a4(-/-) CD8 alpha(-) cDCs show enhanced cytokine production and T-cell priming following Toll-like receptor (TLR)-mediated activation. Furthermore, Clec4a4(-/-) mice exhibit TLR-mediated hyperinflammation. On antigenic immunization, Clec4a4(-/-) mice show not only augmented T-cell responses but also progressive autoimmune pathogenesis. Conversely, Clec4a4(-/-) mice exhibit resistance to microbial infection, accompanied by enhanced T-cell responses against microbes. Thus, our findings highlight roles of Clec4A4 in regulation of the function of CD8 alpha(-) cDCs for control of the magnitude and quality of immune response
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