The Mino-Tanba belt in southwest Japan, a segment of the Cordilleran-type orogenic chain of Jurassic east Asia, is composed mainly of a Middle-Upper Jurassic subduction-accretion complex in which Triassic and Lower Jurassic bedded radiolarian cherts occur as large allochthonous units structurally interlayered with Middle-Upper Jurassic clastic rocks. High-resolution microfossil (conodont and radiolaria) research has identified very low average sedimentation rates of about 0.5 g/cm2/1000 yr in the chert units, similar to those of modern pelagic sediments accumulated in open ocean environments. Judging from the low average sedimentation rate, high purity of biogenic silica, long duration of continuous deposition (>50 m.y.), and wide along-strike extent (> 1000 km), the bedded radiolarian cherts in the Mino-Tanba belt are best understood as ancient pelagic sediments that accumulated in open ocean environments; accordingly, the alleged origin in smaller marginal basins is untenable. Upward lithologic change from bedded chert to overlying siliceous mudstone in the uppermost portion of chert sequences suggests the gradual landward approach of the oceanic plate 1Now at Kyou-ei Kogyo Consulting Company, Paper number 90TC02134. 0278-7407/91]90TC-02134510.00 toward a trench. The tectonic interlayering of these cherts and coarse-grained terrigenous clastics is a secondary feature that was added through duplexingunderplating in the subduction zone. On the basis of the primary stratigraphy and field occurrence of Triassic bedded chert in the Mino-Tanba belt, newly proposed are an idealized oceanic plate stratigraphy and a generalized travel history of a Cordillerantype bedded chert from its birth at a mid-oceanic ridge to its demise at a subduction zone.
Ketoconazole (KCZ) has been shown to exhibit anti-inflammatory effects in addition to its inhibitory effects against fungi; however, the underlying molecular mechanism remains poorly understood. Aryl hydrocarbon receptor (AhR), a receptor that is activated by polycyclic aromatic hydrocarbons (PAHs) and halogenated aromatic hydrocarbons such as dioxin, is a sensor of the redox system against oxidative stress and regulates nuclear factor-erythroid 2-related factor-2 (Nrf2), a master switch of the redox machinery. To clarify whether KCZ modulates AhR-Nrf2 function leading to redox system activation, cultured human keratinocytes were treated with KCZ. Confocal microscopic analysis revealed that KCZ induced AhR nuclear translocation, resulting in the upregulation of CYP1A1 mRNA and protein expression. Furthermore, KCZ actively switched on Nrf2 nuclear translocation and quinone oxidoreductase 1 expression. Tumor necrosis factor-α- and benzo(a)pyrene (BaP)-induced reactive oxidative species (ROS) and IL-8 production were effectively inhibited by KCZ. Knockdown of either AhR or Nrf2 abolished the inhibitory capacity of KCZ on ROS and IL-8 production. In addition, KCZ-induced Nrf2 activation was canceled by AhR knockdown. Moreover, KCZ inhibited BaP-induced 8-hydroxydeoxyguanosine and IL-8 production. In conclusion, the engagement of AhR by KCZ exhibits the cytoprotective effect mediated by the Nrf2 redox system, which potently downregulates either cytokine-induced (AhR-independent) or PAH-induced (AhR-dependent) oxidative stress.
It has been said that 'Necessity is the mother of invention'. Certainly, that old saying applies to the terms phaeohyphomycosis and hyalohyphomycosis. In 1974 [4] and 1982 [2], these were proposed as umbrella terms to cover a growing number of new mycoses caused by moulds whose basic septate mycelial tissue forms were either phaeoid (Gr. 'phaios') or hyaline (Gr. 'hyaleos'), respectively.Primarily, they were intended to stem and counter the growing flood of new generic based disease names derived from the aetiological agents of the emerging opportunistic mycoses. Interestingly, these new mycoses were being encountered in increasing frequency during a period when medical and public health professionals were optimistically predicting that infectious diseases were well on the road to eradication [48]. After all, the incidence and prevalence of the world's killer microbial diseases, such as tuberculosis, polio and malaria, were waning. Was not smallpox on the verge of being obliterated? This hubris was based on the belief that tremendous strides had been made, especially in the Western nations, in reducing the morbidity and mortality caused by infectious diseases. This feat had been accomplished in little more than a century by raising hygiene standards, conducting massive immunization programmes and through the discovery, production and widespread use of antibiotics.It is pertinent to note here that comparable advances, with two exceptions, had not been achieved among the mycoses. One of these exceptional developments occurred in the realm of the cutaneous mycoses that were caused by several anthropophilic dermatophytes. In Europe, the appalling prevalence and incidence of favus among children, as well as adults, infected by Trichophyton schoenleinii and the epidemic of Microsporum audouinii engendered tinea capitis during World War Two, which had erupted and spread rapidly throughout the Western nations, were, to all intents and purposes, eliminated along with the endemic European infections caused by Triehophyton megninii and the post-World War Two epidemic of Trichophyton violaceum infections in Bosnia-Herzegovina [36]. The demise of human ringworm infections in epidemic form became possible when X-ray induced epilation was introduced in 1904 [78, 79] and when the epochal orally administered antifungal agent griseofulvin made its appearance in the late 1950s [8,98]. The second exception was the veterinary triumph of eradicating histoplasmosis farciminosii among equines from the UK and Western Europe by a rigidly enforced quarantine and slaughter policy [14].Ironically, the advances in the control of bacterial, parasitic and viral diseases, as well as in the treatment of non-infectious diseases, such as cancer, made it possible for some of the well known systemic mycoses to proliferate, and for new fungal diseases to emerge in unprecedented varieties and numbers. The therapeutic measures used to cure
Sporotrichosis is caused by a thermo-dependent dimorphic fungus, Sporothrix schenckii. The major clinical manifestations occur in the skin; however, cases of visceral manifestations have also been increasingly reported with some being observed in immune compromised patients. Different virulence of individual S. schenckii strain as well as immune status of the host could contribute to form such different clinical manifestations. Thus, the purpose of the study was to investigate whether different virulence of individual S. schenckii could be a factor for such clinical difference. We investigated the interactions between human monocyte-derived dendritic cells (MoDCs) and S. schenckii, assessed by (i) morphological features, (ii) surface marker expressions, cytokine productions, (iii) signaling pathways and (iv) allostimulatory activity of the activated MoDCs. Immature MoDCs, obtained from peripheral blood monocytes supplemented with granulocyte macrophage colony-stimulating factor and IL-4, were stimulated with S. schenckii strains of both yeasts and conidia forms of different origins (cutaneous isolates: KMU4649, IFM5906 and IFM46010; visceral isolates: KMU4648, IFM41598 and ATCC26331) to be used for various assays. Through the analysis, we found that the cutaneous S. shenckii of cutaneous origins were more potent to activate MoDCs to induce strong T(h)1 response, as evidenced by abundant IFN-gamma production, while the S. shenckii of visceral origins induced only minimal dendritic cell activation and T(h)1 induction. The p38 mitogen-activated protein kinase and c-Jun N-terminal kinase signaling pathways appeared to be associated with the differential activation of the MoDCs by S. schenckii of cutaneous and the visceral origins. Overall, we concluded that the differential activation of MoDCs by S. schenckii of cutaneous and visceral origins to induce T(h)1 response, other than immune status or the host, may be a factor for their different clinical manifestations.
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