• Economic and Environmental Geology
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• v.48 no.4
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• pp.313-324
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• 2015

This study constructed a 3D geological model for Uggi Nuur Fe-Mn mineralization zone in Mongolia, and the 3D geological distribution is cross-analyzed with magnetic anomaly distribution to figure out relationship between ore zone and subsurface geology. As a result of 4 step 3D modeling procedures including geological cross section, surface modeling, foliation modeling and solid modeling, the geology of the both study area is bordered by faults in NW direction with Munguntessj formation being located in the west side of the fault while Yashill formation is located on the other side of the fault. Moreover, the strike direction of foliation in the both formation shows same directional pattern with the NW faults. The magnetic anomaly distribution reveals that higher anomaly values are concentrated to near the ground surface. The analyses of 3 dimensional distribution between subsurface geology and magnetic anomaly indicates that higher anomaly is mainly distributed over the Munguntessj formation as a elongated lens bodies whereas the magnetic anomaly is evenly found in the both of Munguntessj formation and Yashill formation in the study area 2. It infers that volcanic activities associated mineralization occurred during silurian period, and the mineralized zone is thought to be realigned along the geological structures caused by later stage tectonic activities.

• Molecules and Cells
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• v.41 no.8
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• pp.742-752
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• 2018

Parkinson's disease (PD) is a neurodegenerative disease characterized by progressive degeneration of dopaminergic (DAergic) neurons, particularly in the substantia nigra (SN). Although circadian dysfunction has been suggested as one of the pathophysiological risk factors for PD, the exact molecular link between the circadian clock and PD remains largely unclear. We have recently demonstrated that $REV-ERB{\alpha}$, a circadian nuclear receptor, serves as a key molecular link between the circadian and DAergic systems. It competitively cooperates with NURR1, another nuclear receptor required for the optimal development and function of DA neurons, to control DAergic gene transcription. Considering our previous findings, we hypothesize that $REV-ERB{\alpha}$ may have a role in the onset and/or progression of PD. In the present study, we therefore aimed to elucidate whether genetic abrogation of $REV-ERB{\alpha}$ affects PD-related phenotypes in a mouse model of PD produced by a unilateral injection of 6-hydroxydopamine (6-OHDA) into the dorsal striatum. $REV-ERB{\alpha}$ deficiency significantly exacerbated 6-OHDA-induced motor deficits as well as DAergic neuronal loss in the vertebral midbrain including the SN and the ventral tegmental area. The exacerbated DAergic degeneration likely involves neuroinflammation-mediated neurotoxicity. The $REV-erb{\alpha}$ knockout mice showed prolonged microglial activation in the SN along with the over-production of interleukin $1{\beta}$, a pro-inflammatory cytokine, in response to 6-OHDA. In conclusion, the present study demonstrates for the first time that genetic abrogation of $REV-ERB{\alpha}$ can increase vulnerability of DAergic neurons to neurotoxic insults, such as 6-OHDA, thereby implying that its normal function may be beneficial for maintaining DAergic neuron populations during PD progression.