Existence and release of fluid inclusions in bornite and its associated quartz and calcite

The existence and release of fluid inclusions in bornite and its associated minerals, namely, quartz and calcite were investigated and confirmed. The structures, forms, and phases of these large quantities of fluid inclusions were also studied. A mass of fluid inclusions with various sizes, distributions, shapes, and phases exist in bornite and its associated minerals. Their sizes vary from a few micrometers to tens of micrometers, and the forms appear as negative crystals, or elongated, elliptical, and irregular. At room temperature, fluid inclusions were mainly characterized as gas-liquid two- phase. However, small amounts of fluid inclusions with pure gas phase and pure liquid single-phase were also observed in quartz and calcite. These fluid inclusions initially broke during the ore crushing and grinding process and then released into the flotation pulp in the flotation process. The quantitative analysis of fluid inclusions in the solution and the comparisons of mineral dissolution show that the amount of copper and iron released by fluid inclusions in the bornite sample is higher than the amount dissolved by the mineral; fluid inclusions in the associated gangue minerals, quartz, and calcite also make contribution.

Cuprizone-induced demyelination in mice: age-related vulner-ability and exploratory behavior deficit

Schizophrenia is a mental disease that mainly affects young individuals （15 to 35 years old） but its etiology remains largely undefined. Recently, accumulating evidence indicated that demyelination and/or dysfunction of oligodendrocytes is an important feature of its pathogenesis. We hypothesized that the vulnerability of young individuals to demyelination may contribute to the onset of schizophrenia. In the present study, three different age cohorts of mice, i.e. juvenile （3 weeks）, young-adult （6 weeks） and middle-aged （8 months）, were subjected to a 6-week diet containing 0.2% cuprizone （CPZ） to create an animal model of acute demyelination. Then, age-related vulnerability to CPZ-induced demyelination, behavioral outcomes, and myelination-related molecular biological changes were assessed. We demonstrated： （1） CPZ treatment led to more severe demyelination in juvenile and young-adult mice than in middle-aged mice in the corpus callosum, a region closely associated with the pathophysiology of schizophrenia; （2） the higher levels of demyelination in juvenile and young-adult mice were correlated with a greater reduction of myelin basic protein, more loss of CC-1- positive mature oligodendrocytes, and higher levels of astrocyte activation; and （3） CPZ treatment resulted in a more prominent exploratory behavior deficit in juvenile and young-adult mice than in middle-aged mice. Together, our data demonstrate an age-relatedvulnerability to demyelination with a concurrent behavioral deficit, providing supporting evidence for better understanding the susceptibility of the young to the onset of schizophrenia.