Publications by authors named "Xing-Jia Wang"

Agricultural products are a primary pathway for humans to accumulate heavy metals (HMs) via the soil-crop system and should therefore should be included as a crucial part of the food security in our country. Given that previous studies on protection zoning for preventing farmland HM pollution rarely considered agricultural products as a basic element, this study attempted to establish a zoning system for farmland HM prevention, which was based on the perspective of agricultural product pollution. We subsequently took a representative peri-urban area in the black soil region, which was provided with a higher risk of being polluted, as an empirical case.

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We report a rare case of subcutaneous phaeohyphomycosis caused by Cladosporium cladosporioides. A 21-year-old man was presented to our clinic with the history of cysts and nodules on his face and neck for 5 years. He was diagnosed subcutaneous phaeohyphomycosis according to the finding of fungal elements in histopathological examination and direct microscopic examination of cyst pus, which was confirmed by positive culture of the cyst pus.

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Recent studies suggested an involvement of thromboxane A2 in cyclooxygenase-2-dependent inhibition of steroidogenic acute regulatory (StAR) gene expression. The present study further investigated the role of thromboxane A2 receptor in StAR gene expression and steroidogenesis in testicular Leydig cells. The thromboxane A2 receptor was detected in several Leydig cell lines.

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The age-related decline in testosterone biosynthesis in testicular Leydig cells has been well documented, but the mechanisms involved in the decline are not clear. Recent studies have described a cyclooxygenase-2 (COX2)-dependent tonic inhibition of Leydig cell steroidogenesis and expression of the steroidogenic acute regulatory protein (StAR). The present study was conducted to determine whether COX2 protein increases with age in rat Leydig cells and whether COX2 plays a role in the age-related decline in testosterone biosynthesis.

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The decline in blood testosterone concentration during the course of male aging results in decreases in many physiological functions. However, the mechanism(s) responsible for this decline is not clear. Previous observations have suggested the involvement of multiple alterations or defects that inhibit the activities of proteins involved in steroidogenesis and result in reduced testosterone biosynthesis.

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Steroid hormone biosynthesis in steroidogenic cells is regulated through trophic hormone activation of protein kinase A (PKA) signaling pathways. However, many examples of the regulation of steroid synthesis via pathways other than the PKA pathway have been documented. In some cases these pathways act independently of PKA activation whereas in other cases, they act synergistically with it.

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The rate-limiting, committed, and regulatable step in steroid hormone biosynthesis is the transport of cholesterol from the outer to the inner mitochondrial membrane, a process that is mediated by the steroidogenic acute regulatory (StAR) protein. In steroidogenic cells, the StAR protein is regulated by cAMP-dependent mechanisms. However, the StAR promoter lacks a consensus cAMP response-element (CRE), suggesting the involvement of alternate regulatory factor(s) in cAMP responsiveness.

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To understand the mechanism for the role of arachidonic acid (AA) in steroidogenic acute regulatory (StAR) gene transcription, sections of the -1/-966 StAR promoter were deleted to produce constructs of -1/-426, -1/-211, -1/-151, and -1/-110 and inserted into the PGL3 vector to drive luciferase expression. Results indicated that -1/-151 StAR promoter contains the elements that are most responsive to AA. Electrophoretic mobility shift assays using nuclear extracts from AA-treated MA-10 Leydig tumor cells showed that AA enhanced specific binding of the nuclear extract to a 30bp (-67/-96) sequence of the StAR promoter.

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To study the mechanism for the regulatory effect of arachidonic acid (AA) on steroidogenesis, the role of cyclooxygenase (COX) in steroid production and steroidogenic acute regulatory (StAR) gene expression was investigated. Although stimulation with 0.05 mM dibutyryl cAMP (Bt(2)cAMP) did not increase StAR protein or progesterone in MA-10 mouse Leydig cells, the addition of 1 microM of the COX inhibitor indomethacin increased StAR protein expression and progesterone production by 5.

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Steroid hormone biosynthesis in the adrenals and gonads is regulated by the steroidogenic acute regulatory (StAR) protein through its action in mediating the intramitochondrial transport of cholesterol. A role for epidermal growth factor (EGF) in modulating steroidogenesis has been previously determined, but the mechanism of its action remains unknown. The present investigation was designed to explore the potential mechanism of action of mouse EGF (mEGF) in the regulation of steroid biosynthesis and StAR protein expression in mLTC-1 mouse Leydig tumor cells.

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Previous studies have demonstrated that trophic hormone stimulation induced cyclic AMP (cAMP) formation and arachidonic acid (AA) release from phospholipids and that both these compounds were required for steroid biosynthesis and steroidogenic acute regulatory (StAR) gene expression in MA-10 mouse Leydig tumor cells. The present study further investigates the synergistic effects of the AA and cAMP interaction on steroidogenesis. To demonstrate cAMP-induced AA release, MA-10 cells were pre-loaded with 3H-AA and subsequently treated with dibutyryl cyclic AMP (dbcAMP).

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