A novel innovation using modified platelet-rich plasma (mPRP) for preventing urethral stricture recurrence in a rabbit model. [PDF]
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The interplay between neuroinflammation and endothelial dysfunction in cerebral small vessel disease. [PDF]
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Suppression of transforming growth factor-beta1 expression in keloids after cryosurgery
Cryobiology, 2017The biological mechanism underlying cryosurgical treatment of keloids remains unclear. Transforming growth factor-beta1 (TGF-β1) has been implicated in the pathogenesis of keloids and was reported to be the target of several therapeutic modalities. However, the effect of cryosurgery on its expression in keloid tissue has not been yet investigated.
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Expression of Transforming Growth Factor β1 in Ameloblastomas
Journal of Craniofacial Surgery, 2008The aim of the present study was to compare the expression of transforming growth factor (TGF) beta1 in ameloblastomas (AMs) with different risk of recurrence by immunohistochemistry. A total of 29 cases of AMs were evaluated. The tumors were divided into 2 groups: group A (10 cases) composed of unicystic and peripheral AMs, associated with a low risk ...
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Transforming growth factor-beta1 and regulators of apoptosis.
Annals of the New York Academy of Sciences, 2009Growth inhibitory function of transforming growth factor-beta1 (TGF-beta1) is abolished in colorectal cancer cells as a consequence of mutations of various downstream signaling agents, such as p53, which fail to respond to TGF-beta1 stimulation. TGF-beta1 could also suppress T-cell-mediated anticancer immunity.
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The role of transforming growth factor β1 in the vascular system
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Transforming Growth Factor β1: Implications in Adrenocortical Tumorigenesis
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Transforming growth factor-beta1 inhibits steroidogenesis in human trophoblast cells
Molecular Human Reproduction, 2002Transforming growth factor-beta (TGF-beta) is an important regulator of placental development and function. In this study, we have investigated the effect of TGF-beta1 on steroidogenesis, as well as its sites of action in the steroidogenic pathway by using a choriocarcinoma cell line, JEG-3, and a normal trophoblast cell line (NPC).
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