PubMed · 14775598
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A HAGER. [Auricular calcification].. https://pubmed.ncbi.nlm.nih.gov/14775598/
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This paper presents a 3D localization method to register clustered microcalcifications on mammograms from cranio-caudal (CC) and medio-lateral oblique (MLO) views. The method consists of three major components: registration of clustered microcalcifications in CC and MLO views, 3D localization of clustered microcalcifications and 3D visualization of clustered microcalcifications. The registration is performed based on three features, gradient, energy and local entropy codes that are independent of spatial locations of microcalcifications in two different views and are prioritized by discriminability in a binary decision tree. The 3D localization is determined by a sequence of coordinate corrections of calcified pixels using the breast nipple as a controlling point. Finally, the 3D visualization implements a virtual reality modeling language viewer (VRMLV) to view the exact location of the lesion as a guide for needle biopsy. In order to validate our proposed 3D localization system, a set of breast lesions, which appear both in mammograms and in MR Images is used for experiments where the depth of clustered microcalcifications can be verified by the MR images.
X-linked hypophosphatemia (XLH), the most common form of hereditary rickets, is caused by loss-of-function mutations of PHEX gene in osteoblast cells, leading to rachitic bone disease and hypophosphatemia. Available evidence today indicates that the bone defect in XLH is caused not only by hypophosphatemia and altered vitamin D metabolism, but also by locally released osteoblastic mineralization inhibitory factor(s), referred to as minhibin. In our present study, we found that suppression of PHEX expression by PHEX antisense in human osteoblast cells caused an increase in cathepsin D expression at protein, but not mRNA, levels. This was associated with a decrease in cathepsin D degradation and an increased cathepsin D release into culture media. Our results also showed that lowering cathepsin D activity in antisense cell conditioned media abolished their inhibitory effect on osteoblast cell calcification, suggesting the involvement of cathepsin D in mediating the minhibin activity of the antisense cell conditioned media.
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