The ins and outs of male breast and anterior chest wall lesions from childhood to adulthood.

Physiological and pathological processes arising from the breast and anterior chest wall may share similar clinical presentations because of the small volume of male breasts. Therefore, imaging is frequently required to localise and characterise the lesion and guide biopsy when radiological findings are equivocal or suspicious. Mammography or digital breast tomosynthesis (DBT) and ultrasound are the mainstays of breast imaging work-up. Other imaging techniques such as computed tomography (CT), magnetic resonance imaging (MRI) and positron-emission tomography (PET) can sometimes augment the investigation and aid treatment planning. This article reviews the key imaging features of a wide spectrum of benign and malignant conditions that involve the male breast and anterior chest wall across various age groups. Familiarisation with the salient radiological findings is essential for reaching an accurate diagnosis and optimising management.

A low-power VLSI arrhythmia classifier.

The design, implementation, and operation of a low-power multilayer perceptron chip (Kakadu) in the framework of a cardiac arrhythmia classification system is presented in this paper. This classifier, called MATIC, makes timing decisions using a decision tree, and a neural network is used to identify heartbeats with abnormal morphologies. This classifier was designed to be suitable for use in implantable devices and a VLSI (very large scale integration) neural-network chip (Kakadu) was designed so that the computationally expensive neural-network algorithm can be implemented with low power consumption. Kakadu implements a (10,6,4) perceptron and has a typical power consumption of tens of microwatts. When used with the arrhythmia classification system, the chip can operate with an average power consumption of less than 25 nW.

Analysis of the endocytic pathway mediating the infectious entry of mosquito-borne flavivirus West Nile into Aedes albopictus mosquito (C6/36) cells.

The initial interaction between mosquito-borne flavivirus West Nile and mosquito cells is poorly characterized. This study analyzed the endocytic and the associated signaling pathway that mediate the infectious entry of West Nile virus (WNV) into mosquito cell line (C6/36). Pretreatment of C6/36 cells with pharmacological drugs that blocks clathrin-mediated endocytosis significantly inhibited virus entry. Furthermore, the transfection of functional blocking antibody against clathrin molecules and the overexpression of dominant-negative mutants of Eps15 in C6/36 cells caused a marked reduction in WNV internalization. WNV was shown to activate focal adhesion kinase (FAK) to facilitate the endocytosis of virus but not the mitogen-activated protein kinases (ERK1 and ERK2). Subsequent to the internalization of WNV, the virus particles are translocated along the endosomal pathway as revealed by double-immunofluorescence assays with anti-WNV envelope protein and cellular markers for early and late endosomes. Specific inhibitor for protein kinase C (PKC) was shown to be highly effective in blocking WNV entry by inhibiting endosomal sorting event. The disruption of the microtubule network using nocodazole also drastically affects the entry process of WNV but not the disruption of actin filaments by cytochalasin D. Finally, a low-pH-dependent step is required for WNV infection as revealed by the resistance of C6/36 cells to WNV infection in the presence of lysosomotropic agents.

Characterization of plasma membrane-associated proteins from Aedes albopictus mosquito (C6/36) cells that mediate West Nile virus binding and infection.

This study isolated and characterized the West Nile virus (WNV) putative receptor molecule(s) from Aedes albopictus mosquito (C6/36) cells. The binding of WNV to C6/36 cells was saturated with 5000 particles per cell. The entry of WNV into C6/36 cells was strongly inhibited when pretreated with proteinase K and to a lesser extent with sodium periodate. However, pretreatment of C6/36 cells with phospholipases, glycosidases, heparinases and neurimidase had no effect on virus entry. By using virus overlay protein blot assay, WNV was observed to bind to the 140-kDa, 95-kDa, 70-kDa and 55-kDa plasma membrane-associated molecules isolated from C6/36 cells. Murine antibodies generated against the 95-kDa and 70-kDa membrane proteins effectively blocked WNV, Japanese encephalitis virus (JEV) and Dengue virus (DV) serotype 2 infection in C6/36 cells. In addition, the binding of the recombinant-WNV envelope domain III protein to C6/36 cells can be inhibited by the anti-95-kDa and anti-70-kDa membrane protein antibodies. These data strongly supported the possibility that the 95-kDa and 70-kDa plasma membrane-associated proteins are part of a receptor complex for mosquito-borne flaviviruses (WNV, JEV and DV) on mosquito cells.