The human visual process can be studied by examining the computational problems associated with deriving useful information from retinal images. In this paper, we apply this approach to the problem of representing three-dimensional shapes for the purpose of recognition. 1. Three criteria, accessibility, scope and uniqueness , and stability and sensitivity , are presented for judging the usefulness of a representation for shape recognition. 2. Three aspects of a representation’s design are considered, (i) the representation’s coordinate system, (ii) its primitives, which are the primary units of shape information used in the representation, and (iii) the organization the representation imposes on the information in its descriptions. 3. In terms of these design issues and the criteria presented, a shape representation for recognition should: (i) use an object-centred coordinate system, (ii) include volumetric primitives of varied sizes, and (iii) have a modular organization. A representation based on a shape’s natural axes (for example the axes identified by a stick figure) follows directly from these choices. 4. The basic process for deriving a shape description in this representation must involve: (i) a means for identifying the natural axes of a shape in its image and (ii) a mechanism for transforming viewer-centred axis specifications to specifications in an object-centred coordinate system. 5. Shape recognition involves: (i) a collection of stored shape descriptions, and (ii) various indexes into the collection that allow a newly derived description to be associated with an appropriate stored description. The most important of these indexes allows shape recognition to proceed conservatively from the general to the specific based on the specificity of the information available from the image. 6. New constraints supplied by a conservative recognition process can be used to extract more information from the image. A relaxation process for carrying out this constraint analysis is described.

digested by collagenase/trypsin, and the digested cardiac cells were allowed to attach to the plates overnight. The attached cells included macrophages and myofibroblasts (positive for α smooth muscle actin [αSMA]) as well as other cardiac cells (Supplemental Figure 1B). Notably, cardiac myofibroblasts seemed to be more difficult than cardiac macrophages to collect using our isolation method from infarcted hearts because, as revealed by our immunohistochemical analysis, the number of cardiac myofibroblasts was the same as that of cardiac macrophages in the infarcted area (Supplemental Figure 1C). When the overnight-attached cells were cultured in 10% FBS/DMEM for more than 6 days, almost all of the cells on the plates were positive for αSMA and SM22α, 2 myofibroblast marker proteins (18, 19) (>97.9% and >93.8%, respectively) (Supplemental Figure 1, D and E), indicating that the cells were primarily composed of cardiac myofibroblasts. This is probably because only myofibroblasts were able to grow rapidly in the culture medium.Isolated cardiac macrophages and myofibroblasts were allowed to engulf fluorescently labeled apoptotic cells, and we assessed the fluorescence taken up by cardiac macrophages and administration promoted the restoration of cardiac function and morphology after MI, suggesting that MFG-E8 is a new therapeutic target for the treatment of MI.

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Introduction: Autophagy has not been studied extensively in the human placenta. This study was performed to determine whether autophagy is increased in the placentas of women with hypertensive disorders in pregnancy compared to normotensive pregnancies.

Efficient engulfment of apoptotic cells is critical for maintaining tissue homoeostasis. When phagocytes recognize ‘eat me’ signals presented on the surface of apoptotic cells, this subsequently induces cytoskeletal rearrangement of phagocytes for the engulfment through Rac1 activation. However, the intracellular signalling cascades that result in Rac1 activation remain largely unknown. Here we show that G-protein-coupled receptor kinase 6 (GRK6) is involved in apoptotic cell clearance. GRK6 cooperates with GIT1 to activate Rac1, which promotes apoptotic engulfment independently from the two known DOCK180/ELMO/Rac1 and GULP1/Rac1 engulfment pathways. As a consequence, GRK6-deficient mice develop an autoimmune disease. GRK6-deficient mice also have increased iron stores in splenic red pulp in which F4/80+ macrophages are responsible for senescent red blood cell clearance. Our results reveal previously unrecognized roles for GRK6 in regulating apoptotic engulfment and its fundamental importance in immune and iron homoeostasis.

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