Plasma Factor XIII is a zymogen (plasma protransglutaminase) with the tetrametric structure A2B2, whereas the cellular protransglutaminase, i.e. Factor XIII in the platelet and monocyte/macrophage, consists exclusively of A subunits (A2). It is generally accepted that at Ca2+ concentrations comparable with that in plasma the proteolytic removal of an Nterminal activation peptide is the prerequisite for the Ca2+-induced formation of a catalytically active configuration of subunit A. In this study it was demonstrated that at high concentrations NaCl or KCI induced a non-proteolytic activation of cellular (placental macrophage) but not plasma protransglutaminase. The activation depended on time and salt concentration, and Ca2 , in the range 0-20 mm, greatly enhanced the activation process. At 1.25 M-NaCl maximal activation occurred within 60 min in the presence of 2 mM-CaC12, and even at physiological NaCl concentration a slow progressive activation could be observed in the presence of Ca2+. The specific activity of salt-activated Factor XIII was 1.5-2.0-fold higher than that obtained after thrombin activation. The non-proteolytic activation of cellular protransglutaminase was abolished by the addition of subunit B of plasma Factor XIII in stoichiometric amount, which suggests that (one of) the physiological function(s) of the B subunit in plasma Factor XIII is to prevent the slow spontaneous activation of A subunit that would occur in a plasmatic environment. INTRODUCTIONFactor XIII (FXIII) of blood coagulation present in the plasma is a zymogen (plasma protransglutaminase) of tetrameric structure (A2B2). The active site formed in the course of an activation process is located on the A subunit while subunit B remains enzymically inactive. The presence of FXIII has also been verified in platelets [1], monocytes and monocyte-derived macrophages [2][3][4][5][6][7]. In contrast with the plasma FXIII, however, this cellular protransglutaminase consists exclusively of A subunits (A2). The active transglutaminase (FXIIIa) formed from FXIII catalyses an acyl-transfer reaction in which the carboxamide group of a peptide-bound glutamine residue is the acyl

Transglutaminase activity has been detected in the lenses of laboratory animals and in human cataracts. However, its distribution in the lens tissue has not been investigated. Using a monoclonal antibody against tissue transglutaminase, we showed by Western blotting and immunoabsorption that transglutaminase of normal human lens is immunologically related to tissue transglutaminase but has a slightly higher M(r) than the latter enzyme. Using monoclonal or polyclonal antibody against tissue transglutaminase, lens transglutaminase was localized to the epithelial cell layer on the anterior lens surface and to a thin stripe between the capsule and the peripheral cortex on the posterior surface. Lens fibers were not stained with the antibodies. Factor XIII, another transglutaminase, could not be detected in the lens tissue. The localization of transglutaminase in the lens suggests that lens transglutaminase is synthesized in the epithelial cells and secreted into the virtual space between the capsule and the peripheral cortex spreading all around the lens substance.

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PURPOSE: To evaluate the results of photorefractive keratectomy (PRK) for the correction of myopia and myopic astigmatism in megalophthalmos anterior. METHODS: Four eyes of two brothers with megalophthalmos anterior were treated with PRK. In patient 1, best spectacle-corrected visual acuity (BSCVA) was 20/20 in both eyes with a refraction of -4.50 -4.50 x 180? in the right eye and -3.75 -3.00 x 175? in the left eye. In patient 2, BSCVA was 20/25 in both eyes with a refraction of -4.25 x 166? in the right eye and +0.50 -4.00 x 175? in the left eye. RESULTS: Topographic map, slit-lamp, ultrasound biomicroscopy, and postoperative course (no progression), supported with vectorial analysis, demonstrated megalophthalmos anterior. During 24-month follow-up, mild haze was observed and BSCVA was maintained. CONCLUSIONS: Myopia and astigmatism are often observed in this type of nonprogressive corneal dysgenesis. Based on this fact and our results, we recommend PRK in cases of megalophthalmos anterior. [J Refract Surg. 2006;22:408-411.]

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