IgG4-related disease is a newly recognized fibro-inflammatory condition characterized by several features: a tendency to form tumefactive lesions in multiple sites; a characteristic histopathological appearance; andoften but not always-elevated serum IgG4 concentrations. An international symposium on IgG4-related The histopathology of IgG4-related disease was a specific focus of the international symposium. The primary purpose of this statement is to provide practicing pathologists with a set of guidelines for the diagnosis of IgG4-related disease. The diagnosis of IgG4-related disease rests on the combined presence of the characteristic histopathological appearance and increased numbers of IgG4 þ plasma cells. The critical histopathological features are a dense lymphoplasmacytic infiltrate, a storiform pattern of fibrosis, and obliterative phlebitis. We propose a terminology scheme for the diagnosis of IgG4-related disease that is based primarily on the morphological appearance on biopsy. Tissue IgG4 counts and IgG4:IgG ratios are secondary in importance. The guidelines proposed in this statement do not supplant careful clinicopathological correlation and sound clinical judgment. As the spectrum of this disease continues to expand, we advocate the use of strict criteria for accepting newly proposed entities or sites as components of the IgG4-related disease spectrum.

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The purpose ofthis study was to determine the mechanical response of the lamina cribrosa (LC) to elevated intraocular pressure (IOP) so as to identify possible mechanisms of optic nerve damage in early glaucoma. Ten In this paper, we seek to complement previous work by a direct morphometric study of the response of the LC in normal human eyes to acute changes in IOP. We feel that this approach has several advantages. Firstly, a morphometric approach allows both the overall shape and the internal architecture of the LC to be evaluated as a function of pressure. This is in contrast with previous studies of the effects of pressure on the LC which focused on positional changes of the anterior surface of the retina at the ONH or on the topography ofthe ONH. Secondly, the use of normal eyes in acute experiments permits potential assessment of the factors initiating axonal damage, since the effect of IOP on a presumably normal ONH can be studied. This is important since ONH architecture in glaucomatous eyes will be substantially different from that ofnormal eyes, owing to degenerative optic neuropathy.The goals of the present work were: (i) to characterise and quantify acute deformations of the LC as a result of elevated IOP; (ii) to formulate a mechanical model of the stress distribution within the LC which is consistent with clinically and experimentally observed patterns of axonal damage in glaucoma; and (iii) to identify features of the LC which might increase the susceptibility of some eyes to glaucomatous damage. The experimental approach was to fix normal human eyes at either high or low pressure and then to compare morphometrically the LC from the low and high pressure groups.Materials and methods Ten pairs of ostensibly normal human eyes (average age 69 years) from which the corneas had been removed for transplantation were obtained within 24 hours post mortem from the Eye Bank of Ontario. The eyes were hemisected at the equator and the vitreous was carefully removed under an operating microscope. This dissection was performed while suspending the eye in a saline bath to prevent the retina from detaching. Each posterior hemisphere was then mounted onto a plastic perfusion dish'4 which sealed it at the equator and allowed it to be pressurised. Briefly, this dish had a small discshaped elevated region with bevelled edges which effectively matched the inner diameter of the globe at the equator. The eye was then clamped in position by a ring whose inner

This study documents the substantial prevalence of significantly abnormal renal function among patients identified by laboratories as having normal-range SCR: Including calculated estimates of GFR in routine laboratory reporting may help to facilitate the early identification of patients with renal impairment.

Background: Recent evidence suggests that progesterone metabolites play important roles in regulating breast cancer. Previous studies have shown that tumorous tissues have higher 5α-reductase (5αR) and lower 3α-hydroxysteroid oxidoreductase (3α-HSO) and 20α-HSO activities. The resulting higher levels of 5α-reduced progesterone metabolites such as 5α-pregnane-3,20-dione (5αP) in tumorous tissue promote cell proliferation and detachment, whereas the 4-pregnene metabolites, 4-pregnen-3α-ol-20-one (3αHP) and 4-pregnen-20α-ol-3-one (20αDHP), more prominent in normal tissue, have the opposite (anti-cancer-like) effects. The aim of this study was to determine if the differences in enzyme activities between tumorous and nontumorous breast tissues are associated with differences in progesterone metabolizing enzyme gene expression.

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Current classifications of salivary gland tumors separate mucoepidermoid carcinoma from other neoplasms on the basis of a number of histological features, in particular the lack of participation of neoplastic myoepithelial cells. However, ultrastructural examination of low- and intermediate-grade mucoepidermoid carcinomas and pleomorphic adenomas reveals many common organizational and cellular features. Of prime importance is the relationship of intermediate cells to the luminal cells in mucoepidermoid carcinomas, which is remarkably similar to that seen between modified myoepithelial cells and luminal cells in pleomorphic adenomas. The results suggest that intermediate cells of mucoepidermoid carcinoma are the counterpart of the modified myoepithelial cells of pleomorphic adenoma. The generally accepted hypothesis that the former tumor develops from an excretory duct reserve cell, while the latter originates from an intercalated duct stem cell does not seem to be valid; pleomorphic adenoma and mucoepidermoid carcinoma appear to be closely related morphologically.