Abstract-The detection of microaneurysms in digital color fundus photographs is a critical first step in automated screening for diabetic retinopathy (DR), a common complication of diabetes. To accomplish this detection numerous methods have been published in the past but none of these was compared with each other on the same data. In this work we present the results of the first international microaneurysm detection competition, organized in The overall results show that microaneurysm detection is a challenging task for both the automatic methods as well as the human expert. There is room for improvement as the best performing system does not reach the performance of the human expert. The data associated with the ROC microaneurysm detection competition will remain publicly available and the website will continue accepting submissions.

Changes in photosynthetic activity and trehalose levels in field-isolated, natural colonies of the terrestrial cyanobacterium Nostoc commune responding to desiccation and salt stress were investigated. As the water content decreased in N. commune colonies during desiccation, photosynthetic O2-evolving activity decreased and no activity was detected in desiccated colonies. A high level of O2 evolution was restored in the colonies as they absorbed atmospheric moisture, indicating that only a small amount of water is required for reactivation of photosynthesis. No detectable trehalose was found in fully hydrated N. commune colonies; however, trehalose accumulation occurred in response to water loss during desiccation and high levels of trehalose were detected in the airdried colonies. Moreover, a 0.2 M NaCl treatment also induced trehalose accumulation to a level equivalent to that by desiccation. Photosynthetic O2 evolution was inhibited by 0.2 M NaCl, indicating that N. commune can tolerate only low levels of salt. These results suggest that cessation of photosynthesis and trehalose accumulation occur in response to both matric water stress (desiccation) and osmotic water stress (high salt concentration), and that while trehalose may be a less effective osmoprotective compound than others, it is important for the extreme tolerance to desiccation observed in terrestrial cyanobacterium.

Abstract. Hyperoxaluria leads to calcium oxalate (CaOx) crystallization and development of tubulointerstitial lesions in the kidneys. Treatment of hyperoxaluric rats with angiotensin II (Ang II) type I receptor blocker (ARB) reduces lesion formation. Because Ang II mediates osteopontin (OPN) synthesis, which is involved in both macrophage recruitment and CaOx crystallization, it was hypothesized that ARB acts via OPN. Hyperoxaluria was induced in 10-wk-old male Sprague-Dawley rats, and they were treated with ARB candesartan. At the end of 4 wk, kidneys were examined for crystal deposits, ED-1-positive cells, and expression of OPN mRNA. PCR was used to quantify OPN, renin, and angiotensin-converting enzyme (ACE) mRNA in kidneys. RIA was used to determine renal, plasma, and urinary OPN; plasma renin; Ang II and ACE; and renal Ang II. For evaluating oxidative stress, malondialdehyde was measured. Urinary calcium, oxalate, creatinine, and albumin were also determined. Despite similar urinary calcium and oxalate levels, kidneys of hyperoxaluric rats on candesartan had fewer CaOx crystals, fewer ED-1-positive cells, reduced OPN expression, and reduced malondialdehyde than hyperoxaluric rats. Urinary albumin excretion and serum creatinine levels improved significantly on candesartan treatment. mRNA for OPN, renin, and ACE were significantly elevated in hyperoxaluric rats. OPN synthesis and production increased with hyperoxaluria but to a lesser extent in candesartan-treated hyperoxaluric rats. These results show for the first time that oxalate can activate the renal renin-angiotensin system and that oxalate-induced upregulation of OPN is in part mediated via renal renin-angiotensin system.Oxalate, a by-product of metabolism, is normally excreted in the urine and at low concentrations is harmless to the renal epithelial cells. However, elevated oxalate levels and/or calcium oxalate (CaOx) crystals are injurious (1-3). In addition, exposure of renal epithelial cells in vitro to high levels of oxalate and/or CaOx crystals upregulates the production of chemoattractants osteopontin (OPN) (4) and monocyte-chemoattractant protein-1 (MCP-1) (5, 6). Mild idiopathic hyperoxaluria is associated with CaOx nephrolithiasis, whereas hyperoxaluria resulting from jejunal bypass for obesity or genetic defects in oxalate metabolism is nephrotoxic and produces tubulointerstitial lesions. Tubulointerstitial damage is recognized as one of the most important risk factors for the development of chronic renal diseases and eventual renal failure (7).All components of the renin-angiotensin system (RAS) are produced within the kidney, and intrarenal RAS plays pivotal role in renal disease progression (8). Kidneys produce both angiotensinogen and angiotensin-converting enzyme (ACE), and juxtaglomerular apparatus is the main source of circulating renin. Renin catalyzes the production of angiotensin I, which is converted to angiotensin II (Ang II) by the actions of ACE. Ang II acts through two receptors, types 1 (AT1) and 2 (AT2), and mediates many ...

SummaryThe transformation to castration-resistant prostate cancer drives cell plasticity that promotes intra-tumor heterogeneity and contributes to therapeutic resistance.