lectin/атрофия

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Association Study of Mannose-Binding Lectin Levels and Genetic Variants in Lectin Pathway Proteins with Susceptibility to Age-Related Macular Degeneration: A Case-Control Study.

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BACKGROUND In age-related macular degeneration (AMD) the complement system is thought to be activated by chronic oxidative damage with genetic variants identified in the alternative pathway as susceptibility factors. However, the involvement of the lectin pathway of complement, a key mediator of

Lectins can reverse the distal intestinal atrophy associated with elemental diets in mice.

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BACKGROUND Elemental diets cause intestinal atrophy and reduced intestinal integrity, which can lead to significant increases in intestinal permeability and bacterial translocation. Recently, several lectins have been shown to have trophic effects on the intestine. OBJECTIVE We examined the effects

Mannan-binding lectin B allele is associated with a risk of developing more severe gastric mucosal atrophy in Helicobacter pylori-infected Japanese patients.

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OBJECTIVE Mannan-binding lectin (MBL) is an important constituent of the innate immune system, and deficiency of MBL has been reported to increase the overall susceptibility of an individual to infectious disease. Codon 54 G/A variant of exon 1 (B allele) affects MBL2 gene and alters its activity.

Structural changes of the interphotoreceptor matrix in an inherited retinal degeneration: a lectin cytochemical study of progressive rod-cone degeneration.

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OBJECTIVE In the retinal disorder progressive rod-cone degeneration (prcd) in miniature poodle dogs, the photoreceptor layer degenerates slowly in the course of 5 to 7 years. Components of the interphotoreceptor matrix form a continuous extracellular lattice around photoreceptors. The purpose was to

Proteomics-based identification and validation of novel plasma biomarkers phospholipid transfer protein and mannan-binding lectin serine protease-1 in age-related macular degeneration.

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Age-related macular degeneration (AMD) is a major cause of severe, progressive visual loss among the elderly. There are currently no established serological markers for the diagnosis of AMD. In this study, we carried out a large-scale quantitative proteomics analysis to identify plasma proteins that

Cystic adventitial degeneration of the popliteal artery: lectin-histochemical study.

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A case of cystic adventitial degeneration (CAD) of the popliteal artery is presented. Histologically the cyst appeared localised in the adventitia, outside the elastic lamina. A lectin-histochemical study evaluated the following peroxidase conjugated lectins: Peanut agglutinin, Concanavalin A, Ulex

Circulating levels of mannose-binding lectin (MBL) in age-related macular degeneration.

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OBJECTIVE To assess whether the serum levels of mannose-binding lectin of the lectin complement pathway are associated with age-related macular degeneration. METHODS Patients with age-related macular degeneration and age-matched controls underwent full ophthalmologic examination and optical

Lectin binding and desmin expression during necrosis, regeneration, and neurogenic atrophy of human skeletal muscle.

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Changes in the cytoplasm of skeletal muscle fibres during necrosis, regeneration, and neurogenic atrophy have been studied in a wide range of human neuromuscular diseases with a panel of eleven biotinylated lectins and by immunohistochemical staining for the cytoskeletal protein desmin. Increased

Lectin binding pattern of Schwann cells and macrophages in 2,5-hexanedione-induced axonal degeneration in rats.

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The lectin binding pattern of both Schwann cells and macrophages has been studied during axonal degeneration induced in the rat sciatic nerve by chronic administration of 2,5-hexanedione (0.8 ml/kg per day i.p. for 20 days). In particular, the present study aimed to establish a possible relationship

Lectin binding patterns of uterine glands in mares with chronic endometrial degeneration.

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OBJECTIVE To evaluate changes of glycoconjugate in uterine glands of endometrial tissues obtained from mares. METHODS adult mares. METHODS Uterine biopsy samples were collected during the breeding season and analyzed histologically for signs of chronic endometrial degeneration. Stage of the estrous

Labeled lectin studies of renal tubular dysgenesis and renal tubular atrophy of postnatal renal ischemia and end-stage kidney disease.

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Renal tubular dysgenesis (RTD), with hypoplasia especially of renal proximal convoluted tubules and clinical neonatal anuria or oliguria, has been reported as a congenital familial (autosomal recessive) disease, variably with features of oligohydramnios, Potter syndrome, or pulmonary hypoplasia. A

Evidence for Activation of Lectin and Classical Pathway Complement Components in Aqueous Humor of Neovascular Age-Related Macular Degeneration.

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The complement system is activated via 3 different pathways; the lectin pathway (LP), classical pathway (CP), and alternative pathway. To investigate the possible roles for the LP or CP in the development of neovascular age-related macular degeneration (nAMD), we compared aqueous humor

Tubular atrophy in the end-stage kidney: a lectin and immunohistochemical study.

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Atrophic tubules in end-stage renal disease (ESRD) may have various morphologic appearances: some show microscopic features of "classic" atrophic tubules (thick, wrinkled tubular basement membrane and simplified epithelium), others show "thyroidization" (round tubules with simplified epithelium and

Primary degeneration of motor neurons by toxic lectins conveyed from the peripheral nerve.

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In attempts to degenerate motor neurons experimentally by way of retrograde axoplasmic transport, ricinus communis agglutinin (RCA), a potent protein inhibitor, was intraneurally injected into the rat sciatic nerve. Immunohistochemically, RCA was shown to be intra-axonally carried up to motor

Identification of a lectin causing the degeneration of neuronal processes using engineered embryonic stem cells.

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Unlike the mechanisms involved in the death of neuronal cell bodies, those causing the elimination of processes are not well understood owing to the lack of suitable experimental systems. As the neurotrophin receptor p75(NTR) is known to restrict the growth of neuronal processes, we engineered mouse

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