protoporphyrin/atrofi

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Inhibition of ischemia/reperfusion injury and chronic graft deterioration by a single-donor treatment with cobalt-protoporphyrin for the induction of heme oxygenase-1.

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Today, the major problem in organ transplantation is not acute graft rejection but chronic graft deterioration. In addition to alloantigen-specific events, alloantigen independent factors like donor age, previous diseases, consequences of brain death, and perioperative events of ischemia/reperfusion

Expression of the chlI, chlD, and chlH genes from the Cyanobacterium synechocystis PCC6803 in Escherichia coli and demonstration that the three cognate proteins are required for magnesium-protoporphyrin chelatase activity.

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Magnesium-protoporphyrin chelatase catalyzes the first step unique to chlorophyll synthesis: the insertion of Mg2+ into protoporphyrin IX. Genes from Synechocystis sp. PCC6803 with homology to the bchI and bchD genes of Rhodobacter sp. were cloned using degenerate oligonucleotides. The function of

Systemic zinc protoporphyrin administration reduces intracerebral hemorrhage-induced brain injury.

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Hemoglobin degradation products result in brain injury after intracerebral hemorrhage (ICH). Recent studies found that intracerebral infusion of heme oxygenase inhibitors reduces hemoglobin- and ICH-induced brain edema in rats and pigs. The present study examined whether systemic use of zinc

Prevention of chronic deterioration of heart allograft by recombinant adeno-associated virus-mediated heme oxygenase-1 gene transfer.

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BACKGROUND Allograft deterioration is the major obstacle to organ transplantation as a long-term treatment of end-stage heart failure. In this study, we transduced the antioxidant gene, heme oxygenase-1 (HO-1), to heart grafts using a recombinant adeno-associated viral vector (rAAV) in a rat heart

Photosensitization of retinal pigment epithelium by protoporphyrin IX.

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BACKGROUND Clinical evidence of injury to the retinal pigment epithelium is an important feature of age-related macular degeneration, but the mechanism of this injury is unknown. Blue-light-dependent activation of the blood-borne photosensitizer protoporphyrin IX is known to produce free radicals

Protoporphyrin-induced photodynamic effects on transport processes across the membrane of human erythrocytes.

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Previous studies have shown that illumination of erythrocytes with visible light in the presence of protoporphyrin results in cross-linking of membrane proteins and deterioration of several membrane functions, e.g. active transport of K+ and Na+. In the present study it is shown that

Erythrocyte protoporphyrin levels in patients with Friedreich's and other ataxias.

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Of 13 patients with Friedreich's ataxia (Type Ia) and 17 with type IIa recessive ataxias, all were found to have levels of "free erythrocyte protoporphyrin" (FEP) above the normal range. The rise in FEP in Friedreich's ataxia correlated well with the age of the individual and thus appears to be

Mouse model for protoporphyria. I. The liver and hepatic protoporphyrin crystals.

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Outbred albino mice were rendered protoporphyric by a diet containing 2.5% (weight) of griseofulvin. There was a 5-fold increase in liver weight, hepatocellular degeneration and necrosis, cholestasis, ductular proliferation and cirrhosis. Liver protoporphyrin values were elevated and brown pigment

Distribution of protoporphyrin in female broiler chickens affected with protoporphyria.

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One hundred thirty-seven broiler chickens at a poultry meat processing plant had dark green to black livers. Thirty-one chickens of these were collected at random and examined pathologically and biochemically. All of thirty-one chickens were female. The chickens showed mild retarded growth and a

Aminolevulinic acid (ALA)-protoporphyrin IX fluorescence guided tumour resection. Part 1: Clinical, radiological and pathological studies.

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The intraoperative identification and resection of glioma is a significant and important challenge in neurosurgery. Complete resection of the enhancing tumour increases the median survival time in glioblastoma compared to partial glioma resection; however, it is achieved in fewer than half of

Hematogenous photosensitization. A mechanism for the development of age-related macular degeneration.

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Age-related macular degeneration (ARMD) is one of the leading causes of severe visual loss in the United States. Numerous risk factors have been investigated, but the pathogenesis of ARMD has remained elusive. The authors propose that ARMD develops as a direct result of photosensitization of the

Resistance of hepatic lysosomes, mitochondria and microsomes of protoporphyrin-administered rats to peroxidative damage.

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Antioxidative inhibition by protoporphyrin (PP) of peroxidative damage in lysosomes, mitochondria and microsomes of rat liver was investigated at 24 h after an intravenous administration of PP. Using a lysosome-containing (3500 x g) fraction, the release of lysosomal marker enzymes, acid phosphatase

Staurosporine-induced cell death in Tetrahymena thermophila has mixed characteristics of both apoptotic and autophagic degeneration.

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Staurosporine blocks signal transduction associated with cell survival, proliferation and chemosensory behaviour in the ciliated protozoan, Tetrahymena thermophila. Staurosporine inhibits cell proliferation and in vivo protein phosphorylation induced by phorbol ester. It also reduces the in vitro

Preferential Heme Oxygenase-1 Activation in Striatal Astrocytes Antagonizes Dopaminergic Neuron Degeneration in MPTP-Intoxicated Mice.

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Parkinson's disease (PD) is characterized by the loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc) accompanied by increased oxidative damage. Astrocytes, which are the most abundant glial cell types in the brain, possess higher antioxidant potential partially due to

Protoporphyrins enhance oligomerization and enzymatic activity of HtrA1 serine protease.

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High temperature requirement protein A1 (HtrA1), a secreted serine protease of the HtrA family, is associated with a multitude of human diseases. However, the exact functions of HtrA1 in these diseases remain poorly understood. We seek to unravel the mechanisms of HtrA1 by elucidating its

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