aluminum/necrosis

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Biological activities of phthalocyanines. XVII histopathologic evidence for different mechanisms of EMT-6 tumor necrosis induced by photodynamic therapy with disulfonated aluminum phthalocyanine or photofrin.

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The necrosis of EMT-6 mammary murine tumors induced by photodynamic therapy (PDT) with Photofrin (PII) or disulfonated aluminum phthalocyanine (AlPcS2) was studied. Attention was given to the spontaneous evolution of angiogenesis and necrosis of such tumors in order to determine the most appropriate

How do rat cortical cells cultured with aluminum die: necrosis or apoptosis?

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Aluminum (Al) exposure has been implicated as the cause of neural cells loss in several neurodegenerative diseases. Therefore, defining the mechanism of neural cell death in Al toxicity and degenerative diseases might lead to the development of therapeutic agents which promote neural cell survival.

Modulation of tumor necrosis factor alpha expression in mouse brain after exposure to aluminum in drinking water.

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Aluminum, a known neurotoxic substance and a ground-water pollutant, is a possible contributing factor in various nervous disorders including Alzheimer's disease. It has been hypothesized that cytokines are involved in aluminum neurotoxicity. We investigated the alterations in mRNA expression of

Novel interventions targeting on apoptosis and necrosis induced by aluminum chloride in neuroblastoma cells.

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Aluminum chloride induces neuroblastoma cell (SH-SY5Y) death following in vitro exposure. The objective of this study is to define apoptosis and necrosis in an in vitro model system of SH-SY5Y cells, and to investigate appropriate defense mechanisms with caspase-3 small interference RNA (siRNA) and

Evidence for different mechanisms of EMT-6 tumor necrosis by photodynamic therapy with disulfonated aluminum phthalocyanine or photofrin: tumor cell survival and blood flow.

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A comparison was made of photodynamic therapy (PDT) mediated by two photosensitizers, the disulfonated aluminum phthalocyanine (AlPcS2) and Photofrin* (PII) with regard to their mechanism of action on murine tumors. Balb/c mice bearing intradermally growing EMT-6 tumors were injected intravenously

Photodynamic therapy with aluminum-chloro-phthalocyanine induces necrosis and vascular damage in mice tongue tumors.

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In this paper we describe the efficacy of the liposomal-AlClPc (aluminum-chloro-phthalocyanine) formulation in PDT study against Ehrlich tumor cells proliferation in immunocompetent swiss mice tongue. Experiments were conduced in sixteen tumor induced mice that were divided in three control groups:

Aluminum-maltolate induces apoptosis and necrosis in neuro-2a cells: potential role for p53 signaling.

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Aluminum maltolate (Al-malt) causes neurodegeneration following in vivo exposure, and apoptosis plays a prominent role. The objective of this study was to define the form of cell death induced by Al-malt and to establish an in vitro model system amenable to mechanistic investigations of

[Prevention of acidic necrosis of the teeth and parodontal lesions during aluminum production].

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Histomorphological evaluations on the frontal cortex extrapyramidal cell layer following administration of N-Acetyl cysteine in aluminum induced neurodegeneration rat model.

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Aluminum is a potent neurotoxin used in animal models of neurodegenerative diseases like Alzheimer's disease (AD), in which oxidative stress mediates tissue pathogenesis in vivo. N-acetyl cysteine (NAC) is a glutathione precursor with reported antioxidant and neuroprotective potentials. Recent

Aluminum-induced cell death in root-tip cells of barley.

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Aluminum-induced cell death was investigated in root-tip cells of barley (Hordeum vulgare). The growth of roots in 0.1-50 mM Al treatments was inhibited after 8 h treatments, and could not be recovered after 24 h recovery culture without Al. Viable detection with fluorescein diacetate-propidium

Hesperidin and Silibinin Ameliorate Aluminum-Induced Neurotoxicity: Modulation of Antioxidants and Inflammatory Cytokines Level in Mice Hippocampus.

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Mounting evidence suggests that long-term aluminum exposure results in severe toxic effects, including neurobehavioral and neurochemical anomalies. The present study was performed to examine the neuroprotective potential of hesperidin and silibinin against aluminum chloride (AlCl3)-induced

In vivo tests of the concept of photodynamic threshold dose in normal rat liver photosensitized by aluminum chlorosulphonated phthalocyanine.

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In its simplest form, the photodynamic therapy (PDT) threshold dose model states that tissue necrosis due to PDT will occur if the number of photons absorbed by the photosensitizer per unit volume of tissue exceeds a critical value. This threshold is given by the product of photon fluence,

Transcatheter neodymium-yttrium-aluminum-garnet laser coagulation of canine ventricle using a balloon-tipped cardioscope.

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The feasibility of transcatheter laser ablation of the canine left ventricle (LV) was tested using a newly developed cardioscope. In 17 anesthetized dogs, a combined laser-endoscope catheter, consisting of an endoscope encased in a 7-French flexible catheter with an inflatable and transparent

[Effect of necrostatin-1 on apoptosis induced by aluminum and its mechanism].

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OBJECTIVE To study the effect of necrostatin (Nec-1) on apoptosis induced by aluminum (Al), and approach the mechanism. METHODS Neural cell death model was made by 4 mmol/L Al treated neuroblastoma cells (SH-SY5Y). Cell viabilities were detected at different concentrations of Al and/or Nec-1.

A comparison of neodymium: yttrium aluminum garnet and diode laser transscleral cyclophotocoagulation and cyclocryotherapy.

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The cyclodestructive effects of cyclocryotherapy and of the neodymium:yttrium aluminum garnet (Nd:YAG) and diode laser transscleral cyclophotocoagulation were investigated in phakic and pseudophakic cadaver eyes using a modified Miyake posterior-view technique and light microscopy. Cyclocryotherapy

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