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Seite 1 von 162 Ergebnisse
PET imaging of hypoxia-inducible factor-1-active tumor cells with pretargeted oxygen-dependent degradable streptavidin and a novel 18F-labeled biotin derivative.
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OBJECTIVE
We aimed to evaluate the feasibility of using streptavidin-biotin-based pretargeting for positron emission tomography (PET) imaging of hypoxia-inducible factor (HIF)-1-active tumors.
METHODS
We used POS, a genetically engineered form of streptavidin that selectively stabilizes in
Targeting demyelination and virtual hypoxia with high-dose biotin as a treatment for progressive multiple sclerosis.
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Progressive multiple sclerosis (MS) is a severely disabling neurological condition, and an effective treatment is urgently needed. Recently, high-dose biotin has emerged as a promising therapy for affected individuals. Initial clinical data have shown that daily doses of biotin of up to 300 mg can
Hypoxia-directed and activated theranostic agent: Imaging and treatment of solid tumor.
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Hypoxia, a distinguished feature of various solid tumors, has been considered as a key marker for tumor progression. Inadequate vasculature and high interstitial pressures result in relatively poor drug delivery to these tumors. Herein, we developed an antitumor theranostic agent, 4, which is
Inhibition of the mitochondrial unfolded protein response by acetylcholine alleviated hypoxia/reoxygenation-induced apoptosis of endothelial cells.
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The mitochondrial unfolded protein response (UPR(mt)) is involved in numerous diseases that have the common feature of mitochondrial dysfunction. However, its pathophysiological relevance in the context of hypoxia/reoxygenation (H/R) in endothelial cells remains elusive. Previous studies have
A new model of retinal photoreceptor cell degeneration induced by a chemical hypoxia-mimicking agent, cobalt chloride.
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Retinal photoreceptor cell degeneration was induced by cobalt chloride, a chemical hypoxia-mimicking agent in rodents. Time course and dose-response of photoreceptor cell degeneration in mouse retina after intravitreal injection of cobalt chloride were examined by conventional histological analysis
[Expressions of P-JNK in nerve cell apoptosis of A2AR knockout newborn mice after hypoxia/ischemia brain damage].
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OBJECTIVE
To investigate the effect of adenosine A2A receptor knockout (A(2A)RKO) on relationship between continuous activation of phospho-c-Jun N-terminal kinase (P-JNK) and expression of nerve cell apoptosis in hippocampus CA1 domain of newborn mice after hypoxia/ischemia brain damage(HIBD) and
Hypoxia-reoxygenation-induced apoptosis in cultured adult rat myocytes and the protective effect of platelets and transforming growth factor-beta(1).
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The outcome of myocardial ischemia-reperfusion has been partially attributed to the degree of apoptosis in cardiomyocytes. Aggregating platelets by release of transforming growth factor-beta(1) (TGF-beta(1)) protect the isolated heart against ischemia-reperfusion injury and preserve myocardial
Maternal hypoxia increases hippocampal cell susceptibility to ischemia after middle cerebral artery occlusion in rat offspring.
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Introduction: Maternal hypoxia induces an adverse uterine environment and may induce long-term effects in offspring. This study investigated whether maternal hypoxia increases hippocampal cell vulnerability and exacerbates neurological impairments in adult rat offspring following ischemia.
Magnesium pre-treatment reduces neuronal apoptosis in newborn rats in hypoxia-ischemia.
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Hypoxic-ischemic brain damage has significant mortality and morbidity in newborns. Although the role of magnesium in neonatal hypoxic-ischemic brain injury related to N-methyl-D-aspartate receptors has been widely studied; the effects of magnesium on neuronal apoptosis have not been known exactly in
Hypoxic preconditioning protects microvascular endothelial cells against hypoxia/reoxygenation injury by attenuating endoplasmic reticulum stress.
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Endothelial cells (ECs) are directly exposed to hypoxia and contribute to injury during myocardial ischemia/reperfusion. Hypoxic preconditioning (HPC) protects ECs against hypoxia injury. This study aimed to explore whether HPC attenuates hypoxia/reoxygenation (H/R) injury by suppressing excessive
[Effect of endoplasmic reticulum stress in brain injury following chronic intermittent hypoxia in weanling rat].
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OBJECTIVE
To explore the role of endoplasmic reticulum stress in brain injury following chronic intermittent hypoxia (CIH) in weanling rats.
METHODS
A total of 48 male healthy Sprague-Dawley rats (3-4-week-old, 80-100 g) were randomly divided into 4 groups: 2-week-CIH (2IH) group, 4-week-CIH (4IH)
Pharmacologic stabilization of hypoxia-inducible transcription factors protects developing mouse brain from hypoxia-induced apoptotic cell death.
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OBJECTIVE
Accumulation of hypoxia-inducible transcription factors (HIFs) by prolyl-4-hydroxylase inhibitors (PHI) has been suggested to induce neuroprotection in the ischemic rodent brain. We aimed to investigate in vivo effects of a novel PHI on HIF-regulated neurotrophic and pro-apoptotic factors
Antiapoptotic Effect of Gene Therapy with Recombinant Adenovirus Vector Containing Hypoxia-inducible Factor-1α after Cerebral Ischemia and Reperfusion in Rats.
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BACKGROUND
Mounting evidence has demonstrated that hypoxia-inducible factor-1α (HIF-1α) could attenuate brain injuries after cerebral ischemia and reperfusion (CIR). However, few reports have addressed the therapeutic efficacies of a recombinant adenovirus vector containing HIF-1α (AdHIF-1α) gene
Expression of hypoxia-inducible, membrane-bound carbonic anhydrase isozyme XII in mouse tissues.
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Carbonic anhydrase (CA) XII is a membrane-associated enzyme that has been demonstrated to be normally expressed in some human tissues, to be upregulated in some cancers, and to be a hypoxia-inducible gene product. In mouse, CA XII has been recently localized in the kidney. In the present study, we
Apoptosis in a neonatal rat model of cerebral hypoxia-ischemia.
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OBJECTIVE
The mechanisms of excitotoxic cell death in cerebral ischemia are poorly understood. In addition to necrosis, apoptotic cell death may occur. The purpose of this study was to determine whether an established model of cerebral hypoxia-ischemia in the neonatal rat demonstrates any features
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