phenylketonurias/hypoxia

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Tetrahydrobiopterin deficiency increases neuronal vulnerability to hypoxia.

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Tetrahydrobiopterin (BH4) is an essential co-factor for nitric oxide synthases (NOS). The aim of the present work was to study whether BH4 deficiency affects the vulnerability of neurones in primary culture to hypoxia. Intracellular BH4 levels were depleted by pre-incubating neurones with 5 mm

[Effect of chronic hyperphenylalaninemia and hypoxia on the effectiveness of the alpha-ketoglutarate shunt in the brain].

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The effects of hypoxia and chronic hyperphenylalaninaemia (HPA) on the intensity of the alpha-oxoglutarate shunt in rat brain after injection of [5-14C]glutamate were investigated. The reaction of reducing carboxylation of alpha-oxoglutarate was shown to be the rate-limiting step for the whole

Developmental susceptibility of neurons to transient tetrahydrobiopterin insufficiency and antenatal hypoxia-ischemia in fetal rabbits.

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Tetrahydrobiopterin (BH4) is important for normal brain development as congenital BH4 deficiencies manifest movement disorders at various childhood ages. BH4 transitions from very low levels in fetal brains to higher "adult" levels postnatally, with the highest levels in the thalamus. Maternal

Perivascular nitric oxide and superoxide in neonatal cerebral hypoxia-ischemia.

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Decreased cerebral blood flow (CBF) has been observed following the resuscitation from neonatal hypoxic-ischemic injury, but its mechanism is not known. We address the hypothesis that reduced CBF is due to a change in nitric oxide (NO) and superoxide anion O(2)(-) balance secondary to endothelial NO

Development of bladder control in mentally handicapped children.

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OBJECTIVE To analyze the role of mental handicap as a possible source of lack of development of bladder control and to find out the chance of continence to advise future patients. METHODS The parents and relatives of 100 consecutive mentally handicapped patients were inquired by a personal

Apparent diffusion coefficient restriction in the white matter: going beyond acute brain territorial ischemia.

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BACKGROUND Reduction of apparent diffusion coefficient (ADC) values in white matter is not always ischaemic in nature. METHODS We retrospectively analysed our MRI records featuring reduced ADC values in the centrum semiovale without grey matter involvement or significant vasogenic

Pharmacological prevention of eNOS uncoupling.

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Under physiological conditions, nitric oxide (NO) is produced in the vasculature mainly by the endothelial NO synthase (eNOS). This endothelium-derived NO is a protective molecule with antihypertensive, antithrombotic and anti-atherosclerotic properties. Cardiovascular risk factors such as

Uncoupling of endothelial NO synthase in atherosclerosis and vascular disease.

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Nitric oxide (NO) produced by the endothelial NO synthase (eNOS) is an antihypertensive, antithrombotic and anti-atherosclerotic molecule. Hypercholesterolemia leads to a reduction in vascular NO bioavailability. This is attributed to a dysfunction of the eNOS enzyme and a reduced eNOS activity.

SGK1 Mediates Hypoxic Pulmonary Hypertension through Promoting Macrophage Infiltration and Activation.

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Inflammation plays a pivotal role in the development of pulmonary arterial hypertension (PAH). Meanwhile, serum glucocorticoid-regulated kinase-1 (SGK1) has been considered to be an important factor in the regulation of inflammation in some vascular disease. However, the role of SGK1 in

Reptilian behavioural patterns in childhood autism.

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Childhood autism may be caused by damage to three phylogenetically distinct regions of the brain, or their major pathways and connections. Injury to the neocortex results in loss of language and cognitive function, while injury to the limbic cortex results in autistic withdrawal and abolition of

Pivotal role for endothelial tetrahydrobiopterin in pulmonary hypertension.

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BACKGROUND Pulmonary hypertension is a fatal disease characterized by vasoconstriction and vascular remodeling. Loss of endothelial nitric oxide bioavailability is implicated in pulmonary hypertension pathogenesis. Recent evidence suggests that the cofactor tetrahydrobiopterin (BH4) is an important

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