Snijders Blok-Campeau syndrome caused by gene mutation: a case report.

A one-year and two-month old girl indicated large head circumference, widely spaced eyes, narrow palpebral fissures, strabismus on the right eye, broad and low nasal bridge and low-set ears. She had knee over extension and foot eversion on both sides while standing with help. She also had hypotonia and was not able to stand or walk independently.

Zeolites ameliorate asbestos toxicity in a transgenic model of malignant mesothelioma.

Malignant mesothelioma (MM) is an almost invariably fatal cancer caused by asbestos exposure. The toxicity of asbestos fibers is related to their physicochemical properties and the generation of free radicals. We set up a pilot study to investigate the potential of the zeolite clinoptilolite to counteract the asbestos carcinogenesis by preventing the generation of reactive nitrogen and oxygen radicals.

Zeolite protects mice from iron-induced damage in a mouse model trial.

For centuries, zeolites have been used for their utility in binding metals, and they feature in a multitude of agricultural and industrial applications in which the honeycombed zeolite structures form ideal ion exchangers, catalysts and binding agents. Zeolites are currently in a transition period, moving towards implementation in human ailments and diseases. Here, we postulated that zeolites may be able to counter the effects of excess iron and conducted a mouse model trial to gauge the utility of this notion.

Short-term dose-response characteristics of 2-iminobiotin immediately postinsult in the neonatal piglet after hypoxia-ischemia.

Background And Purpose: To determine the optimal dose of 2-iminobiotin (2-IB) for the treatment of moderate to severe asphyxia in a neonatal piglet model of hypoxia-ischemia.

Methods: Newborn piglets were subjected to a 30-minute hypoxia-ischemia insult and randomly treated with vehicle or 2-IB (0.1 mg/kg, 0.

Hypothermia and erythropoietin for neuroprotection after neonatal brain damage.

Background: Both hypothermia and erythropoietin (EPO) are reported to have neuroprotective effects after perinatal hypoxia-ischemia (HI). We investigated a possible additive effect of the use of a combination of hypothermia-EPO in a rat model of neonatal HI.

Methods: At postnatal day 7, rats were subjected to HI and then randomized to 3 h of hypothermia, EPO, or both.

Pharmacological neuroprotection after perinatal hypoxic-ischemic brain injury.

Perinatal hypoxia-ischemia (HI) is an important cause of neonatal brain injury. Recent progress in the search for neuroprotective compounds has provided us with several promising drugs to reduce perinatal HI-induced brain injury. In the early stage (first 6 hours after birth) therapies are concentrated on prevention of the production of reactive oxygen species or free radicals (xanthine-oxidase-, nitric oxide synthase-, and prostaglandin inhibition), anti-inflammatory effects (erythropoietin, melatonin, Xenon) and anti-apoptotic interventions (nuclear factor kappa B- and c-jun N-terminal kinase inhibition); in a later stage stimulation of neurotrophic properties in the neonatal brain (erythropoietin, growth factors) can be targeted to promote neuronal and oligodendrocyte regeneration.

Beneficial effect of erythropoietin on sensorimotor function and white matter after hypoxia-ischemia in neonatal mice.

There are mixed reports on the neuroprotective properties of erythropoietin (EPO) in animal models of birth asphyxia. We investigated the effect of EPO on short- and long-term outcome after neonatal hypoxic-ischemic (HI) brain injury in mice and compared the effect of two different dose regimens of EPO. Nine-day-old mice were subjected to HI, and EPO was injected i.

Pharmacological neuroprotection after perinatal asphyxia.

Recent progress has provided us with several promising neuroprotective compounds to reduce perinatal hypoxic-ischemic (HI) brain injury. In the early post HI phase, therapies can be concentrated on ion channel blockage (Xenon), anti-oxidation (allopurinol, 2-iminobiotin, and indomethacin), anti-inflammation (erythropoietin [EPO], melatonin), and anti-apoptosis (nuclear factor kappa B [NF-κB]and c-jun N-terminal kinase [JNK] inhibitors); in the later phase, therapies should be targeted to promote neuronal regeneration by stimulation of neurotrophic properties of the neonatal brain (EPO, growth factors, stem cells transplantation). Combination of pharmacological interventions with moderate hypothermia, which is the only established therapy for post HI brain injury, is probably the next step to fight HI brain damage in the clinical setting.

The role and regulation of hypoxia-inducible factor-1alpha expression in brain development and neonatal hypoxic-ischemic brain injury.

During neonatal hypoxic-ischemic brain injury, activation of transcription of a series of genes is induced to stimulate erythropoiesis, anti-apoptosis, apoptosis, necrosis and angiogenesis. A key factor mediating these gene transcriptions is hypoxia-inducible factor-1alpha (HIF-1alpha). During hypoxia, HIF-1alpha protein is stabilized and heterodimerizes with HIF-1beta to form HIF-1, subsequently regulating the expression of target genes.