respiratory insufficiency/phosphatase

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Severe hypercalcaemia and respiratory insufficiency associated with infantile hypophosphatasia caused by two novel mutations of the tissue-nonspecific alkaline phosphatase gene.

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We report the case of a male patient with infantile hypophosphatasia associated with severe hypercalcaemia and mild respiratory insufficiency. At the age of 2 months, severe hypercalcaemia, low levels of serum alkaline phosphatase activity, and elevated urinary excretion of calcium and

Neonatal lethal osteochondrodysplasia with low serum levels of alkaline phosphatase and osteocalcin.

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Neonatal lethal skeletal dysplasias are rare and typically involve thoracic malformations and severe limb shortening. We report on a newborn boy manifesting an osteochondrodysplasia associated with fatal respiratory insufficiency who had normal lung volumes and extremity lengths. His disorder

Receptor tyrosine phosphatases control tracheal tube geometries through negative regulation of Egfr signaling.

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The formation of epithelial tubes with defined shapes and sizes is essential for organ development. We describe a unique tracheal tubulogenesis phenotype caused by loss of both Drosophila type III receptor tyrosine phosphatases (RPTPs), Ptp4E and Ptp10D. Ptp4E is the only widely expressed Drosophila

[Determination of placental alkaline phosphatase (PLAP) for detecting the damages of alveolar type I cells caused by smoke inhalation].

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The placental alkaline phosphatase (PLAP) is a marker enzyme of alveolar type I cells. To evaluate the damages of alveolar type I cells and its relations with the development of acute lung injury caused by smoke inhalation, the present study was designed to observe the dynamic changes in PLAP

Respiratory plasticity following intermittent hypoxia: roles of protein phosphatases and reactive oxygen species.

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Plasticity is an important property of the respiratory control system. One of the best-studied models of respiratory plasticity is pLTF (phrenic long-term facilitation). pLTF is a progressive increase in phrenic motor output lasting several hours following acute exposure to intermittent hypoxia.

Pyridoxine-responsive seizures as the first symptom of infantile hypophosphatasia caused by two novel missense mutations (c.677T>C, p.M226T; c.1112C>T, p.T371I) of the tissue-nonspecific alkaline phosphatase gene.

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Pyridoxine-responsive seizures (PRS) and the role of pyridoxine (PN, vitamin B(6)) in hypophosphatasia (HPP) are incompletely understood. Typically, PRS and HPP are rare, independent, metabolic disorders. In PRS, seizures resist standard anticonvulsants apart from PN, yet have a good prognosis. In

Alkaline phosphatase histochemical staining in the study of germinal matrix hemorrhage and brain vascular morphology in a very-low-birth-weight neonate.

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We evaluated the utility of alkaline phosphatase (AP) histochemical staining for studying intraparenchymal vascular morphology in the brain of a 31-wk-gestation (1480 g) neonate who died of respiratory insufficiency after 23 h. In this baby, afferent cerebral vessels (arteries, arterioles, and

Identification of novel missense mutations (Phe310Leu and Gly439Arg) in a neonatal case of hypophosphatasia.

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Hypophosphatasia is associated with a defect of the tissue-non-specific alkaline phosphatase gene. We performed a mutational analysis in a surviving patient diagnosed at birth as having hypophosphatasia, on the basis of a low level of serum alkaline phosphatase (ALP) activity and characteristic

PP2ACα of Alveolar Macrophages Is a Novel Protective Factor for LPS-Induced Acute Respiratory Distress Syndrome.

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Protein phosphatase 2A (PP2A) is one main serine/threonine phosphatase in eukaryotes, and its activation changes have been linked to modulation of numerous pathological processes, such as cancer, inflammation, fibrosis, and neurodegenerative diseases. Acute respiratory distress syndrome (ARDS), the

Clinical Forms and Animal Models of Hypophosphatasia.

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Hypophosphatasia (HPP) is due to mutations of the tissue non-specific alkaline phosphatase (TNAP) gene expressed in the liver, kidney, and bone. TNAP substrates include inorganic pyrophosphate cleaved into inorganic phosphate (Pi) in bone, pyridoxal-5'-phosphate (PLP), the circulating form of

Amitraz poisoning in children: retrospective analysis of 21 cases.

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The clinical and laboratory findings of 21 children with amitraz poisoning were evaluated retrospectively. Poisoning route, signs and symptoms of poisoning, duration of hospitalization and outcome were recorded. The mean age was 3.5 +/- 1.9 years and the ratio of males to females was 1.63. In all

Hypophosphatasia: Novel Mutation Associated With An Atypical Newborn Presentation

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<p>Hypophosphatasia, a rare genetic disease affecting bone metabolism, is characterized by decreased activity of tissue nonspecificalkaline phosphatase (TNAP). The gene encoding TNSP (ALPL) has considerable allelic heterogeneity, which couldexplain different degrees of enzyme activity

Clinico-toxinological characterization of the acute effects of the venom of the marine snail, Conus loroisii.

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The venom of the marine snail, Conus loroisii, was studied to assess its risk and lethal factors in regard of human welfare. The lethality of the crude venom (LD50-5.0 mg/kg via i.p.) in mice was associated with reduced motor activity, asphyxiation, followed by respiratory failure. The effects on

Efficacy and safety of B-mode ultrasound-guided percutaneous transhepatic gallbladder drainage combined with laparoscopic cholecystectomy for acute cholecystitis in elderly and high-risk patients.

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BACKGROUND Standards in treatment of acute cholecystitis (AC) in the elderly and high-risk patients has not been established. Our study evaluated the efficacy and safety of B-mode ultrasound-guided percutaneous transhepatic gallbladder drainage (PTGD) in combination with laparoscopic cholecystectomy

Iron toxicity in sheep.

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The harmful effect of iron excess was studied in an experiment using fifteen adult sheep. The animals were divided into three groups of 5 each. The sheep of the group I were kept as controls, those of the group II and III were supplemented with iron in doses of 80 and 40 mg/kg body weight (BW)/24 h

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