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alkaline phosphatase/atrophy

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Eight children with primary and secondary enteropathy were examined, in whom predominantly advanced partial atrophy and subtotal atrophy of the villous apparatus were established. Enzymic histochemical study of the activity of alkaline phosphatase showed correlation with the degree of villous
To obtain an expression vector that will optimize secretion of proteins with disulfide bridges in Escherichia coli, we fused the phoA gene, encoding the bacterial alkaline phosphatase (PhoA), to the sequence encoding the pectate lyase B signal sequence (PelBSS). We used an extensively degenerate
Objective: The purpose of this study was to determine whether increased alkaline phosphatase (ALP) was associated with early neurological deterioration (END) in patients with atherothrombotic brain infarction (ATBI) attributable to
BACKGROUND There is general agreement that radiation effects on capillary endothelial cells are a leading event in the pathogenesis of late effects of radiation in normal tissues. The mechanism of microvascular involvement however is unclear. In the myocardium, there is not only a decrease in
Alkaline phosphatase (ALP) has been implicated to be associated with poor outcome in ischemic stroke patients, yet its role in aneurysmal subarachnoid hemorrhage (aSAH) patients is unknown. The current study aimed to investigate the on-admission and short-term variation trend of ALP
During maturation from fetal to adult testis, both Sertoli cells (SCs) and germ cells (GCs) switch from an immature to a mature immunophenotype. Immature canine SCs express cytokeratins (CKs), desmin (DES), vimentin (VIM), anti-Müllerian hormone (AMH) and inhibin (INH)-α, while mature SCs retain
Retinal progenitor sheet transplants have been shown to extend neuronal processes into a degenerating host retina and to restore visual responses in the brain. The aim of this study was to identify cells involved in transplant signals to retinal degenerate hosts using computational molecular
Attention has been paid to bone atrophy caused by oral anticonvulsants. Bone atrophy has been judged on X-ray picture in combination with measuring bio-chemical parameters such as serum calcium (Ca), phosphorus (P) and alkaline phosphatase (Alp), and assessing X-ray findings such as bone density and
A single oral dose of di-n-butyl phthalate (DBP) to male rats caused histologically a sloughing of the germ cells at 6 h. On Days 1 and 2 more severe sloughing was seen, followed by atrophy and the dissociation of the germ cells from the Sertoli cells and the spermatogonia. Biochemically, there was
Previous studies have demonstrated a negative correlation between intestinal alkaline phosphatase (IAP) activity and calcium (Ca) absorption in the gut, as IAP acts as a protective mechanism inhibiting high Ca entry into enterocytes, preventing Ca overload. Here we evaluated Ca absorption and bone
Our previous studies demonstrated that estrogen (E2) prevents the development of disuse atrophy of the femur in tail-suspended rats. To elucidate the mechanisms of this E2 action, we investigated the effects of E2 on the expression of alkaline phosphatase (ALP, a marker for bone formation) and

Molecular pathology of Alzheimer neurofibrillary degeneration.

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The most characteristic brain lesion of Alzheimer disease is the accumulation of paired helical filaments (PHF) in the affected neurons. Based on solubility in detergents there are two general populations of PHF, the readily soluble (PHF I) and the sparingly soluble (PHF II) types. The major
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