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Skeletal disease in primary hyperparathyroidism
Most patients with primary hyperparathyroidism in the 1980s do not have evidence of bone disease when they are evaluated by conventional radiography. We sought to determine whether skeletalExpand
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The A2B adenosine receptor protects against inflammation and excessive vascular adhesion.
Adenosine has been described as playing a role in the control of inflammation, but it has not been certain which of its receptors mediate this effect. Here, we generated an A2B adenosineExpand
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Direct identification of PTEN phosphorylation sites
The PTEN tumor suppressor gene encodes a phosphatidylinositol 3′‐phosphatase that is inactivated in a high percentage of human tumors, particularly glioblastoma, melanoma, and prostate andExpand
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Amyloidosis: pathogenesis and new therapeutic options.
The systemic amyloidoses are a group of complex diseases caused by tissue deposition of misfolded proteins that results in progressive organ damage. The most common type, immunoglobulin light chainExpand
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High-Dose Melphalan and Autologous Stem-Cell Transplantation in Patients with AL Amyloidosis: An 8-Year Study
Context AL amyloidosis responds poorly to oral chemotherapy and rarely leads to elimination of plasma cell dyscrasia. Amyloid cardiomyopathy is a particularly fatal complication of the disease.Expand
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Globozoospermia in mice lacking the casein kinase II alpha' catalytic subunit.
Protein kinase casein kinase II (Ck2) is a cyclic-AMP and calcium-independent serine-threonine kinase that is composed of two catalytic subunits (alpha and alpha') and two regulatory beta-subunits.Expand
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Pathway pathology: histological differences between ErbB/Ras and Wnt pathway transgenic mammary tumors.
To study phenotype-genotype correlations, ErbB/Ras pathway tumors (transgenic for ErbB2, c-Neu, mutants of c-Neu, polyomavirus middle T antigene (PyV-mT), Ras, and bi-transgenic for ErbB2/Neu withExpand
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T1alpha, a lung type I cell differentiation gene, is required for normal lung cell proliferation and alveolus formation at birth.
T1alpha, a differentiation gene of lung alveolar epithelial type I cells, is developmentally regulated and encodes an apical membrane protein of unknown function. Morphological differentiation ofExpand
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Repurposing diflunisal for familial amyloid polyneuropathy: a randomized clinical trial.
IMPORTANCE Familial amyloid polyneuropathy, a lethal genetic disease caused by aggregation of variant transthyretin, induces progressive peripheral nerve deficits and disability. Diflunisal, aExpand
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Tal‐1 induces T cell acute lymphoblastic leukemia accelerated by casein kinase IIalpha.
Ectopic activation of the TAL‐1 gene in T lymphocytes occurs in the majority of cases of human T cell acute lymphoblastic leukemia (T‐ALL), yet experiments to date have failed to demonstrate a directExpand
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