Results 151 to 160 of about 34,531 (209)
Chemogenetic Control of Striatal Astrocytes Improves Parkinsonian Motor Deficits in Mice
Main Points Dopamine depletion reduces locomotion‐induced calcium activity in dorsal striatal astrocytes. Chemogenetic activation facilitates astrocyte locomotion responses and improves motor behavior in dopamine lesioned animals. ABSTRACT Parkinson's disease (PD) is characterized by the degeneration of dopaminergic nigrostriatal inputs, which causes ...
Wesley R. Evans+7 more
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Targeted Lung Premetastasis Niche: Mechanisms, Strategies, and Application
Before the cancer cells arrive to the lung through blood vessels, these cancer cells secreted specific factors for two main purposes: first, to recruit bone marrow‐derived cells; and second, to regulate the activation of target cells. Additionally, the unique structure of the lungs provides a comfortable environment. Consequently, the formation of lung
Chenghao Cao+12 more
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Abstracts submitted to the ‘EACR 2025 Congress: Innovative Cancer Science’, from 16–19 June 2025 and accepted by the Congress Organising Committee are published in this Supplement of Molecular Oncology, an affiliated journal of the European Association for Cancer Research (EACR).
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Clinical outcomes in 21-hydroxylase deficiency
Current Opinion in Endocrinology, Diabetes & Obesity, 2021Purpose of review The introduction of synthetic glucocorticoids 70 years ago made survival possible in classic 21-hydroxylase deficiency (21OHD). The currently used glucocorticoid therapy may lead to unphysiological dosing with negative consequencies on health in addition to the problems that may arise due to androgen over ...
Anna Nordenström+2 more
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Annals of the New York Academy of Sciences, 1997
A deficiency of 21-hydroxylase in the adrenal cortex results in insufficient cortisol production. The salt-wasting form of21-hydroxylase deficiency is characterized by inadequate aldosterone production, as well. Because the hypothalamic-adr enal negative feedback system is broken, excess adrenal androgens are produced.
Ron S. Newfield, Maria I. New
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A deficiency of 21-hydroxylase in the adrenal cortex results in insufficient cortisol production. The salt-wasting form of21-hydroxylase deficiency is characterized by inadequate aldosterone production, as well. Because the hypothalamic-adr enal negative feedback system is broken, excess adrenal androgens are produced.
Ron S. Newfield, Maria I. New
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Nonclassic 21-Hydroxylase Deficiency in Croatia
Journal of Pediatric Endocrinology and Metabolism, 2004This is the first report of nonclassic congenital adrenal hyperplasia due to 21-hydroxylase (21-OH) deficiency in Croatia in which the patients have been evaluated clinically, hormonally, and by molecular genetic analysis. Genetic analysis was performed on 18 Croatian patients with nonclassic CAH due to 21-OH deficiency using allele-specific PCR.
Jasenka Ille+10 more
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Epidemiology of 21-Hydroxylase Deficiency in Singapore
Journal of Pediatric Endocrinology and Metabolism, 2002We report the incidence and epidemiology of 21-hydroxylase deficiency in Singapore, based on a retrospective study of all known patients diagnosed with classical 21-hydroxylase deficiency in the past 21 years. The database was obtained from the case registry and questionnaire methodology, with 100% coverage of all practising pediatricians in Singapore.
Loke, K.Y.+3 more
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Late-Onset 21-Hydroxylase Deficiency
Annals of Internal Medicine, 1982Excerpt To the editor: Since our article on the diagnosis of late-onset 21-hydroxylase deficiency was published (1), we have been asked the best way to do the 30-minute adrenocorticotrophic hormone...
Gordon B. Cutler+3 more
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Steroid 21-Hydroxylase Deficiency in Mice*
Endocrinology, 1988The enzyme steroid 21-hydroxylase (21-OHase) plays a key role in adrenal steroidogenesis. Defects in this enzyme are responsible for one of the most common inborn errors of metabolism in humans. Duplicated genes for the enzyme are located in the class III region of the major histocompatibility complex (MHC), HLA.
Hideo Gotoh+4 more
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