sclerosis/hypoxia

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Hypoxia-inducible factor 1a is a Tsc1-regulated survival factor in newborn neurons in tuberous sclerosis complex.

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Tuberous sclerosis complex (TSC) is a genetic disorder caused by mutations in TSC1 or TSC2 resulting in hyperactivity of the mammalian target of rapamycin and disabling brain lesions. These lesions contain misplaced neurons enriched in hypoxia-inducible factor 1a (HIF1a). However, the relationship

Cutaneous hypoxia in patients with systemic sclerosis (scleroderma).

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Measurement of transcutaneous oxygen pressure (TCPO2) is an established and noninvasive way of assessing cutaneous hypoxia. Since the degree of oxygenation modulates fibroblast growth and synthesis, we investigated the presence of cutaneous hypoxia in patients with systemic sclerosis (SS). We

Reduced hypoxia risk in a systemic sclerosis patient with interstitial lung disease after long-term pulmonary rehabilitation.

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Pulmonary rehabilitation is effective for improving exercise capacity in patients with interstitial lung disease (ILD), and most programs last about 8 weeks. A 43-year-old male patient with systemic sclerosis and oxygen saturation (SpO(2)) declining because of severe ILD was hospitalized for

Hypoxia-inducible factor-1a contributes to dendritic overgrowth in tuberous sclerosis.

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Expression of hypoxia-inducible factor 1a (HIF1a) is increased under several pathological conditions such as hyperactive mechanistic target of rapamycin complex 1 (mTORC1) in tuberous sclerosis complex (TSC). Hyperactive mTORC1 and the resulting increased dendritic complexity of neurons are shared

Investigation of hypoxia-inducible factor-1α in hippocampal sclerosis: a postmortem study.

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OBJECTIVE Hypoxia-inducible factor-1α (HIF-1α) is involved in critical aspects of cell survival in response to hypoxia and regulates vascular endothelial growth factor (VEGF) expression. Previous experimental and human studies in epilepsy show up-regulation of VEGF following seizures, although

Increased bone mineral density at the hypoxia prone site of the juxta-articular metacarpal bone in patients with limited systemic sclerosis: a cross-sectional study.

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OBJECTIVE Low levels of oxygen has been shown to be involved in the induction of osteogenesis, particularly in bone repair. It is unknown whether hypoxia leads to osteogenesis at the hypoxia prone skeletal sites in limited systemic sclerosis. This study determined the total and trabecular volumetric

Job strain, hypoxia and risk of amyotrophic lateral sclerosis: Results from a death certificate study.

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Amyotrophic lateral sclerosis (ALS) most likely results from a multifactorial gene-environment interaction. Strenuous physical activity and occupational exposures have been suggested to play a role, and an abnormal response to hypoxia has been proposed in ALS pathogenesis. To test the hypothesis of

Acute effects of whole-body vibration training on neuromuscular performance and mobility in hypoxia and normoxia in persons with multiple sclerosis: A crossover study.

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Whole-body vibration training (WBVT) has been used in people with relapsing-remitting multiple sclerosis (pwMS), showing improvements in different neuromuscular and mobility variables. However, the acute effects of this training are still unknown. The acute effects of WBVT on

A new paraclinical CSF marker for hypoxia-like tissue damage in multiple sclerosis lesions.

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Recent studies on the immunopathology of multiple sclerosis revealed a heterogeneity in the patterns of demyelination, suggesting interindividual differences in the mechanism responsible for myelin destruction. One of these patterns of demyelination, characterized by oligodendrocyte dystrophy and

Thrombospondin 1 in hypoxia-conditioned media blocks the growth of human microvascular endothelial cells and is increased in systemic sclerosis tissues.

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BACKGROUND Systemic sclerosis (SSc) is a chronic inflammatory autoimmune disease characterised by vascular dysfunction and damage, excess collagen deposition and subsequent organ manifestations. Vasculopathy is an early feature of the disease which leads to a chronic hypoxic environment in the

Deregulation of the hypoxia inducible factor-1α pathway in monocytes from sporadic amyotrophic lateral sclerosis patients.

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The clinical course of the degenerative motor neuron disorder amyotrophic lateral sclerosis (ALS) is closely related to hypoxia. The normal response to hypoxia involves two pathways in particular: the hypoxia inducible factor 1α (HIF-1α) pathway (which notably controls the synthesis of vascular

[Mechanisms of deregulated response to hypoxia in sporadic amyotrophic lateral sclerosis: a clinical study].

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Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disorder of upper and lower motorneurons, leading to death in 3 to 5 years. Respiratory insufficiency and hypoxemia are closely linked during the clinical course of ALS. Chronic respiratory insufficiency and hypoxemia generally occur late in

A system out of breath: how hypoxia possibly contributes to the pathogenesis of systemic sclerosis.

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Systemic sclerosis (SSc) is an autoimmune disease characterized by vascular alterations and immunological disturbances and fibrosis, the order of which remains to be fully determined. Clinically, patients show clear signs of hypoxia in skin and internal organs. The low oxygen tension is potentially

6-Deoxyjacareubin, a natural compound preventing hypoxia-induced cell death, ameliorates neurodegeneration in a mouse model of familial amyotrophic lateral sclerosis.

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The central nervous system (CNS) uses a significant amount of oxygen for energy production. Decreased oxygen supply due to impaired blood supply critically damages the CNS. As chronic hypoxic conditions have diverse effects via the excessive production of reactive oxygen species, protection from

Increased expression of ER stress- and hypoxia-associated molecules in grey matter lesions in multiple sclerosis.

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BACKGROUND The endoplasmic reticulum (ER) stress pathway may play a role in the pathogenesis multiple sclerosis (MS), and while ER stress-associated molecules have been demonstrated in white matter (WM) lesions, these have not been analysed in grey matter (GM) demyelination. OBJECTIVE The objective

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