osteochondrodysplasias/hypoxia

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FK228 recovers thiram-induced tibial dyschondroplasia in chicken via hypoxia inducible factor-1α.

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Prijava / prijava

Tibial dyschondroplasia (TD) is a disease of many avian species characterized by an enlarged and avascular lesion in the proximal tibiotarsal bone. The aim of present study was to evaluate the effects of hypoxia-inducible factor-1α(HIF-1α) inhibition on thiram- induced TD using synthetic medicine

Tibial dyschondroplasia is highly related to suppression of the hypoxia inducible factor (HIF)-1ɑ,-2ɑ, and -3ɑ expressions in chickens.

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Prijava / prijava

Tibial dyschondroplasia (TD) cases has not been reported in Tibetan chickens (TBCs), but it is commonly seen in commercial broilers characterized by lameness. The underlying mechanism remains unclear. Hypoxia-inducible factors (HIFs) are important regulators of cellular adaptation to hypoxic

Hypoxia, hypoxia-inducible factor-1alpha (HIF-1alpha), and heat-shock proteins in tibial dyschondroplasia.

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Prijava / prijava

Tibial dyschondroplasia (TD) is one of the most prevalent skeletal abnormalities in avian species; it causes economic losses and is an animal welfare problem. It has been hypothesized that the absence of vasculature in the lesion of the TD growth plates at the ends of the long bones is involved in

PTEN deficiency causes dyschondroplasia in mice by enhanced hypoxia-inducible factor 1alpha signaling and endoplasmic reticulum stress.

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Prijava / prijava

Chondrocytes within the growth plates acclimatize themselves to a variety of stresses that might otherwise disturb cell fate. The tumor suppressor PTEN (phosphatase and tensin homolog deleted from chromosome 10) has been implicated in the maintenance of cell homeostasis. However, the functions of

Tibial dyschondroplasia is highly associated with suppression of tibial angiogenesis through regulating the HIF-1α/VEGF/VEGFR signaling pathway in chickens.

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Prijava / prijava

Tibial dyschondroplasia (TD) is an intractable poultry problem that is characterized by the appearance of non-vascularized and non-mineralized cartilage masses in tibial growth plates (TGPs). However, the role of angiogenesis inhibition in the occurrence of TD remains unknown. In this study, we

The effect of inhibition of heat-shock proteins on thiram-induced tibial dyschondroplasia.

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Prijava / prijava

Tibial dyschondroplasia (TD) is a skeletal abnormality that can cause economic losses and animal welfare concerns. Thiram-induced TD is characterized by enlarged, unvascularized growth plates, low levels of the vascular endothelial growth factor receptor Flk-1, abnormal chondrocyte differentiation,

High altitude hypoxia as a factor that promotes tibial growth plate development in broiler chickens.

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Prijava / prijava

Tibial dyschondroplasia (TD) is one of the most common problems in the poultry industry and leads to lameness by affecting the proximal growth plate of the tibia. However, due to the unique environmental and geographical conditions of Tibet, no case of TD has been reported in Tibetan chickens

Conditional ablation of MAPK7 expression in chondrocytes impairs endochondral bone formation in limbs and adaptation of chondrocytes to hypoxia

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Prijava / prijava

Background: Long bones of limbs are formed through endochondral bone formation, which depends on the coordinated development of growth plates. Our previous studies have demonstrated that dysfunction of mitogen-activated protein kinase 7

Role of Angiopoietin-like 4 on Bone Vascularization in Chickens Exposed to High-altitude Hypoxia.

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Prijava / prijava

The aim of this study was to investigate the role and expression of a novel angiogenic factor (angiopoietin-like 4, ANGPTL4) in tibial growth plates of broiler chickens exposed to high-altitude hypoxia. One-day-old healthy broiler chickens (n = 120) were transported from lowland to a high-altitude

Hypoxia, hypoxia-inducible transcription factors and oxygen-sensing prolyl hydroxylases in bone development and homeostasis.

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Prijava / prijava

To summarize the role of hypoxia signaling in skeletal cells.Hypoxia occurs at several stages during bone development. Skeletal cells, like chondrocytes and osteoblasts, respond to this challenge by stabilizing the hypoxia inducible transcription factor

Cytogenetic investigations in cases of multiple developmental anomalies in children.

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Prijava / prijava

The authors studied 59 children including 48 with multiple developmental anomalies and 11 with disturbances of sexual development. In 11 cases (18.6%) the following chromosomal abnormalities were found: in 5 cases of Down's syndrome, 3 cases of full trisomy G, 1 case of 46XX/47XYG+ mosaicism, and in

A case of achondroplasia with severe pulmonary hypertension due to obstructive sleep apnea.

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Prijava / prijava

Achondroplasia is the most common skeletal dysplasia in children. Achondroplasic patients have a short cranial face and midface hypoplasia. They often have sleep-related respiratory disturbances that lead to hypoxemia caused by midfacial hypoplasia, a small upper airway, hypotonia of airway muscles,

Hsp90 and angiogenesis in bone disorders--lessons from the avian growth plate.

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Prijava / prijava

Thiram-induced tibial dyschondroplasia (TD) and vitamin-D deficiency rickets are avian bone disorders of different etiologies characterized by abnormal chondrocyte differentiation, enlarged and unvascularized growth plates, and lameness. Heat-shock protein 90 (Hsp90) is a proangiogenic factor in

HIF-1α metabolically controls collagen synthesis and modification in chondrocytes.

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Prijava / prijava

Endochondral ossification, an important process in vertebrate bone formation, is highly dependent on correct functioning of growth plate chondrocytes¹. Proliferation of these cells determines longitudinal bone growth and the matrix deposited provides a scaffold for future bone formation.

Cardiopulmonary dysfunction in the Osteogenesis imperfecta mouse model Aga2 and human patients are caused by bone-independent mechanisms.

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Prijava / prijava

Osteogenesis imperfecta (OI) is an inherited connective tissue disorder with skeletal dysplasia of varying severity, predominantly caused by mutations in the collagen I genes (COL1A1/COL1A2). Extraskeletal findings such as cardiac and pulmonary complications are generally considered to be

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