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balkan nephropathy/hypoxia
Saite tiek saglabāta starpliktuvē
8 rezultātiem
[Influence of hypoxia caused by impairment of peritubular capillary on the progression of chronic aristolochic acid nephropathy].
Rakstu tulkošanu var veikt tikai reģistrēti lietotāji
Ielogoties Reģistrēties
OBJECTIVE
To investigate the manifestation of impairment of peritubular capillary (PTC) in chronic aristolochic acid nephropathy (CAAN) and the influence of hypoxia caused by PTC impairment on the progression of CAAN.
METHODS
Fifty-four Wistar rats were randomly divided into 2 groups: Group A (n =
Role of peritubular capillary loss and hypoxia in progressive tubulointerstitial fibrosis in a rat model of aristolochic acid nephropathy.
Rakstu tulkošanu var veikt tikai reģistrēti lietotāji
Ielogoties Reģistrēties
OBJECTIVE
To investigate the effects of peritubular capillary (PTC) loss and hypoxia on the progression of tubulointerstitial fibrosis in a rat model of aristolochic acid nephropathy (AAN).
METHODS
Female Wistar rats received Caulis aristolochiae manshuriensis (CAM) decoction by gavage for 8 weeks,
Protective effect of prostaglandin E1 on renal microvascular injury in rats of acute aristolochic acid nephropathy.
Rakstu tulkošanu var veikt tikai reģistrēti lietotāji
Ielogoties Reģistrēties
BACKGROUND
To investigate the renal microvascular injury in acute aristolochic acid nephropathy (AAN) and the protective effects of prostaglandin E1 (PGE1) in acute AAN.
METHODS
Female Sprague-Dawley rats were randomly divided into three groups. The rats in PGE1 group received Caulis Aristolochia
Characterization of cytotoxic effects of aristolochic acids on the vascular endothelium.
Rakstu tulkošanu var veikt tikai reģistrēti lietotāji
Ielogoties Reģistrēties
Aristolochic acid nephropathy (AAN) is characterized by interstitial fibrosis, proximal tubular atrophy, and hypoxia. A correlation between a reduced peritubular capillary density and the severity of fibrosis has been demonstrated. As calcium, redox and energetic homeostasis are crucial in
Ischemic injury underlies the pathogenesis of aristolochic acid-induced acute kidney injury.
Rakstu tulkošanu var veikt tikai reģistrēti lietotāji
Ielogoties Reģistrēties
Aristolochic acid nephropathy (AAN) is a progressive tubulointerstitial renal disease caused by aristolochic acid intake. To determine the contribution of renal ischemia to the pathogenesis of AAN, we characterized changes in the expression of angiogenic factors and vasoactive substances, and then
[Epidemic of hantavirus disease in Entre-Sambre-et-Meuse: year 1992-1993. Clinical and biological aspects].
Rakstu tulkošanu var veikt tikai reģistrēti lietotāji
Ielogoties Reģistrēties
A multihospital study allowed us to follow a total of 62 serologically proven cases of Nephropathia epidemica (NE) in the Belgian region between Sambre and Meuse during the 1992-1993 period. The clinical picture consisted of sudden high fever (100% of the cases), headache (71%), abdominal or lumbar
[Study on homologous bone marrow mesenchymal stem cells in repairing peri-tubular capillary cluster].
Rakstu tulkošanu var veikt tikai reģistrēti lietotāji
Ielogoties Reģistrēties
OBJECTIVE
To investigate the potential effect of homologous bone marrow mesenchymal stem cells (MSCs) on repairing peri-tubular capillary cluster (PTCC), and on improving renal tubular and mesenchymal hypoxia condition.
METHODS
Monocyte was purified from bone marrow, amplified and identified as MSCs
Aristolochic acid induces renal fibrosis by arresting proximal tubular cells in G2/M phase mediated by HIF-1α
Rakstu tulkošanu var veikt tikai reģistrēti lietotāji
Ielogoties Reģistrēties
Renal tubulointerstitial fibrosis (TIF) is a common pathological feature of aristolochic acid (AA) nephropathy (AAN). G2/M arrest of proximal tubular cells (PTCs) is implicated in renal fibrosis of AAN, but the upstream regulatory molecule remains unknown. Hypoxia inducible factor-1α (HIF-1α)
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