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Sida 1 från 97 resultat
Atypical presentation of mucopolysaccharidosis type IVA.
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A 14 year old patient with short stature, type I diabetes, and cataracts was referred for evaluation of avascular necrosis of the femoral head. Radiography was suggestive of spondyloepiphyseal dysplasia with decreased bone mineral density for age. Targeted molecular and biochemical testing were
Inhibition of chikusetsusaponin IVa on inflammatory responses in RAW264.7 cell line via MAPK pathway
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Chikusetsusaponin IVa (CHS-IVa), a saponin from herb Panacis japonicas, possesses extensive biological activities. However, the roles and underlying mechanisms of CHS-IVa on inflammation have not been fully clarified in the setting of murine macrophages. In this study, we found that CHS-IVa
Lipid IVA inhibits synthesis and release of tumor necrosis factor induced by lipopolysaccharide in human whole blood ex vivo.
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Tumor necrosis factor (TNF) released by lipopolysaccharide (LPS)-stimulated mononuclear phagocytes is a critical mediator of sepsis. We examined the capacities of rough mutant Salmonella typhimurium LPS (Rc) and LPS partial structures lipid A, monophosphoryl lipid A (MPLA), lipid IVA, and lipid X to
Inhibitory effects of Chikusetsusaponin IVa on lipopolysaccharide-induced pro-inflammatory responses in THP-1 cells.
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This study investigated anti-inflammatory effects and possible mechanisms of Chikusetsusaponin IVa (Chi IVa), one of the main bioactive components in saponins from Panacis japonica (SPJ), which is used in traditional Tujia and Hmong Chinese medicine. To this end, changes in the inflammatory profiles
Induction chemoradiotherapy followed by resection for locally advanced Masaoka stage III and IVA thymic tumors.
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BACKGROUND
The treatment of locally advanced thymic tumors is not uniform. Recently, several centers have reported the results of induction chemotherapy followed by resection and then radiation. Our center adopted an alternative strategy and treated locally advanced thymic tumors with induction
Lactosylceramide-Induced Phosphorylation Signaling to Group IVA Phospholipase A2 via Reactive Oxygen Species in Tumor Necrosis Factor-α-Treated Cells.
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The activity of α-type cytosolic phospholipase A2 (cPLA2 α, group IVA PLA2 ), which releases arachidonic acid (AA), is mainly regulated by the Ca2+ -induced intracellular translocation/attachment of the enzyme to substrate membranes and its phosphorylation. We previously reported that tumor necrosis
Comparative study of lipopolysaccharide-, lipid IVa-, and lipid X-induced tumor necrosis factor production in murine macrophage-like cell lines.
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[Long-term survival of a patient with postoperative liver metastasis of stage IVa gallbladder cancer responding to hepatic arterial infusion chemotherapy].
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A 58-year-old man was diagnosed as having advanced gallbladder cancer (T4, P0, H0, N0, stage IVa) with direct invasion to the liver, transverse colon and duodenum. Therefore, extended cholecystectomy and bile duct resection with a partial resection of the transverse colon and the duodenum were
Disruption of group IVA cytosolic phospholipase A(2) attenuates myocardial ischemia-reperfusion injury partly through inhibition of TNF-α-mediated pathway.
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Group IVA cytosolic phospholipase A(2) (cPLA(2)α), which preferentially cleaves arachidonic acid from phospholipids, plays a role in apoptosis and tissue injury. Downstream signals in response to tumor necrosis factor (TNF)-α, a mediator of myocardial ischemia-reperfusion (I/R) injury, involve
Lipopolysaccharides from periodontal pathogens prime neutrophils for enhanced respiratory burst: differential effect of a synthetic lipid a precursor IVA (LA-14-PP).
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When neutrophils are incubated with bacterial lipopolysaccharide (LPS), they become primed for enhanced release of superoxide anion (O2-) in response to stimulation by FMLP. We investigated the human neutrophil-priming activity of LPS from the periodontal pathogens, Porphyromonas gingivalis (Pg),
Paradox of glucocorticoid-induced cytosolic phospholipase A2 group IVA messenger RNA expression involves glucocorticoid receptor binding to the promoter in human amnion fibroblasts.
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Glucocorticoids (GCs) are well-known anti-inflammatory drugs inhibiting prostaglandin production. Paradoxically, GCs are reported to stimulate cytosolic phosphoplipase A2 group IVA (PLA2G4A) and prostaglandin-endoperoxide synthase 2 (PTGS2) expression in human amnion fibroblasts. This study was
Chikusetsu Saponin IVa Ameliorates Cerebral Ischemia Reperfusion Injury in Diabetic Mice via Adiponectin-Mediated AMPK/GSK-3β Pathway In Vivo and In Vitro.
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Diabetes mellitus substantially increases the risk of stroke and enhances brain's vulnerability to ischemia insult. In a previous study, Chikusetsu saponin IVa (CHS) pretreatment was proved to protect the brain from cerebral ischemic in normal stroke models. Whether CHS could attenuate cerebral
Experimental infection studies demonstrating Atlantic salmon as a host and reservoir of viral hemorrhagic septicemia virus type IVa with insights into pathology and host immunity.
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In British Columbia, Canada (BC), aquaculture of finfish in ocean netpens has the potential for pathogen transmission between wild and farmed species due to the sharing of an aquatic environment. Viral hemorrhagic septicemia virus (VHSV) is enzootic in BC and causes serious disease in wild Pacific
Chikusetsusaponin IVa Methyl Ester Isolated from the Roots of Achyranthes japonica Suppresses LPS-Induced iNOS, TNF-α, IL-6, and IL-1β Expression by NF-κB and AP-1 Inactivation.
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We investigated the effect of chikusetsusaponin IVa (CS) and chikusetsusaponin IVa methyl ester (CS-ME) from the roots of Achyranthes japonica NAKAI on lipopolysaccharide (LPS)-induced nitric oxide (NO) and prostaglandin E2 (PGE2) production in RAW264.7 macrophages. CS-ME more potently inhibited
[Arthroscopically assisted therapy of avascular necrosis of the femoral head].
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OBJECTIVE
Preservation of the hip joint function by treatment of the avascular necrosis of the femoral head in adults or at least avoiding progression.
METHODS
Avascular necrosis of the femoral head in adults in Steinberg stages I-III. In patients with Steinberg stage IVa (subchondral collapse ≤ 15%
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