mannose/hemorrhage

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Prevention of cyclophosphamide-induced hemorrhagic cystitis by glucose-mannose binding plant lectins.

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OBJECTIVE Neutrophils are implicated in the physiopathologic alterations of hemorrhagic cystitis (HC). Thus, we decided to test the antiinflammatory activity of glucose-mannose binding lectins extracted from D. violacea and D. guianensis seeds, which showed an inhibitory effect upon neutrophil

Serum mannose-binding lectin levels after aneurysmal subarachnoid hemorrhage.

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BACKGROUND Mannose-binding lectin (MBL) is a key molecule of complement system, which is activated after aneurysmal subarachnoid hemorrhage (aSAH). We investigated the association of serum MBL levels with injury severity and clinical outcomes among aSAH patients. METHODS Serum MBL levels were

Elevated levels of vitamin D and deficiency of mannose binding lectin in dengue hemorrhagic fever.

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BACKGROUND Altered plasma concentrations of vitamin D and mannose binding lectin (MBL), components of innate immunity, have been shown to be associated with the pathogenesis of viral infections. The objective of the present study was to find out whether plasma concentrations of MBL and vitamin D are

Development modulates the serum induced effect on the incorporation of [2-3H]mannose into chick optic lobe protein: the possible role of glia.

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Recently, we described that serum decreases tritiated mannose incorporation into protein in the chick optic lobe at 18 days of embryonic age (Rossi et al., 1990). In this paper, we found a strikingly different response of this serum effect according to age. The data obtained showed no serum induced

[Congenital factor V and factor VIII deficiency discovered in an elderly patient with abnormal bleeding after trauma].

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Congenital combined deficiency of coagulation factor V (FV) and factor VIII (FVIII) (F5F8D) is a rare autosomal recessive bleeding disorder caused by mutations in lectin mannose-binding type 1 (LMAN1) or multiple coagulation factor deficiency 2 (MCFD2) encoding chaperone molecules involved in the

Mannose-binding lectin gene polymorphism and early neonatal outcome in preterm infants.

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BACKGROUND Mannose-binding lectin (MBL) as a component of innate immunity plays an important role in preterm infants in whom adaptive immunity is not sufficiently developed. Polymorphisms in immunoregulatory genes influence the response to infection and subsequent inflammation. Infection and

Case report of mannose-binding lectin (MBL) deficiency and postoperative sepsis and coagulopathy in a patient following total pancreatectomy for chronic pancreatitis.

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BACKGROUND Complement plays a central role against infection and coordinates the activity of coagulation and fibrinolysis. In this report we present a patient that underwent total pancreatectomy experienced sepsis, coagulopathy and bleeding that endangered the postoperative course. METHODS A

High levels of serum mannose-binding lectin are associated with the severity of clinical signs of leptospirosis.

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The clinical heterogeneity observed in leptospirosis may be associated with host factors or bacteria virulence. Human serum mannose-binding lectin (MBL) recognizes many pathogens, and low levels of this lectin are associated with susceptibility to infection. MBL is also implicated in the modulation

Removal of Mannose-Ending Glycan at Asn2118 Abrogates FVIII Presentation by Human Monocyte-Derived Dendritic Cells.

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The development of an immune response against therapeutic factor VIII is the major complication in hemophilia A patients. Oligomannose carbohydrates at N239 and/or N2118 on factor VIII allow its binding to the macrophage mannose receptor expressed on human dendritic cells, thereby leading to factor

Ficolin-1 Levels in Patients Developing Vasospasm and Cerebral Ischemia After Spontaneous Subarachnoid Hemorrhage.

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Activation of the inflammatory generating complement system might play a pathogenic role in spontaneous subarachnoid hemorrhage (SAH). We studied whether plasma and cerebrospinal fluid (CSF) levels of complement proteins were associated with angiographic vasospasm and cerebral ischemic lesions after

Mannose-dependent endoplasmic reticulum (ER)-Golgi intermediate compartment-53-mediated ER to Golgi trafficking of coagulation factors V and VIII.

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The endoplasmic reticulum-Golgi intermediate compartment (ERGIC) is the site of segregation of secretory proteins for anterograde transport, via packaging into COPII-coated transport vesicles. ERGIC-53 is a homo-hexameric transmembrane lectin localized to the ERGIC that exhibits mannose-selective

The soluble mannose receptor is released from the liver in cirrhotic patients, but is not associated with bacterial translocation.

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Intestinal bacterial translocation is involved in activation of liver macrophages in cirrhotic patients. Macrophages play a key role in liver inflammation and are involved in the pathogenesis of cirrhosis and complications. Bacterial translocation may be determined by presence of bacterial DNA and

Mannose-binding lectin-associated serine protease-1 is a significant contributor to coagulation in a murine model of occlusive thrombosis.

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Bleeding disorders and thrombotic complications constitute a major cause of death and disability worldwide. Although it is known that the complement and coagulation systems interact, no studies have investigated the specific role or mechanisms of lectin-mediated coagulation in vivo. FeCl(3)

A zebrafish model of congenital disorders of glycosylation with phosphomannose isomerase deficiency reveals an early opportunity for corrective mannose supplementation.

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Individuals with congenital disorders of glycosylation (CDG) have recessive mutations in genes required for protein N-glycosylation, resulting in multi-systemic disease. Despite the well-characterized biochemical consequences in these individuals, the underlying cellular defects that contribute to

Pristane-induced granulocyte recruitment promotes phenotypic conversion of macrophages and protects against diffuse pulmonary hemorrhage in Mac-1 deficiency.

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Diffuse pulmonary hemorrhage (DPH) is an uncommon but critical complication of systemic lupus erythematosus. Peritoneal administration of 2,6,10,14-tetramethylpentadecane (pristane) can recapitulate a lupus-like syndrome in mice, which can develop into DPH within a few weeks, especially in C57BL/6

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