The effects of Castanospermine, an oligosaccharide processing inhibitor, on mononuclear/endothelial cell binding and the expression of cell adhesion molecules.

Introduction: In this study we aimed to determine whether Castanospermine, a transplant immunosuppressive agent, impaired mononuclear/endothelial cell binding and expression of their cell adhesion molecules.

Methods: The binding of human umbilical vein endothelial cells with peripheral blood mononuclear cells was measured by a binding assay using Chromium 51 label; the membrane expression of cell adhesion molecules was measured by flow cytometry expressed as mean fluorescence intensity ratios.

Results: Castanospermine decreased mononuclear/endothelial cell binding if and only if both cell types were treated with Castanospermine: this impairment occurred if endothelial cells were treated with a range of doses of Castanospermine and mononuclear cells were treated with a constant dose of Castanospermine (p<0.

Synchronous obstructive ureterolithiasis and acute appendicitis.

The differential diagnosis of right lower quadrant abdominal pain includes both ureterolithiasis and acute appendicitis. Surgical treatment can be undergone without confirmatory imaging studies after a clinical diagnosis is made. For this reason, an occult, second abdominal process may be present.

Understanding the role of inflammatory cytokines in malaria and related diseases.

It is now broadly accepted for infectious disease in general that it is not the invading organism, but the body's unbridled response to it--the "cytokine storm"--that causes illness and pathology. Nevertheless, many researchers still regard the harmful effects of falciparum malaria as being governed by oligaemic hypoxia arising from parasitised erythrocytes obstructing blood flow through vulnerable organs, particularly the brain, and we summarise why these notions are no longer tenable. In our view, this harmful sequestration is readily accommodated within the cytokine storm perspective as one of its secondary effects.

Human malarial disease: a consequence of inflammatory cytokine release.

Malaria causes an acute systemic human disease that bears many similarities, both clinically and mechanistically, to those caused by bacteria, rickettsia, and viruses. Over the past few decades, a literature has emerged that argues for most of the pathology seen in all of these infectious diseases being explained by activation of the inflammatory system, with the balance between the pro and anti-inflammatory cytokines being tipped towards the onset of systemic inflammation. Although not often expressed in energy terms, there is, when reduced to biochemical essentials, wide agreement that infection with falciparum malaria is often fatal because mitochondria are unable to generate enough ATP to maintain normal cellular function.

Inhibition of arginase I activity by RNA interference attenuates IL-13-induced airways hyperresponsiveness.

Increased arginase I activity is associated with allergic disorders such as asthma. How arginase I contributes to and is regulated by allergic inflammatory processes remains unknown. CD4+ Th2 lymphocytes (Th2 cells) and IL-13 are two crucial immune regulators that use STAT6-dependent pathways to induce allergic airways inflammation and enhanced airways responsiveness to spasmogens (airways hyperresponsiveness (AHR)).