Molecular cloning and functional analysis of scavenger receptor zebrafish CL-P1.

Background: Scavenger receptors are generally expressed in macrophages and vascular endothelial cells and some scavenger receptors are thought to contribute to the development of atherosclerosis.

Methods: We cloned the cDNA of a zebrafish CL-P1 (collectin placenta 1) and performed a knockdown study using its antisense morpholino oligonucleotides (MO).

Results: Zebrafish CL-P1 (zCL-P1) is 51% identical to human CL-P1 in its amino acid sequence.

Octreotide-treated diabetes accompanied by endogenous hyperinsulinemic hypoglycemia and protein-losing gastroenteropathy.

Occurrence of hypoglycemia in diabetes patients is very rare. We report here a case of frequent hypoglycemic attacks caused by inappropriate endogenous hyperinsulinemia in a female patient with poorly controlled diabetes and protein-losing gastroenteropathy. The blood glucose profiles of the patient were unstable.

The induction of human CL-P1 expression in hypoxia/reoxygenation culture condition and rat CL-P1 after ischemic/reperfusion treatment.

Background: Oxidative stress-induced endothelial dysfunction and oxidized low-density lipoprotein (LDL) might play a key role in the pathogenesis of atherosclerosis. We recently identified a vascular endothelial scavenger receptor, collectin placenta 1 (CL-P1), which acts as a receptor for oxidized LDL as well as for microbes.

Methods: We demonstrate how hypoxic and oxidative stress induced CL-P1 expression and compared their effects with the expression of lectin-like oxidized low-density lipoprotein receptor 1 (LOX-1), an endothelial scavenger receptor expressed by oxidative stress.

Scavenger receptor collectin placenta 1 (CL-P1) predominantly mediates zymosan phagocytosis by human vascular endothelial cells.

Collectin placenta 1 (CL-P1), a recently discovered scavenger receptor, mediates the uptake of oxidized low density lipoprotein and microbes. In this study, we investigated CL-P1-mediated binding and ingestion of yeast-derived zymosan bioparticles using Chinese hamster ovary (CHO) cells stably expressing human CL-P1 (CHO/CL-P1) and human vascular endothelial cells constitutively expressed CL-P1. The uptake of zymosan by CHO/CL-P1 was dependent upon the level of CL-P1 expressed on the membrane and was inhibited by cytochalasin D and wortmannin.

Lipopolysaccharide induces adipose differentiation-related protein expression and lipid accumulation in the liver through inhibition of fatty acid oxidation in mice.

Background: In the present study, we examined the effect of lipopolysaccharide (LPS) on liver histopathology with special reference to lipid metabolism in mice.

Methods: Mice were injected with LPS intraperitoneally, and its effect on the liver was investigated pathologically and biochemically.

Results: Oil-red O staining and adipose differentiation-related protein (ADRP) immunohistochemistry demonstrated that injection of LPS transiently induced lipid accumulation and ADRP expression in hepatocytes, especially around the portal vein.

Identification and characterization of a novel human collectin CL-K1.

Collectins are a family of C-type lectins with two characteristic structures, collagen like domains and carbohydrate recognition domains. They recognize carbohydrate antigens on microorganisms and act as host-defense. Here we report the cloning and characterization of a novel collectin CL-K1.

A system for the calculation and visualisation of radiation field for maintenance support in nuclear power plants.

A system has been developed to improve the efficiency of maintenance work while decreasing the radiation exposure of maintenance personnel in nuclear power plants. The input data for dose rate calculation are automatically generated by using computer-aided design data. Changes for the input data corresponding to the progress of maintenance work, such as installation of a radiation shield and removal of a component, are easily input interactively on a graphical user interface (GUI).

Involvement of MEK-ERK signaling pathway in the inhibition of cell growth by troglitazone in human pancreatic cancer cells.

In the present study, we examined a role of mitogen-activated protein kinases (MAPKs), extracellular signal-related kinase (ERK), c-Jun N-terminal protein kinase, and p38 MAPK in troglitazone-induced inhibition of cell growth in human pancreatic cancer cells. Among the three kinases, troglitazone specifically inhibited the phosphorylation of ERK1/2 in a dose- and time-dependent manner. Troglitazone also down-regulated the protein expression of mitogen-activated protein kinase kinase (MEK)1/2, an upstream molecule that regulates ERK phosphorylation.