Loss of FYCO1 leads to cataract formation.

Autophagy is a degradation process of cytoplasmic proteins and organelles trafficked to degradation vesicles known as autophagosomes. The conversion of LC3-I to LC3-II is an essential step of autophagosome formation, and FYCO1 is a LC3-binding protein that mediates autophagosome transport. The p62 protein also directly binds to LC3 and is degraded by autophagy.

Protamine may have anti-atherogenic potential by inhibiting the binding of oxidized-low density lipoprotein to LOX-1.

Oxidized low-density lipoprotein (ox-LDL) leads to atherosclerosis via lectin-like oxidized lipoprotein receptor-1 (LOX-1), one of the major receptor for ox-LDL. Inhibition of the binding of ox-LDL to LOX-1 decreases the proinflammatory and atherosclerotic events. The aim of the present study was to investigate whether protamine, a polybasic nuclear protein, interferes the binding of ox-LDL to LOX-1.

Zebularine exerts its antiproliferative activity through S phase delay and cell death in human malignant mesothelioma cells.

Malignant mesothelioma is an asbestos-related aggressive tumor and current therapy remains ineffective. Zebularine as a DNA methyltransferase (DNMT) inhibitor has an anti-tumor effect in several human cancer cells. The aim of the present study was to investigate whether zebularine could induce antiproliferative effect in human malignant mesothelioma cells.

Effects of epigallocatechin-3-gallate (EGCG) on A549 lung cancer tumor growth and angiogenesis.

Epigallocatechin 3-gallate (EGCG) has cytotoxic effects in many cancer cells. It has been reported that A549 lung cancer cells are markedly resistant to cell death induced by EGCG. In the present study, the effects of EGCG on A549 lung cancer cell growth and angiogenesis were studied.

EGCG induces human mesothelioma cell death by inducing reactive oxygen species and autophagy.

Malignant mesothelioma is an asbestos-related fatal disease with no effective cure. We studied whether a green tea polyphenol, epigallocathechin-3-gallate (EGCG), could induce cell death in five human mesothelioma cell lines. We found that EGCG induced apoptosis in all five mesothelioma cell lines in a dose-dependent manner.

Dopaminergic modulation of oscillatory network inhibition in the rat basolateral amygdala depends on initial activity state.

The amygdala receives dopaminergic innervation, and dopamine (DA) enhances various activities in cognitive and emotional behaviors. Periodic bursts of spontaneous inhibitory postsynaptic currents (IPSCs) with a low (<1 Hz) inter-event frequency have been observed in projection neurons of the basolateral nucleus of the amygdala (BL). Blockade of ionotropic glutamate receptors or GABA(A) receptors abolishes these oscillatory IPSC bursts in the BL, suggesting that the activity has a network origin.

The value of blood D-dimer test in the diagnosis of walk-in patients with venous thromboembolism.

Venous thromboembolism (VTE) and related pulmonary thromboembolism are life-threatening diseases that require efficient diagnosis and clinical management. While the diagnosis and treatment of VTE in hospitalized patients has been extensively studied, less has been reported on walk-in patients with VTE. Here we report on four outpatients with VTE that were efficiently diagnosed using the blood D-dimer test and successfully treated.

Prohibitin protects against hypoxia-induced H9c2 cardiomyocyte cell death.

We recently demonstrated that short time exposure to hypoxia (15 min) in H9c2 cardiomyocytes protected cells against cell death, and longer exposure to hypoxia induced cell death. To understand the molecular mechanism concerning cell death and survival, it is intriguing to identify survival factors against cell death. Using proteomics analysis, levels of proteins derived from H9c2 cells exposed to hypoxia and normoxia were compared and candidates for survival factor were identified.

High dose of ascorbic acid induces cell death in mesothelioma cells.

Malignant mesothelioma is an asbestos-related fatal disease with no effective cure. Recently, high dose of ascorbate in cancer treatment has been reexamined. We studied whether high dose of ascorbic acid induced cell death of four human mesothelioma cell lines.

In utero and lactational exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) induces disruption of glands of the prostate and fibrosis in rhesus monkeys.

We investigated the effects that 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exposure has on the prostate in rhesus monkey offspring. Dams received 0, 30 or 300 ng/kg TCDD subcutaneously on Day 20 of gestation, and then 5% of the initial dose was injected every 30 days until Day 90 after delivery. The offspring were maintained until reaching sexual maturity, and examined histopathologically.

Inhibition of endostatin/collagen XVIII deteriorates left ventricular remodeling and heart failure in rat myocardial infarction model.

Background: Although therapeutic angiogenesis is a most promising strategy for the treatment of myocardial infarction (MI), it remains unknown if and how endogenous angiogenesis inhibitors, such as endostatin, regulate angiogenesis in MI. In the present study the role of endostatin in left ventricular (LV) remodeling and heart failure was tested in a rat MI model.

Methods And Results: When exposed to hypoxia, rat cardiomyocytes showed increased expression of endostatin.

In utero and lactational exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) induces a reduction in epididymal and ejaculated sperm number in rhesus monkeys.

A long-term developmental toxicity study of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exposure was performed in rhesus monkeys and the effect on male reproductive organs was determined in the second generation. Dams received 0, 30 or 300 ng/kg TCDD subcutaneously on Day 20 of gestation, and then 5% of the initial dose was injected every 30 days until Day 90 after delivery. The offspring were maintained until reaching sexual maturity, and evaluated by semen analysis, and histopathology of the testes and epididymides.

In utero and lactational exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) affects bone tissue in rhesus monkeys.

Bone tissue is one of the target tissues for dioxins and dioxin-like compounds. Therefore, the aim of this study was to investigate effects of in utero and lactational exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), on bone tissue in rhesus monkey, the most human-like experimental model available. Pregnant rhesus monkeys (Macaca mulatta; age 4-10 years) were exposed to TCDD with a total dose of 40.

Protective effect of captopril and enalaprilat, angiotensin-converting enzyme inhibitors, on para-nonylphenol-induced *OH generation and dopamine efflux in rat striatum.

We recently reported that para-nonylphenol, an environmental chemical, induced hydroxyl radical (*OH) formation in rat striatum. In this study we examined the antioxidant effects of angiotensin-converting enzyme inhibitors (captopril or enalaprilat) on para-nonylphenol (nonylphenol) and 1-methyl-4-phenylpyridinium ion (MPP(+))-induced hydroxyl radical (*OH) formation and dopamine (DA) efflux in extracellular fluid of rat striatum, using a microdialysis technique. para-Nonylphenol clearly enhanced *OH formation and DA efflux induced by MPP(+).

Mouse AKR1E1 is an ortholog of pig liver NADPH dependent 1,5-anhydro-D-fructose reductase.

In many organisms, glycogen gives rise to 1,5-anhydro-D-fructose (AF), which is reduced to 1,5-anhydro-D-glucitol (AG). AF reductase, which catalyzes the latter reaction, was purified from pig liver, but mouse ortholog has not yet been reported. In the database, aldo-keto reductase family 1, member E1 (AKR1E1) showed highest homology to pig enzyme.

Polyamine depletion induces G1 and S phase arrest in human retinoblastoma Y79 cells.

Background: Polyamines and ornithine decarboxylase (ODC) are essential for cell proliferation. DL-alpha-difluoromethylornithine (DFMO), a synthetic inhibitor of ODC, induces G1 arrest through dephosphorylation of retinoblastoma protein (pRb). The effect of DFMO on cell growth of pRb deficient cells is not known.

Single-injection ornithine decarboxylase-directed antisense therapy using atelocollagen to suppress human cancer growth.

Background: Substantial evidence supports a direct role of ornithine decarboxylase (ODC) in the development and maintenance of human tumors. Although antisense oligonucleotide therapy targeting various genes are useful for cancer treatment, 1 of the major limitations is the problem of delivery. A novel antisense oligonucleotide delivery method is described that allows prolonged sustainment and release of ODC antisense oligonucleotides in vivo using atelocollagen.

Long-term effects of subcutaneously injected 2,3,7,8-tetrachlorodibenzo-p-dioxin on the liver of rhesus monkeys.

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) accumulates and remains stable in the fatty tissues and liver of rodents for a long time. Considering the pronounced difference between species, long-term, low dose hepatic effects of TCDD were investigated after subcutaneous administration of TCDD into rhesus monkeys during pregnancy. Macroscopic and histopathological examination of the liver carried out 4 y after TCDD administration demonstrated intrahepatic focal fatty changes, infarction, hemorrhage, microthrombi-formation, sinusoidal ectasia, small hepatocyte hyperplasia, and increased number of alpha-smooth muscle actin (alpha-SMA)-positive cells.

Ornithine decarboxylase overexpression enhances ERK and p38 phosphorylation and matrix metalloproteinase-2 expression.

In the present study, we investigated the relationship between ornithine decarboxylase, MAP kinase, and MMP-2 expression in vitro. Overexpression of ornithine decarboxylase cDNA induced MMP-2 expression both at mRNA and protein levels. Promoter analysis and gel shift assay showed that p53 and Ets-1 were involved in MMP-2 expression in ornithine decarboxylase overexpressing transfectants.

Short time exposure to hypoxia promotes H9c2 cell growth.

The effects of short time (15 min) exposure to hypoxia on rat cardiomyocytes (H9c2) were examined. Exposure to hypoxia inhibited cell death via activation of MEK/extracellular signal-regulated kinase (ERK). Further, exposure to hypoxia promoted cell growth by down-regulation of p27 and phosphorylation of cyclin-dependent kinase 2 (CDK2) and retinoblastoma protein (Rb).

Ornithine decarboxylase, mitogen-activated protein kinase and matrix metalloproteinase-2 expressions in human colon tumors.

Aim: To investigate the expressions of ornithine decarboxylase (ODC), MMP-2, and Erk, and their relationship in human colon tumors.

Methods: ODC activity, MMP-2 expression, and mitogen-activated protein (MAP) kinase activity (Erk phosphorylation) were determined in 58 surgically removed human colon tumors and their adjacent normal tissues, using [1-14C]-ornithine as a substrate, ELISA assay, and Western blotting, respectively.

Results: ODC activity, MMP-2 expression, and Erk phosphorylation were significantly elevated in colon tumors, compared to those in adjacent normal tissues.

Exercise-related novel gene is involved in myoblast differentiation.

In this study we tried to identify new genes or proteins in skeletal muscle induced by exercise. We analyzed alterations of protein expression in mouse gastrocnemius muscles induced by swim-exercise using two dimensional gel electrophoresis and mass spectrometry. Nine spots were significantly altered between control and swim groups.