Coarse-grained molecular simulation of the effect of liquid crystal molecular pitch on structure in cylindrical confinement.

Blue phases (BPs) consist of three-dimensional self-assembled structures formed by a double-twisted columnar arrangement of liquid crystal molecules. Although their unique optical and structural properties render BPs particularly useful for applications such as liquid crystal displays, BPs typically appear in a narrow temperature range between the isotropic and nematic phases. This thermodynamic instability impedes their practical applicability.

Effect of the Janus Amphiphilic Wall on the Viscosity Behavior of Aqueous Surfactant Solutions.

The effects of the chemical nature of an interface are one of the key parameters which can affect self-assembly and rheological behavior. To date, several studies have reported self-assembled structures and rheological behaviors in the development of various functional materials. In this study, we investigated the self-assembly and viscosity behavior of aqueous surfactant solutions confined in three types of Janus amphiphilic nanotubes (JANTs), which have two, four, and eight sequential domains, respectively, using molecular simulation.

Cylindrical defect structures formed by chiral nematic liquid crystals in quasi-one-dimensional systems.

Blue phases are three-dimensional self-assembly structures of liquid crystals with a lattice of line defects. They have attracted considerable interest as photonic materials. It is well known that blue phases occur in cholesteric liquid crystals (CLCs) under certain thermodynamic conditions; however, recent studies have indicated that confining surfaces may induce distinctive structural changes.

[Acute hemorrhagic colitis induced by the neuraminidase inhibitor oseltamivir].

A 23-year-old woman had lower abdominal pain, diarrhea and bloody stool was admitted and given a diagnosis of influenza B. Her home doctor had started treatment by neuraminidase inhibitor (oseltamivir) the previous day. Colonoscopic examination revealed an area of hemorrhage and erosion in the left transverse colon.

Repetitive and safe transgene expression in rat liver is achievable by adenoviral infusion into the common bile duct.

To examine the feasibility of adenovirus-mediated gene transfer into the liver, we examined whether adenoviral infusion into the common bile duct could induce repetitive and safe transgene expression in rat livers. Recombinant adenovirus carrying a reporter lacZ gene was repetitively infused retrogradely into the common bile duct of rats. LacZ expression in rat livers was estimated histochemically by X-gal staining and quantitatively by a chemiluminescent reporter gene assay after the first, second and third adenoviral infusion into the common bile duct.

Combination of interferon-beta and angiotensin-converting enzyme inhibitor, perindopril, attenuates the murine liver fibrosis development.

Recent studies have revealed that both interferon (IFN) and angiotensin-converting enzyme inhibitor (ACE-I) exert an anti-fibrotic effect. The aim of this study was to examine the combined effect of the ACE-I and IFN on the murine hepatic fibrosis development. A model of CCl(4)-induced hepatic fibrosis was used to assess the effect of the clinically used ACE-I, perindopril (PE), and IFN-beta.

Involvement of the vascular endothelial growth factor receptor-1 in murine hepatocellular carcinoma development.

Background/aims: The role of the vascular endothelial growth factor receptor-1 (VEGFR-1) in hepatocellular carcinoma (HCC) development has not been elucidated yet. The aim of this study was to examine the role of VEGFR-1 in VEGF-mediated HCC development and angiogenesis as compared to that of VEGFR-2.

Methods: We examined the effects of VEGFR-1, and VEGFR-2 neutralizing monoclonal antibodies (R-1mAb and R-2mAb, respectively) on VEGF-mediated HCC development both in an allograft and orthotopic models.

Halting the interaction between vascular endothelial growth factor and its receptors attenuates liver carcinogenesis in mice.

It has been shown that angiogenesis plays an important role not only in tumor growth, but also in early carcinogenesis. The expression of a potent angiogenic factor, vascular endothelial growth factor (VEGF), increased during the early stage of carcinogenesis. In this study, the effects of the neutralizing monoclonal antibodies R1 mAb and R2 mAb of the VEGF receptors Flt-1 (VEGFR-1) and KDR/Flk-1 (VEGFR-2), respectively, on murine hepatocarcinogenesis induced by diethylnitrosamine (DEN) were examined.

Combination of interferon-beta and the angiotensin-converting enzyme inhibitor, perindopril, attenuates murine hepatocellular carcinoma development and angiogenesis.

Purpose: Angiogenesis is now recognized as a crucial step in the development of tumors, including hepatocellular carcinoma (HCC). The aim of this study was to elucidate the combined effect of the clinically used angiotensin I-converting enzyme (ACE) inhibitor, perindopril (PE), and IFN-beta on the development and angiogenesis of murine HCC at clinically comparable low doses.

Experimental Design: PE and IFN were administered at doses of 2 mg/kg/day and 1 x 10(4) IU/twice a week, respectively.

Angiotensin-II induces the tissue inhibitor of metalloproteinases-1 through the protein kinase-C signaling pathway in rat liver fibrosis development.

It has been shown that tissue inhibitor of metalloproteinases-1 (TIMP-1) plays an important role in the progression of liver fibrosis. TIMP-1 gene expression is regulated by several factors in vivo. Among them, angiotensin-II (AT-II) induces TIMP-1 in endothelial cells (EC) in vitro, however, the interaction between these molecules in liver fibrogenesis has not yet been elucidated.

Vascular endothelial growth factor and receptor interaction is a prerequisite for murine hepatic fibrogenesis.

Background: It has been shown that expression of the potent angiogenic factor, vascular endothelial growth factor (VEGF), and its receptors, flt-1 (VEGFR-1) and KDR/Flk-1 (VEGFR-2), increased during the development of liver fibrosis.

Aims: To elucidate the in vivo role of interaction between VEGF and its receptors in liver fibrogenesis.

Methods: A model of CCl(4) induced hepatic fibrosis was used to assess the role of VEGFR-1 and VEGFR-2 by means of specific neutralising monoclonal antibodies (R-1mAb and R-2mAb, respectively).

The copper-chelating agent, trientine, attenuates liver enzyme-altered preneoplastic lesions in rats by angiogenesis suppression.

It has been shown that angiogenesis plays an important role not only in tumor growth, but also in carcinogenesis. We previously reported that the copper-chelating agent, trientine dihydrochloride (trientine), exerted strong anti-angiogenic activity and inhibited hepatocellular carcinoma (HCC) tumor growth. The aim of the current study was to elucidate the effect of trientine on liver enzyme-altered preneoplastic lesions in rats, especially in conjunction with angiogenesis alteration in the liver.

Extracellular matrix remodeling may predominate over hepatocyte injury in hepatocellular carcinoma development.

It has been suggested that both extracellular matrix (ECM) remodeling and persistent hepatocyte injury play important roles in liver carcinogenesis process. It is, however, still controversial which factor plays a predominant role. The aim of the present study was to examine the role of each factor in the liver enzyme-altered preneoplastic lesions, focusing on the relationship between the hepatocyte injury and fibrosis extension.

Tissue inhibitor of metalloproteinases-1 (TIMP-1) inhibits tumor growth and angiogenesis in the TIMP-1 transgenic mouse model.

The tissue inhibitor of matrix metalloproteinases-1 (TIMP-1) has been recognized as a multifunctional protein. The role of TIMPs in cancer remains the subject of conflicting reports with an antitumor activity or a tumor growth stimulation activity by several mechanisms. The aim of our study is to investigate the effect of ectopic TIMP-1 overexpression on the primary transplanted tumor growth.

Tissue inhibitor of metalloproteinases-1 attenuates spontaneous liver fibrosis resolution in the transgenic mouse.

It has been suggested that the tissue inhibitor of metalloproteinases-1 (TIMP-1) is involved in spontaneous resolution of liver fibrosis. The aim of this study was to investigate whether TIMP-1 altered spontaneous resolution of liver fibrosis in conjunction with matrix metalloproteinases (MMP) inhibition and hepatic stellate cell (HSC) activation. The livers of liver-targeted TIMP-1 transgenic (TIMP-Tg) and control hybrid (Cont) mice were harvested at 0, 3, 7, and 28 days following spontaneous recovery from CCl(4)-induced liver fibrosis.

Development of hepatocytes from ES cells after transfection with the HNF-3beta gene.

We have attempted to generate embryonic stem (ES) cell-derived hepatocytes expressing liver-specific functional properties by use of ES cell technology. It was found that ES cells are allowed to differentiate into hepatocytes possessing high metabolic activities when hepatocyte nuclear factor (HNF)-3beta-transfected ES cells are cultured in alpha-MEM medium supplemented with 10% fetal bovine serum (FBS) and fibroblast growth factor (FGF)-2 in the three-dimensional cell culture system at 5% CO2. The differentiated cells induced albumin, triacylglycerol, urea, and glycogen synthesis as well as further expression of metabolic proteins and serum factors as markers of hepatocytic differentiation for at least 4 months.

Inhibition of renin-angiotensin system attenuates liver enzyme-altered preneoplastic lesions and fibrosis development in rats.

Background/aims: It is suggested that the renin-angiotensin system (RAS) is involved in tumor development and fibrogenesis. The aim of the present study was to examine the effect of RAS inhibition on the liver enzyme-altered preneoplastic lesions and fibrosis development.

Methods: The effects of the clinically used angiotensin-I converting enzyme inhibitor (ACE-I), perindopril (PE), on two different rat model of liver carcinogenesis models induced separately by diethylnitrosamine (DEN) and a choline-deficient L-amino acid-defined (CDAA) diet were studied.

Suppression of the renin-angiotensin system attenuates vascular endothelial growth factor-mediated tumor development and angiogenesis in murine hepatocellular carcinoma cells.

Angiotensin-II (AT-II), which is produced mainly by the renin-angiotensin system (RAS), has been shown to stimulate neovascularization. AT-II induces vascular endothelial growth factor (VEGF), which plays a pivotal role in tumor angiogenesis. The role of AT-II, however, in VEGF-mediated tumor development has not yet been elucidated.

Synergistic effect of basic fibroblast growth factor and vascular endothelial growth factor in murine hepatocellular carcinoma.

The growth of any solid tumor depends on angiogenesis. Among the known angiogenic factors, basic fibroblast growth factor (bFGF) and vascular endothelial growth factor (VEGF), are potent and representative factors involved in tumor development. It has been reported that bFGF and VEGF showed a synergistic effect in both in vitro and in vivo angiogenesis.

The copper-chelating agent, trientine, suppresses tumor development and angiogenesis in the murine hepatocellular carcinoma cells.

Angiogenesis is now recognized as a crucial process in tumor development, including hepatocellular carcinoma (HCC). Since HCC is known as a hypervascular tumor, anti-angiogenesis is a promising approach to inhibit the HCC development. Trientine dihydrochloride (trientine) is used in clinical practice as an alternative copper (Cu)-chelating agent for patients with Wilson's disease of penicillamine intolerance.

Angiotensin-II type 1 receptor interaction is a major regulator for liver fibrosis development in rats.

The renin-angiotensin system (RAS) is frequently activated in patients with chronic liver diseases. Angiotensin-II (AT-II) has been suggested to play an important role in liver fibrogenesis. It induces hepatic stellate cell (HSC) proliferation and up-regulates the transforming growth factor beta(1) (TGF-beta(1)) expression via AT-II type 1 receptor (AT(1)-R) in vitro.

The angiotensin-I-converting enzyme inhibitor perindopril suppresses tumor growth and angiogenesis: possible role of the vascular endothelial growth factor.

Angiotensin-I converting enzyme (ACE) inhibitor is used widely as an antihypertensive agent, and it has been suggested recently that it decreases the risk of cancer (A. F. Lever et al.

A potential approach for electrochemotherapy against colorectal carcinoma using a clinically available alternating current system with bipolar snare in a mouse model.

Background: Although electrochemotherapy appears promising for the treatment of superficial tumors, its usefulness against internal tumors, such as colorectal carcinoma (CRC), has not been well examined. Furthermore, since direct current electric pulses have been used for electropermeabilization of tumors in all in vivo electrochemotherapy studies, including clinical trials, the usefulness of alternating current systems has not been examined at all. In a mouse model it was examined whether the alternating current system with a bipolar snare, which has been employed already as a clinical endoscopic treatment modality, was useful for electrochemotherapy against CRC.

The vascular endothelial growth factor receptor KDR/Flk-1 is a major regulator of malignant ascites formation in the mouse hepatocellular carcinoma model.

The vascular endothelial growth factor-A (VEGF-A), also known as the vascular permeability factor (VPF), has been shown to play an important role in malignant ascites formation. The effects of VEGF-A are mediated through flt-1 and kinase insert domain-containing receptor/fetal liver kinase (KDR/Flk-1) receptors. It has been shown that KDR/Flk-1 is a predominant receptor in solid hepatocellular carcinoma (HCC) development, but the role of this receptor in hepatic ascites formation has not yet been elucidated.