Additive Manufacturing of Wood Composite Panels for Individual Layer Fabrication (ILF).

The renewable resource, wood, is becoming increasingly popular as a feedstock material for additive manufacturing (AM). It can help make those processes more affordable and reduce their environmental impact. Individual layer fabrication (ILF) is a novel AM process conceived for structural applications.

Expression of ECM proteins fibulin-1 and -2 in acute and chronic liver disease and in cultured rat liver cells.

Fibulin-2 has previously been considered as a marker to distinguish rat liver myofibroblasts from hepatic stellate cells. The function of other fibulins in acute or chronic liver damage has not yet been investigated. The aim of this study has been to evaluate the expression of fibulin-1 and -2 in models of rat liver injury and in human liver cirrhosis.

Effect of tumour necrosis factor-alpha and irradiation alone or in combination on the viability of hepatocellular and biliary adenocarcinoma cell lines in vitro.

Background: Tumour necrosis factor alpha (TNF-alpha) may exhibit antitumoral activity and can influence the reaction of both tumour and normal tissue to radiation.

Aims: To test the effect of TNF-alpha and/or irradiation on hepatocellular (HepG2, Hep3B, Sk-Hep1, HuH7) and cholangiocellular (Sk-chA1, Mz-chA1) tumour cell lines.

Methods: Colony formation, apoptosis analysis and trypan blue exclusion were used to assess cell viability.

Irradiation leads to sensitization of hepatocytes to TNF-alpha-mediated apoptosis by upregulation of IkappaB expression.

This study aimed to reveal the pathophysiological signalling responsible for radiation-induced sensitization of hepatocytes to TNF-alpha-mediated apoptosis. IkappaB was upregulated in irradiated hepatocytes. Administration of IkappaB antisense oligonucleotides prior to irradiation inhibited occurrence of apoptosis after TNF-alpha administration.

Irradiation leads to apoptosis of Kupffer cells by a Hsp27-dependant pathway followed by release of TNF-alpha.

In a previous publication, we were able to show that irradiation of Kupffer cells, the liver resident macrophages, leads to an increased TNF-alpha concentration in the culture medium. The pathomechanisms underlying this phenomenon, however, remained to be elucidated. Here, we show that following irradiation of Kupffer cells, the apoptosis rate increased drastically within 48 h.

Decrease of PECAM-1-gene-expression induced by proinflammatory cytokines IFN-gamma and IFN-alpha is reversed by TGF-beta in sinusoidal endothelial cells and hepatic mononuclear phagocytes.

Background And Aim: The mechanisms of transmigration of inflammatory cells through the sinusoids are still poorly understood. This study aims to identify in vitro conditions (cytokine treatment) which may allow a better understanding of the changes in PECAM (platelet endothelial cell adhesion molecule)-1-gene-expression observed in vivo.

Methods And Results: In this study we show by immunohistochemistry, that there is an accumulation of ICAM-1 (intercellular cell adhesion molecule-1) and ED1 positive cells in necrotic areas of livers of CCl4-treated rats, whereas there are few PECAM-1 positive cells observable.

Atorvastatin induces apoptosis by a caspase-9-dependent pathway: an in vitro study on activated rat hepatic stellate cells.

Background: Statins are shown to have cholesterol-independent properties such as anti-inflammation and immunomodulation. Activated hepatic stellate cells (HSCs) acquire the capacity to synthesize matrix proteins in damaged liver. We tested the hypothesis that atorvastatin may be capable of inducing apoptosis in HSCs.

Effect of radiation on gene expression of rat liver chemokines: in vivo and in vitro studies.

The aim of the study was to analyze the effect of a single irradiation on chemokine gene expression in the rat liver and in isolated rat hepatocytes. RNA extracted from livers and from hepatocytes within the first 48 h after irradiation was analyzed by real-time PCR and the Northern blot assay. The chemokine concentrations in the serum of irradiated rats were measured quantitatively by ELISA.

Inflammation and repair in viral hepatitis C.

Hepatitis C viral infection (HCV) results in liver damage leading to inflammation and fibrosis of the liver and increasing rates of hepatic decompensation and hepatocellular carcinoma (HCC). However, the host's immune response and viral determinants of liver disease progression are poorly understood. This review will address the determinants of liver injury in chronic HCV infection and the risk factors leading to rapid disease progression.

Thy-1 is an in vivo and in vitro marker of liver myofibroblasts.

Thy-1, a glycophosphatidylinositol-linked glycoprotein of the outer membrane leaflet, has been described in myofibroblasts of several organs. Previous studies have shown that, in fetal liver, Thy-1 is expressed in a subpopulation of ductular/progenitor cells. The aim of this study has been to investigate whether the liver myofibroblasts belong to the Thy-1-positive subpopulation of the adult liver.

Increase of hepcidin plasma and urine levels is associated with acute proctitis and changes in hemoglobin levels in primary radiotherapy for prostate cancer.

Purpose: To analyse hepcidin serum and urine levels during radiotherapy for prostate cancer.

Methods: In 18 patients undergoing radiotherapy for prostate cancer, blood, plasma, and urine samples were taken before and during radiotherapy. Complete blood cell count, pro-hepcidin-, ferritin-, transferrin-, IL-1beta-, IL-6-, and TNF-alpha concentration was determined.

Inflammation, damage repair and liver fibrosis--role of cytokines and different cell types.

Liver fibrosis is defined as an excessive deposition of extracellular matrix. It is the main complication of chronic liver damage and its endpoint, the liver cirrhosis, is responsible for impressive morbidity and mortality. The accumulation of extracellular matrix proteins in liver fibrosis and cirrhosis is due to different cell types which acquire a myofibroblastic phenotype--the hepatic stellate cells, located in the space of Disse, portal fibroblasts as well as myofibroblasts of the portal and pericentral areas.

x-Irradiation in rat liver: consequent upregulation of hepcidin and downregulation of hemojuvelin and ferroportin-1 gene expression.

Purpose: To prospectively analyze hepcidin, hemojuvelin, and ferroportin-1 expression after x-irradiation of rat liver and isolated rat hepatocytes.

Materials And Methods: The treatment of the rats and this study were approved by the local committee and the public authority on animal welfare. Rat livers in vivo and isolated rat hepatocytes in vitro were irradiated.

Prospero-related homeobox 1 (Prox1) is a stable hepatocyte marker during liver development, injury and regeneration, and is absent from "oval cells".

The aim of this study was to analyse the changes of Prospero-related homeobox 1 (Prox1) gene expression in rat liver under different experimental conditions of liver injury, regeneration and acute phase reaction, and to correlate it with that of markers for hepatoblasts, hepatocytes, cholangiocytes and oval cells. Gene expression was studied at RNA level by RT-PCR, and at protein level by immunohistochemistry. At embryonal stage of rat liver development (embryonal days (ED) 14-16) hepatoblasts were found to be Prox1(+)/Cytokeratin (CK) 19(+) and alpha-fetoprotein (AFP)(+), at this stage Prox1(-)/CK19(+)/AFP(-) small cells (early cholangiocytes?) were identified.

Hepcidin and hemojuvelin gene expression in rat liver damage: in vivo and in vitro studies.

In this work, we used two rat models, partial hepatectomy (PH) and CCl(4) administration, to study the changes in iron pathways in response to hepatic damage. Liver injury induced changes in the hepatic gene expression of hepcidin, hemojuvelin (Hjv), several other proteins of iron metabolism, and several cytokines such as IL-1beta, IL-6, TNF-alpha, and IFN-gamma. Hepcidin gene expression was upregulated between 4 and 8 h with a maximum up to 16 h after surgery.

Identification of genes responsive to gamma radiation in rat hepatocytes and rat liver by cDNA array gene expression analysis.

The mechanisms underlying hepatocellular damage after irradiation are obscure. We identified genes induced by radiation in isolated rat hepatocytes in vitro by cDNA array gene expression analysis and then screened in vivo experiments with those same genes using real-time PCR and Western blotting. Hepatocytes were irradiated and cDNA array analyses were performed 6 h after irradiation.

A phase III randomized, placebo-controlled, double-blind study of misoprostol rectal suppositories to prevent acute radiation proctitis in patients with prostate cancer.

Purpose: Acute radiation proctitis is the most relevant complication of pelvic radiation and is still mainly treated supportively. Considering the negative impact of acute proctitis symptoms on patients' daily activities and the potential relationship between the severity of acute radiation injury and late damage, misoprostol was tested in the prevention of acute radiation-induced proctitis.

Methods And Materials: A total of 100 patients who underwent radiotherapy for prostate cancer were entered into this phase III randomized, placebo-controlled, double-blind study with misoprostol or placebo suppositories.

Interferon-gamma acts proapoptotic on hepatic stellate cells (HSC) and abrogates the antiapoptotic effect of interferon-alpha by an HSP70-dependant pathway.

The activated hepatic stellate cell (HSC) is an important fibrogenic cell type of the liver. Interferon-alpha (IFN-alpha) has recently been shown to elicit an antiapoptotic effect on activated HSC by a JAK-2-dependent inhibition of caspase-8 activation. As JAK-2 has so far been shown to be a member of the IFN-gamma signal transduction pathway we studied the effect of IFN-gamma on apoptosis as well as on its signaling in primary cultured rat HSC.

Irradiation leads to susceptibility of hepatocytes to TNF-alpha mediated apoptosis.

Background And Purpose: The pathogenesis of radiation-induced-liver-disease (RILD) is still unknown. We tested the hypothesis that irradiated liver macrophages influence the viability of radiation stressed hepatocytes.

Patients And Methods: Hepatocytes and liver macrophages were isolated from rat liver, cultured and irradiated with doses of 2, 8, and 25 Gy.

The homeobox transcription factor Prox1 is highly conserved in embryonic hepatoblasts and in adult and transformed hepatocytes, but is absent from bile duct epithelium.

Prox1 is a transcription factor with two highly conserved domains, a homeobox and a prospero domain. It has been shown that Prox1 knock-out mice die during early embryonic stages and display a rudimentary liver. We have studied the expression of Prox1 at RNA and protein levels in chick, rat, mouse and human liver and in transformed and non-transformed hepatic cell lines.

IGF-I induces DNA synthesis and apoptosis in rat liver hepatic stellate cells (HSC) but DNA synthesis and proliferation in rat liver myofibroblasts (rMF).

Several lines of evidence suggest a role of insulin-like growth factor I (IGF-I) in the regulation of apoptosis. Up to now its impact on many specific cells is unknown. We therefore studied the effect of IGF-I on two similar mesenchymal matrix-producing cell types of the liver, the hepatic stellate cells (HSC) and the myofibroblasts (rMF).

Induction of Mx-2 in rat liver by toxic injury.

Background/aims: Mx proteins are supposed to be strictly regulated by viruses or interferon-alpha (IFN-alpha). We used a non-viral model of acute liver injury to study Mx expression.

Methods: We induced toxic liver injury by CCl(4), and studied the expression of IFN-alpha, IFN-gamma, and IFN-inducible antiviral genes (Mx-2; 2'-5' oligoadenylate synthetase, 2-5 A; double-stranded RNA-activated protein kinase, PKR).

Portal tract fibrogenesis in the liver.

The portal area is the 'main entrance' and one of the two main exits of the liver lobule. Through the main entrance portal and arterial blood reach the liver sinusoids. Through the exit the bile flows towards the duodenum.