Adaptations Associated With an After-School Strength and Conditioning Program in Middle-School-Aged Boys: A Quasi-Experimental Design.

High-intensity strength and conditioning programs aimed at improving youth performance are becoming increasingly prevalent. The purpose of this study was to investigate the effects of a 16-week after-school strength and conditioning program on performance and body composition in middle-school-aged boys. Subjects in the training group (n = 16, mean age = 11.

The time course of short-term hypertrophy in the absence of eccentric muscle damage.

Background: It has been proposed that the increase in skeletal muscle mass observed during the initial weeks of initiating a resistance training program is concomitant with eccentric muscle damage and edema.

Purpose: We examined the time course of muscle hypertrophy during 4 weeks of concentric-only resistance training.

Methods: Thirteen untrained men performed unilateral concentric-only dumbbell curls and shoulder presses twice per week for 4 weeks.

Does reactivating a witnessed memory increase its susceptibility to impairment by subsequent misinformation?

In a recent article, Chan and LaPaglia (2013) provided arguments and evidence to support the claim that reactivating a witnessed memory (by taking a test) renders the memory labile and susceptible to impairment by subsequent misinformation. In the current article, we argue that Chan and LaPaglia’s (2013) findings are open to alternative interpretations, and further test the hypothesis that reactivation increases a witnessed memory’s susceptibility to impairment. To this end, the current studies used a different set of materials and a different measure of memory impairment, the Modified Recognition Test (McCloskey & Zaragoza, 1985).

gp120 modulates the biology of human hepatic stellate cells: a link between HIV infection and liver fibrogenesis.

Objective: In patients with hepatitis C virus (HCV)/HIV co-infection, a faster progression of liver fibrosis to cirrhosis has been reported. In this study, an investigation was carried out to determine whether gp120, an HIV envelope protein, modulates the biology of human hepatic stellate cells (HSCs), key cell types in the pathogenesis of fibrosis.

Methods: Myofibroblastic HSCs were isolated from normal human liver tissue.

Long-term outcomes of office-based buprenorphine/naloxone maintenance therapy.

Background: Buprenorphine/naloxone was approved by the FDA for office-based opioid maintenance therapy (OMT), with little long-term follow-up data from actual office-based practice. 18-Month outcome data on the office-based use of buprenorphine/naloxone (bup/nx) and the impact of socioeconomic status and other patient characteristics on the duration and clinical effects of bup/nx are reported.

Methods: This retrospective chart review and cross-sectional telephone interview provide treatment retention of opioid-dependent patients receiving bup/nx-OMT in an office-based setting.

Nuclear localization of TRK-A in liver cells.

The liver represents a site of expression of neurotrophins and their receptors. We have characterized the expression and intracellular localization of the nerve growth factor (NGF) receptor, Trk-A, in liver cells in vivo and in vitro. In both normal and fibrotic liver tissue, Trk-A immunostaining was present in different cell types, including parenchymal cells and cells of the inflammatory infiltrate.

Resistin as an intrahepatic cytokine: overexpression during chronic injury and induction of proinflammatory actions in hepatic stellate cells.

Obesity and insulin resistance accelerate the progression of fibrosis during chronic liver disease. Resistin antagonizes insulin action in rodents, but its role in humans is still controversial. The aims of this study were to investigate resistin expression in human liver and to evaluate whether resistin may affect the biology of activated human hepatic stellate cells (HSCs), key modulators of hepatic fibrogenesis.

Thiazolidinedione treatment inhibits bile duct proliferation and fibrosis in a rat model of chronic cholestasis.

Aim: To investigate the effects of troglitazone (TGZ), an anti-diabetic drug which activates peroxisome proliferator-activated receptor-gamma (PPAR-gamma), for liver tissue repair, and the development of ductular reaction, following common bile duct ligation (BDL) in rats.

Methods: Rats were supplemented with TGZ (0.2% w/w in the pelleted food) for 1 wk before BDL or sham operation.

The chemokine CCL21 modulates lymphocyte recruitment and fibrosis in chronic hepatitis C.

Background And Aims: The chemokines CCL19 and CCL21 bind CCR7, which is involved in the organization of secondary lymphoid tissue and is expressed during chronic tissue inflammation. We investigated the expression of CCL21 and CCR7 in chronic hepatitis C. The effects of CCL21 on hepatic stellate cells (HSCs) were also studied.

Cell adhesion regulates platelet-derived growth factor-induced MAP kinase and PI-3 kinase activation in stellate cells.

The biologic effects of growth factors are dependent on cell adhesion, and a cross talk occurs between growth factors and adhesion complexes. The aim of the present study was to evaluate the influence of cell adhesion on the major intracellular signaling pathways elicited by platelet-derived growth factor (PDGF) in hepatic stellate cells (HSC). PDGF signaling was investigated in an experimental condition characterized by lack of cell adhesion for different intervals of time.

Up-regulated expression of fractalkine and its receptor CX3CR1 during liver injury in humans.

Background/aims: Little is known about the role of fractalkine (CX3CL1) in the liver. The aim of this study was to investigate the expression patterns of fractalkine and its receptor CX3CR1 in normal human liver and in conditions of injury.

Methods: Distribution and expression of fractalkine and its receptor were investigated using immunohistochemistry, in situ hybridization, flow cytometry and reverse transcriptase-polymerase chain reaction.

Ordered array of dendritic cells and CD8+ lymphocytes in portal infiltrates in chronic hepatitis C.

Aims: Despite the importance of dendritic cells in stimulating primary and secondary immune responses by presenting antigens to T-lymphocytes in draining lymph nodes and peripheral tissues, respectively, very limited information is available on the presence and localization of these cells in hepatitis C virus (HCV)-related chronic active hepatitis. Therefore, we addressed the ultrastructure, immunophenotype, distribution and relationships to lymphatics of dendritic cells in portal infiltrates of this disease.

Methods And Results: Part of percutaneous diagnostic liver biopsies (Knodell's histological assessment index: 9-13) was processed for electron microscopy and for immunohistochemical detection of immune system cell membrane antigens and of the lymphatic endothelium marker podoplanin.

Nitrovasodilators inhibit platelet-derived growth factor-induced proliferation and migration of activated human hepatic stellate cells.

Background & Aims: Nitrovasodilators have been proposed for the treatment of portal hypertension alone or in combination with beta-blockers. In addition to their vasodilatory properties, nitric oxide (NO) donors may exert direct antifibrogenic properties. We evaluated the effect of nitroglycerin (NTG) and S-nitroso-N-acetyl penicillamine (SNAP) on the mitogenic and chemotactic properties of platelet-derived growth factor (PDGF)-BB and the modulation of the relative intracellular signaling pathways in fully activated human hepatic stellate cells (HSCs), a cell type that plays an active role in liver fibrogenesis and portal hypertension.

Expression of platelet-derived growth factor in newly formed cholangiocytes during experimental biliary fibrosis in rats.

Background/aims: Chronic cholestasis stimulates a fibroductular reaction which may progress to secondary biliary fibrosis and cirrhosis. Since platelet-derived growth factor has been indicated as a major fibrogenic factor in chronic liver disease, we analyzed its expression and that of its receptor beta subunit in a rat model of chronic cholestasis.

Methods: Liver tissue samples collected at 7, 10, 21, and 28 days after induction of cholestasis obtained by bile duct ligation, were analyzed by immunohistochemistry, in situ hybridization and RNase protection assay for the expression of platelet-derived growth factor (PDGF)-B chain and receptor beta subunit.

Expression of monocyte chemotactic protein-1 precedes monocyte recruitment in a rat model of acute liver injury, and is modulated by vitamin E.

Background: Increased expression of monocyte chemotactic protein-1 (MCP-1) has been indicated as a mechanism underlying leukocyte recruitment after liver injury. In this study we examined the temporal relationship between MCP-1 expression and the appearance of monocyte infiltration during acute liver injury. In addition, we tested the effects of vitamin E, a well known antioxidant, on these parameters.

Increased expression of monocyte chemotactic protein-1 during active hepatic fibrogenesis: correlation with monocyte infiltration.

Monocyte chemotactic protein (MCP)-1 is a chemoattractant and activator for circulating monocytes and T lymphocytes. We investigated MCP-1 protein and gene expression during chronic liver disease at different stages, using immunohistochemistry and in situ hybridization, respectively. In normal liver, a modest expression of MCP-1 was confined to few peri-sinusoidal cells and to bile duct epithelial cells.

Expression of the thrombin receptor in human liver: up-regulation during acute and chronic injury.

Thrombin is generated during tissue damage in several organs, including the liver, and participates in the process of tissue repair through proteolytic activation of a specific thrombin receptor (TR). The aim of this study was to investigate TR expression in human liver by immunohistochemistry and in situ hybridization. In normal liver, immunostaining for TR was present in the endothelial lining of the hepatic sinusoids.

Effect of pentoxifylline on the degradation of procollagen type I produced by human hepatic stellate cells in response to transforming growth factor-beta 1.

1. Pentoxifylline (PTF) may act as a potential antifibrogenic agent by inhibiting cell proliferation and/or collagen deposition in cell type(s) responsible for the accumulation of extracellular matrix. The aim of the present study was to investigate at which level PTF may affect synthesis and degradation of type I collagen in human hepatic stellate cells (HSCs), a key source of connective tissue in fibrotic liver.

Inhibition by pentoxifylline of extracellular signal-regulated kinase activation by platelet-derived growth factor in hepatic stellate cells.

1. It has been proposed that pentoxifylline (PTF) acts an antifibrogenic agent by reducing the synthesis of extracellular matrix components, and this possibility has been confirmed in animal models of hepatic fibrosis. In this study the effects of PTF on the proliferation of extracellular matrix producing cells induced by platelet-derived growth factor (PDGF) were evaluated.

Expression of platelet-derived growth factor and its receptors in normal human liver and during active hepatic fibrogenesis.

Expression of platelet-derived growth factor (PDGF) and its receptor (R) subunits was evaluated in normal human liver and in cirrhotic liver tissue by in situ hybridization and immunohistochemistry. In normal liver, PDGF and PDGF-R subunit expression was limited to a few mesenchymal cells of the portal tract stroma and vessels. In cirrhotic liver, PDGF-A and -B chain mRNA expression was markedly increased and was co-distributed with immunoreactivity for PDGF-AA and -BB in infiltrating inflammatory cells and along vascular structures within fibrous septa.

Involvement of phosphatidylinositol 3-kinase in the activation of extracellular signal-regulated kinase by PDGF in hepatic stellate cells.

Phosphatidylinositol 3-kinase (PI 3-K) is a lipid and protein kinase which associates with the activated platelet-derived growth factor (PDGF) receptor and other tyrosine kinases. We studied the effects of wortmannin, a selective inhibitor of PI 3-K, on the activation of extracellular-signal regulated kinase (ERK) by PDGF in cultured hepatic stellate cells, mesenchymal cells responsible for extracellular matrix synthesis within the liver. Incubation with 100 nM wortmannin, a dose which almost completely blocks PI 3-K, resulted in 50% reduction of ERK activity.

An impression procedure for the severely atrophied mandible.

A procedure is described for the final impression of the severely atrophied mandible. The final impression is developed by use of open- and closed-mouth procedures. The objective is to develop a physiologic impression with maximum support of both hard and soft tissues.

Assessment of oral implant mobility.

Most of the implant literature suggests that successful dental implants are immobile and any detected mobility indicates implant failure. This study evaluated the ability of the Periotest instrument to measure implant mobility in a controlled in vitro model with a sample of 56 in vivo implants. In the in vitro portion of the study, implant model mobility was determined by an axial testing machine (0 to 5 N at 0.

Problem solving in overdenture therapy.

The use of overdentures and the advantages of such are widely documented. Among some of the disadvantages of this treatment modality are overcontour, encroachment of the interocclusal distance and frequency of repair. Listed under major disadvantages of overdentures has been increased incidence of caries, periodontal deterioration of abutment teeth and management of bony undercuts.