Left: The Urograffin enema demonstrating early contrast filling of the stomach and jejunum

, stomach; , jejunum; , transverse colon. Right: The barium meal shows the jejunum and colon simultaneously.<p><b>Copyright information:</b></p><p>Taken from "Gastrojejunocolic fistula after gastrojejunostomy: a case series"</p><p>http://www.jmedicalcasereports.com/content/2/1/193</p><p>Journal of Medical Case Reports 2008;2():193-193.</p><p>Published online 4 Jun 2008</p><p>PMCID:PMC2424061.</p><p></p

Colonoscopic findings reveal two fistulae () at the distal transverse colon

<p><b>Copyright information:</b></p><p>Taken from "Gastrojejunocolic fistula after gastrojejunostomy: a case series"</p><p>http://www.jmedicalcasereports.com/content/2/1/193</p><p>Journal of Medical Case Reports 2008;2():193-193.</p><p>Published online 4 Jun 2008</p><p>PMCID:PMC2424061.</p><p></p

Effects of LPS and MP on the plasma levels of NO (Nitrites+Nitrates) (A), Peroxynitrite (nitrotyrosin) (B), CRP (C), and IL-6 (D).

<p>Data are expressed as mean±s.e. LPS, lipopolysaccharide; MP, methylprednisolone; NO, nitric oxide; CRP, C-reactive protein; IL-6, interleukin-6. (<i>n</i> = 10 in each group).</p

Effects of LPS and MP on aortic characteristic impedance (<i>Z_c</i> in A), systemic arterial compliance at mean aortic pressure (<i>C_m</i> in B), wave reflection factor (<i>R_f</i> in C) and wave transit time (<i>τ</i> in D).

<p>Data are expressed as mean±s.e. LPS, lipopolysaccharide; MP, methylprednisolone. (<i>n</i> = 10 in each group).</p

Up-Regulation of Nerve Growth Factor in Cholestatic Livers and Its Hepatoprotective Role against Oxidative Stress

<div><p>The role of nerve growth factor (NGF) in liver injury induced by bile duct ligation (BDL) remains elusive. This study aimed to investigate the relationship between inflammation and hepatic NGF expression, to explore the possible upstream molecules up-regulating NGF, and to determine whether NGF could protect hepatocytes from oxidative liver injury. Biochemical and molecular detection showed that NGF was up-regulated in cholestatic livers and plasma, and well correlated with systemic and hepatic inflammation. Conversely, systemic immunosuppression reduced serum NGF levels and resulted in higher mortality in BDL-treated mice. Immunohistochemistry showed that the up-regulated NGF was mainly localized in parenchymal hepatocytes. In vitro mechanistic study further demonstrated that TGF-β1 up-regulated NGF expression in clone-9 and primary rat hepatocytes. Exogenous NGF supplementation and endogenous NGF overexpression effectively protected hepatocytes against TGF-β1- and oxidative stress-induced cell death in vitro, along with reduced formation of oxidative adducted proteins modified by 4-HNE and 8-OHdG. TUNEL staining confirmed the involvement of anti-apoptosis in the NGF-exhibited hepatoprotection. Moreover, NGF potently induced Akt phosphorylation and increased Bcl-2 to Bax ratios, whereas these molecular alterations by NGF were only seen in the H₂O₂-, but not TGF-β1-treated hepatocytes. In conclusion, NGF exhibits anti-oxidative and hepatoprotective effects and is suggested to be therapeutically applicable in treating cholestatic liver diseases.</p></div

Effects of LPS and MP on aortic AGEs, RAGE, and iNOS proteins measured by Western blotting technique.

<p>Protein expression was normalized to β-actin. Data are expressed as mean±s.e. LPS, lipopolysaccharide; MP, methylprednisolone; LM, LPS groups treated with MP; iNOS, inducible nitric oxide synthase; AGEs, advanced glycation end products; RAGE, receptor for AGEs. (<i>n</i> = 10 in each group).</p

Effects of LPS and MP on basal heart rate (<i>HR</i> in A), mean aortic pressure (<i>P_m</i> in B), cardiac output (<i>CO</i> in C) and total peripheral resistance (<i>R_p</i> in D).

<p>Data are expressed as mean±s.e. LPS, lipopolysaccharide; MP, methylprednisolone. (<i>n</i> = 10 in each group).</p

Hypothetical scheme showing the regulatory mechanisms and hepatoprotective roles of NGF.

<p>When the liver encounters BDL-induced cholestatic injury, inflammatory signals will induce NGF up-regulation, which can be blocked by systemic MP administration. In vitro study shows that TGF-β1 may be one of the upstream molecules that induce NGF expression in parenchymal hepatocytes. NGF is able to (1) ameliorate hepatocyte cell death caused by exogenous hydrogen peroxide and TGF-β1, (2) enhance pro-survival pathways, including p-Akt and Bcl-2/Bax ratio, (3) decrease intracellular oxidative adduct formation.</p

Effects of LPS and MP on the expression of AGEs (A), RAGE (B), and iNOS (C) in the aortas.

<p>AGEs and RAGE expressions were probed using immunohistochemical staining (400x). The arrows indicated the sites of antibody staining. iNOS expression (red color) was explored using immunocytochemical fluorescence staining (200x). LPS, lipopolysaccharide; MP, methylprednisolone; AGEs, advanced glycation end products; RAGE, receptor for AGEs; iNOS, inducible nitric oxide synthase.</p

In vitro hepatoprotective effects of endogenous NGF overexpression on TGF-β1-induced and oxidative cell death.

<p>Clone-9 hepatocytes were transfected with either pCMS plasmid encoding EGFP (EGFP) or full-length NGF cDNA (NGF) using Lipofectamine reagent for 48 hrs, followed by morphological documentation (A, E, H) and viability determination (B, F, I). <i>Bar</i>  = 50 µm. ELISA showed that NGF gene transfection for 48 hrs significantly induced soluble NGF production in conditioned medium (D). The clone-9 hepatocytes transfected with plasmids were exposed to either TGF-β1 or H₂O₂ for 24 hrs. The MTT cell viability assay showed that NGF overexpression not only prevented transfection- induced cytotoxicity (B) but also reduced TGF-β1 (F) and H₂O₂ (I) cytotoxicity. # and * indicate <i>P</i><0.05 compared with negative control (NC) and between groups, respectively. Western blotting results showed that NGF overexpression attenuated the elevation of cellular oxidative adduct formation, including 4-HNE and 8-OHdG modified proteins, induced by plasmid transfection (C), TGF-β1 (G), and H₂O₂ insults (J). Data are representative results from three independent experiments, and normalized to NC. Density data are expressed as mean±SD. * indicates <i>P</i><0.05 compared with NC; # indicates <i>P</i><0.05 compared with corresponding EGFP- or NGF-transfected group.</p