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Background: Foreign body-induced cancer is a traditional way of understanding cancer development. The induction of cancers by exogenous foreign bodies has been identified in many organs. However, small bowel adenocarcinoma induced by foreign bodies has not been reported in the literature, although the incidence of small bowel adenocarcinoma is increasing globally. Case Presentation: A 70-year-old man was hospitalized for persistent right-sided abdominal pain for 3 months. Abdominal computed tomography revealed localized thickening and clustering of the small bowel wall in the right abdominal cavity. A comminuted fracture of the right 11th rib protruding into the abdominal cavity was observed, with a bone fragment located within the intestinal mass. Exploratory laparotomy was performed, and extensive adhesions were noted among the greater omentum, small bowel, mesentery, and right abdominal wall. Radical resection and lymph node dissection of the affected small bowel and appendix were performed. We also excised the rib end and repaired the abdominal wall to prevent further irritation. The patient was discharged 12 days post-surgery and follow-up assessments revealed no reported discomfort. Conclusion: We first report a case of small bowel adenocarcinoma induced by self-bone tissue, along with successful radical tumor excision and thorough foreign body removal. This case highlights the significant role of chronic inflammation in carcinogenesis. [ABSTRACT FROM AUTHOR]

In this paper we observe that the minimal signless Laplacian spectral radius is obtained uniquely at the kite graph PKn−ω,ω among all connected graphs with n vertices and clique number ω. In addition, we show that the spectral radius μ of PKm,ω (m ≥ 1) satisfies

In this note, we show how the determinant of the q-distance matrix Dq(T) of a weighted directed graph G can be expressed in terms of the corresponding determinants for the blocks of G, and thus generalize the results obtained by Graham et al. [R.L. Graham, A.J. Hoffman and H. Hosoya, On the distance matrix of a directed graph, J. Graph Theory 1 (1977) 85-88]. Further, by means of the result, we determine the determinant of the q-distance matrix of the graph obtained from a connected weighted graph G by adding the weighted branches to G, and so generalize in part the results obtained by Bapat et al. [R.B. Bapat, S. Kirkland and M. Neumann, On distance matrices and Laplacians, Linear Algebra Appl. 401 (2005) 193- 209]. In particular, as a consequence, determinantal formulae of q-distance matrices for unicyclic graphs and one class of bicyclic graphs are presented.

Objective: To explore the effects of recombinant human calcineurin B (rhCNB) on hepatocellular carcinoma in mice. Methods: An in vivo mouse model with hepatocellular carcinoma was established, and the mice were randomized into the rhCNB, positive control and vehicle treatments groups. Tumor growth was assessed via bioluminescence using a small animal imaging system. Relative tumor proliferation rate and tumor growth inhibition were calculated. The expression of p53 and caspase-9 proteins in tumors were detected by immunohistochemistry. In vitro, flow cytometry was used to quantify the cell-cycle stages and rate of apoptosis. Western blotting and quantitative real-time PCR assays were used to evaluate the effects of rhCNB on protein and gene expression of CDK1, cyclin B1, p53 and caspase-9. Results: rhCNB at the higher dose significantly reduced tumor growth in vivo and caused tumor cell apoptosis in vitro. The rhCNB at the higher dose was as effective as cisplatin, and was safer. Conclusions: rhCNB has potent pro-apoptotic effects on tumor cells in vivo and in vitro and is well tolerated in vivo. [ABSTRACT FROM AUTHOR]

Aim: To investigate the anti-apoptotic capability of the hepatitis B virus (HBV) in the HepG2 hepatoma cell line and the underlying mechanisms., Methods: Cell viability and apoptosis were measured by MTT assay and flow cytometry, respectively. Targeted knockdown of manganese superoxide dismutase (MnSOD), AMP-activated protein kinase (AMPK) and hepatitis B virus X protein (HBx) genes as well as AMPK agonist AICAR and antagonist compound C were employed to determine the correlations of expression of these genes., Results: HBV markedly protected the hepatoma cells from growth suppression and cell death in the condition of serum deprivation. A decrease of superoxide anion production accompanied with an increase of MnSOD expression and activity was found in HepG2.215 cells. Moreover, AMPK activation contributed to the up-regulation of MnSOD. HBx protein was identified to induce the expression of AMPK and MnSOD., Conclusion: Our results suggest that HBV suppresses mitochondrial superoxide level and exerts an anti-apoptotic effect by activating AMPK/MnSOD signaling pathway, which may provide a novel pharmacological strategy to prevent HCC.

Aim: To investigate the role of hepatic peroxisome proliferator-activated receptor-γ (PPAR-γ) in increased susceptibility to endotoxin-induced toxicity in rats with bile duct ligation during endotoxemia., Methods: Male Sprague-Dawley rats were subjected to bile duct ligation (BDL). Sham-operated animals served as controls. DNA binding were determined by polymerase chain reaction, Western blotting analysis, and electrophoretic mobility shift assay, respectively. BDL and sham-operated rats received a non-lethal dose of intraperitoneal lipopolysaccharide (LPS) injection (3 mg/kg, i.p.). Additionally, the potential beneficial effects of the PPAR-γ agonist rosiglitazone were determined in BDL and sham-operated rats treated with a non-lethal dose of LPS. Survival was assessed in BDL rats treated with a non-lethal dose of LPS and in sham-operated rats treated at a lethal dose of LPS (6 mg/kg, i.p.)., Results: PPAR-γ activity in rats undergoing BDL was significantly lower than in the sham-controls. Hepatic PPAR-γ gene expression was downregulated at both the mRNA and protein levels. In a parallel group, serum levels of pro-inflammatory cytokines were nearly undetectable in the sham-operated rats. When challenged with a non-lethal dose of LPS (3 mg/kg), the BDL rats had approximately a 2.4-fold increase in serum IL-6, a 2.7 fold increase in serum TNF-α, 2.2-fold increase in serum IL-1 and 4.2-fold increase in serum ALT. The survival rate was significantly lower as compared with that in sham-operated group. Additionally, rosiglitazone significantly reduced the concentration of TNF-α, IL-1β, IL-6 and ALT in sham-operated rats, but not in BDL rats, in response to LPS (3 mg/kg). Also, the survival was improved by rosiglitazone in sham-operated rats challenged with a lethal dose of LPS, but not in BDL rats, even with a non-lethal dose of LPS (3 mg/kg)., Conclusion: Obstructive jaundice downregulates hepatic PPAR-γ expression, which in turn may contribute to hypersensitivity towards endotoxin.

p28(GANK) (also known as PSMD10, p28 and gankyrin) is an ankyrin repeat anti-apoptotic oncoprotein that is commonly overexpressed in hepatocellular carcinomas and increases the degradation of p53 and Rb. NF-kappaB (nuclear factor-kappaB) is known to be sequestered in the cytoplasm by I kappaB (inhibitor of NF-kappaB) proteins, but much less is known about the cytoplasmic retention of NF-kappaB by other cellular proteins. Here we show that p28(GANK) inhibits NF-kappaB activity. As a nuclear-cytoplasmic shuttling protein, p28(GANK) directly binds to NF-kappaB/RelA and exports RelA from nucleus through a chromosomal region maintenance-1 (CRM-1) dependent pathway, which results in the cytoplasmic retention of NF-kappaB/RelA. We demonstrate that all the ankyrin repeats of p28(GANK) are required for the interaction with RelA and that the N terminus of p28(GANK), which contains the nuclear export sequence (NES), is responsible for suppressing NF-kappaB/RelA nuclear translocation. These results suggest that overexpression of p28(GANK) prevents the nuclear localization and inhibits the activity of NF-kappaB/RelA.