sj-pdf-1-imr-10.1177_03000605221109396 - Supplemental material for Confusing delayed hematemesis, unusual arterial hemorrhage after pancreaticoduodenectomy: a case report

Supplemental material, sj-pdf-1-imr-10.1177_03000605221109396 for Confusing delayed hematemesis, unusual arterial hemorrhage after pancreaticoduodenectomy: a case report by Luna Wang, Gaoli Guo, Jianhua Yu, Ling Lin, Jianhui Yang and Baochun Lu in Journal of International Medical Research</p

Data_Sheet_1_Topically applied bacteriophage to control multi-drug resistant Pseudomonas aeruginosa-infected wounds in a New Zealand rabbit model.zip

Pseudomonas aeruginosa (P. aeruginosa) is a widespread, gram-negative, pathogenic bacterium that causes serious internal and external infections in humans and other animals. The increasing antibiotic resistance has complicated bacterial infection treatment, and current antibiotic therapies cannot cure all infections. Owing to this, bacteriophages (phages) have regained attention as potential therapeutics for bacterial infections. In this study, the phage “PaVOA” was isolated from hospital sewage and characterized. Next, a New Zealand rabbit skin infection model was used to determine the therapeutic efficacy of PaVOA as compared to a phage cocktail or the cephalosporin antibiotic ceftriaxone. Characterization results demonstrated that phage PaVOA belongs to the Myoviridae family, has a double-stranded DNA genome, is resistant to low temperatures (−20°C), is most optimal at 40°C, has good acid–base tolerance, and remains stable for 30 min under 20 W ultraviolet (UV) intensity. The optimal multiplicity of infection of PaVOA was 0.1, and a one-step growth curve showed a short latency period (10 min), thus demonstrating its ability to rapidly kill bacteria. Furthermore, the addition of calcium (Ca) and magnesium (Mg) ions significantly increased the PaVOA titer. An in vivo phage kinetic curve showed that PaVOA was rapidly inactivated within the blood of New Zealand rabbits (undetectable after 12 h), and no animals died due to phage treatment. Wound healing studies showed that the phage cocktail induced a high healing rate and an acceleration of the skin remodeling process, and was more efficacious than ceftriaxone. Therefore, phage cocktail therapy represents a novel therapeutic approach in the treatment of traumatic skin infections caused by multi-drug resistant P. aeruginosa.</p

Fangchinoline suppresses the proliferation of GBC cells.

(A) The cell viability curves detected using CCK8 assays after treating GBC-SD and NOZ cells with different fangchinoline concentrations. (B) The colony formation ability of GBC-SD and NOZ cells treated with different fangchinoline concentrations. Data are presented as mean ± SD. *P0.05. **P0.01. ***P0.001, compared with the DMSO group.</p

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Tumor growth in nude mice.

Tumor growth in nude mice.</p

Fangchinoline induces the apoptosis of GBC cells.

(A) Hoechst 33258 staining of GBC cells treated with fangchinoline. (B) TUNEL assay of the apoptosis effect of GBC cells with high fangchinoline concentration. (C) Annexin V/ PI apoptosis assay of GBC-SD. Annexin V (+)/PI (−) or Annexin V (−)/PI (+) were considered as apoptotic cells, Annexin V (−)/PI (−) cells were alive, and Annexin V (+)/PI (+) cells were necrotic.</p

Fangchinoline suppresses the oncogenesis of GBC-SD cells in vivo.

(A) The photograph of nude mice and xenograft tumors. (B) The volume and weight of xenograft tumors were measured. **P < 0.01, compared with the DMSO group.</p

Fangchinoline inhibits the PI3K/Akt/XIAP signaling axis.

(A) Results of FAK, p-FAK (Tyr576/577), Src, p-Src (Tyr527), PI3K, p-PI3K (Tyr458/Tyr199), AKT, p-AKT (Ser473), mTOR, p-mTOR (Ser2448), and XIAP relative protein expression using Western blot. (B) GBC cells were incubated with p-Akt activator SC-79 alone or combined with fangchinoline before lysis for Western blot. Data are presented as mean ± SD. *P0.05. **PP<0.001, compared with the DMSO group.</p