Classic citations in main plastic and reconstructive surgery journals.

BACKGROUND: The number of citations of an article in scientific journals reflects its impact on a biomedical specialty and its recognition in the scientific community. In this study, we identified and analyzed the 100 most highly cited articles published between 1971 and 2011 in journals pertaining to plastic and reconstructive surgery research. METHODS: We selected 6 high-impact journals for literature search in the database of the Science Citation Index (1971 to 2011). We identified the 100 most frequently cited articles published in these journals, and analyzed them. RESULTS: The most cited article received 1007 citations and the least cited article received 165 citations, with a mean of 274 citations per article. These citation classics were published in 5 high-impact journals, led by Plastic and Reconstructive Surgery (76 articles). The articles came from 17 countries, with the United States producing 57 articles. Sixty-two institutions produced these 100 top-cited articles, led by Royal Mountain Hospital, University of Melbourne (7 articles). Twenty-three authors published 2 or more of the top-cited articles, led by Taylor GI who authored 10 classic papers. CONCLUSIONS: This analysis of the top citation classics allows for the recognition of major advances and supplies a historic perspective on the progress of plastic and reconstructive surgery research.

Netrin-1 protects against L-Arginine-induced acute pancreatitis in mice.

Acute pancreatitis (AP) is a common inflammatory disease mediated by damage to acinar cells and subsequent pancreatic inflammation with infiltration of leukocytes. The neuronal guidance protein, netrin-1, has been shown to control leukocyte trafficking and modulate inflammatory responses in several inflammation-based diseases. The present study was aimed toward investigating the effects of netrin-1 in an in vivo model of AP in mice. AP was induced in C57BL/6 mice by administration of two intraperitoneal injections of L-Arginine (4 g/kg). Mice were treated with recombinant mouse netrin-1 at a dose of 1 µg/mouse or vehicle (0.1% BSA) intravenously through the tail vein immediately after the second injection of L-Arginine, and every 24 h thereafter. Mice were sacrificed at several time intervals from 0 to 96 h after the induction of pancreatitis. Blood and tissue samples of pancreas and lung were collected and processed to determine the severity of pancreatitis biochemically and histologically. Immunohistochemical staining demonstrated that netrin-1 was mainly expressed in the islet cells of the normal pancreas and the AP model pancreas, and the pancreatic expression of netrin-1 was down-regulated at both the mRNA and protein levels during the course of AP. Exogenous netrin-1 administration significantly reduced plasma amylase levels, myeloperoxidase activity, pro-inflammatory cytokine production, and pancreas and lung tissue damages. Furthermore, netrin-1 administration did not cause significant inhibition of nuclear factor-kappa B activation in the pancreas of L-Arginine-induced AP. In conclusion, our novel data suggest that netrin-1 is capable of improving damage of pancreas and lung, and exerting anti-inflammatory effects in mice with severe acute pancreatitis. Thus, our results indicate that netrin-1 may constitute a novel target in the management of AP.

Improving the antibacterial property of porcine small intestinal submucosa by nano-silver supplementation: a promising biological material to address the need for contaminated defect repair.

OBJECTIVE: We hypothesize that introduction of nano-silver particles to porcine-derived small intestinal submucosa (NS-PSIS) would lead to significant enhancement in antibacterial property in repairing contaminated abdominal defect. BACKGROUND: Porcine-derived small intestinal submucosa (PSIS) is an acellular and xenogenic biological material intensively used in repairing and regenerating wounded and dysfunctional tissues. Surgical site infection (SSI) remains so far a serious problem and major challenge, particularly in contaminated tissue-deficient repairing. METHODS: Self-assembly was used to fabricate NS-PSIS. The antibacterial property was evaluated in vitro and in vivo by means of repairing full-thickness contaminated abdominal defect in rats. The native PSIS and polypropylene-oxidized regenerated cellulose were served as controls. In addition, changes in biomechanical resistance, morphology and immunohistochemistry for inflammatory reaction and neovasculation in the repaired abdominal wall were analyzed. Biosafety was investigated by pyrogen test, skin irritation test and silver measurement in vivo. RESULTS: NS-PSIS exhibited strong antibacterial activity against Staphylococcus aureus, Staphylococcus epidermidis, Escherichia coli, and Pseudomonas aeruginosa on agar diffusion, with mean diameters of inhibition zone ranging from 11.9 to 23.5 mm. There were significantly lower SSI incidence and a tendency of better abdominal wall resistance in the NS-PSIS group as compared with the PSIS or polypropylene-oxidized regenerated cellulose group after repairing contaminated abdominal defect in rats. Nano-silver modified PSIS did not change the native PSIS property in the tissue recolonization, remodeling and neovascularization. NS-PSIS was not pyrogenic or skin irritated, without silver residual in vivo after repairing contaminated abdominal defect. CONCLUSION: Nano-silver particles to PSIS lead to significant enhancements in antibacterial property in vitro and in vivo without decreasing its biomechanical resistance and biocompatibility. This study provides proof of concept for the use of nano-silver modified naturally derived PSIS as an ideal scaffold for SSI prevention in the contaminated tissue-deficient repair.

The effects of hydrogen-rich saline on the contractile and structural changes of intestine induced by ischemia-reperfusion in rats.

BACKGROUND: Hydrogen has been considered as a novel antioxidant that prevents injuries resulted from ischemia-reperfusion (I/R) injury in various tissues. The study was designed to determine the effect of hydrogen-rich saline on the smooth muscle contractile response to KCl, and on epithelial proliferation and apoptosis of intestine subjected to I/R. METHODS: Intestinal I/R injury was induced in Sprague-Dawley rats using bulldog clamps in superior mesenteric artery by 45 min ischemia followed by 1 h reperfusion. Rats were divided randomly into four groups: sham-operated, I/R, I/R plus saline treatment, and I/R plus hydrogen-rich saline treatment groups. Hydrogen-rich saline (>0.6 mM, 6 mL/kg) or saline (6 mL/kg) was administered, respectively, via tail vein 30 min prior to reperfusion. Following reperfusion, segments of terminal jejunum were rapidly taken and transferred into isolated organ bath and responses to KCl were recorded. Samples of terminal jejunum were also taken for measuring malondialdehyde and myeloperoxidase. Apoptosis in intestinal epithelium was determined with terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling technique (TUNEL). Expression and distribution of proliferating cell nuclear antigen (PCNA) were detected with immunohistochemistry. RESULTS: Hydrogen-rich saline treatment significantly attenuated the severity of intestinal I/R injury, with inhibiting of I/R-induced apoptosis, and promoting enterocytes proliferation. Moreover, Hydrogen-rich saline treatment significantly limited the neutrophil infiltration, lipid oxidation, and ameliorated the decreased contractility response to KCl in the intestine subjected to I/R. CONCLUSIONS: These results suggest that hydrogen treatment has a protective effect against intestinal contractile dysfunction and damage induced by intestinal I/R. This protective effect is possibly due to its ability to inhibit I/R-induced oxidative stress, apoptosis, and to promote epithelial cell proliferation.

Hydrogen-rich saline ameliorates the severity of l-arginine-induced acute pancreatitis in rats.

Molecular hydrogen, which reacts with the hydroxyl radical, has been considered as a novel antioxidant. Here, we evaluated the protective effects of hydrogen-rich saline on the l-arginine (l-Arg)-induced acute pancreatitis (AP). AP was induced in Sprague-Dawley rats by giving two intraperitoneal injections of l-Arg, each at concentrations of 250mg/100g body weight, with an interval of 1h. Hydrogen-rich saline (>0.6mM, 6ml/kg) or saline (6ml/kg) was administered, respectively, via tail vein 15min after each l-Arg administration. Severity of AP was assessed by analysis of serum amylase activity, pancreatic water content and histology. Samples of pancreas were taken for measuring malondialdehyde and myeloperoxidase. Apoptosis in pancreatic acinar cell was determined with terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling technique (TUNEL). Expression of proliferating cell nuclear antigen (PCNA) and nuclear factor kappa B (NF-kappaB) were detected with immunohistochemistry. Hydrogen-rich saline treatment significantly attenuated the severity of l-Arg-induced AP by ameliorating the increased serum amylase activity, inhibiting neutrophil infiltration, lipid oxidation and pancreatic tissue edema. Moreover, hydrogen-rich saline treatment could promote acinar cell proliferation, inhibit apoptosis and NF-kappaB activation. These results indicate that hydrogen treatment has a protective effect against AP, and the effect is possibly due to its ability to inhibit oxidative stress, apoptosis, NF-kappaB activation and to promote acinar cell proliferation.