Two groups were created according to whether they were receiving statin therapy at the time of intervention.

Demographics, lesion morphology, overall mortality, primary and secondary patency, and limb salvage were compared between these groups. Analysis was performed using multivariate regression and Kaplan-Meier analysis.

Results: Between 2004 and 2009, 646 patients, 319 receiving statin therapy and 327 without, underwent an endovascular intervention for CLI. The statin group had significantly higher rates of diabetes mellitus, coronary artery disease, congestive heart failure, previous myocardial infarction, and coronary artery bypass grafting (P < .05). The two groups had similar lesion length, location, lesion type, TransAtlantic Inter-Society buy OSI-027 Consensus (TASC) classification, and primary procedure. At 24 months, the statin-treated group had higher rates of primary patency (43% vs 33%; P = .007), secondary patency (66% vs 51%;

P = .001), limb salvage (83% vs 62%; P = .001), and overall survival (77% vs 62%; P = .038). Statin therapy was also independently associated with improved limb salvage by multivariate regression analysis (hazard Anlotinib manufacturer ratio, 2.55; P < .001).

Conclusions: Patients who were receiving statin therapy when they underwent interventions to treat CLI had significantly improved NADPH-cytochrome-c2 reductase overall survival, primary and secondary patency, and limb salvage rates. Our findings suggest that statins should be part of the periprocedural treatment regimen and support further investigation into the beneficial effects of statins in patients undergoing endovascular treatment of CLI. (J Vase Surg 2012;55:371-80.)”
“Lead (Pb) was one of the first poisons identified, and the developing nervous system is particularly vulnerable to its toxic effects. Relatively low, subclinical doses, of Pb that produce no overt signs of encephalopathy

can affect cognitive, emotional, and motor functions. In the present study, the effects of developmental Pb-exposure on behavioral performance and gene expression in BALB/cAnNTac mice were evaluated. Pups were exposed to Pb from gestational-day (gd) 8 to postnatal-day (pnd) 21 and later evaluated in exploratory behavior, rotarod, Morris water maze, and resident-intruder assays as adults. Pb-exposure caused significant alterations in exploratory behavior and water maze performance during the probe trial, but rotarod performance was not affected. Pb-exposed males displayed violent behavior towards their cage mates, but not to a stranger in the resident-intruder assay. Gene expression analysis at pnd21 by microarray and qRT-PCR was performed to provide a molecular link to the behavior changes that were observed.

Recently, a link between iron starvation and HDP resistance in Yersinia pseudotuberculosis has been shown, supporting the idea that bacteria

can sense when inside a host and coordinate their response accordingly [26]. It has previously been reported that a mutation in S. aureus hssR or hrtA leads to increased virulence [14]. This increase has been suggested to be due to pore formation in the bacterial cell membrane that elicits an increased secretion of immunomodulatory factors, which decreases killing of the bacteria [20]. However, plectasin does not form pores RAD001 ic50 or leads to increased secretion of bacterial compounds. These results indicate that the deletion of hssR affects

the bacteria in a way that improve their ability to survive defensins of the host defence system causing the observed hypervirulence [14]. We did not observe an upregulation of hssR or hrtB when S. aureus was GDC-0449 purchase exposed to plectasin. Previous results have shown a 45 fold upregulation of hrtAB when exposed to exogenous hemin [19]. The lack of plectasin regulation of the systems implies that the TCS does not sense the defensins and the ABC transporter system HrtAB is not involved in exporting the peptides. This suggests that the lack of hssR alleviates a regulation of one or more target genes leading to the resistant phenotype. Modifications of the cell surface Regorafenib order are known to affect HDP resistance and

plectasin targets bacterial cell wall precursor Lipid II, implying a function of HssR on the cell wall synthesis or composition. Change in surface charge is known to affect HDP susceptibility and we have previously shown that mprF and dltA mutations affect S. aureus sensitivity to plectasin, novicidin, protamine and novispirin [7]. However, the effect of the hssR mutation is probably not due to changes in surface charge, since only plectasin and eurocin susceptibilities are altered. A consensus DNA binding sequence for HssR has been predicted and genomic analysis of S. aureus has revealed that, besides the consensus sequence in the hrtAB promoter region, 14 genes have consensus sites containing 3-4 mismatches [16]. Whether one of these genes pentoxifylline is involved in the observed plectasin resistance remains elusive. Further work is needed to clarify whether the hssR mutation has an effect on one of these genes in order to understand the bacterial changes that lead to reduced plectasin sensitivity. Homologues of the HrtAB and HssRS systems are found in several Gram-positive bacterial pathogens [[14], this work]. A possible HssR homologue, RR23, exists in L. monocytogenes. However, a mutation in this response regulator did not affect growth or survival when exposed to the peptides and previous results have shown that RR23 is not important for virulence [22].

Cell 2005, 123:819–831.PubMedCrossRef Competing interests The authors have declared that no competing interests exist. Authors’ contributions

TL and BZ conceived and designed the experiments. LL, JZ and HT performed the experiments. LL, LN and YD analyzed the data. LN and SZ contributed to reagents/materials/analysis tools. LL, TL, BZ, LN wrote the paper. All authors read and approved the final manuscript.”
“Background Drugs that Combretastatin A4 concentration interfere with mitosis are part of the most successful cancer chemotherapeutic compounds currently used in clinical practice [1]. Development of chemotherapeutic drugs that target the mitotic cycle has focused on inhibition of the mitotic spindle through interactions with microtubules [1]. Drugs targeting microtubules such as taxanes and vinca alkaloids are effective

in a wide variety of cancers, however, the hematopoietic and neurological toxicities as well as development of resistance to this class of drugs SAHA HDAC molecular weight severely limit their long term clinical utility [1, 2]. Novel anti-mitotic agents have been designed to target the mitotic apparatus through non-microtubule mitotic mediators such as mitotic kinases www.selleckchem.com/products/empagliflozin-bi10773.html and kinesins [2]. A novel attractive non-microtubule target is Highly Expressed in Cancer 1 (Hec1), a component of the kinetochore that regulates the spindle checkpoint. Hec1 is of particular interest because of its association with cancer progression [3–5]. Hec1 directly interacts with multiple kinetochore components including Nuf2, Spc25, Zwint-1, and with mitotic kinases Nek2 and Aurora B [6, 7] and its expression is tightly regulated in both normal cells and transformed cells during the cell cycle [4, 8]. Rapidly dividing cells express a high level of Hec1, in contrast to very low to undetectable levels of Hec1 in terminally differentiated cells [3]. Hec1 has been demonstrated to overexpress in various human cancers including Phosphatidylethanolamine N-methyltransferase the brain, liver, breast, lung, cervical, colorectal and gastric cancers [3, 9]. From a mechanistic

standpoint, targeted inhibition of Hec1 by RNAi or by small molecules effectively blocks tumor growth in animal models [3, 10]. Therefore, Hec1 emerges as an excellent target for treating cancer clinically. Small molecules targeting the Hec1/Nek2 pathway was first discovered by Drs. Chen in the laboratory of Dr. W.H. Lee using the inducible reverse yeast two-hybrid screening of a library of ~24,000 compounds [3]. A series of compounds was designed based on this published initial hit molecule as the starting template to optimize the potency for drug development (Huang et al., manuscript in preparation). The original template with micromolar in vitro potency was improved to low nanomolar potency, enabling possible clinical utility of the Hec1-targeted compound. This study explores the features and potential of the improved anticancer agent targeting Hec1, TAI-1, for preclinical development and clinical utility.

Secondary incubation of the membrane was then carried out using a 1:5000 dilution of goat antimouse or anti-rabbit IgG tagged with horseradish peroxidase. The blot was developed using Opti-4CN substrate kit (Bio-Rad Laboratories, Hercules, CA). The blots were Danusertib nmr scanned using the Biophotonics system (Biophotonics Corp., Ann Arbor, MI). The band intensity was evaluated using the Intelligent

Quantifier software (Bio Image, Ann Arbor, MI). The overexpression of eIF4E and TLK1B was quantified as x-fold over the samples of benign tissue from noncancer specimens run concurrently on the gel. Analysis of TMAs The first TMA (TMA1) was constructed to optimize antibody dilutions. The second TMA (TMA2) was designed with triplicate specimens to analyze intra-individual variability. In this selleck screening library regard, three separate plugs from each patient were taken from each original block and re-imbedded into TMA2. Replicate breast tumor specimens were AMN-107 mw analyzed for plug-to-plug reproducibility by staining the TMAs immunohistochemically and quantitating them using the ARIOL imaging system (described below). The third TMA (TMA3) was designed to compare eIF4E to its downstream effector

proteins using a larger set of breast cancer specimens. ARIOL Imaging The ARIOL imaging system (Genetix, San Jose, CA) was used to quantify antibody staining of the TMAs. The specimens were scanned at a low resolution (1.25×) and high resolution (20×) using Olympus BX 61 microscope

with an automated platform (Prior). The slides were loaded in the automated slide loader (Applied Imaging SL 50). The images with high resolution were used for training and quantification purpose. The system was trained to select the stained and unstained cells/nuclei by the color of staining and shape of nuclei such that brown staining was considered positive and blue staining was considered negative. The number of cells/nuclei stained was calculated and represented as also percentage of total cells/nuclei stained positively. By measuring both immunostaining intensity and percentage, data obtained are reproducible, objective measurements of immunoreactivity. Because standardizing IHC, from the fixation of tissues to the analysis of IHC results is critical, all immunohistochemistry data were normalized to cytokeratin. To control for the variability in tumor cellularity from one patient to another, and to also control for variations in the number of tumor cells at different TMA spots (intra-tumoral variations), the number of epithelial (tumor) cells present at each TMA spot as highlighted by expression of cytokeratin 7, was used for normalization of each protein expression studied [26]. For each protein, a score was generated based on the area with and the intensity of the brown staining reaction. The scores were then exported to an Excel spreadsheet for analysis.

1, (b) 0.25, and (c) 0.50 ms for 214 fs and 16-W average laser power. The repetition rate and dwell time affect the growth of nanotips in somewhat selleck chemicals llc similar way since both control the number of laser pulses delivered to the target surface. After the breakdown of the target material

has started, it requires a certain number of pulses according to the repetition rate and dwell time to ablate the required amount Y-27632 in vivo of target material into the plasma, as demonstrated in stages 1 to 3 in Figure 8. Before this point in time, the plume does not have enough monomers to start vapor condensation. Once the vapor condensation has started inside the plume, the vapor condensates begin to get deposited onto the hot target surface, as depicted in stage 3. If the machining is stopped little after reaching stage 3, there will not be any more incoming pulses that transfer energy to the plasma species to generate further turbulence. As a result, the plasma species start relaxing by cooling down and mixing with nitrogen gas molecules. The consequence of these phenomena will be that the pressure exerted due PHA-848125 concentration to the plasma species will be relieved and the internal pressure becomes much higher than the external pressure on the deposited plasma condensates due to the hot target surface. At the same time, the deposited condensates experience uneven cooling due to the random flow of nitrogen gas.

As a result, the deposited droplets have regions of high and low surface tension over their entire surface. As a result, the imbalance of pressure pushes the material out of the volume of deposited droplets from regions of low surface tension resulting in the formation of the stem for the nanotips, as depicted in the side figures of stage 3 in Figure 8. Figure 8 Schematic representation of the growth stages of plasma expansion and nanotips’ stem formation. The ablation mechanism somewhat changes from one repetition rate to another due to the

stiripentol difference in threshold energy-per-pulse requirement. The incoming pulses also interact differently with plasma generated from previous pulses for each repetition rate. Thus, the nanostructures generated for even the same dwell time differ for different repetition rates, as seen in Figures 6 and 9. Figure 9 shows SEM images of the glass target irradiated with 4-, 8-, and 13-MHz repetition rates for a dwell time of 0.75 ms. For 8- and 13-MHz repetition rates, the number of nanotips produced is much less compared to 0.50 ms, as seen in Figures 6 and 7. Instead, the presence of many spherical micronanoparticles and molten droplets is observed. This phenomenon can better be understood from the stage 4 of the schematic representation depicted in Figure 8. When the irradiated spot is bombarded with too many pulses as in the case of high repetition rates and high dwell time, an excessive amount of material is added to the plasma.

The clustering analysis was performed using the UPGMA algorithm provided

in the BioNumerics software and the value of Dice predicted similarity of two patterns at settings of 1% optimization and 0.7% position tolerance. Acknowledgements This work was supported by grants DOH94-DC-2025 and DOH94-DC-2026 from the Centers for Disease Control, DOH, Taiwan. References 1. Cunningham MW: Pathogenesis of group A streptococcal infections. Clin Microbiol Rev 2000,13(3):470–511.CrossRefPubMed 2. Espinosa de los Monteros LE, Bustos IM, Flores LV, Avila-Figueroa C: Outbreak of Napabucasin in vivo scarlet fever caused by an erythromycin-resistant MG-132 nmr Streptococcus pyogenes emm 22 genotype strain in a day-care center. Pediatr Infect Dis J 2001,20(8):807–809.PubMed 3. Hsueh PR, Teng LJ, Lee PI, Yang https://www.selleckchem.com/products/VX-770.html PC, Huang LM, Chang SC, Lee CY, Luh KT: Outbreak of scarlet fever at a hospital day care centre: analysis of strain relatedness with phenotypic and genotypic characteristics. J Hosp Infect 1997,36(3):191–200.CrossRefPubMed 4. Yang SG, Dong HJ, Li FR, Xie SY, Cao HC, Xia SC, Yu Z, Li LJ: Report and analysis of a scarlet fever outbreak among adults through food-borne transmission in China. J Infect 2007,55(5):419–424.CrossRefPubMed 5. Beall B, Facklam R, Thompson T: Sequencing emm -specific PCR products for routine and accurate typing of group A streptococci. J Clin Microbiol 1996,34(4):953–958.PubMed 6. Gardiner D, Hartas

J, Currie B, Mathews JD, Kemp DJ, Sriprakash KS: Vir typing: a long-PCR typing method for group A streptococci. PCR Methods Appl 1995,4(5):288–293.PubMed 7. Chiou CS, Liao TL, Wang TH, Chang HL, Liao JC, Li CC: Epidemiology and molecular characterization of Streptococcus pyogenes recovered from scarlet fever patients in central Taiwan from 1996 to 1999. J Clin Microbiol 2004,42(9):3998–4006.CrossRefPubMed 8. O’Loughlin RE, Roberson A, Y-27632 2HCl Cieslak PR, Lynfield R, Gershman K, Craig A, Albanese

BA, Farley MM, Barrett NL, Spina NL, et al.: The epidemiology of invasive group A streptococcal infection and potential vaccine implications: United States, 2000–2004. Clin Infect Dis 2007,45(7):853–862.CrossRefPubMed 9. Yan JJ, Liu CC, Ko WC, Hsu SY, Wu HM, Lin YS, Lin MT, Chuang WJ, Wu JJ: Molecular analysis of group A streptococcal isolates associated with scarlet fever in southern Taiwan between 1993 and 2002. J Clin Microbiol 2003,41(10):4858–4861.CrossRefPubMed 10. Chen YY, Huang CT, Yao SM, Chang YC, Shen PW, Chou CY, Li SY: Molecular epidemiology of group A streptococcus causing scarlet fever in northern Taiwan, 2001–2002. Diagn Microbiol Infect Dis 2007,58(3):289–295.CrossRefPubMed 11. Krause RM: A half-century of streptococcal research: then & now. Indian J Med Res 2002, 115:215–241.PubMed 12. Euler CW, Ryan PA, Martin JM, Fischetti VA: M.SpyI, a DNA methyltransferase encoded on a mefA chimeric element, modifies the genome of Streptococcus pyogenes. J Bacteriol 2007,189(3):1044–1054.CrossRefPubMed 13.

Moreover, in light of the seriousness of the disease, hematologists should be alert to the possibility of such an adverse reaction. This case has been reported to the Italian Health Authority (AIFA) registered as number 212194 on July 2013 and to the manufacturer of the drug (Takeda). Conflict of interest We have no conflicts of interest to disclose. Open AccessThis article is distributed under the terms of buy AZD1480 the Creative Commons Attribution Noncommercial License which permits any noncommercial use, distribution, and reproduction in any medium, provided the original author(s) and the source are credited. References 1. Cotton PB, Lehman G, Vennes J, Geenen

JE, Russell RC, Meyers WC, Liguory C, Nickl N. Endoscopic sphincterotomy complications and their management: an attempt at consensus. Gastrointest Endosc. 1991;37:383–93.PubMedCrossRef 2. Naranjo CA, Busto U, Sellers EM. A method for estimating the probability of adverse

drug reactions. Clin Pharmacol Ther. 1981;30(2):239–45.PubMedCrossRef 3. Carroll JK, Herrick B, Gipson T, Lee SP. Acute pancreatitis: diagnosis, prognosis, and treatment. Am Fam Physician. 2007;75(10):1513–20. 4. Nitsche CJ, Jamieson N, Lerch MM, Mayerle JV. Drug induced pancreatitis. Best Prac Res Clin Gastroenterol. 2010;24:143–55.CrossRef 5. Underwood TW, Frye CB. Drug-induced pancreatitis. Clin Pharm. 1993;12(6):440–448. Momelotinib concentration 6. Tester W, Forbes W, Leighton J. Vinorelbine-induced pancreatitis: a case report. J Natl Cancer Inst. 1997;89(21):1631.PubMedCrossRef”
“1 Amino acid Introduction Setipiprant (ACT-129968, 2-(2-(1-naphthoyl)-8-fluoro-3,4-dihydro-1H-pyrido[4,3-b]indol-5(2H)-yl)acetic acid) is an orally available, selective CRTH2 (chemoattractant receptor-homologous molecule expressed on T helper [Th]-2 cells) antagonist. CRTH2 is a G selleck chemicals protein-coupled receptor for prostaglandin (PGD2). PGD2 is produced by the mast cells and is a key mediator in various inflammatory diseases,

including allergy and asthma [1–3]. Binding of PGD2 to CRTH2, which are expressed on the surface of blood-borne cells, induces chemotaxis of Th2 cells, basophils, and eosinophils, and stimulates cytokine release from these cells [2, 4]. Thus, antagonism of CRTH2 receptors is considered to be a promising therapeutic target for various allergic diseases and asthma. Preclinical data showed that setipiprant potently inhibits migration of eosinophils towards PGD2 in vitro as well as in an in vivo rat model of lung eosinophilia (Actelion Pharmaceuticals Ltd, data on file). In the entry-into-man study in healthy male subjects, single and multiple doses of setipiprant of up to 1,000 mg twice daily (bid) for 6 days showed excellent tolerability and a favorable pharmacokinetic profile (Sidharta et al., unpublished data). The pharmacokinetics of setipiprant were characterized by a rapid absorption with a time to maximum plasma concentration (t max) of 2–4 h, followed by a biphasic elimination pattern.

In this way, 583 proteins were predicted as secreted, 79% of which had unassigned SU5416 ic50 functions. Of the remaining 125 proteins, 18 transporters were found, as well as three procyclins. However, only 13 proteins from this set were found to match our experimental data. Thus, taken together, less than 20% of the secreted proteins from our data set were predicted to have a transit peptide (SignalP) and no transmembrane domain (TMHMM) or to be secreted via the nonclassical pathway (SecretomeP), suggesting that most Trypanosoma secreted proteins purified so far are secreted by a novel mechanism. 2-Possible

exocytosis of microvesicles In Trypanosoma, endocytosis and exocytosis occur through a sequestered organelle called the flagellar pocket (FP), an invagination of the pellicular membrane. This traffic is not fully understood and requires clathrin, actin, and GTPase Rab proteins [24–26]. We found these proteins in the secretome but electronic microscopy pictures clearly indicate Talazoparib supplier a budding of microvesicles at the plasma membrane and flagellum (Figure 7). In human, many types of cells, such as reticulocytes, dendritic cells, tumor cells, neurones, or mast cells, are able to release microvesicles called exosomes. Cross-correlation between

different exosome proteomics studies recently identified a set of 22 proteins commonly associated with Lonafarnib exosomes of various origins [27]. Of these, 13 were found in our data set (clathrin heavy chain, ubiquitin, 14-3-3 proteins, hsp70 and 90, enolase, RAB protein, GAPDH [glyceraldehyde-3-phosphate dehydrogenase], pyruvate kinase, cyclophilin, tubulin α and β, and histone). Moreover,

translationally controlled tumor protein (TCTP) was also shown to be present in small secreted vesicles called exosomes, and participates in inflammatory responses by promoting the release of histamine [28, 29]. We found this protein in both the procyclic (data not shown) and bloodstream form VAV2 of the T. brucei gambiense secretome (see additional file 1, Table S1). Figure 7 Cross-sections of Trypanosoma brucei gambiense purified from infected rat blood by chromatography on DEAE cellulose column and incubation in secretion medium (A, B, C) and directly after cardiac puncture of infected rat (D, E, F). A-C: parasites purified from secretion medium; D-F: parasites purified directly from infected rat blood. A-F: Free vesicles and budding of new vesicles at the coated plasma membrane surface of the parasite, high magnification of vesicle formation (B), budding vesicles at the flagellum (semi-longitudinal section) (C). f flagellum, k kinetoplast, m mitochondrion, n nucleus, pm plasma membrane with surface coat, pmt pellicular microtubules, v vesicle. Scale bars A, D, E 200 nm, B, C, F 100 nm.

The arrows indicate strand direction from 5′ to 3′. The ability of the three ligands to induce structure in the single stranded h-Tel sequence in aqueous solution in the absence of significant AZD6244 concentrations of K+ ions was also investigated. The unfolded h-Tel sequence at 298 K gives a low intensity positive band in the CD spectrum at 265 nm (Figure  4b). However, in the presence of 3.5 molar equivalents of ligand, emergence of the characteristic band at 290 nm was observed, consistent with the ligand-induced formation of

the anti-parallel structures evident in the K+ buffered solution. Thus, under both sets of conditions (with and without stabilising K+ ions), evidence is adduced for ligand selectivity for the anti-parallel quadruplex structure [12, 13]. This analysis was extended to examine the effects of ligand binding on thermal stability by measuring the

unfolding curves at 290 nm of the complexes formed in K+ solution, corresponding to the CD spectra shown in Figure  4a. Monitoring the thermal unfolding transition for h-Tel produces a sigmoidal unfolding curve with a transition mid-point Tm value of 72 ± 3°C (Figure  4c). All three ligands show significant effects in check details enhancing the stability of the quadruplex by shifting the Tm values to higher temperatures RepSox research buy (∆Tm ~ 15-19°C compared to h-Tel without bound ligands) (Table  1). Biological effects of quinoacridinum salts To ascertain if the compounds 2 and 3 maintained the same biological and molecular features of the previously described 1, we firstly evaluated their effect on cell proliferation in a panel of different Rucaparib ic50 histotype tumor cell lines, showing that both compounds maintained an anti-proliferative effect in several human cancer cell lines (Additional file 1). Selectivity for transformed vs normal cells was assessed in the hTERT immortalized BJ human fibroblasts infected or not with the Large T antigen of SV40. Figure  5a and b shows the growth curves of untreated and drug-treated cells, analyzed from day 2 to 8 of culture by using 0.5 μM concentration

of each compound, a dose causing cell death when cells are chronically exposed to the lead compound 1. A time-dependent decrease of cell proliferation was observed in SV40 transformed (BJ-EHLT) cells treated with the ligands reaching the maximum effect at day 6 (for the compounds 1 and 2) or seven (compound 3). Interestingly, as already described for 1, the compounds 2 and 3 did not induce inhibition of cell proliferation in normal telomerized fibroblasts, which were unaffected by the treatment (Figure  5a and b). Even if the mechanism(s) of selectivity towards transformed cells were not identified yet, our results indicate that the new-generated agents 2 and 3, similarly to the lead compound, preferentially limit the growth of cancer cells. Figure 5 Anti-proliferative effect on normal and transformed fibroblasts.

Additionally, many reports list multiple organ failure as a leading cause of death. Does unrecognized shock play a role in these deaths?”" [39]. In conclusion, at the beginning of the 21st century, when NOM for liver and spleen injuries is often advocated beyond the limits of a reasonable

safety and the need for surgery is considered as a defeat or “”failure”". We should not forget in making the best treatment choice, to keep in mind not only the predictors https://www.selleckchem.com/products/poziotinib-hm781-36b.html of NOM failure, such as the injury grade, the presence of associated intra-abdominal injuries and the risk of missing injuries with the subsequent sequelae, of a failed NOM and of delayed surgical treatment, but we must also consider the potential drawbacks of angioembolization, the environmental selleck kinase inhibitor setting and factors, i.e. the level of the hospital (trauma center), availability of Angio Suite and ICU for continuous monitoring, the initiation of NOM during night shift, the need of an eventual time consuming spine surgery in a prone position for a concomitant vertebral fracture, and last but not least, the time needed for complete and safe resumption of normal life (work and Alvocidib manufacturer physical activity). References 1. Feliciano DV, Mattox KL, Jordan GL: Intra-abdominal packing for control of hepatic hemorrhage: a reappraisal. J Trauma 1981, 21:285–290.PubMedCrossRef 2. Pachter HL, Spencer FC, Hofstetter SR, Coppa GF: Experience with the finger fracture technique to achieve intra-hepatic

hemostasis in 75 patients with severe injuries of the liver. Ann Surg 1983,197(6):771–8.PubMedCrossRef 3. Stone HH, Strom PR, Mullins RJ: Management of the major coagulopathy with onset during laparotomy. Ann Surg 1983,197(5):532–5.PubMedCrossRef 4. Lucas CE, Ledgerwood AM: Changing times and the treatment of liver injury. Am Surg 2000,66(4):337–41.PubMed 5. Cogbill TH, Moore EE, very Jurkovich GJ, et al.: Nonoperative management of blunt splenic trauma: a multicenter experience. J Trauma 1989, 29:1312–1317.PubMedCrossRef 6. Pearl RH, Wesson DE,

Spence LJ, Filler RM, Ein SH, Shandling B, Superina RA: Splenic injury: a 5-year update with improved results and changing criteria for conservative management. J Pediatr Surg 1989,24(1):121–4. disc 124–5PubMedCrossRef 7. Rothenberg S, Moore EE, Marx JA, Moore FA, McCroskey BL: Selective management of blunt abdominal trauma in children–the triage role of peritoneal lavage. J Trauma 1987,27(10):1101–6.PubMedCrossRef 8. Pachter HL, Knudson MM, Esrig B, et al.: Status of nonoperative management of blunt hepatic injuries in 1995: a multicenter experience with 404 patients. J Trauma 1996, 40:31–38.PubMedCrossRef 9. Croce MA, Fabian TC, Menke PG, Waddle-Smith L, Minard G, Kudsk KA, Patton JH Jr, Schurr MJ, Pritchard FE: Nonoperative management of blunt hepatic trauma is the treatment of choice for hemodynamically stable patients. Results of a prospective trial. Ann Surg 1995,221(6):744–53. discussion 753–5PubMedCrossRef 10.