PubMed 28. Garnock-Jones KP, Keating GM, Scott LJ: Trastuzumab: a review of its use as adjuvant treatment in human epidermal growth factor receptor 2 (HER2)-positive early breast cancer. Drugs 2010, 70:215–39.PubMedCrossRef 29. Gennari A, Sormani MP, Pronzato P, Puntoni M, Colozza M, Pfeffer

U, Bruzzi P: HER2 status and efficacy of adjuvant anthracyclines in early breast cancer: A pooled analysis of randomized trials. J Natl Cancer Inst 2008, 100:14–20.PubMedCrossRef 30. Sobin LH, Wittekind C: UICC TNM Classification of Malignant Tumours. 6th edition. New York: Wiley-Liss; 2002. 31. Elston C, Ellis I: Pathological prognostic factors in #Selleck Bafilomycin A1 randurls[1|1|,|CHEM1|]# breast cancer. I. The value of histologic grade in breast cancer: experience from a large study with long-term follow-up. Histopatology 1991, 19:403–10.CrossRef 32. The World

Health Organization: Histological typing of breast tumors. Neoplasma 1983, 30:113–23. 33. Clarke SJ, Rivory LP: Clinical pharmacokinetics of docetaxel. Clin Pharmacokinet 1999, 36:99–114.PubMedCrossRef 34. Schiff PB, Fant J, Horwitz SB: Promotion of microtubule assembly in vitro by taxol. Nature 1979, 277:665–67.PubMedCrossRef 35. Ganansia-Leymarie V, Bischoff P, Bergerat GSK872 datasheet JP, Holl V: Signal transduction pathways of taxanes-induced apoptosis. Curr Med Chem Anti-Canc Agents 2003, 3:291–306.CrossRef 36. Verweij JM, Clavel M, Chevalier B: Paclitaxel (Taxol™) and docetaxel (Taxotere™): Not simply two of a kind. Ann Oncol 1994, 5:495–505.PubMed 37. Brugarolas J, Chandrasekaran C, Gordon JI, Beach D, Jacks T, Hannon GJ: Radiation-induced cell cycle arrest compromised by p21 deficiency. Nature 1995, 377:552–557.PubMedCrossRef 38. St Clair S, Manfredi JJ: The dual specificity phosphatase Cdc25C is a direct target for transcriptional repression by the tumor suppressor p53. Cell Cycle 2006, 5:709–713.PubMedCrossRef 39. Deng C, Zhang P, Harper JW, Elledge SJ, Leder P: Mice lacking p21CIP1/WAF1 undergo normal

development, but are defective in G1 checkpoint Thymidylate synthase control. Cell 1995, 82:675–684.PubMedCrossRef 40. Norberg T, Lennerstrand J, Inganas M, Bergh J: Comparison between p53 protein measurements using the luminometric immunoassay and immunohistochemistry with detection of p53 gene mutations using cDNA sequencing in human breast tumors. Int J Cancer 1998, 79:376–383.PubMedCrossRef 41. Bertheau P, Espiè M, Turpin E, Lehmann J, Plassa LF, Varna M, Janin A, de Thè H: TP53 status and response to chemotherapy in breast cancer. Pathobiology 2008, 75:132–139.PubMedCrossRef 42. Berrieman HK, Lind MJ, Cawkwell L: Do β-tubulin mutations have a role in resistance to chemotherapy? Lancet Oncol 2004, 5:158–64.PubMedCrossRef Competing interests The authors declare that they have no competing interests.

30 g/kg lean mass) followed by a 42 days learn more maintenance phase (0.075 g/kg lean mass) of CM or ethyl ester both combined with a resistance training program in 30 novice males with no Selleck SAR302503 previous resistance training experience. The results of this study [65] showed that ethyl ester was not as effective as CM to enhance serum and muscle creatine stores. Furthermore creatine ethyl ester offered no additional benefit for improving body composition, muscle mass, strength, and power. This research did not support the claims of the creatine ethyl ester manufacturers. Polyethylene glycol is a non-toxic, water-soluble polymer

that is capable of enhancing the STA-9090 mw absorption of creatine and various other substances [66]. Polyethylene glycol can be bound with CM to form polyethylene glycosylated creatine.

One study [67] found that 5 g/d for 28 days of polyethylene glycosylated creatine was capable of increasing 1RM bench press in 22 untrained young men but not for lower body strength or muscular power. Body weight also did not significantly change in the creatine group which may be of particular interest to athletes in weight categories that require upper body strength. Herda et al [68] analyzed the effects of 5 g of CM and two smaller doses of polyethylene glycosylated creatine (containing 1.25 g and 2.5 g of creatine) administered over 30 days on muscular strength, endurance,

and power output in fifty-eight healthy men. CM produced a significantly greater improvement in mean power and body weight meanwhile both CM and polyethylene glycosylated form showed a significantly (p < 0.05) greater improvement for strength when compared with control group. These strength increases were similar even though the dose of creatine in the polyethylene glycosylated creatine groups was up to 75% less than that of CM. These results seem to click here indicate that the addition of polyethylene glycol could increase the absorption efficiency of creatine but further research is needed before a definitive recommendation can be reached. Creatine in combination with other supplements Although creatine can be bought commercially as a standalone product it is often found in combination with other nutrients. A prime example is the combination of creatine with carbohydrate or protein and carbohydrate for augmenting creatine muscle retention [5] mediated through an insulin response from the pancreas [69]. Steenge et al [70] found that body creatine retention of 5 g CM was increased by 25% with the addition of 50 g of protein and 47 g of carbohydrate or 96 g carbohydrate when compared to a placebo treatment of 5 g carbohydrate.

Therefore, titanium alkoxides, in this case TBT, can be readily grafted onto the surface of GO through chemical adsorption at the molecular level [28]. On the other hand, it is widely known that titanium alkoxides GW786034 datasheet are extremely sensitive to water. Rapid decomposition

of the titanium precursor would result in the agglomeration of TiO2 crystals as well as hinder the homogeneous growth of TiO2 onto GO. Hence, EG and HAc were introduced into the mixture to co-control the hydrolysis rate of TBT [29]. In addition, the mixtures were also prechilled in an ice bath to further reduce the hydrolysis rate. During the solvothermal treatment, GO was reduced to rGO, and TiO2 nanoparticles formed on the rGO surface simultaneously. The preparation strategy is illustrated in Figure 1. Figure 1 Procedure for the synthesis of rGO-TiO 2 nanocomposites. Characterization of reduced graphene oxide-TiO2 composites The surface morphology and structure of the rGO-TiO2 nanocomposite were characterized using FESEM and HRTEM. From Figure 2a, b, it is observed that the surface of rGO sheets was packed densely with TiO2 nanoparticles, which displayed a good combination of rGO and

TiO2. Despite that, Lazertinib cost the profile of a single TiO2 nanoparticle could be clearly NCT-501 purchase distinguished, indicating that the aggregation of TiO2 was well prevented during the preparation process. The TiO2 particles were also found to exhibit a narrow size distribution with an average crystallite size of 12 nm. The corresponding

HRTEM images (Figure 2c, d) clearly showed the lattice fringes of rGO, which were parallel to the edges of the TiO2 nanoparticles. The lattice spacing of TiO2 was measured to be ca. 0.35 nm, which corresponds to the (101) plane of anatase TiO2 (JCPDS no. 2101272). The rGO sheets were composed of a mixture of two to five layers based on HRTEM observations. Figure 2 Electron microscopy of the rGO-TiO 2 composites. (a) FESEM image, (b, c) HRTEM images, and (d) enlarged HRTEM image of a selected rGO-TiO2 heterojunction. It is known that few-layer rGO sheets have the tendency to aggregate back to the graphite structure due to strong van der Waals interaction [30]. Therefore, the crystallization PD184352 (CI-1040) of TiO2 on the surface of rGO was particularly helpful in overcoming this interaction, which could ultimately alleviate the agglomeration and restacking of the graphene sheets. In addition, the intimate connection would allow the electrons to transfer easily from TiO2 to rGO sheets during the photoexcitation process, which could significantly increase the separation of photoinduced charges and enhance the photocatalytic activity. Raman spectroscopy has been accepted to be a powerful and nondestructive tool to characterize the quality of graphitic materials.

smegmatis. The data present Potential target genes for MtrA in M.smegmatis. (XLS 40 KB) Additional file 6: Homologous target genes recognized by MtrA in M. tuberculosis and M. smegmatis. The data present homologous target genes recognized by MtrA in M. tuberculosis and M. smegmatis. (XLS 18 KB) Additional file 7: Primers used in this study. The data provided primers used in this study. (DOC 28 KB) Additional file 8: Sequences of the DNA substrates used in check details this study. The data provided sequences of the DNA substrates used in this study. (DOC 31 KB) Additional file 9: Primers used for quantitative real time PCR in this study. The data present the primers used for

quantitative real time PCR in this study. (DOC 70 KB) Additional file 10: Classification and percentage of the target genes containing the 7-bp motif recognized by MtrA in M. smegmatis. The data present the categories and percentage of the target genes containing the 7-bp motif recognized by MtrA in M. smegmatis. (DOC 188 KB) Additional file 11: The data present the categories and percentage of the target genes containing the 7-bp motif recognized by MtrA

in M. tuberculosis. The data present the categories and percentage click here of the target genes containing the 7-bp motif recognized by MtrA in M. tuberculosis. (DOC 212 KB) References 1. Johnson R, Streicher EM, Louw GE, Warren RM, van Helden PD, Victor TC: Drug resistance in Mycobacterium tuberculosis . Curr Issues Mol Biol 2006,8(2):97–111.PubMed 2. Wright A, Zignol M, Van Deun A, Falzon D, Gerdes SR, Feldman K, Hoffner S, Drobniewski F, Barrera L, van Soolingen D, Boulabhal F, Paramasivan CN, Kam KM, Mitarai S, Nunn P, Raviglione M, Global Project on Anti-Tuberculosis Drug Resistance Surveillance: Epidemiology of antituberculosis drug resistance 2002–07: an updated analysis of the Global Project on Anti-Tuberculosis Drug Resistance

Surveillance. Lancet 2009,373(9678):1861–1873.PubMedCrossRef 3. Beier D, Gross R: Regulation of bacterial virulence by two-component systems. Curr Opin Microbiol 2006,9(2):143–152.PubMedCrossRef 4. Stock AM, Robinson VL, Goudreau PN: selleck products Two-component signal transduction. Annu Rev Biochem 2000, 69:183–215.PubMedCrossRef 5. Cole ST, Brosch R, Parkhill J, Garnier T, Churcher C, Harris D, Gordon SV, Eiglmeier K, Gas S, Barry CE, Tekaia F, Badcock K, Basham D, Brown D, Chillingworth T, Connor R, Davies R, Devlin K, Feltwell T, Gentles S, Hamlin N, Holroyd S, Hornsby T, Jagels K, Krogh A, McLean J, Moule S, Murphy L, Oliver K, Osborne J, et al.: Deciphering the biology of Mycobacterium tuberculosis from the complete genome sequence. Nature 1998,393(6685):537–544.PubMedCrossRef 6. Zahrt TC, Deretic V: Mycobacterium tuberculosis signal transduction system GDC-0973 research buy required for persistent infections. Proc Natl Acad Sci USA 2001,98(22):12706–12711.PubMedCrossRef 7.

It has to be noted that in trauma patients, concurrent injuries may mislead and delay diagnosis. In our case, fever,

back pain and neurological impairment were at first attributed to superinfection of the retroperitoneal hematoma or possibly to an intra-abdominal abscess, before diagnosis of vertebral osteomyelitis was made. Adequate imaging should also support S3I-201 in vitro the clinical suspicion. In the presented case, CT scan of the abdomen failed to detect vertebral osteomyelitis that was subsequently diagnosed on MRI. Although plain X-ray and CT are frequently used as first step investigation for back pain, MRI is considered to be the gold standard for diagnosis of osteomyelitis. Moreover, MRI is superior to CT in defining involvement of neuronal and soft tissue and extension of the infective process [2]. Every effort should be taken to identify the pathogen, in order to ensure an appropriate antimicrobial therapy and prevent complications such as abscesses, extension of the infection to neuronal tissue, persistence or recurrence of infection, septicemia. Blood cultures have a high rate of positivity, reported to range between 30 and 75% [1]. If negative, percutaneous CT-guided biopsy to obtain material for cultures is generally recommended. Surgical

biopsy in not recommended JQ1 cost unless surgery has already been planned to drain an abscess or to treat spinal instability [2]. In our case, antimicrobial treatment was based on intraoperative cultures of peritoneal liquid whereas www.selleckchem.com/products/srt2104-gsk2245840.html repeated sets of blood cultures remained negative. This therapy demonstrated to be effective and invasive diagnostic procedures were spared. 6 to 8 weeks of antibiotics is the recommended duration for treatment, which should be anyway adjusted according to clinical course. A positive response to therapy is defined by clinical improvement and decrease from in CRP levels within 4 weeks [1]. Repeated MRI is usually unnecessary unless treatment

failure or complications are suspected [2]. Treatment should be also focused towards alleviating symptoms, with extensive use of analgesia and bed rest. An appropriate rehabilitation plan is also advisable. HBOT has been increasingly used as adjuvant therapy for bone infections. Although lacking in high quality evidence, a number of studies have suggested HBOT to be effective in enhancing leukocyte bactericidal activity and antibiotic activity in hypoxic tissues, suppressing anaerobic pathogens, inducing angiogenesis and accelerating wound healing [12]. In our case, HBOT was administered in addition to standard treatment and proved to be beneficial. Appropriate prophylaxis for infective complications in trauma patients has been largely investigated.

Mehta et al [23] reported on survival and neurological outcomes. A follow-up report by Meyers et al. [27] reported specifically on neurocognitive outcomes CX-6258 from the group of patients randomized in the motexafin gadolium trial by Mehta et al

[25] reported on the use of whole brain radiotherapy and supplemental oxygen with or without RSR13 (efaproxiral), a novelty in radiation sensitizer that performs as a modifier of hemoglobin to facilitate oxygen release. Table 1 describes the characteristics of the studies included in this meta-analysis. Table 1 Randomized studies of WBRT and radiosensitizers versus WBRT alone Study Study arms No. of pts randomized Overall median survival Overall survival at 6 months Response (CR + PR) DeAngelis (19) 3000 cGy/10 fr + lonidamine

31 4.0 m NR 37%   3000 cGy/10 fr 27 5.4 m   55% Eyre (20) 3000 cGy/10 fr + metronidazole 57 2.8 m 14 27%   3000 cGy/10 fr 54 3.2 m 13 24% RTOG-7916(21) 3000 cGy/6 fr + misonidazole 220 3.1 m 68 NR   3000 cGy/6 fr 216 4.1 m 83     3000 cGy/10 fr + misonidazole 211 3.9 m 65     3000 cGy/10 fr 212 4.5 m 72   Mehta(23) 3000 cGy/10 fr + MGd 193 5.2 m 82 NR   3000 cGy/10 fr 208 4.9 m 85   RTOG-8905(22) 3750 cGy/15 fr + BrdUrd 35 4.3 m 12 63%   3750 cGy/15 fr 37 6.12 m 20 50% REACH (25) 3000 selleck products cGy/10 fr + RSR13 265 5.4 m 119 48%   3000 cGy/10 fr 250 4.4 m 96 36% RTOG- 0118(26) 3750cGy/15 fr + thalidomide 90     NR   3750 cGy/15 fr 93       SMART(24) 3000 cGy/10 fr + MGd 279 NR NR NR   3000 cGy/10 fr 275       Setting and participants The radiosensitizers studied were lonidamide, metronidazole, misonidazole, motexafin gadolinium, bromodeoxyuridine (BrdU), RSR13 (efaproxiral) and thalidomide. In regards to the outcomes of interest, none of the trials reported on either

proportion of patients who were able to reduce their daily mTOR inhibitor dexamethasone dose or duration of reduced dexamethasone requirements. All trials used WBRT with total dose range 30 – 37.5 Gy in 10–15 fractions. ADP ribosylation factor Overall survival at six months Seven studies reported overall survival as one of the outcomes. Altogether, the analyses included 7 trials with 1763 patients. The overall mortality rates were not decreased for WBRT with radiosensitizer arm (517/878 = 58.8%) compared to WBRT alone arms (519/885 = 58.6%). The test for heterogeneity was not statistically significant with p value 0.28. The overall odds ratio suggests that there is no difference between WBRT with radiosensitizer arms and WBRT alone arms in terms of overall mortality rate with p value 0.77, as demonstrated in figure 2. Figure 2 Overall mortality in the trials included in this meta-analysis comparing WBRT with radisensitizer to WBRT alone. Local brain tumor response Four trials [19, 20, 22, 25] reported on local brain tumor response rates (either complete response (CR) or partial response (PR)).

Typhimurium challenge. Mice immunized with PBS, MT5 and MT4 (n = 5) were treated with ampicillin (25 mg by gavage), challenged with wild-type SB300 (ampr, smr) and sacrificed three days later (day 3 p.c.). Disease parameters like colonization at various host-tissues (A) and cecal pathology (B) were determined. n.s., not significant; *, statistically significant (p < 0.05). Mice immunized with MT4 and MT5 showed equivalent response for both luminal IgA and serum specific IgG Earlier it has been established that immune-protection against S. Typhimurium is based on O-antigen specific luminal

sIgA along with serum IgA, IgM and IgG responses [34]. To validate the immunogenic potential of MT4, the antibody titers of IgG from serum and IgA from gut wash samples of mice vaccinated with MT4 and Momelotinib molecular weight MT5

strains were detected by western blotting at the end of the day 30 p.v. (Figure 4). Fedratinib purchase This experiment relies on the specific antibody binding to specific antigens of the bacterium (wild-type S. Typhimurium) as compared to a bacterium of different serovar (wild-type S. Enteritidis). The intestinal wash and serum samples from mice vaccinated with either MT5 or MT4 exhibited equivalent antibody response of Salmonella specific serum IgG and luminal secretory IgA. We additionally tested the antibody response through flow cytometry analysis and the data supported the finding that MT4 or MT5 vaccination exhibits equivalent antibody response (Additional file 1: Figure S4). The T-cytotoxic and T-helper cells play a critical GPX6 role in the clearance of Salmonella as well as in the production of specific antibodies during the late phase of infection. We analyzed the effect of MT5 and MT4 strains on T-cell population of the mesenteric lymph node. We quantified the CD4+ and CD8+ T-cell population

recovered from the mLN of the vaccinated mice after day 30 p.v. The T-cell population were analyzed by flowcytometry and found to be buy Vorinostat almost equally populated in the vaccinated mice but significantly more in comparison to the PBS treated mice (Additional file 1: Figure S3). This gives a sign that, the MT4 strain has an ability to colonize and induce T-cell mediated innate and adaptive immune response in the wild-type C57BL/6 mice. Figure 4 Validation of antibody response (serum IgG and intestinal sIgA). Serum and gut wash from mice treated with PBS and vaccinated with MT4 and MT5 were collected, diluted to a highest dilution of 1:120 (serum) and 1:9 (gut wash). The presence of Salmonella specific IgG and secretory IgA were detected by Western blots. The representative Western blot analysis of the antibody responses was done by developing the blots of overnight grown cultures of MT5, MT4, SB300 (wild-type S. Typhimurium) and M1525 (S. Enteritidis; negative control) with the serum and gut wash of the immunized mice. Conclusions S. Typhimurium with a nonfunctional SPI-2 is considered as an avirulent and a potential vaccine strain [37].

2%). This trend suggests that an intervention extending beyond 12 weeks may result in significant

changes. Indeed, other studies have reported a beneficial effect of soy consumption alone on serum triglycerides [18, 33, 34]. We attempted to eliminate diet Bucladesine cell line changes other than inclusion of assigned supplements. The percent of calories buy Duvelisib derived from fat decreased significantly (p < 0.05) due to the increase in energy from protein and carbohydrates in spite of no change in total energy intake. It cannot be ruled-out that the dietary fat content played a role in improved lipid profiles but its role would be minor, at best, in view of the fact that total energy and grams of fat did not change significantly. The percent of energy from protein was expected to increase in the whey and soy supplemented groups. The reasons for the increased energy from protein in the placebo group and for energy derived from carbohydrates in all groups are unknown. Community-living subjects may have naturally chosen to alter their food choices and/or lifestyle based on their enthusiasm of

improved health from participation in the study. Study limitations We may not have observed significant changes in body composition and lipid profiles among the different protein supplements because of a type II error and it may be that a longer (>12 weeks) training period is required to show significant changes in body composition and in lipid ratios such as TC:HDL-C and LDL-C:HDL-C. selleck products Meta-analysis Teicoplanin by Zhan et al [32] confirmed that improvements in HDL cholesterol with soy protein supplementation were only observed in studies > 12 weeks in duration. In addition, a diet intervention (for example, limiting daily fat calories to <25%) in combination with the resistance training may have shown more dramatic results in body composition and lipid profile changes. Another

limitation that may have affected the outcome of the study was the difference in initial waist:hip. After randomized enrolment it was observed the soy group had significantly higher waist:hip than the other two groups. It may be that the effect of soy was diminished because of this discrepancy. It should be noted that individuals in the placebo group did modify their diet and this included an increased percentage of energy from protein and carbohydrate sources and a decrease percent of calories from fat sources. The results of training could also be due in part to these diet changes, however; the changes in percent of energy sources as noted in the placebo group do not typically result in such dramatic increases in strength gains. Conclusion Our findings add to the growing evidence that resistance training is beneficial for reducing cardiovascular risk.

Conclusion By constructingSalmonellastrains with a FLAG epitope sequence inserted in

frame into the SPI-1 genesprgI,sipA,sipB,sopE2,spaO, andsptP, and characterizing the expression of the tagged proteinsin vitroandin vivo, we provide direct evidence that PrgI and SipB are expressedin vivoin both MK-4827 the early and late stages of bacterial infection. Furthermore, this study demonstrates that the SpaO protein is preferentially expressed bySalmonellacolonizing the cecum but not the spleen, and that SptP is preferentially expressed bySalmonellacolonizing the spleen but not in the cecum. These results further suggest that different SPI-1 proteins are expressed bySalmonellawhen they colonize specific selleck chemicals tissues and that differential expression of these proteins may play an important role in bacterial pathogenesis in specific tissues. Methods Bacterial strains and growth conditions Bacterial strains and their genotypes are listed in Table1. Strains were grown on LB find more agar or in LB broth. When necessary, the following antibiotics were added at the indicated concentrations: kanamycin, 50 μg/ml; ampicillin, 100 μg/ml. Growth

analysis of bacteria in LB broth was carried out by first inoculating one isolated colony in 2 ml LB broth and culturing at 37°C and 250 RPM overnight (about 16 hours). Thirty microliters of the overnight culture were then inoculated into 3 ml of LB broth and cultured Terminal deoxynucleotidyl transferase at 37°C and 250 RPM. At time points of 0, 2, 4, 6, 8, 10, 12, 14, 16, and 24 hours after inoculation, 100 microliters of bacterial culture were collected and used for analysis by

limiting dilution in sterile 96-well plates, and then plated on LB agar plates to determine their CFU (colony forming unit)/ml. Each sample was analyzed in triplicate and the analysis was repeated at least twice. The average value of CFU/ml was used to generate the growth curve. Construction of plasmids and tagged mutants Plasmid constructs that were used in the study are listed in Table1. Construct pUC-H1PF1 was generated to contain the sequence coding for the FLAG epitope and the kanamycin resistance cassette, and was used as the template to amplify the DNA fragments for homologous targeting inSalmonellaST14028s strain [43]. The primers used to construct the tagged mutants are listed in Table3. For each tagged mutant, a pair of primers was designed to amplify the FLAG epitope and kanamycin resistance gene coding sequences using pUC-H1PF1 as the template [43]. The FLAG epitope is an octapeptide tag (N-DYKDDDDK-C) that has been widely used for tagging a protein, which in turn can be detected and studied using the anti-FLAG antibody [21].

Gupta S, Johnson MM, Murthy R, Ahrar K, Wallace MJ, Madoff DC, McRae SE, Hicks ME, Rao S, www.selleckchem.com/products/srt2104-gsk2245840.html Vauthey JN, Ajani JA, Yao JC: Hepatic arterial embolization and chemoembolization for the treatment of patients with metastatic neuroendocrine tumors: variables affecting response rates and survival. Cancer 2005,104(8):1590–1602.PubMedCrossRef 41. Schell SR, Camp ER, Caridi JG, Hawkins IF Jr: Hepatic artery embolization for control of symptoms, octreotide requirements, and tumor progression in metastatic carcinoid tumors. J Linsitinib research buy Gastrointest Surg 2002,6(5):664–670.PubMedCrossRef 42. Hanssen LE, Schrumpf E, Kolbenstvedt AN, Tausjø J, Dolva LO: Treatment of malignant metastatic midgut carcinoid tumours

with recombinant human alpha2b interferon with or without prior hepatic artery embolization. Scand J Gastroenterol 1989,24(7):787–795.PubMedCrossRef 43. Wangberg B, Westberg G, Tylén U, Tisell L, Jansson S, Nilsson O, Johansson V, Scherstén T, Ahlman H: Survival of patients with disseminated midgut E1 Activating inhibitor carcinoid tumors after aggressive tumor reduction. World J Surg 1996,20(7):892–899. discussion 899PubMedCrossRef

44. Eriksson BK, Larsson EG, Skogseid BM, Löfberg AM, Lörelius LE, Oberg KE: Liver embolizations of patients with malignant neuroendocrine gastrointestinal tumors. Cancer 1998,83(11):2293–2301.PubMedCrossRef 45. Brown KT, Koh BY, Brody LA, Getrajdman GI, Susman J, Fong Y, Blumgart LH: Particle embolization of hepatic neuroendocrine metastases for control of pain Selleckchem CHIR-99021 and hormonal symptoms. J Vasc Interv Radiol 1999,10(4):397–403.PubMedCrossRef 46. Chamberlain RS, Canes D, Brown KT, Saltz L, Jarnagin W, Fong Y, Blumgart LH: Hepatic neuroendocrine metastases: does intervention alter outcomes? J Am Coll Surg 2000,190(4):432–445.PubMedCrossRef 47. Ruutiainen AT, Soulen MC, Tuite CM, Clark

TW, Mondschein JI, Stavropoulos SW, Trerotola SO: Chemoembolization and bland embolization of neuroendocrine tumor metastases to the liver. J Vasc Interv Radiol 2007,18(7):847–855.PubMedCrossRef 48. Ho AS, Picus J, Darcy MD, Tan B, Gould JE, Pilgram TK, Brown DB: Long-term outcome after chemoembolization and embolization of hepatic metastatic lesions from neuroendocrine tumors. AJR Am J Roentgenol 2007,188(5):1201–1207.PubMedCrossRef 49. Kamat PP, Gupta S, Ensor JE, Murthy R, Ahrar K, Madoff DC, Wallace MJ, Hicks ME: Hepatic arterial embolization and chemoembolization in the management of patients with large-volume liver metastases. Cardiovasc Intervent Radiol 2008,31(2):299–307.PubMedCrossRef 50. Pitt SC, Knuth J, Keily JM, McDermott JC, Weber SM, Chen H, Rilling WS, Quebbeman EJ, Agarwal DM, Pitt HA: Hepatic neuroendocrine metastases: chemo- or bland embolization? J Gastrointest Surg 2008,12(11):1951–1960.PubMedCentralPubMedCrossRef 51. Sward C, Johanson V, Nieveen van Dijkum E, Jansson S, Nilsson O, Wängberg B, Ahlman H, Kölby L: Prolonged survival after hepatic artery embolization in patients with midgut carcinoid syndrome. Br J Surg 2009,96(5):517–521.PubMedCrossRef 52.