Ann Surg Oncol 2012, 19:612–619.PubMedCrossRef 10. Dubois RN, Abramson SB, Crofford L, Gupta RA, Simon LS, Van De Putte LB, Lipsky PE: Cyclooxygenase in biology and disease. FASEB J 1998, 12:1063–1073.PubMed 11. Tsujii M, Kawano S, Tsuji S, Sawaoka H, Hori M, DuBois RN: Cyclooxygenase regulates angiogenesis induced by colon cancer cells. Cell 1998, 93:705–716.PubMedCrossRef GDC-0068 cost 12. Dannenberg

AJ, Altorki NK, Boyle JO, Dang C, Howe LR, Weksler BB, Subbaramaiah K: Cyclo-oxygenase 2: a pharmacological target for the prevention of cancer. Lancet Oncol 2001, 2:544–551.PubMedCrossRef 13. Dannenberg AJ, Subbaramaiah K: Targeting cyclooxygenase-2 in human neoplasia: rationale and promise. Cancer Cell 2003, 4:431–436.PubMedCrossRef 14. Chan G, Boyle JO, Yang

EK, Zhang F, Sacks PG, Shah selleck compound JP, Edelstein D, Soslow RA, Koki AT, Woerner BM, Masferrer JL, Dannenberg AJ: Cyclooxygenase-2 expression is up-regulated in squamous cell carcinoma of the head and neck. Cancer Res 1999, 59:991–994.PubMed 15. Gallo O, Franchi A, Magnelli L, Sardi I, Vannacci A, Boddi V, Chiarugi V, Masini E: Cyclooxygenase-2 pathway correlates with VEGF expression in head and neck cancer. Implications for tumor angiogenesis and metastasis. Neoplasia 2001, 3:53–61.PubMedCentralPubMedCrossRef 16. Kyzas PA, Stefanou D, Agnantis NJ: COX-2 expression correlates with VEGF-C and lymph node metastases in patients with head and neck squamous cell carcinoma. Mod Pathol 2005, 18:153–160.PubMedCrossRef 17. Wiese FW, Thompson PA, Kadlubar FF: Carcinogen substrate specificity of human COX-1 and COX-2. Carcinogenesis 2001, 22:5–10.PubMedCrossRef 18. Tsujii M, DuBois RN: Alterations in cellular adhesion and apoptosis in epithelial cells overexpressing prostaglandin endoperoxide synthase 2. Cell 1995, 83:493–501.PubMedCrossRef 19. Sun Y, Tang XM, Half E, Kuo MT, Sinicrope FA: Cyclooxygenase-2 overexpression reduces apoptotic Fenbendazole susceptibility by inhibiting the cytochrome

c-dependent apoptotic pathway in human colon cancer cells. Cancer Res 2002, 62:6323–6328.PubMed 20. Stolina M, Sharma S, Lin Y, Dohadwala M, Gardner B, Luo J, Zhu L, Kronenberg M, Miller PW, Portanova J, Lee JC, Dubinett SM: Specific inhibition of cyclooxygenase 2 restores antitumor reactivity by altering the balance of IL-10 and IL-12 synthesis. J Immunol 2000, 164:361–370.PubMedCrossRef 21. Sharma S, Yang SC, Zhu L, Reckamp K, Gardner B, Baratelli F, Huang M, Batra RK, Dubinett SM: Tumor cyclooxygenase-2/prostaglandin E2-dependent promotion of FOXP3 expression and CD4+ CD25+ T regulatory cell activities in lung cancer. Cancer Res 2005, 65:5211–5220.PubMedCrossRef 22.

L. asiaticus’ has provided information on the metabolic features

of this bacterium and key insights into HLB pathogenesis [11]. In addition, the genome sequence has facilitated the development of DNA markers for genetic analysis; these molecular genetic markers are critical for understanding the genetic diversity of global populations and the epidemiology of HLB. DNA markers have been used for characterization GSK2126458 concentration of microbial populations associated with plant diseases, including RAPDs, SNPs, MLST and SSRs (microsatellites) [12–15]. Molecular genetic markers not only aid in the general characterization of a given population, but can help identify the source of an introduced pathogen [16]. Among RG-7388 concentration the three HLB-associated Liberibacter species, ‘Ca. L. asiaticus’

is the most widespread and is responsible for increasing economic losses of citrus industries. Much attention has been drawn by researchers in the last few years to the importance of understanding the epidemiology and ecology of the disease associated with ‘Ca. L. asiaticus’. ‘Ca. L. asiaticus’ isolates were characterized in some previous studies; most of these studies focused on the Asian continent and utilized conserved genes as genetic markers. For example, southeast Asian isolates were characterized by sequencing the 16S rDNA and 16S/23S regions, omp, the rpl gene cluster, and the bacteriophage-type DNA polymerase [17]. The 16S rDNA was employed for understanding genetic diversity of ‘Ca. L. asiaticus’ in India [18] and a prophage gene was used to reveal variations in China [19]. However, genetic variation within conserved genes has limited discriminatory power to differentiate closely-related isolates within populations. Microsatellite DNA markers associated with hypervariable

Dynein sequence regions can provide sufficient resolution for differentiating closely-related isolates and for tracking genotypes of interest; additionally, these markers may help identify the source of invasive strains. Recently, similar types of markers have been used for differentiating ‘Ca. L. asiaticus’ in Japan [20]. Chen et al. [21] studied populations from Guangdong province in China and Florida in the United States. However, the single variable locus used in that study provided limited characterization of ‘Ca. L. asiaticus’ genetic diversity. Here, we report a panel of seven polymorphic microsatellite markers for conducting genetic analyses of ‘Ca. L. asiaticus’ isolates from Asia (India, China, Cambodia, Vietnam, Thailand, Taiwan, and Japan), North America (Florida, USA) and South America (São Paulo, Brazil). The microsatellite profile for each isolate was compared with all members of the sample set to make predictions on the possible origin and dissemination of HLB in Florida. Results PCR amplification and characteristic of microsatellite loci A total of 287 ‘Ca. L.

Occup Environ Med 61(10):861–866CrossRef Naclerio RM et al (1983) Mediator release BMS-354825 ic50 after nasal airway challenge with allergen. Am Rev Respir Dis 128(4):597–602 Nielsen J, Welinder H, Ottosson H, Bensryd I, Venge P, Skerfving S (1994) Nasal challenge shows pathogenetic relevance of specific IgE serum antibodies for nasal symptoms caused by hexahydrophthalic anhydride. Clin Exp Allergy 24(5):440–449CrossRef Nielsen J, Welinder H, Bensryd I, Rylander LSS (2006) Ocular and airway symptoms related to organic acid anhydride exposure—a prospective stud.

Allergy 61(6):743–774CrossRef Parra FMIJ, Quirce S, Ferrando MC, Martin JA, Losada E (1992) Occupational asthma in a hairdresser caused by persulphate salts. Allergy 47(6):656–660CrossRef Quirce SLC, de Blay F, del Pozo V, Van Gerth Wijk R, Maestrelli P, Pauli G, Pignatti P, Raulf-Heimsoth M, Sastre J, Storaas T, Moscato G (2010) Noninvasive methods for assessment of airway inflammation in occupational settings. Allergy 65(4):445–458CrossRef Riise T, Moen BMN (2003) Occupation, lifestyle factors and health related quality of life The Hordaland Health Stud. J Occup Environ Med 45(3):324–332CrossRef

Ronda E, Hollund BE, Moen this website BE (2009) Airborne exposure to chemical substances in hairdresser salons. Environ Monit Assess 153(1–4):83–93. doi:10.​1007/​s10661-008-0338-y CrossRef Sublett JW, Bernstein DI (2010) Occupational rhinitis. Curr Allergy Asthma Rep 10(2):99–104. doi:10.​1007/​s11882-010-0094-2 CrossRef Sullivan M, Karlsson J (1998) The Swedish SF-36 Health Survey III. Evaluation of criterion-based validity: results from nor native

population. J Clin Epidemiol 51(11):1005–1113CrossRef Sullivan M, Karlssson J, Taft C (2002) SF-36 Hälsoenkät: Svensk Manual Rebamipide och Tolkningsguide, 2:a upplagan (Swedish Manual and Interpretation Guide, 2nd Edition) Taft C, Karlsson J, Sullivan M (2004) Performance of the Swedish SF-36 version 2.0. Qual Life Res 13(1):251–256CrossRef Terreehorst I et al (2004) Comparison of a generic and a rhinitis-specific quality-of-life (QOL) instrument in patients with house dust mite allergy: relationship between the SF-36 and Rhinitis QOL Questionnaire. Clin Exp Allergy 34(11):1673–1677CrossRef Valovirta E, Myrseth S, Palkonen S (2008) The voice of the patients: allergic rhinitis is not a trivial disease. Curr Opin Allergy Clin Immunol 8(1):1–9. doi:10.​1097/​ACI.​0b013e3282f3f42f​ CrossRef van Gerth Wijk R (2002) Allergy: a global problem quality of life. Allergy 57:1097CrossRef van Gerth Wijk R, Patiwael J, de Jong N, de Groot H, Burdorf A (2011) Occupational rhinitis in bell pepper greenhouse workers: determinants of leaving work and the effects of subsequent allergen avoidance on health-related quality of life. Allergy 66(7):903–908. doi:10.​1111/​j.​1398-9995.​2011.

Menopause 2003 May–Jun; 10 (3): 214–7.CrossRefPubMed 27. Demarque D, Jouanny J, Poitevin B, et al. Pharmacologie et matière médicale homéopathique. 3rd ed. Paris: Editions CEDH (Centre d’Enseignement et de Developpement de L’homeopathie), 2003 28. Guermonprez M, Pinkas M, Torck M. Matière médicale homéopathique. 2nd ed. Sainte Foy-lès-Lyon: Edition

Boiron, 1997 29. Relton C, Weatherley-Jones E. Homeopathy service LY294002 manufacturer in a National Health Service community menopause clinic: audit of clinical outcomes. J Br Menopause Soc 2005 Jun; 11 (2): 72–3.CrossRefPubMed 30. Bordet MF, Colas A, Marijnen P, et al. Treating hot flushes in menopausal women with homeopathic treatment: results of an observational study. Homeopathy 2008 Jan; 97 (1): 10–5.CrossRefPubMed www.selleckchem.com/products/NVP-AUY922.html 31. Carpenter JS. The Hot Flash Related Daily Interference Scale: a tool for assessing the impact

of hot flashes on quality of life following breast cancer. J Pain Symptom Manage 2001 Dec; 22 (6): 979–89.CrossRefPubMed 32. Heinemann LAJ, Potthoff P, Schneider HPG. International versions of the Menopause Rating Scale (MRS). Health Qual Life Outcomes 2003 Jul 30; 1: 28.CrossRefPubMed 33. Sloan JA, Loprinzi CL, Novotny PJ, et al. Methodologic lessons learned from hot flash studies. J Clin Oncol 2001 Dec 1; 19 (23): 4280–90.PubMed 34. MacLennan AH, Broadbent JL, Lester S, et al. Oral oestrogen and combined oestrogen/progestogen Edoxaban therapy versus placebo for hot flushes. Cochrane Database Syst Rev 2004 Oct 18;(4):CD002978PubMed 35. Freeman EW, Sherif K. Prevalence of hot flushes and night sweats around the world: a systematic review. Climacteric 2007 Jun; 10 (3): 197–214.CrossRefPubMed 36. Benigni JP, Allaert FA, Desoutter P, et al. The efficiency of pain control using a thigh pad under the elastic stocking in patients following venous stripping: results of a case-control study. Perspect Vasc Surg Endovasc Ther 2011 Dec; 23 (4): 238–43.CrossRefPubMed”
“Attention-deficit hyperactivity disorder (ADHD) is characterized by inattention, hyperactivity, and impulsivity.[2] Globally, ADHD affects approximately

5–10% of children[3] and persists into adolescence in up to 85% of affected individuals.[4] Psychostimulants, such as methylphenidate and amfetamine, are the mainstay of treatment in ADHD.[2] A patch that delivers methylphenidate transdermally (methylphenidate transdermal system; Daytrana®) has been developed for the treatment of ADHD. The patch comprises a backing layer, an adhesive formulation that incorporates methylphenidate and uses DOT Matrix™ technology, and a protective liner, which is removed prior to application.[5] The features and properties of methylphenidate transdermal system (including available patch sizes and the nominal methylphenidate dose delivered by each patch size) are shown in table I. Once applied to the skin, methylphenidate transdermal system releases methylphenidate continuously.

This definition of the moment of inertia is consistent with that defined by Martin et al. [26] and other published

selleck products literature. In the above equations, CSMI u and CSMI v depend on the particular choice of the Cartesian coordinate system (u, v axes) of the 2D slice, which is in turn patient position dependent. CSMI w , although calculated as a sum of the latter two moment terms, is independent of patient position. This can be seen by noting that the distance term (\( \tildeu^2 + \tildev^2 \)) is the square Fluorouracil cell line of the distance to the normal axis (w) and is not affected by the choice of the 2D coordinate system within the slice. Thus, CSMI w , also called the polar CSMI, is the natural choice

for a 2D slice. Therefore, for the primary comparison to CSMIHSA, we have chosen CSMIQCT to be equal to CSMI w . Section modulus (Z) in cubic centimeters is CSMI divided by the distance of the furthest contributing bone pixel from the axis around which CSMI is calculated. Width represents the outer diameter of the bone at the

ROI (Fig. 1). For HSA, this is termed the “sub-periosteal width” and is the distance calculated between the blur-corrected edges of the BMC profile [27]. Blur correction adjusts the DXA image for the apparent increase in size due to the partial volume effect. For the QCT slice, it is the distance between the edges of the bone in the QCT slice at the angle of the DXA PA view. This slice has been extracted from the QCT volume after segmentation, which added minor partial volume artifacts due to an additional interpolation step. As shown in Fig. 1, width is calculated along u to Acesulfame Potassium ensure co-registration with the DXA PA view. Femoral neck axis length (FNAL) assessment did not use co-registration between the DXA image and QCT dataset because minor rotational positioning errors of the femur during PA DXA image acquisition caused errors in the placement of the FNAL when propagated to the QCT dataset. Instead, a plane perpendicular to the narrowest part of the femoral neck was automatically found on the QCT dataset.

4% vs 52.9%, respectively; P = 0.17), and serious adverse events of infections were reported in 3.4% of placebo subjects and 4.1% of denosumab subjects (P = 0.14) [8]. About 40% of the serious adverse events of infection (41.3% with placebo and 44.7% with denosumab) were of mild or moderate severity, although they met the regulatory definition of “serious adverse events.” Usually, the “serious” definition was applied due to hospitalization of the subject. The number of subjects discontinuing the study as a result of adverse events of infection was low and similar Crizotinib in vivo between treatment groups

(four placebo, three denosumab; Table 1). No increased risk for fatal infections was observed with denosumab (six placebo, six denosumab; Table 1). Table 1 Summary of adverse events and serious adverse events of infection   Placebo (N = 3,876), n (%) Denosumab (N = 3,886), n (%) P value Adverse events of infections 2,108 (54.4) 2,055 (52.9) 0.1721 Serious adverse events of infection 133 (3.4) 159 (4.1) 0.1399 Serious opportunistic

infection 3 (<0.1) 4 (0.1) 0.7130 AEs of infection leading to study discontinuation 4 (0.1) 3 (<0.1) 0.6979 Fatal infections 6 (0.2) 6 (0.2) 0.9787 Serious adverse events of infections over CAL-101 chemical structure time The incidence of serious adverse events of infection across the 3 years of study was examined. The rate of infection did not change with increasing duration of denosumab exposure (Table 2). The rates of known bacterial, viral, and fungal infections also did not increase with duration of denosumab exposure (Table 2). Table 2 Incidence of serious adverse events of infections by year of study and microbial classification   Year 1 Year 2 Year 3 Incidence of serious adverse events of infection by year        Placebo 42 (1.1%) 49 (1.3%) 47 (1.4%)  Denosumab 55 (1.4%) 58 (1.6%) 54 (1.5%) Positively identified bacterial infections        Placebo 10 (0.3%) 12 (0.3%)

10 (0.3%)  Denosumab 13 (0.3%) 15 (0.4%) 19 (0.5%) Positively identified viral infections        Placebo 0 (0.0%) 1 (<0.1%) 5 (0.1%)  Denosumab 2 (0.1%) 4 (0.1%) 2 (0.1%) Positively identified fungal infections        Placebo 1 (<0.1%) 0 (0.0%) 0 (0.0%) Ixazomib datasheet  Denosumab 1 (<0.1%) 0 (0.0%) 1 (<0.1%) Opportunistic infections Serious adverse events of opportunistic infections were prospectively identified as events of interest. The incidence of serious adverse events of opportunistic infections was low and similar in the placebo (three [<0.1%]) and denosumab (four [0.1%]) groups [8]. No clear pattern in the type of infections was observed. In the placebo group, all three subjects had tuberculosis (preferred terms of tuberculosis or pulmonary tuberculosis) and one event was fatal. In the denosumab group, the opportunistic infections were tuberculosis (two subjects), aspergillosis of the face, and disseminated herpes zoster.

A p < 0.05 was considered significant, whereas not significant (n.s.) difference was associated with a p ≥ 0.05. Statistics were performed RG7420 in comparison with LPS-stimulated PCT-untreated cells (LPS + SF), and the exact significance index

is indicated on the top of the horizontal line encompassing the two statistically compared bars Figure 4 In vitro effect of different concentrations of PCT on S. typhimurium LPS-induced release of IL-10 evaluated by cytokine biochip array. Human PBMC were cultured for 24 h with the following mixtures which had been pre-incubated at 37°C for 30 min: Sterile saline fluid (SF) plus 50 ng/ml PCT (SF + PCT 50); SF plus 500 ng/ml PCT (SF + PCT 500); SF plus 5000 ng/ml PCT (SF + PCT 5000); LPS of S. typhimurium Selleck BI2536 SL1102 (100 ng/ml) plus SF (LPS + SF); LPS (100 ng/ml) plus 50 ng/ml PCT (LPS + PCT 50); LPS (100 ng/ml) plus 500 ng/ml PCT (LPS + PCT 500); LPS (100 ng/ml) plus 5000 ng/ml PCT (LPS + PCT 5000). Results are presented as means ± SEM

of at least four experiments each carried out in duplicate. Statistical significance between groups was assessed by Student’t test. A p < 0.05 was considered significant. Statistics were performed in comparison with LPS-stimulated PCT-untreated cells (LPS + SF), and the exact significance index is indicated on the top of the horizontal line encompassing the two statistically compared bars. The release of IL-4 was not affected by PCT (data not shown). Direct assay (trypan blue test and acridine orange vital staining) of cellular viability always indicated a percentage of more than 95% viable cells in any experimental group, even after 24 h of PBMC incubation, which would indicate that the observed reduction in cytokine release may not be due to cellular toxicity by PCT, LPS or both. Also cell count was carried out at beginning and at the end of each experiment and

these values were not significantly different. Therefore a decrease of cell number should be excluded as a possible cause of reduced cytokine release, during the experiments which involved PCT. Discussion The main and novel findings of the present study are the PCT-induced decrease of bacterial LPS reactivity and the reduction of LPS- induced release of some cytokines/chemokines by PCT in human Megestrol Acetate PBMC. Previous studies from our group [10, 11] and from other investigators [12], demonstrated that antimicrobial peptides (teicoplanin and magainins) and other biological effective molecules presenting a polycationic structure, can neutralize both the LAL reactivity and other effects of LPS including cytokine release [9, 13]. An examination of the PCT primary structure reveals that relevant polycationic motifs (sequence of at least 2–3 bibasic aminoacids within a sequence of four) are present in the whole molecule. Therefore, the whole PCT molecule may account for binding and neutralizing the LPS as well as inhibiting the LPS-stimulated mediators.

2 eV [17, 24] and if it is possible to obtain a p-type ZnO by thermal oxidation of the n-type Zn3N2 NWs Paclitaxel which would be important for device applications. Conclusion Zn3N2 NWs with

diameters of 50 to 100 nm and a cubic crystal structure have been grown on 1 nm Au/Al2O3 between 500°C and 600°C under a steady gas flow of NH3 containing H2. These exhibited a large optical band gap of 3.2 eV determined from absorption-transmission steady state spectroscopy. The surface oxidation of Zn3N2 is expected to lead to the formation of a Zn3N2/ZnO core-shell NW, the energy band diagram of which was calculated via the self-consistent solution of the Poisson-Schrödinger equations within the effective mass approximation by taking into account a fundamental energy band gap of 1.2 eV for Zn3N2. Uniform Zn3N2 layers were obtained on Au/Si(001), while no deposition took place on plain Si(001), in contrast to the case of ZnO NWs which grow with or without a catalyst on Si(001) via the reaction of Zn with O2. References 1. Othonos A, Zervos M, Pervolaraki M: Ultra fast carrier relaxation of InN nanowires grown by reactive vapor transport. Nanoscale Res Lett 2009, 4:122.CrossRef

2. Tsokkou D, Othonos A, Zervos M: Defect states of CVD grown GaN nanowires: effects and mechanisms in the relaxation of carriers. J Appl Phys 2009, 106:054311.CrossRef 3. Zervos M, Othonos A: Gallium hydride vapor phase epitaxy of GaN nanowires. find more Nanoscale Res Lett 2011, 6:262.CrossRef 4. Wang ZL: Nanostructures of ZnO. Materials Today 2004, 7:26.CrossRef 5. Othonos A, Zervos M, Tsokkou D: Tin oxide nanowires: influence of trap states on ultra fast carrier relaxation. Nanoscale Res Lett 2009, 4:828.CrossRef 6. Zervos M, Othonos A: Synthesis of tin nitride nanowires by chemical vapor deposition. Nanoscale Res Lett 2009, 4:1103.CrossRef 7. Zervos M, Othonos A: Enhanced growth and photoluminescence Idoxuridine properties of Sn x N y ( x > y ) nanowires grown by halide chemical vapor deposition. J Crystal Growth 2011,

316:25.CrossRef 8. Zong F, Ma H, Ma J, Du W, Zhang X, Xiao H, Ji F, Xue C: Structural properties and photoluminescence of zinc nitride nanowires. Appl Phys Lett 2005, 87:233104.CrossRef 9. Zong F, Ma H, Xue C, Du W, Zhang X, Xiao H, Ma J, Ji F: Structural properties of zinc nitride empty balls. Mat Lett 2006, 60:905.CrossRef 10. Khan WS, Cao C, Ping DY, Nabi G, Hussain S, Butt FK, Cao T: Optical properties and characterization of zinc nitride nanoneedles prepared from ball-milled Zn powders. Mat Lett 2011, 65:1264.CrossRef 11. Khan WS, Cao C: Synthesis, growth mechanism and optical characterization of zinc nitride hollow structures. J Crystal Growth 1838, 2010:312. 12. Futsuhara M, Yoshioka K, Akai OT: Structural, electrical and optical properties of zinc nitride thin films prepared by reactive rf magnetron sputtering. Thin Solid Films 1998, 32:274.CrossRef 13.

Biswas C, Zhang Y, DeCastro R, Guo H, Nakamura T, Kataoka H, Nabeshima K: The human tumor cell derived collagenase stimulatory factor (renamed EMMPRIN) is a member of the immunoglobulin superfamily. Cancer Res 1995, 55:434–439.PubMed 42.

Yurchenko V, Pushkarsky T, Li JH, Dai WW, Sherry B, Bukrinsky M: Regulation of CD147 cell surface expression: involvement of the proline residue in the CD147 transmembrane domain. J Biol Chem 2005, 280:17013–17019.PubMedCrossRef 43. Boulos S, Meloni BP, Arthur PG, Majda B, Bojarski C, Knuckey NW: Evidence this website that intracellular cyclophilin A and cyclophilin A/CD147 receptor-mediated ERK1/2 signalling can protect neurons against in vitro oxidative and ischemic injury. Neurobiol Dis 2006, 25:54–64.PubMedCrossRef 44. Zheng J, Koblinski JE, Dutson LV, Feeney YB, Clevenger CV: Prolyl isomerase cyclophilin A regulation of Janus-activated kinase 2 and the progression of human breast cancer. Cancer Res 2008, 68:7769–7778.PubMedCrossRef 45. Kim J, Choi TG, Ding Y, Kim Y, Ha KS, Lee KH, Kang I, Ha J, Kaufman RJ, Lee J, Choe W, Kim selleck chemicals llc SS: Overexpressed cyclophilin B

suppresses apoptosis associated with ROS and Ca2+ homeostasis after ER stress. J Cell Sci 2008, 121:3636–364.PubMedCrossRef 46. Fang F, Flegler AJ, Du P, Lin S, Clevenger CV: Expression of cyclophilin B is associated progression and regulation with malignant of genes implicated in pathogenesis of breast cancer. Am J Pathol 2009,174(1):297–308.PubMedCrossRef Janus kinase (JAK) 47. Gomi S, Nakao M, Niiya F, Imamura Y, Kawano K, Nishizaka S, Hayashi A, Sobao Y, Oizumi K, Itoh K: A cyclophilin B gene encodes antigenic epitopes recognized by HLA-A24-restricted and tumorspecific CTLs.

J Immunol 1999, 163:4994–5004.PubMed 48. Mi Z, Oliver T, Guo H, Gao C, Kuo PC: Thrombin-cleaved COOH-terminal osteopontin peptide binds with cyclophilin C to CD147 in murine breast cancer cells. Cancer Res 2007, 67:4088–4097.PubMedCrossRef 49. Marzo I, Brenner C, Zamzami N, Susin SA, Beutner G, Brdiczka D, Rémy R, Xie ZH, Reed JC, Kroemer G: The permeability transition pore complex: a target for apoptosis regulation by caspases and bcl-2- related proteins. J Exp Med 1998, 187:1261–1271.PubMedCrossRef 50. Lin DT, Lechleiter JD: Mitochondrial targeted cyclophilin D protects cells from cell death by peptidyl prolyl isomerization. J Biol Chem 2002, 277:31134–31141.PubMedCrossRef 51. Halestrap A: Biochemistry: A pore way to die. Nature 2005, 434:578–579.PubMedCrossRef 52. Tanveer A, Virji S, Andreeva L, Totty NF, Hsuan JJ, Ward JM, Crompton M: Involvement of cyclophilin D in the activation of a mitochondrial pore by Ca2+ and oxidant stress. Eur Biochem J 1996, 238:166–172.CrossRef 53. Eliseev RA, Malecki J, Lester T, Zhang Y, Humphrey J, Gunter TE: Cyclophilin D interacts with Bcl2 and exerts an anti-apoptotic effect. J Biol Chem 2009, 284:9692–9699.PubMedCrossRef 54.