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NA, Kapadia NN, de Hoff AL3818 cell line PL, Hirsch AM: Investigations of Rhizobium biofilm formation. FEMS Microbiol Ecol 2006, 56:195–206.PubMedCrossRef 38. Wells DH, Chen EJ, Fisher RF, Long SR: ExoR is genetically coupled to the ExoS-ChvI two-component system and located in the periplasm of Sinorhizobium meliloti. Mol Microbiol 2007, 64:647–664.PubMedCrossRef 39. Yao SY, Luo L, Har KJ, Temozolomide ic50 Becker A, Rüberg S, Yu GQ, Zhu JB, Cheng HP: Sinorhizobium meliloti ExoR and ExoS proteins regulate both succinoglycan and flagellum production. J Bacteriol 2004, 186:6042–6049.PubMedCrossRef 40. Davies BW, Walker GC: Identification of novel Sinorhizobium meliloti mutants compromised for oxidative stress protection and symbiosis. J Bacteriol 2007, 189:2110–2113.PubMedCrossRef 41. Gupta RS: Evolution of the chaperonin families (Hsp60, Hsp10, and Tcp-1) of proteins and the origin of eukaryotic cells. Mol Microbiol 1995, 15:1–11.PubMedCrossRef 42. Movahedi S, Waites W: A two-dimensional protein 6-phosphogluconolactonase gel electrophoresis study of the heat stress response of Bacillus subtilis cells during sporulation. J Bacteriol

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In addition, collaboration with renal medicine is essential to avoid introduction of dialysis. Also we should consider how we could help patients by treatment to live long actively in the society. Open Access This article is distributed under the terms of the Creative Commons Attribution License which permits any use, distribution,

and reproduction in any medium, provided the original author(s) and the source are credited. References 1. Dispenzieri A, et al. Treatment of newly diagnosed NCT-501 concentration multiple myeloma based on Mayo Stratification of Myeloma and Risk-adapted Therapy (mSMART): consensus statement. Mayo Clin Proc. 2007;82:323–41.PubMed 2. Bergsagel DE, et al. Myeloma proteins and the clinical response to melphalan therapy. Science. 1965;148(3668):376–7. 3. Salmon SC, et al. Intermittent

FRAX597 manufacturer high dose prednisone therapy for multiple myeloma. Cancer Chemother Rep. 1967;51:179–87.PubMed 4. Alexanian R, et al. Treatment for multiple myeloma. Combination chemotherapy with different melphalan dose regimens. JAMA. 1969;208(9):1680–5.PubMedCrossRef 5. Kyle RA, et al. A long-term study of prognosis AZD1480 cost in monoclonal gammopathy of undetermined significance. N Engl J Med. 2002;346:564–9.PubMedCrossRef 6. San Miguel JF, et al. Bortezomib plus melphalan and prednisone for initial treatment of multiple myeloma. N Engl J Med. 2008;359(9):906–17. 7. Kumar SK, et al. Improved survival in multiple myeloma and the impact of novel therapies. Blood. 2008;111(5):2516–20.PubMedCrossRef 8. Hideshima T, et al. Intracellular protein degradation and its therapeutic implications. Clin Cancer Res. 2005;11(24 Pt 1):8530–3.PubMedCrossRef 9. Fayers PM, et al. Thalidomide for previously untreated elderly patients with multiple myeloma: meta-analysis of 1685 individual patient data from 6 randomized clinical trials. Blood. 2011;118:1239–47.PubMedCrossRef 10. Richardson PG, et al. Bortezomib or high-dose dexamethasone for relapsed multiple myeloma. N Engl J Med. 2005;352(24):2487–98. 11. San Miguel JF, et

al. ASH2011. http://​myeloma.​org/​pdfs/​ASH2011_​San%20​Miguel_​3619.​pdf. 12. Suzuki K. Discovery research on the effects of giving continuity to the administration of bortezomib in maintenance therapy to target of relapsed and refractory multiple myeloma. J New Rem Clin. Florfenicol 2012;61:1259–69. 13. Durie BGM, et al. International uniform response criteria for multiple myeloma. Leukemia. 2006;20(9):1467–73. 14. Niesvizky R, et al. The relationship between quality of response and clinical benefit for patients treated on the bortezomib arm of the international, randomized, phase 3 APEX trial in relapsed multiple myeloma. Br J Haematol. 2008;143(1):46–53.PubMedCrossRef 15. Harousseau JL, et al. The role of complete response in multiple myeloma. Blood. 2009;114(15):3139–46.PubMedCrossRef 16. Chanan-Khan A, et al. Importance of achieving a complete response in multiple myeloma, and the impact of novel agents. J Clin Oncol. 2010;28(15):2612–24.PubMedCrossRef 17.

A sequence type (ST), based on the allelic profile of the seven amplicons, was assigned to each strain. The sequences of all new alleles and the composition of the new STs identified are available from http://​pubmlst.​org/​sagalactiae/​.​ Strains were grouped into clonal complexes (CCs) with eBURST software [35]. An eBURST clonal complex (CC) was defined as all allelic profiles sharing six identical alleles with at least one other member of the group. The term “”singleton ST”" refers to a ST that did not cluster into a CC. Identification of VNTR loci Tandem repeats were

identified in the sequenced genomes of the three reference strains, NEM316, A909 and 2603 V/R, with the Microbial Tandem Repeats Database http://​minisatellites.​u-psud.​fr[36] and the Tandem https://www.selleckchem.com/products/ca-4948.html Repeats Finder program [37]. AZD1390 datasheet We determined the size of the repeat sequence and the number of repeat units for the three reference strains. BLAST analysis was carried out to determine

whether the repeats were located within or between genes and to identify a hypothetical function for the open reading frame involved. The TR locus name was defined according to the following nomenclature: common name_size of the repeat sequence_size of the amplicon for the reference strain_corresponding number of repeats (Table 1). The primers used for amplification targeted the 5′ and 3′ flanking

regions of selected loci and matched the sequences present at these positions in the Protein kinase N1 genomes of strains NEM316, A909 and 2603 V/R. We initially selected and evaluated 34 tandem repeats with repeat units of more than 9 bp in length. Some TRs were not present in all the strains, some were present in all strains and displayed no polymorphism, and others were too large for amplification in standard conditions. Six TRs were retained for this study, selected on the basis of their greater FHPI price stability and discriminatory power for four of the six (Table 1). Table 1 Characteristics of the 6 VNTR loci selected for MLVA scheme to genotype the 186 strains of S. agalactiae VNTR1 Repeat size bp2 Putative function3 Expected number of repeats4 PCR product bp5 Number of alleles min-max size of amplicons (bp) HGDI 6       2603 V/R A909 NEM316         SAG2_32pb_244pb_3U 32 Non-cds7 3 3 3 244 3 212 – 276 0.474 [0.427 - 0.522] SAG3_24pb_126pb_2U 24 Protein DnaJ 3 2 3 126 2 126 – 150 0.481 [0.452 - 0.511] SAG4_60pb_114pb_1U (SATR1)* 60 Hypothetical protein 3 1 1 114 6 114 – 414 0.713 [0.691 - 0.735] SAG7_18pb_285pb_8U (SATR2)* 18 Hypothetical protein 6 8 – 285 9 231-573 0.745 [0.701 - 0.789] SAG21_48pb_783pb_14U (SATR5)* 48 FbsA – 14 18 783 26 117 – ≈2000 0.893 [0.867 - 0.919] SAG22_159pb_928pb_5U 159 Hypothetical protein 2 5 2 928 7 292 – 1246 0.713 [0.666 – 0.

While the number of OTUs we observed varied little between ATT and SUS bacteria and the two selleck kinase inhibitor groups shared only one-third of their phylogenetic diversity, the archaeal community that colonized our in situ samplers was a distinct subset of the suspended community. Over 90% of ATT archaeal

sequences were from OTUs that were also detected in the SUS fraction, yet 78% of SUS archaeal sequences were not detected in ATT samples (Table 2). This provides strong evidence that the most active and fastest-growing archaeal populations colonized the initially-sterile sediment contained in our in situ samplers. The phylogenetic distinction between ATT and SUS samples (Figure 3) provides further evidence that this is the case, because no such

differentiation of ATT from SUS would be expected if the Staurosporine attachment of cells to the in situ samplers was driven purely by neutral factors such as random adhesion rather than selective colonization [15, 48]. Sequences related to iron-reducing and sulfate-reducing bacteria are much more predominant among the SIS3 cell line ATT communities when compared to their corresponding SUS communities (Figure 6). Geochemical evidence also supports concurrent iron reduction and sulfate reduction processes in this area of the Mahomet aquifer [17, 22]. The near-absence of these functional populations from SUS groundwater samples suggests that their niche is likely

localized to the surface of mineral grains. This makes sense since available ferric iron was associated with the sediment sand used in the traps. This result is not surprising in the case of iron reducers, due to the highly insoluble nature of ferric iron minerals expected in the Mahomet (pH = 7.1–7.9). Iron reducers such as Geobacter require some mechanism of physical attachment to ferric minerals in order to respire [49]. Sulfate, conversely, is highly soluble, cAMP meaning sulfate reducers do not necessarily require attachment to aquifer sediment in order to respire. The greater abundance of apparent sulfate-reducing bacteria in ATT samples relative to SUS may occur because these organisms benefit from proximity to iron reducers, whose generation of ferrous iron prevents toxic sulfide from accumulating in solution [2, 42]. When ferrous iron and sulfide are produced simultaneously, they precipitate as the minerals mackinawite (FeS) and greigite (Fe3S4) [50], limiting the buildup of both reaction products in groundwater and maintaining the thermodynamic drive for each group’s metabolism [51]. Iron reducers have also appeared to benefit from the presence of active sulfate reduction perhaps for the same reason [42]. The predominance of sulfate reducers along with iron reducers in aquifer sediment over groundwater suggests that the two groups may benefit from concurrent respiration.

As seen in Figure 3c, APR-246 cell line the PL spectrum is mainly constituted by the Gaussian peaks around 500 and 575 nm. The visible ZnO emission is due to defects in the sample which can be attributed to the great number of ZnO clusters and the relatively poor ZnO-NC crystallinity, especially at the ZnO-NC/SiO2 interface, as seen in the TEM image (Figure 2a). The ZnO defects are mainly oxygen-related defects. The emission at 417 nm can be assigned to oxygen interstitials [17], while the other visible emissions at 450, 500, and 575 nm can be related

to oxygen vacancies [5, 13, 18]. These defects are consistent with our long annealing data, which will be discussed in the next section. Figure 3 The PL spectra HKI-272 purchase of the samples at various temperatures. (a) Photoluminescence spectra of the ZnO-NCs in the SiO2matrix at various RTP annealing temperatures. (b) The spectrum can be accounted for by two main contributions in the UV-blue and visible regions, respectively. (c) The evolution of various peaks as a function of annealing temperature is shown. For comparison, the volume evolution calculated from the NC size

obtained from the TEM analysis is also shown. The decrease of the signal at high annealing temperature can be roughly accounted for by the decrease of the NC absorption cross section. On the other hand, the few ZnO-NCs that exist in the sample give rise to some UV emission, which results in the broad PL spectrum. At 500°C annealing temperature, the PL spectrum exhibits an overall blueshift which is due to the increase of the UV-blue emission in the sample. As shown in Figure 3c, the RTP annealing at 500°C is accompanied by an increase of the blue and UV emission between 360 and 450 nm and a decrease of defect emissions at higher wavelengths. The drastic change in the emission spectrum of the sample can be attributed to an increase in the ZnO-NCs and the decrease of ZnO clusters in the sample (Figure 2b), which should in turn increase the ZnO near-band-edge emission in the UV region. The emission peak at 378 nm can be related to ZnO near-band-edge (excitonic) emission [19, 20]. The emission peak at 396 nm RAS p21 protein activator 1 could

possibly be related to the electron transition from Zn interstitial to Zn vacancy as reported by Panigrahi et al.[5]. While being relatively weak, it is worth noting the this website appearance of a peak at 360 nm for the smallest NCs for which quantum confinement is expected to occur as already reported in a transmission experiment in solution [16]. Further analysis and especially low-temperature PL measurement are needed to confirm the peak origin. For annealing temperatures higher than 550°C, no drastic change is observed in the shape of the emission spectra, as seen in Figure 3a. Instead, the PL spectra mainly exhibit a decrease in the emission intensity. Indeed the Gaussian fitting analysis shows that the peak amplitudes decreased by the same proportion compared to its value at 500°C.

PubMedCrossRef 26. Park CH, Robicsek A, Jacoby GA, Sahm D, Hooper DC: Prevalence in the United States of aac(6′)-Ib-cr encoding a ciprofloxacin-modifying enzyme. Antimicrob Agents Chemother 2006, 50:3953–3955.PubMedCrossRef 27. Frank T, Gautier V, Talarmin A, Bercion R, Arlet G: Characterization of sulphonamide resistance genes and class 1 integron gene cassettes in Enterobacteriaceae , Central African #Acalabrutinib randurls[1|1|,|CHEM1|]# Republic (CAR). J Antimicrob Chemother 2007, 59:742–745.PubMedCrossRef 28. Carattoli

A, Bertini A, Villa L, Falbo V, Hopkins KL: Identification of plasmids by PCR-based replicon typing. J Microbiol Methods 2005, 63:219–228.PubMedCrossRef 29. Clermont O, Dhanji H, Upton M, Gibreel T, Fox A: Rapid detection of the O25b-ST131 clone of Escherichia coli encompassing the CTX-M-15-producing strains. J Antimicrob Chemother 2009, 64:274–277.PubMedCrossRef

30. Andriamanantena TS, Ratsima E, Rakotonirina HC, Randrianirina F, Ramparany L: Dissemination of multidrug resistant Acinetobacter baumannii in various hospitals of Antananarivo Madagascar. Ann Clin Microbiol Antimicrob 2010, check details 9:17.PubMedCrossRef 31. Pallecchi L, Bartoloni A, Fiorelli C, Mantella A, Di Maggio T: Rapid dissemination and diversity of CTX-M extended-spectrum beta-lactamase genes in commensal Escherichia coli isolates from healthy children from low-resource settings in Latin America. Antimicrob Agents Chemother 2007, 51:2720–2725.PubMedCrossRef 32. Canton R, Coque TM: The CTX-M beta-lactamase pandemic. Curr Opin Microbiol 2006, 9:466–475.PubMedCrossRef 33. Herindrainy P, Randrianirina F, Ratovoson R, Ratsima Hariniana

E, Buisson Y: Rectal carriage of extended-spectrum Beta-lactamase-producing gram-negative bacilli in community settings in madagascar. PLoS One 2011, 6:e22738.PubMedCrossRef 34. Kim J, Kwon Y, Pai H, Kim JW, Cho DT: Survey of Klebsiella pneumoniae strains producing extended-spectrum beta-lactamases: prevalence of SHV-12 and SHV-2a in Korea. J Clin Microbiol 1998, 36:1446–1449.PubMed 35. Lavollay M, Mamlouk K, Frank T, Akpabie A, Burghoffer B: Clonal dissemination of a CTX-M-15 beta-lactamase-producing Escherichia coli strain in the Paris area, Tunis, and Bangui. Antimicrob Agents Chemother 2006, 50:2433–2438.PubMedCrossRef 36. Novais A, Canton R, Moreira R, Peixe L, Baquero F: Emergence and dissemination of Enterobacteriaceae isolates producing CTX-M-1-like enzymes in Spain Diflunisal are associated with IncFII (CTX-M-15) and broad-host-range (CTX-M-1, -3, and −32) plasmids. Antimicrob Agents Chemother 2007, 51:796–799.PubMedCrossRef 37. Nuesch-Inderbinen MT, Kayser FH, Hachler H: Survey and molecular genetics of SHV beta-lactamases in Enterobacteriaceae in Switzerland: two novel enzymes, SHV-11 and SHV-12. Antimicrob Agents Chemother 1997, 41:943–949.PubMed 38. Kasap M, Fashae K, Torol S, Kolayli F, Budak F: Characterization of ESBL (SHV-12) producing clinical isolate of Enterobacter aerogenes from a tertiary care hospital in Nigeria. Ann Clin Microbiol Antimicrob 2010, 9:1.

PT subunits were expressed in E. coli, but unfortunately these failed to assemble into the mature toxin and were insufficiently immunogenic to be considered selleck as potential vaccine candidates

[16]. It is now understood that assembly and secretion of the mature toxin requires several auxiliary genes that were discovered more recently, and these genes are part of the ptl section of the click here ptx-ptl operon [17]. In this publication, we report the construction of recombinant B. pertussis strains expressing increased levels of rPT or rPT and PRN. These strains were generated by a multiple allelic- exchange process: insertion of the mutations that abolish the catalytic activity of subunit S1, insertion of a second copy of the ptx cluster of the five PT structural genes of the ptx-ptl operon with their promoter and terminator into an abandoned gene elsewhere on the chromosome, then insertion of a second copy of the prn gene into a second inactive gene locus. The organization of ptl auxiliary genes present in the ptx-ptl operon was not modified. Enhanced production of rPT and PRN by manipulation of gene copy number has been largely used with multi-copy plasmid vectors and reported to enhance the production of bacterial toxins [18, 19], in particular PT [20]. However,

genes tandemly repeated in this way may have significantly negative consequences on strain genetic stability in a GMP-regulated, vaccine-manufacturing environment. In addition, PRN expression could also be increased by manipulation of the PRN promoter [21]. The allelic-exchange vectors

INCB018424 used in earlier B. pertussis recombinant strains require mutations on the chromosome, particularly the mutation affecting rpsL that results from selection of spontaneous streptomycin-resistant mutants as required in earlier allelic-exchange procedures [22]. Such mutations affecting housekeeping genes may impair virulence, hence the expression of virulence factors including PT, FHA and PRN. In contrary, pSS4245 used in this study harbours streptomycin resistant gene from Tn5 which is functional in B. pertussis but not in E. coli, hence streptomycin was used to select against E. coli donor cell and I-SceI nuclease activity in the plasmid was then functioned as the counter selectable Methane monooxygenase marker in the recombinant B. pertussis through subsequent homologous recombination and does not require or leave auxiliary mutations. The strains reported here produce unaltered levels of the other antigens in particular FHA. These constructs will prove useful for the manufacture of affordable human acellular Pertussis vaccines. Results Mutation of the S1 gene in the B. Pertussis chromosome To introduce the two mutations R9K and E129G into the S1 subunit, a two-stage approach was used to avoid the possibility of recombination in the region between the two mutations that would cause the loss of one of the mutations.

(B, C) The stained membrane after cell invasion demonstrated that Tg737 over expression in HepG2 and MHCC97-H cells led to significantly selleck screening library attenuated cell invasion under hypoxic conditions compared to cells without plasmid transfection under hypoxic conditions. The data are presented as the number of invading cells for each group. (D, Silmitasertib nmr E) The effects of Tg737 over expression on the migration capacity

of hypoxia-treated HCC cells were investigated using a transwell migration assay. The data are presented as the number of migrated cells for each group. I: cells without plasmid transfection; II: cells transfected with pcDNA3.1 (−); III: cells incubated with LipofectamineTM 2000; IV: cells transfected with pcDNA3.1-Tg737. *, P < 0.05 compared to the HepG2 controls; †, P < 0.05 compared to the MHCC97 controls. Original magnification: 200× (B, D). Figure 6 (A, B) HepG2 and MHCC97-H cells were treated as 3-MA in vivo detailed in the legend to Figure 4 . Annexin V assays revealed that the cell viability of HepG2 and MHCC97-H cells transfected

with pcDNA3.1-Tg737 and further incubated with fresh DMEM (1% FBS) for 12 h under hypoxia were not significantly different from cells without plasmid transfection. The data from HepG2 and MHCC97-H cells transfected with pcDNA3.1 (−) or incubated with LipofectamineTM 2000 excluded any liposome/pEGFP-C1-related effects on cell viability.I: cells without plasmid transfection; II: cells transfected with pcDNA3.1 (−); III: cells incubated with LipofectamineTM 2000; IV: cells transfected with pcDNA3.1-Tg737. Polycystin-1, IL-8, and TGF-β1 were associated with the contribution of Tg737 to hypoxia-induced adhesion, migration,

and invasion To further explore the mechanism of action of Tg737 in hypoxia-induced adhesion, migration, and invasion in HCC cells, we examined the effects of Tg737 on the expression/secretion of polycystin-1 and the secretion of IL-8 and TGF-β1, critical regulators of cell invasion and migration. Our data indicated that polycystin-1 protein expression/secretion was downregulated, whereas IL-8 secretion and the active and total TGF-β1 levels were increased by hypoxia treatment. These expression Verteporfin cell line patterns were consistent with Tg737 downregulation compared to normoxia-treated cells. Furthermore, the levels of polycystin-1, IL-8, and TGF-β1 (active and total) in hypoxia-treated HepG2 and MHCC97-H cells could be recovered in both lines by transfection with pcDNA3.1-Tg737. The levels of polycystin-1, IL-8, and TGF-β1 (active and total) were altered with the restored expression of Tg737 (Figure 7A-D). Taken together, these results demonstrated that Tg737 regulated hypoxia-induced adhesion and that migration and invasion capabilities were partially mediated by polycystin-1, IL-8 and, TGF-β1 protein levels, possibly leading to subsequent degradation of the extracellular matrix.

Cancer Biol

Ther 2008, 7:1555–1560.PubMedCrossRef Competing interests The authors declare that they have no competing interests. Authors’ contributions MEI carried out the most experimental work. VH performed the sample collection and Ki67 assays. PM performed the sample collections, provided clinical data. PM, FM, and EW were responsible for the design of the study and its coordination. PM, EW, and FM wrote the manuscript. All authors read and approved the final manuscript.”
“Background Cell proliferation, that represents the essence of cancer disease, involves not only a deregulated control of cell cycle but also adjustments of energy metabolism PSI-7977 in order to fuel cell growth and division. In fact, proliferation of cancer cells is accompanied by glycolysis activation and this altered glucose metabolism is one of the most common hallmark of cancer

[1, 2]. Approximately 60 to 90% of cancers display a metabolic profile, the so-called Warburg phenotype, characterized by their dependence upon glycolysis as the major source of energy, irrespective of the oxygen level [3]. According to the Warburg effect, cancer cells up-regulate glucose transporters, notably GLUT-1, and convert pyruvate, the end-product of glycolysis, into lactate by lactate dehydrogenase (LDH), rather than oxidizing it in mitochondria [4–6]. In this context, the hypoxia inducible factor 1 (HIF-1) has been shown to play a fundamental role [7, 8]. HIF-1 is a transcription factor that consists of Sapanisertib an O2-regulated HIF-1α and a constitutively Carbachol expressed HIF-1β subunit. In cancer cells, HIF-1α is up-regulated and, in turn, activates the expression of glycolytic enzymes (such as LDH) and glucose transporters (such as GLUT-1), and down-regulates the mitochondrial activity through several mechanisms, in particular by inhibiting the conversion of pyruvate to acetyl-CoA via the activation

of the gene encoding pyruvate dehydrogenase kinase 1 [7–10]. Shifting metabolism away from mitochondria (glucose oxidation) and towards the cytoplasm (glycolysis) might suppress apoptosis, a form of cell death that is dependent on mitochondrial energy production [11, 12]. Accordingly, the glycolytic phenotype has been associated to apoptosis resistance and consequently Metabolism inhibitor increased tumor cell proliferation [3, 4, 13]. Understanding the metabolic basis of cancer has the potential to provide the foundation for the development of novel approaches targeting tumor metabolism [14]. In this regard, recent observations suggest that the reversion of the glycolytic phenotype may render tumor cells susceptible to apoptosis and decrease their growth rate [15–17]. With this in mind, we planned to investigate whether the natural supplement Cellfood™ (CF; Nu Science Corporation, CA, USA) might have antiproliferative effects in vitro, limiting cell proliferation and promoting cell death.

Acute tubulointerstitial nephritis associated with autoimmune-related pancreatitis. Am J Kidney Dis. 2004;43:e18–25.PubMedCrossRef 3. Takeda S, Haratake J, Kasai T, Takaeda C, Takazakura E, et al. IgG4-associated idiopathic tubulointerstitial nephritis complicating autoimmune pancreatitis. Nephrol Dial Transplant. 2004;19:474–6.PubMedCrossRef 4. Watson SJ, Jenkins DA, Bellamy JQ-EZ-05 CO. Nephropathy in GSK1210151A research buy IgG4-related systemic disease. Am J Surg Pathol. 2006;30:1472–7.PubMedCrossRef 5. Rudmik L, Trpkov K, Nash C, Kinnear S, Falck V, Dushinski J, et al. Autoimmune pancreatitis associated with renal lesions mimicking metastatic tumours. CMAJ. 2006;175:367–9.PubMedCrossRef

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nephritis successfully treated by high-dose corticosteroid. Mod Rheumatol. 2006;16:176–82.PubMedCrossRef 9. Tsubata Y, Akiyama F, Oya T, Ajiro J, Saeki T, Nishi S, et al. IgG4-related chronic tubulointerstitial nephritis without autoimmune pancreatitis and the time course of renal function. Intern Med. 2010;49:1593–8.PubMedCrossRef 10. Kim F, Yamada K, Inoue D, Nakajima K, Mizushima I, Kakuchi Y, et al. IgG4-related tubulointerstitial nephritis and hepatic inflammatory pseudotumor without hypocomplementemia. Intern Med. 2011;50:1239–44.PubMedCrossRef 11. Saeki T, Nishi S, Imai N, Ito T, Yamazaki M, Kawano M, et al. Clinicopathological characteristics of patients with IgG4-related tubulointerstitial nephritis. Kidney Int. 2010;78:1016–23.PubMedCrossRef 12. Okazaki K, Kawa S, Kamisawa T, Naruse S, Tanaka S, Nishimori I, et al. Clinical diagnostic criteria of autoimmune pancreatitis:

revised proposal. J Gastroenterol. 2006;41:626–31.PubMedCrossRef Ribonucleotide reductase 13. Chari ST, Smyrk TC, Levy MJ, Topazian MD, Takahashi N, Zhang L, et al. Diagnosis of autoimmune pancreatitis: the Mayo Clinic experience. Clin Gastroenterol Hepatol. 2006;4:1010–6.PubMedCrossRef 14. Chari ST, Kloeppel G, Zhang L, Notohara K, Lerch MM, Shimosegawa T. Histopathologic and clinical subtypes of autoimmune pancreatitis: the Honolulu consensus document. Pancreatology. 2010;10:664–72.PubMedCrossRef 15. Deshpande V, Gupta R, Sainani N, Sahani DV, Virk R, Ferrone C, et al. Subclassification of autoimmune pancreatitis: a histologic classification with clinical significance. Am J Surg Pathol. 2011;35:26–35.PubMedCrossRef 16. Yamaguchi Y, Kanetsuna Y, Honda K, Yamanaka N, Kawano M, Nagata M.