MCF-7 cancer

cells in the medium were inoculated subcutan

MCF-7 cancer

cells in the medium were inoculated subcutaneously to mice in the amount of 2 × 106 cells per mouse at the right axilla, and the subcutaneous tumor growth in each mouse was monitored. The length and width of tumors were determined using a vernier caliper, and the tumor volume (V) was calculated as AZD6244 purchase V = d 2 × D / 2, where d and D are the shortest and the longest diameter of the tumor in millimeters, respectively [30]. When the tumor volume reached approximately 50 mm3 (set as the 0 day), treatments were performed. The mice were randomly divided into three groups (each group has five mice, n = 5). The two formulations of paclitaxel, i.e., the drug-loaded CA-PLA-TPGS Fosbretabulin order nanoparticles and Taxol®,

were injected intra-tumorally at a single dose of 10 mg PTX/kg in PBS on days 0, 4, and 8. Physiological saline served as control. Mice were sacrificed by decapitation 12 days after treatment. The terminal tumor weight (mg) was determined and applied to evaluate the antitumor effects. Statistical methods All experiments were performed LGX818 supplier at least three times unless otherwise mentioned. Student’s t test statistical analysis was carried out with SPSS 17.0 software, with P < 0.05 considered to indicate a significant difference. Results and discussions Characterization of CA-PLA-TPGS copolymers In order to confirm the formation of the CA-PLA-TPGS copolymer, 1H NMR spectrum is recorded and is shown in Figure 1A. For the CA-functionalized star-shaped polymer CA-PLA-TPGS, the typical signals from CA moiety, TPGS

moiety, and LA monomer repeating units can be observed. 1H NMR (CDCl3): a (δ = 1.62 ppm, LA repeating unit: -CHCH 3), b (δ = 5.21 ppm, LA repeating unit: -CHCH3), c (δ = 3.65 ppm, TPGS repeating unit: -CH 2CH 2O-), d (δ = 0.50 to 2.40 ppm, CA moiety: -CH 2- and -CH-), e (δ = 4.38 ppm, terminal hydroxyl group of CA-PLA: -CHOH). Figure 1B shows the FTIR spectra of the CA-PLA-TPGS copolymer and TPGS. The carbonyl band of TPGS appears at 1,730 cm-1. For the CA-PLA-TPGS copolymer, the carbonyl band was shifted to 1,755 cm-1. Overlapping of the CH stretching band of PLA at 2,945 cm-1 and that of TPGS at 2,880 cm-1 was observed. The absorption band at 3,400 to 3,650 Megestrol Acetate cm-1 is attributed to the terminal hydroxyl group, and that at 1,050 to 1,250 cm-1 is due to the C-O stretching. The results confirmed that the CA-PLA-TPGS copolymer was synthesized by ring-opening polymerization. Figure 1 1 H NMR and FTIR spectra. (A) Typical 1H NMR spectrum of the CA-PLA-TPGS copolymer. (B) FTIR spectra of the CA-PLA-TPGS copolymer (black) and TPGS (blue). Nanoparticle fabrication PTX-loaded CA-PLA-TPGS nanoparticles were produced by a modified nanoprecipitation method, in which acetone was chosen as an acceptable solvent. Nanoprecipitation could provide a mild, facile, and low energy input method for the fabrication of polymeric nanoparticles [31].

Infect Immun 1997, 65:1172–1180 PubMed

16 Tannaes T, Buk

Infect Immun 1997, 65:1172–1180.PubMed

16. Tannaes T, Bukholm IK, Bukholm G: High relative content of lysophospholipids of Helicobacter pylori mediates increased risk for ulcer disease. FEMS Immunol Med Microbiol 2005, 44:17–23.SGC-CBP30 supplier PubMedCrossRef 17. Marshall BJ, Warren JR: Unidentified curved bacilli in the stomach of patients with gastritis and peptic ulceration. Lancet 1984, 1:1311–1315.PubMedCrossRef 18. You YH, Song YY, Meng FL, He LH, Zhang MJ, Yan XM, et al.: Time-series gene expression profiles in AGS cells stimulated with Helicobacter pylori. Cilengitide research buy World J Gastroenterol 2010, 16:1385–1396.PubMedCrossRef 19. Wang SY, Shen XY, Wu CY, Pan F, Shen YY, Sheng HH, et al.: Analysis of whole genomic expression profiles of Helicobacter pylori related chronic atrophic gastritis with IL-1B-31CC/-511TT genotypes. J Dig Dis 2009, 10:99–106.PubMedCrossRef 20. Shibata W, Hirata Y, Yoshida H, Otsuka M, Hoshida Y, Ogura K, et al.: NF-kappaB and ERK-signaling pathways contribute to the gene expression induced by cag PAI-positive-Helicobacter pylori infection.

World J Gastroenterol 2005, 11:6134–6143.PubMed 21. Sepulveda AR, Tao H, Carloni E, Sepulveda J, Graham MDV3100 order DY, Peterson LE: Screening of gene expression profiles in gastric epithelial cells induced by Helicobacter pylori using microarray analysis. Aliment Pharmacol Ther 2002,16(Suppl 2):145–157.PubMedCrossRef 22. Nagasako T, Sugiyama T, Mizushima T, Miura Y, Kato M, Asaka M: Up-regulated Smad5 mediates apoptosis of gastric epithelial cells induced by Helicobacter pylori infection. J Biol Chem 2003, 278:4821–4825.PubMedCrossRef 23. Maeda S, Otsuka M, Hirata Y, Mitsuno

Y, Yoshida H, Shiratori Y, et al.: cDNA Dolutegravir mw microarray analysis of Helicobacter pylori-mediated alteration of gene expression in gastric cancer cells. Biochem Biophys Res Commun 2001, 284:443–449.PubMedCrossRef 24. Liu YJ, Yan PS, Li J, Jia JF: Expression and significance of CD44s, CD44v6, and nm23 mRNA in human cancer. World J Gastroenterol 2005, 11:6601–6606.PubMed 25. Lim JW, Kim H, Kim KH: Cell adhesion-related gene expression by Helicobacter pylori in gastric epithelial AGS cells. Int J Biochem Cell Biol 2003, 35:1284–1296.PubMedCrossRef 26. Kim N, Park WY, Kim JM, Park YS, Lee DH, Park JH, et al.: Analysis of gene expression profile of AGS cells stimulated by Helicobacter pylori adhesion. Gut Liver 2007, 1:40–48.PubMedCrossRef 27. Han YH, Liu WZ, Shi YZ, Lu LQ, Xiao SD, Zhang QH: Gene expression profile of Helicobacter pylori in response to growth temperature variation. J Microbiol 2009, 47:455–465.PubMedCrossRef 28. Ding SZ, Torok AM, Smith MF Jr, Goldberg JB: Toll-like receptor 2-mediated gene expression in epithelial cells during Helicobacter pylori infection. Helicobacter 2005, 10:193–204.PubMedCrossRef 29. Guillemin K, Salama NR, Tompkins LS, Falkow S: Cag pathogenicity island-specific responses of gastric epithelial cells to Helicobacter pylori infection.

From this band, ten sequences out of 12 obtained were related to

From this band, ten sequences out of 12 obtained were related to the

genus Curvibacter (class of β-proteobacteria), the two other sequences corresponding to the genus Burkholderidia (class of β-proteobacteria) (Table 5). Three other sequenced bands were visible in all treatments but they MK-0457 clinical trial increased significantly in intensity at the end of incubation (both B3 and B4 in Vfinal of LA1, B8 in VFfinal of GSK1120212 solubility dmso LB2). These three excised bands were related to the phylum Actinobacteria (with B3 affiliated to the clade acI) (Figure 4 and Table 5). Finally, the three last bands chosen to be sequenced appeared (B5 in Vfinal and VFfinal of LA2) or disappeared (both B6 and B7 in VFAfinal of LB1) at the end of incubation (Figure 4). These ones were all affiliated to the phylum Actinobacteria

(as were 85% of the sequenced DGGE bands). Note that the excised band B1 (LA1 experiment), related to the phylum Cyanobacteria (Table 5), disappeared at the end of the incubation in both VF and V treatments. Table 5 Phylogenetic information about the OTUs

corresponding BVD-523 to the excised and sequenced DGGE bands Bands N° Number of sequenced clones OTUs Nearest uncultivated species accession no°,% similarity B1 12 Phylum: Picocyanobacteria Synechococcus sp AY224199, 98% B2 10 Class: β-proteobacteria Genus: Curvibacter EU703347, 98 EU642369, 99% B2 1 Class: β-proteobacteria Genus: Burkholderia EU642141, 98% B2 1 Class: β-proteobacteria Genus: Burkholderia EU801155, 97% EU63973669, 96% B3 9 Phylum: Actinobacteria Clade: acI FJ916243, 99% B4 11 Phylum: Actinobacteria Unidentified FN668296, 99% B5 10 Phylum: Actinobacteria Unidentified FN668268, 100% B5 1 Unclassified bacteria Florfenicol   B6 12 Phylum: Actinobacteria Unidentified FJ916291, 99% B7 11 Phylum: Actinobacteria Unidentified DQ316369, 99% B8 8 Phylum: Actinobacteria Unidentified AJ575506, 99% B8 3 Unclassified bacteria   Cluster analyses based on quantification of the band position and intensity (Figure 5) showed that, for each lake, the bacterial community structure was clearly different according to the period (early spring/summer) (Figure 5).

These proteins are considered to be involved in the regulation of

These proteins are considered to be involved in the regulation of paracellular permeability. The TJ effect can be documented by reduction in transepithelial electrical resistance (TER). Some bacterial pathogens manipulate the apical-junctional complex from the apical surface. The cellular cascade induced in Enteropathogenic Escherichia coli (EPEC) infection, which leads to decrease in TER, is not well understood. One such strategy is to target the regulatory elements of the actin cytoskeleton. EPEC infects the apical XAV-939 concentration surface of intestinal epithelial cells and modifies the actin cytoskeleton

by PD-1/PD-L1 targets forming actin-rich pedestals beneath the attached bacteria, firmly anchoring the bacterium to the host cell [5]. Changes in the host cell actin cytoskeleton could lead to a loss of absorptive surfaces in intestinal epithelial cells and account for the persistent diarrhea often associated with EPEC infection. Control of perijunctional actin may be also the final effector mechanism in modulating paracellular permeability

[6]. It is increasingly recognized that Lactobacillus plantarum (L. plantarum) has the ability to protect against EPEC-induced damage of the epithelial monolayer barrier function by preventing changes in host cell morphology, attaching/effacing (A/E) lesion formation, monolayer resistance, and macromolecular permeability [7–10]. In recent years, Moorthy G et al [11] evaluated the effect of L. rhamnosus and L. acidophilus on the maintenance of intestinal membrane integrity during S. dysenteriae 1-induced diarrhea in rats. They found that induced rats showed a significant reduction C-X-C chemokine receptor type 7 (CXCR-7) in the membrane-bound ATPases and reduced expression of TJ proteins in the membrane, coupled with their increased expression in the cytosol, indicating membrane damage. Transmission electron microscopic studies correlated with biochemical parameters. Pretreatment with combination of L. rhamnosus and L. acidophilus significantly prevented these changes. However, the

cellular mechanism involved in this protective effect still remained to be clarified. The aim of this study was to investigate the molecular mechanisms underlying the beneficial effects of the L. plantarum. Moreover, as infections with Enteroinvasive Escherichia coli (EIEC) were accompanied by the disruption of epithelial integrity was also asked whether the presence of L. plantarum would influence the otherwise deleterious barrier disruption of caco-2 cells caused by EIEC bacteria. The permeability, the distribution and expression of tight junction proteins (such as Claudin-1, Occludin, JAM-1 and ZO-1) and the cytoskeleton were examined when infected with EIEC or adhesived of L. plantarum after infection. Results L.

It includes a wide array of symptoms from mild flushing and itchi

It includes a wide array of symptoms from mild flushing and itching to lethal anaphylaxis. The pathogenic mechanisms by which the reactions occur are still unclear, although

they seem to vary SC79 widely among agents. The exact prevalence of these reactions is difficult to evaluate, and such a problems is hindering the establishment of treatments. Previously, pharmacoepidemiological studies have been conducted to confirm that adverse events have accompanied the use of cisplatin, carboplatin, and oxaliplatin [6, 7]. More than a million case reports on adverse events (AERs) submitted to the US Food and Drug Administration (FDA) database Quisinostat nmr were used, and a statistically significant association with an adverse event was detected as a signal, by applying standardized official pharmacovigilance methods [8–14]. This database relies on reports of spontaneous adverse events to the FDA generated

by health professionals, consumers, and manufacturers, and the system is referred ACY-738 to as the Adverse Event Reporting System (AERS). These platinum agents have been proven to cause nausea, vomiting, acute renal failure, neutropenia, thrombocytopenia, and peripheral sensory neuropathy [6]. In terms of susceptibility, their rank-order was consistent with clinical observations, suggesting the usefulness of the AERS database and the data mining method used [6]. The National Cancer Institute Common Terminology Criteria for Adverse Events (NCI-CTCAE) version 4.0 was applied to evaluate the susceptibility to hypersensitivity reactions, and carboplatin

and oxaliplatin were proved to cause mild, GPX6 severe, or lethal reactions [7]. However, the same analytical method failed to detect signals for cisplatin-associated reactions [7]. In the present study, AERs submitted to the FDA were analyzed to detect signals for HSRs caused by paclitaxel, docetaxel, procarbazine, asparaginase, teniposide, and etoposide, in order to more clarify the critical factors to reproduce the clinical observations on HSRs. Additionally, agents thought to be associated with HSRs were also analyzed, including doxorubicin, 6-mercaptopurine, 5-fluorouracil, cyclophosphamide and cytarabine. Methods Data sources Input data for this study were taken from the public release of the FDA’s AERS database, which covers the period from the first quarter of 2004 through the end of 2009. The data structure of AERS is in compliance with international safety reporting guidance, ICH E2B, consisting of 7 data sets; patient demographic and administrative information (DEMO), drug/biologic information (DRUG), adverse events (REAC), patient outcomes (OUTC), report sources (RPSR), drug therapy start and end dates (THER), and indications for use/diagnosis (INDI). The adverse events in REAC are coded using preferred terms (PTs) in the Medical Dictionary for Regulatory Activities (MedDRA) terminology.

The inference of ozone and the timing of this so-called “great ox

The inference of ozone and the timing of this so-called “great oxidation event” (GOE) at 2.4 Ga comes primarily from analyses of sulfur isotopes in the rock record. The analyses and the interpretation, described by Farquhar et al. (2010) is based on the mass independent isotopic fractionation of sulfur. Basically, there are four stable sulfur isotopes, 32S, 33S, 34S and 36S. Virtually all reactions that involve formation or the breaking of this website chemical check details bonds among these isotopes

is mass-dependent, that is the isotope with the smaller mass is reactive (has a higher zero point kinetic energy) and the resulting products are predicted from first principles to be enriched in the lighter isotope. However, up until ~2.4 Ga, the isotopic fractionations in the geologic record are mass independent. SO2 has a UV absorption cross section, peaking at ~200 nm. Breaking of bonds by high energy photons does not lead to mass dependent isotopic fractionation. Hence, one interpretation of the mass independent fractionation is that short wave UV radiation reached the Earth’s surface prior to ~2.4 Ga, but subsequently that radiation was quenched. Stratospheric ozone absorbs short wave UV radiation on the contemporary Earth, and the source of ozone is O2. Hence, the loss of the mass independent isotopic fractionation of sulfur at 2.4 Ga suggests a change in

the oxidation state of Earth’s atmosphere. The mass independent fractionation signal Vistusertib order for S never returned, and hence, it is concluded that the transition from an anaerobic world to an oxidized world occurred once, and only Methane monooxygenase once, in Earth’s history. It should be noted that the concentration of oxygen that arose during the GOE is extremely poorly constrained. Formation of stratospheric ozone is not limited by O2 above ca.

0.1% of the present atmospheric level. Geochemists use other proxies, including N isotopes (Godfrey and Falkowski 2009), transition metal composition and isotopic values (Kaufman et al. 2007) and even mineral composition (Hazen et al. 2008) to further attempt to constrain the concentration of oxygen during the GOE and to understand what controlled the net accumulation of the gas over the ensuing 2.3 billion years. Geological contingencies High concentrations of free molecular oxygen in a planetary atmosphere cannot come about simply by high energy photolysis of water; that reaction is self quenching as UV becomes increasingly blocked. Further, as in all redox reactions, a reductant (the equivalent of hydrogen) is formed. To bring about a change in the oxidation state of the atmosphere, the redox reactions cannot be at equilibrium, but rather the reductant has to be removed and stored for long periods of geological time. Hence, the evolution of oxygenic photosynthesis was a necessary, but not sufficient condition for the oxidation of the planetary surface. In a simple geochemical sense, net production of oxygen on Earth implies the burial and sequestration of reductant.

Chitosan is water soluble in acidic conditions

due to pro

Chitosan is water soluble in acidic conditions

due to protonation of primary amines in the chitosan chains. The Ag NP suspension was also acidic (pH 5.23 to 6.25) [25]. Although the acidity of these two solutions was maintained during mixing, partial precipitation of the Ag NP/Ch composites was observed at all conditions tested, suggesting that Selleck C646 decreased solubility of the chitosan chains was induced by the binding of Ag NPs to URMC-099 the chitosan amino and hydroxyl groups [28]. Addition of excess NaOH completely precipitated the composite. Figure 1 shows a typical SEM micrograph of the composite. Ag NP/Ch composites were obtained as flocculated, aggregated, spherical sub-micrometer particles. The composites were yellow or brown; darker composites were obtained when larger amounts of Ag NPs were reacted with the chitosan. Figure 2 shows UV-visible spectra of the original Ag NP suspension and of the reaction mixes containing high amounts of Ag NP. Since spherical Ag NPs provide a peak near 400 nm [25, 29], the absence of this peak shows that

Ag NPs are not present in the supernatant of the post-reaction mixture and that the Ag NPs were completely bound to the chitosan. Figure 1 A SEM micrograph of chitosan/SN129. Weight ratio of Ag NPs in the composite is 23.5 wt%. Figure 2 UV-visible spectra of the original Ag NP suspension and of the post-reaction mixture supernatant. Akt inhibitor Solid line and dashed line correspond to the original Ag NP suspension and the post-reaction mixture supernatant, respectively. (a) SN35 and the supernatants obtained from 1 mg of chitosan and 328.5 μg of SN35, (b) SN65 and the supernatants obtained from 1 mg of chitosan and 279 g μof SN65, (c) SN129 and the supernatants obtained from 1 mg of chitosan and 308 μg of SN129. The peak due to Ag NPs is marked with a vertical line. The supernatants were obtained from

the post-reaction mixture of 1 mg of chitosan Terminal deoxynucleotidyl transferase and 328.5 μg of SN35 (dotted line), 279 μg of SN65 (short dashed line), and 308 μg of SN129 (long dashed line). The solid line corresponds to the original suspension of SN129. TEM micrographs of the Ag NPs and Ag NP/Ch composites are shown in Figure 3. Compared to Ag NPs before reaction, Ag NPs in the composites are dispersed in the chitosan matrix and appear as uneven gray domains. The thickness of the TEM specimen of the composites is uneven due to the direct casting of the composite floc. Uneven contrast of the chitosan domains is due to the uneven thickness of the specimen. Ag NPs in thick areas of the chitosan matrix are overlapped. Meanwhile, Ag NPs in thin areas appeared non-overlapped. The particle sizes of Ag NPs in the composites are similar to that of the original Ag NPs. Although some minor aggregation of Ag NPs was observed, there was no macroscopic aggregation, showing that the particle size of the Ag NPs in the Ag NP/Ch composites was controlled. Figure 3 TEM micrographs of Ag NPs. (a) SN35, (b) SN65, (c) SN129; Ag NP/Ch composites (d) 24.7 wt% of SN35, (e) 21.

Stud Mycol 64:1–15PubMedCrossRef Seifert RA, Samuels GJ (2000) Ho

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Can J Bot 65:373–405CrossRef Shoemaker RA, Babcock CE (1989a) Bricookea barrae n. sp. compared with Bricookea sepalorum. Stud Mycol 31:165–169 Shoemaker RA, Babcock CE (1989b) Phaeosphaeria. Can J Bot 67:1500–1599CrossRef Oxymatrine Shoemaker RA, Babcock CE (1989c) Diadema. Can J Bot 67:1349–1355CrossRef Shoemaker RA, Babcock CE (1992) Applanodictyosporous LY2603618 mw Pleosporales: Clathrospora, Comoclathris, Graphyllium, Macrospora, and Platysporoides. Can J Bot 70:1617–1658CrossRef Shoemaker RA, Kokko EG (1977) Aglaospora profusa. Fungi Canadenses No.101 Shoemaker RA, LeClair PM (1975) Type studies of Massaria from the Wehmeyer collection. Can J Bot 53:1568–1598CrossRef Silva-Hanlin DMW, Hanlin RT (1999) Small subunit ribosomal RNA gene phylogeny of several loculoascomycetes and its taxonomic implications. Mycol Res 103:153–160CrossRef Simmons EG (1952) Culture studies in the genera Pleospora, Clathrospora, and Leptosphaeria. Mycologia 44:330–365 Simmons EG (1971) Helminthosporium allii as type of a new genus. Mycologia 63:380–386CrossRef Simmons EG (1985, publ. 1986) Perfect states of Stemphylium II. Sydowia 38:284–293 Simmons EG (1986) Alternaria themes and variations (22–26). Mycotaxon 25:287–308 Simmons EG (1989) Perfect states of Stemphylium III. Mem New York Bot Gdn 49:305–307 Simmons EG (1990) Embellisia and related teleomorphs.

The resulting mutant strain was designated 81–176cj0596 To confi

The resulting mutant strain was designated 81–176cj0596. To confirm that mutation of the cj0596 gene did AMN-107 order not alter the expression of the putative co-transcribed cj0597 gene, quantitative real-time RT-PCR was AZD1152 supplier performed on RNA samples harvested from 81–176 and 81–176cj0596. These studies confirmed that mRNA levels downstream of the mutation in 81–176cj0596 were equivalent to those in 81–176, and that the mutation was non-polar (data not shown). However, to ensure that any phenotypes of the cj0596 mutant were specific for cj0596, we subsequently isolated a reversion of the mutation by replacing the rpsl HP /cat cassette with a wild-type cj0596 gene. Analogous to the counterselection system of Dailidiene

et al. [49], use of the H. pylori rpsL gene decreased background gene conversion events and facilitated the recovery of cells in which the mutagenized cj0596 allele was replaced with the wild-type cj0596 gene. This process was extremely efficient, as ~70% of the recovered streptomycin-resistant colonies contained the desired reversions of the cj0596 mutation. Mutation of cj0596 causes a moderate growth defect of C. jejuni in MH broth The role of Cj0596 in Campylobacter growth was studied by comparing the growth rates of C. jejuni 81–176, 81–176cj0596, and 81–176cj0596 + in MH broth (Figure 5). When inoculated at OD600 ~ 0.06 and growth rate was measured by OD600 (Figure 5A), the mutant initially appeared to have a significant

growth defect illustrated both by a slower increase in OD600 and a lower maximum OD600. However, we also found that a ICG-001 research buy similar starting OD600 resulted in a significantly lower starting CFU for the mutant, indicating that Teicoplanin the OD600 did not accurately reflect

the number of cj0596 mutant CFU. We then grew the mutant under two starting conditions: one had the same starting OD600 as the wild-type and revertant (OD600 ~ 0.06) and the other had approximately the same starting CFU (OD600 ~ 0.2) as the wild-type and the revertant. The mutant inoculated at OD600 ~ 0.2 showed a faster initial increase in OD600, but reached a similar maximum OD600 as the mutant inoculated at OD600 ~ 0.06. However, when growth rate was monitored by plating for viable counts (Figure 5B), the mutant had an initial growth rate more similar to that of wild-type, although both mutant cultures yielded final viable counts lower than wild-type. Wild-type growth characteristics were restored in the revertant strain. Together, these data suggest that mutation of cj0596 resulted in a moderate growth defect, especially later in the growth curve, and that the cj0596 mutant had apparent changes in cell characteristics such that the OD600 had poor concordance with CFU measurements. Figure 5 Growth of C. jejuni strains at 37°C in MH broth. Strains 81–176 (black diamonds), 81–176cj0596 (“”low”" inoculum, red triangles) and 81–176cj0596 + (blue squares) were inoculated at an OD600 of ~0.

J Leukoc Biol 2002, 71:669–676 PubMed 28 Nickoloff BJ, Riser BL,

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protein FAT10 forms covalent conjugates and induces apoptosis. J Biol Chem 2001, 276:35334–35343.PubMedCrossRef 36. Xanthou G, Duchesnes CE, Williams TJ, Pease JE: CCR3 functional responses are regulated by both CXCR3 and its ligands CXCL9, CXCL10 and CXCL11. Eur J Immunol 2003, 33:2241–2250.PubMedCrossRef 37. Singal DP, Ye M, Quadr SA: Major histocompatibility-encoded human proteasome LMP2. Genomic organization and a new form of mRNA. J Biol Chem 1995, 270:1966–1970.PubMedCrossRef 38. Mishto M, Bonafe M, Salvioli S, Olivieri F, Franceschi C: Age dependent impact of LMP polymorphisms on TNFalpha-induced apoptosis in human peripheral Amylase blood mononuclear cells. Exp Gerontol 2002, 37:301–308.PubMedCrossRef 39. Zimmerer JM, Lesinski GB, Radmacher MD, Ruppert A, Carson WE 3rd: STAT1-dependent and STAT1-independent gene expression in murine immune cells following stimulation with interferon-alpha. Cancer Immunol Immunother 2007, 56:1845–1852.PubMedCrossRef 40. Schmidtke G, see more Eggers M, Ruppert T, Groettrup M, Koszinowski UH, Kloetzel PM: Inactivation of a defined active site in the mouse 20S proteasome complex enhances major histocompatibility complex class I antigen presentation of a murine cytomegalovirus protein. J Exp Med 1998, 187:1641–1646.PubMedCrossRef 41.