, an alphaproteobacterium Chryseobacterium, Pseudomonas and Serr

, an alphaproteobacterium. Chryseobacterium, Pseudomonas and Serratia were genera common to adult male and female A. stephensi. Figure 1 Percentage abundance diagram of culturable isolates and 16S rRNA gene library clones AZD2014 clinical trial from lab-reared (LR) and field-collected (FC) adult male, female and larvae of Anopheles stephensi. Percentage distribution was calculated on the basis of relative abundance in the total PCR amplification. Table 1 Abundance of isolates and clones within the bacterial

domain derived from the 16S rRNA gene sequences of lab-reared adult A. stephensi. Division Adult Male Culturable Adult Male Unulturable Adult Female Culturable Adult Female Unulturable   OTU a Closest database matches OTU Closest database matches OUT Closest database matches OTU Closest database matches CFB group 4(6)b Chryseobacterium meninqosepticum 3(8) C. meninqosepticum 4(6) C. meninqosepticum 2(6) C. meninqosepticum Firmicutes – - 1(1) Elizabethkingia meninqosepticum – - 1(1) E. meninqosepticum Alpha proteobacteria 1(1) Agrobacterium sp. 2(2) A. tumefaciens – - – - Beta proteobacteria – - – - 2(3) Comamonas sp. – - Gamma proteobacteria 3(4) Pseudomonas mendocina 1(1) P. tolaasii 2(2) P. mendocina – -   3(7) Serratia Foretinib concentration marcescens 4(8) S. marcescens 3(5) S. marcescens 3(15) S. marcescens

  – - 1(1) Klebsiella sp. – - 1(2) Serratia sp. Unclassified Bacteria – - 3(3) Uncultured bacterium click here clone – - – - Total 11 (18) Species = 4 15 (24) Species = 7 11 (16) Species = 4 7 (24) Species = 4 Distribution of the isolates and OTUs in taxonomic groups and their abundance in the individual samples are displayed.

a: Operational Taxonomic Units b: Values in parenthesis corresponds Metformin clinical trial to total number of microbial strains identified. Total number of phylotypes observed: Lab-reared adult male A. stephensi = 26 Lab-reared adult female A. stephensi = 18 Analysis of the 16S rRNA gene clone library from lab-reared adult A. stephensi One hundred clones were screened from each lab-reared adult male and female A. stephensi 16S rRNA gene library, out of which 50 clones from each were analyzed further on the basis of sequencing results. The 16S rRNA gene sequencing data of isolates and clones were used to divide them into broad taxonomic groupings. The relative abundance or percent distribution of the taxonomic groups obtained in lab-reared adult A. stephensi is shown in Figure 1. Analysis of the 16S rRNA gene sequence revealed that the libraries were dominated by sequences related to the genus Pseudomonas and Serratia (71% of the clones examined). The majority of the cultured isolates and the 16S rRNA gene library clones belonged to the gammaproteobacteria class. Diversity of bacteria within the 16S rRNA gene libraries from lab-reared male and female A. stephensi was rather low, with relatively few phylotypes.

Clin Cancer Res 1997, 3: 81–85 PubMed 19 Yousef GM, Diamandis

Clin Cancer Res 1997, 3: 81–85.PubMed 19. Yousef GM, Diamandis Selleckchem Stattic EP: The new human tissue kallikrein gene family: structure, function, and association to disease. Endocr Rev 1992, 22: 184–204.CrossRef 20. Berner A, Nesland JM, Waehre H, Silde J, Fosså SD: Hormone resistant prostatic adenocarcinoma. An evaluation of prognostic factors in pre- and post-treatment specimens. Br J Cancer 1993, 68: 380–384.PubMedCrossRef 21. Lilja H, Christensson A, Dahlén U, Matikainen MT, Nilsson O, Pettersson K, Lövgren T: Prostate-specific antigen in serum occurs predominantly in complex with alpha 1-antichymotrypsin. Clin Chem 1991, 37: 1618–1625.PubMed 22. Williams SA, Singh P, Isaacs JT, Denmeade SR: Does PSA play a

role AZD1390 clinical trial as a promoting agent during the initiation and/or progression of prostate cancer? Prostate 2007, 67: 312–329.PubMedCrossRef 23. Oesterling JE: Prostate specific antigen: a critical assessment of the most useful tumor marker for adenocarcinoma of the prostate. J Urol 1991, 145: 907–923.PubMed 24. Stege R, Grande M, Carlström K, Tribukait B, Pousette A: Prognostic significance of tissue prostate-specific antigen in endocrine-treated prostate carcinomas. Clin Cancer Res 2000, 6: 160–165.PubMed 25. Arakawa A, Soh

S, Chakraborty S, Scardino PT, Wheeler TM: Prognostic significance of angiogenesis in clinically localized prostate cancer (staining for Factor VIII-related antigen and CD34 Antigen. Prostate Cancer and Prostatic Dis 1997, 1: 32–38.CrossRef 26. Conway RE, Petrovic N, Li Z, Heston W, Wu D, Shapiro LH:

Prostate-specific membrane antigen regulates angiogenesis by modulating integrin signal transduction. Mol Cell Biol 2006, 26: 5310–5324.PubMedCrossRef 27. Nielson GK, Sojka K, Trumbull K, Spaulding B, Welcher R: Immunohistochemical characterization old of prostate specific membrane antigen expression in the vasculature of normal and neoplastic tissues. Modern Path 2004, 17: 326A. 28. Laidler P, Dulińska J, Lekka M: Expression of prostate specific membrane antigen in androgen-independent prostate cancer cell line PC-3. Arch Biochem Biophys 2005, 435: 1–14.PubMedCrossRef 29. Moul JW: Angiogenesis, p53, bcl-2 and Ki-67 in the progression of prostate cancer after radical prostatectomy. Eur Urol 1999, 35: 399–407.PubMedCrossRef 30. Mannweiler S, Amersdorfer P, Trajanoski S, Terrett JA, King D, Mehes G: Heterogeneity of prostate-specific membrane antigen (PSMA) expression in prostate carcinoma with distant metastasis. Pathol Oncol Res 2009, 15: 167–172.PubMedCrossRef 31. Heidtmann HH, Nettelbeck DM, Mingels A, Jäger R, Welker HG, Kontermann RE: Generation of angiostatin-like fragments from plasminogen by prostate-specific antigen. Br J Cancer 1999, 81: 1269–1273.PubMedCrossRef 32. Sivridis E, PARP cancer Giatromanolaki A, Koukourakis MI: Tumor Angiogenesis Is Associated with MUC1 Overexpression and Loss of Prostate-specific Antigen Expression in Prostate Cancer. Clin Cancer Res 2001, 7: 1533–1538.PubMed 33.

Conclusion Inflammatory myofibroblastic tumor of the tail of panc

Conclusion Inflammatory myofibroblastic tumor of the tail of pancreas should be included in the differential diagnosis of the etiological causes of massively enlarged spleen and spontaneous splenic rupture. References 1. O’Reilly RA: Splenomegaly in 2,505 patients at a large university medical center from 1913 to 1995. 1963 to 1995: 449 patients. West J Med 1998,169(2):88–97.PubMed 2. Bedu-Addo G, Bates selleckchem I: Causes of massive tropical splenomegaly in Ghana. Lancet 2002,360(9331):449–54.CrossRefPubMed 3. Renzulli P, Hostettler A, Schoepfer AM, Gloor B,

Candinas D: Systematic review of atraumatic splenic rupture. Br J Surg 2009, 96:1114–1121.CrossRefPubMed 4. Pettinato G, Manivel JC, De Rosa N, Dehner LP: Inflammatory myofibroblastic tumor (plasma cell granuloma). Clinicopathologic study of 20 cases with immunohistochemical and ultrastructural observations. Am J Clin Pathol 1990, 94:538–546.PubMed 5. Yamamoto H, Watanabe K, Nagata M, Tasaki K, Honda I, Watanabe S, Soda H, Takenouti T: Inflammatory myofibroblastic tumor (IMT) of the

pancreas. J Hepatobiliary Pancreat Surg 2002, 9:116–119.CrossRefPubMed 6. Dishop MK, Warner BW, Dehner LP, Kriss VM, Greenwood MF, Geil JD, Moscow JA: Successful CYT387 nmr treatment of inflammatory myofibroblastic tumor with malignant transformation by surgical resection and chemotherapy. J Pediatr Hematol 2003, 25:153–158.CrossRef INCB28060 7. Coffin CM, Dehner LP, Meis-Kindblom JM: Inflammatory myofibroblastic tumor, inflammatory fibrosarcoma, and related lesions: an historical review with differential diagnostic considerations. Semin Diagn Pathol 1998, 15:102–110.PubMed 8. Meis JM, Enzinger FM: Inflammatory fibrosarcoma of the

mesentery and retroperitoneum. A tumor closely simulating inflammatory pseudotumor. Am J Surg Pathol 1991, 15:1146–1156.CrossRefPubMed 9. Meis-Kindblom JM, Kjellstrom C, Kindblom LG: Inflammatory fibrosarcoma: update, reappraisal, and perspective on its place in the spectrum of inflammatory myofibroblastic tumors. Semin Diagn Pathol 1998, 15:133–143.PubMed 10. Walsh SV, Evangelista F, Khettry U: Inflammatory myofibroblastic pheromone tumor of the pancreaticobiliary region: morphologic and immunocytochemical study of three cases. Am J Surg Pathol 1998, 22:412–418.CrossRefPubMed 11. Wreesmann V, van Eijck CH, Naus DC, van Velthuysen ML, Jeekel J, Mooi WJ: Inflammatory pseudotumour (inflammatory myofibroblastic tumour) of the pancreas: a report of six cases associated with obliterative phlebitis. Histopathology 2001, 38:105–110.CrossRefPubMed 12. Coffin CM, Watterson J, Priest JR, Dehner LP: Extrapulmonary inflammatory myofibroblastic tumor (inflammatory pseudotumor). A clinicopathologic and immunohistochemical study of 84 cases. Am J Surg Pathol 1995, 19:859–872.CrossRefPubMed 13. Misselevitch I, Podoshin L, Fradis M, Naschitz JE, Yeshurun D, Boss JH: Inflammatory pseudotumor of the neck. Otolaryngol Head Neck Surg 1991, 105:864–867.PubMed 14.

It is worth noting that statins have a well-documented anti-infla

It is worth noting that statins have a well-documented anti-inflammatory effect that is independent of infection. For example, Müller et al., found that simvastatin treatment limited pulmonary endothelial injury, attenuated pulmonary hyperpermeability, prevented the recruitment of leukocytes

to the lung, reduced pulmonary cytokine levels and improved oxygenation in mechanically ventilated mice [28]. Thus our findings for HSD are consistent with those of Müller et al. During pneumonia, neutrophils are the primary effector cell responsible for clearance of extracellular bacteria. It was therefore paradoxical that reduced neutrophil infiltration was observed in HSD mice simultaneously to decreased bacterial burden in their lungs. In our hands, simvastatin does not have antibacterial effects in MK-8931 cell line vitro on S. pneumoniae at in vivo concentrations

4SC-202 [13, 29]. Yet, Jerwood et al. have shown that simvastatin has considerable antimicrobial properties against Staphylococcus aureus[30]. Thus we cannot directly rule out killing by simvastatin in vivo. Possible reasons for the reduction in bacterial burden also include lowered PAFr expression in the lungs that would decrease bacterial adhesion and/or enhanced killing ability by resident alveolar macrophages due to enhanced resistance to the cholesterol-dependent toxin pneumolysin [13]. Although not tested in our study, high dose statins has also been reported to increase killing of S. aureus and S. pneumoniae by enhancing the formation of phagocyte extracellular traps in mice fed pulverized rodent chow supplemented with 500 mg/kg simvastatin [11]. For

S. pneumoniae, killing by extracellular traps remains controversial as other investigators have shown that S. pneumoniae is able to resist neutrophil extracellular traps (NETs) due to the presence of BCKDHA a surface localized endonuclease that degrades the DNA scaffold of NETs [31, 32]. Importantly, the discrepancy in disease severity in mice for S. pneumoniae with simvastatin and for K. pneumoniae with lovastatin, as reported by Fessler et al. [10], raises the possibility that statins facilitate differential outcomes depending on the infectious agent. Neutrophils are a primary mediator of lung injury during pneumonia and a study with neutropenic mice infected with S. pneumoniae demonstrated less lung injury and improved survival [33, 34]. Our findings are consistent with these previous publications. In addition to the differences in the class and delivery of statins used between our study and that of Fessler et al., another CP673451 research buy important consideration is that Gram-negative bacteria do not produce cholesterol-dependent cytolysins, such as pneumolysin. Statins might preferentially protect against Gram-positive bacteria.

Am J Physiol Gastrointest

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Afr J Ecol 37:435–438CrossRef Ottichilo WK, Khaemba WM (2001) Val

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Cryobacterium, Rhodococcus, and

Cryobacterium, Rhodococcus, and Veillonella were identified only in the ovary, whereas Anaerobiospirillum was the only genera unique to the gut. The molecular approach applied in this study allowed us to assess the relative abundance of the microbiota associated with R. microplus. The KU-57788 clinical trial predominant genera in the bacterial communities of the

tick samples analyzed based on an abundance cutoff of 1.0% are shown for each sample in Figure 2. Staphylococcus was relatively abundant (> 18%) in adult males and eggs, but not in adult female ticks. Other prevalent genera were Corynebacterium (> 13%) in eggs and adult males, and EGFR inhibitor Coxiella (> 13%) in tick eggs. Achromobacter (27.7%), Pseudomonas (12.6%), and Sinorhizobium (7.7%) were the predominant genera found in adult female ticks. Among the tissues sampled, Coxiella was the most abundant (98.2%) genus in ovary, whereas Anaerobiospirillum (29.5%) and Brachybacterium (21.9%) predominated in the tick gut. Other

relatively less abundant genera, but worth noting, include Borrelia (7.9%) in the tick gut; Clostridium (3.9%) in adult female ticks; Escherichia (1.5%) in the tick gut; Klebsiella (1.3%) in adult female ticks; Streptococcus in eggs (2.9%) and adult males (1.%); Enterococcus in adult male ticks (1.4%), adult female ticks (2.2%), and tick gut (11.4%); and Wolbachia in adult female ticks (1.8%). Figure 2 Relative abundance of bacterial genera in life stages and tissue samples from R. microplus as detected by bTEFAP pyrosequencing. a) Adult female cattle tick. Mean percentages (n = 2). Values below 1% were grouped as “”Other”" with total value of 9.5%. “”Other”" group includes: Staphylococcus (0.7%), check details Bacillus (0.5%),

Streptococcus (0.7%), Vagococcus (0.3%), Pseudobutyrivibrio (0.7%), Nocardioides (0.2%), Asteroleplasma (0.9%), Ruminococcus (0.4%), Escherichia (0.9%), Acetivibrio (0.3%), Erwinia (0.1%), Pedobacter (0.2%), Dermabacter (0.1%), Ornithinicoccus (0.2%), Oribacterium (0.7%), Alkaliflexus (0.2%), Paludibacter (0.5%), Pantoea (0.2%), Cytophaga (0.1%), Mitsuokella (0.1%), PLEK2 Enterobacter (0.1%), Paucisalibacillus (0.4%), Lachnobacterium (0.1%), Caldithrix (0.2%), Shigella (0.1%), Solirubrobacter (0.1%), Rhodobacter (0.1%), Desulfosporosinus (0.1%). b) Adult male cattle tick. Mean percentages (n = 2). Values below 1% were grouped as “”Other”" with total value of 3.8%. “”Other”" group includes: Coxiella (0.1%), Prevotella (0.3%), Rikenella (0.1%), Pseudomonas (0.2%), Escherichia (0.3%), Hallella (0.3%), Pantoea (0.1%), Moraxella (0.7%), Arthrobacter (0.1%), Enhydrobacter (0.1%), Mogibacterium (0.1%), Kocuria (0.5%), Enterobacter (0.1%), Exiguobacterium (0.2%), Lysinibacillus (0.1%), Belnapia (0.1%). c) Cattle tick egg. Mean percentages (n = 3). Values below 1% were grouped as “”Other”" with total value of 6.9%. “”Other”" group includes: Achromobacter (0.3%), Enterococcus (0.1%), Clostridium (0.1%), Serratia (0.7%), Ruminococcus (0.3%), Propionibacterium (0.4%), Klebsiella (0.2%), Acetivibrio (0.

PubMed 55 Beard J, Tobin B: Iron status and exercise American J

PubMed 55. Beard J, Tobin B: Iron A-1210477 research buy status and exercise. American Journal of Clinical Nutrition 2000,72(2):594S-597S.PubMed 56. Wolfram G: Dietary fatty acids and coronary heart disease. Eur J Med Res 2003,20(8):321–4. 57. Jakobsen MU, Reilly EJ, Heitmann BL, Pereira MA, Bälter K, Fraser GE, Goldbourt U, Hallmans G, Knekt P, Liu S, Pietinen P, Spiegelman D, Stevens J, Virtamo J, Willett WC, Ascherio A: Major types of dietary fat and risk of coronary heart disease: a pooled analysis of 11 cohort studies. Am J Clin Nutr 2009,89(5):1425–1432.PubMedCrossRef

58. Mozaffarian D, Aro A, Willett WC: Health effects of trans-fatty acids: experimental and observational evidence. Eur J Clin Nutr 2009,63(Suppl 2):S5–21.PubMedCrossRef 59. Morrison A, Hokanson JE: The

independent relationship between triglycerides and coronary heart disease. Vasc Health MCC950 order Risk Manag 2009,5(1):89–95.PubMed 60. Sarwar N, Danesh J, Eiriksdottir G, Sigurdsson G, Wareham N, Bingham S, Boekholdt SM, Khaw KT, Gudnason V: Triglycerides and the risk of coronary heart disease: 10,158 incident cases among 262,525 participants in 29 HDAC inhibitor review Western prospective studies. Circulation 2007,115(4):450–8.PubMedCrossRef 61. Siri-Tarino PW, Sun Q, Hu FB, Krauss RM: Saturated fat, carbohydrate, and cardiovascular disease. American Journal of Clinical Nutrition 2010,91(3):502–509.PubMedCrossRef 62. Bazzano LA: Effects of soluble dietary fiber on low-density lipoprotein cholesterol and coronary heart disease risk. Curr Atheroscler Rep 2008,10(6):473–477.PubMedCrossRef

63. Anderson JW, Baird P, Davis RH Jr, Ferreri S, Knudtson M, Koraym A, Waters V, Williams PD184352 (CI-1040) CL: Health benefits of dietary fiber. Nutrition Reviews 2009,67(4):188–205.PubMedCrossRef 64. Jenkinson DM, Harbert AJ: Supplements and sports. Am Family Physician 2008,78(9):1039–46. 65. Tunnicliffe JM, Erdman KA, Reimer RA, Shearer LV: Consumption of dietary caffeine and coffee in physically active populations: physiological interactions. J Appl Physiol Nutr Metab 2008,33(6):1301–10.CrossRef 66. Burke LM: Caffeine and sports performance. Appl Physiol Nutr Metab 2008,33(6):1319–34.PubMedCrossRef 67. Ziegler PJ, Jonnalagadda SS, Nelson JA, Lawrence C, Baciak B: Contribution of meals and snacks to nutrient intake of male and female elite figure skaters during peak competitive season. Am Coll Nutr 2002,21(2):114–9. 68. Giovannini M, Agostoni C, Shamir R: Symposium overview: Do we all eat breakfast and is it important? Crit Rev Food Sci Nutr 2010,50(2):97–9.PubMedCrossRef 69. Farshchi HR, Taylor MA, Macdonald IA: Deleterious effects of omitting breakfast on insulin sensitivity and fasting lipid profiles in healthy lean women. Am J Clin Nutr 2005,81(2):388–96.PubMed 70. Keski-Rahkonen A, Kaprio J, Rissanen A, Virkkunen M, Rose RJ: Breakfast skipping and health-compromising behaviors adolescents and adults. Eur J Clin Nutr 2003,57(7):842–53.PubMedCrossRef 71.

1 ± 1 4 yrs, 174 ± 8 7 cm, 78 5 ± 12 kg,) participated in this st

1 ± 1.4 yrs, 174 ± 8.7 cm, 78.5 ± 12 kg,) participated in this study. All subjects signed informed consent documents and the study was approved by the Baylor University Institutional Review Board for the Protection of Human Subjects prior to any data collection. Subjects were not allowed to participate in this study if they LY333531 reported any of the following: 1) current or past history of anabolic steroid use; 2) any metabolic disorders or taking any thyroid, hyperlipidmeic, hypoglycemic, anti-hypertensive, or androgenic medications; 3) ingested any

ergogenic levels of creatine, HMB, thermogenics, ribose, selleck chemical pro-hormones (i.e., DHEA, androstendione, etc.) or other purported anabolic or ergogenic nutritional supplements within 2 months prior to beginning the study; 4) not taking any additional nutritional supplement or contraindicated check details prescription medication during the protocol. Experimental design The study was conducted in a cross-over, randomized, double-blinded,

and placebo-controlled manner. Participants expressing interest in the study were interviewed on the phone/or via email to determine whether they appear to qualify to participate in this study. Participants believed to meet eligibility criteria were then invited to attend an entry/familiarization session. Once reporting to the lab, participants completed a medical history questionnaire and underwent a general physical examination to determine whether they met eligibility

criteria. RVX-208 Once cleared, participants were familiarized to the study protocol via a verbal and written explanation outlining the study design. All eligible participants who agreed to participate in the study read and signed the university-approved informed consent documents. Participants were familiarized with the angled leg press and leg extension machines, the correct technique in performing each of the exercises, and then performed two low-resistance (30% of body mass) practice/warm-up sets of 10 repetitions on each exercise to familiarize them with the protocol and to also insure that they were able to complete the protocol before being formally admitted to the study. Participants then completed an initial strength test to assess their one repetition maximum (1-RM) for each leg on the angled leg press (Nebula Fitness, Inc., Versailles, OH), and leg extension (Body Masters, Inc., Rayne, LA) exercises using standard guidelines routinely employed our laboratory [29]. Following the practice trials, participants were scheduled to return 48 hours later for testing. Participants were asked to not change their dietary habits in any way throughout the study. This was monitored by having each participant document dietary intake for two days before each testing session.

Gene symbol Gene name GO CCL21B chemokine (C-C motif) ligand 21b

Gene symbol Gene name GO CCL21B chemokine (C-C motif) ligand 21b (serine) 1–2 CD276 CD276 antigen 1–2 SPP1 secreted phosphoprotein 1 1–2 CD24 CD24 antigen 1 C1QG EX-527 complement component 1, q subcomponent, gamma polypeptide 1 CD74 CD74 antigen 1 HLA-DMA major histocompatibility complex, class II, DM alpha 1 HLA-DMB major histocompatibility complex, class II, DM beta 1 DEFB1 defensin beta 1 1 FCGR3 Fc receptor, IgG, low affinity III 1 PLSCR1 phospholipid scramblase 1 1 PRNP prion protein 1 RT1-BA RT1 class II, locus Ba 1 RT1-CE5 RT1 class I, CE5 1

RT1-DA RT1 class II, locus Da 1 RT1-DB1 RT1 class II, locus Db1 1 RT1-BB RT1 class II, locus Bb 1 ANXA1 annexin A1 2 FABP4 fatty acid binding protein 4, adipocyte 2 S100A8 S100 calcium binding protein A8 2 S100A9 S100 calcium JNK-IN-8 clinical trial binding protein A9 2 CDC2A cell division cycle 2 homolog A 3 EGR1 early growth response 1 3 CRYAB crystallin, alpha B 3 CCND1 cyclin D1 3 CD36 cd36 antigen 3 GCLC glutamate-cysteine AC220 cell line ligase, catalytic subunit 3 GGT1 gamma-glutamyltransferase 1 3 GPX2 glutathione peroxidase 2 3 GPX3 glutathione peroxidase 3 3 GSR glutathione reductase 3 GSS glutathione synthetase 3 HSPCB heat shock 90 kDa protein 1, beta 3 LAMC1 laminin, gamma 1 3 MTAP2 microtubule-associated

protein 2 3 NOL3 nucleolar protein 3 (apoptosis repressor with CARD domain) 3 NQO1 NAD(P)H dehydrogenase, quinone 1 3 PDLIM1 PDZ and LIM domain 1 (elfin) 3 SLC25A4 solute carrier family 25 3 TXNRD1 thioredoxin reductase 1 3 NOTE: The numbers from 1–3 indicate immune response, inflammatory response and oxidative stress, respectively. Table 5 The down-regulated DEGs sharing from cirrhosis to metastasis stage relating to the following GO process. Gene Symbol Gene Title filipin GO C5 complement component 5 1–2 IL4RA interleukin 4 receptor, alpha 1–2 MBL2 mannose binding lectin 2 (protein C) 1–3 NOX4 NADPH oxidase 4 2–3 ATRN Attractin 2–3 C1S complement component 1, s subcomponent 1 C4BPB complement component 4 binding protein, beta 1 AZGP1 alpha-2-glycoprotein 1, zinc 1 C6 complement component 6 1 CXCL12 chemokine (C-X-C motif) ligand 12

1 MX2 myxovirus (influenza virus) resistance 2 1 OAS1 2′,5′-oligoadenylate synthetase 1, 40/46 kDa 1 RT1-S3 RT1 class Ib, locus S3 1 VIPR1 vasoactive intestinal peptide receptor 1 1 APOA2 apolipoprotein A-II 2 BCL6_predicted B-cell leukemia/lymphoma 6 (predicted) 2 KLKB1 kallikrein B, plasma 1 2 PROC protein C 2 PTGER3 Prostaglandin E receptor 3 (subtype EP3) 2 MEOX2 mesenchyme homeobox 2 3 CA3 carbonic anhydrase 3 3 ABCB11 ATP-binding cassette, sub-family B (MDR/TAP), member 11 3 ALAD aminolevulinate, delta-, dehydratase 3 CYP2E1 cytochrome P450, family 2, subfamily e, polypeptide 1 3 EGFR epidermal growth factor receptor 3 HAO1 hydroxyacid oxidase 1 3 HNF4A Hepatocyte nuclear factor 4, alpha 3 NOTE: The numbers from 1–3 indicate immune reponse, inflammatory response and oxidative stress, respectively.