Osteoporos Int 14:780–784PubMedCrossRef 9 Elliot-Gibson V, Bogoc

Osteoporos Int 14:780–784PubMedCrossRef 9. Elliot-Gibson V, Bogoch ER, Jamal SA et al (2004) Practice patterns in the diagnosis and treatment of osteoporosis after a fragility fracture: a systematic review. Osteoporos Int 15:767–778PubMedCrossRef 10. Giangregorio L, Papaioannou A, Cranney A et al (2006) Fragility fractures and the osteoporosis care gap: an international phenomenon. Semin Arthritis Rheum 35:293–305PubMedCrossRef 11. Sale JEM, Beaton D, Posen J et al (2010) Systematic review on interventions to improve osteoporosis investigation and treatment in fragility fracture patients. Osteoporos Int. doi:10.​1007/​s00198–011–1544–y 12. McLellan A, Gallacher S, Fraser M et al (2003)

The fracture liaison service: success of a program for the evaluation and management of patients with osteoporotic fracture. Osteoporos Int #LY2874455 randurls[1|1|,|CHEM1|]# 14:1028–1034PubMedCrossRef RAD001 order 13. McLellan AR, Wolowacz SE, Zimovetz EA et al (2010) Fracture liaison services for the evaluation and management of patients with osteoporotic fracture: a cost–effectiveness evaluation based on data collected over 8 years of service provision. Osteoporos Int. doi:10.​1007/​s00198–011–1534–0 14. Torgerson D, Iglesias C, Reid D (2011) The economics of fracture prevention.

In: Barlow D, Francis RM, Miles A (eds) The effective management of osteoporosis. Aesculapius Medical Press, London, pp 111–121 15. Marsh D, Åkesson K, Beaton DE et al (2011) Coordinator-based systems for secondary prevention in fragility fracture patients. Osteoporos Int. doi:10.​1007/​s00198–011–1642-x PubMed 16. Harrington JT (2006) Dilemmas in providing osteoporosis care for fragility fracture patients. US Musculoskeletal Review-Touch Briefings. http://​www.​touchbriefings.​com/​cdps/​cditem.​cfm?​nid=​2162&​cid=​5#Osteoporosis Accessed 31 January 2011 17. The global coalition

on aging http://​www.​globalcoalitiono​naging.​com/​v1/​ Accessed 31 January 2011 18. Dell R, Greene D, Schelkun SR et al (2008) Osteoporosis disease management: the role of the orthopaedic surgeon. Astemizole J Bone Joint Surg Am 90:188–194PubMedCrossRef”
“Introduction Osteoporotic fractures represent a major growing public health issue. The number of fractures in the elderly is expected to increase mainly due to the world’s ageing population [1]. Bone mineral density (BMD) measured by dual energy X-ray absorptiometry (DXA) scan alone is not sufficient to provide an accurate prediction of fracture risk. Other clinical, non-BMD risk factors are known to be important for estimating an adequate probability of fracture [2, 3]. A previous fracture doubles the risk for future fractures and vertebral fractures quadruple this risk [4, 5] and even more so at short-term [6–10]. Recently, the World Health Organization developed a fracture risk assessment (FRAX) tool to evaluate the 10-year fracture risk of patients [11].

Hall J, Hammerich K, Roberts P: New paradigms in the management o

Hall J, Hammerich K, Roberts P: New paradigms in the management of diverticular disease. Curr Probl Surg 2010,47(9):680–735. doi:10.1067/j.cpsurg.2010.04.005. PubMed PMID: 20684920PubMedCrossRef 50. Radiology ACo: ACR Appropriateness Criteria. 2008. Available from: http://​www.​acr.​org/​ac 51. Soumian S, LY3023414 cost Thomas S, Mohan PP, Khan N, Khan Z, Raju T: Management of Hinchey II diverticulitis. World J Gastroenterol: WJG 2008,14(47):7163–7169. PubMed PMID: 19084929; PubMed Central PMCID: PMC2776873PubMedCrossRef 52. Lameris W, van Randen A, Bipat S, Bossuyt PM, Boermeester MA, Stoker J: Graded compression

ultrasonography and computed tomography in acute colonic diverticulitis: meta-analysis of test accuracy. Eur Radiol 2008,18(11):2498–2511. doi:10.1007/s00330–008–1018–6. VS-4718 PubMed PMID: 18523784PubMedCrossRef Autophagy activity 53. Destigter KK, Keating DP: Imaging update: acute colonic diverticulitis. Clin Colon Rectal Surg 2009,22(3):147–155. doi:10.1055/s-0029–1236158; PubMed PMID: 20676257; PubMed Central PMCID: PMC2780264PubMedCentralPubMedCrossRef 54. Dellinger RP, Levy MM, Carlet JM, Bion

J, Parker MM, Jaeschke R, Reinhart K, Angus DC, Brun-Buisson C, Beale R, Calandra T, Dhainaut JF, Gerlach H, Harvey M, Marini JJ, Marshall J, Ranieri M, Ramsay G, Sevransky J, Thompson BT, Townsend S, Vender JS, Zimmerman JL, Vincent JL, International Surviving Sepsis Campaign Guidelines C, et al.: Surviving Sepsis Campaign: international guidelines for management of severe sepsis and septic shock: 2008. Crit Care Med 2008,36(1):296–327. doi:10.1097/01.CCM.0000298158.12101.41. PubMed PMID: 18158437PubMedCrossRef 55. Moore LJ, Moore FA: Epidemiology of sepsis in surgical patients. Surg Clin North Am 2012,92(6):1425–1443. doi:10.1016/j.suc.2012.08.009. PubMed PMID: 23153877PubMedCrossRef 56. Byrnes MC, Mazuski JE: Antimicrobial therapy for acute colonic diverticulitis. Surg Infect 2009,10(2):143–154. doi:10.1089/sur.2007.087. PubMed PMID: 19226204CrossRef 57. Sartelli M, Viale P, Catena F, Ansaloni L, Moore E, Malangoni

M, Moore FA, Velmahos G, Coimbra R, Ivatury R, Peitzman A, Koike K, Leppaniemi A, Biffl W, Burlew CC, Balogh ZJ, Boffard K, Bendinelli C, Gupta S, Kluger Y, Agresta F, Di Saverio S, Wani Loperamide I, Escalona A, Ordonez C, Fraga GP, Junior GA, Bala M, Cui Y, Marwah S, et al.: 2013 WSES guidelines for management of intra-abdominal infections. World J Emerg Surg: WJES 2013,8(1):3. doi:10.1186/1749–7922–8-3. PubMed PMID: 23294512; PubMed Central PMCID: PMC3545734PubMedCrossRef 58. Ambrosetti P, Chautems R, Soravia C, Peiris-Waser N, Terrier F: Long-term outcome of mesocolic and pelvic diverticular abscesses of the left colon: a prospective study of 73 cases. Dis Colon Rectum 2005,48(4):787–791. doi:10.1007/s10350–004–0853-z. PubMed PMID: 15747071PubMedCrossRef 59. Durmishi Y, Gervaz P, Brandt D, Bucher P, Platon A, Morel P, Poletti PA: Results from percutaneous drainage of Hinchey stage II diverticulitis guided by computed tomography scan.

Grain boundaries can probably offer location for most of the oxyg

Grain boundaries can probably offer location for most of the oxygen impurities out of post-oxidization, where the oxygen atoms can incorporate the dangling bonds along the grain boundaries. On the other hand, the incorporation of oxygen impurities in the films is effectively

influenced by H radicals. The mechanism is that H radicals generated in the plasma during the growth process of the films are accelerated by the RF power and impinge onto the growing surface of the films with a certain kinetic energy. Those H radicals with enough kinetic energy can passivate the dangling bonds along the grain boundaries and effectively prevent the oxygen impurities from post-oxidization. The bonded H located at grain boundaries can form hydrides with a certain type of TGF-beta inhibitor PF477736 bonding configuration, which can be identified from the deconvoluted peaks of the Si-H stretching mode of the peak at 2,090 cm-1 as mentioned in Figure  2a. These hydrides with different types of bonding configurations were then investigated in this part to help us accurately understand the spatial correlation between the hydrogen-related microstructures and oxygen impurities. The spectrum of a representative sample with R H = 98.2% was chosen to be deconvoluted into eight Gaussian absorption peaks as presented in Figure  5a, standing for several types of different bonding configurations. The buy Eltanexor frequency position of the deconvoluted

peaks depends on the unscreened eigen-frequency of the hydride, bulk screening, local hydride density, and possible mutual dipole interactions of the hydrogen incorporation configuration [31]. The low stretching mode (LSM; 1,980 to 2,010 cm-1) originating from the a-Si:H tissue is often in an isolated Si-H form in the bulk. The middle stretching mode (MSM; 2,024 to 2,041 cm-1) due to the Si-H stretching vibrations is located at the platelet-like configuration of the amorphous-crystalline

interface with massive defect states. The high stretching click here mode (HSM; 2,086 to 2,094 cm-1) responsible for Si-H2 at the internal surface of microvoids [32] is also related to a number of unsaturated dangling bonds. The extreme HSM (EHSM; 2,140 to 2,150 cm-1) arises from the trihydrides in the film prepared under high hydrogen dilution conditions. Three narrow HSMs (NHSMs; at 2,097, 2,109, and 2,137 cm-1) represent mono-, di-, and trihydrides, respectively, on the crystalline surface. Lastly, the stretching mode at approximately 2,250 cm-1 corresponds to the hydride O x Si-H y vibration with oxygen atoms back-bonded to the silicon atoms [33]. Figure 5 Deconvoluted Si-H stretching mode and correlation between the integrated intensity of MSM and oxygen content. (a) Typical deconvoluted Si-H stretching mode of the nc-Si:H thin film under R H = 98.2%. The solid curves are the overall fitting results using eight Gaussian peaks.

CrossRef 11 Araki H, Kubo Y, Mikaduki A, Jimbo K, Maw WS, Katagi

see more CrossRef 11. Araki H, Kubo Y, Mikaduki A, Jimbo K, Maw WS, Katagiri H, Yamazaki selleck M, Oishi K, Takeuchi A: Preparation of Cu 2 ZnSnS 4 thin films by sulfurizing electroplated precursors. Sol Energy Mater Sol Cells 2009, 93:996–999.CrossRef 12. Jimbo K, Kimura R, Kamimura T, Yamada S, Maw WS, Araki H, Oishi K, Katagiri H: Cu 2 ZnSnS 4 -type thin film solar cells using abundant materials. Thin Solid Films 2007, 515:5997–5999.CrossRef

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(mrkD) of Klebsiella species is not conserved among all fimbriate strains. Infect Immun 1994, 62:4186–4191.PubMed 35. Low AS, Holden N, Rosser T, Roe AJ, Constantinidou C, Hobman JL, Smith DGE, Low JC, Gally DL: Analysis of fimbrial gene clusters and their expression selleck inhibitor in enterohaemorrhagic Escherichia coli many O157:H7. Environ Microbiol 2006, 8:1033–1047.PubMedCrossRef 36. Korea C-G, Ghigo J-M, Beloin C: The sweet connection: Solving the riddle of multiple sugar-binding fimbrial adhesins in Escherichia coli: Multiple E. coli fimbriae form a versatile arsenal of sugar-binding lectins potentially involved in surface-colonisation and tropism. BioEssays 2011, 33:300–311.PubMedCrossRef 37. Struve C, Krogfelt KA: Pathogenic potential of environmental Klebsiella pneumoniae isolates. Environ Microbiol 2004, 6:584–590.PubMedCrossRef 38. Schembri MA, Blom J, Krogfelt KA, Klemm P: Capsule and fimbria interaction in Klebsiella pneumoniae. Infect Immun 2005, 73:4626–4633.PubMedCrossRef 39.

Struve C, Krogfelt KA: Role of capsule in Klebsiella pneumoniae virulence: lack of correlation between in vitro and in vivo studies. FEMS Microbiol Lett 2003, 218:149–154.PubMedCrossRef 40. Lawlor MS, Hsu J, Rick PD, Miller VL: Identification of Klebsiella pneumoniae virulence determinants using an intranasal infection model. Mol Microbiol 2005, 58:1054–1073.PubMedCrossRef 41. Lau HY, Clegg S, Moore TA: Identification of Klebsiella pneumoniae genes uniquely expressed in a strain virulent using a murine model of bacterial pneumonia. Microb Pathog 2007, 42:148–155.PubMedCrossRef 42. Valenski ML, Harris SL, Spears PA, Horton JR, Orndorff PE: The Product of the fimI gene is necessary for Escherichia coli type 1 pilus biosynthesis.

Man SQ, Pun EYB, Chung PS: Upconversion luminescence of Er3+ in a

Appl Phys Let 2002,80(10):1752–1754.CrossRef 2. Man SQ, Pun EYB, Chung PS: Upconversion luminescence of Er3+ in alkali bismuth gallate glasses. Appl Phys Lett 2000,77(4):483–485.CrossRef 3. Zhang HX, Kam CH, Zhou Y, Han XQ, Buddhudu S, Xiang Q, Lam YL, Chan YC: Green upconversion luminescence in Er 3+ :BaTiO 3 films. Appl Phys Lett 2000,77(5):609–611.CrossRef 4. Luo XX, Cao WH: Upconversion luminescence of holmium and ytterbium co-doped yttrium Adriamycin cell line oxysulfide phosphor. Mater Lett 2007,61(17):3696–3700.CrossRef 5. Zhan J, Shen H, Guo W, Wang S,

Zhu C, Xue F, Hou J, Su H, Yuan Z: An upconversion NaYF 4 :Yb3+, Er3+/TiO 2 core-shell nanoparticle photoelectrode for improved efficiencies of dye-sensitized solar cells. J Power Sources 2013, 226:47–53.CrossRef 6. Ming C, Song F, Ren X: Color variety of up-conversion emission of Er 3+ /Yb 3+ co-doped phosphate glass ceramics. Curr Appl Phys 2013,13(2):351–354.CrossRef 7. Liu G, Chen X: Spectroscopic properties of lanthanides in nanomaterials. In Handbook on the Physics and Chemistry of Rare Earths. Edited by: Gschneide KAJr, Bünzli J-CG, Pecharsky VK. Amsterdam: Elsevier; 2007:99–169. 8. Sivakumar S, van Veggel FCJM, May PS: Near-infrared (NIR) to red and green up-conversion emission

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Therefore, CP673451 in vitro optimal protein intakes for bodybuilders during contest preparation may be significantly higher than existing recommendations. In support of this notion, Butterfield et al. [22] found that male athletes running five to 10 miles per day during a slight caloric deficit were in a significant negative nitrogen balance despite consuming 2 g/kg of protein daily. Celejowa et al. [39] showed that five out of 10 competitive weight lifters achieved a negative nitrogen balance over the course of a training camp while consuming an average protein intake of

2 g/kg. Out of these five, as many as three were in a caloric deficit. The authors concluded that a protein intake of 2–2.2 g/kg under these conditions only allows for a small margin of error before nitrogen losses occur. Walberg et al. [32] examined the effects of two energy restricted isocaloric diets of differing protein intakes in 19 lean (9.1-16.7% body fat), male, non-competitive body builders. One group consumed a protein intake of 0.8 g/kg and higher carbohydrates, while the other consumed 1.6 g/kg of protein with lower carbohydrates. The length of the intervention was only one week, but nonetheless nitrogen losses occurred only in the lower protein group and LBM decreased by a mean of 2.7 kg in the 0.8 g/kg protein group and by a mean of 1.4 kg in the 1.6 g/kg SBE-��-CD molecular weight protein group. While the high protein group

mitigated LBM losses compared to the low protein group, they were not eliminated. A recent study by Mettler et al. [29] employed the same basic methodology as Walberg et al. [32]. However, one group consumed a protein intake of 1 g/kg, while the other consumed 2.3 g/kg. The high-protein group lost significantly less LBM (0.3 kg) over the course of the two week intervention compared to the low-protein group (1.6 kg). Unlike Walberg et al. [32] calorie balance between diets was maintained by reducing dietary fat as opposed to carbohydrate

to allow for the increase in protein. While it appears that the 2.3 g/kg Vitamin B12 protein intervention in Mettler et al. [29] was superior for maintaining LBM compared to 1.6 g/kg in Walberg et al. [32] a recent study by Pasiakos et al. [40] found a trend towards the opposite. In this study, a non-significant trend of greater LBM retention occurred when subjects consumed 1.6 g/kg of protein compared to 2.4 g/kg of protein. However, the participants were Selleck Epacadostat intentionally prescribed low volume, low intensity resistance training “”to minimize the potential of an unaccustomed, anabolic stimulus influencing study outcome measures”". Thus, the non-anabolic nature of the training may not have increased the participants’ protein requirements to the same degree as the participants in Mettler et al. [29] or to what would be expected among competitive bodybuilders. Maestu et al. [6] did not observe a significant loss of LBM in a group of drug free bodybuilders consuming 2.5-2.

Case study of contrast-induced nephropathy using cardiac

Case study of contrast-induced nephropathy using cardiac click here catheterization. Jpn Circ J. 2001;65(Suppl III):750 (in Japanese) [IVb]. 74. Fujisaki K, Nakayama M, Yoshimitsu T, Doi T, Tanaka R, Yamada A,

et al. Incidence of contrast-induced nephropathy using cardiac catheterization: a case report. Jpn J Nephrol. 2002;44:315 (in Japanese) [IVb]. 75. Abe M, Kimura T, Morimoto T, Furukawa Y, Kita T. Incidence of and risk factors for contrast-induced nephropathy after cardiac catheterization in Japanese patients. Circ J. 2009;73:1518–22 [IVb].PubMedCrossRef 76. Laskey WK, Jenkins C, Selzer F, Marroquin OC, Wilensky RL, Glaser R, NHLBI Dynamic Registry Investigators, et al. Volume-to-creatinine clearance ratio: a pharmacokinetically based risk factor for prediction of early creatinine increase learn more after percutaneous coronary intervention. J Am Coll Cardiol. 2007;50:584–90

[IVb].PubMedCrossRef 77. Gurm HS, Dixon SR, Smith DE, Share D, Lalonde T, Greenbaum A, BMC2 (Blue Cross Blue Shield of Michigan Cardiovascular Consortium) Registry, et al. Renal function-based contrast dosing to define safe limits of radiographic contrast media in patients undergoing percutaneous coronary interventions. J Am Coll Cardiol. 2011;58:907–14 [IVb].PubMedCrossRef 78. Chong E, Poh KK, Liang S, Soon CY, Tan HC. Comparison of risks and clinical predictors of contrast-induced nephropathy in patients undergoing emergency versus nonemergency percutaneous coronary interventions. J Interv Cardiol. 2010;23:451–9 [IVa].PubMedCrossRef 79. Machino-Ohtsuka T, Seo Y, Ishizu T, Sekiguchi Y, Sato A, Tada H, et al. Combined

assessment of carotid vulnerable plaque, renal insufficiency, eosinophilia, and hs-CRP for predicting risky aortic plaque of Pexidartinib supplier Cholesterol crystal embolism. Circ J. 2010;74:51–8 [IVb].PubMedCrossRef 80. Fukumoto Y, Tsutsui H, Tsuchihashi M, Masumoto A, Takeshita A, Cholesterol Embolism Study (CHEST) Investigators. The incidence and risk factors of cholesterol embolization syndrome, a complication of cardiac catheterization: a prospective study. J Am Coll Cardiol. 2003;42:211–6 [IVb].PubMedCrossRef 81. Funabiki K, Masuoka H, Shimizu Fludarabine clinical trial H, Emi Y, Mori T, Ito M, et al. Cholesterol crystal embolization (CCE) after cardiac catheterization: a case report and a review of 36 cases in the Japanese literature. Jpn Heart J. 2003;44:767–74 [IVb].PubMedCrossRef 82. Modi KS, Rao VK. Atheroembolic renal disease. J Am Soc Nephrol. 2001;12:1781–7 [IVb].PubMed 83. Scolari F, Tardanico R, Zani R, Pola A, Viola BF, Movilli E, et al. Cholesterol crystal embolism: a recognizable cause of renal disease. Am J Kidney Dis. 2000;36:1089–109 [IVb].PubMed 84. Belenfant X, Meyrier A, Jacquot C. Supportive treatment improves survival in multivisceral cholesterol crystal embolism. Am J Kidney Dis. 1999;33:840–50 [IVb].PubMedCrossRef 85. Thadhani RI, Camargo CA Jr, Xavier RJ, Fang LS, Bazari H. Atheroembolic renal failure after invasive procedures.

We observed significant

We observed significant Selleckchem Alvocidib aggregation of proline in P. formosus associated plants growing under salinity stress, suggesting a decline in ionic influx inside the cellular masses and rescuing cucumber plants to maintain its osmotic balance. Similarly, higher nitrogen uptake by endophyte-inoculated plants under salinity suggested the regulation of sodium ion toxicity to indirectly maintain chlorophyll and osmotic

balance [47]. Sodium and chloride ion toxicity can trigger the formation of ROS which can damage cellular functioning [45–48]. Resultantly, accumulation of antioxidants inside plant can extend greater resistance to oxidative damage [48]. Higher DPPH radical scavenging activity in P. formosus inoculated plants suggest greater oxidative selleck inhibitor stress regulation than non-inoculated

plants [4]. Several studies have suggested that fungal symbiosis helps plants to mitigate stress by increasing Baf-A1 datasheet antioxidant activities [29, 46, 48]. Under salinity stress, phytohormones like ABA can protect plants by stomatal closure to minimize water loss and then mediates stress damage [49]. It is widely described that ABA contents in plants increase under salt stress [1, 50]. However, our finding shows significantly lower ABA level in endophyte-associated plants as compared to endophyte-free plants. Previously, Jahromi et al. [51] observed the same findings after association of Glomus intraradices with lettuce plants. Similarly, when soybean were given salinity stress in the presence of phytohormones producing endophytic fungi (Penicillium funiculosum and Aspergillus fumigatus), ABA levels were declined [15, 16], whilst the plants experienced lesser amount of stress. Since ABA is involved in the regulation of stress signalling during plant growth therefore, its biosynthesis can be affected by acetylcholine the presence of fungal interaction in abiotic stress. Although other studies suggests that fungal inoculation have increased the ABA content in leaves

and roots compared with non-inoculation control plants [52]. However, the effect may fluctuate among difference class of microorganisms and plant species as some earlier reports have elaborated this [44, 53]. There are several studied which narrates the same findings of low ABA levels under stress and fungal association [44]. Exogenous application of GA3 improved soybean salinity stress tolerance by increasing plant biomass while accumulating lesser ABA [54]. Iqbal and Ashraf [55] observed that GA3 application can results in altered level of ABA under salinity stress in Triticum aestivum L. Although, higher ABA in salinity is correlated with inhibition of leaf expansion and shoots development in different species [56] however, P.

PCADM-1 was over-expressed in human PCa and not found in

PCADM-1 was over-expressed in human PCa and not found in benign (BPH), high grade prostatic intraepithelial neoplasia (HGPIN), or seminal vesicle (SV) tissue. Likewise, the normal RPS2 gene was found to be over-expressed by malignant prostate lines (i.e. PC-3 ML and LNCaP cells), and by early stage prostate cancer cell lines (HGPIN, CPTX-1532). The data suggest that PCADM-1 and/or RPS2 might be novel bio-markers and excellent prognostic indicators for human prostate cancer. More importantly, PCADM-1 or RPS2 might be novel therapeutic targets for treating the

disease. In this paper, we have examined the importance of the RPS2 gene for proliferation and survival of malignant C188-9 order and normal learn more prostate cell lines in vitro

and in vivo. We have developed a ‘ribozyme-like’ oligonucleotide, DNAZYM-1P, which specifically targets RPS2 and found that DNAZYM-1P treatment of PC-3ML, LNCaP, and CPTX-1532 cells induced a click here significant increase in cellular apoptosis and death (i.e. > 95% after 48 hr). Mouse tumor modeling studies further revealed that DNAZYM-1P delivered locally or systemically, eradicated primary and metastatic tumors of PC-3ML cells in SCID mice. More importantly, treatment dramatically increased mice disease free survival rates by 100%. For the first time, we have convincingly demonstrated that tumors which over express the RPS2 protein can be eradicated with a DNAZYM-1P targeting this gene. Methods Cell cultures LNCaP, DU145, CRW22R1 and mouse 3T3 fibroblasts were obtained from ATCC (Bethesda, MD) and grown according to their instructions. PC-3 ML cells were maintained in DMEM plus 10% fetal bovine serum according to published methods

[5]. CPTX-1532 and NPTX-1532 cells were derived from malignant and normal tissue of the same human prostate tissue, respectively [6]. BPH-1 cells [7] were a gift from Donna Peehl (Stanford Univ.). CPTX-1532, NPTX-1532, and BPH-1 cells were each immortalized with human papillomavirus serotype 16 [8]. IBC-10a [9] cells were primary ‘intermediate basal cell’ cultures Prostatic acid phosphatase derived from a Gleason score 6 prostate cancers by our lab. IBC-10a cells were subsequently immortalized with hTERT (courtesy of Johng Rhim, Bethesda, MD). The IBC-10a cells were also transfected with a pBABE-c-myc puromycin vector (courtesy of Dr. Sell, Drexel Univ., Philadelphia, PA)(the pBABE vector was purchased from Clonetics Inc., Boston, MA)) and stable clones selected for 2 weeks with 2 ug/ml puromycin. The CPTX-1532 and NPTX-1532, BPH-1, and IBC-10a were maintained at low passage (< 10) in Keratinocyte serum free media (SFM) (Life Technologies, Inc., Grand Island, NY) containing 5 ng/mL epidermal growth factor, 50 μg/mL bovine pituitary extract, plus 100 units/mL penicillin G sodium and 100 μg/mL streptomycin sulfate. Cells were cultured at 37°C in a humidified atmosphere of 95% air and 5% CO2.