Microelectron J 2005, 36:673 CrossRef 5 Koynov S, Brandt MS, Stu

Microelectron J 2005, 36:673.CrossRef 5. Koynov S, Brandt MS, Stutzmann M: Black nonreflecting silicon surfaces for solar cells. Appl Phys Lett 2006, 88:203107.CrossRef 6. Huang MJ, Yang CR, Chiou YC, Lee RT: Fabrication of nanoporous antireflection surfaces on silicon. Sol Energy

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produced by 3.5 GeV Xe ion irradiation and their distribution along ion tracks in single-crystal silicon: an infrared study. J Phys: Condens Matter 2002, 14:L57. 11. Varichenko VS, Zaitsev AM, Kazutchits NM, Chelyadinskii AR, Penina NM, Martinovich VA, Latushko YI, Fahrner WR: Defect production in silicon irradiated with 5.68 GeV Xe ions. Nucl Instrum Methods Phys Res, Sect B 1996, 107:268.CrossRef 12. Li XC, Li JS, Chen T, Tay BK, Wang JX, Yu HY: Periodically aligned si nanopillar arrays as efficient antireflection layers for solar cell applications. Nanoscale Res Lett 2010, 5:1721.CrossRef 13. Chen ST, Li ZC, Zhang ZJ: Anisotropic

Ti PI-1840 x Sn 1-x O 2 nanostructures prepared by magnetron sputter deposition. Nanoscale Res Lett 2011, 6:1. 14. Su SM, Lin LH, Li ZC, Feng JY, Zhang ZJ: The fabrication of large-scale sub-10-nm core-shell silicon nanowire arrays. Nanoscale Res Lett 2013, 8:1.CrossRef 15. Wood DL, Tauc JS: Weak absorption tails in amorphous semiconductors. Phys Rev B 1972, 5:3144.CrossRef 16. Van Buuren T, Dinh LN, Chase LL, Siekhaus WJ, Terminello LJ: Changes in the electronic properties of Si nanocrystals as a function of particle size. Phys Rev Lett 1998, 80:3803.CrossRef Competing interests The authors declare that they have no competing interests. Authors’ contributions FY carried out the studies and drafted the manuscript. ZL participated in the design of the study and helped revise the manuscript. TZ participated in the experiments and data analysis. WM and ZZ gave suggestions on the analysis of results. All the authors read and approved the final manuscript.”
“Background Nanofluids, suspensions of nanoparticles, are increasingly being used in various industrial [1, 2] and medical applications [3].

Veiga H, Jorge AM, Pinho MG: Absence of nucleoid occlusion effect

Veiga H, Jorge AM, Pinho MG: Absence of nucleoid occlusion effector Noc impairs formation of orthogonal FtsZ rings during Staphylococcus aureus cell division. Mol Microbiol 2011, 80:1366–1380.PubMedCrossRef

24. Arnaud M, Chastanet A, Debarbouille M: New vector for efficient allelic replacement in naturally nontransformable, low-GC-content, gram-positive bacteria. Appl Environ Microbiol 2004, 70:6887–6891.PubMedCrossRef 25. Pereira PM, Veiga H, Jorge AM, Pinho MG: Fluorescent reporters for studies of cellular localization of proteins in Staphylococcus aureus. Appl Environ Microbiol 2010, 76:4346–4353.PubMedCrossRef 26. Pinho MG, Filipe SR, de Lencastre H, Tomasz A: Complementation of the essential peptidoglycan transpeptidase function of penicillin-binding protein 2 (PBP2) by the drug resistance protein PBP2A in Staphylococcus aureus. J Bacteriol 2001, 183:6525–6531.PubMedCrossRef 27. Atilano ML, Pereira PM, Yates J, Reed P, Veiga H, Pinho MG, Filipe SR: Teichoic acids are SC79 mouse temporal and spatial regulators

of peptidoglycan cross-linking in Staphylococcus aureus. Proc Natl CA4P molecular weight Acad Sci U S A 2010, 107:18991–18996.PubMedCrossRef 28. Veiga H, Pinho MG: Inactivation of the SauI type I restriction-modification system is not sufficient to generate Staphylococcus aureus strains capable of efficiently accepting foreign DNA. Appl Environ Microbiol 2009, 75:3034–3038.PubMedCrossRef 29. Oshida T, Tomasz A: Isolation and characterization of a Tn551-autolysis mutant of Staphylococcus aureus. J Bacteriol 1992, 174:4952–4959.PubMed 30. Jana M, Luong TT, Komatsuzawa H, Shigeta M, Lee CY: A method for demonstrating gene essentiality in Staphylococcus aureus. Plasmid 2000, 44:100–104.PubMedCrossRef 31. Reed P, Veiga H, Jorge AM, Terrak M, Pinho MG: Monofunctional transglycosylases are not essential for Staphylococcus aureus cell wall synthesis.

J Bacteriol 2011, 193:2549–2556.PubMedCrossRef 32. Iyer VN, Szybalski W: A molecular mechanism of mitomycin action: linking of complementary DNA strands. Proc 17-DMAG (Alvespimycin) HCl Natl Acad Sci U S A 1963, 50:355–362.PubMedCrossRef 33. Peak MJ, Peak JG, Moehring MP, Webb RB: Ultraviolet action spectra for DNA dimer induction, lethality, and mutagenesis in Escherichia coli with emphasis on the UVB region. Photochem Photobiol 1984, 40:613–620.PubMedCrossRef 34. Wu LJ, Errington J: GSK-3 inhibitor Bacillus subtilis SpoIIIE protein required for DNA segregation during asymmetric cell division. Science 1994, 264:572–575.PubMedCrossRef 35. Sharpe ME, Errington J: Postseptational chromosome partitioning in bacteria. Proc Natl Acad Sci U S A 1995, 92:8630–8634.PubMedCrossRef 36. Britton RA, Grossman AD: Synthetic lethal phenotypes caused by mutations affecting chromosome partitioning in Bacillus subtilis. J Bacteriol 1999, 181:5860–5864.PubMed 37. Kaimer C, Gonzalez-Pastor JE, Graumann PL: SpoIIIE and a novel type of DNA translocase, SftA, couple chromosome segregation with cell division in Bacillus subtilis. Mol Microbiol 2009, 74:810–825.PubMedCrossRef 38.

LDL, particularly oxidized LDL, is incorporated by mesangial cell

LDL, particularly P505-15 cost oxidized LDL, is incorporated by mesangial cells with scavenger receptors, forming foam cells. The foam cells and induced macrophages express various inflammatory cytokines and chemokines and cause tissue damage (Fig. 1) [2]. In addition, a large amount of protein leaks into the urine, but detached tubular cells that

have absorbed fat are often observed. These reabsorbed excess lipids are considered to damage tissues by intensifying GF120918 concentration oxidative stress in the renal tubules [3]. Typical findings such as the frequent appearance of interstitial foam cells are observed in FSGS, in which dyslipidemia persists. Fig. 1 Lipid nephrotoxicity Anti-nephropathic effect of the correction of hyperlipidemia associated with nephrotic syndrome The secondary dyslipidemia mentioned above can be corrected by statins over a long period, but by LDL-A if an acute effect is expected. In LDL-A using a dextran sulfate column (Liposorber, Kaneka), which is prepared by coating porous Sepharose beads with dextran sulfate, LDL-cholesterol is adsorbed due to an electrostatic interaction between negatively charged dextran sulfate and positively charged apoprotein

B on the surface of lipoprotein. VLDL and LDL are selectively adsorbed, but no HDL-cholesterol with ApoA or other plasma components including albumin is adsorbed. Liposorber can purify 3–4,000 ml of plasma in 2–3 h. When Sakai et al. first carried out this treatment many for FSGS in 1988 in Japan, not only the click here correction of hyperlipidemia, but also rapid resolution of NS was observed, so coverage by national health insurance was extended to its application to FSGS with hyperlipidemia (LDL-cholesterol >250 mg/dl) in 1989. Evaluation of the mechanism of the effects of LDL-A (Table 1) Effects of adsorption of LDL, particularly oxidized LDL

The infiltration of lesions by macrophages induces cytokines and chemokines such as TNFα and IL-8, which are elevated in the serum of nephrotic patients, and causes inflammation and the activation of mesangial cells. LDL scavenger receptors present in these macrophages are likely to be hyperstimulated by an increase in LDL-cholesterol, particularly oxidized LDL, in the circulation. Evaluation of the effect of LDL-A on LPS-stimulated IL-8 production by peripheral monocytes by its comparison between before and after treatment revealed significant suppression of the responsiveness compared with that in healthy subjects before treatment, but this was significantly recovered after treatment [6]. This is considered to have been due to the recovery of macrophage function caused by the rapid elimination of LDL. Table 1 Hypothetical mechanism of action of LDL-A on refractory NS 1. Direct effect of lipid (LDL, VLDL, oxLDL) adsorption (1) Reduction of macrophage stimulation by ox-LDL (2) Amelioration of macrophage dysfunction (3) Reduction of inflammatory cytokine 2.

Figure  2c showed the morphology and the size distribution of sil

Figure  2c showed the morphology and the size distribution of silica-coated Tariquidar mouse GNRs; the sGNRs were approximately spherical with a size of about 80 nm. The sGNRs exhibited monodispersed, well-defined core-shell structures. The GNR core, with 50 nm in length and 20 nm in width, was prepared by seed-mediated template-assisted method. The silica shell has a thickness of 10 to 20 nm. Figure  2d is the HR-TEM image of an individual

sGNR, showing that the silica shell has a well-ordered mesopore structure. Figure  2e,f showed that the sGNRs combined on the CX-6258 manufacturer surface of MWNTs mainly along their sidewalls, highly suggesting that sGNRs successfully attached to MWNTs. The well-distributed sGNRs deposited onto the surface of MWNTs showed that the CNT pre-treatment was effective, which resulted in many active sites on the MWNTs. Figure  2f showed that the structure and the crystallinity of MWNTs and sGNRs did not change after the cross-link. Almost 90% of sGNRs were successfully cross-linked with MWNTs; the average size of RGD-sGNRs/MWNTs was almost 300 nm in length and 50 nm in width. Figure 2 TEM and HR-TEM images. (a, b) MWNTs, (c, d) sGNRs, and (e,

f) MWNTs/sGNRs. Binding sites of sGNRs and MWNTs Figure  3 showed TEM images of the different binding sites of sGNRs and MWNTs. According to the TEM observations, the sGNRs decorated the surface of MWNTs SYN-117 mainly along their sidewalls (Figure  3a) and partly connected to the WNT ends (Figure  3b), which may be attributed to the fact that the amount of amino groups

on the long axis of GNRs is more than the amount on the short axis of GNRs. Figure 3 TEM images of the different binding sites of sGNRs and MWNTs. (a) sGNRs attached on the surface of WNT along the sidewalls. (b) sGNRs attached on the end of WNT. UV-vis spectra of gold nanorods Figure  4 showed the UV-vis absorbance spectra of GNR-CTAB, GNR-SiO2, and sGNRs in the wavelength PtdIns(3,4)P2 range of 400 ~ 900 nm. The spectrum of GNR-CTAB showed that GNR-CTAB had two absorption bands: a weak short-wavelength band around 515 nm and a strong long-wavelength band around 715 nm. Moreover, we observed that the plasmon peaks of GNR-SiO2 exhibited no significant changes in peak width or position, so the silica modification could improve only the biocompatibility of GNRs and did not change the two absorption bands of GNRs. After being modified with the second amino silane coupling agent, the special absorption peaks of sGNRs exhibited a little redshift (approximately 6 nm), which may be attributed to the fact that the coated silica layer became thick and the size of sGNRs became big.Figure  5 showed the UV-vis absorbance spectra of MWNTs and sGNRs/MWNTs. MWNTs exhibited a relative low absorption peak at NIR, and after MWNTs covalently bound with sGNRs, the sGNRs/MWNTs exhibited marked NIR absorption enhancement.

Motorcycle drivers

were requested to wear hearing protect

Motorcycle drivers

were requested to wear hearing protection during driving and be present at the lab at least half an hour before the tests would start. We decided to include all these participants into the analysis. Audiological tests Participants were H 89 price subjected to an extended audiological test battery containing tests on audiometric thresholds, loudness perception, diplacusis, tinnitus, speech perception in noise, and otoacoustic emissions. The tests were performed at the ENT-/audiological department of the Academic Medical Centre. Before testing the otoacoustic emissions, the participant had otoscopic inspection in order to check for cerumen. If present, the cerumen was removed by an ENT-doctor. Audiometric thresholds (PTA) Pure-tone air-conduction thresholds at 0.25, 0.5, 1, 2, 3, 4, 6, and 8 kHz were measured using an Interacoustics AC40 audiometer with TDH39 headphones. The audiometer was calibrated according to ISO 389 (1991). Pure-tone measurements were all performed in a sound–isolated booth. Bone-conduction thresholds were measured at 0.5, 1 this website and 2 kHz when air-conduction thresholds exceeded 20 dB. All audiometric thresholds were KPT-330 order assessed with adequate masking

and were expressed in dB HL, according to standards of diagnostic audiometry. Loudness perception We used an adaptive procedure for categorical loudness scaling ACALOS (Adaptive, Categorical Loudness Scaling) as described by Brand and Hohmann (2002) for three different stimuli: octave-band noises with 0.75 and 3 kHz as the centre frequency, and a wide band noise with a speech-shaped spectrum. Each stimulus was presented for 1,000 ms in a free-field condition. The participant was

seated at 1 m from the speaker producing the noise. For safety purposes, the maximum output was limited to 105 dB (SPL), according to the JBL control1X specifications. Based on the participant’s judgment of Phospholipase D1 the loudness of the test sound for various intensities, an individual loudness curve was fitted. Thus, the dynamic range and the increase of loudness within this dynamic range can be assessed in a single measurement. Diplacusis An adaptive procedure was used to compare the pitch of tonal signals presented alternating to the right and left ear by headphones on three different frequencies: 1, 2 and 4 kHz. First, participants had to match the loudness of the tone in the left ear to the tone in the right ear, presented at 60 dB HL. Then, the musician was asked to match the pitch of the tone in the left ear to that of the right ear. Adjustment on the basis of the participants’ feedback on both loudness and pitch was done by the test leader, changing the presentation level or the frequency of the tone presented to the left ear in steps of 1 dB or 1 Hz, respectively. Tinnitus When participants suffered from tinnitus at the time of testing, a tinnitus matching procedure was conducted. First, the tinnitus was localized (i.e.

I consider this to be very important information and welcome more

I consider this to be very important information and welcome more “news of difference” that may inform all aspects of the marriage and family therapy profession.”
“As a Professor in a School of Social Work I act as a bridge between professions, licensed as both a marriage and family therapist (MFT) and a clinical social worker

and teaching systems theory and family therapy to social work students. As I write this editorial I am continuing in that role only now I am doing so in a very different context. As part of a sabbatical leave I am spending the month of October as a Visiting Professor in the Department of Social Work at the National Wnt/beta-catenin inhibitor University of Singapore. Go6983 ic50 Thus, I also am something of a bridge between cultures, one Western and one Eastern. However, despite the many distinctions between these two cultures, I find that here, as at home, the students with whom I have the opportunity to work are very similar in terms of both their eagerness to learn

and the challenges they experience as they encounter and attempt to internalize a new way of thinking. I suspect that over time we tend to forget what it was like to enter the unfamiliar new world of systems theory and family therapy. Certainly I see it in the eyes of students wherever I teach, but that is not the same as living it. However, I now am reminded every day, at least metaphorically, of this experience as I attempt to find my way around an enormous campus with its maze Baf-A1 order of buildings, learn to use appliances that work differently, adapt electrical sockets to accommodate my computer and cell phone, negotiate on foot through traffic that flows in a direction that is opposite to what I am used to, and eat food (delicious by the way) that

is totally unfamiliar to me. Being a stranger in a strange land is a marvelous experience for many reasons. Relative to the marriage and family therapy profession it certainly has been significant for me. On the one hand it is helping me to remain mindful of the confusion and muddled feelings most of us experienced during our initial training. It also reminds me that in some small way this experience is probably AZD4547 in vivo isomorphic to what the original creators of our field encountered as they introduced and began to practice using a totally different paradigm. And on the other hand, it helps me to remain cognizant of how far we have come both as individuals and as a field in terms of our comfort level with systemic thinking and our sophistication as practitioners, theorists, and researchers. This certainly seems evident in the wealth of information provided in this issue of the journal. The initial focus is on training issues as described in two articles.

This taxonomic concept whereby the unifying structures are the fl

This taxonomic concept whereby the unifying structures are the flagellar hairs, is broader and more appropriate for the oomycetes and their related groups. The first proposal for stramenopiles was not formally presented as a kingdom but Dick (2001) did propose that the name kingdom Straminipila be applied. Unfortunately,

there has been a fairly significant amount of confusion in the correct spelling of this name. There have been numerous combinations of vowels applied in the name as well as the incorrect usage of the Selleckchem R406 suffix “philes” instead of “piles” (Table 1). This becomes a serious impediment in this day and age of digital document searches. This is an example where having a community clearly unified under one international scientific society would help settle these technical issues by consensus or votes. However, the current usage trend should be an acceptable situation for a majority rule decision. The original colloquial name “stramenopiles” as proposed by Patterson (1989) and currently used by the NCBI taxonomy is by far the most commonly used term. The more formal kingdom name Straminipila given by

Dick (2001) and its derived adjective straminipilous are together the second most commonly used names. Table 1 Google hits (June 2011) of different spelling for the stramenopile group of organisms first proposed see more by Patterson (1989) Name searched Number of hitsa Stramenopile(s) 187,000 Straminipila 15,990 Straminipilous 54,600 Stramenopila 24,600 Straminipile(s) 9,410 Stramenophile(s) 6,360 Straminopile(s) 3,040 Stramenophila 2,740 Straminopila 1,320 Straminopilous 696 Stramenopilous 108 Stremenopile(s) 51 Stramenipile(s) 4 Stramenipilous 3 Straminiphila 3 Straminophila 3 awith or without capital letters and total number of hits for singular or plural names Ultrastructure of the zoospore The oomycete community has been proactive

in making judicious usage of technological advances that can help answer important questions, Apoptosis antagonist Pictilisib ic50 regardless of the challenges that needed to be overcome to adapt the technology to oomycetes. The usage of transmission electron microscopy to look at the ultrastructure of motile zoospores is an excellent example of a challenging technological advance. The development of this technique was done with the chytrids (Barr and Hartmann 1976; Chong and Barr 1973). The first detailed study of the ultrastructure of the flagellar apparatus of oomycete zoospores was performed by Holloway and Heath (1977). Additional species of oomycetes, hyphochytrids and thraustochytrids were studied by Barr and Allan (1985). The main features of the apparatus are the two different flagella, the basal bodies or kinetosomes, a transitional zone between these regions, and the roots which anchor the flagella. Within this apparatus defined by regions, there are conserved and more variable areas such as the flagellar roots.

48 ± 2 35), and the difference was significant with P < 0 05 Liv

48 ± 2.35), and the difference was significant with P < 0.05. Livin expression ARN-509 order was inhibited meanwhile Caspas 3 expression was increased after transfection with Livin ASODN Livin immunohistochemistry showed that the majority of tumor cells in the tumor tissues of MSODN injection group were stained dark brown, while the tumor cell nucleus

of ASODN injection group was stained pale yellow and the number of stained cells was small (Fig. 9a, b). Figure 9 Livin and caspase 3 expression level in tumor tissue of nude mice. After injection of Livin ASODN, the Livin expression level in tumor tissue was significantly inhibited (a control group compare b ASOND group) and Caspase 3 expression was significantly increased (c control group compare with d ASOND

group). Caspas 3 immunohistochemical staining showed that the majority of tumor cells in the tumor tissues of ASODN injection group were stained dark brown, while the tumor cell caspas 3 staining of MSODN injection Selleck CRT0066101 group was relatively light, and the number of stained cells was relatively small (Fig. 9c, d). Discussion In recent years, using EST clone containing the BIR sequences, Vucic D, Kasof GM, etc. found Livin–a new member of this gene family in human fetal kidney cDNA library according to the IAPs homologous sequences [12, 13]. Livin produces two kinds of mRNA isomers in the transcription process due to the different ways of splicing. They have 1351 and 1297 base pairs, respectively. In spite of the 54 bp difference in length, properties of these two different mRNAs are exactly the same. The proteins coded by Resveratrol them were 298 and 280 amino acids with the molecular weight of about 33 kD and 30 kD, and were respectively termed as Livin α and Livin β [14]. For normal adults, most tissues do not express Livin at all (except placenta), but in some cancer cell lines such as melanoma cell lines (G361 and SK-Mel29), lymphoma, HaCat cells, and MCF7 breast cancer

cells [14], Livin is highly expressed. In spite of that, Livin was also highly expressed in a number of tumor tissues, such as BV-6 supplier bladder cancer [10], lymphoma [13], lung cancer [15], hepatocellular carcinoma[16], and renal carcinoma[17, 18]. Gazzaniga et al screened the apoptosis-related genes in bladder transitional cell carcinoma tumor tissues, including Livin, Survivin, BCL-X and BCL-2/BAX and so on, and then performed a four-year follow-up visit. Results showed that only Livin was related to bladder cancer recurrence in these genes[10]. The tumor average recurrence time of the patients with positive Livin expression after surgery (3.5 months) was much less than the one of the patients with negative Livin expression (27.2 months). The significant differences of recurrence intervals indicated that Livin expression is a sign of poor prognosis of early superficial bladder cancer and it can be used as indicators for monitoring recurrence of bladder cancer.

In the study to be described, we used this semi-automated

In the study to be described, we used this semi-automated

fluorometric method to study EtBr transport in M. smegmatis, using the wild-type strain mc2155 and mutant strains carrying in-frame deletions of genes coding for porins MspA and MspC, the efflux pump LfrA and its repressor LfrR, and correlated this information with the corresponding antibiotic profile. Since many efflux pumps of M. smegmatis have their homologues in Mycobacterium tuberculosis, the use of M. smegmatis as a model mycobacterium may provide data that will help to understand efflux-mediated drug resistance in M. tuberculosis and other mycobacteria that infect the human [15]. Results and Discussion MspA as a major pathway for EtBr in M. smegmatis The M. smegmatis strains used in this study are described in Table 1. The accumulation of increasing concentrations of EtBr by strains SMR5, MN01 (Δ mspA) and ML10 ICG-001 solubility dmso (Δ mspA ΔmspC) is presented by Figure 1. Accumulation of EtBr under conditions that maximize efflux (presence of glucose and incubation at 37°C) begins to take place at a concentration of 1 mg/L in the case of M. smegmatis SMR5. This concentration of EtBr marginally exceeds the ability of the intrinsic efflux system of SMR5 to extrude the substrate. In the

case of the SMR5 derived porin mutants MN01 (Δ mspA) and ML10 (Δ mspA Δ mspC), the marginal concentration that results in accumulation of EtBr is increased to 2 and 4 mg/L, respectively (Figure 1) and considered to be the result of a decreased influx rate of EtBr due to the deletion Tipifarnib nmr of porins in these strains [3, 5]. These concentrations were selected to test the

effect of the efflux inhibitors chlorpromazine, thioridazine and verapamil in the accumulation of EtBr by these strains. This is to ensure that the increase of accumulation of EtBr is due to Fer-1 manufacturer inhibition of efflux pumps and not to the use of an EtBr concentration that the cell’s efflux system cannot extrude. As shown by Figure 2, the efflux inhibitors chlorpromazine, thioridazine and verapamil, used at ½ the minimum inhibitory concentration (MIC; see Table 1), increased Interleukin-3 receptor accumulation of EtBr, although only marginally in strain ML10. We interpret these results as indicating that because of the absence of both porins in ML10, little EtBr enters the cell, accumulation does not take place, and hence, there is no EtBr subject for extrusion. Table 1 Description of M. smegmatis strains used in this study and corresponding MICs determined for EtBr and efflux inhibitors M. smegmatis strain Description [Reference] MICs (mg/L)     EtBr CPZ TZ VP mc 2 155 Wild-type [34] 6.25 25 12.5 200 SMR5 mc2155 derivative; resistant to streptomycin due to a mutation in ribosomal protein S12 (rpsL) [29] 6.25 25 12.5 400 MN01 SMR5 Δ mspA [5] 6.25 25 25 400 ML10 SMR5 Δ mspA Δ mspC [28] 12.5 25 25 250 XZL1675 mc2155 Δ lfrA [15] 0.4 25 6.25 125 XZL1720 mc2155 Δ lfrR [15] 6.25 25 12.

References 1 Shreck GL, Toalson TW: Delayed presentation of trau

References 1. Shreck GL, Toalson TW: Delayed presentation of traumatic rupture of the diaphragm. J Okla State Medical Association 2003,96(4):181–183. 2. Disler DG, Deluca SA: Traumatic rupture of the find more diaphragm and herniation of the liver. Am Fam Physician 1992,46(2):453–456.PubMed 3. Rossetti G, Brusciano L, Maffetone V, Napolitano V, Sciaudone G, DelGenio G, Russo G, DelGenio A: Giant right post-traumatic diaphragmatic hernia: laparoscopic repair without a mesh. Chir Ital 2005,57(2):243–246.PubMed 4. Pappas-Gogos G, Karfis E, Kakadellis J, Tsimoyiannis EC: Intrathoracic cancer of the splenic flexure. Hernia 2007,11(3):257–259.CrossRefPubMed

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11. Walchalk LR, Stanfield SC: Delayed Presentation of Traumatic Diaphragmatic Rupture. Journal of Emergency Medicine 2008, in press. 12. Sirbu H, Busch T, Spillner J, Schachtrupp A, Autschbach R: Late bilateral diaphragmatic rupture: Thiamet G challenging diagnostic and surgical repair. Hernia 2005,9(1):90–92.CrossRefPubMed 13. Faul JL: Diaphragmatic rupture presenting forty years after injury. Injury 1998,29(6):479–480.CrossRefPubMed 14. Grimes OF: Traumatic injuries of the diaphragm. Diaphragmatic hernia. Am J Surg 1974,128(2):175–181.CrossRefPubMed 15. Launey Y, Geeraerts T, Martin L, Duranteau J: Delayed traumatic right diaphragmatic rupture. Anesth Analg 2007,104(1):224–225.CrossRefPubMed 16. Kelly J, Condon E, Kirwan W, Redmond H: Post-traumatic tension faecopneumothorax in a young male: case report. World Journal Emergency Surgery 2008, 3:20.CrossRef 17. Pojarliev T, Tzvetkov I, Blagov J, Radionov M: Laparoscopic repair of traumatic rupture of the left diaphragm cupola with prosthetic mesh. Surg Endosc 2003,17(4):660.PubMed 18. Al-Mashat F, Sibiany A, Kensarah A, Eibany K: Delayed presentation of traumatic diaphragmatic rupture.