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PubMedCrossRef 5. Shah N, Sukumar S: The Hox genes and their roles in oncogenesis. Nat Rev Cancer 2010,10(5):361–371.PubMedCrossRef 6. Mukai Y, Ohno-Yamashita Y, Oshima Y, Harashima S: The role of cysteine residues in the homeodomain protein Mat alpha 2 in mating-type control of Saccharomyces cerevisiae. Mol Gen Genet 1997,255(2):166–171.PubMedCrossRef 7. Kelly M, Burke J, Smith M, Klar A, Beach D: Four mating-type genes control sexual differentiation in the fission yeast. EMBO J 1988,7(5):1537–1547.PubMed 8. Kronstad JW, Staben C: Mating type in filamentous fungi. Annu Rev Genet NSC23766 molecular weight 1997, 31:245–276.PubMedCrossRef 9. Burglin

TR: The yeast regulatory gene PHO2 encodes a homeo box. Cell 1988,53(3):339–340.PubMedCrossRef 10. Torres-Guzman JC, Dominguez A: HOY1, a homeo gene required for learn more hyphal formation in Yarrowia lipolytica. Mol Cell Biol 1997,17(11):6283–6293.PubMed 11. Aligianni S, Lackner DH, Klier S, Rustici G, Wilhelm BT, Marguerat S, Codlin S, Brazma A, de Bruin RA, Bahler J: The fission yeast homeodomain protein Yox1p binds to MBF and confines MBF-dependent cell-cycle transcription to G1-S via negative feedback.

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Allen JM, Garcia E, Thomas LR, Gregory ID, Voth WP, Whelihan K, Rolfes RJ, Stillman DJ: Mutations in the pho2 (bas2) transcription factor that differentially affect activation with its partner proteins bas1, pho4, and swi5. J Biol Chem 2002,277(40):37612–37618.PubMedCrossRef 16. Hannum C, Kulaeva OI, Sun H, Urbanowski JL, Wendus A, Stillman DJ, Rolfes RJ: Functional mapping of Bas2. Identification of activation and Bas1-interaction domains. J Biol Chem 2002,277(37)):34003–34009.PubMedCrossRef 17. Matsuyama A, Arai R, Yashiroda Y, Shirai A, Kamata A, Sekido S, Kobayashi Y, Hashimoto A, Hamamoto M, Hiraoka Y, et al.: ORFeome cloning and global analysis of protein localization in the fission yeast Schizosaccharomyces pombe. Nat Biotechnol 2006,24(7):841–847.PubMedCrossRef 18. Vivancos AP, Jara M, Zuin A, Sanso M, Hidalgo E: Oxidative stress in Schizosaccharomyces pombe: different H2O2 levels, different response pathways. Mol Genet Genomics 2006,276(6):495–502.PubMedCrossRef 19. Herman PK: Stationary phase in yeast. Curr Opin Microbiol 2002,5(6):602–607.PubMedCrossRef 20.

, Davie, FL) or PLA. Research personnel watched as each participant

CA3 in vivo consumed the supplement on all training days. In addition, participants were given single servings of SYNTH or PLA to consume on non-training days. Laboratory testing took place only before and after the six-week intervention. Participants returned for post-testing at least 36 hours following the final training session in order to minimize the effects of delayed onset muscle soreness and post-exercise reduced maximal torque [23] on testing data, as well as to ensure that any changes were due to chronic training and supplementation rather than acute changes from the final RT session. Participants continued to consume a serving of SYNTH (1x/day) after training had ended until the day of (but not including) post-testing. Resistance training protocol For the duration of the study, three sets of each exercise were completed as a percentage of baseline 1RM. For the first two weeks, participants completed 10 repetitions at 70-75% of 1RM. For weeks three and four, resistance was increased to six repetitions at 80-85% 1RM. For the final two weeks, participants completed four repetitions per set at 85-90% of CX-5461 mw 1RM. Each major muscle group was trained once per week using at least one exercise. The six-week training program was designed to target every major muscle group in a three-day split and was modified from previously published research

[24, 25]. The exercises for day one, designed to work the biceps, triceps, and shoulders were performed in the following order:

shoulder military press, dumbbell incline biceps curl, cable overhead French press, straight bar curls, cable triceps press down, and dumbbell reverse fly. The exercises for day two, designed to work the muscles of the legs and core, were (in order): leg press (LP), straight leg dead lift, dumbbell lunge, leg curls, standing calf Ribonucleotide reductase raises, abdominal crunch, and core planks. The third and final day of the rotation was designed to work the muscles of the chest and back with the following exercises (in order): flat chest press (CP), cable pull down, incline CP, cable low row (neutral grip), dumbbell chest flys, and dumbbell shrugs. Three sets of each exercise were performed for prescribed number of repetitions or to failure, selleck compound whichever came first, with resting times of 60–90 seconds between sets. If a participant was unable to perform the prescribed weight for an exercise, the weight was adjusted to yield failure at or near the specified number of repetitions. The emphasis placed on consistent lifting form in this study, coupled with researcher supervision from certified personal trainers through the National Strength and Conditioning Association (NSCA), helped ensure full participant compliance with training as well as reduce variability due to inter-subject differences or deficiencies in form. Testing sessions Laboratory testing was completed on two occasions.

Eur J Radiol 2007,61(30):433–441.PubMedCrossRef 21. Suo BJ, Zhou LY, Ding SG, Guo CJ, Gu F, Zheng YA: Analysis of etiological

and related factors responsible for acute gastrointestinal hemorrhage. Zhonghua Yi Xue Za Zhi 2011,91(25):1757–1761.PubMed 22. Aschoff AJ, Stuber G, Becker BW, Hoffmann MHK, Schmitz BL, Schelzig H, Jaeckle T: Evaluation of acute mesenteric ischemia: accuracy of biphasic mesenteric multi-detector CT angiography. Abdom Imaging 2009, 34:345–357.PubMedCrossRef Competing interests The authors declare that they have no competing interests. Authors’ contributions IEK, who was the attending surgeon, designed the study and drafted the manuscript. AB helped to draft the manuscript. MS and IG performed the literature search using the PubMEd database. Temsirolimus molecular weight AS critically revised the manuscript. MKD coordinated the study. All authors read and approved the final version.”
“Introduction Prosthetic

abdominal wall surgical repair is a common procedure [1, 2]. Actually, about one million prostheses per year for abdominal wall repair are used worldwide [3]. Since the first description of a mesh use for abdominal mTOR inhibitor wall repairing [4] plenty of new material have been introduced, first synthetic, but later biologic. Indications for repair are well established and widely diffused [5]. However controversies still exist about the indication in using the different materials and principally about the biological ones. More than a dozen of biological prosthesis (BP) are currently available (Table  1). All of them are derived from human or mammalian tissues [6]. It has already been noted the major variability among human dermis

prosthesis than among the animal ones in terms of mechanical and physical properties [6]. In fact xenograft products are obtained from a more uniform animal population with similar age and life histories, this allows producers to obtain more consistent implants than from humans donors [6]. Table 1 Biological prosthesis Exoribonuclease currently on the market Name Manufacturer Tissue source Material X-linking Alloderm LifeCell Human Acellular dermis No AlloMax Bard Human Acellular dermis No Flex HD Ethicon/MTF¥ Human Acellular dermis – DermaMatrix MTF¥ Human Acellular dermis No Permacol Covidien Porcine Acellular dermis Yes CollaMend Davol/Bard Porcine Acellular dermis Yes Strattice KCI/LifeCell Porcine Acellular dermis No XenMatrix Brennan Medical Porcine Acellular dermis No Surgisis Cook Porcine Small intestine submucosa No Surgisis Gold Cook Porcine Small intestine submucosa No Lyosis Cook Porcine Lyophilized small intestine submucosa No FortaGen Organogenesis Porcine Small intestine submucosa Yes SurgiMend TEI bioscience Bovine Fetal dermis No Periguard Synovis Bovine find more Pericardium Yes Veritas Synovis Bovine Pericardium No Tutomesh Tutogen Bovine Pericardium No Tutopatch Tutogen Bovine Pericardium No ¥ MTF: Muscoloskeletal Transplant Foundation.

Can J Fish Aquat Sci 62:863–871CrossRef Girvetz EH, Zganjar C, Raber GT, Maurer EP, Kareiva P, Lawler JJ (2009) Androgen Receptor Antagonist nmr Applied climate-change analysis: the AG-881 mouse climate Wizard tool. PLoS ONE 4. doi:10.​1371/​journal/​pone.​0008320

Glick P, Stein B (2010) Scanning the conservation horizon: a guide to climate change vulnerability assessment. National Wildlife Federation, Washington DC Grantham HS, Bode M, McDonald-Madden E, Game ET, Knight AT, Possingham HP (2010) Effective conservation planning requires learning and adaptation. Front Ecol Environ 8:431–437CrossRef Groves CR (2003) Draft a conservation blueprint: a practitioners guide to planning for biodiversity. Island Press, Washington DC Groves CR, Jensen DB, Valutis LL, Redford KH, Shaffer ML, Scott M, Baumgartner JV, Higgins JV, Beck MW, Anderson MG (2002) Planning for biodiversity conservation: putting conservation science into practice. BioScience 52:499–512CrossRef Hale LZ, Meliane I (2009) Ecosystem-based adaptation in marine and coastal ecosystems. Renew Res PRIMA-1MET in vitro J 25:21–28 Halpin PN (1997) Global climate change and natural area protection: management responses and research directions. Ecol Appl 7:828–843CrossRef Hansen L, Hoffman JR, Drew C, Mieelbirecht

(2010) Designing climate-smart conservation: guidance and case studies. Conserv Biol 24:63–69 Heller NE, Zavaleta ES (2009) Biodiversity management in the face of climate change: a review of 22 years of recommendations. Biol Conserv 142:14–32CrossRef Higgins J, Bryer M, Khoury M, Fitzhugh

T (2005) A freshwater classification approach for biodiversity conservation planning. Conserv Biol 19:432–445CrossRef Hilty J, Lidicker W Jr, Merenlender AM (2006) Corridor ecology: the science and practice of linking landscapes for biodiversity conservation. Island Press, Washington DC Hodgson JA, Thomas CD, Wintle BA, Moilanen selleck kinase inhibitor A (2009) Climate change, connectivity and conservation decision making: back to basics. J Appl Ecol 46:964–969CrossRef Hunter ML, Jacobson TLJ, Web T III (1988) Paleoecology and the coarse filter approach to maintaining biological diversity. Conserv Biol 2:375–385CrossRef IPCC (2007a) Climate change 2007: synthesis report. Contribution of working groups I, II and III to the fourth assessment report of the intergovernmental panel on climate change. IPCC, Geneva, Switzerland IPCC (2007b) Climate change 2007: impacts, adaptation and vulnerability. Contribution of working group II to the fourth assessment report of the intergovernmental panel on climate change. Cambridge University Press, Cambridge, UK Jackson CR, Pringle CM (2010) Ecological benefits of reduced hydrologic connectivity in intensively developed landscapes. Biosci 60:37–46. doi:10.​1525/​bio.​2010.​60.​1.​8 CrossRef Jetz W, Rahbeck C (2002) Geographic range size and determinants of avian species richness.

Schwarzenbach H, Chakrabarti G, Paust HJ, Mukhopadhyay AK: Gonadotropin-mediated regulation of the murine VEGF expression in MA-10 Leydig cells. J Androl 2004, 25 (1) : 128–139.PubMed 37. Jones A, Fujiyama C, Turner K, Fuggle S, Cranston D, Turley H, Valtola R, Bicknell R, Harris AL: Angiogenesis and lymphangiogenesis in stage 1 germ cell tumours of the testis. BJU Int 2000, 86 (1) : 80–86.CrossRefPubMed 38. Wulff C, Wilson H, Largue P, Duncan WC, Armstrong DG, Fraser HM: Angiogenesis in the human corpus luteum: localization and changes in angiopoietins, tie-2, and vascular endothelial growth factor messenger ribonucleic acid. J Clin Endocrinol Metab 2000, 85: 4302–4309.CrossRefPubMed 39. Haggstrom

Rudolfsson S, Johansson A, Franck Lissbrant I, Wikstrom P, Bergh A: Localized expression of angiopoietin 1 and 2 may explain unique characteristics of the rat testicular microvasculature. Biol Reprod 2004, 69: 1231–1237.CrossRef 40. Aigner A, Brachmann Ro 61-8048 P, Beyer J, Jäger R, Raulais D, Vigny M, Neubauer A, Heidenreich A, Weinknecht S, Czubayko F, Zugmaier G: Marked increase of the growth factors pleiotrophin and fibroblast growth factor-2 in serum of testicular cancer patients. Ann Oncol 2003, 14 (10) : 1525–1529.CrossRefPubMed 41. DNA Synthesis inhibitor Reisinger K, Baal N, McKinnon T, Mûnsteed K, Zygmunt M: The gonadotropins: AZ 628 ic50 tissue-specific

angiogenic factors? Mol Cell Endocrinol 2007, 269 (1–2) : 65–80.CrossRefPubMed Competing interests The authors declare that they have no competing interests. Authors’ contributions OA design and conception of the study, analysis of data, revision of the

manuscript, RMM acquisition and analysis of data, draft and revision of the manuscript, JAS acquisition of data, CVG critically revised the manuscript and also contributed to the analysis, AAS supervised the immunohistochemistry, revised the manuscript, JGCV checked the immunohistochemistry, revised the final version, EAO revised the data, ALG carried out the immunohistochemistry, MAJ critical revision of the manuscript and JLA conception of the study and revision of the manuscript. All authors have read and approved the final version of the manuscript.”
“Background Soft Tissue Sarcomas (STS) are malignant tumors that develop within mesenchymal connective tissue and can occur in any Carnitine palmitoyltransferase II part of the body, most commonly in the limbs, which represent over 45% of occurrences [1]. STS growth does not usually cause any noticeable symptoms in early stages, making early detection uncommon. Some STS such as synovial sarcoma, malignant fibrous histiocytoma, rhabdomyosarcoma and certain neurogenic sarcomas tend to invade peripheral tissues, such as nerves, vessels and bones, and are thus have a relatively poor prognosis and are difficult to cure [2]. The treatment of limb STS have traditionally included surgery, which can involve extensive muscle excision or resection [3].

aureus. GSK2126458 results YsxC is essential in S. aureus To test whether ysxC was essential in S. aureus, a strain containing a single chromosomal copy of ysxC under the control of a regulatable promoter (Pspac), repressed by LacI and requiring the inducer IPTG for expression was constructed

as indicated in Material and Methods (See also Figure 1). Growth of LC109 (SH1000 Pspac~ysxC/pGL485) at several IPTG concentrations (0 μM, 5 μM, 10 μM and 500 μM) was analysed on BHI agar plates supplemented with chloramphenicol to ensure maintenance of the lacI-containing plasmid (Figure 2A). Strong growth can be seen on the plate containing 500 μM IPTG with distinctive single colonies, which are absent on the plate without Selumetinib mw IPTG. The phenotype on solid medium was further confirmed in liquid medium (Figure 2B). In a different

experiment it was shown that the presence or absence of IPTG does not affect growth of the wild type SH1000 strain (data not shown), while growth of LC109 (SH1000 Pspac~ysxC/pGL485) is IPTG concentration dependent (Figure 2B). No distinguishable alterations were observed on YsxC-depleted cells under light or transmission electron microscopy (data not shown). The number of viable counts on LC109 incubated in the absence of IPTG remained virtually unchanged, while in the presence of 1 mM IPTG it increased by 2 logs. Interestingly, even at 1 mM IPTG, LC109 (SH1000 Pspac~ysxC/pGL485) had a growth defect when compared to the wild type SH1000 strain (2.8×108 and 7.3×109 CFU after 7 h, respectively).

These results demonstrate that ysxC is apparently ID-8 essential for growth of S. SBE-��-CD solubility dmso aureus in these conditions. Figure 1 Detailed scale representation of the P spac ~ ysxC (LC108/LC109) and ysxC ::TAP-tag (LC103) chromosomal constructs. λred recombination allowed highly specific chimera construction resulting in the Tet-T-Pspac or TAP-tag-kan cassette insertions. The relevant sequence junctions are shown for both constructs. Chromosomal sequence is shown in italics and relevant features generated by λred recombination are underlined. Figure 2 YsxC requirement for S. aureus growth. A) Strain LC109 (SH1000 Pspac~ysxC/pGL485) was grown on BHI agar plates containing 20 μg ml-1 Cam and 500 μM, 10 μM, 5 μM or 0 μM IPTG overnight. B) Exponentially growing cultures of strains SH1000 (●) and LC109 (SH1000 Pspac~ysxC/pGL485) (○,τ,ρ) were washed and resubcultured to approximately 1×106 CFU ml-1 in BHI (●) or in BHI supplemented with 20 μg ml-1 Cam plus different concentration of IPTG: 0 (○), 10 μM (▼) or 1 mM (△). Growth was monitored as CFU/ml. c) Western blot using anti-YsxC polyclonal antibodies. Strains SH1000 and LC109 (SH1000 Pspac~ysxC/pGL485) were grown to an OD600 = 0.5 in BHI and BHI plus 20 μg ml-1 Cam, respectively. Cells were harvested by centrifugation, the membrane protein fraction extracted and samples were separated by 12% (w/v) SDS-PAGE.

Most species within the Salmonella and Shigella genera do not have the ability to ferment lactose. However, Shigella sonnei may ferment lactose, but only after extended incubation [31]. ChromID ESBL, Brilliance ESBL and BLSE agar are available as “ready to use” plates from the producers, while CHROMagar ESBL is sold as a powder base. Statistical analyses The calculation of the sensitivity for detecting ESBL-carrying isolates for each screening agar was based on a total of 87 isolates, NVP-BSK805 51 isolates carrying ESBLA genotypes and 36 carrying AmpC genotypes. The single isolate which was

both ESBLA – and AmpC positive was counted as an AmpC in the statistical analysis. For each agar plate the total sensitivity was calculated (ESBLA + AmpC) (n = 87), as well as the sensitivity for ESBLA and AmpC alone (n = 51 and n = 36, respectively). A 95% confidence interval (95% CI) for each value was manually calculated using binomial proportions’ confidence interval. Results The ESBL genotyping results are shown in Tables 2 and 3. The genotypic characterisation enabled prediction of growth and color selleck screening library of the colonies growing on the various media. The expected outcome was compared with the observed results. The expected colony colours for Salmonella spp. and Shigella sonnei on each ESBL screening agar are shown in Figure 1. The grading of growth for the 87 isolates is presented in Tables 4 and 5, respectively. The calculated sensitivity is presented

in Table 6. Table 2 Distribution of ESBL-genes in the 87 isolates   ESBL A ESBL A + AmpC AmpC Total   CTX-M SHV-12 CTX-M −15 + SHV-12 TEM-63 + CMY-2 CMY-2 DHA-1   Salmonella 26 3 4 1 33 1 68 Shigella 18 0 0 0 1 0 19 Total 44 3 4 1 34 1 87 Table 3 Genotypes within the CTX-M-isolates   Salmonella Shigella CTX-M-1 1 0 CTX-M-3 during 0 1 CTX-M 3/22 1 0 CTX-M-9 1 0 CTX-M 14/17/18 7 1 CTX-M 15 16 15 CTX-M-27 0 1   26 18 Figure 1 Picture of normal

growth of Salmonella (left) and Shigella sonnei (right) with ESBL genotypes. All ESBL positive isolates were mixed with a fecal suspension controlled for the absence of Salmonella, Shigella and any other ESBL-producing bacteria, before being inoculated onto the screening agars. The Lactose and XLD agars (top) were used as RG7112 mw controls. a = Salmonella, b = Shigella sonnei, 1 = Lactose + XLD (control agars), 2 = BLSE agar, 3 = Brilliance ESBL, 4 = ChromID ESBL, 5 = CHROMagar ESBL. Table 4 Grading of growth of 68 ESBL A – and/or AmpC-producing Salmonella isolates (n=68) Growth Excellent Good Poor No growth   ESBL A AmpC ESBL A AmpC ESBL A AmpC ESBL A AmpC Brilliance ESBL 31 9 1 5 1 17   4 BLSE agar* – Drigalski 31 35 1       1   BLSE agar* – Mac Conkey 31 34   1 1   1   CHROMagar ESBL 32 4 1 4   14   13 ChromID ESBL 33 12   16   4   3 All ESBL-producing isolates were mixed with a fecal suspension controlled for the absence of Salmonella, Shigella and any other ESBL-producing bacteria, before being inoculated on the screening agars.

The earliest report of CA-MRSA infections involved indigenous people living in remote communities in the sparsely populated Kimberley region of Western Australia (WA) [20]. Approximately 50% of selleckchem the people in this region are indigenous, many of whom live in poor socioeconomic conditions. Infected skin lesions and staphylococcal sepsis occur frequently and empirical antistaphylococcal therapy is often prescribed. Colloquially known as “”WA-MRSA”", the early isolates have a similar pulsed-field gel electrophoresis (PFGE) pattern and have subsequently been characterized as a single clone; PVL-negative WA5 (ST8-IV/spa t008) [21]. By 2006 22 CA-MRSA clones were identified in WA, with PVL-negative WA 1 (ST1-IV [2B]/t127)

replacing WA5 as the predominant clone [22]. At this time CA-MRSA from indigenous people

living in remote areas outside of WA were reported in the Northern Territory [23], Queensland [24] and Central Australia [25]. As may be expected in a geographically large country with relatively few dense concentrations of population, often separated by large areas of desert, different CA-MRSA clones evolved in these learn more communities. In 1982 colonization or infection with MRSA became a notifiable condition in WA. For infection control purposes all MRSA isolated in the state since 1997 have been referred to the Australian Collaborating Centre for Enterococcus and Staphylococcus Species (ACCESS) Typing and Research where based on many molecular markers they are characterized as either HA-MRSA or CA-MRSA [26]. Although a state-wide policy of screening all patients and healthcare workers who have lived outside the state for MRSA has prevented HA-MRSA from becoming endemic in Western Australian hospitals, it has not prevented CA-MRSA from becoming PCI-32765 clinical trial established in the community. In WA the public health system is divided into two metropolitan health regions and seven country health regions. The state encompasses an area of 1.02 million square miles and has a population of approximately 2.24 million people. In 1983, the overall rate of MRSA notifications

was 10 per 100,000 persons in the rural country health regions and 7/100,000 in the metropolitan regions [27]. By 2006 notifications rates throughout the state had increased to 179/100,000 persons of which 144/100,000 were CA-MRSA. In the metropolitan health regions the CA-MRSA notification rate was 134/100,000 whilst in the Kimberley health region the CA-MRSA notification rate had increased 40-fold to 391/100,000 [18]. CA-MRSA is thought to emerge when a locally prevalent strain of methicillin susceptible S. aureus (MSSA) acquires a SCCmec element and utilizes mobile genetic elements and single nucleotide polymorphisms to establish local and geographic niches [28]. As WA is a remote region in which all MRSA isolates are referred to a central typing laboratory it is an ideal environment to study the emergence and evolution of CA-MRSA.

The natural oxide layer worked as an etching mask at 25 min. While the heights of the pre-processed areas were exactly the same as those before etching, the area

pre-processed at 40-μN load was enlarged by the plastic KU-57788 solubility dmso deformation.Figure  12 shows the topography and cross-sectional profiles of the pre-processed areas after 30-min etching. The etching also advanced in the unprocessed area. The etching depth of the area processed at 1.5 μN progressively increased to 210 nm, while that of the unprocessed area increased to 140 nm. This implied that only the high-loaded processed area was not etched because of the mechanochemical oxide layer. The height obtained this website at 10-μN load was slightly higher than that at 40-μN load.Figure  13 shows the etching profile of pre-processed areas after 40-min etching. The etching depths of both the low-load processed and unprocessed areas were approximately 530 nm. In contrast, the areas processed at high loads of 10 and 40 μN were not etched. This experimentally confirmed that high-loaded processed protuberate areas show superior etching resistance towards

KOH solution due to formation of a high-density VS-4718 supplier oxide layer.Figure  14 shows the dependence of relative etching depth on KOH solution etching time. The standard plane is the unprocessed area. The plane heights of the areas pre-processed at 10- and 40-μN load from the standard plane are denoted as A and B. The corresponding height of the area pre-processed at 1.5-μN load is C. Between 10 and 20 min, there was little change in the topography of each area. From 25- to 30-min etching, it was observed that the etched depths significantly increased in the 1.5-μN-load pre-processed area. However, etching was hardly observed in the 10- and 40-μN-load

pre-processed areas. Etching of the unprocessed area was hardly observed until 25 min. After 30-min etching, the unprocessed area was progressively etched owing to the removal of the natural oxide layer. Figure 10 Etching profile of processed parts after 20 min. (a) Surface profile. (b) Section profile (10 and 40 μN). Figure 11 Etching profile of processed parts after 25 min. (a) Surface profile. (b) Section Liothyronine Sodium profile (10 and 40 μN). Figure 12 Etching profile of processed parts after 30 min. (a) Surface profile. (b) Section profile (10 and 40 μN). Figure 13 Etching profile of processed parts after 40 min. (a) Surface profile. (b) Section profile. Figure 14 Dependence of relative etching depth on etching time at different loads. From 35 to 40 min, the etching depths of both the unprocessed and 1.5-μN-load pre-processed areas were larger than those of the areas processed at higher load. The area mechanically pre-processed at higher load exhibited resistance to etching owing to mechanochemical oxidation layer formation.