The purpose of this study is to review operative results and dura

The purpose of this study is to review operative results and durability of open AAA repair and EVAR in octogenarians.

Methods: From May 1996 to August 2006, 150 patients aged 80 years underwent elective repair of their Epigenetics inhibitor infrarenal AAA. Eighty-one underwent EVAR and 69 had open repair. Demographic data, aneurysm specifics, comorbidities, operative morbidity, and mortality, intensive care unit and hospital length of stay, and late outcomes were analyzed.

Results: In the EVAR

group, 27 of 81 (33%) patients died during a mean follow-up of 25 months. In the open repair group, 34 of 69 (49%) patients died during a mean follow-up of 43 months. The median survival time for EVAR was 350 weeks (range, 145-404 weeks) compared with 317 weeks (range, 233-342 weeks) for the open repair group. A Kaplan-Meier log-rank analysis showed no difference in early or long-term survival between EVAR and open repair (P = .13). EVAR was associated with decreased blood loss, decreased length of intensive care unit and hospital stays, and a greater number of patients discharged to home.

Conclusions. EVAR and open repair are comparable in safety and efficacy in octogenarians. Operative repair outcomes remain acceptable. Mid-and long-term survival are similar, indicating no survival advantage of one procedure compared with AC220 in vitro the

other.”
“Background: Increased biomechanical stresses within the abdominal aortic aneurysm (AAA) wall contribute to its rupture. Calcification and intraluminal thrombus can be commonly found in AAAs, but the relationship between calcification/intraluminal thrombus and AAA wall stress is not completely described.

Methods: Patient-specific three-dimensional

AAA geometries were reconstructed from computed tomographic images of 20 Oxaprozin patients. Structural analysis was performed to calculate the wall stresses of the 20 AAA models and their altered models when calcification or intraluminal thrombus was not considered. A nonlinear large-strain finite element method was used to compute the wall stress distribution. The relationships between wall stresses and volumes of calcification and intraluminal thrombus were sought.

Results: Maximum stress was not correlated with the percentage of calcification, and was negatively correlated with the percentage of intraluminal thrombus (r = -0.56; P = .011). Exclusion of calcification from analysis led to a significant decrease in maximum stress by a median of 14% (range, 2%-27%; P < .01). When intraluminal thrombus was eliminated, maximum stress increased significantly by a median of 24% (range, 5%-43%; P < .01).

Conclusion: The presence of calcification increases AAA peak wall stress, suggesting that calcification decrease the biomechanical stability of AAA. In contrast, intraluminal thrombus reduces the maximum stress in AAA. Calcification and intraluminal thrombus should both be considered in the evaluation of wall stress for risk assessment of AAA rupture.

Rates of restenosis (defined by duplex ultrasound

Rates of restenosis (defined by duplex ultrasound INCB018424 in vitro imaging at the 1-year follow-up) were estimated using life-table analysis. Cox proportional hazards models were used to identify multivariable predictors of postoperative

restenosis <= 1 year.

Results: Across 58 surgeons and 11 hospitals, we studied 2611 conventional CEAs (88% of all CEAs) and 370 eversion CEAs (12% of all CEAs). Median follow-up was 12.8 months (range, 1-35 months). The proportion of conventional CEAs performed with patching increased from 87% to 96% (P < .001) between 2003 and 2008, whereas eversion CEA declined from 18% to 5% (P < .001). Restenosis occurred in 303 patients (10%); by life-table analysis, the restenosis rate at 1 year was 6.2% (95% confidence interval [CI], 4.7%-6.8%). Restenoses were most commonly noncritical: 50%-79% restenosis in 7.9%, 80%-99% restenosis in 1.7%, and occlusion in 0.5%. Univariate analyses showed significant differences in 80% to 100% restenosis by procedure type (2% in conventional CEA, 6% in eversion CEA, P < .002), the year of procedure (3.2% in 2003, 0% in 2008; P <

.03), and use of patching in conventional CEA (2.9% no patch, 1% with patch; P < .008). By multivariable analysis, absence of patching (hazard ratio [HR], 3.2; 95% CI, 1.5-7.0), contralateral internal carotid artery stenosis >80% (HR, 4.1; 95% CI, 1.4-11.5), and dialysis dependence (HR, 3.5; 95% CI, click here 1.2-9.8) were independently associated with a higher risk of an 80% to 100% restenosis. Of the 51 patients with 80% to 99% restenosis, 14 underwent reintervention <= 1 year, comprising 4 reoperations and 10 carotid artery stent procedures. Of the 15 patients with a carotid occlusion <= 1 year, transient ischemic attacks occurred in 2 and a disabling stroke in 1.

Conclusions: In our region, restenosis after CEA, especially clinically significant restenosis <= 1 year after surgery, decreased slightly over time. This improvement in outcome was associated with several

factors, including an increase in patching after conventional Gemcitabine price CEA, a process of care that was studied and encouraged within our vascular study group. These results highlight the utility of regional quality-improvement efforts in improving outcomes in vascular surgery. (J Vase Surg 2010;52:897-905.)”
“Background: Despite the current Centers for Medicare and Medicaid Services coverage criteria for carotid artery stenting (CAS), consensus regarding its appropriateness in patients with carotid artery stenosis has not been reached. This is one of the first population-based studies to use a dedicated administrative convention for the endovascular procedure to address whether there is a cohort of patients in whom CAS is more beneficial than carotid endarterectomy (CEA).

The predicted 88, 123 and 99 amino acid (aa) sequences of Hyd1, H

The predicted 88, 123 and 99 amino acid (aa) sequences of Hyd1, Hyd2 and Hyd3, respectively, all contained a 60-65 aa core structure that contained the Cys residues. The conserved domain analysis of translated aa sequences using Simple Modular Architecture Research Tool (SMART) identified a single hydrophobin_2 domain (Pfam 06766) between aa positions 21-86, 21-85 and 30-91for Hyd1, Hyd2 and Hyd3, respectively. This structure was further confirmed by InterproScan and Conserved Domain Search (CDS) analyses. Signal P predicted 16-18 aa long

secretion signal peptides in the N-termini https://www.selleckchem.com/products/gsk1838705a.html of each C. rosea hydrophobin. The highest similarity of Hyd1 was with cerato-ulmin of Geosmithia spp. and Ophistoma nova-ulmi (e-value 3e-07; identity 33%), of Hyd2 with T. atroviride hydrophobin and spore related hydrophobin of T. viride (e-value 3e-10; identity 41%), and of Hyd3 with hydrophobin from Fusarium

spp. (e-value 3e-32; CCI-779 nmr identity 73%). In addition, aa similarity between Hyd1, Hyd2 and Hyd3 were below 20%. Hyd1 and Hyd2 contained eight Cys in their protein sequences, while Hyd3 contained only seven as the Cys residue closest to the C-terminus was replaced by a glutamine (Gln) (Figure 1). This replacement was similar to the T. harzianum hydrophobin QID3 that also contained seven Cys [30], although Hyd3 did not show the extended N-terminus of QID3. The Cys spacing of Hyd1, Hyd2 and Hyd3 conformed to the pattern of Class II (Figure 1). Furthermore, the hydropathy patterns of Hyd1, Hyd2 and Hyd3 were all indicative of class II hydrophobins (data not shown). Taken together, these analyses suggest that C. rosea Hyd1, Hyd2 and Hyd3 encode putative class II hydrophobins. Figure 1 Sequence alignment of C . rosea hydrophobins. Amino acid sequence alignment of C. rosea hydrophobins with class II hydrophobins from Trichoderma spp. and additional representatives of known class II hydrophobins. The amino acid sequences from first Cys to eight Cys residues were used for the alignment. Conserved residues in a column are indicated in white and boxed in black; two different

conserved residues in a column are highlighted by grey boxes; gaps are indicated by dashes. Conserved Cys residues are indicated G protein-coupled receptor kinase by asterisks. A phylogenetic tree was constructed with Hyd1, Hyd2 and Hyd3 together with class II hydrophobins from Trichoderma spp. and additional representatives of known class II hydrophobins (Additional file 1: Table S1). The result from the phylogenetic analysis click here showed that Hyd1, Hyd2 and Hyd3 do not represent recent gene duplicates as they clustered in different parts of the tree (Figure 2). Figure 2 Phylogenetic analysis of C . rosea hydrophobins. Phylogenetic analysis of class II hydrophobins using maximum likelihood methods implemented in PhyML-aBayes. Pleurotus ostreatus hydrophobins are used as out group.

This plasmid was introduced into L monocytogenes EGD by electrop

This plasmid was introduced into L. monocytogenes EGD by electroporation and gene replacement was performed as described previously [30]. Chloramphenicol-sensitive clones were screened for the presence of the hly deletion by PCR with primers llo-1 and llo-4. A shorter PCR product was amplified from strains that had undergone allelic exchange to introduce

the deleted version of the wild-type allele selleck inhibitor on the chromosome. The hly deletion was further verified by DNA sequencing and the absence of a hemolytic phenotype during growth of bacteria on BHI agar medium supplemented with 5% sheep blood. The hly gene preceded by its ribosome binding site was amplified by PCR from strain EGD chromosomal DNA using the primer pair Hly-1 and Hly-2. DNA Polymerase pfu (Fermentas) was

used in the PCR. The amplified fragment was digested with BamHI and SalI and cloned using the corresponding restriction sites into the high-copy-number E. coli-gram positive bacteria shuttle vector pAT28 [31] to produce plasmid pAT28-hly. The hly sequence cloned in pAT28-hly, used for the generation of libraries, was confirmed by DNA sequencing. Four genomic DNA libraries were constructed Ruxolitinib ic50 in pAT28-hly. Chromosomal DNA from L. monocytogenes EGD was mechanically sheared using a nebulizer according to the manufacturer’s instructions (Invitrogen) or was partially digested with restriction endonucleases BsuRI, Bsh1236I or simultaneously with BsuRI and Bsh1236I. In each case, the fragmented DNA was separated by gel electrophoresis and fragments with a size distribution from 500 to 2000 bp were excised from the gel and purified. In the case of the DNA fragments obtained by nebulization, the ends were blunted by treatment with T4 DNA polymerase (Fermentas). All four DNA fragment pools were then cloned into the SmaI site of pAT28-hly using a two-step ligation SAHA HDAC procedure [32]. After purification,

each plasmid library was introduced into L. monocytogenes strain EGDΔhly by electroporation. The transformants were plated on BHI-SPC agar supplemented with 5% defibrinated sheep blood and penicillin G (0.03 μg/ml), and incubated overnight at 37°C. Approximately 2.3 × 103, 1 × 104, heptaminol 3 × 103 and 6.7 × 103 recombinant L. monocytogenes were obtained for the libraries created using DNA fragmented by nebulization, BsuRI, Bsh1236I or simultaneous BsuRI and Bsh1236I digestion, respectively. Among these clones, the frequencies of hemolytic colonies were 0.6%, 1.1%, 2.6% and 0.9%, respectively. The total number of hemolytic clones identified was 259. All hemolytic clones were replica plated on BHI-SPC agar supplemented with 5% defibrinated sheep blood alone, and on BHI-SPC agar supplemented with 5% defibrinated sheep blood plus penicillin G (0.03 μg/ml). After overnight incubation at 37°C, the diameter of zones of hemolysis created by each clone during growth on plates with and without penicillin G was compared.

p i with higher loads of murinised Lmo-InlA-mur-lux bacteria, th

p.i. with higher loads of murinised Lmo-InlA-mur-lux bacteria, these differences were not further detectable at 5 and 7 days p.i.. We therefore conclude that at least in our infection system, InlA-Cdh1 Veliparib order interactions do not play a role in the dissemination of L. monocytogenes to the brain. Moreover, even in different mouse genetic backgrounds no evidence for InlA-mediated CNS infection was found. Table 1 Neurological symptoms in mouse inbred strains after oral infection with Lmo-InlA-mur-lux and

Lmo-EGD-lux L. monocytogenes strain Mouse inbred strain Total number of mice infected Number of mice displaying neurological abnormalities Symptoms occurrence time post infection [days] Lmo-InlA-mur-lux C3HeB/FeJ 40 0     A/J OlaHsd 30 1 7   BALB/cJ 30 0     C57BL/6J 30 1 7     ∑ 130 ∑ 2   Lmo-EGD-lux C3HeB/FeJ 40 0     A/J OlaHsd 40 0     BALB/cJ 40 1 7   C57BL/6J RGFP966 order 40 0       ∑ 160 ∑ 1   Discussion In vivo bioluminescence imaging is an important technology for the spatial-temporal monitoring of infection processes that underlie microbial pathogenesis and host defence mechanisms [30, 36]. Importantly, BLI allows repeated non-invasive imaging of pathogen dissemination to target organs and was used to identify the murine gallbladder as a novel

organ of infection and as a host reservoir for extracellular Listeria replication and pathogen shedding [19, 37]. In the present study, we have combined an InlA and Anidulafungin (LY303366) InlB permissive mouse infection model of L. monocytogenes[12] with BLI, bacterial growth, and histopathology. We accurately compared resistance of mouse strains of different genetic backgrounds to orally acquired murinised and non-murinised Listeria. We identified the C3HeB/FeJ, A/J, and BALB/cJ strains as being susceptible to oral L. monocytogenes challenge whereas C57BL/6J mice were resistant. BLI analysis was more sensitive than bacterial culture or histopathology at detecting differences in pathogenesis between the murinised and non-murinised Listeria strains, and demonstrated that in the susceptible mouse inbred

strains Lmo-InlA-mur-lux spread to internal organs more quickly and in higher APR-246 numbers when compared to Lmo-EGD-lux infected animals. Thus, murinised Listeria can efficiently be used with mice of different genetic backgrounds for studies on mechanisms of orally acquired listeriosis. Importantly, once the intestinal barrier has been overcome by the pathogen, patterns of L. monocytogenes host resistance that have been previously determined by using systemic infection models are very similar to those that were observed in our present study. C57BL/6J mice are resistant to both oral and intravenous L. monocytogenes infection challenge, whereas C3HeB/FeJ, A/J and BALB/cJ mice are highly susceptible in both mouse infection models [38–42]. We show here that the host resistance of C57BL/6J mice to intragastric L.

Treatment

Treatment www.selleckchem.com/products/Acadesine.html holiday was not allowed. Median time to progression with first treatment with cetuximab was 10 months, the median interval time between last cycle of first cetuximab-based therapy and first cycle of the following cetuximab retreatment was 6 months. Caspase Inhibitor VI manufacturer Moreover, ORR was 53.8% with 19 partial responses (48.7%) and 2

complete responses (5.1%). The median time to progression (TTP) was 6.6 months, stable disease (SD) was obtained in 35.9% of patients and progression in 4 (10.2%), and 18 patients (46.1%) showed the same type of response (SD, partial response or complete response) during cetuximab retreatment when compared with the response obtained during the first cetuximab-based therapy. Then stable disease lasting at least 6 months and partial response during the first cetuximab-based therapy have been demonstrated to predict clinical benefit after cetuximab retreatment [30]. Conversely, a subsequent phase II prospective GSK1210151A clinical trial study, including twenty patients treated with panitumumab after progression on prior cetuximab-based therapy, did not show any response to panitumumab being stable disease (no progression for at least two cycles) the best response in 45% of patients [31]. This study showed that panitumumab has a minimal effect

after disease progression on cetuximab; however, no interval therapy or treatment holiday were permitted between cetuximab and panitumumab administration. Diaz Jr et al. evaluated the variation of circulating tumor DNA (ctDNA) in serum of 24 patient receiving single-agent therapy

with panitumumab. K-Ras mutations were recorded in 38% of cases between 5–6 months following treatment and mathematical modelling indicated that mutations were present in expanded subclones before the initiation of treatment. These results suggest that the emergence Phenylethanolamine N-methyltransferase of KRAS mutations is a mediator of acquired resistance to EGFR blockade [32]. Consistently, another small study showed that point mutations of K-Ras are casually associated with the onset of acquired resistance to anti-EGFR therapy. In fact analysis of metastasis from ten patients who developed resistance to cetuximab or panitumumab showed the emergence of K-Ras mutant alleles were detectable in the blood months before the radiographic documentation of disease progression, and the in vitro model confirmed the hypothesis of continuing mutagenesis under the pressure of anti-EGFR therapy [33]. These studies underlined the possibility of late acquisition of K-Ras secondary mutations under anti EGFR therapy but still do not confute the possibility of a rechallenge.

2 Minor glomerular abnormalities 216 25 1 408 37 5 624 32 0 Mesan

2 Minor glomerular abnormalities 216 25.1 408 37.5 624 32.0 Mesangial proliferative glomerulonephritis 167 19.4 86 7.9 253 13.0 Focal segmental Peptide 17 nmr glomerulosclerosis 113 13.1 149 13.7 262 13.4 Membranoproliferative glomerulonephritis (types I and III) 48 5.6 51 4.7 99 5.1 Crescentic and necrotizing glomerulonephritis 19 2.2 18 1.7 37 1.9 Endocapillary

proliferative glomerulonephritis 8 0.9 24 2.2 32 1.6 Chronic interstitial nephritis 7 0.8 3 0.3 10 0.5 Sclerosing glomerulonephritis 7 0.8 3 0.3 10 0.5 Nephrosclerosis 5 0.6 7 0.6 12 0.6 Acute interstitial nephritis 1 0.1 0 – 1 0.1 Acute tubular necrosis 0 – 1 0.1 1 0.1 Others 11 1.3 9 0.8 20 1.0 Total 861 AZD6244 cost 100.0 1,089 100.0 1,950 100.0 In the patients with nephrotic syndrome as classified by the clinical diagnosis, primary glomerular disease other than IgAN was the predominant diagnosis in both 2009 and 2010, followed by diabetic nephropathy, Epigenetics inhibitor which was the same order as in 2007 and 2008 (Table 9). In 2010, minor glomerular abnormalities were the leading diagnosis, followed by MN, FSGS, and MPGN (types I and III) (Table 10). Table 9 The frequency of pathological diagnoses as classified by pathogenesis in nephrotic syndrome in native kidneys in J-RBR 2009 and 2010 Classification 2009 2010 Total n % n % n % Primary glomerular disease (except IgA nephropathy) 442 62.3 696 Bumetanide 66.7 1,138 64.9 Diabetic nephropathy 85 12.0 78 7.5 163 9.3 IgA nephropathy 30 4.2 36 3.5 66 3.8 Lupus nephritis 30 4.2 58 5.6 88 5.0 Amyloid nephropathy 27 3.8 41 3.9 68 3.9 Infection-related nephropathy 6 0.8 7 0.7 13 0.7 Hypertensive nephrosclerosis 6 0.8 10 0.9 16 0.9 Purpura nephritis 4 0.6 8 0.8 12 0.7 Alport syndrome 3 0.4 0 – 3 0.2 Thrombotic microangiopathy 1 0.1 1 0.1 2 0.1 PR3-ANCA positive nephritis 1 0.1 0 – 1 0.1 MPO-ANCA positive nephritis 1 0.1 2 0.2 3 0.2 Others 74 10.4 106 10.2 180 10.3 Total 710 100.0

1,043 100.0 1,753 100.0 MPO myeloperoxidase, ANCA anti-neutrophil cytoplasmic antibody, PR3 proteinase 3 Table 10 The frequency of pathological diagnoses as classified by histopathology in primary glomerular disease except IgA nephropathy in nephrotic syndrome in native kidneys in J-RBR 2009 and 2010 Classification 2009 2010 Total n % n % n % Membranous nephropathy 178 40.3 227 32.6 405 35.6 Minor glomerular abnormalities 172 38.9 348 50.0 520 45.7 Focal segmental glomerulosclerosis 47 10.6 82 11.8 129 11.3 Membranoproliferative glomerulonephritis (types I and III) 25 5.7 18 2.6 43 3.8 Mesangial proliferative glomerulonephritis 11 2.5 13 1.9 24 2.1 Crescentic and necrotizing glomerulonephritis 2 0.5 2 0.3 4 0.4 Sclerosing glomerulonephritis 2 0.5 0 – 2 0.

However, the process of cancer initiation, metastasis and recurre

However, the process of cancer initiation, metastasis and recurrence is sequential and selective, and consists of a series of independent steps with interlinks [3–6]. Reportedly, CD133 expressing cells in glioblstoma and colorectal cancers include, Selleck Pexidartinib but are apparently not limited to, the small subpopulation of tumor cells

termed as cancer stem cells (CSCs) which mediate tumor initiation, metastasis and recurrence [4–6], and possess the unique self-renewal properties, the multiple differentiating potential, the proliferating aptitude and the carcinogenesis [5, 7, 8]. In addition to being considered as the tumor initiating cell population, CSCs have also been demonstrated to resistance to chemotherapy and radiotherapy implying that they are responsible for tumor recurrence [9, 10]. At the same time, CD133 has been considered as a CSCs marker in many kinds of tumors such as colorectal [5, 6], brain [4, 7], prostate [8], pancreatic [11] and gastric cancers [12]. One of the aims in this study was to investigate the expression

levels of CD133 CH5183284 nmr protein and CD133 mRNA in primary lesion of gastric adenocarcinoma (GC) and to compare these expressive levels with clinicopathological characteristics and survival time after curative resection. Additionally, we explored the relation of CD133 mRNA expression level with lymphatic vessel infiltration, lymph node metastasis and metastatic lymph node ratio [13] which factors reflected the status of lymphatic metastasis demonstrated wildly as one of the main risk factors for the prognosis. At the same time, immunostaining for Ki-67, a kind of cellule nucleus protein, and its labeling index

(LI) were applied to assess the proliferating ability of tumor cells with higher or lower CD133 mRNA level and the relation of this proliferating ability of tumor cells sharing higher or lower CD133 mRNA level were evaluated. Methods LY2835219 mw patients A total of 99 patients who underwent radical gastrectomy (D2 or D3; R0 or R1) for primary GC at our hospital from July 2004 to July 2009 were registered Nintedanib (BIBF 1120) for immunohistochemical staining in this study. The median age of the patients was 62.0 years old (range 29~83 years old) in this group of patients. Among them, a total of 31 patients from May 2008 to July 2009 were also assessed by semi-quantitative RT-PCR for detecting CD133 mRNA in primary lesion and in noncancerous gastric tissue (NCGT), which was identified by pathological observation, at > 5 cm distance adjacent to primary lesion, and by immunohistochemical staining for Ki-67 expression in tumor cells. In this group of patients, the median age of the patients was 64.0 years old (range 34~83 years old). None of them accepted any preoperative chemotherapy or radiotherapy. All of the cases received postoperative adjuvant chemotherapy. The diameter of tumors was ranged from 1 to 10 cm; median 5.0 cm.

J Antimicrob Chemother 2009,64(6):1175–1180 PubMedCrossRef 38 Ch

J Antimicrob Chemother 2009,64(6):1175–1180.PubMedCrossRef 38. Chamot D, Owttrim GW: Regulation of cold shock-induced RNA helicase gene expression in the Cyanobacterium anabaena sp. strain PCC 7120. J Bacteriol 2000,182(5):1251–1256.PubMedCrossRef 39. Chinni SV, Raabe CA, Zakaria R, Randau G, Hoe CH, Zemann A, Brosius J, Tang TH, Rozhdestvensky TS: Experimental identification and characterization of 97 novel npcRNA candidates in Salmonella enterica

serovar Typhi. Nucleic Acids Res 2010,38(17):5893–5908.PubMedCrossRef 40. Rosenblum R, Khan E, Gonzalez G, Hasan R, Schneiders T: Genetic regulation of the ramA locus and its expression in clinical isolates of Klebsiella pneumoniae. Int J Antimicrob Agents 2011,38(1):39–45.PubMedCrossRef 41. Horiyama T, Nikaido E, Yamaguchi A, Nishino K: Roles of Salmonella CP673451 purchase multidrug efflux pumps in tigecycline

resistance. J Antimicrob Chemother 2011,66(1):105–110.PubMedCrossRef 42. Tjaden B: TargetRNA: a tool for predicting targets of small RNA action in bacteria. Nucleic Acids Res 2008,36(Web Server issue):W109–113.PubMedCrossRef 43. Darwin AJ: The phage-shock-protein response. Mol Microbiol 2005,57(3):621–628.PubMedCrossRef selleck products 44. Santiviago CA, Reynolds MM, Porwollik S, Choi SH, Long F, Andrews-Polymenis HL, McClelland M: Analysis of pools of targeted Salmonella deletion mutants identifies novel genes affecting fitness during competitive infection in mice. PLoS Pathog 2009,5(7):e1000477.PubMedCrossRef 45. Papenfort K, Pfeiffer V, Lucchini S, Sonawane A, Hinton JC, Vogel J: Systematic deletion of Salmonella small RNA genes identifies CyaR, a conserved CRP-dependent riboregulator of OmpX synthesis. Mol Microbiol 2008,68(4):890–906.PubMedCrossRef

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With regard to international recommendations, guidelines and repo

With regard to international recommendations, guidelines and reports, Sequeiros et al. (2012) concluded that a common consensus definition of genetic testing does not exist. The authors argue that a clear set of precise definitions may help create a common language among geneticists and other health professionals, and that a clear context-dependent, operative definition should always be given. Sirpa Soini’s presentation covers genetic testing legislation. Five countries have enacted genetic-specific laws, and three have comprehensive provisions pertaining to genetic testing in their biomedical legislation.

Central provisions cover the informed consent, autonomy and integrity of the person tested, further uses of tests Apoptosis inhibitor results, and quality requirements of the personnel and facilities involved. The notion Selleckchem GSK1904529A of genetic exceptionalism was characteristic to the normative reactions in the legal

acts, but Soini (2012) questions how justified this is. Acknowledgments Research grants making this series of lectures possible have been received from: the Erik-Philip Sörensen Foundation for Research in Medicine and the Humanities, the Karin and Hjalmar Tornblad Foundation, the Fahlbeck Foundation and the Nilsson-Ehle Foundations of the Royal Physiographic Society in Lund. All contributors to this special issue are acknowledged for their contributions making this special volume possible. Seminars 11 and 12 were held in collaboration with the Learning U0126 purchase and Media Technology Studio (LETStudio),

University EPZ5676 of Gothenburg. References Abraham J, Ballinger R (2012) Power, expertise and the limits of representative democracy: genetics as scientific progress or political legitimation in carcinogenic risk assessment of pharmaceuticals? J Community Genet. doi:10.​1007/​s12687-011-0060-2 Cornel MC, van Carla G, El CG, Dondorp WJ (2012) The promises of genomic screening: 1 building a governance infrastructure. J Community Genet. doi:10.​1007/​s12687-011-0056-y Gottweis H, Lauss G (2012) Biobank governance: heterogeneous modes of ordering and democratization. J Community Genet. doi:10.​1007/​s12687-011-0070-0 Howard H, Borry P (2012) Is there a doctor in the house? The presence of physicians in the direct-to-consumer genetic testing context. J Community Genet. doi:10.​1007/​s12687-011-0062-0 Nuffield Council on Bioethics (2002) Genetics and human behaviour—the ethical context. http://​www.​nuffieldbioethic​s.​org/​sites/​default/​files/​Genetics%20​and%20​human%20​behaviour.​pdf Sequeiros J, PanequeM GB, Rantanen E, Javaher P, Nippert I, Schmidtke J, Kääriäainen H, Kristoffersson U, Cassiman J-J (2012) The wide variation of definitions of genetic testing in international recommendations, guidelines and reports. J Community Genet. doi:10.​1007/​s12687-012-0084-2 Soini S (2012) Genetic testing legislation in the Western Europe—a fluctuating regulatory target. J Community Genet. doi:10.