However, overexpression of NME1 and NME2 genes was found only in

However, overexpression of NME1 and NME2 genes was found only in SH-SY5Y cells after combined treatment

with ATRA and inhibitors. The overexpression of this gene family was reported to be associated with more differentiated phenotypes in human and murine neuroblastoma cell lines [33–35]. Similar changes were observed in the SH-SY5Y cell line and in the expression of the CDKN1A gene after combined treatment with ATRA and both inhibitors; the CDKN1B gene was overexpressed in SH-SY5Y cells with a combination of ATRA and CX only. An increase in the expression of cyclin kinase inhibitors by RA alone and in combination with histone deacetylase inhibitors was Selleck Captisol reported [36]. Moreover, inhibition of cdk activity was repeatedly confirmed to be a determinant of neuronal differentiation [37]. The same expression pattern was found in SH-SY5Y cells and for the NINJ1 gene; this gene encodes adhesion molecules promoting find more neurite outgrowth [38]. RA-induced differentiation of neuroblastoma

cells is also associated with the overexpression of tumor necrosis factor receptors (TNFRs) [39]. In SH-SY5Y cells, we noted JPH203 order an increase in the expression of the TNFRST10B gene after treatment both with 10 μM ATRA alone and with all combinations of ATRA and inhibitors. To summarize, in addition to the genes generally overexpressed in both cell lines after combined treatment, as listed above, we also identified other genes that are specifically influenced in specific cell lines, including SK-N-BE(2) or SH-SY5Y. These genes are also known to be involved in the process of neuronal differentiation in neuroblastoma cells; however, their regulation is obviously cell Metalloexopeptidase type-specific and is independent of the inhibitor type. Nevertheless, we also determined sets of genes influenced specifically

by combined treatment with ATRA and CA in both SK-N-BE(2) and SH-SY5Y cell lines; but changes in the gene expression of such genes may differ between these cell lines. In contrast, the very same increase of AKT1 gene expression in both cell lines treated with the combination of 1 μM ATRA and CA was observed. Published results on SH-SY5Y cells suggest that the PI3K/Akt signaling pathway is activated during RA-induced differentiation [40]. We also identified genes influenced specifically by the combined treatment with ATRA and CX in both SK-N-BE(2) and SH-SY5Y cell lines. The most interesting finding is the overexpression of the HMGA1 gene in both cell lines after combined treatment with ATRA and CX in a concentration-dependent manner. According to published data, retinoic acid may increase HMGA1 expression in RA-resistant neuroblastoma cells, but it inhibits this expression in cells undergoing RA-induced neuronal differentiation [41].

Thus, the genetic family would be limited to blood relatives and

Thus, the genetic DNA Damage inhibitor family would be limited to blood relatives and spouses

and would exclude adopted children as well as same sex and cohabitating partners or others who may have a need to know the information aside from their own personal health. While on the surface this definition appears unequivocal in identifying who is a genetic family member, it is problematic as there is potentially no limit to the degree of biologic relation that could be included, however far removed. This disregards the practical realities of family dynamics, by asking patients to disclose genetic information to distant blood relatives with whom the patient has little to no preexisting social relationship. Sapitinib price It also ignores the interests of non-blood relations. Further, it ignores the contribution that other family members could make in disseminating family history information (Koehly

et al. 2009). In contrast, there is a broad view of the genetic family that accounts for both biological and social interests. According to this biosocial model, in the absence of a biological relationship, a preexisting social relationship could substitute as the defining criteria for identifying a family member (Gilbar 2005). As a consequence, a wide range of relationships would qualify as familial relationships, such as same SC79 concentration sex partners. In addition, in the complete absence of a preexisting social relationship, this model could excuse

individuals from classification as family members, even if there is a biological relationship. This, for example, would allow for exclusion of a sperm donor from family or distant cousins who have never met. The emphasis on the sociological aspect, however, is not without criticism. One can question the reasoning or fairness of refusing to communicate with close family members in families that are in the midst of breakdown or with whom a patient has never had a personal relationship (assuming the patient knows of the family members and has PDK4 the means and knowledge to contact them). This disadvantage aside, the flexibility afforded by the biosocial model represents a key advantage, as the model is capable of adapting to the myriad of legal and social relationships found within today’s modern family. Recognizing the unique challenges brought about through knowledge of genetic information, many organizations, including ethics and medical genetics groups and physician and patient advocacy groups, have attempted to acknowledge both the familial and individual nature of genetic information (Forrest et al. 2007). Some European bodies have addressed the definition of the family directly and have adopted either narrow or broad views of the family.

J Clin Endocrinol Metab 2004,89(2):632–7 PubMedCrossRef 289 Wagn

J Clin Endocrinol Metab 2004,89(2):632–7.PubMedCrossRef 289. Wagner G, Kindrick S, Hertzler S, DiSilvestro RA: Effects of various Ku 0059436 forms of calcium on body weight and bone turnover markers in women participating in a weight loss program. J Am Coll Nutr 2007,26(5):456–61.PubMed 290. Yanovski JA, Parikh SJ, Yanoff LB, Denkinger BI, Calis KA, Reynolds JC, Sebring NG, McHugh T: Effects of calcium supplementation on body weight and adiposity in overweight and obese adults: a randomized trial. Ann Intern Med 2009,150(12):821–9. W145–6PubMed 291. Zemel M, Thompson

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Assignment to a family or subfamily within the TC system often al

Assignment to a family or subfamily within the TC system often allows prediction of substrate type with confidence [13, 20, 135–137]. When an expected transport protein constituent of a multi-component transport system could not be identified with BLASTP, tBLASTn was performed because such expected proteins are sometimes undetectable by BLASTP due to sequencing errors, sequence divergence, or pseudogene formation. Transport proteins thus Selleckchem Tubastatin A obtained were systematically analyzed for unusual properties using published [132] and unpublished in-house software. Unusual properties can result from events such as genetic deletion and fusion, sometimes resulting in the gain or loss of extra domains or the generation of multifunctional

proteins. Such results can be reflective of the actual protein sequence, but can also be artifactual, due to sequencing errors or incorrect initiation codon assignment. In the latter cases, but not the former, click here the protein sequences were either corrected when possible or eliminated from our study. This theoretical bioinformatics study does not contain any experimental

research that requires the approval of an ethics committee. Acknowledgements We thank Carl Welliver and Maksim Shlykov for valuable assistance in the preparation of this manuscript. This work was supported by NIH Grant GM077402. Electronic supplementary material Additional file 1: Table S1: Sco transport proteins. Detailed description of Sco 4SC-202 concentration transport proteins and their homologues in TCDB, including comparison scores obtained via G-Blast and GSAT, oxyclozanide substrate, substrate class, organism, phylum, and organismal domain. Proteins are organized from lowest to highest TC#. (DOCX 205 KB) Additional file 2: Table S2: Mxa transport proteins. Detailed description of Mxa transport proteins and their homologues in TCDB, including comparison scores obtained via G-Blast and GSAT, substrate, substrate class, organism, phylum, and organismal domain. Proteins are organized from lowest to highest TC#. (DOCX 133 KB) Additional file 3: Table S3: Chromosomal

distribution of Sco transporters. Sco transport proteins distributed by chromosomal arms and core. (DOCX 21 KB) References 1. de Hoon MJ, Eichenberger P, Vitkup D: Hierarchical evolution of the bacterial sporulation network. Curr Biol 2010,20(17):R735–745.PubMedCentralPubMed 2. Flardh K, Buttner MJ: Streptomyces morphogenetics: dissecting differentiation in a filamentous bacterium. Nat Rev Microbiol 2009,7(1):36–49.PubMed 3. Gogolewski RP, Mackintosh JA, Wilson SC, Chin JC: Immunodominant antigens of zoospores from ovine isolates of Dermatophilus congolensis. Vet Microbiol 1992,32(3–4):305–318.PubMed 4. Setubal JC, dos Santos P, Goldman BS, Ertesvag H, Espin G, Rubio LM, Valla S, Almeida NF, Balasubramanian D, Cromes L, et al.: Genome sequence of Azotobacter vinelandii, an obligate aerobe specialized to support diverse anaerobic metabolic processes.

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K, Hepel M: Resonance elastic light scattering (RELS) spectroscopy of fast non-Langmuirian ligand-exchange in glutathione-induced gold nanoparticle assembly. J Colloid Interface Sci 2010, 350:168–177.CrossRef 39. Jadzinsky PD, Calero G, Ackerson CJ, Bushnell DA, Kornberg RD: Structure of a thiol monolayer-protected gold nanoparticle at 1.1 Å resolution. Science 2007, 318:430–433.CrossRef 40. Cho CE, Zhang Q, Xia Y: The effect of sedimentation and diffusion on cellular uptake of gold nanoparticles. Nat Nanotechnol 2011, 6:385–391.CrossRef Adriamycin 41. Mosmann T: Rapid colorimetric assay for cellular growth and survival: application to proliferation and cytotoxicity assays. J Immunol Methods 1983, 65:55–63.CrossRef 42. Borenfreund E, Puerner JA: Toxicity determined in vitro by morphological alterations and neutral red absorption. Toxicol Lett 1985, 24:119–124.CrossRef 43. O’Brien J, Wilson I, Orton T, Pognan F: Investigation of the alamar blue (resazurin) fluorescent dye for the assessment of mammalian cell cytotoxicity. Eur J Biochem 2000,

267:5421–5426.CrossRef 44. why Wang H, Joseph AJ: Quantifying cellular oxidative stress by dichlorofluorescein assay using microplate reader. Free Radical Bio Med 1999, 27:612–616.CrossRef 45. Allen S, Shea JM, Felmet T, Gadra J, Dehn PF: A kinetic microassay for glutathione in cells plated on 96-well microtiter plates. Methods Cell Sci 2001, 22:305–312.CrossRef 46. Krpetic Z, Nativo P, Porta F, Brust M: A multidentate peptide for stabilization and facile bioconjugation of gold nanoparticles. Bioconjug Chem 2009, 20:619–624.CrossRef 47. Liu X, Atwater M, Wang J, Huo Q: Extinction coefficient of gold nanoparticles with different sizes and different capping ligands. Colloids Surf B 2007, 58:3–7.CrossRef 48. Si S, Dinda E, Mandal TK: In situ synthesis of gold and silver nanoparticles by using redox-active amphiphiles and their phase transfer to organic solvents. Chem Eur J 2007, 13:9850–9861.CrossRef 49.

Both can be administered more quickly and can provide more rapid

Both can be administered more quickly and can provide more rapid reversal of warfarin anticoagulation GW3965 research buy as defined by normalization of the INR [10–14]. The doses of PCC and rFVIIa administered in these reports has varied widely and thus the optimal dose for reversal of warfarin anticoagulation with these products is unknown. Additionally, there is little information about potential differences in the efficacy and safety of rFVIIa when compared with PCC. There is limited data in the literature reporting a comparison of PCC and rFVIIa for warfarin anticoagulation reversal [14]. Our institution uses both a 3 factor PCC (PCC3) weight based doses at 20 units/kg regardless of INR and low dose rFVIIa (LDrFVIIa) 1000

mcg or 1200 mcg for serious and life-threatening bleeding in patients anticoagulated with warfarin. To evaluate these QNZ chemical structure therapies,

we reviewed the charts of patients who required emergent reversal of warfarin anticoagulation and who received either PCC as a 3 factor product (PCC3) or LDrFVIIa to compare the safety and efficacy of these coagulation factor products. Our hypothesis was that PCC3 and LDrFVIIa are equally effective and PF-3084014 mw safe for warfarin anticoagulation reversal. Methods Institutional review board approval was obtained and a retrospective chart review was conducted at North Memorial Medical Center, an American College of Surgeons verified level 1 trauma center. The electronic medical record database was searched to identify all patients who received either PCC or rFVIIa from August 29th, 2007 to October 10th, 2011. A review of the electronic medical record of those patients was conducted to identify patients

who met the following inclusion criteria: Clear documentation of warfarin usage prior to admission, a need for emergent reversal of warfarin anticoagulation and a pre-reversal INR of 1.6 or greater, received either prothrombin complex concentrate (PCC3, 20 units/kg rounded to nearest 500 units) or low-dose recombinant Factor VIIa (LDrFVIIa, 1000 or 1200 mcg), and at least one INR obtained pre and one INR obtained Inositol monophosphatase 1 post coagulation factor administration. Fresh frozen plasma and vitamin K were administered at provider discretion. Patients were excluded if they had no pre or post coagulation factor INR, a pre-reversal INR of 1.5 or less, received both PCC3 and LDrFVIIa, received more than one PCC3 or rFVIIa dose before follow-up INR, or received any single rFVIIa dose greater than 1200 mcg. The PCC3 product used was Profilnine® SD (Grifols Biologicals Inc., Los Angeles, CA) and the rFVIIa product was NovoSeven® or NovoSeven RT® (Novo Nordisk Inc., Princeton, NJ). The following data were collected: 1) Demographic: age, gender, indication for warfarin, and indication for reversal; 2) Coagulation parameters: INR pre and post administration of either PCC3 or LDrFVIIa, change in INR (absolute and percent change), achievement at INR of 1.5 or less, and time to reach INR 1.

Methods Study subjects and data collection In this hospital-based

Methods Study subjects and data collection In this hospital-based case-control study, the case group consisted of 285 diagnosed nonsmoking female patients (between January 2002 and November 2007) with histologically confirmed lung adenocarcinoma. At the same time controls

were selected from cancer-free patients with other lung diseases but free of cancer history and symptom. Selleckchem Liproxstatin 1 Controls were all non-smoking females and frequency matched to cases on age (± 5 years). Controls suffered mainly from bronchitis, pneumonias, fibrosis, sarcoidosis, chronic obstructive pulmonary disease and emphysema. The human investigations were approved by the Institutional Review Board of China Medical University, and informed consent was obtained from each participant or each participant’s representatives if direct consent could not be obtained. All patients were all unrelated ethnic PF-573228 ic50 Han Chinese. Each participant donated 10 ml venous blood and was interviewed to collect demographic data and environmental exposures at the time they were admitted to the hospital. Information concerning demographic characteristics, passive smoking, cooking oil fume exposure, fuel smoke exposure, family history of cancer, occupational exposure and dietary habit was obtained for each case and control by trained interviewers. Individual with a total

of 100 cigarettes in his lifetime was defined as a smoker, otherwise he was considered as a non-smoker. For cooking oil fume exposure, participants were asked about the frequency of cooking and types of oils. Subjects were also asked “”How often did the air in your kitchen become filled with oily ‘smoke’ during cooking?”" For each of these questions, there were four possible responses ranging from “”never”", “”seldom”", Thiamet G “”sometimes”", to “”frequently”". Exposure for cooking oil fume was categorized as an indicator variable equal to 1 if participants reported

frequently or sometimes, and equal to 0 otherwise. DNA isolation and genotyping Genomic DNA samples were isolated by guanidine hydrochloride (GuHCl) method. SNPs were analyzed by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method as described previously [5]. The PCR primers (Takara Biotechnology Dalian Co. Ltd., China) for amplifying DNA fragment containing the ERCC2 751Lys/Gln, 312Asp/Asn, and ERCC1 118Asn/Asn were 751 F5′-GCC CGC TCT GGA TTA TAC G-3′ and R5′-CTA TCA TCT CCT GGC CCC C-3′, 312 F5′-CTG TTG GTG GGT GCC CGT ATC TGT TGG TCT-3′ and R5′-TAA TAT CGG GGC TCA CCC TGC AGC ACT TCC T-3′, 118 F5′-AGG ACC ACA GGA CAC GCA GA-3′ and R5′-CAT AGA ACA GTC CAG AAC AC-3′, respectively. The PCR products were digested with restriction enzyme (New England Biolabs, Beverly, MA) PstI (for Lys751Gln), StyI (for Asp312Asn), and BsrdI (for Asn118Asn) to determine the genotypes.

The second DNA fragment was amplified using the forward primer: F

The second DNA fragment was amplified using the forward primer: F2Nc-β-gal GGCAAGCGTTTTCCAAGCGG, and and reverse primer: R32c-β-gal CCCCGTCGACTTTTCTAGA TCAGTCCTCCGCGATCAC (containing SalI recognition site, underlined). The start and stop codons are given in bold. mTOR inhibitor For the NcoI sticky end generation the second forward F2Nc-β-gal primer contains only one nucleotide of the start codon. Each PCR reaction mixture contained: 0.2 μM of each primer, 0.2 μg of pBADmycHisALibB32c DNA, 250 μM of each dNTP, 1 U of DNA polymerase (Hypernova, DNA-Gdańsk, Poland) in 1 × PCR buffer (20 mM Tris-HCl pH 8.8, 10 mM KCl, 3.4 mM MgCl2, 0.15% Triton X-100).

The reaction mixtures were incubated for 3 min at 95°C, followed by 5 cycles at 95°C for 1 min, 50°C for 1 min, 72°C for 2 min and 25 cycles at 95°C for 1 min, 60°C for 1 min, 72°C for 2 min and a final incubation for 5 min at 72°C using a Mastercycler Gradient (Eppendorf, Germany). Both amplification reaction products were purified and mixed together at ratio 1:1. This mixture was denaturated at 95°C NSC 683864 for 3 min and cooled down to room temperature at 0.2°C/s. Roscovitine research buy Afterwards DNA were purified by ethanol precipitation, digested with SalI endonuclease and cloned into pBAD/Myc/HisA (Invitrogen) vector pre-cutted with NcoI and SalI endonucleases. The resulting recombinant plasmid

pBAD/Myc/HisA-β-gal32c containing the Arthrobacter sp. 32c β-D-galactosidase gene under control of the pBAD promoter was used to transform chemically competent E. coli LMG194 plysN cells [29] Expression of the recombinant β-D-galactosidase gene in E. coli The recombinant plasmid pBAD/Myc/HisA-32cβ-gal was used for the expression of the putative β-D-galactosidase gene in E. coli LMG 194 plysN under the control of pBAD promoter. The cells were grown overnight at 37°C in LB medium containing chloramphenicol IMP dehydrogenase (34 μg/ml) and ampicillin (100 μg/ml) in air shaker at 220 rpm. The preculture was inoculated (1%) into fresh 1 liter of LB medium containing the same antibiotics and cultivation was continued at 37°C to OD600

of 0.5. The culture was then supplemented with 0.02% (w/w) arabinose (final concentrations) and grown for 4 h at 37°C to achieve the overexpression of β-D-galactosidase gene. Pichia pastoris expression plasmids construction The primers used for amplification of the Arthrobacter sp. 32c β-D-galactosidase gene were: F32c-β-gal ATGGGCAAGCGTTTTCCAAGCGGC and R32c-β-gal CCCCGTCGAC TTTTCTAGA TCAGTCCTCCGCGATCAC (containing SalI and XbaI recognition sites, underlined) (reaction A). The start and stop codons are given in bold. The second PCR reaction was performed to obtain a linear form of DNA vectors using primers: Phos-alfa-factor phos-TCTTTTCTCGAGAGATACCCCTTCTTCTTTAGCAGCAATGC and AOX1-res-insert-ATTTGAATTCTCTAGACTTAAGCTTGTTTGTAGCCTTAGACATGACTGTT CCTCAGTTCAAGTTG and pPICZαA (reaction B) or pGAPZαB (reaction C) plasmid DNA as DNA template. Each PCR reaction mixture contained: 0.

5 M), sorbitol

(1 5 M) or caffeine (0 2%) Conidia spread

5 M), sorbitol

(1.5 M) or caffeine (0.2%). Conidia spread on only PDA plates served as control. For cold stress experiments, conidia at a concentration of 1e + 06 ml-1 in sterile water was incubated at 4°C for 3 days, 6 days or 9 days and then spread on PDA plates. Frequency of conidial germination was determined post 16 h of spreading by counting the number of germinating and non-germinating conidia using microscope. Two hundred to three hundred conidia were counted for each treatment. Each experiment had 3 biological replicates and was repeated 2 times. Mycelial hydrophobicity of C. rosea strains were assayed on PDA plates post 3 days or 10 days of inoculation using water or SDS following the procedure described before [34]. The hydrophobicity check details of conidia was assayed using MATH [34], and hydrophobic index was calculated following the formula described before [10]. For extracellular AZD8186 in vitro protein concentration determination, fungal strains were grown for 10 days in liquid PDB medium at 25°C, mycelial debris were removed by filtering through four layers of Miracloth, followed by protein precipitation using an acetone precipitation protocol as described elsewhere. The protein Duvelisib ic50 pellets

were dissolved in water and total extracellular protein concentration was determined using the quick start Bradford protein assay kit following the manufacturer’s instruction (Bio-Rad, Hercules, CA). Antagonism test Antagonistic behaviour against phytopathogenic fungi B. cinerea, F. graminearum and R. solani was tested using an in vitro plate confrontation assay on PDA medium. An agar plug of C. rosea was inoculated 2 cm from the edge in a 9 cm PDA plate. After 7 days of incubation at 25°C, a plug of B. cinerea, F. graminearum or R. solani was placed

at equal distance to the opposite edge of plate. To test the tolerance of C. rosea WT, deletion or complemented strains against secreted factors of B. cinerea, F. graminearum and R. solani, agar plugs of phytopathogenic fungi were inoculated on PDA plates covered with cellophane and incubated at 25°C in darkness. The plates covered with cellophane, without inoculation, were used as control. The cellophane was removed when fungal mycelia covered the plates, followed by inoculation with C. rosea WT, deletion or complementation strains. Linear growth OSBPL9 was recorded daily in 3 replicates. For secretion assay, C. rosea strains were grown for 10 days in liquid PDB medium on rotary shaker at 25°C. Culture filtrate was collected after removing mycelia by filtering through four layers of Miracloth. The filtrate was further purified by passing through a 0.45 μM pore size nylon membrane. Agar plugs of B. cinerea, F. graminearum or R. solani was inoculated in conical flasks (50 ml) with 20 ml culture filtrate and incubated at 25°C under constant shaking condition (100 rpm). Biomass production in culture filtrates was analysed by determining mycelial dry weight post 3 days of inoculation. Detached leaf bioassay B.

Figure 1 shows an SEM image of a Ni-filled PS sample with deposit

Figure 1 shows an SEM image of a Ni-filled PS sample with deposits of approximately 100 nm in size. Details of the fabrication process

of the PS/Ni nanocomposite can be found in an earlier publication [15]. The light-dark transient SPV was employed using a broad-spectrum incident white light, which included super-bandgap wavelengths. The surface was first allowed #LGK-974 randurls[1|1|,|CHEM1|]# to saturate in light, and then to reach equilibrium in the dark. SPV signal was monitored using the Kelvin probe method, a non-contact technique utilized to measure contact potential difference (CPD) between the sample surface and the probe [8]. Characterization of a bare PS and a Ni-filled PS using SPV transients for different environments were performed in high vacuum as well as in O2, N2 and Ar. Figure 1 SEM image of a Ni-filled PS sample. SEM image (formed by back-scattered electrons) of a Ni-filled PS sample with a high density of Ni-particles in the pores with an average size of 100 nm.

Results and discussion SPV transients for both types of samples in different gases show anomalous spikes of SPV during both ‘light-on’ and ‘light-off’ events (Figure 2). Similar behavior is observed for all three gaseous environments. After obtaining the SPV transients in these gas ambients, the experimental chamber was evacuated and then the SPV transients were obtained in vacuum. As a result, we observed that the PS surface was very sensitive to the experimental ambient, as one can see from Figure 3. In vacuum, the sharp SPV spikes disappeared whereas PXD101 the light-on and light-off saturation

times became dissimilar. Resolving the SPV transients obtained in gaseous environments on the logarithmic time scale (cf. Figure 4), one can see that these curves contain both fast and slow components with opposite contributions to charge dynamics. The initial fast process in the case of light-on and light-off events in the gaseous environments occurs over a time scale of tens of seconds, whereas the entire event until saturation is in the range of thousands of seconds. However, the transients observed in vacuum revealed only one relatively fast process. Since the fast Racecadotril process is always present regardless of the ambient conditions, we believe that it is related to the charge recombination occurring in PS. On the other hand, the slow process is present only in the gaseous environments suggesting that it might be related to the non-vacuum ambient. Figure 2 SPV transients in gaseous environments. (a) Bare PS in N2. (b) Ni-filled PS in O2. Figure 3 SPV transients in vacuum. (a) Bare PS. (b) Ni-filled PS. Figure 4 SPV transients in different gas environments for Ni-filled PS on a logarithmic time scale. (a) ‘Light-on’ transient. (b) ‘Light-off’ transient. A detailed discussion of fast and slow SPV transients can be found in ref. [9]. Coexisting slow and fast charge transfer processes were reported for wide-bandgap materials and analyzed theoretically by Reschikov et al.