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Germ-line mutations in epidermal growth factor receptor (EGFR) are rare but may contribute to oncogenesis: A novel germ-line mutation in EGFR detected in a patient with lung adenocarcinoma

  • Irene Centeno1,
  • Pilar Blay2,
  • Iñigo Santamaría1,
  • Aurora Astudillo3, 4,
  • Ana S Pitiot1,
  • Fernando G Osorio5,
  • Patricia González-Arriaga6,
  • Fernando Iglesias1, 4,
  • Primitiva Menéndez3,
  • Adonina Tardón6,
  • Jose M Freije5 and
  • Milagros Balbín1Email author
BMC Cancer201111:172

Received: 7 December 2010

Accepted: 16 May 2011

Published: 16 May 2011

A subset of lung cancer patients harbour EGFR somatic mutations in their tumours and are candidates for treatment with EGFR tyrosine kinase inhibitors. In a few cases EGFR mutations have also been found in the germ line, suggesting a role in lung carcinogenesis. Objetives of this study were: 1) To analyze the EGFR gene mutations in a population diagnosed with lung adenocarcinoma from Northern Spain. 2) To determine the frequency of a new germ-line mutation found in our laboratory as well as the frequency in our population of three other EGFR germ-line mutations detected by other authors. 3) To determine whether the novel mutation detected may have a functional effect on the EGFR protein.

Tumour DNA samples were obtained from frozen or paraffin embedded tumour tissues. Samples of DNA from peripheral blood cells were obtained from 912 individuals with lung cancer recruited from the CAPUA study [1, 2], 477 unrelated healthy donor individuals and 32 individuals with other types of cancer. EGFR gene exons 18 to 21 were studied by direct standard dideoxy sequencing. Specific mutations were determined either by direct sequencing or by specific RFLP analysis. Cell lines were transfected with EGFR-mutant plasmids and analysed by western blot with antibodies specific for total or phosphorylated-EGFR.

We found EGFR mutation in 12 of the 71 tumour samples (17%). One tumour contained two mutations. One mutation (p.R776G) was present as a germ line. Using an RFLP analysis, this mutation was not found in 954 alleles from healthy individuals studied, concluding that it is not a polymorphism. The mutation was not found either in genomic DNA from 912 lung cancer patients. Three additional EGFR germ-line mutations that were already described were not found in any of the studied samples. These observations show that EGFR mutated alleles are rare in the population. In vitro studies revealed that tyrosine autophosphorylation is enhanced in p.R776G-mutant EGFR when compared with wild-type EGFR. This enhanced autophosphorylation in the absence of ligand may be associated with a proliferative advantage.

Germ-line mutations in EGFR are rare but may contribute to oncogenesis

Epidermal Growth Factor ReceptorEpidermal Growth Factor Receptor GeneEpidermal Growth Factor Receptor Tyrosine KinaseEpidermal Growth Factor Receptor Tyrosine Kinase InhibitorEpidermal Growth Factor Receptor Protein

One of the main goals of cancer research is to find a way of selecting the appropriate patients for specific therapies. A promising result regarding lung cancer was the discovery that somatic activating mutations in the tyrosine kinase domain of the EGFR gene identified a subset of non-small cell lung cancer (NSCLC) patients that may respond to tyrosine kinase inhibitors [35]. After this seminal discovery, evidence accumulated in recent years has supported the idea that patients harbouring these mutations in their tumours show response to EGFR tyrosine kinase inhibitors [6, 7]. Based on the results of the latest phase III trials [8, 9] gefitinib, an EGFR tyrosine kinase inhibitor, has been approved in Europe for first line treatment of adult patients with locally advanced or metastatic NSCLC carrying activating EGFR somatic mutations. Thus, introduction of mutational screening of somatic mutations into clinical care is already a requirement for taking therapeutic decisions [10].

As recorded in the Sanger Institute Catalogue of Somatic Mutations in Cancer data-base (COSMIC v49 Release) [11, 12], curated from the recent literature, a total of 22489 samples from lung cancer tumours have been analyzed for EGFR tyrosine kinase domain mutations. The number of samples with mutations is 4722, with 5055 mutations detected, being p.L858R missense mutation and in frame-deletions in exon19 the most frequently detected alterations in EGFR. Resequencing studies provide an opportunity to find novel variants that may be involved in the activity of the protein, and may also allow us to find germ line alterations that support implication of these genes in familial carcinogenesis.

In the course of our EGFR mutational screening in lung adenocarcinoma patients from the area of Asturias, Northern Spain, we found a tumour sample with a double somatic mutation in EGFR gene; one of the changes was demonstrated to be present as a germ-line mutation. We have determined the frequency in our population of the new germ-line mutation as well as the frequency of three additional EGFR germ-line mutations described earlier, and we have investigated the impact of the novel mutation on the biochemical properties of the EGFR protein.

Tissue procurement

Lung adenocarcinoma samples were obtained from frozen or paraffin embedded tumour tissues and their paired normal tissues deposited in the Tumour Bank of Hospital Universitario Central de Asturias (HUCA). Samples were evaluated for tumour content prior to use for nucleic acid extraction. RNA and DNA were purified using Trizol method (Invitrogen) following manufacturer's instructions. In addition, genomic DNA was obtained from peripheral blood cells of 912 individuals with lung cancer recruited from the CAPUA study [1, 2], 477 unrelated healthy donor individuals aged 21-65 years recruited through the Blood Bank of HUCA and 32 individuals with other types of cancer. All samples were obtained with informed consent. The study was approved by the ethical committee of the hospital and the research was done conformed to the Helsinki Declaration.

Mutational analyses

EGFR exons 18 to 21 were amplified from genomic DNA and EGFR tyrosine kinase domain was amplified from cDNA when possible. Standard sequencing PCR was set up with kit Big Dye Terminator ® v1.1 (Applied Biosystems) and analyzed in an ABIPrism310 (Applied Biosystems). Primers used for the different PCRs are listed in Table 1.
Table 1

Primers used for EGFR PCR analysis

Sequence 5' to 3'

1 (EGFR Exon 18R)

2 (EGFR Exon 19R)

3 (EGFR Exon 20F)

4 (EGFR Exon 20R)

5 (EGFR Exon 18F)

6 (EGFR Exon 19F2)

7 (EGFR Exon cDNA)

8 (EGFR Exon cDNA)

9 (EGFR Exon 21F2)

10 (EGFR Exon 21R2)

11 (EGFR Exon 20F)

12 (EGFR Exon 20F)

13 (EGFR Exon 19F)

14 (EGFR Exon 19R FAM*)

15 (EGFR Exon cDNA)

16 (EGFR Exon 21R Hex*)

17 (EGFR Exon 21 ASO L858R)

Detection of specific mutations in EGFR exons 20 and 21

EGFR exon 20 p.R776G mutation and exon 21 p.V843I and p.P848L were detected by specific RFLP analysis since nucleotide changes affect restriction sites for HaeIII, RsaI and PstI respectively. All restriction fragments were visualized on a 2% agarose gel. If no matching restriction enzyme could be found, samples were analyzed by direct sequencing. In addition, high sensibility mutation detection methods were also developed to perform a mutational screening study for the most frequent EGFR activating mutations. Briefly, an EGFR exon 19 hot spot region was amplified from 50 ng of genomic DNA using primers 13 and 14 (Table 1). A 24 cycle-PCR was done in standard conditions with 10 μmol of fluorescent reverse primer and 20 μmol of the direct one, in a final volume of 50 μL. Products were analyzed through capillary electrophoresis in an automatic sequencer ABIPrism310 (Applied Biosystems) and software GenMapper. For detection of the p.L858R mutation, an allele specific oligonucleotide multiple PCR was performed. Primers 15 and 16 amplify the region encompassing the mutation; the reverse primer is marked with 5'HEX. Primer 17 is 858R allele-specific. A multiple 26-cycle PCR was done in standard conditions using 10 μmol of direct and reverse primers and 40 μmol of the allele-specific primer, in a final volume of 50 μL. Products were analyzed through capillary electrophoresis the same way as exon 19 deletions.

Construction of expression vectors encoding mutant EGFR

Vectors for mammalian expression containing human EGFR were kindly donated by W. Pao (Memorial Sloan-Kettering Cancer Center, NY). Plasmids containing p.R776G mutation were constructed by inserting a BstXI fragment obtained by PCR amplification of an EGFR segment from a cDNA carrying this mutation into a BstXI-digested pcDNA3-EGFR vector. All constructs were fully sequenced to confirm the absence of unwanted additional mutations in the EGFR region.

Cell transfections and western blot analysis

HEK293T and COS-7 cells were transiently transfected, using Lipofectamine™ LTX with PLUS™ (Invitrogen), with the indicated plasmids and with a vector containing the green fluorescent protein to check transfection efficiency by fluorescence microscopy. Forty-eight hours after transfection, lysates of these cells were used to quantify levels of phosphorylated EGFR. Total cell protein, extracted using RIPA buffer, were resolved by SDS-PAGE (8%) in parallel duplicated gels, transferred to nitrocellulose membranes and incubated with primary antibody ((Phospho-EGFR Tyr-1045, or total EGFR; Cell Signalling Technology) diluted 1/1000 in 5% BSA in TBS-T overnight at 4°C. Loading control gels were run in additional electrophoresis gels, blotted to nitrocellulose membrane and incubated with antibodies to beta-actin. Membranes incubated with primary antibody were washed and incubated 1 hour at RT with peroxidase labelled goat antirabbit antibody 1/2000 diluted in TBS-T containing 5% non-fat milk. Signals were visualized with ECL system (Amersham Biosciences) and lumino-image analyzer LAS3000 (Fujifilm), following the manufacturer's instructions.

Analysis of EGFR gene mutations in a lung cancer population from Northern Spain

We selected a group of 62 frozen lung adenocarcinomas and their corresponding normal matching tissue from patients that were subjected to surgery from years 2001 to 2006 at HUCA and completely sequenced EGFR exons 18 to 21. In addition, 9 samples from transbronchial biopsies were also analyzed for mutational status of the EGFR Tyrosine kinase domain. Results of the detected mutations are shown in Table 2. The obtained results showed mutation in 12 of the 71 tumour samples (17%), one of which contained two mutations. Regarding smoking status, gender and mutation presence, 7 out of 13 detected mutations were found in lung tumours from women; 6 of them were non smokers and the remaining one was a former smoker. In the male group, 6 mutations were detected, 4 of which corresponded to non smokers and the 2 remaining mutations were detected in the same patient, a smoker male. Therefore, in our cohort, EGFR mutations are more frequent in women and patients who have never smoked, as reported in previous studies [13].
Table 2

Distribution of EGFR somatic mutation's frequency from lung adenocarcinoma tissues and transbronchial biopsies, depending on gender and smoking condition

EGFR mutations

Smoking status

Exon 19

Exon 20

Exon 21

Male (n = 55)

Yes (n = 47)

1 (p.R776G)

1 (p.L858R)

No (n = 8)

2 (p.E746_A750del)

1 (p.E746_S752del)

1 (p.L858R)

Female (n = 16)

Yes (n = 7)

1 (p.E746_A750del)

No (n = 9)

2 (p.E746_T751del)

1 (p.E746_S752delinsV)

1 (p.D761_E762insEAFQ)

2 (p.L858R)

Detection of a novel germ-line mutation and population frequency study

One of the tumour samples harboured two coexistent EGFR mutations c.2326C > G p.R776G in exon 20 and c.2573T > G p.L858R in exon 21. Analysis of matched non tumoral tissue and available DNA from peripheral blood revealed that one of the mutations (p.R776G) was present as a germ-line alteration, since it was present both in the tumoral and non tumoral tissue as well as in genomic DNA obtained from peripheral blood. This sample belonged to a 47 year-old man with a 50 pack-year smoking history, who was diagnosed with a stage IIIA (pT3N2M0) undifferenciated lung adenocarcinoma. He was initially treated with surgery, but died of metastatic disease one year later. Genealogical information of this patient revealed that one of his siblings died of cancer but unfortunately no samples were available to study and no other healthy family members were requested to be analyzed, for ethical reasons.

To determine if this germ-line mutation was a polymorphism present in the population, we analysed 477 available healthy donor individuals using a RFLP analysis with HaeIII restriction enzyme. The mutation was not found in 954 alleles from control individuals studied. We also searched for the presence of this mutation in genomic DNA from another group of 912 lung cancer patients, 285 of them with familial cancer history and a cohort of 32 patients with other types of cancer. We did not find any additional sample harbouring the p.R776G EGFR mutation as a germ-line alteration, so it can be concluded that p.R776G mutation is a rare event.

Three more EGFR germ-line mutations have been recently described: p.T790M [14, 15] in exon 20, and p.V843I and p.P848L in exon 21 [16, 17]. We analyzed the frequency of these germ-line mutations in a set of 285 samples of our group from NSCLC patients with familial cancer antecedents. Table 3 shows the samples analyzed for each mutation. None of these mutations were detected in our studied population, neither the control population nor the group of samples from lung cancer patients. It can be concluded that p.R776G, as well as p.T790M, p.V843I and p.P848L are rare mutant EGFR alleles.
Table 3

Number of patients analyzed for p.R776G, p.T790M, p.V843I and p.P848L mutation presence in genomic DNA

Analyzed samples

Healthy donors

NSCLC: non small cell lung cancer; FCH: familiar cancer history; NFCH: no familiar cancer history; SS: smoking status; NSS: non smoking status; Other: patients with other types of cancer.

In vitro EGFR p.R776G analysis

To determine if both EGFR alleles were affected in the tumour sample where a double mutation was found, we first determined if both mutations were located in cis or in trans. Figure 1 depict the strategy developed to determine if p.R776G and p.L858R were located in the same strand of DNA. Thus, taking into account that c.2326C > G mutation causing p.R776G amino acid change generates a new HaeIII restriction site, when an exon 21 PCR fragment containing these mutations was digested with HaeIII, two different bands could be distinguished from the heterozygous tumour sample: one 276 bp fragment (wt for p.R776) and one 248 bp fragment (mutated for p.R776G). Sequence analysis of both fragments revealed that the base change yielding an Arg at position 858 was present in the same band as the mutation yielding Gly at position 776. It was concluded then that both mutations were located in cis, that is, they occurred in the same allele.
Figure 1

Strategy developed to resolve if p.R776G and p.L858R were located in cis. Taking into account that c.2326C > G mutation causing p.R776G amino acid change generates a new HaeIII restriction site, when an exon 21 PCR fragment containing these mutations was digested with HaeIII, two different bands could be distinguished from the heterozygous tumour sample: one 276 bp fragment (wt for the position c.2326) and one 248 bp fragment (mutated at this position). Sequence analysis of 248 bp fragment revealed that the p.L858R mutation was present in the same band as the p.R776G mutation.

EGFR mutant vector constructions were performed based on a pcDNA3.1 plasmid containing human wild-type EGFR cDNA; the EGFR tyrosine kinase domain was replaced with the corresponding p.R776G mutant variant and the resultant construction was used to transfect 293EBNA and COS7 cells. Forty-eight hours after transfection cell lysates were analyzed by western blot using primary antibodies anti Phospho-EGFR. In vitro analyses showed that in the absence of ligand (EGF), an enhanced tyrosine autophosphorylation can be observed in cells transfected with the plasmid containing EGFR-R776G when compared to those transfected with wild-type EGFR (Figure 2).
Figure 2

Anti-Phospho-EGFR immunoblot analysis. COS-7 and 293 EBNA cells were transiently transfected as described. All EGFR constructs are expressed at similar levels. EGFR activity (phospho-EGFR level) is increased in p.R776G mutant, both in presence or in absence of ligand.

In recent years, mutational screening and re-sequencing of potential oncogenes in tumours allowed the identification of hot spots for mutations and also new genes not previously involved in tumour genesis [12, 18]. Identification of somatic mutations in exons coding for tyrosine kinase domain of EGFR in tumours from patients with NSCLC and their association with response with targeted therapies, has led to the introduction of mutational screening of tumours in the clinic. A substantial number of tumours have already been studied and in addition to somatic mutations, few germ line mutations have been found.

In this work we have described the identification of a new germ line mutation p.R776G in EGFR in a patient suffering from NSCLC. In order to rule out that this mutation could be a polymorphism, we analysed 954 alleles from healthy donors and did not find this variation. In addition, we have searched for the presence of this mutation in 285 genomic DNA samples from patients with lung cancer and some history of familial cancer, and 627 samples from patients with lung cancer and no familial cancer antecedents. We have not found this mutation in any other patient. Three other germ line mutations in EGFR have been described: the first is p.T790M, that has been found in at least five families [14, 15, 19, 20], p.V843I, described in two cases [17, 21] and p.P848L [22]. It is interesting to mention that p.T790M was the first mutation in NSCLC associated with resistance to therapy with tyrosine kinase inhibitors [2325]. We also studied if these mutations were present in our cohort of individuals with lung cancer and familial history of cancer but we did not find any of them. Moreover, the sequencing of the entire exon 20 of EGFR did not reveal any other alteration in this gene. Vikis et al [26] also analyzed a number of families with high susceptibility to lung cancer for the presence of p.T790M mutation and did not find this alteration in any of 237 probands. Girard et al [20] found p.T790M as germ-line in 2 of 369 cases of never smokers with NSCLC, both patients with a family history significant for lung cancer. Concerning p.V843I and p.P848L no studies with a large group of samples was performed previously to the present work. From these results, we can conclude that p.R776G, p.T790M, p.V843I and p.P848L are rare EGFR alleles that have been found in germ line from patients suffering lung cancer.

Regarding the possibility that these mutations can represent cancer susceptibility alleles, several studies have been performed on p.T790M allele (reviewed by Suda et al [27]). Its detection as a somatic mutation in tumours supports this option. Moreover, this mutation has also been found together with the activating p.L858R mutation, both in tumours and in cell lines that never were in contact with tyrosine kinase inhibitor treatments, suggesting that p.T790M might be also growth promoting. Bell et al [14] observed that this mutation seems to occur in cis with the p.L858R activating mutation. Kinase activity of EGFR p.T790M mutant has been reported as indistinguishable from wild-type EGFR [23, 25], but Vikis et al [26] reported that p.T790M mutation alone causes increased phosphorylation levels. Godin-Heymann et al have shown that, although p.T790M mutation has a moderate effect on EGFR function, when combined with p.L858R or p.746_750del show a remarkable enhancement of EGFR activity [28]. Finally, animal models generated to inducibly express the p.T790M mutation have been also shown to develop lung tumours [29]. The latency of developing tumours is longer in those mice with p.T790M mutation alone than those bearing both p.T790M and p.L858R.

In relation to p.R776G, the novel germ line mutation revealed in this work, some lines of evidence similar to the p.T790M mutation would also support its possible role as a cancer susceptibility allele. Mutations at this position in the EGFR gene have also been discovered in tumours as somatic mutations [30]. In the tumour sample analyzed in this work, the p.R776G mutation was found together with a p.L858R activating somatic mutation in cis. A double mutation p.R776G/p.L858R was found by Wu et al [30] and the patient harbouring these two mutations did not respond to tyrosine-kinase inhibitor therapy. Alterations at R776 position giving rise to a different amino acid substitution (p.R776C) have also been described as somatic mutations and in conjunction with p.L858R [5, 31]. Preliminary studies by transfection of cell lines with EGFR mutant constructs revealed that in the absence of ligand (EGF), an enhanced tyrosine autophosphorylation can be observed in cells harbouring the plasmid containing EGFR-R776G when compared with wild-type EGFR, providing biochemical evidence of the functional relevance of this mutation.

Further analysis encompassing single and double mutant constructs will help to clarify the role of these alterations on EGFR function and in tumour genesis. It is tempting to speculate that, since p.R776G has appeared as germ-line mutation, it would have a weaker effect on EGFR functions than the double mutations detected within the tumours. Functional analyses of these mutants need to be evaluated by cellular assays, for example with tagged constructs [32], by transformation assays and by tumorigenicity studies in animal models. It will also be interesting to test the sensibility of these mutants to TK inhibitors in order to gain information of clinical value.

Mutations in genes coding for proteins with tyrosine kinase activity have been one of the genetic alterations most frequently detected in cancer over the last years [33]. Pathways activated by these proteins usually lead to proliferative advantages, thus they have received much consideration, given their association with malignant proliferation. Regarding the role of receptor tyrosine kinase alterations in familial carcinogenesis, germ line mutations in KIT have been described in familial gastrointestinal stromal tumours (GIST), RET mutations are involved familial medullary thyroid cancers and other endocrine cancer predisposition syndromes and MET mutations have been found in papillary renal cancer syndrome among others [34]. Somatic mutations in these genes have also been described in sporadic tumours and in the case of GIST, activating mutations in KIT are predictors of response to targeted therapy with imatinib [3537].

Taking these examples as precedent, it is reasonable to hypothesize that germ-line mutations in the EGFR gene could be involved in lung cancer pathogenesis, and probably in other tumours in whose development EGFR deregulation can play a role. Although there have been reported some evidences of mendelian inheritance in the pathogenesis of lung cancer [38], the intrinsic genetic factors controlling susceptibility to this malignancy might be hidden by strong environmental factors like cigarette smoking and air pollution, implicated in the mutagenesis of many other genes controlling pathways involved in the development of these tumours [18, 39].

More studies are needed in large cohorts of cancer patients with familiar history of cancer in order to link EGFR germ-line mutations to development of the disease, but these results and precedent observations do suggest that EGFR is a candidate to be involved in familial oncogenesis.

Germ-line mutations in EGFR gene are rare but may contribute to oncogenesis.

This work was supported by grants from Fundación Mutua Madrileña and Fundación Caja Rural de Asturias. We thank Dr. C. López-Otín (Dept. of Biochemistry and Molecular Biology, University of Oviedo) and Dr. C. Suarez-Nieto (Instituto Universitario de Oncología del Principado de Asturias IUOPA) for support and advice, Dr. M.V. Alvarez (Laboratory of Genetics, Hospital Universitario Central de Asturias) for genomic DNA samples from unrelated healthy individuals and Dr. W. Pao (Memorial Sloan-Kettering Cancer Center, NY) for EGFR-containing mammalian expression plasmids. A.T. is member of Centro de Investigación Biomédica en Red (CIBER) de Epidemiología y Salud Pública. IUOPA is supported by RTICC and Obra Social Cajastur.

Authors’ Affiliations

Laboratorio de Oncología Molecular, Instituto Universitario de Oncología del Principado de Asturias, Hospital Universitario Central de Asturias, Oviedo, Spain
Unidad de Cáncer Familiar, Servicio de Oncología Médica, Instituto Universitario de Oncología del Principado de Asturias, Hospital Universitario Central de Asturias, Oviedo, Spain
Servicio de Anatomía Patológica, Hospital Universitario Central de Asturias, Oviedo, Spain
Banco de Tumores, Instituto Universitario de Oncología del Principado de Asturias, Hospital Universitario Central de Asturias, Oviedo, Spain
Departamento de Bioquímica y Biología Molecular, Instituto Universitario de Oncología del Principado de Asturias, Universidad de Oviedo, Oviedo, Spain
Unidad de Epidemiología Molecular, Instituto Universitario de Oncología del Principado de Asturias, Facultad de Medicina, Universidad de Oviedo, Oviedo, Spain

  1. Fernandez-Rubio A, Lopez-Cima MF, Gonzalez-Arriaga P, Garcia-Castro L, Pascual T, Marron MG, Tardon A: The TP53 Arg72Pro polymorphism and lung cancer risk in a population of Northern Spain. Lung Cancer. 2008, 61 (3): 309-316. 10.1016/j.lungcan.2008.01.017.View ArticlePubMedGoogle Scholar
  2. Lopez-Cima MF, Gonzalez-Arriaga P, Garcia-Castro L, Pascual T, Marron MG, Puente XS, Tardon A: Polymorphisms in XPC, XPD, XRCC1, and XRCC3 DNA repair genes and lung cancer risk in a population of northern Spain. BMC Cancer. 2007, 7: 162-10.1186/1471-2407-7-162.View ArticlePubMedGoogle Scholar
  3. Lynch TJ, Bell DW, Sordella R, Gurubhagavatula S, Okimoto RA, Brannigan BW, Harris PL, Haserlat SM, Supko JG, Haluska FG, Louis DN, Christiani DC, Settleman J, Haber DA: Activating mutations in the epidermal growth factor receptor underlying responsiveness of non-small-cell lung cancer to gefitinib. N Engl J Med. 2004, 350 (21): 2129-2139. 10.1056/NEJMoa040938.View ArticlePubMedGoogle Scholar
  4. Paez JG, Janne PA, Lee JC, Tracy S, Greulich H, Gabriel S, Herman P, Kaye FJ, Lindeman N, Boggon TJ, Naoki K, Sasaki H, Fujii Y, Eck MJ, Sellers WR, Johnson BE, Meyerson M: EGFR mutations in lung cancer: correlation with clinical response to gefitinib therapy. Science. 2004, 304 (5676): 1497-1500. 10.1126/science.1099314.View ArticlePubMedGoogle Scholar
  5. Pao W, Miller V, Zakowski M, Doherty J, Politi K, Sarkaria I, Singh B, Heelan R, Rusch V, Fulton L, Mardis E, Kupfer D, Wilson R, Kris M, Varmus H: EGF receptor gene mutations are common in lung cancers from "never smokers" and are associated with sensitivity of tumors to gefitinib and erlotinib. Proc Natl Acad Sci USA. 2004, 101 (36): 13306-13311. 10.1073/pnas.0405220101.View ArticlePubMedPubMed CentralGoogle Scholar
  6. Sequist LV, Engelman JA, Lynch TJ: Toward noninvasive genomic screening of lung cancer patients. J Clin Oncol. 2009, 27 (16): 2589-2591. 10.1200/JCO.2008.20.4875.View ArticlePubMedGoogle Scholar
  7. Sharma SV, Bell DW, Settleman J, Haber DA: Epidermal growth factor receptor mutations in lung cancer. Nat Rev Cancer. 2007, 7 (3): 169-181. 10.1038/nrc2088.View ArticlePubMedGoogle Scholar
  8. Mitsudomi T, Morita S, Yatabe Y, Negoro S, Okamoto I, Tsurutani J, Seto T, Satouchi M, Tada H, Hirashima T, Asami K, Katakami N, Takada M, Yoshioka H, Shibata K, Kudoh S, Shimizu E, Saito H, Toyooka S, Nakagawa K, Fukuoka M: Gefitinib versus cisplatin plus docetaxel in patients with non-small-cell lung cancer harbouring mutations of the epidermal growth factor receptor (WJTOG3405): an open label, randomised phase 3 trial. The lancet oncology. 11 (2): 121-128.Google Scholar
  9. Mok TS, Wu YL, Thongprasert S, Yang CH, Chu DT, Saijo N, Sunpaweravong P, Han B, Margono B, Ichinose Y, Nishiwaki Y, Ohe Y, Yang JJ, Chewaskulyong B, Jiang H, Duffield EL, Watkins CL, Armour AA, Fukuoka M: Gefitinib or carboplatin-paclitaxel in pulmonary adenocarcinoma. N Engl J Med. 2009, 361 (10): 947-957. 10.1056/NEJMoa0810699.View ArticlePubMedGoogle Scholar
  10. Pirker R, Herth FJ, Kerr KM, Filipits M, Taron M, Gandara D, Hirsch FR, Grunenwald D, Popper H, Smit E, Dietel M, Marchetti A, Manegold C, Schirmacher P, Thomas M, Rosell R, Cappuzzo F, Stahel R: Consensus for EGFR mutation testing in non-small cell lung cancer: results from a European workshop. J Thorac Oncol. 2010, 5 (10): 1706-1713. 10.1097/JTO.0b013e3181f1c8de.View ArticlePubMedGoogle Scholar
  11. Bamford S, Dawson E, Forbes S, Clements J, Pettett R, Dogan A, Flanagan A, Teague J, Futreal PA, Stratton MR, Wooster R: The COSMIC (Catalogue of Somatic Mutations in Cancer) database and website. Br J Cancer. 2004, 91 (2): 355-358.PubMedPubMed CentralGoogle Scholar
  12. Forbes SA, Bindal N, Bamford S, Cole C, Kok CY, Beare D, Jia M, Shepherd R, Leung K, Menzies A, Teague JW, Campbell PJ, Stratton MR, Futreal PA: COSMIC: mining complete cancer genomes in the Catalogue of Somatic Mutations in Cancer. Nucleic Acids Res. 2010Google Scholar
  13. Rosell R, Moran T, Queralt C, Porta R, Cardenal F, Camps C, Majem M, Lopez-Vivanco G, Isla D, Provencio M, Insa A, Massuti B, Gonzalez-Larriba JL, Paz-Ares L, Bover I, Garcia-Campelo R, Moreno MA, Catot S, Rolfo C, Reguart N, Palmero R, Sanchez JM, Bastus R, Mayo C, Bertran-Alamillo J, Molina MA, Sanchez JJ, Taron M: Screening for epidermal growth factor receptor mutations in lung cancer. N Engl J Med. 2009, 361 (10): 958-967. 10.1056/NEJMoa0904554.View ArticlePubMedGoogle Scholar
  14. Bell DW, Gore I, Okimoto RA, Godin-Heymann N, Sordella R, Mulloy R, Sharma SV, Brannigan BW, Mohapatra G, Settleman J, Haber DA: Inherited susceptibility to lung cancer may be associated with the T790M drug resistance mutation in EGFR. Nat Genet. 2005, 37 (12): 1315-1316. 10.1038/ng1671.View ArticlePubMedGoogle Scholar
  15. Prudkin L, Tang X, Wistuba II: Germ-line and somatic presentations of the EGFR T790M mutation in lung cancer. J Thorac Oncol. 2009, 4 (1): 139-141. 10.1097/JTO.0b013e3181915f92.View ArticlePubMedPubMed CentralGoogle Scholar
  16. Sequist LV, Joshi VA, Janne PA, Bell DW, Fidias P, Lindeman NI, Louis DN, Lee JC, Mark EJ, Longtine J, Verlander P, Kucherlapati R, Meyerson M, Haber DA, Johnson BE, Lynch TJ: Epidermal growth factor receptor mutation testing in the care of lung cancer patients. Clin Cancer Res. 2006, 12 (14 Pt 2): 4403s-4408s.View ArticlePubMedGoogle Scholar
  17. Ikeda K, Nomori H, Mori T, Sasaki J, Kobayashi T: Novel germline mutation: EGFR V843I in patient with multiple lung adenocarcinomas and family members with lung cancer. Ann Thorac Surg. 2008, 85 (4): 1430-1432. 10.1016/j.athoracsur.2007.10.012.View ArticlePubMedGoogle Scholar
  18. Ding L, Getz G, Wheeler DA, Mardis ER, McLellan MD, Cibulskis K, Sougnez C, Greulich H, Muzny DM, Morgan MB, Fulton L, Fulton RS, Zhang Q, Wendl MC, Lawrence MS, Larson DE, Chen K, Dooling DJ, Sabo A, Hawes AC, Shen H, Jhangiani SN, Lewis LR, Hall O, Zhu Y, Mathew T, Ren Y, Yao J, Scherer SE, Clerc K, et al: Somatic mutations affect key pathways in lung adenocarcinoma. Nature. 2008, 455 (7216): 1069-1075. 10.1038/nature07423.View ArticlePubMedPubMed CentralGoogle Scholar
  19. Tibaldi C, Giovannetti E, Vasile E, Boldrini L, Gallegos-Ruiz MI, Bernardini I, Incensati R, Danesi R, Cappuzzo F, Peters GJ, Fontanini G: Inherited germline T790M mutation and somatic epidermal growth factor receptor mutations in non-small cell lung cancer patients. J Thorac Oncol. 2011, 6 (2): 395-396. 10.1097/JTO.0b013e3182059a6f.View ArticlePubMedGoogle Scholar
  20. Girard N, Lou E, Azzoli CG, Reddy R, Robson M, Harlan M, Orlow I, Yatabe Y, Nafa K, Ladanyi M, Viale A, Kris MG, Riely G, Miller V, Klein RJ, Matsuo K, Pao W: Analysis of genetic variants in never-smokers with lung cancer facilitated by an Internet-based blood collection protocol: a preliminary report. Clin Cancer Res. 2011, 16 (2): 755-763.View ArticleGoogle Scholar
  21. Ohtsuka K, Ohnishi H, Kurai D, Matsushima S, Morishita Y, Shinonaga M, Goto H, Watanabe T: Familial Lung Adenocarcinoma Caused by the EGFR V843I Germ-Line Mutation. J Clin Oncol. 2011, 29 (8): e191-192. 10.1200/JCO.2010.31.4492.View ArticlePubMedGoogle Scholar
  22. Sequist LV, Dziadziuszko R: Update on epidermal growth factor receptor inhibitor development in lung cancer. J Thorac Oncol. 2006, 1 (7): 740-743. 10.1097/01243894-200609000-00029.PubMedGoogle Scholar
  23. Kobayashi S, Ji H, Yuza Y, Meyerson M, Wong KK, Tenen DG, Halmos B: An alternative inhibitor overcomes resistance caused by a mutation of the epidermal growth factor receptor. Cancer Res. 2005, 65 (16): 7096-7101. 10.1158/0008-5472.CAN-05-1346.View ArticlePubMedGoogle Scholar
  24. Kwak EL, Sordella R, Bell DW, Godin-Heymann N, Okimoto RA, Brannigan BW, Harris PL, Driscoll DR, Fidias P, Lynch TJ, Rabindran SK, McGinnis JP, Wissner A, Sharma SV, Isselbacher KJ, Settleman J, Haber DA: Irreversible inhibitors of the EGF receptor may circumvent acquired resistance to gefitinib. Proc Natl Acad Sci USA. 2005, 102 (21): 7665-7670. 10.1073/pnas.0502860102.View ArticlePubMedPubMed CentralGoogle Scholar
  25. Pao W, Miller VA, Politi KA, Riely GJ, Somwar R, Zakowski MF, Kris MG, Varmus H: Acquired resistance of lung adenocarcinomas to gefitinib or erlotinib is associated with a second mutation in the EGFR kinase domain. PLoS Med. 2005, 2 (3): e73-10.1371/journal.pmed.0020073.View ArticlePubMedPubMed CentralGoogle Scholar
  26. Vikis H, Sato M, James M, Wang D, Wang Y, Wang M, Jia D, Liu Y, Bailey-Wilson JE, Amos CI, Pinney SM, Petersen GM, de Andrade M, Yang P, Wiest JS, Fain PR, Schwartz AG, Gazdar A, Gaba C, Rothschild H, Mandal D, Kupert E, Seminara D, Viswanathan A, Govindan R, Minna J, Anderson MW, You M: EGFR-T790M is a rare lung cancer susceptibility allele with enhanced kinase activity. Cancer Res. 2007, 67 (10): 4665-4670. 10.1158/0008-5472.CAN-07-0217.View ArticlePubMedPubMed CentralGoogle Scholar
  27. Suda K, Onozato R, Yatabe Y, Mitsudomi T: EGFR T790M mutation: a double role in lung cancer cell survival?. J Thorac Oncol. 2009, 4 (1): 1-4. 10.1097/JTO.0b013e3181913c9f.View ArticlePubMedGoogle Scholar
  28. Godin-Heymann N, Bryant I, Rivera MN, Ulkus L, Bell DW, Riese DJ, Settleman J, Haber DA: Oncogenic activity of epidermal growth factor receptor kinase mutant alleles is enhanced by the T790M drug resistance mutation. Cancer Res. 2007, 67 (15): 7319-7326. 10.1158/0008-5472.CAN-06-4625.View ArticlePubMedPubMed CentralGoogle Scholar
  29. Regales L, Balak MN, Gong Y, Politi K, Sawai A, Le C, Koutcher JA, Solit DB, Rosen N, Zakowski MF, Pao W: Development of new mouse lung tumor models expressing EGFR T790M mutants associated with clinical resistance to kinase inhibitors. PLoS One. 2007, 2 (8): e810-10.1371/journal.pone.0000810.View ArticlePubMedPubMed CentralGoogle Scholar
  30. Wu JY, Wu SG, Yang CH, Gow CH, Chang YL, Yu CJ, Shih JY, Yang PC: Lung cancer with epidermal growth factor receptor exon 20 mutations is associated with poor gefitinib treatment response. Clin Cancer Res. 2008, 14 (15): 4877-4882. 10.1158/1078-0432.CCR-07-5123.View ArticlePubMedGoogle Scholar
  31. Kosaka T, Yatabe Y, Endoh H, Kuwano H, Takahashi T, Mitsudomi T: Mutations of the epidermal growth factor receptor gene in lung cancer: biological and clinical implications. Cancer Res. 2004, 64 (24): 8919-8923. 10.1158/0008-5472.CAN-04-2818.View ArticlePubMedGoogle Scholar
  32. de Gunst MM, Gallegos-Ruiz MI, Giaccone G, Rodriguez JA: Functional analysis of cancer-associated EGFR mutants using a cellular assay with YFP-tagged EGFR intracellular domain. Mol Cancer. 2007, 6: 56-10.1186/1476-4598-6-56.View ArticlePubMedPubMed CentralGoogle Scholar
  33. Stratton MR, Campbell PJ, Futreal PA: The cancer genome. Nature. 2009, 458 (7239): 719-724. 10.1038/nature07943.View ArticlePubMedPubMed CentralGoogle Scholar
  34. Garber JE, Offit K: Hereditary cancer predisposition syndromes. J Clin Oncol. 2005, 23 (2): 276-292. 10.1200/JCO.2005.10.042.View ArticlePubMedGoogle Scholar
  35. Demetri GD, von Mehren M, Blanke CD, Van den Abbeele AD, Eisenberg B, Roberts PJ, Heinrich MC, Tuveson DA, Singer S, Janicek M, Fletcher JA, Silverman SG, Silberman SL, Capdeville R, Kiese B, Peng B, Dimitrijevic S, Druker BJ, Corless C, Fletcher CD, Joensuu H: Efficacy and safety of imatinib mesylate in advanced gastrointestinal stromal tumors. N Engl J Med. 2002, 347 (7): 472-480. 10.1056/NEJMoa020461.View ArticlePubMedGoogle Scholar
  36. Heinrich MC, Corless CL, Demetri GD, Blanke CD, von Mehren M, Joensuu H, McGreevey LS, Chen CJ, Van den Abbeele AD, Druker BJ, Kiese B, Eisenberg B, Roberts PJ, Singer S, Fletcher CD, Silberman S, Dimitrijevic S, Fletcher JA: Kinase mutations and imatinib response in patients with metastatic gastrointestinal stromal tumor. J Clin Oncol. 2003, 21 (23): 4342-4349. 10.1200/JCO.2003.04.190.View ArticlePubMedGoogle Scholar
  37. Hirota S, Isozaki K, Moriyama Y, Hashimoto K, Nishida T, Ishiguro S, Kawano K, Hanada M, Kurata A, Takeda M, Muhammad Tunio G, Matsuzawa Y, Kanakura Y, Shinomura Y, Kitamura Y: Gain-of-function mutations of c-kit in human gastrointestinal stromal tumors. Science. 1998, 279 (5350): 577-580. 10.1126/science.279.5350.577.View ArticlePubMedGoogle Scholar
  38. Sellers TA, Bailey-Wilson JE, Elston RC, Wilson AF, Elston GZ, Ooi WL, Rothschild H: Evidence for mendelian inheritance in the pathogenesis of lung cancer. J Natl Cancer Inst. 1990, 82 (15): 1272-1279. 10.1093/jnci/82.15.1272.View ArticlePubMedGoogle Scholar
  39. Pleasance ED, Stephens PJ, O-Meara S, McBride DJ, Meynert A, Jones D, Lin ML, Beare D, Lau KW, Greenman C, Varela I, Nik-Zainal S, Davies HR, Ordonez GR, Mudie LJ, Latimer C, Edkins S, Stebbings L, Chen L, Jia M, Leroy C, Marshall J, Menzies A, Butler A, Teague JW, Mangion J, Sun YA, McLaughlin SF, Peckham HE, Tsung EF, et al: A small-cell lung cancer genome with complex signatures of tobacco exposure. Nature. 463 (7278): 184-190.Google Scholar
  40. Pre-publication history

    1. The pre-publication history for this paper can be accessed here:

© Centeno et al; licensee BioMed Central Ltd. 2011

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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Boland-de Vries
The website of the Boland Family.
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This website is mainly in English, but there are some Dutch sections
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mostly Asia Pacific and China in particular

Photo series 2000-2011

China, where we lived,
China, where we worked,
China, where we traveled,
China, with our friends
China, with our art
China, our newspapers,
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Dinky Toys
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almost every boy in those years owned a few

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still being updated

  1. Ceramic artwork:The tomb of my parents
  2. Aerial Pictures taken over Zeeland, August 30, 2005
  3. De Sermoen van den Onderpaster van St Gilles Fake-Flemish sermon about Adam and Eve"'

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10 Most Insane Festivals Around The World

The world is full festivals and joys and we just need a excuse to celebrate something. There are so many festivals each are really insane and dangerous but still large number of people celebrate them every year.

1. The Thaipuism Festival

This Hindu festival is typically celebrated in southern India and involves some of the most intense body piercings known to man.

2. Tunarama

Originally meant to promote Australia’s fledling tuna industry, this festival has now come to be known for it’s highlight event…the tuna toss.

3. La Tomatina

The largest tomato fight in the world. It happens every year in the small Spanish town of Bunyol and over the course of about 1 hour the town gets so covered in tomatos that the fire department has to come in and spray everything down.

4. Boryeong Mud Festival

Taking place every summer in the town of Boryeong, South Korea this international mud fight attracts millions of visitors from all over the world.

5. Holi

You might want to pay India a visit during the springtime festival of Holi. At the very least you’ll probably end up with a pretty cool looking tie-dye shirt.

6. Fiesta de Santa Marta de Ribarteme

Also known as the Near Death Festival, this celebration is held annually in the town of Las Nieves, Spain. Hundreds of people attend mass in honor of Saint Marta de Ribarteme, the Patron saint of resurrection.

7. Argungu Fishing Festival

Every year in the town of Argungu, Nigeria all the local men compete to see who can pull the largest fish out of the river using nothing but their bare hands.

8. Pamplona Bull Run

the Pamplona Bull Run in Spain is actually part of the Fiesta San Fermin which takes place every July. The only requirements to participate are that you have to be at least 18 years old and sober.

9. The Redneck Games

In 1996 when the Olympics were held in Atlanta, some locals took offense to the fact that the international media portrayed them as a “bunch of rednecks holding a sporting event.” As a result they ended up doing just that. Some of the events include toilet seat throwing, hubcap hurling, and the armpit serenade.

10. Burning Tar Barrel Festival

For hundreds of years people in the town of Devon, England have been running through the streets carrying burning battles of tar.

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Psychologist; Theodore M. Newcomb Distinguished University Professor, University of Michigan; author, Mindware: Tools for Smart Thinking

The first time I had occasion to think about what thinking machines might do to human existence was at a talk decades ago by a computer scientist at a Yale Psychology Department colloquium. The talk’s topic was “What will it mean to humans’ conception of themselves, and to their well-being, if computers are ever able to do everything better than humans can do—beat the greatest chess player, compose better symphonies than humans?”

“I want to make two things clear at the outset,” the speaker said. “First, I don’t know whether machines will ever be able to do those things. Second, I’m the only person in the room with the right to an opinion about that question.” The latter statement was met with gasps and nervous laughter.

Decades later, it’s no longer a matter of opinion that computers can do many of the astonishing things the speaker mentioned. And I’m worried that the answer to his question about what this will mean to us is that we’ll feel utterly sidelined and demoralized by machines. I was sorry that Deep Blue beat Garry Kasparov at chess. I was momentarily depressed when Watson, its successor, defeated both its human Jeopardy! competitors. And of course we know that machines can already compose works that beat the socks off John Cage for interest and listenability!

We do have to worry about a devastating morale problem, when any work we might do can be done better by machines. What does it mean to airplane pilots that a machine can do their job better than they can? How long will it be before that occupation, like hundreds of others already, is made obsolete by machines? What will it mean to accountants, financial planners, and lawyers when machines can carry out, at the very least, nearly all of their bread-and-butter tasks more effectively and infinitely faster than they can? To physicians, physicists, and psychotherapists?

What will it mean when there’s simply no meaningful work for any of us to do? When unsupervised machines plant and harvest crops? When machines can design better machines than any human could even think of? Or be a more entertaining conversationalist than even the cleverest of your friends?

Steve Jobs told us that it wasn’t the customers’ job to know what they want. Computers may be able to boast that it’s not the job of humans to know what they want.

Like you, I love to read, listen to music, see movies and plays, experience nature. But I also love to work—to feel that what I do is fascinating, at least to me, and might possibly improve the lives of others. What would it mean to people like you and me if our work were simply pointless and there were only the other enjoyable things to do?

We already know what machine-induced obsolescence has meant to some of the world’s peoples. It’s no longer necessary for anyone to make their own bows and arrows and hunt animals, for any purpose other than recreation. Or to plant, cultivate, and harvest corn and beans. Some cultures built around such activities have collapsed and lost their meaning to the people who were shaped by them. Think, for example, of Southwestern Indian tribes, or rural whites in South Dakota, Alabama, New Mexico, with their ennui, lassitude, and drug addiction. We have to wonder whether the world’s people can face with equanimity the possibility of there being nothing to do other than to entertain themselves.

Which isn’t to say that cultures couldn’t evolve in some way as to make the absence of work acceptable, even highly satisfying. There are cultures in which there has been little to do in the way of work for eons, and people seem to have gotten along just fine. In some South Pacific cultures, people could get by with little other than waiting for a coconut to drop or wading into a lagoon to catch a fish. In some West African cultures, men didn’t do anything you’d be likely to classify as work except for a couple of weeks a year, when they were essential for the planting of crops. And then there were the idle rich of, say, early twentieth-century England, with their endless rounds of card playing, the putting on of different costumes for breakfast, lunch, and dinner, and serial infidelities with really rather attractive people. Judging from PBS fare, that was pretty enjoyable.

So maybe the most optimistic possibility is that we’re headed toward evolving cultures that will enable us to enjoy perpetual entertainment with no meaningful, productive work to do. However repellent that may seem to us, we have to imagine—hope, even—that it may seem a delightful existence to our great-great-grandchildren, who will pity us for our cramped and boring lives. Some would say the vanguard is already here: Portland, Oregon, has been described as the place where young people go to retire.


text:
Curriculum and Assessment

Front Cover
David Scott
Greenwood Publishing Group, 2001 - Education - 190 pages
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Curriculum and Assessment is the first volume of a new series International Perspectives on Curriculum. This edited book examines the relationship between curriculum, pedagogy and assessment, and, as with subsequent volumes, adopts a cross-sector and comparative approach. Contributors make reference to a number of important debates in the fields of curriculum and assessment: summative versus formative assessment; differentiation versus inclusion; psychometric versus holistic theorising; decontextualised versus contextualised assessment; symbol-processing versus situated learning approaches; integrated versus connected assessment; and high stakes versus low stakes assessment. The rationale for this volume is not to reach an agreement about assessment and curriculum frameworks, but to air the various debates referred to above and develop new frameworks for understanding these important issues.

This volume and the series is timely as administrators and policy-makers in different parts of the world have taken an increased interest in education, and as moves to centralise curriculum provision have gathered pace. This has in some cases driven a wedge between curriculum theory and curriculum practice, as policy-makers have developed and implemented proposals without referring to academic debates about these issues. It therefore is an important task to reassert the need to discuss and debate the curriculum in a critical manner before implementation occurs. This volume sets about that task, addressing policy-makers, administrators, teachers and the research community.

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Formative Assessment and Curriculum Consequences
Differentiation and Assessment Mary Simpson
Pupil Assessment and Classroom Culture A Comparative Study of the Language of Assessment in England and France
Portfolio Assessment in Teacher Education
Examination Techniques Issues of Validity and Effects on Pupils Performance
Professional Doctorates and Assessment Issues
Scottish Perspectives on the Curriculum and Assessment
Conceptual Frameworks to Accommodate the Validation of Rapidly Changing Requirements for Assessments
An Overview of the Relationship Between Assessment and the Curriculum
About the Editor and Contributors

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About the author (2001)

DAVID SCOTT is a Senior Lecturer in the Centre for Curriculum and Teaching Studies at the Open University in the United Kingdom. He has published widely in the fields of curriculum, assessment and research methodology. His most recent books include Reading Educational Research and Literacy, Realism and Educational Research: New Perspectives and Possibilities and (with Robin Usher) Researching Education. Data, Methods and Theory in Educational Enquiry. He is the current editor of The Curriculum Journal.

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Iowa Long a Leader in Civil Rights; Marriage Equaltiy Advocates Hopeful About State Supreme Court Case

by Kilian Melloy
Tuesday Dec 9, 2008

Oral arguments began Dec. 9 in a marriage equality case that has gone before the Iowa state Supreme Court. The fact that the case is being heard in Iowa--with its long tradition of leadership in civil rights--has given heart to gay and lesbian families still shocked at the revocation of marriage parity by majority vote in California last month.

A Dec. 9 article in the Des Moines Register offered a synopsis of the state's history at the forefront of civil rights, from an 1839 ruling that enabled an escaped slave to retain his freedom (nearly two decades before the U.S. Supreme Court's Dred Scott decision trumped the state court's finding) to an 1868 court decision, eight decades in advance of the state court's federal counterpart issuing its ruling in Brown v. Board of Education, that struck down segregated schooling in Iowa.

The article then identified the crux of the case: the claim by the plaintiffs that to deny gay and lesbian couples in Iowa the right to marry is contrary to the Iowa constitution's guarantee of equality under the law.

The Register article quoted from the Bill of Rights section of the Iowa state constitution, which states, "the General Assembly shall not grant to any citizen, or class of citizens, privileges or immunities, which, upon the same terms shall not equally belong to all citizens."

The article also recalled that the court had previously found marriage to be fundamental as a right, though opponents of marriage parity promptly took the stance that only mixed-gender couples should have the opportunity to claim that right.

Not so, countered pro-marriage advocates. Rights are universal to all citizens, and are not dependent upon gender.

Similar arguments brought about marriage equality in Massachusetts in 2004, and in California and Connecticut earlier this year.

Other states have approached the issue from the legislative branch of government, with New York's Assembly having approved a bill to extend marriage equality to gay and lesbian families in that state; the New York senate, until now controlled by Republicans, did not allow the matter to come up for a vote.

And in Vermont, legislators have examined whether the state's eight-year-old, first-in-the-union Civil Unions law is adequate to the needs of gay and lesbian families there, or whether only marriage comprehensively guarantees rights and responsibilities to families.

For other states--thirty of them--quite a different response has met the notion of full-fledged equality for gay and lesbian families.

In every state where a constitution amendment has been put to voters to re-write the basis of state law and pointedly exclude some families from marriage, voters have approved those changes.

Only once, in 2006, did voters defeat such an amendment, and then it was from a fear that the broadly-worded amendment would impact the finances of unmarried heterosexual couples. When the amendment was rewritten so as only to target gay families, and put before Arizona voters once more in 2008, it passed handily.

Only once to date has a state taken the step of granting marriage equality, only for voters to subsequently approve an amendment that would rescind that right; California's Proposition 8 may have set a new legal precedent, or it may be found by the California Supreme Court to have gone too far, revising, rather amending, that state's constitution.

But observers do not believe that Iowans will be faced with a vote on a constitutional amendment even if the Supreme Court there rules in favor of the plaintiffs and strikes down anti-gay-family laws as inconsistent with the current version of the Iowa constitution.

A Dec. 9 article in the Iowa City Press Citizen referenced the University of Iowa's David Redlawsk, a professor of political science, who thought it improbable that such an amendment would clear the state's legislature given its current political makeup.

Moreover, Redlawsk argued that courts as a mirror for general social attitudes. Redlawsk pointed to recent polls that show marriage equality is becoming more widely accepted.

Another tack that opponents may take if the Supreme Court finds in favor of the plaintiffs is to seek a repeal of marriage equality through the state's lawmakers, though any such law runs the risk of being struck down under the same equal protection clause upon which the current case turns.

But Iowa's judicial legacy, and the reputation it has given the state, play perhaps the biggest role when it comes to trying to guess the outcome.

The Citizen Press quoted Lambda Legal attorney Camilla Taylor, who said, "I don't want to sound presumptuous, but I am optimistic because of the Iowa cases we are relying on."

Taylor is the plantiffs' lead counsel.

Kilian Melloy serves as EDGE Media Network's Assistant Arts Editor. He also reviews theater for WBUR. His professional memberships include the National Lesbian & Gay Journalists Association, the Boston Online Film Critics Association, The Gay and Lesbian Entertainment Critics Association, and the Boston Theater Critics Association's Elliot Norton Awards Committee.

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Where to Stand

October 13, 2015

Gallant Ship

Filed under: Calligraphy — Tags: , , , — breckenrcook @ 10:15 PM

imageI mixed this blue gouache to look like waves of the ocean. The hand is a gothicized pointed pen that I learned from Lee Sims at a Utah Calligraphic Artists meeting. The tight bounce again mimics the waves.

On a personal note, I love this hymn. I was trying to memorize it for a performance when we had a family emergency. I was driving to the hospital, not sure what I would find, when the line “No danger can the heart appall when Jesus stoops to reign” finally clicked. I burst into tears–full of fear, but I knew that we weren’t facing the event alone, and that if it were ultimately a tragedy we would be scooped up in His hands and carried through. Thankfully, there was a full recovery, and our fears were dispelled the way we had hoped.image

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  1. So beautiful

    Comment by Mon Ange — October 14, 2015 @ 12:31 AM

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Hello again,

Just thought I’d share a fab idea and some equally fabulous, statement head pieces!

Evangeline Rose Bridal boutique based in leafy Surrey, England features some of the most beautiful, stylish bridal wear and accessory collections by Britain’s top designers.

I love their new ‘Something Borrowed‘ service ~ basically brides can ‘borrow’ {hire} some of their gorgeous bridal accessories, headpieces and veils by designers including Polly Edwards, Joyce Jackson and Vivienne Sheriff.

It’s a great idea for fashionista brides on a tight budget and, let’s face it, there’s only one day in your life you can wear a veil {without looking extremely OTT!} so why pay a fortune?

Here’s a selection of my favourite pieces from the collection…

That Joyce Jackson bow veil is darling!

Prices start from £40 for a three-day loan. How great is that?!

You can view the entire collection available for hire here and while you’re there why not check out the beautiful bridal dresses in the sale too!


text:
Six people file complaint after Minneapolis officer shoots into car during downtown brawl

The officer now faces an internal affairs investigation over his use of force.

Elizabeth Flores, Star TribuneChief Janee Harteau met with those involved after the incident.

Six people have filed formal complaints with the city after a Minneapolis police officer fired on their vehicle during a downtown scuffle last weekend.

The officer, who is now facing a standard internal affairs investigation, was responding to the scene of a large brawl near Target Field around bar close early Sunday that left two men with noncritical gunshot wounds, according to police. Amid the chaos, a car trying to back away struck the officer’s squad. He then fired one round, hitting the side of the vehicle with six people inside.

Neither the officer nor the passengers were injured in the incident, authorities said.

But activists and family members of those in the car that night condemned the officer’s actions as careless, contending that he put the four women and two men at risk.

Caylea Wade, the 23-year-old driver, was trying to leave the area with her friends after a night on the town, said her father, Lou Wade. An officer told the group to reverse the vehicle and return the way they came, he said, when a squad car approached from behind and the vehicles collided. A shot suddenly rang out, striking the driver’s side door, and the occupants were surrounded.

“They weren’t suspects. It’s unfortunate that they put my girl in harm’s way,” said Lou Wade, who met with Police Chief Janeé Harteau about the incident on Monday, where he said she apologized but offered few answers. “At the end of the day, we just can’t have police officers on the force like that. I think it’s negligence.”

A police spokesman confirmed that six people were in the vehicle that night, but declined to comment on whether they were detained or considered suspects, as an investigation is pending.

The chaos began just after 2 a.m. on Nov. 20, when police responded to a report that 30 to 40 people were fighting in the 400 block of 3rd Avenue N. At the scene, officers heard gunshots and found a man who had been shot in the ankle.

During that time, another man showed up at Hennepin County Medical Center after being shot in the arm. No arrests have been made.

Lou Wade said his daughter was detained for several hours because of the collision. Her car was impounded for four days before it was returned to the family with a bullet hole.

The Minneapolis NAACP demanded punishment for the officer involved in the “unnecessary and dangerous shooting,” said Jason Sole, NAACP chapter president. “What would have happened had one of the young passengers been wounded or killed?” Sole said in a statement.

The passengers, their family members and activists from advocacy groups like Black Lives Matter and the General Defense Committee, held a rally outside City Hall on Monday. The group filed complaints shortly after, Wade said, and the family plans to meet with Mayor Betsy Hodges this week.

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Howard Hospital Cops Dumped Wheelchair Bound Woman at Bus Stop

May 30
Howard University officials have fired two campus police officers and their supervisor involved with dumping a female patient from a wheelchair and leaving her lying on the ground at a bus stop near the university hospital.Two of the officers, a male and female, were terminated; a third, a male supervisor who ordered that the woman be taken from the hospital, also was fired, according to Gabriel Adegoke, president of the Metropolitan Campus Police Officers Union, which represents the officers.

The incident, which occurred last month and was captured on video, appears to show a male officer pushing the barefoot woman in the chair along Georgia Avenue. The woman’s legs are flung in the air when the officer stops abruptly and she tumbles out of the chair. A second male officer and a female officer watched as the woman hits the ground. The female officer throws up her gloved hand and tells the male officers to “leave her there.”

The second male officer was not terminated, Adegoke said.

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Posts Tagged ‘perl’

Project-Builder.org reaches 0.13.2

Before leaving for a 15 days trip to the US, I’ve published the latest version 0.13.2 of project-builder.org.

It will be very useful for my colleagues and friends working on python-redfish to make local packages for testing that module, and then to publish it in upstream distributions such as Mageia and Fedora to start with.

That version improves git support, ssh support with ECDSA (for RHEL 7 distributions which have removed DSA by default), provides Fedora 22 and 23 support as well (with dnf).

Of course, project-builder.org is available for 160 distribution tuples because it uses project-builder.org to make that possible ! And if I can do that for this project, then you can probably do it as well for yours. The goal again is to help upstream projects to provide upstream packages for various distributions to help users, testers to install the software on their system. And so is the tool itself, you can download it easily and test it following the instructions described in the Lab document.

I have the intention to work next on improving the conf files to support regular expressions for the labels (to allow making conf entries such as minosdep fedora-2[0-9] = ….), looking at transforming them to use JSON instead of their own format (JSON wasn’t an option when I started back in 2005) and also looking at the Swagger2 perl module to help build a RESTful API around project-builder.org

As usual, that’s not the lack of idea which is preventing all that to arrive but the lack of time. So don’t hold your breath if you plan to do GET/POST request to build your packages with project-builder.org but it will come. And now this version is available, back to MondoRescue to fix the UEFI support !

Random thoughts after 3 days down under and 1 around Linux.conf.au

Australia !
Back to Australia !
Shark Bay
Just after my arrival in Perth last Friday, I had a bit of time to walk in the city in order to have a view on it and feel the atmosphere.
View from the hotel
It’s an interesting mix of modern buildings and a bit less modern buildings !
Mix of buildings
Of course, Australia is a young country, with (from my point of view) mostly young people around (that’s where I see I’m getting old !). People are very nice, friendly and always ready to help with a smile. It’s my third time here, and it’s always been like that, that’s probably why I like coming back here.
Australian Steak
I had a dinner in what I found a strange place, the shed, where I had to show my ID before entering, which was pretty empty despite the size. Maybe because it was a bit early. The dinner was good, but I really felt alone !
That's where Perth performs savant music

It was then time to go back to the hotel for some mail, and the preparation of my Monday presentation.

Being in Australia during europe winter time is just great. As great that you can receive too much sun on your head 😉 Especially when you go to such a nice place as Fremantle !
Main Fremantle Street
I did that on Saturday (for once I had time around an event) in that city which is similar to a french mediteranean city like Cagnes sur mer e.g. (more from a climate perspective than an architectural one)
Hall Town
and so I passed the full day around, enjoying the view on the Indian Ocean (my first time),
Site seeing from Round House
and beach (nearly empty as very windy)
Fremantle beach
and the nice food you can eat on the harbour
View on the harbour
(remember that as french we put a lot of emphasis on this, and even more because it’s me ;-))

One of the main building of Fremantle is their prison, which has been added to the World Heritage List of Unesco as a testimony of the role of convicts/prisoners sent to Australia to work there. One of the oldest building of the region, even if it’s just less than 200 years (old european reaction ;-))
Fremantle prison

It’ was also interesting to see that Fremantle uses Wikipedia to document their sites. They are adding QRCodes pointing to Wikipedia pages in order to make your visit more rich. That’s the first time I see that usage BTW.
Wikipedia QR code

Sunday was passed doing more preparation around project-builder.org release 0.12.3 and the presentation. I just took some time in the afternoon to go back in the city
Skyline view some strange trees in parks
and bells tower
Bells tower
before recognizing the itinerary to go to Linux.conf.au
LCA2014 Banner
hosted at the University of Western Australia
where we could register.
UWA main building
Despite not being at LCA for the first time, I attended Rusty Nelsson session on first timer LCA attendees, which was a nice way to start the event.First time session
After some more discussion at a nearby bar, it was time to finalize my presentation, and work on the demo. Took me up to 3AM, but was still not finished as I wanted !

On monday, LCA was starting.
Start of LCA
The first keynote was about Whistle-blowing (les lanceurs d’alerte for my french audience who like me would not happen to know what it is) and how their perception is changing in our post-Snowden era.
Dr Suelette Dreyfus
That was an interesting presentation of her finding through a survey they organized to gather data. Especially after having seen the keynote at LinuxCon EMEA around Living in a Surveillance State by Mikko Hypponen, which I highly recommend to watch,as it’s a very enlightning one.
Dr Suelette Dreyfus
However, during the Q&A session, I found a bit strange that the audience didn’t want to listen to the question from a doctor around how to determine what is good and what is bad, which was much more interesting that what they felt it could be. And I think he was right, as this is a real concern that should rather be dealt with, instead of just asking the person to shut up. The limit of what can be disclosed or not whether you are in a government or a private company wrt ethic aspects is really a difficult topic to solve and more debate should be left so more interesting input could be heard and answers brought to improve the quality of the debate.

And also it’s interesting that the spot is now only on the NSA, whereas we tend to forget that some months ago, we had the same questions around Facebook. Of course, people give willingly their info to Facebook while theydon’t to the NSA, and that’s a bad thing. However, it doesn’t rmove the other threat from companies like Facebook which should continue to be explained to all IT users and consumers.

There was a remark on the fact that US own 5 millions records of autralian citizens who have travelled to the US. Again, it’s easy to avoid that: do not travel to the US. If you want to go there, it seems normal to me they can ask for info beofre to protect themselves. Of course, the level of what is asked should be reasonable wrt the effect researched, and people have modification right son it and insurance it won’t be provided to other entities. But here I think they are in their own right to gather them. Of course, again nothing to do with what we’re learning regularly thanks to E. Snowden revelations with what the NSA is doing.

I passed the rest of the day mostly in the Continuous Integration miniconf which was also hosting my talk with the exception of a presentation around ansible and vagrant I wanted to follow in the sysadmin mini-conf. It turned out that this presentation wasn’t so interesting due to the lack of demo (no network). Too bad as I’m also testing ansible as time permits on my side and would have like to get insights.

So after that I took some time to finish my slidset for the pres of the afternoon and the demo I wanted to make. I think I’ll never been able to finish a presentation days in advance completely. Don’t get me wrong, I have plenty of material availblle and I can make any 3 days workshop on the fly just using what I already have. However, I like to tailor the presentation to the audience, the context, polish one or two stuff, remove slides and some new ones… And same with the demo. So even if I started early before coming, I just finished to publish project-builder.org 0.12.3 the morning (time for all packages to build), realized that some feature that I hadn’t tested enough were not working, so making just a last patch (c) to have my demo shiny !

So I missed some sessions in between and went back to the CI miniconf and really heard Anita Kuno’s talk on 3rd party testing with OpenStack (a good one on latest aspects of the project I wasn’t aware of – this one is moving soooo fast !).
Geology Building at UWA

And finally all went well (at least from my point of view of course, ask one of the around 40 people of the the audience for objective feedback !). Demo worked as expected (thanks for preparation ;-)) and as usual I din’t had enough time to cover all what I wanted to address. Will see now if my Continuous Packaging approach is supported more in Australia, and if project-builder.org gets adopted there to create more upstream packages for some projects. Those interested can find my presentation on SlideShare. The video is also available.
Perth Lighted building
End of day was dedicated to the CI BoF and a dinner with a lot of HP peers working on OpenStack on various aspects (always amazed to meet so many people involved in it as time passes that I wasn’t knowing before).

But that’s not the end ! More “awesome” presentations to see the days coming. And more pictures are available at https://plus.google.com/photos/112434061686721373729/albums/5966194867275136465

It starts as a happy new year indeed

Well, would you really be surprised if i say that the begining of 2014 looks as promising (and as busy of course) as the end of 2013 was ?

While travelling to Linux.conf.au in Perth (28 hours door to door but could it be a better start for 2014 !) I had some time to look at Project-Builder.org, subject of my conference on Monday and also to MondoRescue.

For Project-Builder.org, I’ll publish a new version for LCA (0.12.3) which will fix rpmbootstrap for lastest Fedora (18-20), Mageia 3 and also other recent distros. Also as SVK is now broken on Mageia 3, I’m using git-svn to work on my laptop when remote, and thus pb supports it now. Some various fixes since last year release will also be done (better printing with VM/VE name for logs, improved ntp support, pbdistrogetparam command to easy shell interface…), but globally the software is pretty stable for my usage, so now it’s your turn to tell me what would be useful for you in it. I also need to make a newer presentation for Monday with a short demo.

For MondoRescue I’m not ready yet to publish a final version, so I have made for now a first beta for the 3.2.0 version. First this will be a new 3;x version as there are lots of changes in the code that may make it less reliable due to the adoption of dynamic memory allocation instead of static in a lot of functions. If I compare 3.0 and 3.2:

  • 3.0
    • total mr_asprintf usage : 646
    • total sprintf usage : 674
    • total strcpy usage : 560
    • total fgets usage : 79
    • total malloc_string usage : 367
    • total MAX_STR_LEN usage : 370
  • 3.2
    • total mr_asprintf usage : 1223
    • total sprintf usage : 166
    • total strcpy usage : 388
    • total fgets usage : 28
    • total malloc_string usage : 129
    • total MAX_STR_LEN usage : 221

Which means that a lot has been done in code changes between 3.0 and 3.2. But also a lot remains to do if we want to have no malloc_string nor MAX_STR_LEN at all. And also if I made mistakes in the mr_malloc/mr_asprintf/mr_free usage, the commands will crash. THat’s why I need your tests here ! I’ve made a full bakup restore cycle (which has revealed some issues that I fixed), but I’m far from being confident in the result.

Another consequence is that this version will probably have less fixes than previous ones as most of the time has been passed on code modernization.

And it will require new mindi and mindi-busybox versions. And these versions should finally work for systemd crazyness of removing /bin and /sbin (which broke MondoRescue for a too long time now). And you’ll need new perl modules in order to have it work correctly as I finally rewrote some bash mindi functions into perl to have what I consider better code.
Which means Fedora 18-20, Mageia 3 should work out of the box (at least my Mageia 3 now works correctly).

And expect again more pacthes to MondoRescue durnig the 28+ hours back home at the end of next week 😉

So I wish to all readers a happy new year 2014 and hope it will start for you as it has for me !

Meeting at Linux.conf.au in Perth

I’m again lucky to be able to fly in a plane for 20+ hours the first week of January to attend Linux.conf.au ! (And of course the 20+ hours of fly back ;-))

I’ll talk on Monday 06 January 2014 during the miniconf dedicated to Developer, Testing, Release and Continuous integration Automation of project-builder.org and the idea of Continuous packaging.

This has been possible only thanks to HP‘s support, its Open Source investment council, and the kindness of our VP & Deputy General Counsel, Cloud Computing and Open Source Eileen Evans who continues to support my travels at many Open Source conferences, and should be greatly thanked for that.

I’ll make a new version of the tool available to celebrate this, not that a lot has changed, but some fixes should be made available as packages, and it’s a long time since I published the last one. In fact, for me the tool is pretty stable and usable. I recently added git-svn support, as svk is broken with latest perl versions such as on my Mageia 3 😦 So learning slowly git, and still not liking it that much, but I have not a lot of other choices.

I still need to improve rpmbootstrap for the latest Fedora which changed their mirroring structure. Hopefully this will be done on time.

And as I’m on it, Merry Christmas and Happy New Year to you all readers !

Finally time to publish pb 0.12.2

As you can see with the few messages I had time to post on this blog, the end of 2012 start of 2013 has been pretty busy, and I’m late in delivering the 2 projects I’m leading. So this week, I decided it was time to make a 0.12.2 version of pb, and make it available. Was asked by my colleagues of FOSSology, specially to add Fedora 18 support, so I also build my VMs to make packages on this distro.

BTW, a bit of ranting for Fedora once more: no perl by default :-(, and no ifconfig nor route command either which is breaking MondoRescue of course, and I guess tons of other software around. These guys don’t care about past, but don’t provide compatibility tools either !! So I’ll have to make new patches, just to do the same as what was done, but with another command again. Not to speak of systemd which I still have issues to deal with 😦 That doesn’t make stuff go faster !

Anyway, the version is now out, no official bugs fixed, but a lot of small stuff here and there which were desrving a release. No time to test Fedora 17/18 VE yet, so you’ll have to do that yourself if you want. I also had a look at virsh usage in combination with pb, and it’s again not as easy as it could seem to be. Especially port redirection I’m easily using by launching qemu-kvm manually with the -redir or hostfwd option doesn’t seem to be possible with the user mode network through virsh (neither manager nor CLI). Will have to post on their ML to see how they do that, if they can !

And MondoRescue has been very late. I really need to publish a verion, but I still have some blocking bugs I really would like to get rid of: CTRL+ALT+DEL not working anymore during restore, some LVM issues on RHEL, some grub issues on SLES… Hopefully at the end of next week I’ll have made progresses.

Of course patches are much easy to integrate, but I receive more bug reports than them 😉

And also back to preparing the HP internal TES event, Solutions Linux confs, submitting to LinuxCon, working on an FLOSS ITIL stack, learning more OpenStack, looking at Intel’s TXT…. so many things I’d like to do or learn and will never have time to ! Maybe at least I’ll talk about that another time.

About to publish project-builder.org 0.12.1

When I looked at the date of the current project-builder.org current stable version, I had a shock ! It has been nearly a year since I published that version. I should not stay that long without providing updates 😦 But you know what it is, you always think that you should still add that latest cool feature, and then that other, + fix this problem, … and you end up one year later with a great development version, but still no public stable one so others could benefit from your work.

So it’s time ! Especially as I have committed a lot of patches from an HP colleague, Eric Anderson, who is using the tool (and in its devel version !) to support packaging projects he is working on for HP. So I worked hard since the 8th of May to integrate what he has made available on github, since he got HP’s approval through the OSRB. And I have integrated I think more than 90% of his enhancements, which now will make 0.12.1 even more appealing than before.

But I’m not as a good guy as some think 😉 Some of the patches seemed strange to me, or could have an impact which I wasn’t completely sure of, so there is still some work Eric did, that has been left appart for the moment. Sorry for that, but I’m a slow guy, using this project on a daily basis, so I really need to be convinced before accepting a patch. But I was convinced by a lot 😉 I’ll now contact him back through the project mailing list, and see how we can work on these remaining points for 0.12.2 so he has a tool working much better for him. Among the nice stuff Eric has brought is clearly a much improved GIT support (read working !), and Debian/Ubuntu support as well (as he is using them natively). He also added support for stopping with the first error, or not as this is an option. Plus lots of improvements all around.

And he will also beneft from my own modifications, which hopefully improved the tool as well ! The last one, being with the configuration file management, now fully done in memory, instead of re-reading all conf file each time (which could also have some advantages, but speed improvement is what I was looking for here). In particular, in this version, the documentation has been improved a lot and should help more beginners. I have added a new getconf option to help following the value of configuration items (useful as pb uses lots of config files !), checkssh to verify what has been delivered on the repository, wrt what should have been, cleanssh to clean up the remote repository for test versions. A new -t option has been added to create local packages more quickly (when only the local distro will be used). Patches support has also been extended to .deb distributions. I have also introduced a new script, pbmkbm, which is aimed at creating customized boot media (project-builder.org make boot media), that will be the basis of an evolution of mindi in the MondoRescue project (doesn’t work as of now, and more on that later on). Some enhancement requests and bug fixes have also been done (#99, #585, #93, #522, #103, #105, new distro support for Fedora 15 and 16, Ubuntu 11.10, 12.04, OpenSuSE 11.4, 12.1 at least). #101 is the last on the list for 0.12.1 and as soon as it’s mostly done, I’ll publish it. Promised !

Stay tuned as usual 😉

md2mb.pl improved to better support migration from Kmail to Thunderbird

It’s just incredible how the Open Source world works. You could never believe it before being yourself part of it.

It started with a simple poor small script I wrote for myself to support the migration of my kids to Thunderbird from KMail. And I blogged about it, as I thought it could be interesting as I didn’t found myself a working tool to do it.

It turned out it was the most read article of this blog ! Grumph ! I thought people could be interested by MondoRecue or Continuous Packaging, my bad 😉

Of course, when I have something to do, I prefer to write a script. Because old guy like me know perfectly you’ll have to do the stuff twice, and thus a script is useful !! And it was prooved again when I migrated my last kid with it again. And the script was improved at the same time. But I knew there were still some flaws, as one colleague found it as well, and had an issue with it (some mails not seen correctly even if imported in subfolders) !

So last month I received feedback from another user, who took that script and improved it greatly, fixing btw the above mentioned problem. And so that small script has now as many contributors as Mondorescue and twice as many as project-builder.org.
Edward Baudrez did a great job to improve the script, adding lots of CLI options capabilities to make it more versatile, fixing mail import in subfolders, error message handling, adding POD doc, …

I still have one or two improvements I’ll discuss with him to try making it even better, but that’s already quite an interesting piece of code !

So as it’s now even more useful than before, those interested by that migration should download and test it in their environment, and continue to send patches 😉 and make me more mazaed by the power of our community, for large as well as small stuff !

The project-builder.org Fosdem Vidéo is now available

The presentation I made at Fosdem this year has been video taped by the great video team during that event. It’s now available online for you to replay (as well as on the project’s ftp server). If you want the associated slideset, just download it !

The latest development have been around fixing the bug on file names, improving test versions build. And we now have new requests on the devel mailing list and, even more interesting, patches proposals to improve pb work with Git and other bug fixes, that should make their way before I issue 0.12.1.

Let’s meet at Fosdem 2012 in Brussels

I’ll attend Fosdem again this year next week-end in Brussels. I’ll deliver a talk on Project-Builder.org as a support for a Continuous Packaging cross Operating Systems development.

There are some news with the tool, and hopefully a new version, and some future evolution that I’d like to communicate. I also plan to present less slides, and have a more concrete demo to help people see the value of the approach.

While not presentting, I’ll probably be around near the Mageia booth or around my HP colleagues attending the event as well (Bdale Garbee, Martin Michlmayr, Hugo Roy). Don’t hesitate to come and chat !

Migrating from KMail to Thunderbird: The revenge

After migrating 2 of my kids and my wife from Kmail to Thunderbird last year, I finally decided this week-end to finish the last migration for my first daughter on her Mageia distribution.

I previously made unsuccessful tries, as her environement was different, with many more subdirectories, and special chars, so it didn’t work with the previous version of the script.

Now with the revisions 1389 and 1390 of the md2mb.pl script, I have successfully migrated her environment, without any manual intervention.

Hopefully, seeing the number of times the previous post was looked at, it will be again useful (even more now that it works better:-)) for others. I even clarified the license in revision 1391 for you to use more easily.

Happy migration !


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