Cellular cobalamin defects are a locus and allelic heterogeneous disorder. The gold standard for coming to genetic diagnoses of cobalamin defects has for some time been gene-by-gene Sanger sequencing of individual DNA fragments. Enzymatic and cellular methods are employed before such sequencing to help in the selection of the gene defects to be sought, but this is time-consuming and laborious. Furthermore some cases remain undiagnosed because no biochemical methods have been available to test for cobalamin absorption and transport defects.
This paper reports the use of massive parallel sequencing of DNA (exome analysis) for the accurate and rapid genetic diagnosis of cobalamin-related defects in a cohort of affected patients. The method was first validated in an initial cohort with different cobalamin defects. Mendelian segregation, the frequency of mutations, and the comprehensive structural and functional analysis of gene variants, identified disease-causing mutations in 12 genes involved in the absorption and synthesis of active cofactors of vitamin B12 (22 cases), and in the non-cobalamin metabolism-related genes ACSF3 (in four biochemically misdiagnosed patients) and SUCLA2 (in one patient with an unusual presentation). We have identified thirteen new variants all classified as pathogenic according to the ACGM recommendation but four were classified as variant likely pathogenic in MUT and SUCLA2. Functional and structural analysis provided evidences to classify them as pathogenic variants.
The present findings suggest that the technology used is sufficiently sensitive and specific, and the results it provides sufficiently reproducible, to recommend its use as a second-tier test after the biochemical detection of cobalamin disorder markers in the first days of life. However, for accurate diagnoses to be made, biochemical and functional tests that allow comprehensive clinical phenotyping are also needed.
Cellular cobalamin problems are caused by nutritional deficiency or genetic defects that affect either the absorption or cellular uptake of the vitamin or the synthesis from it of methylcobalamin (MeCbl) and adenosylcobalamin (AdoCbl). The latter are, respectively, a cofactor of methionine synthase (MS EC_2.1.1.13), which catalyzes the remethylation of homocysteine (Hcys) to methionine in the cytoplasm, and of methylmalonyl-CoA mutase (MUT EC_5.4.99.2), which catalyzes the mitochondrial isomerization of L-methylmalonyl-CoA (MMACoA) to succinyl-CoA. Defects in the synthesis of AdoCbl or the conversion of MMACoA to succinyl-CoA lead to elevated methylmalonic acid (MMA) concentrations, while defects in the synthesis of MeCbl or the remethylation of Hcys to methionine cause elevated Hcys (HC). Defects in the absorption and transport of vitamin B12, and in the cytosolic synthesis of the above cofactors, cause methylmalonic aciduria with homocystinuria (MMA&HC) [1, 2].
After its intake, cobalamin is first bound to haptocorrin (encoded by TCN1) and then to the intrinsic factor (IF) encoded by GIF. To date, only one pathogenic mutation and one functional polymorphism (p.Asp301Tyr in TCN1) have been described [3, 4]. Cubilin and amnionless, encoded by CUBN and AMN respectively, form the cubam dimer which functions as the receptor of IF-Cbl in the ileum . The IF is then degraded and vitamin B12 appears in the blood stream associated with transcobalamin II (TCII) [2, 5]. Inherited malabsorption of cobalamin causes haematological and neurological abnormalities that can be fatal .
Still bound to TCII, the vitamin enters cells via transcobalamin receptor (TCblR)-mediated endocytosis. This receptor is encoded by CD320, for which only one mutation has been described . The cobalamin is then released into the cytosol, an event impaired in people with defects in LMBRD1 (cblF complementation group, MIM #277380) . LMBRD1 protein interacts with ABCD4 protein, which is also involved in the release of Cbl into the cytoplasm from the lysosomes (a defect which falls into complementation group cblJ) . The most common form of cobalamin defect, complementation group cblC (MIM#277400), is caused by mutations affecting MMACHC . Patients with mutations in the Host Cell Factor 1 (HCFC1) locus (MIM 309541), located on the X chromosome, have a phenocopy of cblC disease  since HCFC1 encodes a transcriptional co-regulator of MMACHC. Recently additional defects have been described that affect transcription factors involved in the regulation of Cbl pathway: ZNF143  and THAP11 . In addition new variants in PRDX1 also affect the expression of MMACHC, named epi-cblC cases. Thus, these patients result from pathogenic variants in MMACHC and one in PRDX1 which force the antisense transcription of MMACHC and thereby a possible methylation mark .
Cellular cobalamin processing occurs via two major pathways - the cytosolic and mitochondrial pathways. The protein thought to be responsible for sorting cobalamin for these pathways is MMADHC (cblD complementation group, MIM #611935). This complementation group is the most complex of all since patients present with biochemical heterogeneity ranging from isolated homocystinuria (cblD variant 1) or isolated methylmalonic aciduria (cblD variant 2) through to methylmalonic aciduria combined with homocystinuria (cblD) depending on the nature and location of the mutations present .
The cytosolic pathway is involved in the synthesis of MeCbl by MS, encoded by MTR (defects give rise to complementation group cblG), while the enzyme methionine synthase reductase encoded by MTRR is involved in the reactivation of MS (defects give rise to complementation group cblE). Both cblG (MIM#250940) and cblE (MIM#236270) defects, lead to elevated Hcys, hypomethioninaemia, and megaloblastic anaemia [1, 2].
Inactive cob(II)alamin entering the mitochondria is converted into AdoCbl via a reductive adenosylation reaction catalysed by an adenosyltransferase (ATR) encoded at the cblB locus (MIM#251110) . MUT is encoded at the MUT locus and two different phenotypes have been described: mut0 and mut− (MIM#251100). Finally MMAA is the gene associated with complementation group cblA defects (MIM# 607481). It encodes a protein of the same name which may be involved in transferring AdoCbl from ATR to MUT protein as well as maintaining MUT's functional integrity [5, 17].
Mildly elevated MMA also occurs in patients with mutations affecting SUCLA2 (MIM#612073) and SUCLG1 (MIM#245400) which lead to infantile mitochondrial encephalopathic depletion syndrome. These genes encode either the ß-subunit of ADP-forming or the α-subunit of GDP-forming succinyl-CoA synthetases. The accumulated succinyl-CoA inhibits the metabolism of MMACoA to succinyl-CoA, leading to the accumulation of MMA in body fluids. Mutations in SUCLA2 give rise to typical (though rare) early onset dystonia combined with deafness [18, 19]. An increase in MMA is also seen in patients with mutations in ACSF3 (MIM# 614265), in whom malonic acid levels may also be elevated (combined malonic and methylmalonic aciduria, CMAMMA) . ACSF3 encodes a mitochondrial acyl-CoA synthetase considered to have malonyl-CoA and MMACoA synthetase activities.
The diagnosis of an intracellular cobalamin metabolism disorder in a symptomatic individual is based on both clinical suspicion and biochemical analyses [1, 21]. Since expanded newborn screening potentially allows early detection of certain disorders of intracellular cobalamin metabolism, some affected individuals may be diagnosed prior to the onset of clinical symptoms. Diagnosis is based on elevated propionylcarnitine (C3), a high propionylcarnitine to acetylcarnitine ratio (C3/C2), high heptadecanoylcarnitine (C17), and/or reduced methionine concentrations . After symptomatic or asymptomatic detection, a differential diagnosis is needed to help identify the gene that might be involved. Confirmatory testing is based on measuring Hcys and MMA in plasma and/or urine, enzyme analyses, the incorporation of [1-14C] propionate and [5-14C] methyl-THF into proteins in fibroblasts cultured in basal and hydroxocobalamin-supplemented media, and in some cases by cellular complementation assays . However, biochemical analysis cannot pinpoint a genetic defect, making diagnosis complicated. Fortunately, recent developments in high-throughput sequence capture have made next generation sequencing (NGS) a rapid and accurate means of analysing genetic locus and allele heterogeneous disorders [23–25].
The main purpose of clinical laboratory testing is to support medical decision-making. Clinical genetic testing is generally used to identify or confirm the cause of a disease and, if possible, to provide ideas for personalized treatment. Massive parallel sequencing is the starting point of a complex process for identifying pathogenic variants as well as the description of new functions for a gene product . The aim of the present work was to assess the use of genetic studies as second-tier tests following the detection of cobalamin disorders in biochemical newborn screening. The usefulness of massive parallel sequencing in the identification of the mutated genes responsible for cobalamin and related defects was analyzed, and the structural and functional analysis of the novel variants identified undertaken.
Patient-derived fibroblasts, blood samples or dried blood spots from 27 patients with elevated MMA and/or Hcys or vitamin B12 deficiency were referred to our laboratory for genetic analysis. Another 9 samples from patients with cobalamin defects, previously diagnosed in our laboratory, were included for validation purposes. The diagnosis of these cases was made by biochemical, cellular and genetic studies. Fourteen cases were detected through expanded newborn screening programs; the others were diagnosed after clinical presentation (neonatal or late onset). The study was approved by the ethics committee of the Universidad Autónoma de Madrid. The participants or their legal guardians gave their signed, informed consent to be included.
High purity DNA was extracted from whole blood, fibroblasts or dried blood spot samples using the MagNA Pure Compact Kit (Roche Applied Biosciences, Indianapolis, IN) following the manufacturer's protocol. Two massive parallel sequencing panels were used: targeted customized exome sequencing to capture the exome of 120 genes involved in metabolic disorders (Nextera Nature Capture, Illumina, San Diego, California, USA) (the list of genes included can be sent upon request), and an extended panel (Clinical-Exome Sequencing TruSight™ One Gene Panel, Illumina) that included all the known (in 2013) disease-associated genes described in the OMIM database (Mendeliome panel). For genetic analysis in the validation cohort both panels were used. For genetic analysis in discovery cohort either of the two panels was used, except in cases P24-P27 where both panels were used. After gene capture and alignment with the reference genome, variant callings were made using a virtual panel that included all cobalamin metabolism and related genes. Incidental findings in genes unrelated to the clinical/biochemical phenotypes were ignored. Additional files 1 and 2 describes the coverage of the genes. With both panels, the libraries generated were sequenced using 150 bp paired-end reads employing the Illumina MiSeq or Nextseq500 NGS platforms. SNVs was annotated and subsequently filtered as previously described . Variants were always confirmed by conventional Sanger sequencing employing both patient genomic DNA and that of their parents if available. Pathogenic prediction was assessed by Alamut Visual software. Variants were classified following the ACMG recommendation guidelines [27, 28].
To assess the isolated effect of the recently described mutation c.1084-10A > G in MUT , the splicing profile was analyzed ex vivo using a minigene assay. Briefly, exon 6 and the corresponding flanking intronic regions from patient P10 were amplified as previously described and cloned into pSPL3 vector . Transcriptional profile analysis was performed as described elsewhere .
The oxygen consumption rate (OCR) was measured using the XF24 Extracellular Flux Analyzer (Seahorse Bioscience, Billerica, MA, USA) as previously described  in cells transduced with lentiviral particles incorporating wild-type cDNA of SUCLA2 (NM_003850) or the respective negative control. Modulating compounds such as oligomycin inhibitor of the ATP synthase (OL, 6 μM), carbonyl cyanide 4-(trifluoromethoxy) phenyl-hydrazone a potent uncoupler of oxidative phosphorylation in mitochondria (FCCP, 50 μM), rotenone inhibitor of complex I (RO, 1 μM) and antimycin A inhibitor of complex III (AT, 1 μM) were used to assess the bioenergetic profile and were sequentially added to the cells. The calibration plate for these compounds was prepared according to the manufacturer's protocol. The data obtained were used to determine basal OCR, the maximum respiratory rate, ATP-linked respiration, mitochondrial reserve capacity, proton leakage and non-mitochondrial respiration. Briefly, for OCR determinations, patient-derived skin fibroblasts (5 × 104 each), were seeded per well in 24-well tissue culture microplates and incubated with 100 μl DMEM supplemented galactose (1 g/L g/l, DMEM-Gal) instead of glucose at 37 °C for 2–5 h. After the incubation period, up to 250 μl of the corresponding medium was added and incubated overnight at 37 °C. On the next day, the medium was removed and the cells washed with phosphate saline buffer (PBS). 700 μl of the corresponding medium DMEM-Gal without bicarbonate were then added and the plates incubated at 37 °C for 1 h.
The novel intronic and exonic SNVs identified were analyzed using Alamut Visual software, which includes a number of functional predictors. The two SUCLA2 variants (p.Gly326Arg, p.Ile312Thr) were mapped to a homology model of the human protein based on the known X-ray structure of SUCLG2 (S. scrofa; PDB code: 2fp4) . The percentage sequence identity between these proteins was 54% .
To assess the sensitivity of the proposed assay in the detection of pathogenic mutations, all mapped sequence reads from the nine samples (VC1–9) with previously defined mutations in TCN2, MTR, MTRR, MMACHC, MMADHC, MUT, MMAA and MMAB (Table 1) (11 known and three unknown mutations detected by conventional Sanger sequencing) were inspected blind. Samples for the validation cohort were selected to include different types of Cbl deficiency. All the previously known mutations in all samples were detected in their correct heterozygous/homozygous state.
Adult with slight anemia and low serum vit B12.
The discovery cohort consisted of samples received for cobalamin genetic diagnosis, for which no mutations were previously known. Variant changes were identified in the cobalamin transport genes i.e., TCN1, GIF and AMN, in genes causing isolated MMA i.e., MMAA, MUT and MMAB, in genes causing MMA&HC i.e., CD320, MMACHC, MMADHC, in genes causing HC i.e., MTRR, and in two MMA metabolism-related genes SUCLA2 and ACSF3 (Table 1). Some variants in MMACHC, MMADHC, MUT, MTRR and ACSF3 were detected in several samples. In some cases DNA from blood spots was used in parallel; the coverage compared to whole blood was similar.
Overall, 33 variations were identified in 12 different genes. All the new exonic non-synonymous SNVs (nsSNVs) were predicted to be pathogenic or likely pathogenic (Additional files 1 and 3).
Among 27 samples with biallelic nucleotide changes, 21 showed at least one described (HGMD® professional release professional release 2018.1) or one new LoF mutation. Three samples (P6, P9 and P23) presented two new variants in MUT or SUCLA2. A previously described functional SNP in TCN1 was detected in two samples (P1 and P2) . Although this disease-associated polymorphism was not detected in the in-house control samples analysed, this variation is present close to 9% in all data base consulted (ExAc, gnomAD and Spanish data) with presence of homozygous cases. Therefore this change alone in TCN1 is unlikely to be responsible for the clinical picture in P1 and P2.
P11 (identified by newborn screening) presented the previously described nonsense mutation p.Arg152Ter in MUT, plus the disease-associated polymorphism in TCN1 described above. Both changes were present in the paternal sample. No other exonic or described intronic mutation were detected. Mean coverage allowed to rule out a large genomic deletion. It was not possible to rule out the presence of deep intronic mutations.
Four patients (P24, P25, P26 and P27) referred for analysis of genes related to isolated MMA in fact had mutations in ACSF3. After the genetic diagnosis, a slight increase in urinary malonic acid was confirmed by GC-MS in three of them.
The effect of mutation c.1084-10A > G identified in P10 on the splicing process was addressed using an ex vivo minigene system. The results indicate the insertion of a 9 nt sequence upstream of the normal 3′ splice site, as recently described by transcriptional profile analysis in patient-derived fibroblasts . A shorter transcript was also observed, resulting from the deletion of 135 nt from exon 6. This was detected as a heteroduplex along with the normal transcript. This deletion was generated by the activation of an internal exonic cryptic 3'splice with a higher splicing score than normal, plus two exonic splicing enhancer sequences (Fig. 1).This deletion would likely translate into the elimination of 45 amino acid residues from the protein.
To assess the bioenergetic profile of patient P23, and to determine whether mitochondrial function could be restored by the transfection of patient-derived fibroblasts with a lentiviral construct bearing wild-type SUCLA2 cDNA, the oxygen consumption rate (OCR) of control and patient derived-fibroblasts (transduced or not with the lentiviral construct) was analyzed. In order to force the functioning of the electron transport chain, this experiment was performed in a medium supplemented with galactose. Fig. 2a shows that P23-derived fibroblasts had a diminished bioenergetic profile compared to control cells. Basal respiration was significantly reduced (Fig. 2b). The addition of FCCP to the medium resulted in increased electron flow through the mitochondrial respiratory chain and allowed the maximum respiration rate to be calculated. Figure 2b shows this variable to also be significantly reduced in P23 fibroblasts. Oligomycin-sensitive respiration (OSR), which represents the ATP-linked oxygen consumption (Fig. 2c), was also reduced in P23 cells, indicating reduced oxidative phosphorylation.
The transduction of patient dermal fibroblasts with an empty construct (Lv-Co) did not influence the bioenergetic profile, except for an increase in the maximum respiration rate which was still below control levels. Transduction with the lentiviral construct bearing wild-type SUCLA2 cDNA, however, was able to restore the bioenergetic profile (Fig. 2a). Both basal and maximal respiration rates were restored to control levels (Fig. 2b). As shown in Fig. 2c, oligomycin-sensitive respiration was also significantly increased, suggesting the restoration of oxidative phosphorylation. These results indicate that the bioenergetic deficit observed in the cells from P23 could be caused by defects in SUCLA2.
Structural analysis of the SUCLA2 variants was performed for prediction of protein dysfunction at the molecular level.
The functional and in silico analyses of the two SUCLA2 variants also suggested them to be damaging. Only AlignGVGD gave a nearly neutral score for p.Ile312Thr. It should be noted that the pathogenicity score for this variant was closer to the threshold between neutral and damaging replacements, suggesting a milder effect (Additional file 1). This observation agrees with the results of the structural analysis. The wild type residues Gly326 and Ile312 were identified in a homology model of SUCLA2, obtained using pig SUCLG2. Visual analysis of the structures (Fig. 3) showed that both loci fell near the protein's "phosphate shuttle" loop , indicating that the replacement of the wild-type residue might interfere with the functional role of this loop. This was particularly noticeable for Gly326, which lies in close contact with residue His299 of the loop, and occurs at a packed location in the structure. The replacement of glycine by the bulkier arginine would undoubtedly create some steric clashes. Gly326 was found to be highly conserved in multiple sequence alignments of the SUCLA2 family, supporting the idea that it may have a functional role. Finally, Ile312 was involved in a dense network of residue interactions, although no close contact (<5Angs) with the residues from the functional "phosphate shuttle" loop was observed. This indicates, once again, that replacement of Ile312 may have a milder impact on function. This agrees with the less strict conservation pattern seen in multiple sequence alignments. In summary, agreement was seen between in silico predictions and structural analyses for both variants, indicating that the observed replacements are pathogenic, although p.Gly326Arg probably causes more severe problems than p.Ile312Thr.
The gold standard for coming to genetic diagnoses of cobalamin defects has for some time been gene-by-gene Sanger sequencing of individual DNA fragments. Enzymatic and cellular methods are employed before such sequencing to help in the selection of the gene defects to be sought, but this is time-consuming and laborious . Further, no biochemical methods have been available to test for cobalamin absorption and transport defects, and while plasma B12 concentrations are tentatively used to help in the selection of genes to be sequenced, this has probably led to the under-recognition of cases . This costly, stepwise, and time-consuming methodology is gradually being replaced by NGS technologies, which offer higher throughput and scalability, cost less per sequenced nucleotide and have shorter turnaround times . The present work reports the NGS analysis of a cohort of patients suspected of having cobalamin defects (plus the corresponding structural/functional analyses for some of the defects involved) and shows it to be quick and reliable.
A 100% correct diagnostic rate was returned with the validation cohort, with exonic and intronic nucleotide changes and small deletions (c.271dupA in MMACHC or c.57_64del8 in MMADHC) all successfully detected. With the clinical exome massive parallel sequencing system used, the depth and breadth of coverage of the cobalamin metabolism-related genes was > 30× and 99% respectively. The sensitivity and specificity of the method appeared to be very good and the results reproducible (several mutations were detected in more than one unrelated mutant allele i.e., c.271dupA in MMACHC, c.671_678dupAATTTATG in MUT, c.748C > T in MMADHC etc.). Thus, even though the use of smaller, specific panels is recommended  so that secondary incidental findings are avoided, the present work shows clinical exome sequencing to be successful. It could be used in sequencing analyses of single patients as well groups of patients whose members have other, unrelated disorders.
The LoF mutations detected in GIF and AMN were found to affect the absorption of cobalamin. GIF and AMN, in addition to CUBN and TCN1, are not usually captured in the available panels offered by genetic companies but the results reported in the present work have demonstrated they should be analyzed [19, 34].
The potential missense changes p.Ala302Pro and p.Ala676Thr, identified in MUT, were predicted to be damaging by several bioinformatic algorithms. The present detection of the associated mutations in combination with functional cellular studies provided a rational basis for tailored treatment. Indeed, the cellular uptake of 14C-propionate revealed that p.Ala302Pro is a mut0 mutation, while p.Ala676Thr located in the C-terminal of the cobalamin binding domain is likely a mut− mutation. Based on these results, patient P6 might not be responsive to the pharmacological administration of the vitamin, while P9 would likely respond. Case P11 inherited a described LoF mutation in MUT and the functional polymorphism p.Asp301Tyr in TCN1, probably an incidental finding of no clinical significance. This asymptomatic individual was detected in newborn screening. No other mutations were detected in the coding region of MUT, not even in the deep intronic sequence reported to bear an intronic pathogenic mutation [30, 37]. Although massive parallel sequencing exome analysis cannot rule out the presence of other nucleotide changes in promoter or intronic sequences, both the absence of clinical symptoms and the slight abnormal levels of urinary MMA in case P11 suggested he/she was a carrier of the disease.
Variations in genes that do not encode cobalamin metabolism-related proteins (ASCF3 and SUCLA2) were also detected in the present work. Both were associated with slightly increased urinary MMA. The two new variants of SUCLA2 (p.Gly326Arg and p.Ile312Thr) detected are probably damaging changes; both were predicted to be so in bioinformatic and structural analyses. Neither was found to be present in database control populations nor in the in-house control samples. Structural analysis suggested that the replacement of Ile312 may have a mild functional impact, which agrees with the less strict conservation pattern seen in multiple sequence alignments. Importantly, the mitochondrial dysfunction in deficient fibroblasts from P24 was rescued via the stable expression of the SUCLA2 protein through lentiviral transduction. This suggests that SUCLA2 is the gene likely affected in this patient, although his/her symptoms were atypical [18, 38]. With respect to ASCF3, individuals P24, P25, P26 and P27 were diagnosed as having isolated MMA since the urinary malonic acid that identifies CMAMMA can be easily missed . Given the difficulty in diagnosing CMAMMA, several of the present patients were originally diagnosed during genetic analyses, e.g., exome sequencing . Even though a new method for the rapid metabolic diagnosis of CMAMMA has recently been reported , diagnoses by genetic analysis would be improved by second tier genetic testing after newborn screening. In some cases ACSF3 defects only cause biochemical conditions such as short-chain acyl-CoA dehydrogenase deficiency  or 3-methylcrotonylglycinuria , and symptoms appear only during viral infections etc. [39, 43]. In other cases, as reported in the present work, patients can show neurological damage . Prompt diagnosis would avoid unnecessary treatment with vitamin B12.
The use of massive parallel sequencing in a new era of newborn screening would avoid the time-consuming biochemical and enzymatic methods presently used to help identify which genes might be causing isolated MMA, MMA&HC, HC or CMAMMA. The rapid return of an accurate genetic diagnosis would allow the prescription of an appropriate treatment just a few days after birth. This report illustrates the clinical usefulness of massive parallel sequencing in the diagnosis of cobalamin and related defects. This powerful technology could improve the detection of these under-recognized or rare vitamin B12 defect conditions.
This work provides evidence supporting the use of massive parallel sequencing as second tier test for confirming cobalamin defects following their detection in newborn screening. Biochemical and cellular analyses and additionally comprehensive phenotyping are needed for an accurate classification of variants for making fully useful clinical reports.
Sandra Brasil, Fátima Leal, Begoña Merinero and Belén Pérez contributed equally to this work.
An institutional grant from the Fundación Ramón Areces to the Centro de Biología Molecular Severo Ochoa, and funding from the European Regional Development Fund, are gratefully acknowledged.
This work was funded by grants PI13/01239-PI16/00573; Fundación Isabel Gemio-Fundación La Caixa (LCF/PR/PR16/11110018).
SB, FL, AV, RN, MJE carried out the functional and genetic studies; CR, NP, XC, participated in the structural studies; MLC, EMH, AM, CP, LPQ, MR, NE, IT IV, RY: clinical diagnosis; follow-up pf the cases; PRP, LR, MU, CPC participated in the biochemical diagnosis; BM and BP conceived the study, participated in its design and coordination, interpreted of results and writing the manuscript. All authors read and approved the final manuscript.
The study was approved by the ethics committee of the Universidad Autónoma de Madrid (CEI48–919). The participants or their legal guardians gave their signed, informed consent to be included.


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NextRevisiting the Kingdom: Ten Years After "Desiring the Kingdom"
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Learning in Quarantine
E. J. Hutchinson	on March 19, 2020
On 9/11, I was a senior in college. It was my birthday, in fact. After sleeping in (as I said, it was my birthday), I came downstairs in my off-campus apartment. I couldn't find anyone. It was a ghost town.
As it turned out, my roommates were in the next apartment, watching commercial jets flying into skyscrapers. Overnight, the world had changed.
The coronavirus feels similar, only in slow motion. Whether it is in reality, time will tell.
A day or two before 9/11, I went to a lecture on totalitarianism and the carnage of the wars of the twentieth century. The speaker predicted that this would never happen again. We had learned our lesson.
A day or two after 9/11, I went to a lecture on C.S. Lewis's sermon "Learning in War-Time" (originally called "None Other Gods: Culture in War Time"), preached at Oxford in the fall of 1939 in the shadow of Adolf Hitler and the Second World War and later included in The Weight of Glory and Other Addresses. As I recall, the lecture had been planned before 9/11, but its relevance was suddenly as subtle as a sledgehammer. We had not learned our lesson.
We are once again in a similar situation, but this time the enemy is even more viscerally one of flesh and blood: the sour grapes of a virus that has set the world's teeth on edge. My institution, like many others, has suspended its in-person classes. And the question can easily arise: Why bother learning? People are dying. More people are going to die. Reading a book seems to be at best a ridiculous self-indulgence, at worst a repudiation of trying at least to do something useful.
On that score, what Lewis had to say in 1939—mutatis mutandis, ceteris paribus, and all the rest of it—has something to say to us now. For he had to face the same question. Given Hitler, given Mussolini, given all of it, why go to school? How can one justify it? "Is it not like fiddling," Lewis asks, "while Rome burns?" The way in which he responds to this question is at once incisive and illuminating.
The first thing he does is to set the war, and the way it might make one radically rethink his priorities, against a deeper, broader, and more cosmic backdrop. That is to say, the drama of life occurs in the midst not only of temporal concerns like war or disease, but also of eternal ones, namely heaven and hell. Everyone is on his way to one or the other. Thus "every Christian who comes to a university must at all times face a question compared with which the questions raised by the war are relatively unimportant." The last enemy is not one of flesh and blood.
This is not to say that the war is completely unimportant, but rather that it is not–cannot be–the most important thing. Lewis is not attempting to be callous or to perform what is known on Twitter as a "Jesus juke." His point is that "[i]f human culture can stand up to that [i.e. the question of one's eternal destiny], it can stand up to anything." If we think that culture and learning are important even when taking the last things and eternity into account, then they are a fortiori important when taking earthly calamity into account.
After all, war and disease do not create death where there was no death before. We were already mortal. What they do instead is "simply [to] aggravate the permanent human situation so that we can no longer ignore it. Human life has always been lived on the edge of a precipice. Human culture has always had to exist under the shadow of something infinitely more important than itself." And if we waited to "search for knowledge" until we had solved the problem of death, "the search would never have begun."
When we think about death, we realize that "[l]ife has never been normal." For death is the ever present abnormality that taints everything, even in the best of times. To repurpose Melville–but only slightly–it "touch[es] all objects, even tulips and roses, with its own blank tinge." Men have never waited for the ideal moment to pursue culture and learning. The ideal moment will never come; for the ideal moment is an illusion. Whereas insects seek "material welfare" first, Lewis says,
Men are different. They propound mathematical theorems in beleaguered cities, conduct metaphysical arguments in condemned cells, make jokes on scaffolds, discuss, the last new poem while advancing to the walls of Quebec, and comb their hair at Thermopylae. This is not panache; it is our nature.
We seek knowledge and beauty, Lewis claims, because we are made to do it. We cannot not do it.
But what if this is only a product of our fallen nature? And perhaps it is still selfish, given that the world, too, is fallen; perhaps we should only be concerned about the salvation of souls. Lewis's response is twofold.
First, even if that accusation were true and no one should do anything but evangelize, that's not going to happen. Human beings are still human beings, and they will still do what they naturally do. There is that scene in King of the Hill in which Hank says to the Christian rocker who wants to use music only for preaching, "Can't ya see ya aren't makin' Christianity better, you're just makin' rock 'n roll worse?" What Lewis is saying is similar: "If you attempted…to suspend your whole intellectual and aesthetic activity, you would only succeed in substituting a worse cultural life for a better."
Second, the accusation rests on a specious opposition between the "spiritual" and the "secular." "It is clear," Lewis remarks, "that Christianity does not exclude any of the ordinary human activities." It simply directs them to a new end. As the apostle Paul says, "Do all things to the glory of God." Grace restores and perfects nature. It does not obliterate it. There is therefore "no essential quarrel between the spiritual life and the human activities as such." The life of the monk is not "more spiritual" than the life of the factory worker.
There is an error on the other side, too, however, and that is the idea that it is the work of culture and learning that is the more spiritual. Lewis has a word here that all who work at Christian liberal arts institutions need to hear:
I reject at once an idea which lingers in the mind of some modern people that cultural activities are in their own right spiritual and meritorious — as though scholars and poets were intrinsically more pleasing to God than scavengers and bootblacks. I think it was Matthew Arnold who first used the English word spiritual in the sense of the German geistlich, and so inaugurated this most dangerous and most antiChristian error. Let us clear it forever from our minds.
The life of the scholar is not "more spiritual" than the life of the factory worker.
Where, then, does the truth lie? It lies, as Aristotle might say, in the middle. Everyone has a vocation. Some are called to one kind of work, some to another. And the vocation of the student is to study. How do you know if that is your vocation? Well: Are you enrolled in college? Then that is your vocation.
And if it is your vocation, it is also your duty. "If our parents have sent us to Oxford, if our country allows us to remain there, this is prima facie evidence that the life which we, at any rate, can best lead to the glory of God at present is the learned life." This does not make you, as a student, better than anyone else. It only shows you what your calling is, and you had best leave to others their own calling. As Lewis puts it, "The intellectual life is not the only road to God, nor the safest, but we find it to be a road, and it may be the appointed road for us."
It is a difficulty that this all sometimes must occur under the shadow of catastrophe. This makes us anxious, and that is not surprising. But Lewis counsels that you "not let your nerves and emotions lead you into thinking your present predicament is more abnormal than it really is." To return to an earlier point, conditions will never be ideal, and "[i]f we let ourselves, we shall always be waiting for some distraction or other to end before we can really get down to our work." But the truth is that "[t]he only people who achieve much are those who want knowledge so badly that they seek it while the conditions are still unfavorable. Favorable conditions never come."
Does that mean that conditions now are no more unfavorable than they were two weeks ago? Of course not. That would be absurd. Disease, just like war, "does do something to death. It forces us to remember it. The only reason why the cancer at sixty or the paralysis at seventy-five do not bother us is that we forget them." Now, we cannot forget death. Now, we cannot ignore it. Now, we cannot hide from mortality and the reality of the human condition.
What then? So be it. After 9/11, I was milling around in what used to be the Student Union on campus. It was packed. The president of the college came by unannounced. This is what he said:
We must go on with our work. We've all got a job to do, just like everyone else in America. London continued to function (after it was bombed!). We're going to act like that, too. We have to have the strength to keep ourselves together. In the meantime, each one of us should do his part.
Now is no different. We must do our work. We must do it in unfavorable conditions. We must do it before the specter of Death's hooked and gnarled finger. But this is what we must always do. "We must," Lewis says, "do the best we can."
Posted in: Current Politics, Featured, Health
Tagged in: COVID-19
Posted by	E. J. Hutchinson
E.J. Hutchinson is Associate Professor of Classics at Hillsdale College, where he also directs the Collegiate Scholars Program. He is the editor and translator of Niels Hemmingsen's On the Law of Nature: A Demonstrative Method.
Show comments	Hide comments
Susan Francino	 March 20, 2020 at 4:51 pm
Liberty for All : A Response
Revisiting the Kingdom: Ten Years After "Desiring the Kingdom"
Augustine Amongst the Strong Gods

redpajama_set_name: RedPajamaCommonCrawl


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Q: Performing join given complex entity relationships in hibernate I'm having difficulty establishing an association between two entities in Hibernate.  The relationship is complicated.
We have a table (lets call it Translations) that contains translations used within our program whose primary key is the base text and the language code.  This means there are several lines with the same base text but with differing language codes.
Translations:
   BaseText
   LanguageCode

I have a second table (lets call it Usage) which indicates, for each distinct BaseText in Translations table, where it is used in the program.  The same text can be used in multiple places within the program, so there are potentially several lines with the same text but with differing programs.
Usage:
  Text
  Program

The one field that ties them both together is Text in Usage and BaseText in Translations.  If I wanted to write a query that selects translations pertaining to a specific Program (as indicated in Usage table), I would probably write something like:
select * from Translations inner join Usage on Translations.BaseText = Usage.Text where Usage.Program = ?

However, I'm using hibernate and JPA to do this.  I see many examples for creating a Parent-Child association between two entities, however this relationship is clearly a bit dysfunctional.  This would probably be better represented with a middle table and a many-to-many relationship, however to make things more complicated, this is a legacy program using a legacy database, and thus I can't really add any tables.
The closest question that I could find related to my problem I found here, however it deals with a much cleaner Parent-Child type relationship.  If I use only the one JoinColumn, it complains that the whole primary key is not satisfied.
Using annotations, how should I structure my entities so that I can optionally query Translation entities by Usage.program (if at least one line exists in Usage with a given program, I would like to retrieve its corresponding Translation line)?
This is what I have currently:
@Entity
public class Translation
    @Id
    private String baseText;

    @Id
    private String languageCode;

    @ManyToOne(fetch=FetchType.LAZY)
    @JoinColumn(name="baseText", referencedColumnName="text", nullable=false, insertable = false, updatable = false)
    private Usage usage;

    // .. getters and setters
}

@Entity
public class Usage {
    @Id
    private String text;

    @Id
    private String program;

    // .. getters and setters
    // OneToMany counterpart added, but I removed it because it seemed to
    // make Usage the "owner" entity of the relationship, which isn't my case
}

I appreciate any help you can provide.

redpajama_set_name: RedPajamaStackExchange


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Married at First Sight 2019: Dan tells 'Talking Married' about the moment he nearly confessed to his affair
By Claire Knight| 10 months ago
MAFS groom's close call
His relationship with Jessika has become the latest sordid secret amongst the Married at First Sight group, and it turns out that Dan was ready to spill the beans about the entire affair during this week's dinner party.
Speaking to Talking Married on Wednesday night, the cheating groom reflected on the moment that saw fiery bride Cyrell come "very close" to busting their whole charade wide open.
"When Cyrell came storming in, I was just like, 'she's found out'," Dan recalled, speaking of the bride's heated argument with Jessika over her attraction to him.
"So, when I heard her coming through the doors, the heart started bouncing, and I'm like, 'alright, I gotta face the music here.'"
Cyrell comes for Jessika (Nine)
After Cyrell accused Jess of saying that she wanted to sleep with Dan, the red-faced groom admitted that he was about to come clean to the group about their secret meetups, phone calls and texts.
"I was nearly just going to say it there and then… I'm like, 'I better break it to them now I suppose'," he said.
Unfortunately for us viewers, we're yet to see that bubble burst, as Dan decided to stay quiet. But why?
"I didn't feel like it was the right time, I was a bit intoxicated as were a few people there, so it might've gotten a bit out of hand," he explained.
What Tamara really thinks of Jess's dinner party behaviour
Melissa's strange bedroom habit revealed
MAFS bride Ning defends herself against online haters
EXCLUSIVE: Ines explains her boat breakdown
Considering the fireworks that had already lit up the explosive dinner party, it was probably a wise decision.
Speaking of his covert catch-ups with the blonde model, Dan described his rendezvous with Jess as "the stressfulest [sic] nights ever", and revealed that sneaking around wasn't very fun.
"I was nervous the whole time doing it, it was just outside the dinner party, so it wasn't too far," he said.
"Sometimes we were gone for a little bit and I thought, 'this is shocking'. I felt like I needed to go back in and say something to the group."
Dan and Jessika sneak away from the MAFS dinner party (Nine)
Hindsight is a beautiful thing, and the Queensland dad has been hit with it in spades, revealing that he "definitely" messed up in regards to his relationship with Tamara.
Tamara and Dan during a MAFS commitment ceremony (Nine)
"It's a tricky situation… I've definitely gone about things the wrong way, behind Tam's back. It's something that goes against who I am [but] I was following my heart," he told the panel.
"Looking back now, I probably didn't give Tam the respect and attention that she deserves," he added.
Something tells us Tamara would probably agree with him.
So, will the truth come out? Find out when Married at First Sight continues this Sunday on Nine at 7pm.
For more exclusives, tune in to 9Life every Wednesday at 9.00pm, right after MAFS.
You can also stream episodes of MAFS and Talking Married for free on 9Now.
Auto news: Mercedes' bold plan to sidestep price negotiation on new cars - caradvice.com.au


The T-shirt's are printed very well , dispatched in a very quick time , found sweets inside the bag ??and voucher as well I'm so impressed , strongly recommend.!!!
T-shirt arrived very quickly and exactly as ordered. Love it!


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South Africas legal war over Gaza
by MRN | Jan 1, 2013 | Archive 2012 | 0 comments
South Africans 'fought in Gaza war'
Efforts to prosecute those who may have committed war crimes in Israel's war on Gaza have spread beyond the Middle East.
A lawyer in South Africa has identified 75 South African nationals who he says were fighting with the Israeli army in the war earlier this year.
Feroze Boda, based in Johannesburg and working on behalf of two local pro-Palestinian organisations, says the soldiers should face court action for their involvement.
Imran Garda reports from Johannesburg
(source: Al-Jazeera)
The Goldstone report on last winter's Gaza war has become something of a fixture in the media since its publication in September.
But for South Africans, it is another investigation carried out by the distinguished judge Richard Goldstone – a commission that exposed the brutality of Apartheid security forces in the early 1990s – that looms large in their minds.
That investigation, which came as South Africa moved towards democracy, gave Goldstone hero status in the country.
Now a group of South African lawyers are confident that his recent Gaza report has paved the way for a legal case that could see uncomfortable questions about the conflict asked much closer to home.
They want to investigate South African citizens who may have fought for the Israeli army during the war on Gaza in December and January, with a view to prosecuting them on South African soil for war crimes and crimes against humanity.
The lawyers are representing two civic organisations, The Media Review Network and the Palestinian Solidarity Alliance. Working from a Johannesburg office, they are building a case known as the Gaza docket which seeks to bring the South African soldiers to justice for their role in the Gaza war.The lawyers are all Muslims, but deny they are only taking on the case to defend their co-religionists."This is not a Muslim-Jew thing. No religion condones the killing of innocents. No religion condones the killing of 1,400 people, or the use of white phosphorus on a civilian population," says Feroze Boda, the group's spokesman.
More than rumours
Boda is well-versed in all 3,500 pages of the Gaza docket and says he has presented the evidence to South Africa's police and National Prosecution Authority. "There's always been rumours within the community in South Africa that local South African citizens fight in the IDF, and you would attend mass meetings for example and you would have spokespersons who would say they were interrogated at a border point or in Jerusalem by Israeli soldiers and that soldier spoke Afrikaans," he said. But legal cases, especially ones containing such explosive allegations, need to be based on more than hearsay to succeed.The docket relies heavily on the testimony of UN workers, human rights groups, journalists, and doctors who treated the wounded. The information was gathered by the lawyers on a fact-finding mission to Egypt and Gaza earlier this year. It features hundreds of pages that detail the aftermath of the use of white phosphorus in urban areas, eyewitness accounts of civilian casualties, and evidence of UN schools hit by Israel during the war. Crucially, the lawyers say the docket also contains evidence that South Africans took part in the fighting. "We've identified about 75 South Africans who we believe served in the IDF at one point or the other," Boda says. "We believe that there is prima facae evidence against all of them. We have informants from South African police stations, whose identity we are currently protecting for their safety, who have pinpointed which of their fellow South African police force reservists went to Gaza to fight in the war. We have pictorial evidence as well." Evidence online
The lawyers say some of their evidence can be found on public profiles on social networking sites like Facebook. Al Jazeera logged on to Facebook and quickly found photographs of South Africans proudly showing off their stints fighting for the Israeli army. One 23-year-old man from Johannesburg had posted photographs that made it clear he had fought in the Gaza war. And he is not alone.
There is a dizzying array of similar photographs on the website, featuring smiling young men striking gladiatorial poses with weapons that, according to Goldstone, belonged to an army committing war crimes in the Gaza Strip. Beneath the pictures are captions such as: "These are the presents we sent the Gaza residents daily." As a signatory to the Rome Statute, South Africa could theoretically arrest and prosecute these individuals for alleged war crimes and crimes against humanity – which is why lawyers like Boda are confident they can set up a war crimes court in South Africa.They have the backing of another South African legal heavyweight, John Dugard, the former UN special rapporteur for human rights, who is acting as legal counsel to the Gaza docket team. One of the high profile targets for the lawyers is South African-born Lieutenant Colonel David Benjamin, who served as a legal advisor in the Israeli Military Advocates Corps during the war. Luis Moreno Ocampo, the International Criminal Court's chief prosecutor, has signaled that he too is keen to investigate Benjamin, who gave statements to the media in January hinting that he was one of the legal masterminds behind "Operation Cast Lead". He has since distanced himself from those remarks.
Alternative charges Even if war crimes and crimes against humanity cannot be proven, there is another more obvious charge for South Africans who fought for Israel. A South African law, the Regulation of Foreign Military Assistance Act, bars any citizen from fighting for a foreign force without express government permission. South Africa's most influential Jewish organisation, the Jewish Board of Deputies, strongly condemned the Goldstone report and has been quick to dismiss the Gaza docket. They gave Al Jazeera a brief statement, insisting that they need time to talk to their lawyers. "While we believe that the 'Gaza docket' has no merit, we are investigating this further, and will provide more comment as soon as we have done so," the statement said. The war on Gaza may have taken place on a tiny, densely populated strip of land thousands of kilometres away, but Goldstone's involvement in the subsequent investigations has meant that South Africa has already been touched by its repercussions. If Feroze Boda and the other lawyers have their way, the next act in the drama of the war's aftermath will be played out in South Africa's courtrooms – and the Gaza docket will join the Goldstone commission as a landmark case that South Africans will remember for years to come.


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text:
General Synod: Changes to faculty rules more than 'tweaks'
Madeleine Davies, Adam Becket, and Tim Wyatt report from the General Synod in York
SAM ATKINS/CHURCH TIMES
The Dean of the Arches, the Rt Worshipful Charles George QC
THE Faculty Jurisdiction (Amendment) Rules 2019 were approved after a debate.
The Dean of the Arches, the Rt Worshipful Charles George QC, introduced a raft of changes to rules after, he said, an extensive consultation over the past year. As well as many "tweaks" to what was on List A and List B, there were also significant procedural changes, most notably front-loading the consultation requirements in the faculty process to avoid delays between the formal commencement of faculty proceedings and the diocesan chancellor's decision.
Also, documents that had to be inspected in person at the church could now be inspected online. Finally, any objector was no longer able to require holding an oral hearing rather than simply a written one; that power would now rest with the Chancellor alone. The aim throughout had been to simplify the process by moving as many changes to a church to List A as possible, and some had been removed from the process entirely where very minor. If the Synod approved the new rules, further guidance on their operation would be produced.
The Archdeacon of Oxford, the Ven. Martin Gorick (Oxford), noted how his diocese had both more parishes than any other, and more faculty applications also: more than 100 in just the past month. He commended the proposals, saying that they echoed some changes already implemented in Oxford diocese which were working well and preventing lengthy and frustrating delays. His one concern was that the changes to List A and B could lead parishes to undertake unwise mortar repairs and repoint with inappropriate materials.
The Revd Paul Ayers (Leeds) said that he broadly welcomed the changes, but did have some concerns, similar to Archdeacon Gorick's, as well as issues concerning boilers and sound systems. He was also worried about the new need for the diocesan advisory committees to not send advice when all the consultees have replied, which could compromise their independence.
The Revd Timothy Goode (Southwark) said that he and the diocesan advisory committee of which he was a member fully supported the hope of making the faculty system more efficient and effective. Any remaining concerns could, no doubt, be picked up by the forthcoming advice from the Church Buildings Commission. He had similar worries about the front-loading of the consultation requirements and asked for clarification on some finer points of the new process.
Julie Dziegiel (Oxford) said that she often had to defend the existence of the faculty system, which was seen by parishes as a "right royal pain in the behind". But, thanks to it, the Church of England was exempt from most planning-permission requirements and the need for listed-building consent, also. It was, in fact, a "huge privilege", and the Church should be thankful for it. The Synod must support these new simpler procedures wholeheartedly
The Archdeacon of Halifax, the Ven. Dr Anne Dawtry (Leeds), commended the new rules to the Synod, as part of the simplification of the system, which had occurred throughout this quinquennium. There was a helpful distinction between those needed in an unlisted church and a listed church. "The rules on trees caused great confusion in 2016, and the simplification of these is much welcome," she said.
Read full coverage of the General Synod here
Call for transition liturgy
Synod: Citizenship 'should be about loyalty, not wealth'
Synod: Law on suicide and unbaptised altered
From the archive: The day the Church said yes to women
General Synod discussions to go nuclear in York
General Synod: pattern of future meetings
Church in Wales falls under IICSA's scrutiny as Archbishop and Provincial Secretary are questioned
Synod votes for collaborative efforts to stem youth violence
General Synod: Methodist union legislation a bridge too far for now
WorldCommentFeatures
Team Rector (Designate)
Is God calling you to our growing commuter-belt market town in South Essex?
Bishops' Chaplain and Canon Theologian
The Bishop of St Edmundsbury and Ipswich and The Bishop of Dunwich seek an ordained BISHOPS' CHAPLAIN AND CANON THEOLOGIAN to assist them in their diocesan and national responsibilities.
We have an exciting opportunity for a minister to lead us in effective evangelism to a diverse and growing population close to Basingstoke.
We are seeking an energetic and mission-focused priest to lead these two parishes of a central tradition in a beautiful part of rural Cheshire.


Often when I am speaking to a group I will say; "The biggest challenge we all face in both our personal and professional lives is communication." Think about it. How often do you have issues with family, friends or at work, and the cause of the problem was poor communication. It is not at all uncommon.
There are three main types of communication: Verbal, nonverbal, and written or visual communication. I am going to discuss the first two types of communication in this article.
Effective communication is a key interpersonal skill. Learning how to improve your oral communication has many benefits. Interpersonal is defined as relating to relationships or communication between people. Interpersonal skills are the skills used to properly interact with others. In the business world the term refers to an employee's ability to get along with others while getting the work done. Good interpersonal skills are a prerequisite for a good manager.
Oral communication is a two way process. Improving oral communication involves both how we send and how we receive messages. Thoughts, feelings and ideas must be clearly articulated and shared to achieve mutual understanding. All this seems simple; speak, be heard, and be understood. However, ensuring that understanding is achieved is actually an art. Following are four steps to achieve productive and meaningful oral communication.
Be clear on the message you wish to convey and what you are trying to achieve. Make sure you understand the outcome you want. Stick to the point, as fewer words mean less chance for misunderstanding.
The tone in which your deliver a message is very important. A harsh verbal tone will undermine a positive message. A cheery tone can take away the seriousness of a disciplinary message.
A barrier in oral communication is anything that can potentially interfere with the accurate delivery of a message. Potential barriers include; stress, defensiveness, past interactions, environmental distractions, timing of the conversation and information overload. You should think ahead about potential barriers that might stand in the way of relaying your message clearly and accurately and make an effort to avoid or minimize them.
Look for nonverbal clues in communication such as nodding, facial expressions and body language. If appropriate, ask the listener to paraphrase what you have said. Address inconsistencies or misunderstandings immediately. Listening is an important part of communication. Listen without interrupting. Finding out how your message impacts the other person can help you improve for the future and clear up any misunderstandings at the time.
A majority of what you communicate to people on a daily basis is done without words. Nonverbal communication is anything besides words, such as gestures, facial expressions, appearance and body language which when seen communicates something. Think of the phrase "it is not what you say but how you say it" or the saying "actions speak louder than words." People send, receive and interpret nonverbal messages the same way they do oral communication. Because nonverbal communication is often without consideration, inconsistencies between oral and nonverbal communication can occur. It is important to ensure consistency between your oral communication and you nonverbal communications.


Everyone loves to save some money. But, not everyone knows how to do it! Because, they find it difficult to figure out simple ways to save money and how to use savings to pursue their financial goals. Here are few steps that can help you to develop a realistic savings plan.
The best way to save money is to have a budget. A good budget can always help you to spend your money in an effective way. With a good budget, you can plan your spending, limit over-spending and make sure that you put money away in an emergency savings fund.
It's very important for one to record all the expenses. This gives you a control over your money. You can track your money, like where you are spending more or maybe if you are incurring some unnecessary expenses. Start doing it for a month, then you can organize the same by categories like – gas, groceries, mortgage etc. and get the total amount for each.
The next plan for you is to have a savings plan. Considering your monthly expenses and earnings, create a savings category within your budget. If your expenses are't letting you save that much, it might be time to cut back. Look out for the least important things in your expense list and decide to cut down some expenses like entertainment or outings, that you think can be avoided.
When it comes to savings, different people have different priorities. So you must decide which savings goals are most important for you. Accordingly, you can plan how much money to put into your different savings plans.
You can begin by setting few short term goals. Those goals may be set for 1-3 years, which may include – savings for a vacation, to buy a new car or even you can save for your tax payment. Long term savings goals are generally set for several years, which include – savings for retirement, money for children's education or for marriages etc.


text:
Jewłasze (, Jeułaszy; , Jewłaszy) – wieś na Białorusi, w obwodzie brzeskim, w rejonie janowskim, w sielsowiecie Brodnica, nad Filipówką i w pobliżu jej ujścia do Piny.

Historia
W XIX i w początkach XX w. położone były w Rosji, w guberni mińskiej, w powiecie pińskim, w gminie Duboj. Były wówczas własnością Kurzenieckich.

W dwudziestoleciu międzywojennym leżały w Polsce, w województwie poleskim, w powiecie pińskim, w gminie Brodnica. W 1921 wieś liczyła 298 mieszkańców, zamieszkałych w 57 budynkach. Wszyscy oni byli Białorusinami. 289 mieszkańców było wyznania prawosławnego i 9 mojżeszowego.

Po II wojnie światowej w granicach Związku Sowieckiego. Od 1991 w niepodległej Białorusi.

Przypisy

Bibliografia

Wsie w rejonie janowskim (Białoruś)

redpajama_set_name: RedPajamaWikipedia


text:
Bijzondere biologie is een wat oudere term voor de biologische vakgebieden die betrekking hebben op de systematiek van de soorten van bepaalde taxonomische groepen.

Onderdelen
Bijzondere biologie beschrijft van bepaalde taxonomische groepen als soorten, geslachten of families de (bio)systematiek, de morfologie en de anatomie, de ecologie en het gedrag (bij dieren).

Onder (bio)systematiek vallen de natuurlijke verwantschapsbetrekkingen, inclusief de levenscyclus en de voortplanting, de afstammingsgeschiedenis (de fylogenie of de evolutie) en de soorten, het verspreidingsgebied, hun plaats in het systeem (soort, geslacht, familie, verwanten) en hun naamgeving: de taxonomie en de nomenclatuur

Voorbeelden
Voorbeelden van de vakgebieden en de bestudeerde groepen in de "klassieke" indeling zijn:

Biologie


text:
Disability rights in the UK: updated submission to the UN Committee on the Rights of Persons with Disabilities
This submission provides information on the extent to which the UK is putting the UN Convention on the Rights of Persons with Disabilities (CRPD) into effect. It provides an update on our earlier submission to the CRPD Committee in February 2017.
This report has been produced by the United Kingdom Independent Mechanism (UKIM), which is made up of:
•Equality and Human Rights Commission (EHRC)
•Equality Commission for Northern Ireland (ECNI)
•Northern Ireland Human Rights Commission (NIHRC)
•Scottish Human Rights Commission (SHRC)
UKIM is tasked with promoting, protecting and monitoring implementation of the CRPD across the UK.
https://www.equalityhumanrights.com/en/publication-download/disability-rights-uk-updated-submission-un-committee-rights-persons
contact@equalityaction.org.uk
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It's that time of year again! StartUp Maryland has announced the dates and route of their 2016 STRT1UP Road Show, their 5th annual tour of Maryland that celebrates entrepreneurship and gives startups the opportunity to hone their pitch.
Since the launch of the road show in 2012, more than 1000 Maryland startup companies have participated. Citing the huge variety of industry sectors that Maryland startups have entered, Startup Maryland CEO Michael Binko explains that the STRT1UP Road Show "proudly shines a spotlight on the diversity of our innovation categories and the ecosystem supporting them.
At each stop along the tour, Startup Maryland and their partners and sponsors host rallies and events sharing information about Maryland entrepreneurship. Startups and entrepreneurs are given the chance to step aboard the Startup Maryland bus and pitch their idea in the bus' mobile studio. The pitches are then uploaded to Startup Maryland's YouTube channel where the public can view them and vote on their favorites as part of the Pitch Across Maryland competition.
To learn more about Startup Maryland and view dates and stops, visit StartupMD.org.


Opinions about Google+ differ a lot. Some love it because of all the interaction they are getting there (more comments), others have lost interest all together. Fact is that as a social network it still has a long way to go.
But if you did lose interest because your feed kept showing the same people and you figured others would have lost interest too, you might be wrong. Experian Hitwise, who always checks the numbers, reported a few days ago that Google+ is not suffering at all. On the contrary, at least in the US. The month December 2011 was the "biggest month to date" for Google+.
Hitwise says December saw an increase of no less than 55% increase over November 2011. This would indicate the huge growth is back.
Why December was such a good month is a guessing game. Maybe its because Google really pushed Google+ in all different ways they can, maybe some updates on the mobile front helped interaction. Or maybe it was the integration of Google+ into other products like search which pushed traffic.
Now beware: traffic doesn't tell us everything. Many tend to think that more traffic means success. There might be more traffic to Google+, that doesn't mean it is actually used more than before. It could be people checking out the service, or less people making more use of the service. These numbers do not 'tell all'.
Still, Google+ will continue to be a discussion trigger for marketeers in 2012. Should we or should we not use it. My personal thought is that even though as a social network it has a long way to go. It will be very dominant in what Google is doing. So you better not ignore it.
Yeah, there were even ads below the search box on Google.com which led to a page displaying four products, Google+ among them. No wonder there is growth.
One Gmail Account is All you need online!
G+ is a great site!
I have come to really enjoy being on Google+ and I despise social networks.
This network will have a bright future.
Have too agree, not one for social networks myself!


text:
Kemranggen is een bestuurslaag in het regentschap Purworejo van de provincie Midden-Java, Indonesië. Kemranggen telt 903 inwoners (volkstelling 2010).

Plaats in Midden-Java


text:
EU3 - After Action Reports (AAR)
A Venice Divine Wind 5.1 AAR
Thread starter diegoami
Well, I guess some archangel appeared and told them to convert. This is the only reasonable explenation...
The thing that irritates me a lot is that there is no mechanism which makes Muslims around the world royally pissed off once somebody takes their holy city. It would be fun if, like, 80% of them declared war stimultainiously with "reconquest of Mecca" cb. Other then that, how do you make the missions love you so much? Yes, I know that having 2 integrate missions in a row is worse then a integrate-vassalise-integrate chain, but still...
vasziljevics
hm... that's ridiculous indeed... my idea that just came to my mind would be a new factor in religious conversions, something that measures how 'embedded' the actual religion is - for example by the 1500 Muslim faith would have nearly 900 years of that in Mecca while Catholicism would have only 200-300 years in regions like the Baltic. so converting the latter to a whole new faith should be easier. also there should be differences between converting to a 'heretic' belief and converting to an entirely new religion (Sunni-Shiite vs. Sunni-Catholic in this case). but that's just my idea.
anyway, do you plan to claim all of the New World for Venice or dividing it into spheres of countries would be enough?
diegoami
Memento Mori said:
I like the idea, taking and converting the Mecca seemed too easy
What should I say about missions ? This is what helped me get some good missions, I think.
- Low infamy all the time. Which means I have good relationships with most countries and I seldom get the missions "Improve relations with X". Not sure if you are likelier to get good missions if your infamy is low.
- Big land army and navy. No missions "Naval Race" and "Army Race"
- Focus on missions. The more missions you accomplish, the likelier it is to get a good one. Kind of obvious.
- Having a long border. Bordering many small countries. Being in a fragmented region.
- And most important of all, creating the conditions for this kind of missions. I made Austria release Styria and Tirol, the Papal state release Urbino and Siena, Milan release Pisa, Bavaria release Augsburg. I got missions on all these small countries.
- No point in canceling a mission. You will get the same mission over and over.
Completed (EU IV, 1.28.3) : Succeeding with Ottomans playlist (Completed)
Finished (EU3 5.2) : Venice Reloaded - a 1453 Venice DW 5.2 AAR - Interrupted in 1639
Finished (V2 2.31) : Born to colonize - a straightforward Portugal AAR (AHD 2.31)
Completed (EU3 5.1) : War is the extension of commerce - A Venice Divine Wind 5.1 AAR
Completed (V2 2.31) : A tale of two Kaisers : a gameplay Prussia AAR (AHD 2.31) (Tied for 3rd - AArland AwAAds 2012_Q4)
Read my Victoria 2 analysis threads to learn more about the game.
vasziljevics said:
Yeah I don't think there is an easy solution for this. Several approaches have been tried. Making entrenched religions harder to dislodge is a good idea, but there are religions which are much harder to dislodge than others. The Incas have all been converted in a generation, while I don't know of any province in history who has been converted peacefully from Muslim to Christian. I mean, without kicking them out, like the Moriscos in Spain.
- In EU2 I think you can only convert provinces who have low population
- In Magna Mundi conversions are much harder
- In Vicky 2 you have Pops. It models the world better, you have several religions in a province. But it is much harder to understand and follow.
Anyway, Spain has a lot of provinces in Africa and I even helped them there. I consider all of America Venice's sphere of influence. But that will be decided on the battlefield. The only provinces I will leave alone are the cities who will not border Venice's colonies in America ever, like Trinidad for instance.
1521-1526 : Colonial growth and Imperial Integrity
Gold is still waiting for us in Zimbabwe. War is declared on the Musape in March 1521.
And on the Chimu and the Inca as well.
Zimbabwe is annexed in June 1521.
Chanchan is annexed in October 1521.
And we get one province more from the Incas, Arequipa.
So this is the situation in South America in November 1521. Portugal has founded another colony, Antioquia.
We keep converting the heathen provinces. We always have enough missionaries. Meanwhile Protestantism keeps spreading in Europe.
In November 1522, we connect our COT in Mohawk to the coast in North America, thanks to the founding of Mahican.
Our doge dies and we elect a new one. I choose a diplomatic one. There is diplomatic work to do.
Land Tech 16 is researched. We found a new colony in North America, Massachussets. Since we have a core on Loango, we can also claim Cape. A colony is founded there too.
In November 1523, I can choose a new National Idea. I choose "Land of Opportunity" : 33% Global Colonial Growth more. My other NIs are Press Gangs, National Bank and Quest for the New World.
In December 1523, I find out that our economy is more than twice bigger than Spain's.
I am not afraid of taking on Spain 1-on-1, but there are other countries who might intervene. There are three more things that I want to do before war is declared : join the HRE, improve relations with Great Britain and annex Pisa, which will be possible in August 1526. Our relations with Austria, the current Emperor, have improved lately. We are both Catholic, although Austria's capital is now Protestant.
Our relations with Great Britain are improved as well. They have military access and should not declare war out of the blue. And we still have trade rights on their iron, which we bought like - 70 years ago ?
Meanwhile the colony in Cape has been founded, but colonization in Little Karoo fails even if it was 99% likely.
In September 1524, the Holy Roman Emperor accepts our request to join the Empire. Will I regret that ? If I had to annex a country like Croatia now I might not be able to keep all of the provinces...
But the bonus is very good and cannot be ignored. Imperial Integrity. Actually, I should have joined the Empire before.
We got called to arms from the Iroquois against the Huron. In February 1526, Nav Technology 16 is researched.
A new colony is founded in Sayultecas, in Mexico, who has a very high tax base.
And we strike gold in Cape ! Little Karoo, meanhwhile, has been succesfully colonized.
A new colony is founded in North America as well, Lenape.
meh... if in need of it you can leave the HRE anytime
on the former topic: yeah, the Vicky-system of pops is probably the best (out of the ones that have been tried yet) but it complicates the game to a scale which could be rejected by a large part of EU players. anyway it was just an idea.
1526-1529 : Pisa annexed.
Our ally Syria is having some trouble. He is at war with several Muslim countries
We give them war subsidies, we need to be at peace to annex Pisa.
But of course, Syria calls us to arms soon.
As soon as we enter the war, we are offered white peace. In August 1526, we white peace the Mameluks.
Peace is made with Benin as well. In March 1527, we are all at peace and we can annex Pisa.
Our next mission will be colonize Timucua.
Meanwhile, we get a core on an Inca province, Tumbes.
Spain has founded another colony in North America, Pamlico, and has sent a colonist to Santee.
In October 1527, a colony is founded in Timucua.
Next mission will be turn Mahican into a city.
Of course, we need to get back to stability 1 as well. Netherlands for some reason expanded in Eastern Europe and is snaking into the Golden Horde territory.
Spain keeps expanding in South America as well. There are quite a few colonies we could grab now. Havana has already turned into a city so it is about time we declare war on Spain.
They have the same land and naval technology as Venice : 16. They are at war with the Golden Horde and have some War Exhaustion. We infiltrate Spain's administration.
In January 1529, War is declared on Spain using the Colonialism casus belli. Allies will be called to arms manually, since not all of them can join (e.g. Syria).
Here are the diplomatic maps right after the declaration of war.
ok - the Netherlands is a country which I haven't seen yet conquering the GH but in EU3 all things has to come sooner or later... wow!
now let's see what the Spaniards have...
Malurous
Whee, major conflict coming up! Certainly looks interesting in the New World.
DIP 9, ADM 8? That's one heck of a Doge.
This! Hopefully they'll win the race to the steppes, would be awesome.
Read my Cuzco MEIOU AAR Children of the Sun! (ongoing)
AARland Choice AwAARd: EU Gameplay Q1 & Q2 2011, Weekly AAR Showcase 17-10-2010, ●
Follow Gentlemen in Germany - a Brunswick AAR! (ongoing)
Participating in 1001 Sultans - A Jalayirids Succession AAR (ongoing)
WritAAR of the Week 24-5-2011, Fan of the Week 3-12-2009 & 15-1-2012
Speed - A Castille (mini-?)AAR (finished)
Took part in the HT Succession Game (finished)
Malurous said:
Yeath... but I am worried too. Imagine the quantities of cannabis they will start to grow, if given the access to the steppes
As far as I know, hemp was common all over Europe in the EU timeframe...
1529 : War with Spain (1)
Spain is present also in the Middle East. One more reason to attack them, the Eastern Mediterranean is definitely Venice's sphere of influence.
The first engagements are obviously naval. We ambush a fleet in the Straits of Gibraltar.
There are no Spanish troops in North America and it is easy to grab their colonies.
Major naval engagements are fought in the Mediterranean. We called most of our vassals to arms by now. The ones who have a fleet.
Havana is occupied as well, but regrettably cannot be seized because it is a city - with no fort though.
By middle of February 1529, a first batch of Spanish colonies in North America has been seized.
But we get surprised in Judea by a major Spanish stack. We have to retreat to Syria.
The Byzantines are taking care of Spanish possessions in Turkey.
On the 21th of February 1529, in a surprising turn of events, Austria declares war on us.They cite "Imperial Liberation" as their casus belli ! I guess they never forgave us that we took several provinces out of the HRE. I thought I had covered my back there. This is actually the scenario I feared.
They take a bunch of countries into the war as well. So Venice is now at war with Spain, Portugal, Austria, Bavaria, Savoy, Dauphine and Bosnia. Isn't that great ?
Difficult times call for extreme measures. A loan has to be taken. There are virtually no Venetian troops in Italy and the vassals cannot match the enemys' stacks.
The naval war with Spain seems to turn bad as well. We lose a major engagement in the Meditarranean sea.
But Spain has no troops on the Mainland and Naples and Sicily are invading it ! That is going to put some serious pressure on them.
The situation in Italy is getting very dangerous. Austria has two major stacks and is assaulting Krain, while Bavary is invading Tirol with a big stack. To add insult to injury, the vassals Augsburg and Styria are not allied with Venice any longer - they cancelled their alliance after going Protestant and it takes some time before it is restored and they are called to arms as well.
One of our major problems is that we don't have generals - apart from our doge. We have a pretty low military tradition, around 30%. We brought reinforcements to Judea but it looks like we will be defeated there.
Savoy also joins the fray and sends a major stack to Milan. We have no answer to that.
When I thought think things could not get worse, I spot a big Dauphine stack heading to Milan as well.
At least in America things are going well. We are grabbing colonies in South America....
In North America....
And we achieved naval superiority.
Poulern
Pretty much what i feared did happen, more planning in terms of HRE provinces would have been helpful before joining, although i will say the bonus is kickass. Its always good to dismantle the spanish colonies, they totally ruined my attempt at a complete americas empire. If all else fails, i always found that the AI rarely completely occupies you in the pennisula, and leaves about half of my provinces alone, so you might benefit from that.
Ricardo Rolo
Austria always gets in the way ,isn't it ?
This look good enough on the Americas, and even the situation in Spain is quite good. Italy, on the other hand, is in dire straits :/ I guess it is time to get what you can from the Spanish war and focus on driving the Emperor back to his lair, since Italy is your power base and all those armies around are not doing it any good . Too bad you can't be the Emperor yourself ... this would be easily averted if you could.
Poulern said:
I didn't know about this game mechanics, I thought that being in the Empire would make the Emperor LESS likely to declare war on you. You live and learn.
Ricardo Rolo said:
This is exactly my plan right now. I have to be a republic, that is a house rule, so I cannot be the Emperor of course
For reasons I don't know, Bavaria offers us a white peace. I am happy to accept it, since this takes more than 20k troops out of the war.
As expected, the troops in Judea are defeated and retreat to Syria. Luckily the Spanish cannot follow us there.
In Morocco a Venetian and Spanish stack are about to meet. We are more than them, but they have a general while we don't. I am taking attrition in Ifni, this is why I am eager to meet them.
The naval war seems to turn back to our favour and we win two major engagements in the Mediterranean sea.
Spain has no answer to the invasion by Sicily and Naples. This might win the war for us.
By the end of April 1529, Milan falls and Liguria is under siege as well.
In May, we win another major naval engagement in Cape Bon.
But devastating news comes from Rio de Oro. Our Army of Morocco has been soundly defeated. That puts a even bigger drain on our depleted manpower. I guess I have shown you how not to do it, their great general made a big difference. I should have avoided engagement and let the Spanish take attrition in Ifni / Sus.
It is a very little consolation that Bosnian troops are defeated in Zeta.
In America, we have moved to the next phase of "colony seizing" and we are about to grab the Spanish colonies in Colombia and Central America.
By the end of June 1526, Spain offers us a white peace, just as they are about to wipe out our Army of Morocco. But they want out of this war as well, they have high War Exhaustion and risks of revolt even on the Mainland, Spain is being invaded and they are about to lose all of their colonies.
We accept, even if that means we are not achieving all of our war goals. But Italy is being invaded and that needs to be taken care of. We are now at war with Austria, Savoy, Dauphine and Bosnia. We should be able to handle that.
Our freshly recruited regiments, joined by the troops we withdrew from Africa, meet the Dauphine stack who has ventured too deep into Italy. The Austrian and Savoy stacks remain unchallenged in Slovenia and Liguria. The smaller Austrian stack in Krain has been wiped out by our vassals after they foolishly tried assaulting the fort.
A much needed victory is achieved.
Of course our vassals will bring the war to their countries as well. A small Byzantium stack lands in Dauphine. All of Austria is already under siege.
Bosnia and Dauphine offer a white peace. We accept Bosnia's offer, but not Dauphine's. The tide is turning and we will make them pay for attacking us when they thought we were weak.
Dauphine's stack is wiped out in Görz.
In September 1529 we can move a slider and we go Mercantilism - we will found the East India Company sooner or later.
I challenge the Austrian stack in Slavonia hoping that my vassals will come and join the fight - but they don't. They just walk around it.
My bigger stack, who got other reinforcements from overseas, is tackling Savoy's stack in Liguria.
Without help, though, our outnumbered troops have to retreat from Slavonia.
1529-1531 : War with Austria
But in Liguria we win and Savoy's stack is not going to survive this.
Their stack is wiped out in Nice, while Dauphine is begging for a peace they are not going to get. The road to the invasion of Savoy and Dauphine is open.
While our main stack is tackling the Austrian stack another time and this time we are going to win the battle. Our vassals have invaded Austria as well.
We win, but not as decisively as I hoped. Our losses hurt and we are now very low on manpower.
In April 1530, our war score with Savoy is high enough to make them release Sardinia and their colony Hausa.
In Osjek we win another major costly battle. I really need better generals.
The war is pretty much decided, so we start another one, against the Inca.
Which is immediately over after the occupation of Tumbes, which is a Venice core.
In Bosnia, who conveniently gave us military access, the Austrian stack is routed. Our losses are horrific, though. Austria is very tough.
During the war with Spain, we didn't notice they have a colony south of Loango. In our rage we declare war on Kongo.
Dauphine is soundly defeated.
We make them release Provence.
It is Austria who has to be punished. They have to cede Graz, even if we have no core on them and will be unlawful.
But Styria suddenly gets a core on it. I am sure it was not there last time I checked. That is very convenient, Graz will be sold to Styria.
After this war, which cost us so many brave men, our manpower is depleted but our economy is booming. Spain's economy has been damaged, but they are still strong. The newly acquired colonies will have to be assimilated in our culture, which will cost us some colonists.
Venice's performance in this war was mixed. We made several mistakes, which I hope we won't repeat in the next war. There are still colonies in the New World to seize.
Well done all things considered - that was quite a coalition you were up against at one point. The colonial race is certainly looking worse for Spain now.
It's typically not a good idea to fight without a general. Even a bad one can make somewhat of a difference and those are easy enough to get...
Smart move going to mercantilism, being so large seems to make everyone envy you and that decreases your trade chances significantly even with low infamy. At least that is my experience, and it is kinda annoying.


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Home » England » Matthew Kneale » English Passengers
Matthew Kneale: English Passengers
Kneale tells a fascinating story – or, rather, several fascinating stories that intertwine and illuminate a little known part of English history. There are really four main stories that merge and influence one another. The first two concern British colonisation of Tasmania. One is about the aboriginals of Tasmania and how they are exploited and then slaughtered by the British settlers. Related to this is the story of the convicts sent to penal settlements in Tasmania. In particular, we follow the story of Jack Harp, a former convict still living in Tasmania. Seeking female company, he captures a Tasmanian woman, tethers her up and sexually exploits her. However, this woman (who, apparently, is based on a real Tasmanian woman) is a strong, formidable woman. She escapes and then leads a band of Tasmanians against the settlers. She has two children but it is Peevay, her son by Harp, who we follow most and whom she utterly despises (to the chagrin of Peevay.)
The second set of stories concerns a group of Manxmen, led by Captain Illiam Quillian Kewley who endeavour to cleverly smuggle contraband to England. Inevitably things go wrong and then worse and they are forced to leave England in a hurry. Linked to this is an expedition led by the Reverend Geoffrey Wilson, a Yorkshire vicar, who has determined that the Garden of Eden is in Tasmania and manages to persuade a rich man to fund an expedition to confirm this. Unfortunately, at the last minute the ship they were to use is diverted to help fight the Indian Mutiny. Fortunately, Kewley and his ship are available, uniting two unlikely groups.
Kneale tells the story through the voices of the main characters – over twenty of them – which gives a vivid and varied picture of the expedition, the ship and, in particular, Tasmania. And a fine story it is. He manages to give us the voices of the exploited aboriginals and their struggle for survival, the voices of his fellow Manxmen (who consider themselves very different from the English), the voices of both the convicts and those guarding them and, of course, the voices of the expedition members. All sorts of things go wrong, of course, and, inevitably, the surviving Tasmanians meet the expedition members. Kneale manages to keep the story going, tell it with great humour and gusto and painting a picture of the savagery of the times. That his sympathy is with the exploited – the Tasmanians and the Manxmen – is clear, with most of the English being at best weak and often mad, bad or both. And that is, to a least some extent, what make the story enjoyable.
First published 2000 by Hamish Hamilton


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Associated Press of Pakistan (APP) is the main news agency in Pakistan. It began its operations in 1947. In 1961, APP was taken over by the government on the pretext of financial difficulties. It offers news in English, Urdu, Sindhi, Pashto, Balochi, Brahvi, Seraiki and Arabic languages. Being a government organisation allows APP greater access than any other Pakistani news agency can muster. It gives disproportionately more coverage to the engagements and statements of cabinet ministers and government functionaries. The news content generally gives more favourable coverage to the government. APP has news exchange agreements with 37 foreign news agencies.
There are a number of privately owned news agencies as well. The main ones include Network News International, which was established in 1992 and provides services in English and Urdu. Online International News Network initiated its operations in 1999 and also offers news services in English and Urdu. Pakistan Press International (PPI) was established in 1956 as Pakistan Press Association (PPA) and renamed as PPI in 1968. PPI offers text, photo and audio news services in English and Urdu.
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