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Graesse II, Nagler XX, Not in Adams. Published by Wien, Carl Gerold's Sohn, Erste Ausgabe, mit Verfasserwidmung und einigen Textkorrekturen in Bleistift. Diese Ausgabe des Epos aus dem Baden, 3. Rabenlechner I, Rypka Published by Wien, Mechitharisten, About this Item: Wien, Mechitharisten, XIV, 2 , 80 SS. Bedruckte Originalbroschur. Erste Ausgabe. Kalemkiar S. Chauvin II, S. Small folio. LXVII, 1 , 4 , , 1 pp. Publisher's original blue printed wrappers.

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The first critical edition of Abu'l-Fida's great tabular geography "Taqwim al-buldan", edited and introduced by Joseph Toussaint Reinaud and Mac Guckin de Slane, two of de Sacy's most eminent students, based on the Paris and Leyden manuscripts. The crater Abulfeda on the Moon is named after him. The author speaks of its various regions, of the equator and the seven 'climes', describing each in detail. He establishes their geographical positions and addresses conditions in each of them. He describes their sizes and their boundaries, and also mentions their seas and lakes and rivers and mountains" The Arabic Books Printed in Europe.

Wrappers stained and chipped with large flaws to spine. GAL II, 46, no. Zenker OCLC Published by Berlin, Julius Bard, About this Item: Berlin, Julius Bard, With frontispiece, title vignette and 9 illustrations, all in original hand colour. Contemporary full red calf with giltstamped spine title. Top edge gilt. Number of a limited edition of copies: an appealing, complete edition of the satirical narrative by Hoffmann , who was prosecuted for the work.

A partly censored first edition appeared in The illustrations were created by the stage designer and graphic artist Stern , whom Max Reinhardt had hired for the Deutsches Theater in Berlin in Binding lightly scuffed.

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From the library of the Viennese collector Werner Habel, with his signed and stamped ownership to flyleaf, dated Voerster Grutzmacher For Stern cf. Vollmer IV, f. Published by Altenburg, Paul Emanuel Richter, Title printed in red and black. With engraved frontispiece and 5 engraved portraits. All edges gilt; front pastedown with colourful floral design.

Contemporary blindstamped calf over boards. A well-preserved devotional containing prayers, chants and psalms, also offering an index of authors and songs. Since the foreword by Carl Andreas Redel dates from , it probably derives from the first edition. The portraits depict five men: Matthias Bel, a Lutheran theologian who translated the Bible into Bohemian; three members of the Serpilius family, two of whom were pastors in Sopron and Pozsony and one of whom, Johannes Serpilius, was town judge of Sopron, and finally Johann Christoph Burgstaller, senator in Hungary's Pozsony County.

Apart from motives of Christian devotion, the frontispiece shows a small view of the city of Altenburg as well as the city arms and the coat of arms of the Wettin family, who ruled Altenburg in late medieval times. Christoph Ziegler to his sister Susanna in , as stated on the upper flyleaf. With separate title-page after the index and the first portrait "Das Geistliche Altenburg in seinem Bethen [.

Altenburg, Paul Emanuel Richter, ". From the library of the Viennese collector Werner Habel, with his ownership stamp to flyleaf. VD 18, ed. Published by Bruck, in Commission bei Ignaz Strobl, Small 8vo. Wants the plates. Contemporary black boards with ornaments stamped in relief. First edition. Includes various prayers and litanies to the Virgin Mary and other saints as well as a brief of indulgence by Pope Pius IX. Hinges damaged, binding loosened and scuffed. From the library of the Viennese collector Werner Habel, with his signed and stamped ownership, dated , to front pastedown.

Schlossar Title page printed in red and black with engraved vignette. Title page printed in red and black. With engraved frontispiece. Contemporary vellum over boards with handwritten spine title. Bound after this is a similar work giving advice on sore throats and bad breath, but also on childbed fever and baby care and even on what to do when poisoned.

XIV, pp. With 23 illustrations maps, diagrams and genealogical tables , including 3 folding plates. Original publisher's white cloth. Provides a "general overview of the societies", followed by chapters on their history, religion and social structure. Another chapter is devoted solely to the oil industry of the area. Westervelt with his ownership to front flyleaf.

Folio ca. Title-page printed in red and black. With additional engraved title-page, one engraved portrait and engraved illustrations in the text. Contemporary giltstamped oxydized calf over wooden boards with giltstamped spine and spine title spine rebacked. Two ribbon bookmarks. Modern marbled endpapers. The first engraved edition of the Mainz Bible, published several times since , based on the translation by Caspar Ulenberg With ownership to the flyleaf. Paper evenly browned and brownstained throughout. An ink stain to p. From the library of the Viennese collector Werner Habel, with his signed and stamped ownership, dated , to the flyleaf.

Graesse I, note. E VD 18, Published by Antwerp, About this Item: Antwerp, As noted in the title, the map was prepared by Gerard De Jode's and is largely identical to Giacomo Gastaldi's highly influential map of De Jode's delineation of Arabia is vastly superior to the contemporary maps of Ortelius, showing far more accuracy and detail.

Extending from the Nile to Afghanistan and centered on the Arabian Peninsula and Persian Gulf, the map depicts what was then still among the most important trading centers of the commercial world. The present example is from the first edition of De Jode's work, which can be distinguished from the second edition by the pagination on the verso VII for the edition; 9 for the edition. At least one commentator has opined that as few as 11 known examples of the first edition are known to have survived, making separate maps from this first edition very rare on the market.

Karrow described him as "one of the most important cartographers of the sixteenth century. He was certainly the greatest Italian mapmaker of his age. A large number of maps were published throughout this period with the geography credited to Gastaldi, but it is often difficult to know what role Gastaldi played in their creation.

As a practice, he did not sign himself as publisher, although his name may be found in the title, dedication, or text to the reader. Frequently where there is no imprint one may assume that Gastaldi was the publisher.

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A further clue may be that many of the maps attributable to Gastaldi as publisher seem to have been engraved by Fabius Licinius. In other cases, where publication is credited to another, it is not always certain whether Gastaldi was commissioned by the publisher to compile the map, whether another less-enterprising publisher merely copied his work and attribution, or simply added Gastaldi's name in the title to add authority to the delineation. His name clearly commanded the same sort of respect that the Sanson name had in the last years of the seventeenth century, and as Guillaume de L'Isle's had in the first half of the eighteenth century.

Gastaldi's first published map was of Spain, engraved on four sheets, and issued in The following year he published a map of Sicily, among the most widely copied of all his maps. In the course of a prolific career, Gastaldi subsequently produced a number of maps of Italy, and individual parts of the peninsula, with his general map of Italy, and the map of Piedmont also being very influential.

Among the most important of his maps, however, were of areas outside Italy. Principal among these was his map of the World, published in , a four sheet map of the countries of south-eastern Europe, published in , and his series of three maps of the Middle East, Southern Asia, and South-East Asia with the Far East, issued between and In , Gastaldi issued a two-sheet map of the Kingdom of Poland, and in , a magnificent eight-sheet map of Africa.

Tibbetts, Arabia in Early Maps Published by Nuremberg, Endter, ]. About this Item: Nuremberg, Endter, ]. With engraved title. Lacks the red and black letterpress title-page. With engraved and several woodcut illustrations in the text as well as 10 numbered engraved plates. Title-page printed in red and black title and preliminaries erroneously bound with prelims of the first work.

With woodcut title-vignette and 6 engraved illustrations in the text. Later binding remboitage using contemporary blindstamped calf over wooden boards with two clasps; new endpapers. Includes information on common illnesses and remedies, as well as on child care and education. The engraved illustrations show typical works on noble estates throughout the year, while also including a view of the Austrian town of Eisenerz p. The plates show various patterns for arranging flower gardens.

Pagination jumps from to ; text continuous. Severe flaws to the engraved title, which is glued to the second flyleaf. Numerous flaws and tears to several other pages, mostly affecting the lower margins, some rebacked with paper strips, some with significant loss of text fol. VD 17, A. Lindner Kress I, Lipperheide Pc 4 see note. Krzymowski Humpert ed. Graesse III, ed. Published by Basle, Hieronymus Froben d. About this Item: Basle, Hieronymus Froben d. With woodcut illustrations within the text, 85 of which full-page.

Woodcut printer's devices to title-page and final page verso. Gentium et familiarum Romanarum stemmata. With woodcut title-vignette. Contemporary full vellum. Graesse , a "state handbook of the military and civil organisation of the late Roman Empire" cf.

Compiled anonymously around , the classical text and illustrations were passed on in several manuscripts, first appeared in print in abridged form in and were published in the present version by the classicist Gelen ca. The woodcut illustrations were created by Conrad Schnitt , except for pp.

They show, inter alia, allegoric depictions of parts of the Empire, the insignia of court, civil and military authorities, as well as statues, small buildings and books. The genomic coordinates hg19 on chromosomal region 8q24 are given as x axis on the top. Blue arrows in MYC gene indicate the transcriptional orientation on the forward strand.

The scale of the y axis indicates the mean expression of the respective MYC transcript across the cases using a maximum scale of 55 normalized value of the expression. Note that due to the resolution not all neighboring mutations can be clearly distinguished. The box plots give the range of the fractions per somatic SNV of translocated allele vs total MYC expression per case.

Remarkably, more than one type of fusion transcript with maximum of 4 was detected from both derivative chromosomes in 5 of 9 cases as consequence of the IGH- MYC translocation. We could determine the orientation of those fusion transcripts in five cases and interestingly all of them appeared to be an antisense transcript.


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Thus, the identified antisense fusion transcription might be attributed to the generation of the translocation breakpoints by this enzyme. Overall, we found that MYC transcription is mainly driven from the translocated allele, on which the BCL6BS suppressive element is either translocated away or disrupted, and that class I breakpoints lead to expression of an alternative MYC transcript. Of these, occurred in cases expressing the canonical and 30 in cases expressing the alternative MYC transcript; the remaining SNVs were in cases where the transcript could not be classified, due to the unavailability of RNA.

These, did not affect the overexpressed MYC transcript. We also detected 7 small indels in 7 patients, and 7 SVs 3 duplications, 3 deletions, and one inversion involving MYC in five BL; three of them were located in the coding region. A total of 10 exonic positions were recurrently mutated with 8 of them showing exactly the same base change. LeuVal in the protein sequence P—1 encoded by both canonical and alternative transcript corresponding to position for P—2 isoform, only encoded by the canonical transcript.

This might be of relevance for common diagnostics, because the immunogen for a widely used antibody clone Y69 are the first aa of the protein. Mutational analysis on MYC gene and protein. Note that the isoform 2 of the MYC protein Uniprot: P harbors 15 N-terminal amino acids which are not present in the canonical isoform 1.

Since phosphorylation is required for ubiquitination and degradation of the MYC protein by the proteasome, abolition of phosphorylation could lead to a decrease of protein degradation and hence, increase the stability of the MYC protein It was not possible to determine the timing of the events in the cases with two IGH breakpoints directly from the sequencing data due to the short sequencing reads and the distances of the breakpoint on the IGH locus.

Thus, though rare cases of light-chain revision in germinal center B-cell lymphomas have been described, this event more likely occurred in an early stage of B-cell development in the bone marrow compartment, when the cell attempted to perform an IGKV to IGKJ recombination 32 , HECW2 is an ubiquitin-protein ligase that mediates ubiquitination of the tumor suppressor protein TP73 , a member of the p53 family of transcription factors, and also degrades ATR Finally, CCNG1 is a cyclin which is thought to play a role in growth regulation, participates in pdependent G 1 -S and G 2 checkpoints and might function as an oncogenic protein in ovarian carcinoma Unfortunately, we could not analyze the expression of the new partners due to lack of RNA in those cases.

IG-non- MYC translocations. The arrows indicate the genomic regions of each chromosomal partner and the discontinued line the exact breakpoint of the translocation. Between both sequences the presence of N-nucleotides was observed. Besides oncogene activation by enhancer hijacking as in the case of IG-translocations, the generation of fusion genes is a common mechanism through which SVs can contribute to oncogenesis. In recent years, additional genes besides MYC have been described as recurrently mutated in BL, usually as a consequence of point mutations 15 , 16 , 17 , To elucidate the genes involved in BL lymphomagenesis, we performed an integrative analysis of the different somatic genomic alterations potentially resulting in gene deregulation, namely SNVs, indels, SVs, and copy number aberrations CNAs.

The mean number of gained or lost regions per case was only 2. Incorporating all data on genomic alterations, we identified 49 coding genes affected in at least three cases Fig. Correlating the number of mutations per gene to its replication timing in lymphoblastoid B-cell lines showed that many recurrently mutated genes replicate rather early in B-cells Fig. All cases exhibited mutations in at least one driver gene. Gene dysregulation in BL. The Fig. Losses are indicated in blue, gains in orange, and copy neutral losses of heterozygosity LOH as red line.

The events in recurrently affected genes are shown independent of the transcript form. The affected genes are ordered by frequency, as well as gene name and the cases are displayed according to the BL subgroups solBL in gray, leukBL in red, and pleuraBL in orange. The lncRNA cancer susceptibility candidate 2 CASC2 , is recurrently deleted in solid tumors, suggesting a tumor suppressor function 41 , Taken together, these findings suggest that RFX7 could be a transcription factor regulating genes in cell cycle control including CCND3.

The precise role of this putative cell-cycle related process in BL will require additional investigation. Mutual exclusivity analysis. Heat-map showing the mutual exclusivity of recurrently altered genes in BL. The colors indicate the p -value of the mutual exclusivity analysis. A low p -value indicates that both genes of the respective gene pair are mutated together less frequently than expected.

At the genomic level the mutations in TCF3 observed in our cohort and described previously 17 , 37 are located in the helix-loop-helix B-HLH DNA binding and dimerization domain of the E47 splice isoform, but remarkably not in the E12 encoding part of the gene. We correlated the expression of both TCF3 isoforms to the mutational status of its negative regulator ID3.

The isoform E47 contains 4 negatively charged residues less than isoform E12, showing an overall more positive charge at the DNA-binding groove Fig. TCF3 splicing. On the top, the ENST Below, the RefSeq annotations for the isoforms E47 and E12 are shown. Each isoform includes only one of the alternative exons.

The numbers indicate the amount of spliced reads between the connected exons. The red arc marks the isoform that includes both alternative exons. Note the slight difference in expression levels between the three plots. The location of the domain is inferred by sequence similarity to the structure from protein databank code 2ypa chain A a heterodimeric complex involving an equivalent domain from human TAL1 in complex with DNA. Differences between the sequences are highlighted uncolored and bold for uncharged amino acids; red for negatively charged and blue for positively charged amino acids.

Note that many changes alter the charge in one isoform relative to the other, leading to a net gain of four negative charges in isoform E12 relative to isoform E The surface of E47 has a more positive electrostatic potential blue. The loss of these four negative charges also means that the E47 isoform is relatively more positively charged.

Given that a recent study has identified differential expression of the E12 and E47 TCF3 isoforms in pluripotent human embryonic stem cells ESCs compared to differentiated cells we extended our analysis to published data from ESCs and induced pluripotent stem cells iPSCs 49 , 50 Supplementary Fig. Here, expression of isoform 2 which lacks amino acids 1—61 and — of the canonical form was preferentially expressed in BL.

This pathway is regulated by GNAS-coupled G-protein coupled receptors, for which mutations in colorectal cancer have been shown to activate cAMP signaling Moreover, the IG translocation associated breakpoints in CBFA2T3 in the case described above and in another, previously published pediatric mature B-cell leukemia diagnosed morphologically as B-AL 34 disrupts isoform 1 and should lead to preferential expression of isoform 2. Several germline mutations predisposing individuals to particular cancers are known, but to date only few have been described for BL Aiming at clearly damaging changes we focused on protein-truncating germline mutations in known cancer predisposition genes in the present BL cohort The frameshift mutation in CHEK2 leads to a truncated protein p.

The BLM mutations were compound heterozygous, leading to biallelic inactivation. Indeed, clinical features of the patient were in line with the phenotype of Bloom syndrome OMIM: but the diagnosis was not made prior to the current study. Individuals with Bloom Syndrome, which is a rare autosomal recessive disorder characterized by genomic instability, have been described to carry a higher risk of developing cancers including lymphomas. In addition to the known cancer predisposition genes we also investigated the presence of germline mutations in genes showing somatic alterations in BL.

We observed co-occurrence of germline and somatic mutations in the same gene in two patients, indicating double hits affecting these genes FOXO1 and RYR2. After filtering for allele frequency of the mutations in a public database gnomAD, Germline events and mutational signatures. The affected genes are ordered by the incidences as well as names and the BL cases are displayed according to their subgroups solBL in gray, leukBL in red, and pleuraBL in orange.

The nucleotide changes are labeled using different colors. The x axis encodes the genomic coordinate and the y axis the log-scaled intermutation distance. The mutational signatures are labeled with different colors and the BL cases are displayed according to their subgroups solBL in gray, leukBL in red, and pleuraBL in orange. The cases are also annotated for the age group.

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Heights of the stacked bar plots correspond to the number of SNVs associated to the respective mutational signatures. Germline mutations in some cancer predisposing genes have been linked to certain mutational signatures in the tumor cells. Remarkably and in contrast to other GCB-lymphomas we did not identify further regions of recurrent kataegis. Two of these latter signatures may be attributed to the action of AID; one with a low degree of modulation by altered repair pathways and associated with CSR L1 and one with a high degree of modulation and associated with SHM L2.

However, we did not find the patients with germline mutations to differ in the mutational patterns of the tumor cells. In the present work, we used up-to-date integrated sequencing analyze to study the mechanisms underlying Burkitt lymphomagenesis. In depth characterization of IG- MYC breakpoint sequences, the MYC mutations, and MYC transcripts allowed us to reassess the mechanisms leading to generation of the IG- MYC translocations and to identify a complex interplay of mutational, regulatory, transcriptional, and possibly post-transcriptional mechanisms leading to enhanced MYC activity.

This very much underscores the central role for MYC in BL pathogenesis and how pathogenetic alterations at various levels contribute to the deregulation of MYC activity. We also revealed a series of mechanisms cooperating with MYC in lymphomagenesis, caused by a wide variety of changes, including germline mutations, somatic mutations, and structural aberrations associated with enhancer hijacking and intron retention as well as alternative splicing. This conclusion is also supported by the clinical observation that sBL frequently presents in lymphatic tissue of the ileocoecal region, i.

In contrast, there is a considerable overlap with regard to genes affected in eBL despite some differences in mutation frequencies 18 , 69 Supplementary Fig. On the other hand, pediatric sBL and eBL, although developing in different continents and having distinct key co-factors for their pathogenesis association with malaria infection of the children and much higher frequency of tumor cell infection with EBV in eBL show a similar landscape of genetic lesions, and thus a closely related pathogenesis. This seemingly functional simplicity on the basis of a marked aberrational complexity renders BL a good candidate for both ex vivo modeling and in vivo targeted therapy.

In addition, sorted germinal center B-cells GCB and naive B-cells from non-neoplastic tonsils were included. Tumor samples were reviewed by expert hematopathologists and classified according to the WHO guidelines. A consensus diagnosis was achieved by a single independent microscope analysis if at least five of seven pathologists agreed by discussion. For discrepant cases, a consensus was obtained after discussing the respective cases at a multiheaded microscope. The immunophenotypic and morphologic characteristics were evaluated on formalin-fixed and paraffin-embedded tissue sections of the diagnostic tumor biopsies.

Immunohistochemical staining for Ki was assessed as the percentage of positive tumor cells on FFPE material. In addition, in situ hybridization staining for Epstein—Barr encoding region was done in tissue sections. Moreover, in the cases with leukemic presentation, the immunophenotype data was obtained using flow cytometry exploring the same immunophenotype markers as described above.

All of the probes were provided by Abbott Molecular Diagnostics. Digital image acquisition, processing, and evaluation were performed using ISIS digital image analysis version 5. The signal distribution was evaluated by two independent observers. Using these criteria a total of 39 patients entered this study. Seventeen cases were previously published 16 , 19 , 70 , The study was performed in accordance with the ICGC guidelines www. The experimental procedures for DNA and RNA extraction, the detection and sequencing of immunoglobulin have been published previously 16 , Initial candidate variants for SNVs in the tumor were generated by samtools and bcftools version 0.

To enable calling of variants with low allele frequency we disabled the Bayesian model by setting -p 2. Thus, all positions containing at least one high quality non-reference base are reported as candidate variant. The resulting raw calls were categorized into putative somatic variants and others artifacts, germline based on the presence of variant reads in the matched normal sample. The frequency of all putative somatic variants was then refined by checking for potential redundant information due to overlapping reads and precise base counts for each strand were determined.

The confidence for each variant was then determined by a heuristic punishment scheme taking the aforementioned tracks into account. In addition variants with strong read biases according to the strand bias filter were removed. High-confidence variants were used for further analysis. To identify indel events tumor and matched control samples were analyzed by Platypus 76 version 0. High-confidence somatic variants were required to either have the Platypus filter flag PASS or pass custom filters allowing for low variant frequency using a scoring scheme.

Additionally, combinations of Platypus non-PASS filter flags, bad quality values, low genotype quality, very-low variant counts in the tumor, and presence of variant reads in the control were not tolerated. In order to remove recurrent artifacts and misclassified germline events, somatic indels that were identified as germline in at least two patients in the ICGC MMML-seq cohort were excluded. For two samples , tumors and their matched controls were sequenced on different Illumina instruments Hiseq and HiseqX.

To prevent technology-specific artefacts, the standard SNV and indel calling workflow was extended with filters developed for samples without matched control. We additionally removed mutations found in ExAC version 0. For some samples , , , , , increased SNV artefact rates were detected, which were related to higher base quality scores for wrongly called bases. For these samples the base quality threshold was increased from 13 to 20 and low mutant allele frequency MAF penalty was switched off i.

SNVs classified as splicing, nonand accurate short read alignment with Burrowssynonymous changes, stop-gains, and stop-losses were predicted to affect protein function. Allele-specific copy number alterations were detected using ACEseq allele-specific copy number estimation from whole-genome sequencing; unpublished data. ACEseq determines absolute allele-specific copy numbers as well as tumor ploidy and tumor cell content based on coverage ratios of tumor and control as well as the B-allele frequency BAF of heterozygous single-nucleotide polymorphisms SNPs.

Ploidies were manually checked and compared with FISH results. Adjustments were made if necessary. Final copy number segments were further smoothed to calculate the total number of gains and losses. Neighboring segments were merged if they rounded to the same copy number and deviated by less than 0. Based on the resulting segments the number of gains and losses was estimated. SVs aberrations with scores from 3 to 5 were used for all the analysis, with the exception of IG translocations.

Repli-Seq scores 80 were used to investigate the replication timing of mutations.

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Unsupervised analysis of mutational signatures. This unsupervised method has high requirements on statistical power, i. The factorization rank was varied from 2 to The optimal factorization rank was obtained by simultaneously minimizing the Frobenius error, maximizing the cophenetic correlation coefficient and minimizing the Amari distance. For every factorization rank, iterations over different random initializations were performed.

For every initial condition, iteration over update equations was performed at most times. Supervised analysis of mutational signatures. Using YAPSA, a linear combination decomposition of the mutational catalog with known and predefined signatures was computed with the function LCD complex cutoff by non-negative least squares NNLS using functions implemented in the R package lsei In order to increase specificity, LCD complex cutoff applies the NNLS algorithm twice: once proposing all signatures supplied by the user to the decomposition, and then after the first execution, only those signatures whose exposures, i.

As detectability of the different signatures may vary, the cutoffs were chosen to be signature-specific. The following cut-offs were employed - AC1: 0;AC2: 0.

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IntoGen version 3. For larger SVs only genes that were directly hit by a breakpoint were considered. To capture the precise target focal SVs and CNAs were combined and local maxima of overlapping regions with more than one event were identified. We employed freebayes v1.

High impact i. Putative damaging germline mutations were removed if the estimated minor allele frequency MAF in at least one continental population was above 0. Finally, all germline mutations were excluded from the analysis if annotated as benign in ClinVar. The telomere content was determined from whole-genome sequencing data using the software tool TelomereHunter www. In the case of tumor samples, the telomere content was further corrected for the tumor purity as estimated by ACEseq using the following formula:.

Transcriptome data were mapped with segemehl 0. US rental company W. UK based outrigger mat specialist Outriggerpads has launched four new mats for heavy cranes and Hinowa spiders. A mobile crane clipped a vehicle stopped on the hard shoulder of a highway in Melbourne, Australia. One of our readers, working on a scale model of Smith C Crawler Crane would like to find a parts book for it. A few photos covering some of the new products at Platformers Days the event continues today on fine weather.

We have learnt more on the cause of the load drop in the fatal Melbourne crane incident last week. Dutch mobile self erecting tower crane manufacturer Spierings is upgrading its UK service and support. WorkSafe Victoria has released a statement concerning the fatal tower crane incident in Melbourne last week. Contact us.