Exotic glass types and the intensity of recycling in the northwest Quarter of Gerasa (Jerash, Jordan)

Major and trace elements are presented for 149 glass fragments ranging in date from the Roman to Early Islamic periods (1st – mid-8th centuries CE), excavated during the Danish-German Jerash Northwest Quarter Project's fieldwork between 2011 and 2016. The results confirm a clear dominance of Levantine glass types, but also reveal 12 glasses of Egyptian and Mesopotamian compositions recovered from two houses destroyed by the major earthquake which hit parts of the Levant in January 749 CE. These closed and undisturbed contexts from the final phase of occupation reveal the presence of relatively more pristine Levantine as well as imported material that is less visible in earlier contexts in the Gerasa assemblage, where the recycling indexes are high and chemical signatures of any exotic glass were largely lost due to remelting and their dilution by the overwhelming quantities of glass produced in the Levantine region. This emphasizes that imported glass may frequently be underestimated or even invisible in glass compositional studies, depending on the archaeological context sampled and the approach taken to artifact quantification. Levantine glass was attributed to Roman, Late Roman (Jalame) and Byzantine/Early Islamic (Apollonia) productions based primarily on MnO, Al_{2}O_{3} and Na_{2}O concentrations, which offered an advantage over previous approaches. While colorants in weakly colored glass indicate recycled material, their concentrations are sensitive to context, with higher concentrations in the early periods when the use of intentionally colored glass was more frequent. We have therefore developed the concept of the intensity of recycling, which was estimated using components modified during prolonged melting, such as K_{2}O, P_{2}O_{5} and Cl. A pronounced enrichment in CaO, also dependent upon the intensity of recycling, may affect the assignment to compositional groups and should be taken into consideration in future. Recycling in Gerasa appears to have been more intensive than was the case for cities closer to the primary production centers on the Mediterranean coast, consistent with the view that the dependency on recycling increases further away from the source of the primary material. In contrast, the cities in the coastal plain could readily exploit the marine transportation network, which appears to have played a major role in the distribution of raw glass

Roman and Byzantine burials at Yavneh-Yam : new insights into the site’s settlement history

This paper discusses Roman and Byzantine tombs and burial caves at Yavneh-Yam (the harbor site of ancient Iamnia) excavated in the 1960s and 1980s. It focuses on the finds recovered during these excavations as a means to enhance our knowledge on the site’s social and religious history vis-à-vis the inhabited site’s recent excavations and studies. More specifically, the discussed funerary remains reflect the changes in the site’s social composition between Early Roman to Byzantine times. While in the Early Roman period Yavneh-Yam was probably predominantly Jewish, in Late Roman and mainly Byzantine times it was developed into a large and thriving harbor town whose mixed population was composed of polytheists, Jews, Samaritans and Christians

Genetic loci associated with chronic obstructive pulmonary disease overlap with loci for lung function and pulmonary fibrosis

Chronic obstructive pulmonary disease (COPD) is a leading cause of mortality worldwide. We performed a genetic association study in 15,256 cases and 47,936 controls, with replication of select top results (P < 5 × 10(-6)) in 9,498 cases and 9,748 controls. In the combined meta-analysis, we identified 22 loci associated at genome-wide significance, including 13 new associations with COPD. Nine of these 13 loci have been associated with lung function in general population samples, while 4 (EEFSEC, DSP, MTCL1, and SFTPD) are new. We noted two loci shared with pulmonary fibrosis (FAM13A and DSP) but that had opposite risk alleles for COPD. None of our loci overlapped with genome-wide associations for asthma, although one locus has been implicated in joint susceptibility to asthma and obesity. We also identified genetic correlation between COPD and asthma. Our findings highlight new loci associated with COPD, demonstrate the importance of specific loci associated with lung function to COPD, and identify potential regions of genetic overlap between COPD and other respiratory diseases

Author Correction:New genetic signals for lung function highlight pathways and chronic obstructive pulmonary disease associations across multiple ancestries

Correction to: Nature Genetics https://doi.org/10.1038/s41588-018-0321-7, published online 25 February 2019

Author Correction:New genetic signals for lung function highlight pathways and chronic obstructive pulmonary disease associations across multiple ancestries (Nature Genetics, (2019), 51, 3, (481-493), 10.1038/s41588-018-0321-7)

Correction to: Nature Geneticshttps://doi.org/10.1038/s41588-018-0321-7, published online 25 February 2019. In the version of the article initially published, unconsented individuals were erroneously included in SPIROMICS consortium results. The analysis has now been repeated with the unconsented individuals removed. The change in the results does not affect the conclusions in the paper. The corrections required to the paper are as follows: In the third paragraph of the “Association with FEV1/FVC and COPD in multiple ancestries” section: “(n = 6,979 cases and 3,915 controls)”, should be “(n = 6,964 cases and 3,904 controls)” and “P = 2.87 × 10–75” should be “P = 2.21 × 10–75”. In the fourth paragraph of the “Association with FEV1/FVC and COPD in multiple ancestries” section: “4.73 (95% CI: [3.79, 5.90]), P = 3.00 × 10−43”, should be “4.71 (95% CI: [3.77, 5.87]), P = 7.24 × 10−43”. In the Fig. 3b table, the SPIROMICS row: “1.54, 1.38, 1.72, 4.47 × 10–14, 988, 537”, should be “1.55, 1.39, 1.74, 6.80 × 10–14, 973, 526”; and the Meta-analysis row: “1.55, 1.48, 1.62, 1.48 × 10–75, 6,979, 3,915”, should be “1.55, 1.48, 1.62, 2.21 × 10–75, 6,964, 3,904”. In the final paragraph of the Discussion: “The 279-variant GRS we constructed was associated with a 4.73-fold increased relative risk…”, should be “The 279-variant GRS we constructed was associated with a 4.71-fold increased relative risk…” In the fifth paragraph of the “Effect of genetic risk score on COPD susceptibility in multiple ancestries” section in the Methods: “SPIROMICS (988 cases, 537 controls)”, should be “SPIROMICS (973 cases, 526 controls)”. In the third paragraph of the “Association with FEV1/FVC and COPD in multiple ancestries” section: “(n = 6,979 cases and 3,915 controls)”, should be “(n = 6,964 cases and 3,904 controls)” and “P = 2.87 × 10–75” should be “P = 2.21 × 10–75”. In the fourth paragraph of the “Association with FEV1/FVC and COPD in multiple ancestries” section: “4.73 (95% CI: [3.79, 5.90]), P = 3.00 × 10−43”, should be “4.71 (95% CI: [3.77, 5.87]), P = 7.24 × 10−43”. In the Fig. 3b table, the SPIROMICS row: “1.54, 1.38, 1.72, 4.47 × 10–14, 988, 537”, should be “1.55, 1.39, 1.74, 6.80 × 10–14, 973, 526”; and the Meta-analysis row: “1.55, 1.48, 1.62, 1.48 × 10–75, 6,979, 3,915”, should be “1.55, 1.48, 1.62, 2.21 × 10–75, 6,964, 3,904”. In the final paragraph of the Discussion: “The 279-variant GRS we constructed was associated with a 4.73-fold increased relative risk…”, should be “The 279-variant GRS we constructed was associated with a 4.71-fold increased relative risk…” In the fifth paragraph of the “Effect of genetic risk score on COPD susceptibility in multiple ancestries” section in the Methods: “SPIROMICS (988 cases, 537 controls)”, should be “SPIROMICS (973 cases, 526 controls)”. The correction is due to 26 unconsented SPIROMICS samples being originally included in the analysis. The analyses that previously included these samples have been rerun with data from these 26 samples removed. Supplementary Information accompanies the online version of this amendment and includes: Updated Supplementary Text and Figures wherein we have changed: On page 23 (description of SPIROMICS cohort) the number of COPD cases has been changed from 988 to 973 and controls from 537 to 526. Supplementary Figure 9 – the forest plots have been updated for the new results for association with 279 variants after reanalysis of SPIROMICS. Supplementary Table 20 – the demographics for SPIROMICS have been updated. Supplementary Table 21 – the results rows for the SPIROMICS and “Meta-analysis of 5 European-ancestry study groups” have been updated. Supplementary Table 22 – The “Meta-analysis of 5 European cohorts” columns have been updated after SPIROMICS reanalysis. Updated Supplementary Tables wherein we have changed: Supplementary Table 29 – columns X–Z (“Meta-analysis of 5 external European-ancestry COPD cohorts (Cases = 6,964; Controls = 3,904)”) after reanalysis of SPIROMICS data. Updated Supplementary Text and Figures wherein we have changed: On page 23 (description of SPIROMICS cohort) the number of COPD cases has been changed from 988 to 973 and controls from 537 to 526. Supplementary Figure 9 – the forest plots have been updated for the new results for association with 279 variants after reanalysis of SPIROMICS. Supplementary Table 20 – the demographics for SPIROMICS have been updated. Supplementary Table 21 – the results rows for the SPIROMICS and “Meta-analysis of 5 European-ancestry study groups” have been updated. Supplementary Table 22 – The “Meta-analysis of 5 European cohorts” columns have been updated after SPIROMICS reanalysis. Updated Supplementary Tables wherein we have changed: Supplementary Table 29 – columns X–Z (“Meta-analysis of 5 external European-ancestry COPD cohorts (Cases = 6,964; Controls = 3,904)”) after reanalysis of SPIROMICS data

New genetic signals for lung function highlight pathways and chronic obstructive pulmonary disease associations across multiple ancestries

Abstract Reduced lung function predicts mortality and is key to the diagnosis of chronic obstructive pulmonary disease (COPD). In a genome-wide association study in 400,102 individuals of European ancestry, we define 279 lung function signals, 139 of which are new. In combination, these variants strongly predict COPD in independent populations. Furthermore, the combined effect of these variants showed generalizability across smokers and never smokers, and across ancestral groups. We highlight biological pathways, known and potential drug targets for COPD and, in phenome-wide association studies, autoimmune-related and other pleiotropic effects of lung function–associated variants. This new genetic evidence has potential to improve future preventive and therapeutic strategies for COPD