Explore the vast range of titles available.

\"This is a history of twentieth-century architecture, written with close critical attention to the theories that lie behind the works described. Importantly, unlike other historical accounts, it does not take sides and urge the reader to identify with one strand of thinking or style of architecture at the expense of others, but presents a dispassionate view, with persuasive arguments on behalf of different positions. It pursues the history of European and American architecture chronologically. But the history is interwoven with the philosophical ideas that informed both writers and architects and are essential for its understanding\"-- Provided by publisher.

Inland waters play a major role in global greenhouse gas (GHG) budgets. The smallest of these systems (i.e., ponds) have a particularly large—but poorly constrained—emissions footprint at the global scale. Much of this uncertainty is due to a poor understanding of temporal variability in emissions. Here, we conducted high‐resolution temporal sampling to quantify GHG exchange between four temperate constructed ponds and the atmosphere on an annual basis. We show these ponds are a net source of GHGs to the atmosphere (564.4 g CO2‐eq m−2 yr−1), driven by highly temporally variable diffusive methane (CH4) emissions. Diffusive CH4 release to the atmosphere was twice as high during periods when the ponds had a stratified water column than when it was mixed. Ebullitive CH4 release was also higher during stratification. Building ponds to favor mixed conditions thus presents an opportunity to minimize the global GHG footprint of future pond construction. Plain Language Summary Ponds are an important contributor to global greenhouse gas emissions, but there is still much uncertainty associated with global emissions estimates. To clarify this uncertainty, we investigated seasonal patterns of greenhouse gas emissions from four constructed ponds in a temperate region of the northeastern United States. We found that methane made up most of pond greenhouse gas emissions on an annual basis, leading the ponds to be a net source of greenhouse gases to the atmosphere. Methane and carbon dioxide exchange between ponds and the atmosphere followed clear seasonal patterns, with highest rates of methane release to the atmosphere during warm summer months. Ponds consumed carbon dioxide during warm months when aquatic plants were growing rapidly. We also found high variability in methane and carbon dioxide emissions over weekly time periods that was associated with whether the water column in the pond was mixed or stratified. When ponds were stratified, methane emissions were higher than during mixed conditions, possibly due to low availability of oxygen near sediments where methane is produced by micro‐organisms that require low oxygen conditions. These results provide a path forward to better estimating pond greenhouse gas emissions at a global scale. Key Points Constructed ponds are a net source of global greenhouse gass to the atmosphere on annual basis CO2 and CH4 exchange between ponds and the atmosphere show strong seasonal trends, with CH4 highly variable within season Summertime diffusive CH4 release dominates annual emissions budget

\"Nicholas Dylan Ray grew up next to an American national park, whose mountains and forests he explored to escape his troubled home. As ayoung man, he left the United States, and aged twenty-two set out on a six-month journey from France to Tibet, travelling through Turkey. That journey forms the first chapter of this book, and led to a career working with the Middle East. In middle age, the author returned to the road, travelling throughout Turkey. In the six subsequent chapters, one for each journey, he recounts his adventures, discusses the archaeology and history of the places visited, and the people met along the way. In Konya he is transported by the beauty of an Arabic quotation from the Qur'an inscribed on Rumi's tomb. In Istanbul, among Syrian refugees, he considers the concept of charity in Islam. In Antalya, just after the Islamic State terrorist attack in his home country of France, he analyses the textual foundations of jihadism in Islamic law. Within earshot of the shelling in Syria, he contemplates genocide, and climbs Musa Dagh mountain, the last redoubt of the Armenians who fought the Ottoman troops in 1915. In the coastal region of the Black Sea, he examines the monastic urge in religion and experiments with fasting during Ramadan. And finally, on the north-western Mediterranean coast, he visits two battlefields, Troy and Gallipoli, before returning to Istanbul for a last visit to Sultanahmet, the centre of the Islamic world for five centuries. During these wanderings Nicholas Dylan Ray shares with the reader his deep knowledge of Islamic religion, culture and history, discussing the foundational texts and their role in current events in the Middle East. He also takes note of those who have travelled these lands before him and reflects on the mixed experience of travel itself.\" --Provided by publisher.

The genetic component of early-onset Alzheimer disease (EOAD), accounting for ~10% of all Alzheimer’s disease (AD) cases, is largely unexplained. Recent studies suggest that EOAD may be enriched for variants acting in the lipid pathway. The current study examines the shared genetic heritability between EOAD and the lipid pathway using genome-wide multi-trait genetic covariance analyses. Summary statistics were obtained from the GWAS meta-analyses of EOAD by the Alzheimer’s Disease Genetics Consortium ( n =19,668) and five blood lipid traits by the Global Lipids Genetics Consortium ( n =1,320,016). The significant results were compared between the EOAD and lipids GWAS and genetic covariance analyses were performed via SUPERGNOVA. Genes in linkage disequilibrium (LD) with top EOAD hits in identified regions of covariance with lipid traits were scored and ranked for causality by combining evidence from gene-based analysis, AD-risk scores incorporating transcriptomic and proteomic evidence, eQTL data, eQTL colocalization analyses, DNA methylation data, and single-cell RNA sequencing analyses. Direct comparison of GWAS results showed 5 loci overlapping between EOAD and at least one lipid trait harboring APOE , TREM2 , MS4A4E , LILRA5 , and LRRC25 . Local genetic covariance analyses identified 3 regions of covariance between EOAD and at least one lipid trait. Gene prioritization nominated 3 likely causative genes at these loci: ANKDD1B , CUZD1 , and MS4A64 .The current study identified genetic covariance between EOAD and lipids, providing further evidence of shared genetic architecture and mechanistic pathways between the two traits.

Ponds are globally abundant and important to the global carbon cycle. Although ponds have large greenhouse gas emissions, they also sequester carbon in their sediments. Here, we studied organic carbon (OC) burial rates in 22 temperate experimental ponds with negligible watersheds, where carbon sequestration derives solely from autochthonous primary production. The ponds were built identically in 1964 and have since experienced different management strategies, allowing us to test how management actions influence burial rates. On average, the ponds accumulated 67.1 g OC m−2 yr−1 (range 38.3–113.6 g OC m−2 yr−1)—about double the global average burial rate for lakes and similar to global averages for wetlands. Carbon burial rates were higher in ponds with macrophytes, fish, and higher N : P loads. We contend that the global carbon sink for inland waters may be substantially underestimated due to the undervaluation of OC burial in natural and artificial ponds.

Background Alzheimer's disease (AD) and kidney function share multiple risk factors and pathogenic mechanisms, particularly through impaired clearance of AD‐related biomarkers. Recent clinical evidence suggests kidney function directly influences AD pathophysiology independent of cardiovascular factors. We aimed to explore this relationship through genetic analyses to minimize confounders like age and lifestyle. Method We investigated genome‐wide and local genetic correlations (rg) between AD and estimated glomerular filtration rate (eGFR) in European (EUR) and African (AFR) ancestries using LDSC, cond/conjFDR, and LAVA utilizing summary statistics from large‐scale genome‐wide association studies. LAVA measures the strength and direction of local correlations, while cond/conjFDR increases power for pleiotropic variant detection by leveraging conditional false discovery rates. Result Genome‐wide correlations between AD and eGFR were nonsignificant (rg values ≈ 0.07) in both ancestries, with regions of strong local correlations observed. In EUR, 52 regions showed significant local correlations (Bonferroni‐corrected), and heritability (AD: h² = 0.05, p ≈ 0.025; eGFR: h² = 0.10, p < 1E‐10). These regions exhibited balanced bidirectional correlations (26 loci each; positive range: 0.32 to 1.00; negative range: ‐1.00 to ‐0.69), with strongest signals on chr9 (rg = 0.77, p = 2.9E−10) and chr5 (rg = −0.66, p = 1.34E‐10). The identified loci were linked to genes involved in vascular, cognitive, and inflammatory pathways. Cond/conjFDR analysis identified 15 loci containing 372 SNPs with significant pleiotropy (conjFDR < 0.05), mapped to genes like PICALM, SPI1, and TOMM40 with previously reported AD associations. In AFR, three loci showed significant negative local correlations (range: ‐0.9 to ‐1), with one AFR‐specific locus on chr11 containing several key genes: CD81 (inflammation), STIM1 (calcium signaling and neurodegeneration), KCNQ1 (potassium channels), and RRM1 (nephron development and neuronal DNA repair). Conclusion Our findings reveal components of shared genetic architecture between AD and kidney function, characterized by a mixture of concordant and discordant associations that are likely driven by specific biological pathways rather than genome‐wide effects. We will focus on refining these associations to determine directionality and causality, identifying key genes driving strong local genetic correlations and their biological pathways, and integrating chronic kidney disease associations alongside eGFR to capture phenotypic variability.

Alzheimer's disease (AD) and kidney function share multiple risk factors and pathogenic mechanisms, particularly through impaired clearance of AD-related biomarkers. Recent clinical evidence suggests kidney function directly influences AD pathophysiology independent of cardiovascular factors. We aimed to explore this relationship through genetic analyses to minimize confounders like age and lifestyle. We investigated genome-wide and local genetic correlations (r ) between AD and estimated glomerular filtration rate (eGFR) in European (EUR) and African (AFR) ancestries using LDSC, cond/conjFDR, and LAVA utilizing summary statistics from large-scale genome-wide association studies. LAVA measures the strength and direction of local correlations, while cond/conjFDR increases power for pleiotropic variant detection by leveraging conditional false discovery rates. Genome-wide correlations between AD and eGFR were nonsignificant (r values ≈ 0.07) in both ancestries, with regions of strong local correlations observed. In EUR, 52 regions showed significant local correlations (Bonferroni-corrected), and heritability (AD: h² = 0.05, p ≈ 0.025; eGFR: h² = 0.10, p < 1E-10). These regions exhibited balanced bidirectional correlations (26 loci each; positive range: 0.32 to 1.00; negative range: -1.00 to -0.69), with strongest signals on chr9 (r = 0.77, p = 2.9E-10) and chr5 (r = -0.66, p = 1.34E-10). The identified loci were linked to genes involved in vascular, cognitive, and inflammatory pathways. Cond/conjFDR analysis identified 15 loci containing 372 SNPs with significant pleiotropy (conjFDR < 0.05), mapped to genes like PICALM, SPI1, and TOMM40 with previously reported AD associations. In AFR, three loci showed significant negative local correlations (range: -0.9 to -1), with one AFR-specific locus on chr11 containing several key genes: CD81 (inflammation), STIM1 (calcium signaling and neurodegeneration), KCNQ1 (potassium channels), and RRM1 (nephron development and neuronal DNA repair). Our findings reveal components of shared genetic architecture between AD and kidney function, characterized by a mixture of concordant and discordant associations that are likely driven by specific biological pathways rather than genome-wide effects. We will focus on refining these associations to determine directionality and causality, identifying key genes driving strong local genetic correlations and their biological pathways, and integrating chronic kidney disease associations alongside eGFR to capture phenotypic variability.

Genome-wide association studies (GWAS) of complex traits often implicate genetic loci spanning thousands of variants. Statistical fine-mapping refines a GWAS locus to a smaller set of likely causal variants facilitating interpretation and functional validation. Ancestry-informed fine-mapping can further improve resolution by capitalizing on the genomic diversity across ancestries (e.g., smaller LD blocks in African populations). We employed cross-ancestry fine-mapping at top loci recently identified in a transethnic meta-analysis of non-Mendelian early-onset Alzheimer's Disease (EOAD; Bradley et al. 2025) to identify population-specific causative variants associated with this type of AD. Bradley et al. (2025) identified 13 distinct disease-associated loci, 8 of these for the first time reported in EOAD. Capitalizing on the individual ancestry-specific summary statistics from individuals of European (NHW) and African American (AA) ancestry (NHW: 6,282 cases, 13,386 controls; AA: 782 cases, 3,663 controls) for the top loci, we employed MESuSiE to model shared and ancestry-specific causal variants. MESuSie accounts for LD structure in multiple ancestries and accommodates causal effect size similarity and heterogeneity. Loci prioritized by MESuSiE were followed up in whole-genome sequencing data of NHW (N = 6,225) and AA individuals (N = 4,376) from the ADSP. Multi-ancestry fine-mapping identified regulatory variant rs6733839 in BIN1 (transethnic EOAD GWAS p-value: 1.73E-10) as the most likely causative variant associated with EOAD at this locus and suggests that it is shared across NHW and AA populations (PIP EUR: 0.0002; PIP AFR: 0.0001; PIP EUR_AFR: 0.99). Notably, while the associated haplotypes in both ancestries overlapped, the AA haplotype was much narrower, in line with the smaller extent of LD in individuals of African ancestry and pinpointing a much more concise locus harboring the causative variant. Individual analysis of WGS data from individuals of European and African ancestry from the ADSP validated rs6733839 as disease-associated in both ancestral population groups. Multi-ancestry fine-mapping pinpoints rs6733839 as a likely causative variant associated with non-Mendelian EOAD and suggests that it is shared across individuals of European and African ancestry. These findings elucidate the etiology of this type of AD in these populations and demonstrate the value of ancestry-informed fine-mapping for identification of population-specific causative variants.

Background Genome‐wide association studies (GWAS) of complex traits often implicate genetic loci spanning thousands of variants. Statistical fine‐mapping refines a GWAS locus to a smaller set of likely causal variants facilitating interpretation and functional validation. Ancestry‐informed fine‐mapping can further improve resolution by capitalizing on the genomic diversity across ancestries (e.g., smaller LD blocks in African populations). We employed cross‐ancestry fine‐mapping at top loci recently identified in a transethnic meta‐analysis of non‐Mendelian early‐onset Alzheimer's Disease (EOAD; Bradley et al. 2025) to identify population‐specific causative variants associated with this type of AD. Method Bradley et al. (2025) identified 13 distinct disease‐associated loci, 8 of these for the first time reported in EOAD. Capitalizing on the individual ancestry‐specific summary statistics from individuals of European (NHW) and African American (AA) ancestry (NHW: 6,282 cases, 13,386 controls; AA: 782 cases, 3,663 controls) for the top loci, we employed MESuSiE to model shared and ancestry‐specific causal variants. MESuSie accounts for LD structure in multiple ancestries and accommodates causal effect size similarity and heterogeneity. Loci prioritized by MESuSiE were followed up in whole‐genome sequencing data of NHW (N = 6,225) and AA individuals (N = 4,376) from the ADSP. Result Multi‐ancestry fine‐mapping identified regulatory variant rs6733839 in BIN1 (transethnic EOAD GWAS p‐value: 1.73E‐10) as the most likely causative variant associated with EOAD at this locus and suggests that it is shared across NHW and AA populations (PIP EUR: 0.0002; PIP AFR: 0.0001; PIP EUR_AFR: 0.99). Notably, while the associated haplotypes in both ancestries overlapped, the AA haplotype was much narrower, in line with the smaller extent of LD in individuals of African ancestry and pinpointing a much more concise locus harboring the causative variant. Individual analysis of WGS data from individuals of European and African ancestry from the ADSP validated rs6733839 as disease‐associated in both ancestral population groups. Conclusion Multi‐ancestry fine‐mapping pinpoints rs6733839 as a likely causative variant associated with non‐Mendelian EOAD and suggests that it is shared across individuals of European and African ancestry. These findings elucidate the etiology of this type of AD in these populations and demonstrate the value of ancestry‐informed fine‐mapping for identification of population‐specific causative variants.

Oysters enhance benthic–pelagic coupling in coastal systems by moving large quantities of suspended particulates to the sediments, stimulating biogeochemical processes. Recent research efforts have focused on quantifying the impact of oysters on coastal biogeochemical cycling, yet there is little consensus on how oysters influence processes across systems. A potential driver of this variance is availability of organic material suspended in the water column and subsequent loading to sediment by oysters. Here, we measured fluxes of sediment di-nitrogen (N₂-N), ammonium (NH₄ ⁺), combined nitrate-nitrite (NOₓ), and phosphate (PO₄ 3−) in spring, summer, and fall at 2 oyster reefs and 1 farm in a temperate estuary (Narragansett Bay, Rhode Island). We then linked these fluxes with patterns of water column primary production. Nitrogen removal from the system was highest in spring, when we detected net sediment denitrification (48.8 μmol N₂-N m−2 h−1) following a winter–spring diatom bloom. In contrast, we measured sediment N₂ fixation in fall (−44.8 μmol N₂-N m−2 h−1) at rates nearly equivalent to spring denitrification. In the summer, we measured a nearly net zero sediment N₂-N flux (−2.7 μmol N₂-N m−2 h−1). Recycling of nitrogen to the water column was consistent across seasons, composed almost exclusively of NH₄ ⁺. These results demonstrate that sediment nitrogen cycling in oyster habitats is dynamic and can change rapidly based on seasonal patterns of productivity. At carrying capacity, the impact of oysters on nitrogen cycling is large and should be considered during efforts to increase oyster populations through aquaculture or reef restoration.