Acute kidney injury (AKI) is the leading cause of nephrology consultation and is associated with high mortality rates. The primary causes of AKI include ischemia, hypoxia or nephrotoxicity. An underlying feature is a rapid decline in GFR usually associated with decreases in renal blood flow. Inflammation represents an important additional component of AKI leading to the extension phase of injury, which may be associated with insensitivity to vasodilator therapy. It is suggested that targeting the extension phase represents an area potential of treatment with the greatest possible impact. The underlying basis of renal injury appears to be impaired energetics of the highly metabolically active nephron segments (i.e., proximal tubules and thick ascending limb) in the renal outer medulla, which can trigger conversion from transient hypoxia to intrinsic renal failure. Injury to kidney cells can be lethal or sublethal. Sublethal injury represents an important component in AKI, as it may profoundly influence GFR and renal blood flow. The nature of the recovery response is mediated by the degree to which sublethal cells can restore normal function and promote regeneration. The successful recovery from AKI depends on the degree to which these repair processes ensue and these may be compromised in elderly or CKD patients. Recent data suggest that AKI represents a potential link to CKD in surviving patients. Finally, earlier diagnosis of AKI represents an important area in treating patients with AKI that has spawned increased awareness of the potential that biomarkers of AKI may play in the future.

Infectious and inflammatory diseases have repeatedly shown strong genetic associations within the major histocompatibility complex (MHC); however, the basis for these associations remains elusive. To define host genetic effects on the outcome of a chronic viral infection, we performed genome-wide association analysis in a multiethnic cohort of HIV-1 controllers and progressors, and we analyzed the effects of individual amino acids within the classical human leukocyte antigen (HLA) proteins. We identified >300 genome-wide significant single-nucleotide polymorphisms (SNPs) within the MHC and none elsewhere. Specific amino acids in the HLA-B peptide binding groove, as well as an independent HLA-C effect, explain the SNP associations and reconcile both protective and risk HLA alleles. These results implicate the nature of the HLA–viral peptide interaction as the major factor modulating durable control of HIV infection.

Animals encountering nutritionally imbalanced foods should release elements in excess of requirements in order to maintain overall homeostasis. Quantifying these excesses and predicting their fate is, however, problematic. A new model of the stoichiometry of consumers is formulated that incorporates the separate terms in the metabolic budget, namely, assimilation of ingested substrates and associated costs, protein turnover, other basal costs, such as osmoregulation, and the use of remaining substrates for production. The model indicates that release of excess C and nonlimiting nutrients may often be a significant fraction of the total metabolic budget of animals consuming the nutrient-deficient forages that are common in terrestrial and aquatic systems. The cost of maintenance, in terms of not just C but also N and P, is considerable, such that food quality is important even when intake is low. Many generalist consumers experience short-term and unpredictable fluctuations in their diets. Comparison of model output with data for one such consumer, Daphnia, indicates that mechanisms operating postabsorption in the gut are likely the primary means of regulating excess C, N, and P in these organisms, notably respiration decoupled from biochemical or mechanical work and excretion of carbon and nutrients. This stoichiometrically regulated release may often be in organic rather than inorganic form, with important consequences for the balance of autotrophic and heterotrophic processes in ecosystems.

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Turkey is moving westward relative to Eurasia, thereby accommodating the collision between Arabia and Eurasia. This motion is mostly taken up by strike‐slip deformation along the North and East Anatolian Faults. The Sea of Marmara lies over the direct westward continuation of the North Anatolian Fault zone. Just east of the Sea of Marmara, the North Anatolian Fault splits into three strands, two of which continue into the sea. While the locations of the faults are well constrained on land, it has not yet been determined how the deformation is transferred across the Sea of Marmara, onto the faults on the west coast of Turkey. We present results from a seismic reflection survey undertaken to map the faults as they continue through the three deep Marmara Sea basins of Çlnarclk, Central Marmara and Tekirdag, in order to determine how the deformation is distributed across the Sea of Marmara, and how it is taken up on the western side of the sea. The data show active dipping faults with associated tilting of sedimentary layers, connecting the North Anatolian Fault to strike‐slip faults that cut the Biga and Gallipoli Peninsulas.