New data on mollusks from the Miocene (Tarkhanian-Chokrakian) of northern Sinop Province,Turkey

An insufficiently known bivalve and gastropod assemblage from the Early-Middle Miocene (Tarkhanian-Chokrakian) of northern Sinop Province (Turkey), is analyzed. Environments of the assemblage are reconstructed for the Chokrakian as subtidal, with prevailing lime and sandy bottom and good aeration, and partially well vegetated. Impoverishment of the mollusk biocoenose in this part of the marine basin (only 18 bivalve and 22 gastropod species recorded) compared to other areas, including the closest regions, Bulgaria on the west and Georgia on the east, is emphasized. The relatively low diversity of the fauna is probably connected not only with insufficient collecting, but with special hydrological conditions. A special aspect of the fauna is highlighted by the presence of the bivalve Circomphalus foliaceolamellosus subplicatus (Orb.), which is rare in the Chokrakian.     

Interleukin-1α Activity in Necrotic Endothelial Cells Is Controlled by Caspase-1 Cleavage of Interleukin-1 Receptor-2: IMPLICATIONS FOR ALLOGRAFT REJECTION*

Inflammation is a key instigator of the immune responses that drive atherosclerosis and allograft rejection. IL-1α, a powerful cytokine that activates both innate and adaptive immunity, induces vessel inflammation after release from necrotic vascular smooth muscle cells (VSMCs). Similarly, IL-1α released from endothelial cells (ECs) damaged during transplant drives allograft rejection. However, IL-1α requires cleavage for full cytokine activity, and what controls cleavage in necrotic ECs is currently unknown. We find that ECs have very low levels of IL-1α activity upon necrosis. However, TNFα or IL-1 induces significant levels of active IL-1α in EC necrotic lysates without alteration in protein levels. Increased activity requires cleavage of IL-1α by calpain to the more active mature form. Immunofluorescence and proximity ligation assays show that IL-1α associates with interleukin-1 receptor-2, and this association is decreased by TNFα or IL-1 and requires caspase activity. Thus, TNFα or IL-1 treatment of ECs leads to caspase proteolytic activity that cleaves interleukin-1 receptor-2, allowing IL-1α dissociation and subsequent processing by calpain. Importantly, ECs could be primed by IL-1α from adjacent damaged VSMCs, and necrotic ECs could activate neighboring normal ECs and VSMCs, causing them to release inflammatory cytokines and up-regulate adhesion molecules, thus amplifying inflammation. These data unravel the molecular mechanisms and interplay between damaged ECs and VSMCs that lead to activation of IL-1α and, thus, initiation of adaptive responses that cause graft rejection.     

Immunopathological Changes in the Brain of Immunosuppressed Mice Experimentally Infected with Toxocara canis

Toxocariasis is a soil-transmitted helminthozoonosis due to infection of humans by larvae of Toxocara canis. The disease could produce cognitive and behavioral disturbances especially in children. Meanwhile, in our modern era, the incidence of immunosuppression has been progressively increasing due to increased incidence of malignancy as well as increased use of immunosuppressive agents. The present study aimed at comparing some of the pathological and immunological alterations in the brain of normal and immunosuppressed mice experimentally infected with T. canis. Therefore, 180 Swiss albino mice were divided into 4 groups including normal (control) group, immunocompetent T. canis-infected group, immunosuppressed group (control), and immunosuppressed infected group. Infected mice were subjected to larval counts in the brain, and the brains from all mice were assessed for histopathological changes, astrogliosis, and IL-5 mRNA expression levels in brain tissues. The results showed that under immunosuppression, there were significant increase in brain larval counts, significant enhancement of reactive gliosis, and significant reduction in IL-5 mRNA expression. All these changes were maximal in the chronic stage of infection. In conclusion, the immunopathological alterations in the brains of infected animals were progressive over time, and were exaggerated under the effect of immunosuppression as did the intensity of cerebral infection.     

An evaluation of semi‐automated methods for collecting ecosystem‐level data in temperate marine systems

Historically, marine ecologists have lacked efficient tools that are capable of capturing detailed species distribution data over large areas. Emerging technologies such as high‐resolution imaging and associated machine‐learning image‐scoring software are providing new tools to map species over large areas in the ocean. Here, we combine a novel diver propulsion vehicle (DPV) imaging system with free‐to‐use machine‐learning software to semi‐automatically generate dense and widespread abundance records of a habitat‐forming algae over ~5,000 m² of temperate reef. We employ replicable spatial techniques to test the effectiveness of traditional diver‐based sampling, and better understand the distribution and spatial arrangement of one key algal species. We found that the effectiveness of a traditional survey depended on the level of spatial structuring, and generally 10–20 transects (50 × 1 m) were required to obtain reliable results. This represents 2–20 times greater replication than have been collected in previous studies. Furthermore, we demonstrate the usefulness of fine‐resolution distribution modeling for understanding patterns in canopy algae cover at multiple spatial scales, and discuss applications to other marine habitats. Our analyses demonstrate that semi‐automated methods of data gathering and processing provide more accurate results than traditional methods for describing habitat structure at seascape scales, and therefore represent vastly improved techniques for understanding and managing marine seascapes.     

Resistance to radial expansion limits muscle strain and work

The collagenous extracellular matrix (ECM) of skeletal muscle functions to transmit force, protect sensitive structures, and generate passive tension to resist stretch. The mechanical properties of the ECM change with age, atrophy, and neuromuscular pathologies, resulting in an increase in the relative amount of collagen and an increase in stiffness. Although numerous studies have focused on the effect of muscle fibrosis on passive muscle stiffness, few have examined how these structural changes may compromise contractile performance. Here we combine a mathematical model and experimental manipulations to examine how changes in the mechanical properties of the ECM constrain the ability of muscle fibers and fascicles to radially expand and how such a constraint may limit active muscle shortening. We model the mechanical interaction between a contracting muscle and the ECM using a constant volume, pressurized, fiber-wound cylinder. Our model shows that as the proportion of a muscle cross section made up of ECM increases, the muscle’s ability to expand radially is compromised, which in turn restricts muscle shortening. In our experiments, we use a physical constraint placed around the muscle to restrict radial expansion during a contraction. Our experimental results are consistent with model predictions and show that muscles restricted from radial expansion undergo less shortening and generate less mechanical work under identical loads and stimulation conditions. This work highlights the intimate mechanical interaction between contractile and connective tissue structures within skeletal muscle and shows how a deviation from a healthy, well-tuned relationship can compromise performance.