Geophysical survey at Talos Dome, East Antarctica: the search for a new deep-drilling site

Talos Dome is an ice dome on the edge of the East Antarctic plateau; because accumulation is higher here than in other domes of East Antarctica, the ice preserves a good geochemical and palaeoclimatic record. A new map of the Talos Dome area locates the dome summit using the global positioning system (GPS) (72˚47’ 14’’S, 159˚04’ 2’’E; 2318.5m elevation (WGS84)). A surface strain network of nine stakes was measured using GPS. Data indicate that the stake closest to the summit moves south-southeast at a few cma–1. The other stakes, located 8 km away, move up to 0.33ma–1. Airborne radar measurements indicate that the bedrock at the Talos Dome summit is about 400m in elevation, and that it is covered by about 1900m of ice. Snow radar and GPS surveys show that internal layering is continuous and horizontal in the summit area (15 km radius). The depth distribution analysis of snow radar layers reveals that accumulation decreases downwind of the dome (north-northeast) and increases upwind (south-southwest). The palaeomorphology of the dome has changed during the past 500 years, probably due to variation in spatial distribution of snow accumulation, driven by wind sublimation. In order to calculate a preliminary age vs depth profile for Talos Dome, a simple one-dimensional steady-state model was formulated. This model predicts that the ice 100m above the bedrock may cover one glacial–interglacial period.Published423-4323.8. Geofisica per l'ambienteJCR Journalreserve

A tissue engineered osteochondral composite for cartilage repair: an in vivo study

This work aimed to validate the efficacy of a tissue engineered osteochondral composite for the treatment of cartilage lesion produced in adult pigs. The osteochondral composite was manufactured by combining an osteo-compatible cylinder and a neocartilagineous tissue obtained by seeding swine articular chondrocytes into a collagen scaffold. Articular cartilage was harvested from the trochlea of six adult pigs and was enzymatically digested to isolate the chondrocytes [Deponti D.et al. 2005]. The cells were then expanded in monolayer culture in chondrogenic medium and seeded onto a collagen scaffold. The collagen scaffold was preintegrated in vitro, macroscopically and microscopically, to a an osteo-compatible cylinder. The seeded osteochondral scaffolds were left in standard culture condition for 3 weeks with the addition of growth factors. At the end of culture time the osteochondral scaffolds were surgically implanted in osteochondral lesion performed in the trochlea of the same pigs from which the cartilage was initially harvested. As control, some osteochondral lesions were treated with acellular scaffolds and others were left untreated. After 3 months, the repair tissue of the three experimental groups was macroscopically analyzed and processed for histological and biochemical analysis. The hystologic ICRS II scale showed a statistically significant difference between the three experimental groups only in the parameters regarding the cell morphology and the surface/superficial assessment: the lesion treated with the unseeded osteochondral scaffolds showed higher values in chondrocytes morphology and in the superficial layer recovery, with respect to the lesions treated with the seeded scaffolds or left untreated. The biochemical analysis showed a higher DNA content in the lesion repaired with cellular scaffold and a higher GAGs/DNA ratio in the lesions with a spontaneous repair. The result of this study demonstrate that an osteochondral scaffold was able to repair an osteochondral lesion in an in vivo model of adult pigs, showing a good integration with the surrounding tissue. The quality of the repair was higher when the scaffold was not seeded with chondrocytes, but filled with cells migrated from subchondral bone. This tissue engineered osteochondral composite could represent a valuable model for further in vivo studies on the repair of chondral/osteochondral lesion

Necdin Controls Proliferation of White Adipocyte Progenitor Cells

White adipose tissues are composed mainly of white fat cells (adipocytes), which play a key role in energy storage and metabolism. White adipocytes are terminally differentiated postmitotic cells and arise from their progenitor cells (preadipocytes) or mesenchymal stem cells residing in white adipose tissues. Thus, white adipocyte number is most likely controlled by the rate of preadipocyte proliferation, which may contribute to the etiology of obesity. However, little is known about the molecular mechanisms that regulate preadipocyte proliferation during adipose tissue development. Necdin, which is expressed predominantly in postmitotic neurons, is a pleiotropic protein that possesses anti-mitotic and pro-survival activities. Here we show that necdin functions as an intrinsic regulator of white preadipocyte proliferation in developing adipose tissues. Necdin is expressed in early preadipocytes or mesenchymal stem cells residing in the stromal compartment of white adipose tissues in juvenile mice. Lentivirus-mediated knockdown of endogenous necdin expression in vivo in adipose tissues markedly increases fat mass in juvenile mice fed a high-fat diet until adulthood. Furthermore, necdin-null mutant mice exhibit a greater expansion of adipose tissues due to adipocyte hyperplasia than wild-type mice when fed the high-fat diet during the juvenile and adult periods. Adipose stromal-vascular cells prepared from necdin-null mice differentiate in vitro into a significantly larger number of adipocytes in response to adipogenic inducers than those from wild-type mice. These results suggest that necdin prevents excessive preadipocyte proliferation induced by adipogenic stimulation to control white adipocyte number during adipose tissue development

Micromechanical study of the load transfer in a polycaprolactone-collagen hybrid scaffold when subjected to unconfined and confined compression

Scaffolds are used in diverse tissue engineering applications as hosts for cell proliferation and extracellular matrix formation. One of the most used tissue engineering materials is collagen, which is well known to be a natural biomaterial, also frequently used as cell substrate, given its natural abundance and intrinsic biocompatibility. This study aims to evaluate how the macroscopic biomechanical stimuli applied on a construct made of polycaprolactone scaffold embedded in a collagen substrate translate into microscopic stimuli at the cell level. Eight poro-hyperelastic finite element models of 3D printed hybrid scaffolds from the same batch were created, along with an equivalent model of the idealized geometry of that scaffold. When applying an 8% confined compression at the macroscopic level, local fluid flow of up to 20 [Formula: see text]m/s and octahedral strain levels mostly under 20% were calculated in the collagen substrate. Conversely unconfined compression induced fluid flow of up to 10 [Formula: see text]m/s and octahedral strain from 10 to 35%. No relevant differences were found amongst the scaffold-specific models. Following the mechanoregulation theory based on Prendergast et al. (J Biomech 30:539-548, 1997. https://doi.org/10.1016/S0021-9290(96)00140-6 ), those results suggest that mainly cartilage or fibrous tissue formation would be expected to occur under unconfined or confined compression, respectively. This in silico study helps to quantify the microscopic stimuli that are present within the collagen substrate and that will affect cell response under in vitro bioreactor mechanical stimulation or even after implantation

Necdin, a p53-Target Gene, Is an Inhibitor of p53-Mediated Growth Arrest

In vitro, cellular immortalization and transformation define a model for multistep carcinogenesis and current ongoing challenges include the identification of specific molecular events associated with steps along this oncogenic pathway. Here, using NIH3T3 cells, we identified transcriptionally related events associated with the expression of Polyomavirus Large-T antigen (PyLT), a potent viral oncogene. We propose that a subset of these alterations in gene expression may be related to the early events that contribute to carcinogenesis. The proposed tumor suppressor Necdin, known to be regulated by p53, was within a group of genes that was consistently upregulated in the presence of PyLT. While Necdin is induced following p53 activation with different genotoxic stresses, Necdin induction by PyLT did not involve p53 activation or the Rb-binding site of PyLT. Necdin depletion by shRNA conferred a proliferative advantage to NIH3T3 and PyLT-expressing NIH3T3 (NIHLT) cells. In contrast, our results demonstrate that although overexpression of Necdin induced a growth arrest in NIH3T3 and NIHLT cells, a growing population rapidly emerged from these arrested cells. This population no longer showed significant proliferation defects despite high Necdin expression. Moreover, we established that Necdin is a negative regulator of p53-mediated growth arrest induced by nutlin-3, suggesting that Necdin upregulation could contribute to the bypass of a p53-response in p53 wild type tumors. To support this, we characterized Necdin expression in low malignant potential ovarian cancer (LMP) where p53 mutations rarely occur. Elevated levels of Necdin expression were observed in LMP when compared to aggressive serous ovarian cancers. We propose that in some contexts, the constitutive expression of Necdin could contribute to cancer promotion by delaying appropriate p53 responses and potentially promote genomic instability

Current surgical options for articular cartilage repair

The articular cartilage lesions represent one of the major unsolved problems in the orthopaedic surgery. This is because articular cartilage has a limited capacity of self-repair following trauma. The aim of this study is to review the different surgical options for articular cartilage repair. They can be divided into three groups: techniques without transplant of cells or tissues; techniques based on the transplantation of tissues; the tissue engineering techniques. The first group includes the joint debridement and the techniques based on the bone marrow-stimulation principle. The second group includes the transplantation of periosteum and the transplantation of autologous or allogeneic osteochondral plugs. The tissue engineering techniques could be further divided as follows: methods based on the transplantation of cells either in solution, or in the form of microspheres, or carried on a biocompatible scaffold; the transplant of cartilage fragments; the cell-free techniques, based on the use of an acellular scaffold, able to entrap the reparative cells recruited from the host tissue and to guide their differentiation toward a chondral phenotype. In this work we present various options for the treatment of chondral or osteochondral lesions. Today, however, due to the lack of comparative studies, it is not always possible to define the best treatment choice for the different cartilage pathologies

Photoinduced hydrogen evolution by a pentapyridine cobalt complex: elucidating some mechanistic aspects

A new hydrogen evolving cobalt catalyst 1 based on a pentapyridine ligand has been synthesized and characterized. Its photocatalytic activity in the presence of a Ru(bpy)3 2+ sensitizer and ascorbic acid as a sacrificial electron donor has been screened in purely buffered aqueous solutions showing TONs and TOFs strongly dependent on both catalyst concentration and pH with the best results obtained at 50 μM 1 and at pH 4 (TON = 187, TOF = 8.1 min−1). The photochemical mechanism, as revealed by flash photolysis, involves reaction of the excited sensitizer with ascorbic acid to yield Ru(bpy)3 + as a primary photogenerated reductant, capable of electron transfer to 1 with a remarkable rate (bimolecular rate constant k = 5.7 (±0.7) × 109 M−1 s−1). For hydrogen generation, two one-electron photochemical reduction steps of 1 are needed along with hydride formation and protonation. Under the experimental conditions used, hydrogen evolution is mainly limited by partial decomposition of both the sensitizer and the catalyst. Moreover, accumulation of the oxidation product of the ascorbic acid donor, dehydroascorbic acid, is observed to strongly decrease the hydrogen production yield. As shown by flash photolysis, this species is capable of quenching the reduced ruthenium species (k = 4.4 (±0.5) × 107 M−1 s−1) thus competing with electron transfer to the catalys

Distribution of ghrelin-producing cells in the gastrointestinal tract of pigs at different ages

Ghrelin is involved in many biological processes, ranging from appetite regulation and the release of growth hormone to the regulation of gastrointestinal motility and secretion processes. Ghrelin expression is not homogenously distributed throughout the gastrointestinal tract; expression is species-specific and can also depend on the animal age. This study was performed to investigate ghrelin immunolocalization in the gastrointestinal tract of pigs at different ages: 1 day (birth), 28 days (weaning), 2 months, 4 months, and 7 months (pre-puberty). Tissue samples were collected along the entire gastrointestinal tract and were examined by immunohistochemistry and double-immunofluorescence. Histometry was performed by counting the number of endocrine ghrelin immunopositive cells in the gastrointestinal mucosa. Ghrelin was found to be present along the swine alimentary canal from the stomach to the caecum. In all regions of the alimentary canal of the animals studied, ghrelin-immunoreactive (IR) cells co-localized with chromogranin-A and were therefore identified as endocrine cells. In the gastric fundus, ghrelin-immunoreactivity was partially detected in co-localization with H-K-adenosine triphosphatase and pepsinogen. Ghrelin-IR endocrine cells were abundant in the oxyntic mucosa but less present in the small intestine and rare in the large intestine. The cell density of the ghrelin-IR endocrine cells was lowest in the oxyntic mucosa of 1-day-old pigs. We can conclude that gastric ghrelin expression is not related merely to age but could also potentially be influenced by food intake