A Novel Triangle-based Method for Scattered Data Interpolation

Abstract Local numerical methods for scattered data interpolation often require a smart subdivision of the domain in geometrical polyhedral structures. In particular triangulations in the plane (2D) and tetrahedrizations in the space (3D) are widely used to define interpolation models. In this paper we give a short survey on the main methods for the scattered data problem and we recall preliminaries on triangulations and their related properties. Finally, combining two well-known ideas we present a new triangle-based interpolation method and show its application to a case study. Mathematics Subject Classification: 41A05, 65D05, 68U0

A role for apoptosis in temporomandibular joint disc degeneration. A contemporary review

The temporomandibular joint (TMJ) connects the mandible to the skull. TMJ disorders induce degenerative tissue changes in TMJ disc that are largely the result of maladaption to abnormal joint loading. Histopathological studies have documented an association between TMJ arthropathy and loss of tissue cellularity, via apoptosis-related processes, that result in diminished extracellular matrix generation, organization, and repair. However, the exact molecular mechanisms underpinning the development and progression of such degenerative changes are still unclear. We review the most recent findings regarding the involvement of apoptotic mechanisms in TMJ disc degeneration. Although a number of aspects of TMJ disc degeneration have been thoroughly investigated, data on the involvement of apoptotic mechanisms and their mediators are few and quite recent; indeed most of the research conducted on fibrous cartilage apoptosis has focused on the intervertebral disc

Induction of tissue plasminogen activator (tPA) by pituitary adenylate cyclase-activating polypeptide (PACAP) in Schwann cell-like cultures

Peripheral nerve regeneration is dependent on the ability of regenerating neurites to migrate through cellular debris and altered extracellular matrix at the injury site, grow along the residual distal nerve sheath conduit, and reinnervate synaptic targets. In cell culture, growth cones of regenerating axons secrete PACAP, a peptide known to induce the expression of the protease tPA1. Here we tested the hypothesis that PACAP might also stimulate peripheral glial cells to release tPA to participate in nerve regeneration. More specifically, we addressed whether PACAP promoted the release and expression of tPA in the Schwann cell-like culture RT4-D6P2T, which shares biochemical and physical properties with Schwann cells2. We found that PACAP dose- and time-dependently stimulated tPA expression. Maxadilan, a potent PACAP receptor agonist, mimicked the effect of PACAP, whereas VIP, a PACAP-related peptide, produced only a moderate response. PACAP ability to stimulate tPA expression seemed to be dependent on the Akt/CREB signaling cascade, as inhibition using the PI3K/Akt blocker wortmannin or the TrkA/B inhibitor K252a both significantly dampened PACAP-evoked tPA expression. A similar effect was obtained in cells treated with the PACAP/VIP receptor antagonist PACAP6-38. We conclude that PACAP through the Akt/CREB intracellular pathway, acts as a potent inducer of tPA expression and release in Schwann-cell like cultures

Dopamine D3 receptor, neurofibromin and amyloid precursor protein expression during learning

Among dopamine receptors, the Dopamine D3 receptor (D3R) has been extensively characterized. It is distributed with highest densities in the limbic system and plays an important role in cognitive, emotional and endocrine functions. Like D3R, NF1 and APP genes are also involved in memory processes. Neurofibromin is a large tumor suppressor protein encoded by Neurofibromatosis type I gene (NF1). Amyloid precursor protein (APP) is the precursor of the amyloid-beta (Aβ) peptides involved in the pathogenesis of Alzheimer’s disease. Previously, it has been proposed that neurofibromin forms a binding complex with APP that interacts with D3R (Donarum EA et al., 2006). In addition, we have demonstrated that the absence of D3R is correlated to modifications in the expression of both NF1 and APP. Since these genes are all involved in cognitive processes, we have investigated whether such correlation is also present during a specific learning task. D3R, NF1 and APP expression levels were assessed in hyppocampi of mice subjected to the passive avoidance test. Animals were divided into four groups: naive, unconditioned stimulus trained (USTA), conditioned stimulus trained (CSTA) and conditioned (CA). mRNA and protein levels were analyzed by quantitative real time PCR and Western blot. Results showed that hyppocampal D3R expression was significantly increased in CA as compared to naive and, to a greater extent, in CSTA and USTA. Concurrently, increased NF1 expression was also found in CA and CSTA, but not in USTA. APP expression was unchanged both in CA, in CSTA and USTA as compared to naive animals. In conclusion, these data suggest that D3Rs may be correlated to passive avoidance-related learning, whereas both NF1 and APP do not seem to be directly linked to D3Rs during the acquisition of this specific learning task

Beneficial effects of PACAP in osteoarthritis cartilage. An “in vivo” and an “in vitro” morphological and biochemical study

Osteoarthritis (OA); the most common form of degenerative joint disease; is associated with variations in pro-inflammatory growth factor levels; inflammation and hypocellularity resulting from chondrocyte apoptosis (1). Pituitary adenylate cyclaseactivating polypeptide (PACAP) is a neuropeptide endowed with a range of trophic effects in several cell types; including chondrocytes (2). However; its role in OA has not been studied. To address this issue; we investigated whether PACAP expression is affected in OA cartilage obtained from experimentally-induced OA rat models; and then studied the effects of PACAP in isolated chondrocytes exposed to IL-1β in vitro to mimic the inflammatory milieu of OA cartilage. OA induction was established by histomorphometric and histochemical analyses. Changes in PACAP distribution in cartilage or its concentration in synovial fluid (SF) were assessed by immunohistochemistry and ELISA. Results showed that PACAP abundance in cartilage tissue and SF was high in healthy controls. OA induction decreased PACAP levels both in affected cartilage and SF. In vitro; PACAP prevented IL-1β-induced chondrocyte apoptosis; as determined by MTT assay; Hoechst staining and western blots of apoptotic-related proteins. These changes were also accompanied by decreased i-NOS and COX-2 levels; suggesting an anti-inflammatory effect. Altogether, these findings support a potential role for PACAP as a chondroprotective agent for the treatment of OA

Treatment of Cutaneous Melanoma Harboring SMO p.Gln216Arg Mutation with Imiquimod: An Old Drug with New Results

: Melanoma is the most lethal form of skin cancer and its incidence is growing worldwide. In the last ten years, the therapeutic scenario of this disease has been revolutionized by the introduction of targeted therapies and immune-checkpoint inhibitors. However, in patients with many lesions and bulky tumors, in which surgery is no longer feasible, there is a need for new treatment options. Here we report, for the first time to our knowledge, a clinical case where a melanoma patient harboring the SMO p.Gln216Arg mutation has been treated with imiquimod, showing a complete and durable response. To better explain this outstanding response to the treatment, we transfected a melanoma cell line (MeWo) with the SMO p.Gln216Arg mutation in order to evaluate its role in response to the imiquimod treatment. Moreover, to better demonstrate that the antitumor activity of imiquimod was due to its role in suppressing the oncogenic SMO signaling pathway, independently of its immune modulating function, an in vivo experiment has been performed. This clinical case opens up a new scenario for the treatment of melanoma patients identifying a new potentially druggable target

The effects of physical activity (treadmill and vibration stimulation training) on RANKL and OPG expression in bone cells, in rats with glucorticoid-induced osteoporosis

The aim of this study was to investigate bone tissue and plasma levels of RANKL and OPG in rats with prednisolone-induced osteoporosis and to evaluate the outcomes of physical activity on the skeletal system by treadmill and vibration platform training. Osteoporosis is a disease characterised by low bone mass and structural deterioration of bone tissue leading to bone fragility. Vibration exercise is a new and effective measure to prevent muscular atrophy and osteoporosis. The animals were divided into 5 groups. 1: control rats; 2: rats with osteoporosis receiving prednisolone; 3: rats receiving prednisolone and treadmill training; 4: rats receiving prednisolone and vibration stimulation training; 5: rats receiving prednisolone, treadmill training and vibration stimulation training. Bone evaluations used whole-body scans, histology and histomorphometric analysis. RANKL and OPG expression was evaluated by immunohistochemistry and biochemical analysis. After treatment, our data demonstrated that RANKL expression was significantly increased in groups 2 and 3 and decreased in groups 4 and 5. Conversely, OPG expression was significantly decreased in groups 2 and 3 and increased in groups 4 and 5. In conclusion, our findings suggest that mechanical stimulation inhibits the activity of RANKL. This finding provides new insights into the occurrence and progression of osteoporosis

Mesenchymal stem cell-based tissue engineering strategy for cartilage regeneration: A morphomolecular study

Articular cartilage is an avascular and aneural tissue with poor self-repair capacity. Pathological conditions leading to the cartilage degeneration, such as osteoarthritis (OA), have prompted the development of strategies aimed to its regeneration, such as mesenchymal stem cells (MSCs)-based tissue engineering approach. The aim of this study was to investigate if chondrocytes, differentiated from rat adipose tissue derived-MSCs (AMSCs) and seeded on Collagen Cell Carrier (CCC) scaffolds, are able to constitute a morphologically and biochemically healthy hyaline cartilage. To this purpose the AMSCs were primarily differentiated in chondrocytes through chondrogenic medium and subsequently cultured for 6 weeks on CCC scaffolds. The expression of osteoblast (Runt-related transcription factor 2 (RUNX2) and osteocalcin), chondrocyte (collagen I, II and lubricin) and apoptosis (caspase-3) biomarkers were evaluated in undifferentiated AMSCs, AMSCs-derived chondrocytes cultured in monolayer and AMSCs-derived chondrocytes seeded on CCC scaffolds, by different techniques such as immunohistochemistry, ELISA, Western blot and gene expression analyses. AMSCs-derived chondrocytes cultured on CCC scaffolds showed the increased expression of collagen II and lubricin, whereas the expression of collagen I, RUNX2, osteocalcin and caspase-3 resulted decreased when compared to the other groups. In conclusion, the results of this study suggest a possible role of AMSCs and the use of CCC scaffolds for therapeutic strategies aimed to the articular cartilage regeneration