Low-frequency modes in the Raman spectrum of sp-sp2 nanostructured carbon

A novel form of amorphous carbon with sp-sp2 hybridization has been recently produced by supersonic cluster beam deposition showing the presence in the film of both polyynic and cumulenic species [L. Ravagnan et al. Phys. Rev. Lett. 98, 216103 (2007)]. Here we present a in situ Raman characterization of the low frequency vibrational region (400-800 cm-1) of sp-sp2 films at different temperatures. We report the presence of two peaks at 450 cm-1 and 720 cm-1. The lower frequency peak shows an evolution with the variation of the sp content and it can be attributed, with the support of density functional theory (DFT) simulations, to bending modes of sp linear structures. The peak at 720 cm-1 does not vary with the sp content and it can be attributed to a feature in the vibrational density of states activated by the disorder of the sp2 phase.Comment: 15 pages, 5 figures, 1 tabl

Collagenated heterologous cortico-cancelleus bone mix stimulated dental pulp derived stem cells

Collagenated heretologous cortico-cancelleus bone mix (CHCCBM) is largely employed in maxillary and dental surgery for regeneration procedures, and is similar to human bone from chemical and physical point of view and promotes osteogenesis. In order to get more inside how this biomaterial induces osteoblast gene expression to promote bone formation, the mRNA levels of bone related genes were compared in human osteoblasts and dental pulp stem cells, using real time RT-PCR. The obtained results demonstrated that CHCCBM enhance stem cells differentiation and deposition of matrix by the activation of osteoblast related genes SP7, FOSL1 and SPP1

Free flap loss caused by heparin-induced thrombocytopenia and thrombosis (HITT) : a case report and literature review = Trombocitopenia eparino-indotta e trombosi (HITT): Una causa sottostimata di fallimento di lembi liberi : Case report e revisione della letteratura

Heparin-induced thrombocytopenia and thrombosis (HITT) represents a dramatic condition that is difficult to diagnose because of nuanced clinical presentation. Therefore, in every case of microvascular thrombosis during heparin-therapy prompt suspicion about HITT is necessary to avoid flap necrosis. We present a case of HITT which, as the 8 other articles reviewed, clearly shows that HITT is difficult to diagnose and complex to manage. Microvascular reconstruction is the first choice in head and neck reconstruction; unfortunately, dramatic outcomes in free flap surgery due to unpredictable thrombotic events are still reported in the English literature. More knowledge is required about HITT and reaching a consensus about thrombotic prevention in microsurgery could be helpful. Furthermore, a careful anamnesis can help minimise unexpected situations

Free flap loss caused by heparin-induced thrombocytopenia and thrombosis (HITT): a case report and literature review

La trombocitopenia eparino-indotta con trombosi rappresenta una complicanza che può portare a esiti drammatici nella chirurgia ricostruttiva microvascolare, tanto più che il suo riconoscimento non è sempre semplice. In ogni caso di trombosi microvascolare, in corso di terapia eparinica, il sospetto di HITT deve subito insorgere, così da poter intercettare e trattare la catena di eventi che porterebbe alla necrosi del lembo ricostruttivo. Presentiamo un caso che dimostra quanto possa essere difficile la diagnosi di HITT, così come appare negli altri reports reperibili in letteratura internazionale. I lembi microvascolari sono il gold standard nella chirurgia ricostruttiva cervico-facciale: purtroppo però il successo della metodica può essere inficiato da eventi trombo-embolici imprevedibili. Crediamo che una maggior divulgazione e la formulazione di domande anamnestiche specifiche possano essere utili nel limitare le conseguenze devastanti della HITT

Model for tumour growth with treatment by continuous and pulsed chemotherapy

Peer reviewedPreprin

Nucleolar retention of a translational C/EBPα isoform stimulates rDNA transcription and cell size

The messenger RNA of the intronless CEBPA gene is translated into distinct protein isoforms through the usage of consecutive translation initiation sites. These translational isoforms have distinct functions in the regulation of differentiation and proliferation due to the presence of different N-terminal sequences. Here, we describe the function of an N-terminally extended protein isoform of CCAAT enhancer-binding protein α (C/EBPα) that is translated from an alternative non-AUG initiation codon. We show that a basic amino-acid motif within its N-terminus is required for nucleolar retention and for interaction with nucleophosmin (NPM). In the nucleoli, extended-C/EBPα occupies the ribosomal DNA (rDNA) promoter and associates with the Pol I-specific factors upstream-binding factor 1 (UBF-1) and SL1 to stimulate rRNA synthesis. Furthermore, during differentiation of HL-60 cells, endogenous expression of extended-C/EBPα is lost concomitantly with nucleolar C/EBPα immunostaining probably reflecting the reduced requirement for ribosome biogenesis in differentiated cells. Finally, overexpression of extended-C/EBPα induces an increase in cell size. Altogether, our results suggest that control of rRNA synthesis is a novel function of C/EBPα adding to its role as key regulator of cell growth and proliferation

Tissue Specific Roles for the Ribosome Biogenesis Factor Wdr43 in Zebrafish Development

During vertebrate craniofacial development, neural crest cells (NCCs) contribute to most of the craniofacial pharyngeal skeleton. Defects in NCC specification, migration and differentiation resulting in malformations in the craniofacial complex are associated with human craniofacial disorders including Treacher-Collins Syndrome, caused by mutations in TCOF1. It has been hypothesized that perturbed ribosome biogenesis and resulting p53 mediated neuroepithelial apoptosis results in NCC hypoplasia in mouse Tcof1 mutants. However, the underlying mechanisms linking ribosome biogenesis and NCC development remain poorly understood. Here we report a new zebrafish mutant, fantome (fan), which harbors a point mutation and predicted premature stop codon in zebrafish wdr43, the ortholog to yeast UTP5. Although wdr43 mRNA is widely expressed during early zebrafish development, and its deficiency triggers early neural, eye, heart and pharyngeal arch defects, later defects appear fairly restricted to NCC derived craniofacial cartilages. Here we show that the C-terminus of Wdr43, which is absent in fan mutant protein, is both necessary and sufficient to mediate its nucleolar localization and protein interactions in metazoans. We demonstrate that Wdr43 functions in ribosome biogenesis, and that defects observed in fan mutants are mediated by a p53 dependent pathway. Finally, we show that proper localization of a variety of nucleolar proteins, including TCOF1, is dependent on that of WDR43. Together, our findings provide new insight into roles for Wdr43 in development, ribosome biogenesis, and also ribosomopathy-induced craniofacial phenotypes including Treacher-Collins Syndrome

IGF-I activates caspases 3/7, 8 and 9 but does not induce cell death in colorectal cancer cells

Background: Colorectal cancer is the third most common cancer in the western world. Chemotherapy is often ineffective to treat the advanced colorectal cancers due to the chemoresistance. A major contributor to chemo-resistance is tumour-derived inhibition or avoidance of apoptosis. Insulin-like growth factor I (IGF-I) has been known to play a prominent role in colorectal cancer development and progression. The role of IGF-I in cancer cell apoptosis is not completely understood.Methods: Using three colorectal cancer cell lines and one muscle cell line, associations between IGF-I and activities of caspase 3/7, 8 and 9 have been examined; the role of insulin-like growth factor I receptor (IGF-IR) in the caspase activation has been investigated.Results: The results show that exogenous IGF-I significantly increases activity of caspases 3/7, 8 and 9 in all cell lines used; blocking IGF-I receptor reduce IGF-I-induced caspase activation. Further studies demonstrate that IGF-I induced caspase activation does not result in cell death. This is the first report to show that while IGF-I activates caspases 3/7, 8 and 9 it does not cause colorectal cancer cell death.Conclusion: The study suggests that caspase activation is not synonymous with apoptosis and that activation of caspases may not necessarily induce cell death