A FACIAL ANIMATION FRAMEWORK WITH EMOTIVE/EXPRESSIVE CAPABILITIES

LUCIA is an MPEG-4 facial animation system developed at ISTC-CNR.. It works on standard Facial Animation Parameters and speaks with the Italian version of FESTIVAL TTS. To achieve an emotive/expressive talking head LUCIA was build from real human data physically extracted by ELITE optotracking movement analyzer. LUCIA can copy a real human by reproducing the movements of passive markers positioned on his face and recorded by the ELITE device or can be driven by an emotional XML tagged input text, thus realizing a true audio/visual emotive/expressive synthesis. Synchronization between visual and audio data is very important in order to create the correct WAV and FAP files needed for the animation. LUCIA\u27s voice is based on the ISTC Italian version of FESTIVAL-MBROLA packages, modified by means of an appropriate APML/VSML tagged language. LUCIA is available in two different versions: an open source framework and the "work in progress" WebG

A 3d talking head for mobile devices based on unofficial ios webgl support

In this paper we present the implementation of a WebGL Talking Head for iOS mobile devices (Apple iPhone and iPad). It works on standard MPEG-4 Facial Animation Parameters (FAPs) and speaks with the Italian version of FESTIVAL TTS. It is totally based on true real human data. The 3D kinematics information are used to create lips articulatory model and to drive directly the talking face, generating human facial movements. In the last year we developed the WebGL version of the avatar. WebGL, which is 3D graphic for the web, is currently supported in the major web browsers for desktop computers. No official support has been given for mobile device main platforms yet, although the Firefox beta version enables it on android phones. Starting from iOS 5 WebGL is enabled only for the advertisement library class (which is intended for placing ad-banners in applications). We have been able to use this feature to visualize and animate our WebGL talking head

LUCIA: An open source 3D expressive avatar for multimodal h.m.i.

LUCIA is an MPEG-4 facial animation system developed at ISTC-CNR . It works on standard Facial Animation Parameters and speaks with the Italian version of FESTIVAL TTS. To achieve an emotive/expressive talking head LUCIA was build from real human data physically extracted by ELITE optotracking movement analyzer. LUCIA can copy a real human by reproducing the movements of passive markers positioned on his face and recorded by the ELITE device or can be driven by an emotional XML tagged input text, thus realizing a true audio/visual emotive/expressive synthesis. Synchronization between visual and audio data is very important in order to create the correct WAV and FAP files needed for the animation. LUCIA\u27s voice is based on the ISTC Italian version of FESTIVAL-MBROLA packages, modified by means of an appropriate APML/VSML tagged language. LUCIA is available in two dif-ferent versions: an open source framework and the "work in progress" WebGL

Tracking the 2015 Gastrointestinal Cancers Symposium: bridging cancer biology to clinical gastrointestinal oncology

The 2015 Gastrointestinal Cancers Symposium (San Francisco, CA, USA; January 15–17) is the world-class conference co-sponsored by the American Society of Clinical Oncology, the American Society for Radiation Oncology, the American Gastroenterological Association Institute, and the Society of Surgical Oncology, in which the most innovative research results in digestive tract oncology are presented and discussed. In its twelfth edition, the meeting has provided new insights focusing on the underpinning biology and clinical management of gastrointestinal malignancies. More than 3,400 health care professionals gathered from all over the world to share their experiences on how to bridge the recent novelties in cancer biology with everyday medical practice. In this article, the authors report on the most significant advances, didactically moving on three different anatomic tracks: gastroesophageal malignancies, pancreatic and biliary cancers, and colorectal adenocarcinomas

Mastectomy with immediate breast reconstruction during "phase 1" COVID-19 emergency: An Italian experience.

n/

Stearoyl-CoA desaturase 1 and paracrine signal involvement in the promotion of breast cancer cell migration induced by cancer-associated fibroblasts

Despite the acknowledged impact of the tumor stroma on breast cancer development and progression, the molecular basis of such effects remain partially unexplained. We previously reported that breast cancer-associated fibroblasts (CAFs) induced epithelial-mesenchymal transition and an increase in cell membrane fluidity and migration speed in poorly (MCF-7) and highly invasive (MDA-MB-231) breast cancer cells. More recently, in order to better define the mechanisms responsible for the CAF-promoted tumor cell migration, we investigated the role of Stearoyl-CoA desaturase 1 (SCD1), the main enzyme regulating membrane fluidity, and demonstrated its CAF-triggered up-regulation as well as its crucial role in the migratory ability of the above tumor cells. Besides SCD1 induction, a CAF-promoted enhancement in the protein level and/or activity of the SCD1 transcription factor, the sterol regulatory element-binding protein 1 (SREBP1), was observed. Moreover, the influence of stroma-derived signals in cancer cell migration speed was proved by cell tracking analysis in the presence of neutralizing antibodies to hepatocyte growth factor, transforming growth factor-β or basic fibroblast growth factor, where a marked reduction or abolishment of the fibroblast-triggered increase in cancer cell migration speed was observed. In the last part of this study, in order to verify if soluble CAF-derived factors stimulate breast cancer cell migration in a SCD1-dependent manner, tumor cells were exposed to CAF-conditioned medium (CM) and their migration evaluated by scratch assay in the presence of a small molecule inhibitor of SCD1. Moreover, to assess if the induction of SCD1 expression by CAFs might occur via SREBP1, the desaturase levels were also determined in SREBP1-inhibited tumor cells. These latest investigations indicate that SCD1 contributes to the promotion of breast cancer cell migration by CAF-derived soluble factors, since the desaturase inhibition completely suppressed the stimulatory effect of CAF-CM on tumor cell migration. SREBP1 inhibition impaired CAF-mediated up-regulation of SCD1 in poorly invasive but not in highly invasive tumor cells, in which SREBP1-independent mechanisms may account for the enhancement of SCD1 levels. These results provide further insights in understanding the role of CAFs in promoting tumor cell migration, which may help to design new stroma-based therapeutic strategies

Breast cancer-associated fibroblasts promote tumor cell migration: crucial role of Stearoyl CoA Desaturase1 and paracrine signalings

The key role played by the stroma in breast cancer development and progression has been widely recognized. Recently, we reported that the cross-talk between epithelial and stromal cells affects structural and functional features correlated with the invasive phenotype of breast cancer cells by co-culturing mammary cancer cells with different metastatic potential (MDA-MB-231>MCF-7) with fibroblasts isolated from breast healthy skin (normal fibroblasts, NFs) or breast tumor stroma (cancer-associated fibroblasts, CAFs) [1].This study was designed to deepen the knowledge of the role played notably by CAFs in promoting breast tumor cell migratory skill through the analysis of the expression/activity of downstream potential target molecules and of the contribution of paracrine signalings. Thus, we investigated the influence of fibroblasts on the expression of Stearoyl- CoA desaturase 1 (SCD1), the main enzyme regulating membrane fluidity, as well as on the level and activity of its transcription factor, SREBP1, in breast cancer cells. The ability of CAFs to promote a 2-3 fold increase in SCD1 mRNA and protein expression as well as an induction of SREBP1 DNA binding activity has been shown in the two cancer cell lines. Both siRNA-mediated and pharmacological inhibition of SCD1 impaired tumor cells migration. To clarify the possible role of tumor-stroma paracrine interaction in the previously reported improvement of cancer cell migratory ability, cocultures were set up in presence of neutralizing antibodies against hepatocyte growth factor, transforming growth factor-β or basic fibroblast growth factor. Cell tracking analysis demonstrated that the CAF-mediated increase in tumor cell migration speed was reduced or abolished by neutralizing the above soluble factors. These results provide new insights in understanding the role of CAFs in promoting tumor cell invasiveness and may help to devise new targeted therapeutic approaches

Breast cancer-associated fibroblasts promote tumor cell migration: crucial role of Stearoyl CoA Desaturase1 and paracrine signalings

The key role played by the stroma in breast cancer development and progression has been widely recognized. Recently, we reported that the cross-talk between epithelial and stromal cells affects structural and functional features correlated with the invasive phenotype of breast cancer cells by co-culturing mammary cancer cells with different metastatic potential (MDA-MB-231>MCF-7) with fibroblasts isolated from breast healthy skin (normal fibroblasts, NFs) or breast tumor stroma (cancer-associated fibroblasts, CAFs) [1].This study was designed to deepen the knowledge of the role played notably by CAFs in promoting breast tumor cell migratory skill through the analysis of the expression/activity of downstream potential target molecules and of the contribution of paracrine signalings. Thus, we investigated the influence of fibroblasts on the expression of Stearoyl- CoA desaturase 1 (SCD1), the main enzyme regulating membrane fluidity, as well as on the level and activity of its transcription factor, SREBP1, in breast cancer cells. The ability of CAFs to promote a 2-3 fold increase in SCD1 mRNA and protein expression as well as an induction of SREBP1 DNA binding activity has been shown in the two cancer cell lines. Both siRNA-mediated and pharmacological inhibition of SCD1 impaired tumor cells migration. To clarify the possible role of tumor-stroma paracrine interaction in the previously reported improvement of cancer cell migratory ability, cocultures were set up in presence of neutralizing antibodies against hepatocyte growth factor, transforming growth factor-β or basic fibroblast growth factor. Cell tracking analysis demonstrated that the CAF-mediated increase in tumor cell migration speed was reduced or abolished by neutralizing the above soluble factors. These results provide new insights in understanding the role of CAFs in promoting tumor cell invasiveness and may help to devise new targeted therapeutic approaches

Stearoyl-CoA desaturase 1 and paracrine diffusible signals have a major role in the promotion of breast cancer cell migration induced by cancer-associated fibroblasts

Background: Despite the recognised contribution of the stroma to breast cancer development and progression, the effective targeting of the tumor microenvironment remains a challenge to be addressed. We previously reported that normal fibroblasts (NFs) and, notably, breast cancer-associated fibroblasts (CAFs) induced epithelial-to-mesenchymal transition and increases in cell membrane fluidity and migration in well- (MCF-7) and poorly-differentiated (MDA-MB-231) breast cancer cells. This study was designed to better define the role played, especially by CAFs, in promoting breast tumor cell migration. Methods: Fibroblast/breast cancer cell co-cultures were set up to investigate the influence of NFs and CAFs on gene and protein expression of Stearoyl-CoA desaturase 1 (SCD1), the main enzyme regulating membrane fluidity, as well as on the protein level and activity of its transcription factor, the sterol regulatory element-binding protein 1 (SREBP1), in MCF-7 and MDA-MB-231 cells. To assess the role of SREBP1 in the regulation of SCD1 expression, the desaturase levels were also determined in tumor cells treated with an SREBP1 inhibitor. Migration was evaluated by wound-healing assay in SCD1- inhibited (by small-interfering RNA (siRNA) or pharmacologically) cancer cells and the effect of CAF-conditioned medium was also assessed. To define the role of stroma-derived signals in cancer cell migration speed, cell-tracking analysis was performed in the presence of neutralising antibodies to hepatocyte growth factor, transforming growth factor-b or basic fibroblast growth factor. Results: A two to three fold increase in SCD1 mRNA and protein expression has been induced, particularly by CAFs, in the two cancer cell lines that appear to be dependent on SREBP1 activity in MCF-7 but not in MDA-MB-231 cells. Both siRNA-mediated and pharmacological inhibition of SCD1 impaired tumor cells migration, also when promoted by CAF-released soluble factors. Fibroblast-triggered increase in cancer cell migration speed was markedly reduced or abolished by neutralising the above growth factors. Conclusion: These results provide further insights in understanding the role of CAFs in promoting tumor cell migration, which may help to design new stroma-based therapeutic strategies