Abstract
We propose a technical solution that enables 3D video-based in-bore movement quantification to be acquired synchronously with the BOLD function magnetic resonance imaging (fMRI) sequences. Our solution relies on in-bore video setup with 2 cameras mounted in a 90 degrees angle that allows tracking movments while acquiring fMRI sequences. In this study we show that using 3D motion quantification of a simple finger opposition paradigm we were able to map two different finger positions to two different BOLD response patterns in a typical block design protocol. The motion information was also used to adjust the block design to the actual motion start and stop improving the time accuracy of the analysis. These results reinforce the role of video based motion quantification in fMRI analysis as an independent regressor that allows new findings not discernable when using traditional block designs.

Abstract
The non-invasive assessment of hemodynamic parameters has been a permanent challenge posed to the scientific community. The literature shows many contributions to this quest expressed as algorithms dedicated to revealing some of its characteristics and as new probes or electronics, featuring some enhanced instrumental capability that can improve their insight. A test system capable of replicating some of the basic properties of the cardiovascular system, especially the ones related with the propagation of the arterial pressure wave (APW), is a powerful tool in the development of those probes and in the validation of the various algorithms that extract clinically relevant information from the data that they can collect. This work describes a test bench system, based on the combination of a new programmable pressure wave generator with a flexible tube, capable of emulating some of these properties. It discusses its main characterization issues and demonstrates the system in a relevant case study. Two versions of the system have been set up: one that generates a short duration pulse-like pressure wave from an actuator operated in a switched mode, appropriate to system characterization; a second one, using a long stroke actuator, linearly operated under program control, capable of generating complex, including cardiac-like, pressure waveforms. This configuration finds its main use in algorithm test and validation. Tests with a new piezoelectric probe, designed to collect the APW at the major artery sites are shown, demonstrating the possibility of non-invasive precise recovery of the pressure waveform.

Abstract
Local pulse-wave velocity (PWV) is an accurate indicator of the degree of arteriosclerosis (stiffness) in an artery, providing a direct characterization of the properties of its wall. Devices currently available for local PWV measurement are mainly based on ultrasound systems and have not yet been generalized to clinical practice since they require high technical expertise and most of them are limited in precision, due to the lack of reliable signal processing methods. The present work describes a new type of probe, based on a double-headed piezoelectric (PZ) sensor. The principle of PWV measurement involves determination of the pulse transit time between the signals acquired simultaneously by both PZs, placed 23 mm apart. The double probe (DP) characterization is accomplished in three main studies, carried out in a dedicated test bench system, capable of reproducing a range of clinically relevant properties of the cardiovascular system. The first study refers to determination of the impulse response (IR) for each PZ sensor, whereas the second one explores the existence of crosstalk between both transducers. In the last one, DP time resolution is inferred from a set of three different algorithms based on (a) the maximum of cross-correlation function, (b) the maximum amplitude detection and (c) the zero-crossing point identification. These values were compared with those obtained by the reference method, which consists of the simultaneous acquisition of pressure waves by means of two pressure sensors. The new probe demonstrates good performance on the test bench system and results show that the signals do not exhibit crosstalk. A good agreement was also verified between the PWV obtained from the DP signals (19.55 +/- 2.02 ms(-1)) and the PWV determined using the reference method (19.26 +/- 0.04 ms(-1)). Although additional studies are still required, this probe seems to be a valid alternative to local PWV stand-alone devices.

Abstract
We developed and tested the performance of a new wavelet based algorithm for Augmentation Index (AIx) determination. The evaluation method relies on reference cardiac-like pulses that are synthesized using a weighted combination of exponentially shaped sub-pulses that represent the three main components of real pulses: the systolic stroke, its reflected replica and the carotid reservoir or windkessel effect. The pulses are parameterized so as to reproduce the main types of cardiac waveforms. The values of AIx yielded by the new algorithm are compared with the ones computed directly from the synthesized waveform and with the values produced by standard Probability Density Function (PDF) analysis.

Abstract
The fitting of physical dynamical models to stimulus-response data such as the chemical concentration measured after a gas has been released to the environment, or the plasma concentration measured after an intravenous or oral input of a drug, are important problems in the area of system identification. Using models of different structures, one can obtain relevant statistical information on the parameters of the model from an array of software packages available in the literature. A meaningful interpretation of these parameters requires that in the presence of error-free data and an error-free model structure, a unique solution for the model parameters is guaranteed. This problem is known as a priori identifiability. Once the model is deemed identifiable, the parameters are then obtained, usually via a nonlinear least squares technique. In addition to identifiability, there is the problem of convergence of the parameters to the true values. It is a known fact that nonlinear parameter estimation algorithms do not always converge to the true parameter set. This is due to the fact that estimating the parameters of a nonlinear model can at times be an ill-conditioned problem. In this paper we use the same state space analysis techniques used to determine identifiability, to estimate the model parameters in a linear fashion. We approach the problem from a system identification point of view and then take advantage of the similarity transformation between the physical model and the identified model. We formulate the similarity relations and then transform them into a null space problem whose solution leads to the physical parameters. The novelty of our approach is in the use of a state space system identification algorithm to identify a black-box system, followed by a physical parameter extraction step using robust numerical tools such as the singular value decomposition.

Abstract
Meiotic and early-embryonic cell divisions in vertebrates take place in the absence of transcription and rely on the translational regulation of stored maternal messenger RNAs. Most of these mRNAs are regulated by the cytoplasmic-polyadenylation-element-binding protein (CPEB), which mediates translational activation and repression through cytoplasmic changes in their poly(A) tail length. It was unknown whether translational regulation by cytoplasmic polyadenylation and CPEB can also regulate mRNAs at specific points of mitotic cell-cycle divisions. Here we show that CPEB-mediated post-transcriptional regulation by phase-specific changes in poly(A) tail length is required for cell proliferation and specifically for entry into M phase in mitotically dividing cells. This translational control is mediated by two members of the CPEB family of proteins, CPEB1 and CPEB4. We conclude that regulation of poly(A) tail length is not only required to compensate for the lack of transcription in specialized cell divisions but also acts as a general mechanism to control mitosis.