Experimental evaluation of synergy-based in-hand manipulation

In this paper, the problem of in-hand dexterous manipulation has been addressed on the base of postural synergies analysis. The computation of the synergies subspace able to represent grasp and manipulation tasks as trajectories connecting suitable configuration sets is based on the observation of the human hand behavior. Five subjects are required to reproduce themost natural grasping configuration belonging to the considered grasping taxonomy and the boundary configurations for those grasps that admit internal manipulation. The measurements on the human hand and the reconstruction of the human grasp configurations are obtained using a vision-based mapping method that assume the kinematics of the robotic hand, used for the experiments, as a simplified model of the human hand. The analysis to determine the most suitable set of synergies able to reproduce the selected grasps and the relative allowed internal manipulation has been carried out. The grasping and in-hand manipulation tasks have been reproduced bymeans of linear interpolation of the boundary configurations in the selected synergies subspace and the results have been experimentally tested on the UB Hand IV

Towards a Twisted String Actuated Haptic Device: Experimental Testing of a 2-D Virtual Environment and Teleoperation Interface

In the article, a first stage implementation of a haptic device towards a complete 3-D workspace twisted-string actuated haptic interface is discussed. In the present work, a 2-D setup is presented, with the aim of preliminarly testing the behaviour of this novel haptic system, especially with respect to the adopted cable-based actuation solution. In particular, the component descriptions, kinematics of the planar device and the controller for teleoperation purposes are illustrated. Results regarding the behaviour of the system in rendering a virtual environment and in a robot teleoperation scenario with haptic force feedback are reported. The experimental outcomes show that the designed and implemented system is suitable for teleoperation with haptic interfaces, providing positive perspectives for the realization of the fully functional 3-D haptic interface in the future work

Rtg signaling sustains mitochondrial respiratory capacity in hog1-dependent osmoadaptation

Mitochondrial RTG-dependent retrograde signaling, whose regulators have been characterized in Saccharomyces cerevisiae, plays a recognized role under various environmental stresses. Of special significance, the activity of the transcriptional complex Rtg1/3 has been shown to be modu-lated by Hog1, the master regulator of the high osmolarity glycerol pathway, in response to osmotic stress. The present work focuses on the role of RTG signaling in salt-induced osmotic stress and its interaction with HOG1. Wild-type and mutant cells, lacking HOG1 and/or RTG genes, are compared with respect to cell growth features, retrograde signaling activation and mitochondrial function in the presence and in the absence of high osmostress. We show that RTG2, the main upstream regulator of the RTG pathway, contributes to osmoadaptation in an HOG1-dependent manner and that, with RTG3, it is notably involved in a late phase of growth. Our data demonstrate that impairment of RTG signaling causes a decrease in mitochondrial respiratory capacity exclusively under os-mostress. Overall, these results suggest that HOG1 and the RTG pathway may interact sequentially in the stress signaling cascade and that the RTG pathway may play a role in inter-organellar metabolic communication for osmoadaptation

An Overview of Mitochondrial Protein Defects in Neuromuscular Diseases

none8noNeuromuscular diseases (NMDs) are dysfunctions that involve skeletal muscle and cause incorrect communication between the nerves and muscles. The specific causes of NMDs are not well known, but most of them are caused by genetic mutations. NMDs are generally progressive and entail muscle weakness and fatigue. Muscular impairments can differ in onset, severity, prognosis, and phenotype. A multitude of possible injury sites can make diagnosis of NMDs difficult. Mitochondria are crucial for cellular homeostasis and are involved in various metabolic pathways; for this reason, their dysfunction can lead to the development of different pathologies, including NMDs. Most NMDs due to mitochondrial dysfunction have been associated with mutations of genes involved in mitochondrial biogenesis and metabolism. This review is focused on some mitochondrial routes such as the TCA cycle, OXPHOS, and β-oxidation, recently found to be altered in NMDs. Particular attention is given to the alterations found in some genes encoding mitochondrial carriers, proteins of the inner mitochondrial membrane able to exchange metabolites between mitochondria and the cytosol. Briefly, we discuss possible strategies used to diagnose NMDs and therapies able to promote patient outcomeopenMarra Federica, Lunetti Paola, Curcio Rosita, Lasorsa Francesco Massimo, Capobianco Loredana, Porcelli Vito, Dolce Vincenza, Fiermonte Giuseppe and Scarcia PasqualeMarra, Federica; Lunetti, Paola; Curcio, Rosita; Lasorsa Francesco, Massimo; Capobianco, Loredana; Porcelli, Vito; Dolce, Vincenza; Fiermonte Giuseppe and Scarcia, Pasqual

Identification of mitochondrial carriers in Saccharomyces cerevisiae by transport assay of reconstituted recombinant proteins".

The inner membranes of mitochondria contain a family of carrier proteins that are responsible for the transport in and out of the mitochondrial matrix of substrates, products, co-factors and biosynthetic precursors that are essential for the function and activities of the organelle. This family of proteins is characterized by containing three tandem homologous sequence repeats of approximately 100 amino acids, each folded into two transmembrane α-helices linked by an extensive polar loop. Each repeat contains a characteristic conserved sequence. These features have been used to determine the extent of the family in genome sequences. The genome of Saccharomyces cerevisiae contains 34 members of the family. The identity of five of them was known before the determination of the genome sequence, but the functions of the remaining family members were not. This review describes how the functions of 15 of these previously unknown transport proteins have been determined by a strategy that consists of expressing the genes in Escherichia coli or Saccharomyces cerevisiae, reconstituting the gene products into liposomes and establishing their functions by transport assay. Genetic and biochemical evidence as well as phylogenetic considerations have guided the choice of substrates that were tested in the transport assays. The physiological roles of these carriers have been verified by genetic experiments. Various pieces of evidence point to the functions of six additional members of the family, but these proposals await confirmation by transport assay. The sequences of many of the newly identified yeast carriers have been used to characterize orthologs in other species, and in man five diseases are presently known to be caused by defects in specific mitochondrial carrier genes. The roles of eight yeast mitochondrial carriers remain to be established. © 2006 Elsevier B.V. All rights reserved

KRAS-regulated glutamine metabolism requires UCP2-mediated aspartate transport to support pancreatic cancer growth

The oncogenic KRAS mutation has a critical role in the initiation of human pancreatic ductal adenocarcinoma (PDAC) since it rewires glutamine metabolism to increase reduced nicotinamide adenine dinucleotide phosphate (NADPH) production, balancing cellular redox homeostasis with macromolecular synthesis1,2. Mitochondrial glutamine-derived aspartate must be transported into the cytosol to generate metabolic precursors for NADPH production2. The mitochondrial transporter responsible for this aspartate efflux has remained elusive. Here, we show that mitochondrial uncoupling protein 2 (UCP2) catalyses this transport and promotes tumour growth. UCP2-silenced KRASmut cell lines display decreased glutaminolysis, lower NADPH/NADP+ and glutathione/glutathione disulfide ratios and higher reactive oxygen species levels compared to wild-type counterparts. UCP2 silencing reduces glutaminolysis also in KRASWT PDAC cells but does not affect their redox homeostasis or proliferation rates. In vitro and in vivo, UCP2 silencing strongly suppresses KRASmut PDAC cell growth. Collectively, these results demonstrate that UCP2 plays a vital role in PDAC, since its aspartate transport activity connects the mitochondrial and cytosolic reactions necessary for KRASmut rewired glutamine metabolism2, and thus it should be considered a key metabolic target for the treatment of this refractory tumour

Jón Guđmundsson Lӕrđ's True Account and the Massacre of Basque Whalers in Iceland in 1615

On the night of September 20, 1615, the eve of the feast of St. Matthew, an expedition of Basque whalers lost their ships in a fjord near Trékyllisvik, Iceland, during a terrible storm. This led to a series of events that culminated in their October massacre at hands of the islanders. The Basque mariners' bodies, dismembered, would not be buried. However, not all Icelanders saw that massacre with good eyes. One of them, Jón Guđmundsson, better known as Jón lӕrđi (1574-1658) or "the wise man", wrote an essay on those events in defense of the victims titled "SöThis book reveals Jón Guđmundsson Lӕrđ's account of the massacre of the Basque whalers in Iceland in 1615.This book was published with generous financial support from the Basque Government