Evidence of robust 2D transport and Efros-Shklovskii variable range hopping in disordered topological insulator (Bi2Se3) nanowires

We report the experimental observation of variable range hopping conduction in focused-ion-beam (FIB) fabricated ultra-narrow nanowires of topological insulator (Bi2Se3). The value of the exponent in the hopping equation was extracted as ~ 1/2 for different widths of nanowires, which is the proof of the presence of Efros-Shklovskii hopping transport mechanism in a strongly disordered system. High localization lengths (0.5nm, 20nm) were calculated for the devices. A careful analysis of the temperature dependent fluctuations present in the magnetoresistance curves, using the standard Universal Conductance Fluctuation theory, indicates the presence of 2D topological surface states. Also, the surface state contribution to the conductance was found very close to one conductance quantum. We believe that our experimental findings shed light on the understanding of quantum transport in disordered topological insulator based nanostructures.Comment: 14pages, 4 figure

Satellite cell depletion in degenerative skeletal muscle

Adult skeletal muscle has the striking ability to repair and regenerate itself after injury. This would not be possible without satellite cells, a subpopulation of cells existing at the margin of the myofiber. Under most conditions, satellite cells are quiescent, but they are activated in response to trauma, enabling them to guide skeletal muscle regeneration. In degenerative skeletal muscle states, including motor nerve denervation, advanced age, atrophy secondary to deconditioning or immobilization, and Duchenne muscular dystrophy, satellite cell numbers and proliferative potential significantly decrease, contributing to a diminution of skeletal muscle's regenerative capacity and contractility. This review will highlight the fate of satellite cells in several degenerative conditions involving skeletal muscle, and will attempt to gauge the relative contributions of apoptosis, senescence, impaired proliferative potential, and host factors to satellite cell dysfunction.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/44390/1/10495_2004_Article_5150572.pd

17β-estradiol abrogates apoptosis inhibiting PKCδ, JNK and p66Shc activation in C2C12 cells

17β-Estradiol (E2) protects several non-reproductive tissues from apoptosis, including skeletal muscle. Previously, we showed that E2 at physiological concentrations prevented apoptosis induced by H2O2 in skeletal myoblasts. As we have also demonstrated a clear beneficial action of this hormone on skeletal muscle mitochondria, the present work further characterizes the signaling mechanisms modulated by E2 that are involved in mitochondria protection, which ultimately result in antiapoptosis. Here, we report that E2 through estrogen receptors (ERs) inhibited the H2O2-induced PKCδ and JNK activation, which results in the inhibition of phosphorylation and translocation to mitochondria of the adaptor protein p66Shc. In conjunction, the inhibition by the hormone of this H2O2-triggered signaling pathway results in protection of mitochondrial potential membrane. Our results provide basis for a putative mechanism by which E2 exerts beneficial effects on mitochondria, against oxidative stress, in skeletal muscle cells. J. Cell. Biochem. 116: 1454-1465, 2015.Fil: la Colla, Anabela Belén. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Centro Cientifico Tecnológico Bahia Blanca. Instituto de Ciencias Biologicas y Biomedicas del Sur; ArgentinaFil: Boland, Ricardo Leopoldo. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Centro Cientifico Tecnológico Bahia Blanca. Instituto de Ciencias Biologicas y Biomedicas del Sur; ArgentinaFil: Vasconsuelo, Andrea Anahi. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Centro Cientifico Tecnológico Bahia Blanca. Instituto de Ciencias Biologicas y Biomedicas del Sur; Argentin

Farasha: A Provable Permutation-based Parallelizable PRF

The pseudorandom function Farfalle, proposed by Bertoni et al. at ToSC 2017, is a permutation based arbitrary length input and output PRF. At its core are the public permutations and feedback shift register based rolling functions. Being an elegant and parallelizable design, it is surprising that the security of Farfalle has been only investigated against generic cryptanalysis techniques such as differential/linear and algebraic attacks and nothing concrete about its provable security is known. To fill this gap, in this work, we propose Farasha, a new permutation-based parallelizable PRF with provable security. Farasha can be seen as a simple and provable Farfalle-like construction where the rolling functions in the compression and expansion phases of Farfalle are replaced by a uniform almost xor universal (AXU) and a simple counter, respectively. We then prove that in the random permutation model, the compression phase of Farasha can be shown to be an uniform AXU function and the expansion phase can be mapped to an Even-Mansour block cipher. Consequently, combining these two properties, we show that Farasha achieves a security of min(keysize, permutation size/2). Finally, we provide concrete instantiations of Farasha with AXU functions providing different performance trade-offs. We believe our work will bring new insights in further understanding the provable security of Farfalle-like constructions

Double free-flap reconstruction of massive defects involving the lip, chin, and mandible

Two patients with massive, composite defects of the total lower lip, chin, and anterior mandible underwent double free-flap reconstruction. A fibular osteoseptocutaneous flap was used to reconstruct the mandible and floor of the mouth and a radial forearm fasciocutaneous composite flap, including the palmaris longus tendon, was used for total lower lip and chin reconstruction. Postoperatively, both patients had acceptable cosmesis, were orally competent, and recovered adequate mandibular function. Double free-flap reconstruction is indicated only in those circumstances in which composite tissue requirements or massive tissue defects preclude reconstruction with a single free-tissue transfer. © 1998 Wiley-Liss, Inc. MICROSURGERY 18:372–378, 1998Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/38479/1/6_ftp.pd

Human Cord Blood Stem Cell Therapy for Treatment of Stress Urinary Incontinence

Our objective in this study was to evaluate the safety and efficacy of transurethral cord blood stem cell injection for treatment of stress urinary incontinence in women. Between July 2005 and July 2006, 39 women underwent transurethral umbilical cord blood stem cell injection performed by one operator at a single hospital. All patients had stress urinary incontinence. The patients were evaluated 1, 3, and 12 months postoperatively. No postoperative complications were observed. 28 patients (77.8%) were more than 50% satisfied according to the Patient's Satisfaction results after 1 month, 29 patients (83%) were more than 50% satisfied according to the Patient's Satisfaction results after 3 months, and 26 (72.2%) continuously showed more than 50% improvement after 12 months. Intrinsic sphincter deficiency and mixed stress incontinency improved in the ten patients evaluated by urodynamic study. Our results suggest that transurethral umbilical cord blood stem cell injection is an effective treatment for women with all types of stress urinary incontinence

Skeletal muscle stem cells express anti-apoptotic ErbB receptors during activation from quiescence

To be effective for tissue repair, satellite cells (the stem cells of adult muscle) must survive the initial activation from quiescence. Using an in vitro model of satellite cell activation, we show that erbB1, erbB2 and erbB3, members of the EGF receptor tyrosine kinase family, appear on satellite cells within 6 h of activation. We show that signalling via erbB2 provides an anti-apoptotic survival mechanism for satellite cells during the first 24 h, as they progress to a proliferative state. Inhibition of erbB2 signalling with AG825 reduced satellite cell numbers, concomitant with elevated caspase-8 activation and TUNEL labelling of apoptotic satellite cells. In serum-free conditions, satellite cell apoptosis could be largely prevented by a mixture of erbB1, erbB3 and erbB4 ligand growth factors, but not by neuregulin alone (erbB3/erbB4 ligand). Furthermore, using inhibitors specific to discrete intracellular signalling pathways, we identify MEK as a pro-apoptotic mediator, and the erbB-regulated factor STAT3 as an anti-apoptotic mediator during satellite cell activation. These results implicate erbB2 signalling in the preservation of a full compliment of satellite cells as they activate in the context of a damaged muscle