Continuous cardiac autonomic and haemodynamic responses to isometric exercise in females

Purpose: Hypertension is associated with impaired haemodynamic control mechanisms and autonomic dysfunction. Isometric exercise (IE) interventions have been shown to improve autonomic modulation and reduce blood pressure (BP) in predominantly male participants. The physiological responses to IE are under explored in female populations; therefore, this study investigated the continuous cardiac autonomic and haemodynamic response to a single bout of IE in a large female population. Methods: Forty physically inactive females performed a single, individually prescribed isometric wall squat training session. Total power spectral density of heart rate variability (HRV) and associated low frequency (LF) and high-frequency (HF) power spectral components, were recorded in absolute (ms2) and normalised units (nu) pre, during and post an IE session. Heart rate (HR) was recorded via electrocardiography and baroreceptor reflex sensitivity (BRS) via the sequence method. Continuous blood pressure was recorded via the vascular unloading technique and stroke volume via impedance cardiography. Total peripheral resistance (TPR) was calculated according to Ohm’s Law. Results: During IE, there were significant reductions in HRV (p<0.001) and BRS (p<0.001), and significant increases in heart rate (p<0.001), systolic, mean and diastolic BP (p<0.001 for all). In recovery following the IE session, cardiac autonomic parameters returned to baseline (p=0.974); however, total peripheral vascular resistance significantly reduced below baseline (p<0.001). This peripheral vascular response was associated with significant reductions in systolic (-17.3±16.5 mmHg, p<0.001), mean (-18.8±17.4 mmHg, p<0.001) and diastolic BP (-17.3±16.2 mmHg, p<0.001), below baseline. Conclusion: A single IE session is associated with improved haemodynamic cardiovascular responses in females. Cardiac autonomic responses return to baseline values, which suggests alternative mechanisms are responsible for the post exercise haemodynamic improvements in females. Future mechanistic research is required to investigate the acute and chronic effects of IE in female populations with different resting BP profiles

From Skew-Cyclic Codes to Asymmetric Quantum Codes

We introduce an additive but not $\mathbb{F}_4$-linear map $S$ from $\mathbb{F}_4^{n}$ to $\mathbb{F}_4^{2n}$ and exhibit some of its interesting structural properties. If $C$ is a linear $[n,k,d]_4$-code, then $S(C)$ is an additive $(2n,2^{2k},2d)_4$-code. If $C$ is an additive cyclic code then $S(C)$ is an additive quasi-cyclic code of index $2$. Moreover, if $C$ is a module $\theta$-cyclic code, a recently introduced type of code which will be explained below, then $S(C)$ is equivalent to an additive cyclic code if $n$ is odd and to an additive quasi-cyclic code of index $2$ if $n$ is even. Given any $(n,M,d)_4$-code $C$, the code $S(C)$ is self-orthogonal under the trace Hermitian inner product. Since the mapping $S$ preserves nestedness, it can be used as a tool in constructing additive asymmetric quantum codes.Comment: 16 pages, 3 tables, submitted to Advances in Mathematics of Communication

Possible Localized Modes in the Uniform Quantum Heisenberg Chains of Sr2CuO3

A model of mobile-bond defects is tentatively proposed to analyze the "anomalies" observed on the NMR spectrum of the quantum Heisenberg chains of Sr2CuO3. A bond-defect is a local change in the exchange coupling. It results in a local alternating magnetization (LAM), which when the defect moves, creates a flipping process of the local field seen by each nuclear spin. At low temperature, when the overlap of the LAM becomes large, the defects form a periodic structure, which extends over almost all the chains. In that regime, the density of bond-defects decreases linearly with T.Comment: 4 pages + 3 figures. To appear in Physical Review

Amp\`ere-Class Pulsed Field Emission from Carbon-Nanotube Cathodes in a Radiofrequency Resonator

Pulsed field emission from cold carbon-nanotube cathodes placed in a radiofrequency resonant cavity was observed. The cathodes were located on the backplate of a conventional $1+\frac{1}{2}$-cell resonant cavity operating at 1.3-GHz and resulted in the production of bunch train with maximum average current close to 0.7 Amp\`ere. The measured Fowler-Nordheim characteristic, transverse emittance, and pulse duration are presented and, when possible, compared to numerical simulations. The implications of our results to high-average-current electron sources are briefly discussed.Comment: 5 pages, 6 figures; submitted to Applied Physics Letter

Polarized distribution of HCO3- transport in human normal and cystic fibrosis nasal epithelia

The polarized distribution of HCO3− transport was investigated in human nasal epithelial cells from normal and cystic fibrosis (CF) tissues. To test for HCO3− transport via conductive versus electroneutral Cl−/HCO3− exchange (anion exchange, AE) pathways, nasal cells were loaded with the pH probe 2′,7′-bis(carboxyethyl)-5(6)-carboxyfluorescein and mounted in a bilateral perfusion chamber. In normal, but not CF, epithelia, replacing mucosal Cl− with gluconate caused intracellular pH (pHi) to increase, and the initial rates (ΔpH min−1) of this increase were modestly augmented (∼26 %) when normal cells were pretreated with forskolin (10 μm). Recovery from this alkaline shift was dependent on mucosal Cl−, was insensitive to the AE inhibitor 4,4′-diisothiocyanatodihydrostilbene-2,2′-disulfonic acid (H2DIDS; 1.5 mm), but was sensitive to the cystic fibrosis transmembrane conductance regulator (CFTR) channel inhibitor diphenylamine-2-carboxylate (DPC; 100 μm). In contrast, removal of serosal Cl− caused pHi to alkalinize in both normal and CF epithelia. Recovery from this alkaline challenge was dependent on serosal Cl− and blocked by H2DIDS. Additional studies showed that serosally applied Ba2+ (5.0 mm) in normal, but not CF, cells induced influx of HCO3− across the apical membrane that was reversibly blocked by mucosal DPC. In a final series of studies, normal and CF cells acutely alkaline loaded by replacing bilateral Krebs bicarbonate Ringer (KBR) with Hepes-buffered Ringer solution exhibited basolateral, but not apical, recovery from an alkaline challenge that was dependent on Cl−, independent of Na+ and blocked by H2DIDS. We conclude that: (1) normal, but not CF, nasal epithelia have a constitutively active DPC-sensitive HCO3− influx/efflux pathway across the apical membrane of cells, consistent with the movement of HCO3− via CFTR; and (2) both normal and CF nasal epithelia have Na+-independent, H2DIDS-sensitive AE at their basolateral domain

Polarized Signaling via Purinoceptors in Normal and Cystic Fibrosis Airway Epithelia

Airway epithelia are confronted with distinct signals emanating from the luminal and/or serosal environments. This study tested whether airway epithelia exhibit polarized intracellular free calcium (Ca2+i) and anion secretory responses to 5′ triphosphate nucleotides (ATP/UTP), which may be released across both barriers of these epithelia. In both normal and cystic fibrosis (CF) airway epithelia, mucosal exposure to ATP/UTP increased Ca2+i and anion secretion, but both responses were greater in magnitude for CF epithelia. In CF epithelia, the mucosal nucleotide–induced response was mediated exclusively via Ca2+i interacting with a Ca2+-activated Cl− channel (CaCC). In normal airway epithelia (but not CF), nucleotides stimulated a component of anion secretion via a chelerythrine-sensitive, Ca2+-independent PKC activation of cystic fibrosis transmembrane conductance regulator. In normal and CF airway epithelia, serosally applied ATP or UTP were equally effective in mobilizing Ca2+i. However, serosally applied nucleotides failed to induce anion transport in CF epithelia, whereas a PKC-regulated anion secretory response was detected in normal airway epithelia. We conclude that (1) in normal nasal epithelium, apical/basolateral purinergic receptor activation by ATP/UTP regulates separate Ca2+-sensitive and Ca2+-insensitive (PKC-mediated) anion conductances; (2) in CF airway epithelia, the mucosal ATP/UTP-dependent anion secretory response is mediated exclusively via Ca2+i; and (3) Ca2+i regulation of the Ca2+-sensitive anion conductance (via CaCC) is compartmentalized in both CF and normal airway epithelia, with basolaterally released Ca2+i failing to activate CaCC in both epithelia

Tetramerisation of a frustrated spin-1/2 chain

We investigate a model of a frustrated spin-1/2 Heisenberg chain coupled to adiabatic phonons with a general form of magnetoelastic coupling. For large enough frustration and lattice coupling a new tetramerised phase with three different bond lengths is found. We argue that the zig-zag spin-1/2 chain LiV$_2$O$_5$ might be a good candidate to observe such a phase

RLZAP: Relative Lempel-Ziv with Adaptive Pointers

Relative Lempel-Ziv (RLZ) is a popular algorithm for compressing databases of genomes from individuals of the same species when fast random access is desired. With Kuruppu et al.'s (SPIRE 2010) original implementation, a reference genome is selected and then the other genomes are greedily parsed into phrases exactly matching substrings of the reference. Deorowicz and Grabowski (Bioinformatics, 2011) pointed out that letting each phrase end with a mismatch character usually gives better compression because many of the differences between individuals' genomes are single-nucleotide substitutions. Ferrada et al. (SPIRE 2014) then pointed out that also using relative pointers and run-length compressing them usually gives even better compression. In this paper we generalize Ferrada et al.'s idea to handle well also short insertions, deletions and multi-character substitutions. We show experimentally that our generalization achieves better compression than Ferrada et al.'s implementation with comparable random-access times

On the Asymptotic Stability of De-Sitter Spacetime: a non-linear perturbative approach

We derive evolution and constraint equations for second order perturbations of flat dust homogeneous and isotropic solutions to the Einstein field equations using all scalar, vector and tensor perturbation modes. We show that the perturbations decay asymptotically in time and that the solutions converge to the De-Sitter solution. By induction, this result is valid for perturbations of arbitrary order. This is in agreement with the cosmic no-hair conjecture of Gibbons and Hawking.Comment: 11 pages, 2 figure

The Mitochondrial Barriers Segregate Agonist-induced Calcium-dependent Functions in Human Airway Epithelia

In airway epithelia, purinergic receptor (P2Y2-R) stimulation of intracellular calcium (Ca2+i)–regulated ion transport is restricted to the membrane domain ipsilateral to receptor activation, implying compartmentalization of Ca2+i signaling. Because mitochondria can spatially restrict cellular Ca2+i signals, immunocytochemical, electron microscopic, and fluorescent studies of mitochondria localization were performed in human airway epithelia. Although concentrated at the apical domain, mitochondria were found distributed at both the apical and the basolateral poles and in close association with the endoplasmic reticulum. The role of mitochondria in locally restricting P2Y2-R–induced Ca2+i signals was investigated by measuring changes in mitochondrial Ca2+ (Ca2+m) in human airway epithelial monolayers. P2Y2-R activation induced Ca2+m accumulation in mitochondria confined to the domain ipsilateral to P2Y2-R stimulation, which was blocked by mitochondrial uncoupling with 1 μM CCCP and 2.5 μg/ml oligomycin. The role of mitochondria in restricting the cellular cross-talk between basolateral P2Y2-R–dependent Ca2+i mobilization and apical membrane Ca2+-activated Cl− secretion was investigated in studies simultaneously measuring Ca2+i and Cl− secretion in cystic fibrosis human airway epithelial monolayers. Activation of basolateral P2Y2-Rs produced similar increases in Ca2+i in monolayers without and with pretreatment with uncouplers, whereas Ca2+i-activated Cl− secretion was only efficiently triggered in mitochondria-uncoupled conditions. We conclude that (a) mitochondria function as a Ca2+i-buffering system in airway epithelia, compartmentalizing Ca2+i-dependent functions to the membrane ipsilateral to receptor stimulation; and (b) the mitochondria provide structural barriers that protect the airway epithelia against nonspecific activation of Ca2+i-modulated functions associated with Ca2+i signals emanating from the apical or the basolateral membrane domains