bluuebunny/crossref_metadata_2025 huggingface dataset:
LncRNA‐ATB mediated E‐cadherin repression promotes the progression of colon cancer and predicts poor prognosis
Authors: Yue Ben , Qiu Shenglong , Zhao Senlin , Liu Chenchen , Zhang Dongyuan , Yu Fudong , Peng Zhihai , Yan Dongwang
Published: October 2015

Background

Long non‐coding RNA‐activated by TGF‐β (lncRNA‐ATB) promotes the invasion–metastasis cascade in hepatocellular carcinoma via downregulating E‐cadherin (E‐cad) and inducing epithelial‐to‐ mesenchymal transition (EMT) and is clinically significant in human colon cancer. However, its molecular mechanisms in colon cancer progression remain unclear. This study aimed to elucidate the role of lncRNA‐ATB and its clinical value in colon cancer.

Methods

Expression levels of lncRNA‐ATB in colon cancer tissues and colon cancer cell lines were evaluated using quantitative real‐time polymerase chain reaction. The clinicopathological significance and prognostic value of lncRNA‐ATB were investigated, and roles of lncRNA‐ATB in regulating E‐cad and other EMT‐related markers expression and colon cancer progression were evaluated in vitro. Expression levels of lncRNA‐ATB and E‐cad in human plasma were evaluated.

Results

Long non‐coding RNA‐activated by TGF‐β was upregulated in colon cancer tissues compared with adjacent mucosa (P < 0.001). LncRNA‐ATB levels were also higher in metastatic cancer tissues (P < 0.001). Among the three highly invasive colon cancer cell lines, lncRNA‐ATB levels were relatively higher with concurrent low levels of E‐cad compared with levels in the three low‐invasive cell lines. LncRNA‐ATB expression correlated with pN stage (P < 0.01) and American Joint Committee on Cancer stage (P < 0.01). Striking differences were observed in overall survival and disease‐free survival in cases with both high lncRNA‐ATB expression and low E‐cad expression. Reduction of lncRNA‐ATB increased expression of epithelial markers E‐cad, ZO‐1, and decreased expression of mesenchymal markers ZEB1 and N‐cadherin (N‐cad), and significantly influenced colon cancer cell progression. Plasma lncRNA‐ATB was upregulated in colon cancer patients one month after surgery (P < 0.05).

Conclusions

Long non‐coding RNA‐activated by TGF‐β may act on colon tumorigenesis by suppressing E‐cad expression and promoting EMT process, and lncRNA‐ATB inhibition may provide a promising therapeutic option for suppressing colon cancer progression.
The pleiotropic ABNORMAL FLOWER AND DWARF1 affects plant height, floral development and grain yield in rice
Authors: Ren Deyong , Rao Yuchun , Wu Liwen , Xu Qiankun , Li Zizhuang , Yu Haiping , Zhang Yu , Leng Yujia , Hu Jiang , Zhu Li , Gao Zhenyu , Dong Guojun , Zhang Guangheng , Guo Longbiao , Zeng Dali , Qian Qian
Published: October 2015

Moderate plant height and successful establishment of reproductive organs play pivotal roles in rice grain production. The molecular mechanism that controls the two aspects remains unclear in rice. In the present study, we characterized a rice gene, ABNORMAL FLOWER AND DWARF1 (AFD1) that determined plant height, floral development and grain yield. The afd1 mutant showed variable defects including the dwarfism, long panicle, low seed setting and reduced grain yield. In addition, abnormal floral organs were also observed in the afd1 mutant including slender and thick hulls, and hull‐like lodicules. AFD1 encoded a DUF640 domain protein and was expressed in all tested tissues and organs. Subcellular localization showed AFD1‐green fluorescent fusion protein (GFP) was localized in the nucleus. Meantime, our results suggested that AFD1 regulated the expression of cell division and expansion related genes.
Evaluation of Mandibular Movement Functions Using Instrumental Ultrasound System
Authors: Sójka Anna , Huber Juliusz , Kaczmarek Elżbieta , Hędzelek Wiesław
Published: October 2015

Purpose

The article deals with routinely performed instrumental temporomandibular joint (TMJ) examinations and interpretation of findings obtained from the Arcus Digma ultrasound device in individuals with or without clinical symptoms of temporomandibular disorders (TMD). The aim of this study was to analyze mandibular movement functions and the relationship between incisors and condylar movement parameters during jaw opening, which may be helpful for clinical evaluation in these patients.

Materials and methods

The study group consisted of 84 young students with no dental problems and other serious acute or chronic diseases in the medical history; the students were examined both clinically and with the Arcus Digma ultrasound device.

Results

Helkimo Di = I was the most common score in 49 participants, and Helkimo Di = II in a significantly (p < 0.01, Di = I vs. Di = II) smaller number of participants. Medical history revealed symptoms of unilateral mastication in 15 participants and a statistically significant increased (p < 0.02, participants with symptoms of unilateral mastication vs. asymptomatic) condylar range of motion parameter during retrusion. Also a significant decrease (p < 0.03, participants with symptoms of unilateral mastication vs. asymptomatic) of the incisal and condylar ranges of motion during mouth opening was found. Limitation of mouth opening, defined as a decrease of inter‐incisal distance, appeared in 19 participants (22.6%) and in 25 participants (29.8%) measured instrumentally with the Arcus Digma device. A comparison of instrumental result examinations of the right and left TMJs showed positive correlations of the range of mandible opening movement with the Posselt opening movement (r = 0.75) and opening/closing movements with the Posselt closing movements (r = 0.70). A correlation was demonstrated (r = 0.81) between the condylar range of motion studied on the left and on the right TMJ during mandible opening movement. Correlations were also found between opening‐closing movements and the condylar range of motion of the left TMJ, and between the opening‐closing movement and the condylar range of motion of the right TMJ during the opening movement.

Conclusions

According to the results of this study with instrumental Arcus Digma ultrasound device measurements of mandibular movements, data were provided on irregularities in TMJ function not detected in participants with or without clinical symptoms of TMD.
Impact of land cover changes and topography on soil quality in the Kasso catchment, Bale Mountains of southeastern Ethiopia
Authors: Warra Hussein Haycho , Ahmed Mohammed Assen , Nicolau Melanie D.
Published: October 2015

This study assessed land cover change and topographic elevation on selected soil quality parameters in the Kasso catchment, southeastern Ethiopia. Twenty‐seven soil samples collected from 0–30cm depth under four land cover types across three elevation gradients were analysed for selected soil quality parameters. Results indicated that soil particle size distribution is different (p<0.001) in the catchment because of the effect of land cover change and elevation. Most cultivated lands occupy lower elevations where clay accumulates as a result of its movement from higher to lower elevations. Ploughing accentuates weathering, making cultivated lands richer in finer materials. Cation exchange capacity and exchangeable magnesium and potassium negatively correlated with elevation, total nitrogen and available phosphorous. Conversion of natural vegetation to cropland contributed to changes in pH (p<0.05), exchangeable calcium (p<0.01), potassium (p<0.001), available phosphorous (p<0.01) and nitrogen (p<0.01) contents. Parameter soil degradation index results showed that soil organic carbon, nitrogen, available phosphorous and exchangeable potassium contents declined and bulk density increased because of the land cover change. This negative effect on agricultural development and environmental health of the catchment makes an integrated land resource management approach indispensable for sustaining agricultural productivity and the environmental health of the Kasso catchment.
Burn depth assessments by photoacoustic imaging and laser Doppler imaging
Authors: Ida Taiichiro , Iwazaki Hideaki , Kawaguchi Yasushi , Kawauchi Satoko , Ohkura Tsuyako , Iwaya Keiichi , Tsuda Hitoshi , Saitoh Daizoh , Sato Shunichi , Iwai Toshiaki
Published: October 2015

Diagnosis of burn depths is crucial to determine the treatment plan for severe burn patients. However, an objective method for burn depth assessment has yet to be established, although a commercial laser Doppler imaging (LDI) system is used limitedly. We previously proposed burn depth assessment based on photoacoustic imaging (PAI), in which thermoelastic waves originating from blood under the burned tissue are detected, and we showed the validity of the method by experiments using rat models with three different burn depths: superficial dermal burn, deep dermal burn and deep burn. On the basis of those results, we recently developed a real‐time PAI system for clinical burn diagnosis. Before starting a clinical trial, however, there is a need to reveal more detailed diagnostic characteristics, such as linearity and error, of the PAI system as well as to compare its characteristics with those of an LDI system. In this study, we prepared rat models with burns induced at six different temperatures from 70 to 98 °C, which showed a linear dependence of injury depth on the temperature. Using these models, we examined correlations of signals obtained by PAI and LDI with histologically determined injury depths and burn induction temperatures at 48 hours postburn. We found that the burn depths indicated by PAI were highly correlative with histologically determined injury depths (depths of viable vessels) as well as with burn induction temperatures. Perfusion values measured by LDI were less correlative with these parameters, especially for burns induced at higher temperatures, being attributable to the limited detectable depth for light involving a Doppler shift in tissue. In addition, the measurement errors in PAI were smaller than those in LDI. On the basis of these results, we will be able to start clinical studies using the present PAI system.
Proteolytic fragmentation of inositol 1,4,5‐trisphosphate receptors: a novel mechanism regulating channel activity?
Authors: Wang Liwei , Alzayady Kamil J. , Yule David I.
Published: October 2015

Inositol 1,4,5‐trisphosphate receptors (IP3Rs) are a family of ubiquitously expressed intracellular Ca2+ release channels. Regulation of channel activity by Ca2+, nucleotides, phosphorylation, protein binding partners and other cellular factors is thought to play a major role in defining the specific spatiotemporal characteristics of intracellular Ca2+ signals. These properties are, in turn, believed pivotal for the selective and specific physiological activation of Ca2+‐dependent effectors. IP3Rs are also substrates for the intracellular cysteine proteases, calpain and caspase. Cleavage of the IP3R has been proposed to play a role in apoptotic cell death by uncoupling regions important for IP3 binding from the channel domain, leaving an unregulated leaky Ca2+ pore. Contrary to this hypothesis, we demonstrate following proteolysis that N‐ and C‐termini of IP3R1 remain associated, presumably through non‐covalent interactions. Further, we show that complementary fragments of IP3R1 assemble into tetrameric structures and retain their ability to be regulated robustly by IP3. While peptide continuity is clearly not necessary for IP3‐gating of the channel, we propose that cleavage of the IP3R peptide chain may alter other important regulatory events to modulate channel activity. In this scenario, stimulation of the cleaved IP3R may support distinct spatiotemporal Ca2+ signals and activation of specific effectors. Notably, in many adaptive physiological events, the non‐apoptotic activities of caspase and calpain are demonstrated to be important, but the substrates of the proteases are poorly defined. We speculate that proteolytic fragmentation may represent a novel form of IP3R regulation, which plays a role in varied adaptive physiological processes.

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Essential role of carbonic anhydrase XII in secretory gland fluid and HCO3− secretion revealed by disease causing human mutation
Authors: Hong Jeong Hee , Muhammad Emad , Zheng Changyu , Hershkovitz Eli , Alkrinawi Soliman , Loewenthal Neta , Parvari Ruti , Muallem Shmuel
Published: October 2015

Key points

Fluid and HCO3− secretion is essential for all epithelia; aberrant secretion is associated with several diseases.

Carbonic anhydrase XII (CA12) is the key carbonic anhydrase in epithelial fluid and HCO3− secretion and works by activating the ductal Cl−–HCO3− exchanger AE2.

Delivery of CA12 to salivary glands increases salivation in mice and of the human mutation CA12(E143K) markedly inhibits it.

The human mutation CA12(E143K) causes disease due to aberrant CA12 glycosylation, and misfolding resulting in loss of AE2 activity.

Aberrant epithelial fluid and HCO3− secretion is associated with many diseases. The activity of HCO3− transporters depends of HCO3− availability that is determined by carbonic anhydrases (CAs). Which CAs are essential for epithelial function is unknown. CA12 stands out since the CA12(E143K) mutation causes salt wasting in sweat and dehydration in humans. Here, we report that expression of CA12 and of CA12(E143K) in mice salivary glands respectively increased and prominently inhibited ductal fluid secretion and salivation in vivo. CA12 markedly increases the activity and is the major HCO3− supplier of ductal Cl−–HCO3− exchanger AE2, but not of NBCe1‐B. The E143K mutation alters CA12 glycosylation at N28 and N80, resulting in retention of the basolateral CA12 in the ER. Knockdown of AE2 and of CA12 inhibited pancreatic and salivary gland ductal AE2 activity and fluid secretion. Accordingly, patients homozygous for the CA12(E143K) mutation have a dry mouth, dry tongue phenotype. These findings reveal an unsuspected prominent role of CA12 in epithelial function, explain the disease and call for caution in the use of CA12 inhibitors in cancer treatment.
Intrinsic muscle clock is necessary for musculoskeletal health
Authors: Schroder Elizabeth A. , Harfmann Brianna D. , Zhang Xiping , Srikuea Ratchakrit , England Jonathan H. , Hodge Brian A. , Wen Yuan , Riley Lance A. , Yu Qi , Christie Alexander , Smith Jeffrey D. , Seward Tanya , Wolf Horrell Erin M. , Mula Jyothi , Peterson Charlotte A. , Butterfield Timothy A. , Esser Karyn A.
Published: October 2015

Key points

The endogenous molecular clock in skeletal muscle is necessary for maintenance of phenotype and function.

Loss of Bmal1 solely from adult skeletal muscle (iMSBmal1−/−) results in reductions in specific tension, increased oxidative fibre type and increased muscle fibrosis with no change in feeding or activity.

Disruption of the molecular clock in adult skeletal muscle is sufficient to induce changes in skeletal muscle similar to those seen in the Bmal1 knockout mouse (Bmal1−/−), a model of advanced ageing.

iMSBmal1−/− mice develop increased bone calcification and decreased joint collagen, which in combination with the functional changes in skeletal muscle results in altered gait.

This study uncovers a fundamental role for the skeletal muscle clock in musculoskeletal homeostasis with potential implications for ageing.

Disruption of circadian rhythms in humans and rodents has implicated a fundamental role for circadian rhythms in ageing and the development of many chronic diseases including diabetes, cardiovascular disease, depression and cancer. The molecular clock mechanism underlies circadian rhythms and is defined by a transcription–translation feedback loop with Bmal1 encoding a core molecular clock transcription factor. Germline Bmal1 knockout (Bmal1 KO) mice have a shortened lifespan, show features of advanced ageing and exhibit significant weakness with decreased maximum specific tension at the whole muscle and single fibre levels. We tested the role of the molecular clock in adult skeletal muscle by generating mice that allow for the inducible skeletal muscle‐specific deletion of Bmal1 (iMSBmal1). Here we show that disruption of the molecular clock, specifically in adult skeletal muscle, is associated with a muscle phenotype including reductions in specific tension, increased oxidative fibre type, and increased muscle fibrosis similar to that seen in the Bmal1 KO mouse. Remarkably, the phenotype observed in the iMSBmal1−/− mice was not limited to changes in muscle. Similar to the germline Bmal1 KO mice, we observed significant bone and cartilage changes throughout the body suggesting a role for the skeletal muscle molecular clock in both the skeletal muscle niche and the systemic milieu. This emerging area of circadian rhythms and the molecular clock in skeletal muscle holds the potential to provide significant insight into intrinsic mechanisms of the maintenance of muscle quality and function as well as identifying a novel crosstalk between skeletal muscle, cartilage and bone.
Viscoplastic Modeling of the Green Anode Paste Compaction Process
Authors: Chaouki H. , Picard D. , Ziegler D. , Azari K. , Alamdari H. , Fafard M.
Published: October 2015

The aim of this work is to simulate the forming process of green anodes. For this purpose, a nonlinear compressible viscoplastic constitutive law is presented. The concept of natural reference configuration is considered. Within an isothermal thermodynamic framework, a Helmholtz free energy is proposed to take into account the nonlinear compressible deformation process occurring between natural reference configuration and current configuration. A dissipation potential is introduced in order to characterize the irreversible aspect of compaction process. The constitutive law is thus formulated through two equations: (1) an expression of Cauchy stress tensor and (2) a differential equation characterizing the evolution of the natural reference configuration. Material parameters are assumed to be a function of the apparent green density. An experimental study is carried out in order to characterize the compaction behavior of the anode paste. A user's material VUMAT subroutine for finite-element dynamic explicit analysis has been developed and implemented in the abaqus commercial software. To evaluate the model predictive capability, numerical simulations of the compaction forming process of anode paste were performed. Simulation results show that the constitutive law predicts the experimental trends and gives insight of physical responses. This constitutes a first step toward characterizing the anode paste behavior and making a benchmark with experimental results on the forming process of anode paste.
An Emulator-Based Prediction of Dynamic Stiffness for Redundant Parallel Kinematic Mechanisms
Authors: Luces Mario , Boyraz Pinar , Mahmoodi Masih , Keramati Farhad , Mills James K. , Benhabib Beno
Published: October 2015

The accuracy of a parallel kinematic mechanism (PKM) is directly related to its dynamic stiffness, which in turn is configuration dependent. For PKMs with kinematic redundancy, configurations with higher stiffness can be chosen during motion-trajectory planning for optimal performance. Herein, dynamic stiffness refers to the deformation of the mechanism structure, subject to dynamic loads of changing frequency. The stiffness-optimization problem has two computational constraints: (i) calculation of the dynamic stiffness of any considered PKM configuration, at a given task-space location, and (ii) searching for the PKM configuration with the highest stiffness at this location. Due to the lack of available analytical models, herein, the former subproblem is addressed via a novel effective emulator to provide a computationally efficient approximation of the high-dimensional dynamic-stiffness function suitable for optimization. The proposed method for emulator development identifies the mechanism's structural modes in order to breakdown the high-dimensional stiffness function into multiple functions of lower dimension. Despite their computational efficiency, however, emulators approximating high-dimensional functions are often difficult to develop and implement due to the large amount of data required to train the emulator. Reducing the dimensionality of the approximation function would, thus, result in a smaller training data set. In turn, the smaller training data set can be obtained accurately via finite-element analysis (FEA). Moving least-squares (MLS) approximation is proposed herein to compute the low-dimensional functions for stiffness approximation. Via extensive simulations, some of which are described herein, it is demonstrated that the proposed emulator can predict the dynamic stiffness of a PKM at any given configuration with high accuracy and low computational expense, making it quite suitable for most high-precision applications. For example, our results show that the proposed methodology can choose configurations along given trajectories within a few percentage points of the optimal ones.
Static Load Distribution and Axial Stiffness in a Planetary Roller Screw Mechanism
Authors: Abevi Folly , Daidie Alain , Chaussumier Michel , Sartor Marc
Published: October 2015

In this paper, an original approach is proposed to calculate the static load distribution and the axial stiffness of a planetary roller screw (PRS) mechanism. Assuming that the external loading is shared equally over an arbitrary number of rollers, only a sector of the system is represented to save on computing time. The approach consists in using a structure of bars, beams, and nonlinear springs to model the different components of the mechanism and their interactions. This nonlinear model describes the details of the mechanism and captures the shape of the nut as well as the bending deformation of the roller. All materials are assumed to operate in the elastic range. The load distribution and the axial stiffness are determined in three specific configurations of the system for both compressive and tensile loads. Further, the influence of the shape of the nut is studied in the case of the inverted PRS. The results obtained from this approach are also compared to those computed with a three-dimensional finite-element (3D FE) model. Finally, since the calculations appear to be very accurate, a parametric study is conducted to show the impact of the bending of the roller on the load distribution.
Research Trends in Adapted Physical Activity Quarterly From 2004 to 2013
Authors: Haegele Justin A. , Lee Jihyun , Porretta David L.
Published: October 2015

The purpose of this documentary analysis was to examine trends in research published in Adapted Physical Activity Quarterly (APAQ) over a 10-yr span. A total of 181 research articles published from 2004 to 2013 were coded and analyzed using the following categories: first-author country affiliation, theoretical framework, intervention, research methods, disability categories, and topical focus. Results indicate high frequencies of nonintervention and group-design studies, as well as a low frequency of studies that describe a theoretical or conceptual framework. Trends in disability of participants and topical focus reflect current interests of researchers publishing in APAQ. While some scholars have suggested that changes in research on adapted physical activity would occur, the results of this analysis suggest that many of these categories remain largely unchanged for research published in APAQ. This study calls attention to similarities between the results of the current analysis and previous ones.
The Role of Physical Activity and Physical Function on the Risk of Falls in Older Mexican Americans
Authors: Lewis Zakkoyya H. , Markides Kyriakos S. , Ottenbacher Kenneth J. , Al Snih Soham
Published: October 2015

We investigated the relationship between physical activity and physical function on the risk of falls over time in a cohort of Mexican-American adults aged 75 and older from the Hispanic Established Population for the Epidemiologic Study of the Elderly (H-EPESE). Participants were divided into four groups according to their level of physical activity and physical function: low physical activity and low physical function (n = 453); low physical activity and high physical function (n = 54); high physical activity and low physical function (n = 307); and high physical activity and high physical function (n = 197). Using generalized linear equation estimation, we showed that participants with high physical activity and low physical function had a greater fall risk over time, followed by the high physical activity and high physical function group. Participants seldom took part in activities that improve physical function. To prevent falls, modifications to physical activity should be made for older Mexican Americans.
Effect of triiodothyronine (T3) excess on fatty acid metabolism in the soleus muscle from endurance-trained rats
Authors: Górecka M. , Synak M. , Brzezińska Z. , Dąbrowski J. , Żernicka E.
Published: October 2015

We studied whether short-term administration of triiodothyronine (T3) for the last 3 days of endurance training would influence the rate of uptake of palmitic acid (PA) as well as metabolism in rat soleus muscle, in vitro. Training per se did not affect the rate of PA uptake by the soleus; however, an excess of T3increased the rate of this process at 1.5 mmol/L PA, as well as the rate that at which PA was incorporated into intramuscular triacylglycerols (TG). The rate of TG synthesis in trained euthyroid rats was reduced after exercise (1.5 mmol/L PA). The rate of PA oxidation in all of the trained rats immediately after exercise was enhanced by comparison with the sedentary values. Hyperthyroidism additionally increased the rate of this process at 1.5 mmol/L PA. After a recovery period, the rate of PA oxidation returned to the control values in both the euthyroid and the hyperthyroid groups. Examination of the high-energy phosphate levels indicated that elevated PA oxidation after exercise-training in euthyroid rats was associated with stable ATP levels and increased ADP and AMP levels, thus reducing energy cellular potential (ECP). In the hyperthyroid rats, levels of ADP and AMP were increased in the sedentary as well as the exercise-trained rats. ECP levels were high as a result of high levels of ATP and decreased levels of ADP and AMP in hyperthyroid rats after the recovery period. In conclusion, short-term hyperthyroidism accelerates PA utilization in well-trained soleus muscle.
Efficiency Re-Climbing in High-Current Droop Regime for Gallium-Nitride-based Light-Emitting Diodes
Authors: Lin Guan-Bo , Schubert E. Fred
Published: October 2015

The efficiency droop in GaInN/GaN blue light-emitting diodes (LEDs) usually commences at current density around 10 A/cm2 and the efficiency decreases monotonically after the droop onset. GaN-based LEDs suffer seriously, at typical operating current densities (10–100 A/cm2), by the efficiency droop. Efficiency re-climbing is observed in the typical droop regime at cryogenic temperatures below 125K. The “efficiency re-climbing” coincides with a distinct increase in device conductivity, which is mainly attributed to an enhancement in p-type conductivity due to field ionization of acceptors. The “efficiency re-climbing” phenomenon implies an approach of solving efficiency droop by enhancing hole injection by external electric field.
High Speed All Optical Logic Gates Using Binary Phase Shift Keyed Signal Based On QD-SOA
Authors: Li Wenbo , Hu Hongyu , Zhang Xiang , Dutta Niloy K.
Published: October 2015

A scheme to realize all-optical Boolean logic functions, XOR, AND and NAND operations using binary phase shift keyed (BPSK) signal based on quantum-dot semiconductor optical amplifiers (QD-SOA) has been designed and studied. Nonlinear dynamics including carrier heating and spectral hole-burning are taken into account together with the rate equations. We demonstrate XOR, AND and NAND operations at 250Gb/s using a pair of QD-SOA Mach-Zehnder interferometers. Results show that this scheme is suitable for high speed all-optical Boolean logic operations and can improve the output quality comparing with the system using on-off-keyed (OOK) signal.
The framed Standard Model (I) — A physics case for framing the Yang–Mills theory?
Authors: Chan Hong-Mo , Tsou Sheung Tsun
Published: October 2015

Introducing, in the underlying gauge theory of the Standard Model, the frame vectors in internal space as field variables (framons), in addition to the usual gauge boson and matter fermions fields, one obtains:

the standard Higgs scalar as the framon in the electroweak sector; a global [Formula: see text] symmetry dual to colour to play the role of fermion generations.

Renormalization via framon loops changes the orientation in generation space of the vacuum, hence also of the mass matrices of leptons and quarks, thus making them rotate with changing scale [Formula: see text]. From previous work, it is known already that a rotating mass matrix will lead automatically to:

CKM mixing and neutrino oscillations, hierarchical masses for quarks and leptons, a solution to the strong-CP problem transforming the theta-angle into a Kobayashi–Maskawa phase.

Here in the framed standard model (FSM), the renormalization group equation has some special properties which explain the main qualitative features seen in experiment both for mixing matrices of quarks and leptons, and for their mass spectrum. Quantitative results will be given in Paper II. The present paper ends with some tentative predictions on Higgs decay, and with some speculations on the origin of dark matter.
Analysis of the Zc(4200) as axial-vector molecule-like state
Authors: Wang Zhi-Gang
Published: October 2015

In this paper, we assume the [Formula: see text] as the color octet–octet type axial-vector molecule-like state, and construct the color octet–octet type axial-vector current to study its mass and width with the QCD sum rules. The numerical values [Formula: see text] and [Formula: see text] are consistent with the experimental data [Formula: see text] and [Formula: see text], and support assigning the [Formula: see text] to be the color octet–octet type molecule-like state with [Formula: see text]. Furthermore, we discuss the possible assignments of the [Formula: see text], [Formula: see text] and [Formula: see text] as the diquark–antidiquark type tetraquark states with [Formula: see text].
Emergence of Lowenstein–Zimmermann mass terms for QED3
Authors: Upadhyay Sudhaker , Dwivedi Manoj Kumar , Mandal Bhabani Prasad
Published: October 2015

In this paper we consider a super-renormalizable theory of massless QED in (2 + 1) dimensions and discuss their BRST symmetry transformation. By extending the BRST transformation, we derive the Nielsen identities for the theory. Further, we compute the generalized BRST (so-called FFBRST) transformation by making the transformation parameter field dependent. Remarkably, we observe that the Lowenstein–Zimmermann mass terms, containing Lowenstein–Zimmermann parameter which plays an important role in the BPHZL renormalization program, along with the external sources coupled to the nonlinear BRST variations appear naturally in the theory through an FFBRST transformation.
Semiclassical intrinsic localized modes in the β-Fermi–Pasta–Ulam lattice model with first- and second-nearest neighbor interactions
Authors: Yao Ying-Bo , Li De-Jun , Tang Bing
Published: October 2015

We present an analytical study on intrinsic localized modes (ILMs) in the quantum [Formula: see text]-Fermi–Pasta–Ulam lattice model with first- and second-nearest neighbor interactions by means of the semiclassical approach. We quantize the lattice model Hamiltonian by introducing vibron creation and annihilation operators, and retaining only number conserving terms. The coherent state representation is considered as the basic representation of the quantum lattice system. In order to obtain the ILM solutions, we adopt the multiple scales method combined with a quasidiscreteness approximation. It is found that, when the system parameters satisfy [Formula: see text], at the Brillouin zone (BZ) boundary, a bright ILM occurs above the top of the harmonic wave frequency band. While for [Formula: see text], our results indicate that at wave number [Formula: see text] a bright ILM occurs above the top of the harmonic wave frequency band and at the BZ boundary, the system support a dark intrinsic localized resonant mode.
2-Methoxyestradiol blocks the RhoA/ROCK1 pathway in human aortic smooth muscle cells
Authors: Rigassi Lisa , Barchiesi Bozzolo Federica , Lucchinetti Eliana , Zaugg Michael , Fingerle Jürgen , Rosselli Marinella , Imthurn Bruno , Jackson Edwin K. , Dubey Raghvendra K.
Published: October 2015

2-Methoxyestradiol (2-ME), a metabolite of estradiol with little affinity for estrogen receptors, inhibits proliferation of vascular smooth muscle cells; however, the molecular mechanisms underlying this effect are incompletely understood. Our previous work shows that 2-ME inhibits initiation (blocks phosphorylation of ERK and Akt) and progression (reduces cyclin expression and increases expression of cyclin inhibitors) of the mitogenic pathway and interferes with mitosis (disrupts tubulin organization). Because the RhoA/ROCK1 pathway (RhoA → ROCK1 → myosin phosphatase targeting subunit → myosin light chain) is involved in cytokinesis, herein we tested the concept that 2-ME also blocks the RhoA/ROCK1 pathway. Because of the potential importance of 2-ME for preventing/treating vascular diseases, experiments were conducted in female human aortic vascular smooth muscle cells. Microarray transcriptional profiling suggested an effect of 2-ME on the RhoA/ROCK1 pathway. Indeed, 2-ME blocked mitogen-induced GTP-bound RhoABC expression and membrane-bound RhoA, suggesting interference with the activation of RhoA. 2-ME also reduced ROCK1 expression, suggesting reduced production of the primary downstream signaling kinase of the RhoA pathway. Moreover, 2-ME inhibited RhoA/ROCK1 pathway downstream signaling, including phosphorylated myosin phosphatase targeting subunit and myosin light chain; the ROCK1 inhibitor H-1152 mimicked these effects of 2-ME; both 2-ME and H-1152 blocked cytokinesis. 2-ME also reduced the expression of tissue factor, yet another downstream signaling component of the RhoA/ROCK1 pathway. We conclude that 2-ME inhibits the pathway RhoA → ROCK1 → myosin phosphatase targeting subunit → myosin light chain, and this likely contributes to the reduced cytokinesis in 2-ME treated HASMCs.
Ingestion of glucose or sucrose prevents liver but not muscle glycogen depletion during prolonged endurance-type exercise in trained cyclists
Authors: Gonzalez Javier T. , Fuchs Cas J. , Smith Fiona E. , Thelwall Pete E. , Taylor Roy , Stevenson Emma J. , Trenell Michael I. , Cermak Naomi M. , van Loon Luc J. C.
Published: October 2015

The purpose of this study was to define the effect of glucose ingestion compared with sucrose ingestion on liver and muscle glycogen depletion during prolonged endurance-type exercise. Fourteen cyclists completed two 3-h bouts of cycling at 50% of peak power output while ingesting either glucose or sucrose at a rate of 1.7 g/min (102 g/h). Four cyclists performed an additional third test for reference in which only water was consumed. We employed 13C magnetic resonance spectroscopy to determine liver and muscle glycogen concentrations before and after exercise. Expired breath was sampled during exercise to estimate whole body substrate use. After glucose and sucrose ingestion, liver glycogen levels did not show a significant decline after exercise (from 325 ± 168 to 345 ± 205 and 321 ± 177 to 348 ± 170 mmol/l, respectively; P > 0.05), with no differences between treatments. Muscle glycogen concentrations declined (from 101 ± 49 to 60 ± 34 and 114 ± 48 to 67 ± 34 mmol/l, respectively; P < 0.05), with no differences between treatments. Whole body carbohydrate utilization was greater with sucrose (2.03 ± 0.43 g/min) vs. glucose (1.66 ± 0.36 g/min; P < 0.05) ingestion. Both liver (from 454 ± 33 to 283 ± 82 mmol/l; P < 0.05) and muscle (from 111 ± 46 to 67 ± 31 mmol/l; P < 0.01) glycogen concentrations declined during exercise when only water was ingested. Both glucose and sucrose ingestion prevent liver glycogen depletion during prolonged endurance-type exercise. Sucrose ingestion does not preserve liver glycogen concentrations more than glucose ingestion. However, sucrose ingestion does increase whole body carbohydrate utilization compared with glucose ingestion. This trial was registered at https://www.clinicaltrials.gov as NCT02110836.
Mechanisms for greater insulin-stimulated glucose uptake in normal and insulin-resistant skeletal muscle after acute exercise
Authors: Cartee Gregory D.
Published: October 2015

Enhanced skeletal muscle and whole body insulin sensitivity can persist for up to 24–48 h after one exercise session. This review focuses on potential mechanisms for greater postexercise and insulin-stimulated glucose uptake (ISGU) by muscle in individuals with normal or reduced insulin sensitivity. A model is proposed for the processes underlying this improvement; i.e., triggers initiate events that activate subsequent memory elements, which store information that is relayed to mediators, which translate memory into action by controlling an end effector that directly executes increased insulin-stimulated glucose transport. Several candidates are potential triggers or memory elements, but none have been conclusively verified. Regarding potential mediators in both normal and insulin-resistant individuals, elevated postexercise ISGU with a physiological insulin dose coincides with greater Akt substrate of 160 kDa (AS160) phosphorylation without improved proximal insulin signaling at steps from insulin receptor binding to Akt activity. Causality remains to be established between greater AS160 phosphorylation and improved ISGU. The end effector for normal individuals is increased GLUT4 translocation, but this remains untested for insulin-resistant individuals postexercise. Following exercise, insulin-resistant individuals can attain ISGU values similar to nonexercising healthy controls, but after a comparable exercise protocol performed by both groups, ISGU for the insulin-resistant group has been consistently reported to be below postexercise values for the healthy group. Further research is required to fully understand the mechanisms underlying the improved postexercise ISGU in individuals with normal or subnormal insulin sensitivity and to explain the disparity between these groups after similar exercise.
Impact of maternal undernutrition around the time of conception on factors regulating hepatic lipid metabolism and microRNAs in singleton and twin fetuses
Authors: Lie Shervi , Morrison Janna L. , Williams-Wyss Olivia , Suter Catherine M. , Humphreys David T. , Ozanne Susan E. , Zhang Song , MacLaughlin Severence M. , Kleemann David O. , Walker Simon K. , Roberts Claire T. , McMillen I. Caroline
Published: October 2015

We have investigated the effects of embryo number and maternal undernutrition imposed either around the time of conception or before implantation on hepatic lipid metabolism in the sheep fetus. We have demonstrated that periconceptional undernutrition and preimplantation undernutrition each resulted in decreased hepatic fatty acid β-oxidation regulators, PGC-1α ( P < 0.05), PDK2 ( P < 0.01), and PDK4 ( P < 0.01) mRNA expression in singleton and twin fetuses at 135–138 days gestation. In singletons, there was also lower hepatic PDK4 ( P < 0.01), CPT-1 ( P < 0.01), and PKCζ ( P < 0.01) protein abundance in the PCUN and PIUN groups and a lower protein abundance of PDPK-1 ( P < 0.05) in the PCUN group. Interestingly, in twins, the hepatic protein abundance of p-AMPK (Ser485) ( P < 0.01), p-PDPK-1 (Ser41) ( P < 0.05), and PKCζ ( P < 0.05) was higher in the PCUN and PIUN groups, and hepatic PDK4 ( P < 0.001) and CPT-1 ( P < 0.05) protein abundance was also higher in the PIUN twin fetus. We also found that the expression of a number of microRNAs was altered in response to PCUN or PIUN and that there is evidence that these changes may underlie the changes in the protein abundance of key regulators of hepatic fatty acid β-oxidation in the PCUN and PIUN groups. Therefore, embryo number and the timing of maternal undernutrition in early pregnancy have a differential impact on hepatic microRNA expression and on the factors that regulate hepatic fatty acid oxidation and lipid synthesis.
Prefrontal spatial working memory network predicts animal's decision making in a free choice saccade task
Authors: Mochizuki Kei , Funahashi Shintaro
Published: October 2015

While neurons in the lateral prefrontal cortex (PFC) encode spatial information during the performance of working memory tasks, they are also known to participate in subjective behavior such as spatial attention and action selection. In the present study, we analyzed the activity of primate PFC neurons during the performance of a free choice memory-guided saccade task in which the monkeys needed to choose a saccade direction by themselves. In trials when the receptive field location was subsequently chosen by the animal, PFC neurons with spatially selective visual response started to show greater activation before cue onset. This result suggests that the fluctuation of firing before cue presentation prematurely biased the representation of a certain spatial location and eventually encouraged the subsequent choice of that location. In addition, modulation of the activity by the animal's choice was observed only in neurons with high sustainability of activation and was also dependent on the spatial configuration of the visual cues. These findings were consistent with known characteristics of PFC neurons in information maintenance in spatial working memory function. These results suggest that precue fluctuation of spatial representation was shared and enhanced through the working memory network in the PFC and could finally influence the animal's free choice of saccade direction. The present study revealed that the PFC plays an important role in decision making in a free choice condition and that the dynamics of decision making are constrained by the network architecture embedded in this cortical area.
Proteomic Study to Survey the CIGB-552 Antitumor Effect
Authors: Rodríguez-Ulloa Arielis , Gil Jeovanis , Ramos Yassel , Hernández-Álvarez Lilian , Flores Lisandra , Oliva Brizaida , García Dayana , Sánchez-Puente Aniel , Musacchio-Lasa Alexis , Fernández-de-Cossio Jorge , Padrón Gabriel , González López Luis J. , Besada Vladimir , Guerra-Vallespí Maribel
Published: October 2015

CIGB-552 is a cell-penetrating peptide that exertsin vitroandin vivoantitumor effect on cancer cells. In the present work, the mechanism involved in such anticancer activity was studied using chemical proteomics and expression-based proteomics in culture cancer cell lines. CIGB-552 interacts with at least 55 proteins, as determined by chemical proteomics. A temporal differential proteomics based on iTRAQ quantification method was performed to identify CIGB-552 modulated proteins. The proteomic profile includes 72 differentially expressed proteins in response to CIGB-552 treatment. Proteins related to cell proliferation and apoptosis were identified by both approaches. In line with previous findings, proteomic data revealed that CIGB-552 triggers the inhibition of NF-κB signaling pathway. Furthermore, proteins related to cell invasion were differentially modulated by CIGB-552 treatment suggesting new potentialities of CIGB-552 as anticancer agent. Overall, the current study contributes to a better understanding of the antitumor action mechanism of CIGB-552.
Tau Hyperphosphorylation and Oxidative Stress, a Critical Vicious Circle in Neurodegenerative Tauopathies?
Authors: Alavi Naini Seyedeh Maryam , Soussi-Yanicostas Nadia
Published: October 2015

Hyperphosphorylation and aggregation of the microtubule-associated protein tau in brain, are pathological hallmarks of a large family of neurodegenerative disorders, named tauopathies, which include Alzheimer’s disease. It has been shown that increased phosphorylation of tau destabilizes tau-microtubule interactions, leading to microtubule instability, transport defects along microtubules, and ultimately neuronal death. However, although mutations of theMAPTgene have been detected in familial early-onset tauopathies, causative events in the more frequent sporadic late-onset forms and relationships between tau hyperphosphorylation and neurodegeneration remain largely elusive. Oxidative stress is a further pathological hallmark of tauopathies, but its precise role in the disease process is poorly understood. Another open question is the source of reactive oxygen species, which induce oxidative stress in brain neurons. Mitochondria have been classically viewed as a major source for oxidative stress, but microglial cells were recently identified as reactive oxygen species producers in tauopathies. Here we review the complex relationships between tau pathology and oxidative stress, placing emphasis on (i) tau protein function, (ii) origin and consequences of reactive oxygen species production, and (iii) links between tau phosphorylation and oxidative stress. Further, we go on to discuss the hypothesis that tau hyperphosphorylation and oxidative stress are two key components of a vicious circle, crucial in neurodegenerative tauopathies.
Depression and Anxiety among Patients with Epilepsy and Multiple Sclerosis: UAE Comparative Study
Authors: Alsaadi Taoufik , El Hammasi Khadija , Shahrour Tarek M. , Shakra Mustafa , Turkawi Lamya , Nasreddine Wassim , Raoof Mufeed
Published: October 2015

Depression and anxiety are highly prevalent in patients with epilepsy (PWE), with prevalence rates ranging from 20% to 55%. The cause of this increased rate is multifactorial. Depression and epilepsy are thought to share the same pathogenic mechanism. Anxiety, on the other hand, seems to have a prevalence rate among PWE comparable to, or even higher than, those reported for depression, and it is closely linked to epilepsy. To test this hypothesis, we screened for depression and anxiety 186 and 160 patients attending the epilepsy and MS clinics, respectively, using standardized screening tools to determine the rates of both depression and anxiety, comparing these rates to 186 age, sex matched controls. Among the three groups, only patients with epilepsy were at increased risk of having depression (OR = 1.9), whereas anxiety was not. This finding could point to the shared pathogenic mechanisms hypothesis between depression and epilepsy.
Serum Oxidative Stress Markers and Genotoxic Profile Induced by Chemotherapy in Patients with Breast Cancer: A Pilot Study
Authors: Júnior Antonio Luiz Gomes , Paz Marcia Fernanda Correia Jardim , Silva Laís Iasmin Soares da , Carvalho Simone da Costa e Silva , Sobral André Luiz Pinho , Machado Kátia da Conceição , Ferreira Paulo Michel Pinheiro , Satyal Prabodh , Freitas Rivelilson Mendes de , Cavalcante Ana Amélia de Carvalho Melo
Published: October 2015

The aim of this study was to evaluate the oxidative parameters of erythrocytes and genotoxicity in leukocytes of patients with breast cancer. Oxidative parameters were detected by spectrophotometry and genotoxic damage by single cell gel electrophoresis. Twenty-eight women with breast cancer were monitored before chemotherapy and after the second and fourth cycles of therapy with cyclophosphamide and doxorubicin. After the fourth cycle, increases (P<0.05) in the reactive substances to thiobarbituric acid levels, nitrite content, and superoxide dismutase activity and high rates of DNA damage in leukocytes were observed when compared with healthy women group and baseline levels. Similarly, after the second cycle, the same parameters were increased (P<0.05) when compared with baseline levels. Increase in catalase activity was detected only after the fourth cycle and reduced glutathione levels and glutathione peroxidase activity were decreased in all cycles when compared with healthy women, as well as after the second and fourth chemotherapy cycles compared to baseline (P<0.05). Patients with breast cancer presented an indicative of oxidative stress before, during, and after chemotherapy, as well as increased genotoxic damage in all stages of treatment, demonstrating the clinical applicability of this investigation.