bluuebunny/crossref_metadata_2025_split huggingface dataset:
Bipolar resistive switching in p-type Co3O4 nanosheets prepared by electrochemical deposition
Authors: Younis Adnan , Chu Dewei , Lin Xi , Lee Jiunn , Li Sean 
Published: January 2013

Abstract
Metal oxide nanosheets have potential applications in novel nanoelectronics as nanocrystal building blocks. In this work, the devices with a structure of Au/p-type Co3O4 nanosheets/indium tin oxide/glass having bipolar resistive switching characteristics were successfully fabricated. The experimental results demonstrate that the device have stable high/low resistance ratio that is greater than 25, endurance performance more than 200 cycles, and data retention more than 10,000 s. Such a superior performance of the as-fabricated device could be explained by the bulk film and Co3O4/indium tin oxide glass substrate interface effect.
Effect of TiO2 rutile nanorods on the photoelectrodes of dye-sensitized solar cells
Authors: Jung Young Hee , Park Kyung-Hee , Oh Jeong Seok , Kim Do-Heyoung , Hong Chang Kook 
Published: January 2013

Abstract
In order to enhance the electron transport on the photoelectrodes of dye-sensitized solar cells, one-dimensional rutile nanorods were prepared using electrospun TiO2 nanofibers. The grain size of the nanorods increased with increasing temperature. Electrochemical impedance spectroscopy measurements revealed reduced interface resistance of the cells with the one-dimensional rutile nanorods due to the improved electron transport and the enhanced electrolyte penetration. Intensity-modulated photocurrent/photovoltage spectroscopy showed that the one-dimensional rutile nanorods provided the electrons with a moving pathway and suppressed the recombination of photogenerated electrons. However, an excessive quantity of rutile nanorods created an obstacle to the electrons moving in the TiO2 thin film. The photoelectrode with 7 wt.% rutile nanorods optimized the performance of the dye-sensitized solar cells.
Porcine epidemic diarrhea virus E protein causes endoplasmic reticulum stress and up-regulates interleukin-8 expression
Authors: Xu Xingang , Zhang Honglei , Zhang Qi , Dong Jie , Liang Yabing , Huang Yong , Liu Hung-Jen , Tong Dewen 
Published: January 2013

AbstractBackgroundPorcine epidemic diarrhea virus (PEDV) is an important pathogen in swine and is responsible for substantial economic losses. Previous studies suggest that the PEDV E protein plays an important role in the viral assembly process. However, the subcellular localization and other functions of PEDV E protein still require more research.MethodsThe subcellular localization and function of PEDV E protein were investigated by examining its effects on cell growth, cell cycle progression, interleukin-8 (IL-8) expression and cell survival.ResultsThe results show that plenty of PEDV E protein is localized in the ER, with small quantities localized in the nucleus. The PEDV E protein has no effect on the intestinal epithelial cells (IEC) growth, cell cycle and cyclin A expression. The cells expressing PEDV E protein express higher levels of IL-8 than control cells. Further studies show that PEDV E protein induced endoplasmic reticulum (ER) stress and activated NF-κB which is responsible for the up-regulation of IL-8 and Bcl-2 expression.ConclusionsThis study shows that the PEDV E protein is localized in the ER and the nucleus and it can cause ER stress. The PEDV E protein had no effect on the IEC growth and cell cycle. In addition, the PEDV E protein is able to up-regulate IL-8 and Bcl-2 expression.
Autosomal dominant cerebellar ataxia type III: a review of the phenotypic and genotypic characteristics
Authors: Fujioka Shinsuke , Sundal Christina , Wszolek Zbigniew K 
Published: January 2013

Abstract
Autosomal Dominant Cerebellar Ataxia (ADCA) Type III is a type of spinocerebellar ataxia (SCA) classically characterized by pure cerebellar ataxia and occasionally by non-cerebellar signs such as pyramidal signs, ophthalmoplegia, and tremor. The onset of symptoms typically occurs in adulthood; however, a minority of patients develop clinical features in adolescence. The incidence of ADCA Type III is unknown. ADCA Type III consists of six subtypes, SCA5, SCA6, SCA11, SCA26, SCA30, and SCA31. The subtype SCA6 is the most common. These subtypes are associated with four causative genes and two loci. The severity of symptoms and age of onset can vary between each SCA subtype and even between families with the same subtype. SCA5 and SCA11 are caused by specific gene mutations such as missense, inframe deletions, and frameshift insertions or deletions. SCA6 is caused by trinucleotide CAG repeat expansions encoding large uninterrupted glutamine tracts. SCA31 is caused by repeat expansions that fall outside of the protein-coding region of the disease gene. Currently, there are no specific gene mutations associated with SCA26 or SCA30, though there is a confirmed locus for each subtype. This disease is mainly diagnosed via genetic testing; however, differential diagnoses include pure cerebellar ataxia and non-cerebellar features in addition to ataxia. Although not fatal, ADCA Type III may cause dysphagia and falls, which reduce the quality of life of the patients and may in turn shorten the lifespan. The therapy for ADCA Type III is supportive and includes occupational and speech modalities. There is no cure for ADCA Type III, but a number of recent studies have highlighted novel therapies, which bring hope for future curative treatments.
Analysis of prevalence of PTSD and its influencing factors among college students after the Wenchuan earthquake
Authors: Fu Yan , Chen Yongshun , Wang Jin , Tang Xiaohui , He Jieyun , Jiao Miaorui , Yu Chunhua , You Guiying , Li Junying 
Published: January 2013

Abstract

Background
This study explored the prevalence and severity of post-traumatic stress disorder (PTSD) in college students who lived in earthquake center one year after the Wenchuan earthquake on May 12, 2008, the factors affecting the prevalence of PTSD was also investigated.

Methods
2987 students studying at the senior normal school in Tibetan autonomous region which was one of the most devastated regions were selected for this study. The PTSD Checklist-Civilian Version (PCL-C) was used as a screening instrument.

Results
A total of 420 cases (14.1%) were diagnosed with PTSD, among which mild, moderate, severe and extreme symptoms were reported in 122, 185, 106 and 7 cases, respectively. The PTSD prevalence in college students lived in the severely affected area was significantly higher than that in the less severe area (P < 0.001). According to the multivariate logistic regression analysis, the students who were injured in the earthquake, those lost their first degree relative, and those confronted with dead bodies were more likely to express PTSD. Male students were more prone than female students to develop PTSD. However, the students who received psychological tutorship were less prone to express PTSD.

Conclusions
At one year after the earthquake, the PTSD rate in college students in the severely affected area was high. The social support, psychological help and rehabilitation project should be strengthened to improve their ability to cope with the trauma.
A comparative study on the antioxidant activity of methanolic extracts from different parts of Morus alba L. (Moraceae)
Authors: Khan Muhammad Ali , Rahman Aziz Abdur , Islam Shafiqul , Khandokhar Proma , Parvin Shahnaj , Islam Md Badrul , Hossain Mosharrof , Rashid Mamunur , Sadik Golam , Nasrin Shamima , Mollah M Nurul Haque , Alam AHM Khurshid 
Published: January 2013

Abstract

Background
Antioxidants play an important role to protect damage caused by oxidative stress (OS). Plants having phenolic contents are reported to possess antioxidant properties. The present study was designed to investigate the antioxidant properties and phenolic contents (total phenols, flavonoids, flavonols and proanthrocyanidins) of methanolic extracts from Morus alba (locally named as Tut and commonly known as white mulberry) stem barks (TSB), root bark (TRB), leaves (TL) and fruits (TF) to make a statistical correlation between phenolic contents and antioxidant potential.

Methods
The antioxidant activities and phenolic contents of methanolic extractives were evaluated by in vitro standard method using spectrophotometer. The antioxidant activities were determined by total antioxidant capacity, DPPH (1,1-diphenyl-2-picrylhydrazine) radical scavenging assay, hydroxyl radical scavenging assay, ferrous reducing antioxidant capacity and lipid peroxidation inhibition assay methods.

Results
Among the extracts, TSB showed the highest antioxidant activity followed by TRB, TF and TL. Based on DPPH and hydroxyl radical scavenging activity, the TSB extract was the most effective one with IC50 37.75 and 58.90 μg/mL, followed by TRB, TF and TL with IC50 40.20 and 102.03; 175.01 and 114.63 and 220.23 and 234.63 μg/mL, respectively. The TSB extract had the most potent inhibitory activity against lipid peroxidation with IC50 145.31 μg/mL. In addition, the reducing capacity on ferrous ion was in the following order: TSB > TRB > TL > TF. The content of phenolics, flavonoids, flavonols and proanthocyanidins of TSB was found to be higher than other extractives.

Conclusion
The results indicate high correlation and regression (p-value <0 .001) between phenolic contents and antioxidant potentials of the extracts, hence the Tut plant could serve as effective free radical inhibitor or scavenger which may be a good candidate for pharmaceutical plant-based products. However, further exploration is necessary for effective use in both modern and traditional system of medicines.
Non-autoimmune subclinical hypothyroidism due to a mutation in TSH receptor: report on two brothers
Authors: Cerbone Manuela , Agretti Patrizia , De Marco Giuseppina , Improda Nicola , Pignata Claudio , Santamaria Francesca , Tonacchera Massimo , Salerno Mariacarolina 
Published: January 2013

Abstract
Subclinical hypothyroidism (SH) is a condition characterized by a mild persistent thyroid failure. The main cause is represented by autoimmune thyroiditis, but mutations in genes encoding proteins involved in TSH pathway are thought to be responsible for SH, particularly in cases arising in familial settings. Patients with the syndrome of TSH unresponsiveness may have compensated or overt hypothyroidism with a wide spectrum of clinical and morphological alterations depending on the degree of impairment of TSH-receptor (TSH-R) function. We describe the case of two brothers with non autoimmune SH carrying the same heterozygous mutation in the extracellular domain of TSH-R and presenting with different clinical, biochemical and morphological features. The first one had only a slight persistent elevation of TSH, a normal thyroid ultrasound and did never require l- thyroxine (L-T4) replacement treatment. The second one had a neonatal persistent moderate TSH levels increase associated with a thyroid gland hypoplasia and was treated with L-T4 since the first months of life.
These two cases support the recent association of TSH-R mutations inheritance as an autosomal dominant pattern with variable expressivity and suggest that the decision to start replacement therapy in patients with persistent SH due to TSH resistance should be individualized.
Empowerment assessment and influential factors among patients with type 2 diabetes
Authors: Tol Azar , Baghbanian Abdolvahab , Mohebbi Bahram , Shojaeizadeh Davoud , Azam Kamal , Shahmirzadi Sima Esmaeeli , Asfia Abolghasem 
Published: January 2013

Abstract
Background
Diabetic patients need high awareness of disease prevention to adopt self-management behaviors in their daily life. Central to this activity is patients’ empowerment. Current study was conducted to assess empowerment score and its related factors among type 2 diabetic patients.

Method
A cross-sectional study carried out over a period of nine months during 2010–2011. All patients with a diagnosis of type 2 diabetes including those referring to four hospitals affiliated with Tehran University of Medical Sciences were recruited. A total of 688 diabetic patients were identified who met the inclusion criteria and were all included in the study. Patients’ empowerment was measured by Diabetes Empowerment Scale reflecting three dimensions including managing psychosocial aspect of diabetes, assessing dissatisfaction and readiness to change and Setting and achieving diabetes goal. Collected data was analysed using SPSS software version 11.5.

Results
As total, 688 were available for analysis, ranging from 37–81 years old with mean of 54.41 years (SD = 8.22). The Mean duration of the disease was approximately 6.67 years (SD = 4.58). Dimensions of ‘managing the psychosocial aspect of diabetes’, ‘assessing dissatisfaction and readiness to change’ and ‘setting and achieving diabetes goal’ were all measured and scored for each patient. The mean score for each domain was 25.75 ± 5.55, 24.78 ± 7.54, 27.63 ± 7.90, respectively. Data analysis revealed a statistically significant reverse relationship between age and ‘assessing dissatisfaction and readiness to change’ and ‘setting and achieving diabetes goal’. In addition, disease duration had a statistically significant reverse relationship with ‘assessing dissatisfaction and readiness to change’.

Conclusion
Patients with type 2 diabetes have the potential to be empowered to manage their chronic disease if they are actively informed and educated.
Limk2 mediates semaphorin signalling in cortical interneurons migrating through the subpallium
Authors: Andrews William D. , Zito Arianna , Memi Fani , Jones Gareth , Tamamaki Nobuaki , Parnavelas John G. 
Published: January 2013

Summary
En route to the neocortex, interneurons migrate around and avoid the developing striatum. This is due to the chemorepulsive cues of class 3 semaphorins (Sema3A and Sema3F) acting through neuropilin and plexin co-receptors expressed in interneurons. In a recent genetic screen aimed at identifying novel components that may play a role in interneuron migration, we identified LIM-kinase 2 (Limk2), a kinase previously shown to be involved in cell movement and in Sema7A-PlexinC1 signalling. Here we show that Limk2 is differentially expressed in interneurons, with a higher expression in the subpallium compared to cortex, suggesting it may play a role in their migration through the subpallium. Chemotactic assays, carried out with small interfering RNAs (siRNAs), revealed that Limk2-siRNA transfected interneurons are less responsive to Sema3A, but respond to Sema3F. Lack of responsiveness to Sema3A resulted in their aberrant invasion of the developing striatum, as demonstrated in brain slice preparations and in in utero electroporated mouse embryos with the same siRNAs. Our results reveal a previously unknown role for Limk2 in interneuron migration and Sema3A signalling.
Mitochondrial NDUFS3 regulates the ROS-mediated onset of metabolic switch in transformed cells
Authors: Suhane Sonal , Kanzaki Hirotaka , Arumugaswami Vaithilingaraja , Murali Ramachandran , Ramanujan V. Krishnan 
Published: January 2013

SummaryAerobic glycolysis in transformed cells is an unique metabolic phenotype characterized by a hyperactivated glycolytic pathway even in the presence of oxygen. It is not clear if the onset of aerobic glycolysis is regulated by mitochondrial dysfunction and, if so, what the metabolic windows of opportunity available to control this metabolic switch (mitochondrial to glycolytic) landscape are in transformed cells. Here we report a genetically-defined model system based on the gene-silencing of a mitochondrial complex I subunit, NDUFS3, where we demonstrate the onset of metabolic switch in isogenic human embryonic kidney cells by differential expression of NDUFS3. By means of extensive metabolic characterization, we demonstrate that NDUFS3 gene silencing systematically introduces mitochondrial dysfunction thereby leading to the onset of aerobic glycolysis in a manner dependent on NDUFS3 protein levels. Furthermore, we show that the sustained imbalance in free radical dynamics is a necessary condition to sustain the observed metabolic switch in cell lines with the most severe NDUFS3 suppression. Together, our data reveal a novel role for mitochondrial complex I subunit NDUFS3 in regulating the degree of mitochondrial dysfunction in living cells, thereby setting a “metabolic threshold” for the observation of aerobic glycolysis phenotype within the confines of mitochondrial dysfunction.
Establishment and mitotic characterization of newDrosophilaacentriolar cell lines fromDSas-4mutant
Authors: Lecland Nicolas , Debec Alain , Delmas Audrey , Moutinho-Pereira Sara , Malmanche Nicolas , Bouissou Anais , Dupré Clémence , Jourdan Aimie , Raynaud-Messina Brigitte , Maiato Helder , Guichet Antoine 
Published: January 2013

SummaryIn animal cells the centrosome is commonly viewed as the main cellular structure driving microtubule (MT) assembly into the mitotic spindle apparatus. However, additional pathways, such as those mediated by chromatin and augmin, are involved in the establishment of functional spindles. The molecular mechanisms involved in these pathways remain poorly understood, mostly due to limitations inherent to current experimental systems available. To overcome these limitations we have developed six new Drosophila cell lines derived from Drosophila homozygous mutants for DSas-4, a protein essential for centriole biogenesis. These cells lack detectable centrosomal structures, astral MT, with dispersed pericentriolar proteins D-PLP, Centrosomin and γ-tubulin. They show poorly focused spindle poles that reach the plasma membrane. Despite being compromised for functional centrosome, these cells could successfully undergo mitosis.Live-cell imaging analysis of acentriolar spindle assembly revealed that nascent MTs are nucleated from multiple points in the vicinity of chromosomes. These nascent MTs then grow away from kinetochores allowing the expansion of fibers that will be part of the future acentriolar spindle. MT repolymerization assays illustrate that acentriolar spindle assembly occurs “inside-out” from the chromosomes. Colchicine-mediated depolymerization of MTs further revealed the presence of a functional Spindle Assembly Checkpoint (SAC) in the acentriolar cells. Finally, pilot RNAi experiments open the potential use of these cell lines for the molecular dissection of anastral pathways in spindle and centrosome assembly.
Essential role of grim-led programmed cell death for the establishment of corazonin-producing peptidergic nervous system during embryogenesis and metamorphosis in Drosophila melanogaster
Authors: Lee Gyunghee , Sehgal Ritika , Wang Zixing , Nair Sudershana , Kikuno Keiko , Chen Chun-Hong , Hay Bruce , Park Jae H. 
Published: January 2013

Summary
In Drosophila melanogaster, combinatorial activities of four death genes, head involution defective (hid), reaper (rpr), grim, and sickle (skl), have been known to play crucial roles in the developmentally regulated programmed cell death (PCD) of various tissues. However, different expression patterns of the death genes also suggest distinct functions played by each. During early metamorphosis, a great number of larval neurons unfit for adult life style are removed by PCD. Among them are eight pairs of corazonin-expressing larval peptidergic neurons in the ventral nerve cord (vCrz). To reveal death genes responsible for the PCD of vCrz neurons, we examined extant and recently available mutations as well as RNA interference that disrupt functions of single or multiple death genes. We found grim as a chief proapoptotic gene and skl and rpr as minor ones. The function of grim is also required for PCD of the mitotic sibling cells of the vCrz neuronal precursors (EW3-sib) during embryonic neurogenesis. An intergenic region between grim and rpr, which, it has been suggested, may enhance expression of three death genes in embryonic neuroblasts, appears to play a role for the vCrz PCD, but not for the EW3-sib cell death. The death of vCrz neurons and EW3-sib is triggered by ecdysone and the Notch signaling pathway, respectively, suggesting distinct regulatory mechanisms of grim expression in a cell- and developmental stage-specific manner.
Light-activation of the Archaerhodopsin H+-pump reverses age-dependent loss of vertebrate regeneration: sparking system-level controls in vivo
Authors: Adams Dany Spencer , Tseng Ai-Sun , Levin Michael 
Published: January 2013

Summary
Optogenetics, the regulation of proteins by light, has revolutionized the study of excitable cells, and generated strong interest in the therapeutic potential of this technology for regulating action potentials in neural and muscle cells. However, it is currently unknown whether light-activated channels and pumps will allow control of resting potential in embryonic or regenerating cells in vivo. Abnormalities in ion currents of non-excitable cells are known to play key roles in the etiology of birth defects and cancer. Moreover, changes in transmembrane resting potential initiate Xenopus tadpole tail regeneration, including regrowth of a functioning spinal cord, in tails that have been inhibited by natural inactivity of the endogenous H+-V-ATPase pump. However, existing pharmacological and genetic methods allow neither non-invasive control of bioelectric parameters in vivo nor the ability to abrogate signaling at defined time points. Here, we show that light activation of a H+-pump can prevent developmental defects and induce regeneration by hyperpolarizing transmembrane potentials. Specifically, light-dependent, Archaerhodopsin-based, H+-flux hyperpolarized cells in vivo and thus rescued Xenopus embryos from the craniofacial and patterning abnormalities caused by molecular blockade of endogenous H+-flux. Furthermore, light stimulation of Arch for only 2 days after amputation restored regenerative capacity to inhibited tails, inducing cell proliferation, tissue innervation, and upregulation of notch1 and msx1, essential genes in two well-known endogenous regenerative pathways. Electroneutral pH change, induced by expression of the sodium proton exchanger, NHE3, did not rescue regeneration, implicating the hyperpolarizing activity of Archaerhodopsin as the causal factor. The data reveal that hyperpolarization is required only during the first 48 hours post-injury, and that expression in the spinal cord is not necessary for the effect to occur. Our study shows that complex, coordinated sets of stable bioelectric events that alter body patterning—prevention of birth defects and induction of regeneration—can be elicited by the temporal modulation of a single ion current. Furthermore, as optogenetic reagents can be used to achieve that manipulation, the potential for this technology to impact clinical approaches for preventive, therapeutic, and regenerative medicine is extraordinary. We expect this first critical step will lead to an unprecedented expansion of optogenetics in biomedical research and in the probing of novel and fundamental biophysical determinants of growth and form.