Miracle-dz/UniFAR-FTUs huggingface dataset:
Social Media and Public Administration in Spain: A Comparative Analysis of the Regional Level of Government

The chapter investigates the employment of digital social media by Spanish regional administrations: its presence, the factors that determine that presence, as well as the self-perception of those responsible for its management. This study raises the following questions: What are the key factors that explain the use of social media in public administrations? What is the self-perception of those responsible for the management of digital social media about its current level of development within their organisations? What are the main inhibitors-facilitators for the development of digital social media in public administrations? What are the next steps to promote digital social media in the sphere of public organisations? This chapter is based on a questionnaire that was responded to by those responsible for the management of digital social media in the Spanish regional administrations. This research shows that Web 2.0 tools are more oriented to explore potential changes in the relations between the public administrations and citizens, than to innovate the functioning of public sector organisations. In sum, this chapter offers a relevant analysis, although it is of an exploratory character because of the almost total absence of systematic studies about the diffusion of digital social media within Spanish public administrations. DOI: 10.4018/978-1-4666-4173-0.ch014
Mapping the alterations in glutamate with GluCEST MRI in a mouse model of dopamine deficiency

Glutamate chemical exchange saturation transfer (GluCEST) MRI was used to measure metabolic changes in mice treated with 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP) by mapping regional cerebral glutamate. The GluCEST contrast following MPTP treatment was correlated with 1H‐MR spectroscopy, motor function, and immunohistochemical measures. The GluCEST contrast was found to be significantly higher in the striatum and motor cortex of mice treated with MPTP than in controls (p < 0.001), which was confirmed by localized 1H‐MR spectroscopy. Elevated striatal GluCEST was positively associated with local astrogliosis measured by immunohistochemistry for glial fibrillary acidic protein. Additionally, a negative correlation was found between motor function, measured by the four‐limb grip strength test, and GluCEST of the striatum (R = −0.705, p < 0.001) and the motor cortex (R = −0.617, p < 0.01), suggesting a role of elevated glutamate in the abnormal cerebral motor function regulation. The GluCEST contrast and glial fibrillary acidic protein immunostaining were unaltered in the thalamus indicating glutamate elevation was localized to the striatum and the motor cortex. These findings suggest that in addition to measuring spatial changes in glutamate, GluCEST may serve as an in vivo biomarker of metabolic and functional changes that may be applied to the assessment of a broad range of neuropathologies.
The ETS Domain Transcription Factor ELK1 Directs a Critical Component of Growth Signaling by the Androgen Receptor in Prostate Cancer Cells*

Background: Mechanisms that redirect androgen receptor signaling to primarily support prostate tumor growth are poorly understood. Results: Prostate cancer cells were addicted to ELK1, which tethered AR to activate growth genes in hormone-dependent and castration-recurrent PC without ELK1 phosphorylation. Conclusion: ELK1 directs a critical arm of transcriptional growth signaling by AR that is preserved in CRPC. Significance: The ELK1-AR interaction offers a functionally tumor-selective drug target. The androgen receptor (AR) is essential for diverse aspects of prostate development and function. Molecular mechanisms by which prostate cancer (PC) cells redirect AR signaling to genes that primarily support growth are unclear. A systematic search for critical AR-tethering proteins led to ELK1, an ETS transcription factor of the ternary complex factor subfamily. Although genetically redundant, ELK1 was obligatory for AR-dependent growth and clonogenic survival in both hormone-dependent PC and castration-recurrent PC cells but not for AR-negative cell growth. AR required ELK1 to up-regulate a major subset of its target genes that was strongly and primarily enriched for cell growth functions. AR functioned as a coactivator of ELK1 by association through its A/B domain, bypassing the classical mechanism of ELK1 activation by phosphorylation and without inducing ternary complex target genes. The ELK1-AR synergy per se was ligand-independent, although it required ligand for nuclear localization of AR as targeting the AR A/B domain to the nucleus recapitulated the action of hormone; accordingly, Casodex was a poor antagonist of the synergy. ELK3, the closest substitute for ELK1 in structure/function and genome recognition, did not interact with AR. ELK1 thus directs selective and sustained gene induction that is a substantial and critical component of growth signaling by AR in PC cells. The ELK1-AR interaction offers a functionally tumor-selective drug target.
Promoting well‐being and independence for people with dementia

This paper reviews the research evidence relating to non‐pharmacological interventions with people with dementia aiming to improve well‐being and independence. There have been a number of attempts to improve the person's level of independent functioning through programmes training and supporting self‐care skills, mobility, continence, orientation and participation in activities. Well‐being has been less often directly addressed, although recently studies have begun to specifically target aspects of it. Increased independence does not necessarily lead to greater well‐being, and it is clear that the greatest potential for increasing function is in tackling the excess disability which many care giving situations in effect impose on the person with dementia. In carrying out research in this area, the limitations of randomized controlled trials are evident, and there is much to be said for the reporting of series of carefully controlled single‐case studies in addition to group studies. Further development of methods of measuring well‐being in people with dementia is also required. Copyright © 1999 John Wiley & Sons, Ltd.
Human airway smooth muscle responsiveness in neonatal lung specimens.

The mechanical activity of proximal airways isolated from human lung specimens obtained at autopsy from 11 neonates was studied in response to the following compounds: carbachol, histamine, potassium chloride (KCl), neurokinin A (NKA) (both in the presence and in the absence of the neutral endopeptidase inhibitor phosphoramidon) and isoproterenol. Isometric responses to the various concentrations of each of the compounds were expressed as both raw values of force normalized to smooth muscle cross-sectional area (SMCSA), i.e., muscle stress and percentages of the maximal response to acetylcholine. Maximal active muscle stress of human neonatal bronchi was induced by carbachol and averaged 95 +/- 25 mN/mm2 SMCSA (n = 8). The rank of maximal force induced by the contractile agonists was carbachol > histamine > KCl > NKA, and the rank of the concentration of drug producing one-half of the maximum effect (EC50) was NKA < carbachol < histamine < KCl. The EC50 value for isoproterenol was the lowest, although it generated the smallest mechanical response. When compared with results obtained under identical experimental conditions in the human adult lung, except for carbachol and isoproterenol, general trends were an increase in force generation with age and little changes in EC50 values. There was a decrease in carbachol-induced force with age, whereas the opposite was observed with isoproterenol. We conclude that most of the mechanisms that control airway tone in humans are already present in the neonate. Alterations in the response to agonists with the maturational process may have implications in the pharmacologic modulation of bronchial obstruction in neonates.
SDR structure based CFO estimation and compensation circuit for OFDM systems using reconfigurable CORDIC FPGA modules

In this paper, a software defined radio (SDR) structure based carrier frequency offset (CFO) estimation and compensation circuit is designed for an orthogonal frequency division multiplexing (OFDM) system using the reconfigurable coordinate rotation digital computer (CORDIC) field programmable gate array (FPGA) rotation and vectoring circuit modules. The SDR architecture of the CFO estimation and compensation circuit and the program flow of the CORDIC FPGA modules are presented. The required processing time and hardware reconfiguration function are our major design considerations. The experimental results demonstrate that the designed CFO estimation and compensation circuit implemented with a 10 MHz clock FPGA chip can reduce the residual CFO to an acceptable range within 1. 5µsec.
Cooperation of transmembrane segments during the integration of a double‐spanning protein into the ER membrane

While membrane insertion of single‐spanning membrane proteins into the endoplasmic reticulum (ER) is relatively well understood, it is unclear how multi‐spanning proteins integrate. We have investigated the cotranslational ER integration of a double‐spanning protein that is derived from leader peptidase. Both transmembrane (TM) segments are inserted into the membrane by the Sec61 channel. While the first, long and hydrophobic TM segment (TM1) inserts into the lipid bilayer on its own, the second, shorter TM anchor (TM2) collaborates with TM1 during its integration. TM1 diffuses away from the Sec61 complex in the absence of TM2, but is close to Sec61 when TM2 arrives inside the channel. These data suggest that the exit of a weak TM segment from the Sec61 channel into the lipid phase can be facilitated by its interaction with a previously integrated strong and stabilizing TM anchor.
[Treatment strategies for auditory verbal hallucinations].

BACKGROUND Auditory verbal hallucinations (AVH) are experienced not only by patients diagnosed with schizophrenia, but also by patients with other disorders (some of which may be psychiatric) and in the general population. The ensuing affliction may be severe and can sometimes result in dangerous behaviour. Although various treatment options are available for AVH, only a few have been investigated in randomised placebo-controlled trials. AIM To provide an overview of the literature relating to the effectiveness of antipsychotics, cognitive-behavioural therapy (CBT), electroconvulsive therapy (ect), and transcranial magnetic stimulation (TMS) in the treatment of avh. METHOD This review paper is based on the Ph.D. study of the first author; in addition, a literature search was carried out using PubMed. RESULTS Antipsychotics have never been studied specifically with regard to their effect on AVH, but they are known to lead to a significant decrease in the severity and frequency of hallucinations in general. cbt can reduce the torment caused by AVH, but not the severity or frequency. ect can be helpful in the treatment of drug-resistant psychosis, but it has never been studied specifically with regard to its effect on avh or on other types of hallucinations. tms is effective for the treatment of drug-resistant AVH, but in the cases where it has been used so far, the beneficial effects seem to have been of limited duration. CONCLUSION Very few of the available treatment strategies have been used specifically to relieve the distress caused by avh. tms and cbt have proved reasonably effective, but there is a need for further research into additional treatment strategies, particularly into those involving TMS.
University of Birmingham Characterization of mutations in the PAS domain of the EvgS sensor kinase selected by laboratory evolution for acid resistance in Escherichia coli

Summary Laboratory-based evolution and whole-genome sequencing can link genotype and phenotype. We used evolution of acid resistance in exponential phase Escherichia coli to study resistance to a lethal stress. Iterative selection at pH 2.5 generated ﬁve populations that were resistant to low pH in early exponential phase. Genome sequencing revealed multiple mutations, but the only gene mutated in all strains was evgS ,partofatwo-componentsystemthathasalready been implicated in acid resistance.All these mutations were in the cytoplasmic PAS domain of EvgS, and were shown to be solely responsible for the resistant phenotype, causing strong upregulation at neutral pH of genes normally induced by low pH. Resistance to pH 2.5 in these strains did not require the transporter GadC, or the sigma factor RpoS. We found that EvgS-dependent constitutive acid resistance to pH 2.5 was retained in the absence of the regulators GadE or YdeO, but the also A deletion in the domain of abolished the response to low pH, but not the activity of the constitutive mutants. On the basis of these results we propose a model for how EvgS may become activated by low pH.
REDUCED VASCULAR RESPONSE TO PHENYLEPHRINE DURING EXPOSURE TO LIPOPOLYSACCHARIDE IN VITRO INVOLVES NITRIC OXIDE AND ENDOTHELIN 1

Nitric oxide (NO) and endothelin 1 (ET-1) increase significantly during the first 4 h of Escherichia coli lipopolysaccharide (LPS) exposure. The aim of this study was to investigate the role of these mediators in the reduced response to phenylephrine treatment. We used male rat saphenous arteries (internal relaxed diameter, 63-152 &mgr;m; n = 48), mounted on a wire myograph and subsequently treated with LPS. At 1 h, LPS (dose, 50 µg mL−1) significantly (P < 0.05) inhibited constriction to phenylephrine (concentration, 10−1M to 10−6M) (LPS concentration required for half maximal response [EC50], 10.82 ± 1.08&mgr;M; Control EC50, 5.07 ± 0.34&mgr;M). However, by removing the endothelium (denuded) or adding N&ohgr;-nitro-L-arginine methyl ester (L-NAME; concentration, 10−4M), the response to phenylephrine treatment was significantly improved compared with LPS only-treated arteries (LPS + denuded EC50, 7.04 ± 1.12&mgr;M; LPS + L-NAME EC50, 2.64 ± 0.63&mgr;M). On the other hand, denudation did not restore constriction to phenylephrine at 2 and 4 h. However, L-NAME and the nonspecific ET-1 receptor antagonist bosentan (concentration, 10−5M) improved constriction to phenylephrine in LPS-treated arteries (P < 0.05) at 4 h (LPS EC50, 998.50 ± 447.10&mgr;M; LPS + L-NAME EC50, 65.23 ± 25.61&mgr;M; LPS + bosentan EC50, 63.65 ± 25.33&mgr;M). We conclude that endothelium-dependent mechanisms have an early role in the reduced responsiveness of vascular smooth muscle to vasoconstrictors during simulated septic conditions. Shortly after exposure to LPS (duration, 1 h), endothelium-derived NO seemed to have a role in reduced arterial constriction to phenylephrine, but later (4 h) ET-1 and endothelium-independent increase in NO seemed to contribute further to the loss of response.
Blood Pressure Responses to Lifestyle Physical Activity Among Young, Hypertension-Prone African-American Women

Background: Physical inactivity and obesity increase the risk for hypertension, and both are more prevalent in African-American than Caucasian women. Regular physical activity serves as an important intervention for reducing cardiovascular risk, yet the ideal physical activity profile to meet the needs of young, sedentary African-American women remains unclear. We performed a randomized, parallel, single-blind study to examine the effect of lifestyle physical activity (LPA) on blood pressure indices in sedentary African-American women aged 18 to 45 years with prehypertension or untreated stage 1 hypertension. Methods: The primary intervention was an 8-week individualized, home-based program in which women randomized to Exercise (n = 14) were instructed to engage in lifestyle-compatible physical activity (eg, walking, stair climbing) for 10 minutes, 3 times a day, 5 days a week, at a prescribed heart rate corresponding to an intensity of 50% to 60% heart rate reserve. Women in the No Exercise group (n = 10) continued with their usual daily activities. Mean changes in cuff, ambulatory, and pressure load indices were compared using paired t tests, and physical activity adherence was expressed as percentages. Results: Women in the Exercise group had a significant reduction in systolic blood pressure (−6.4 mm Hg, P = .036), a decrease in diastolic blood pressure status to the prehypertensive level (90.8 vs 87.4 mm Hg), and greater reductions in nighttime pressure load compared with the No Exercise group. Adherence to LPA was exceedingly high by all measures (65%-98%) and correlated with change in systolic blood pressure (r = −0.620, P = .024). Conclusion: The accumulation of LPA reduced cuff, ambulatory, and pressure load. The accumulation of LPA appears well tolerated and feasible in this sample of young African-American women, demonstrated by the overall high adherence rates. Given the excess burden of pressure-related clinical sequelae among African Americans and the strong correlation between pressure load and target organ damage, LPA may represent a practical and effective strategy in this population.
Amelioration of symptoms by enhancement of proprioception in patients with joint hypermobility syndrome.

OBJECTIVE Joint hypermobility syndrome (JHS) is characterized by an association between joint hypermobility and musculoskeletal pains, the latter occurring in the absence of any objective indicator of rheumatic disease. The lack of a recognizable disease marker makes this condition difficult to identify and manage. We previously observed that patients with JHS have impaired proprioception compared with that of a matched control group. The purpose of this study was to investigate whether a home-based exercise program could produce objective enhancement of proprioception as well as alleviate symptoms in JHS. METHODS A threshold detection paradigm was used to assess knee joint proprioception, balance was assessed using a balance board, and quadriceps and hamstring strength were measured by an isokinetic dynamometer. A visual analog scale was used to assess musculoskeletal pain, and quality of life was evaluated by a Short Form 36 questionnaire. Assessments were performed before and after an 8-week program of progressive closed kinetic chain exercises. RESULTS Following the exercise program, proprioceptive acuity increased in 16 of 18 subjects and was very significantly improved overall (P < 0.001). There was a comparable improvement in performance on the balance board (P < 0.001), and quadriceps and hamstring strength also increased significantly. Symptomatic improvement also occurred, in terms of both pain (P = 0.003) and quality-of-life (P = 0.029 for physical functioning; P = 0.008 for mental health) scores. CONCLUSION Appropriate exercises lead not only to symptomatic improvement, but also to demonstrable enhancement of objective parameters such as proprioception.
Community structures and activities of nitrifying and denitrifying bacteria in industrial wastewater‐treating biofilms

The bacterial community structure, in situ spatial distributions and activities of nitrifying and denitrifying bacteria in biofilms treating industrial wastewater were investigated by combination of the 16S rRNA gene clone analysis, fluorescence in situ hybridization (FISH) and microelectrodes. These results were compared with the nitrogen removal capacity of the industrial wastewater treatment plant (IWTP). Both nitrification and denitrification occurred in the primary denitrification (PD) tank and denitrification occurred in the secondary denitrification (SD) tank. In contrast, nitrification and denitrification rates were very low in the nitrification (N) tank. 16S rRNA gene clone sequence analysis revealed that the bacteria affiliated with Alphaproteobacteria, followed by Betaproteobacteria, were numerically important microbial groups in three tanks. The many clones affiliated with Alphaproteobacteria were closely related to the denitrifying bacteria (e.g., Hyphomicrobium spp., Rhodopseudomonas palustris, and Rhodobacter spp.). In addition, Methylophilus leisingeri affiliated with Betaproteobacteria, which favorably utilized methanol, was detected only in the SD‐tank to which methanol was added. Nitrosomonas europaea and Nitrosomonas marina were detected as the ammonia‐oxidizing bacteria affiliated with Betaproteobacteria throughout this plant, although the dominant species of them was different among three tanks. Nitrifying bacteria were mainly detected in the upper parts of the PD‐biofilm whereas their populations were low in the upper parts of the N‐biofilm. The presence of denitrifying bacteria affiliated with Hyphomicrobium spp. in SD‐ and N‐biofilms was verified by FISH analysis. Microelectrode measurements showed that the nitrifying bacteria present in the N‐ and PD‐biofilms were active and the bacteria present in the SD‐biofilm could denitrify. © 2006 Wiley Periodicals, Inc.
Intestinal ischemia/reperfusion enhances microglial activation and induces cerebral injury and memory dysfunction in rats*

Objective: The mortality of critically ill patients associated with intestinal ischemia/reperfusion remains very high, which results from multiorgan dysfunction or failure due to intestinal injury induced by intestinal ischemia/reperfusion. This study was carried out to investigate whether intestinal ischemia/reperfusion can cause cerebral injury and concomitant memory dysfunction, and explore the potential mechanisms. Design: Prospective, controlled, and randomized animal study. Setting: University research laboratory. Subjects: Male, adult Sprague-Dawley rats (weighing 250–300 g). Interventions: Intestinal ischemia/reperfusion was established by clamping the superior mesenteric artery for 90 mins followed by different reperfusion durations (2, 6, 12, 24, or 48 hrs). The sham surgical preparation including isolation of the superior mesenteric artery without occlusion was performed as control. Measurements and Main Results: In comparison with sham control, intestinal ischemia/reperfusion caused severe intestinal injury, accompanied by notable cerebral damage evidenced by increased wet-to-dry brain weight ratio reflecting brain edema and neuronal cell apoptosis manifested by increased apoptotic cell number and cleaved caspase-3 protein expressions. All these changes were concomitant with reduced survival rates as well as impaired memory function determined by Morris water maze test at 24 and 48 hrs after reperfusion. In addition, intestinal ischemia/reperfusion resultedin significant increases in the levels of tumor necrosis factor-&agr; and interleukin-6 both in the serum and in cortices and hippocampal Cornu Ammonis area 1 regions, concomitant with the activation of microglia, a key cellular mediator involved in neuroinflammation and neurodegeneration, which was evidenced by increased protein expressions of ionized calcium binding adaptor molecule 1. Furthermore, the releases of reactive oxygen species evidenced by increased malondialdehyde levels and decreased superoxide dismutase activities in cortices and hippocampal Cornu Ammonis area 1 regions were found after reperfusion. Conclusions: These findings indicate that intestinal ischemia/reperfusion-induced intestinal injury can lead to cerebral damage and memory dysfunction partly via microglia activation which further facilitates oxidative injury, inflammatory response, and neuronal cell apoptosis.