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University participation has increased in many countries in recent years in response to the requirement for a strong knowledge economy. While this has provided additional access opportunities, not all students enter university with the same transferrable social capital. To counter this, educational institutions could play a strategic role in the development of networks and connections that provide students with valuable information, support and a sense of belonging. This research project explored the development of social capital, and its impact upon university life satisfaction and wellbeing, within an Australian university course undertaken by all first-year students regardless of programme or discipline. A survey of students was conducted three times over one semester. The results suggested that peer-level social capital indicators of trust, social support and relatedness changed over the semester, while other social capital indicators begin high and remain stable. Bridging social capital and peer social support predicted university life satisfaction. The relationship between social capital and wellbeing was found to be more complex. In a competitive, global tertiary environment, institutions could maximise the satisfaction and success of increasingly diverse student cohorts through strategies that facilitate social capital development.

The ventricular folds, also called false vocal folds or vestibular folds, are two laryngeal structures located above and in the vicinity of the vocal folds. As illustrated in Figure 1a, [...], Purpose: In this study, the authors aimed (a) to provide a classification of the ventricular-fold dynamics during voicing, (b) to study the aerodynamic impact of these motions on vocal-fold vibrations, and (c) to assess whether ventricular-fold oscillations could be sustained by aerodynamic coupling with the vocal folds. Method: A 72-sample database of vocal gestures accompanying different acoustical events comprised high-speed cinematographic, audio, and electroglottographic recordings of 5 subjects. Combining the physiological correlates with a theoretical model of phonation, the vocal-ventricular aerodynamic interactions were investigated. Results: A ventricular-fold motion is found during (de)crescendos, shout, throat singing, yodel, growls, and glides with transitions between registers. Three main types of dynamics are identified: slow nonoscillatory motion and fast oscillatory motion with aperiodical or periodical vibrations. These patterns accompany a change in voice quality, pitch, and/or intensity. Alterations of glottal-oscillatory amplitude, frequency, and contact were predicted. It is shown that a ventricular oscillation can be initiated and sustained by aerodynamic coupling with the vocal folds. Conclusions: Vocal-ventricular aerodynamic interactions can alter, enhance, or suppress vocal-fold vibrations or leave them unchanged, depending on the ventricular-fold dynamics involved. Depending on its variation in time, a similar level of ventricular-fold adduction impacts the glottal vibratory magnitude and contact much differently. Keywords: voice, ventricular folds, aerodynamics, high-speed cinematography, phonation modeling

Introduction Pruritus (itch) is a common symptom of numerous dermatologic, allergic, and autoimmune diseases and tumors, but its molecular and cellular basis is still poorly understood (1). Itch is an [...], In humans, pruritus (itch) is a common but poorly understood symptom in numerous skin and systemic diseases. Endothelin 1 (ET-1) evokes histamine-independent pruritus in mammals through activation of its cognate G protein-coupled receptor endothelin A receptor (ETAR). Here, we have identified neural endothelin-converting enzyme 1 (ECE-1) as a key regulator of ET-1-induced pruritus and neural signaling of itch. We show here that ETAR, ET-1, and ECE-1 are expressed and colocalize in murine dorsal root ganglia (DRG) neurons and human skin nerves. In murine DRG neurons, ET-1 induced internalization of ETAR within ECE-1-containing endosomes. ECE-1 inhibition slowed ETAR recycling yet prolonged ET-1-induced activation of ERK1/2, but not p38. In a murine itch model, ET-1-induced scratching behavior was substantially augmented by pharmacological ECE-1 inhibition and abrogated by treatment with an ERK1/2 inhibitor. Using iontophoresis, we demonstrated that ET-1 is a potent, partially histamine-independent pruritogen in humans. Immunohistochemical evaluation of skin from prurigo nodularis patients confirmed an upregulation of the ET-1/ETAR/ECE-1/ERK1/2 axis in patients with chronic itch. Together, our data identify the neural peptidase ECE-1 as a negative regulator of itch on sensory nerves by directly regulating ET-1-induced pruritus in humans and mice. Furthermore, these results implicate the ET-1/ECE-1/ERK1/2 pathway as a therapeutic target to treat pruritus in humans.

Introduction Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia and is a significant contributor to cardiovascular morbidity and possibly mortality. Emerging evidence suggests an important role for abnormal [...], Atrial fibrillation (AF), the most common human cardiac arrhythmia, is associated with abnormal intracellular [Ca.sup.2+] handling. Diastolic [Ca.sup.2+] release from the sarcoplasmic reticulum via 'leaky' ryanodine receptors (RyR2s) is hypothesized to contribute to arrhythmogenesis in AF, but the molecular mechanisms are incompletely understood. Here, we have shown that mice with a genetic gain-of-function defect in Ryr2 (which we termed [Ryr2.sup.R176Q/+] mice) did not exhibit spontaneous AF but that rapid atrial pacing unmasked an increased vulnerability to AF in these mice compared with wild-type mice. Rapid atrial pacing resulted in increased [Ca.sup.2+]/calmodulin-dependent protein kinase II (CaMKII) phosphorylation of RyR2, while both pharmacologic and genetic inhibition of CaMKII prevented AF inducibility in [Ryr2.sup.R176Q/+] mice. This result suggests that AF requires both an arrhythmogenic substrate (e.g., RyR2 mutation) and enhanced CaMKII activity. Increased CaMKII phosphorylation of RyR2 was observed in atrial biopsies from mice with atrial enlargement and spontaneous AF, goats with lone AF, and patients with chronic AF. Genetic inhibition of CaMKII phosphorylation of RyR2 in [Ryr2.sup.S2814A] knockin mice reduced AF inducibility in a vagotonic AF model. Together, these findings suggest that increased RyR2-dependent [Ca.sup.2+] leakage due to enhanced CaMKII activity is an important downstream effect of CaMKII in individuals susceptible to AF induction.

Triadin is involved in the regulation of cardiac excitation-contraction coupling. However, the extent of its contribution to the regulation of sarcoplasmic reticulum (SR) Ca release remains unclear, because overexpression of triadin in single-transgenic mice was associated with the downregulation of its homologous protein, junctin. In the present study, this problem was circumvented by cross-breeding of mice with heart-directed overexpression of triadin and junctin (JxT). This resulted in a stable approximately threefold expression of total triadin but unchanged junctin protein. Transgenic mice exhibited cardiac hypertrophy and structural abnormalities of myofibrils. Measurement of cardiac function by echocardiography and edge detection in myocytes revealed an impaired relaxation in JxT mice. The stimulation of [beta]-adrenergic receptors resulted in a depressed contractility and an impaired relaxation in catheterized hearts and myocytes of JxT mice. The use of a maximum stimulation frequency (5 Hz) was associated with both a lower shortening and relengthening in isolated myocytes of JxT mice. The contractile effects in JxT myocytes were paralleled by similar changes of the intracellular Ca concentration ([[Ca].sub.i]) peak amplitude and Ca transient decay kinetics at basal conditions, under administration of isoproterenol, and with high-frequency stimulation. Finally, we found a higher caffeine-induced [[Ca].sub.i] peak amplitude in JxT myocytes. Our data show that the stable expression of triadin, independent of junctin expression, resulted in cardiac hypertrophy, prolonged basal relaxation, a depressed response to [beta]-adrenergic agonists, and altered Ca transients. Thus the maintenance of triadin expression is essential for normal SR Ca cycling and contractile function. transgenic mice; sarcoplasmic reticulum; hypertrophy; Ca signaling; cardiac function; force-frequency relationship; [beta]-adrenergic receptor stimulation

Junctin is a transmembrane protein located at the cardiac junctional sarcoplasmic reticulum (SR) and forms a quaternary complex with the [Ca.sup.2+] release channel, triadin and calsequestrin. Impaired protein interactions within this complex may alter the [Ca.sup.2+] sensitivity of the [Ca.sup.2+] release channel and may lead to cardiac dysfunction, including hypertrophy, depressed contractility, and abnormal [Ca.sup.2+] transients. To study the expression of junctin and, for comparison, triadin, in heart failure, we measured the levels of these proteins in SR from normal and failing human hearts. Junctin was below our level of detection in SR membranes from failing human hearts, and triadin was downregulated by 22%. To better understand the role of junctin in the regulation of [Ca.sup.2+] homeostasis and contraction of cardiac myocytes, we used an adenoviral approach to overexpress junctin in isolated rat cardiac myocytes. A recombinant adenovirus encoding the green fluorescent protein served as a control. Infection of myocytes with the junctin-expressing virus resulted in an increased RNA and protein expression of junctin. [Ca.sup.2+] transients showed a decreased maximum [Ca.sup.2+] amplitude, and contractility of myocytes was depressed. Our results demonstrate that an increased expression of junctin is associated with an impaired [Ca.sup.2+] homeostasis. Downregulation of junctin in human heart failure may thus be a compensatory mechanism. junctin; adenovirus; cardiac myocytes; calcium transient; sarcoplasmic reticulum doi:10.1152/ajpheart.01187.2006

The article discusses the formation of the Berlin Sharpshooter's Association in 1862 by the left-wing Berliner Volkszeitung that was amplified by a clever use of publicity created through festivals, public exercises and the press is illustrated.

A concept enabling larger photonic band gaps in simple cubic structures, the manufacturing of which is nevertheless is based on macroporous silicon, is evaluated. Combining the anisotropic posttreatment with the isotropic one and keeping the arbitrarily adjustable initial pore shape of the macroporous silicon in mind establishes a versatile sculpturing technique of complex three-dimensional structures in silicon that might be used in future photonic crystal applications.

Preventive diagnosis and maintenance of transformers have become more and more popular in recent times in order to improve the reliability of electric power systems. Dielectric testing techniques such as return voltage measurement (RVM) and polarization-depolarization current (PDC) measurement are being investigated as potential tools for condition assessment of transformer insulation. A better understanding and analysis of the dielectric test results are only possible with a clear understanding of the physical behavior of the insulation system in response to moisture and aging. A circuit model, which describes the dielectric behavior of the transformer's main insulation system, has been parameterized in this paper. The values of the parameters of the model have been identified from the dielectric tests. A correlation has been developed between the physical condition of the insulation and the equivalent model parameters that enable a clear and transparent interpretation of the dielectric test results. Index Terms--Depolarization current, dielectric response, equivalent circuit, modeling, polarization current, return voltage, transformer insulation.

Author(s): Sven Matthias; Frank Müller (corresponding author) The brownian motion of mesoscopic particles is ubiquitous and usually random. But in systems with periodic asymmetric barriers to movement, directed or 'rectified' [...]

Due to intensive intracellular metabolism of short-chain fatty acids, ruminal epithelial cells generate large amounts of D-[beta]-hydroxybutyric acid, acetoacetic acid, and lactic acid. These acids have to be extruded from the cytosol to avoid disturbances of intracellular pH ([pH.sub.i]). To evaluate acid extrusion, [pH.sub.i] was studied in cultured ruminal epithelial cells of sheep using the pH-sensitive fluorescent dye 2', 7'-bis(2-carboxyethyl)-5(6)-carboxyfluorescein. Extracellular addition of D-[beta]-hydroxybutyrate, acetoacetate, or lactate (20 mM) resulted in intracellular acidification. Vice versa, removing extracellular D-[beta]-hydroxybutyrate, acetoacetate, or lactate after preincubation with the respective monocarboxylate induced an increase of [pH.sub.i]. Initial rate of phi decrease as well as of [pH.sub.i] recovery was strongly inhibited by pCMBS (400 [micro]M) and phloretin (20 [micro]M). Both cultured cells and intact ruminal epithelium were tested for the possible presence of proton-linked monocarboxylate transporter (MCT) on both the mRNA and protein levels. With the use of RT-PCR, mRNA encoding for MCT1 isoform was demonstrated in cultured ruminal epithelial cells and the ruminal epithelium. Immunostaining with MCT1 antibodies intensively labeled cultured ruminal epithelial cells and cells located in the stratum basale of the ruminal epithelium. In conclusion, our data indicate that MCT1 is expressed in the stratum basale of the ruminal epithelium and may function as a main mechanism for removing ketone bodies and lactate together with [H.sup.+] from the cytosol into the blood. intracellular pH; short-chain fatty acids; intracellular metabolism

Author(s): David R. Stevens [1]; Reinhard Seifert [2]; Bernd Bufe [3]; Frank Müller [2]; Elisabeth Kremmer [4]; Renate Gauss [2]; Wolfgang Meyerhof [3]; U. Benjamin Kaupp [2]; Bernd Lindemann (corresponding [...]

Glutamic-acid-rich proteins (GARPs) exist as GARP1 and GARP2, and as a large cytoplasmic domain of the beta-subunit of the cyclic GMP-gated channel. GARPs have been identified as multivalent proteins interacting with those involved in cGMP signalling, phosphodiesterase and guanylate cyclase, and with a retina-specific ATP-binding cassette transporter.