Mockup einer Betriebsleitstelle für automatisierte Shuttlebusse - Konzeption und Design eines universellen, visuellen und auditiven Interfaces

Derzeit sind automatisierte Shuttlebusse beim Einsatz auf einen Operator an Bord angewiesen. Damit sich dies nicht erst beim vollständig autonomen Fahren ändert, bedarf es weiterer Lösungsansätze. Eine Möglichkeit ist die Überwachung der Busse aus einer Betriebsleitstelle. Allerdings können mit den Betriebsleitstellen von Verkehrsgesellschaften nach heutigem technologischem Stand keine Fahrfunktionen übernommen werden. Um diese Forschungslücke zu schließen, wurde im Rahmen dieses Beitrags ein Mockup für eine Betriebsleitstelle von automatisierten Shuttlebussen entwickelt. Das Hauptaugenmerk bei der Konzeption dieses Interfaces liegt in der Anforderungsanalyse. Zu diesem Zweck wurden Experten aus Wirtschaft und Wissenschaft eingebunden. Als Ergebnis ist ein Mockup mit einer interaktiven Karte, einer Ereignisliste und einer Ansicht zur Übernahme der Fahrfunktionen entstanden

Theorization as institutional work: The dynamics of roles and practices

This study unpacks the construct of theorization – the process by which organizational ideas become delocalized and abstracted into theoretical models to support their diffusion across time and space. We adopt an institutional work lens to analyze the key components of theorization in contexts where institutional work is in transition from creating institutions to maintaining them. We build on a longitudinal inductive study of theorization by the Fair Labor Association (FLA), a private regulatory initiative which created and then enforced a code of conduct for working conditions in apparel factories. Our study reveals that when institutional work shifts from creating to maintaining an institutional arrangement of corporate social responsibility, there is a key change in how the FLA theorizes roles and practices related to this arrangement. We observe that theorization on key practices largely remain intact, whereas the roles of different actors are theorized in a dramatically different manner. Our findings contribute to a better understanding of the work involved in the aftermath of radical change by demonstrating the relative plasticity of roles over the rigidity of practices

I. Hautkrankheiten

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Extracorporeal Chloride Removal by Electrodialysis (CRe-ED): A Novel Approach to Correct Acidemia

RATIONALE: Acidemia is a severe condition among critically ill patients. Despite lack of evidence, sodium bicarbonate is frequently used to correct pH. However, its administration is burdened by several side effects. We hypothesized that the reduction of plasma chloride concentration could be an alternative strategy to correct acidemia. OBJECTIVES: To evaluate feasibility, safety, and effectiveness of a novel strategy to correct acidemia through Extracorporeal Chloride Removal by Electrodialysis (CRe-ED). METHODS: Ten swine (6 treatments, 4 controls) were sedated, mechanically ventilated and connected to an electrodialysis extracorporeal device capable of removing selectively chloride. In random order, an arterial pH of 7.15 was induced either through reduction of ventilation (respiratory acidosis) or through lactic acid infusion (metabolic acidosis). Acidosis was subsequently sustained for 12-14 hours. In treatment pigs, soon after reaching target acidemia, electrodialysis was started in order to restore pH. MEASUREMENTS AND MAIN RESULTS: During respiratory acidosis, electrodialysis reduced plasma chloride concentration by 26\ub15 mEq/L within 6 hours (final pH=7.36\ub10.04). Control animals exhibited incomplete and slower compensatory response to respiratory acidosis (final pH=7.29\ub10.03, p<0.001). During metabolic acidosis, electrodialysis reduced plasma chloride concentration by 15\ub13 mEq/L within 4 hours (final pH=7.34\ub10.07). No effective compensatory response occurred in controls (final pH=7.11\ub10.08; p<0.001). No complications occurred. CONCLUSIONS: We described the first in-vivo application of an extracorporeal system targeted to correct severe acidemia by lowering plasma chloride concentration. The CRe-ED proved to be feasible, safe, and effective. Further studies are warranted to assess its performance in presence of impaired respiratory and renal functions

Allosteric mechanism of Ca2+ activation and H+-inhibited gating of the MthK K+ channel

MthK is a Ca2+-gated K+ channel whose activity is inhibited by cytoplasmic H+. To determine possible mechanisms underlying the channel’s proton sensitivity and the relation between H+ inhibition and Ca2+-dependent gating, we recorded current through MthK channels incorporated into planar lipid bilayers. Each bilayer recording was obtained at up to six different [Ca2+] (ranging from nominally 0 to 30 mM) at a given [H+], in which the solutions bathing the cytoplasmic side of the channels were changed via a perfusion system to ensure complete solution exchanges. We observed a steep relation between [Ca2+] and open probability (Po), with a mean Hill coefficient (nH) of 9.9 ± 0.9. Neither the maximal Po (0.93 ± 0.005) nor nH changed significantly as a function of [H+] over pH ranging from 6.5 to 9.0. In addition, MthK channel activation in the nominal absence of Ca2+ was not H+ sensitive over pH ranging from 7.3 to 9.0. However, increasing [H+] raised the EC50 for Ca2+ activation by ∼4.7-fold per tenfold increase in [H+], displaying a linear relation between log(EC50) and log([H+]) (i.e., pH) over pH ranging from 6.5 to 9.0. Collectively, these results suggest that H+ binding does not directly modulate either the channel’s closed–open equilibrium or the allosteric coupling between Ca2+ binding and channel opening. We can account for the Ca2+ activation and proton sensitivity of MthK gating quantitatively by assuming that Ca2+ allosterically activates MthK, whereas H+ opposes activation by destabilizing the binding of Ca2+

A Kir6.2 mutation causing severe functional effects in vitro produces neonatal diabetes without the expected neurological complications

AIMS/HYPOTHESIS: Heterozygous activating mutations in the pancreatic ATP-sensitive K+ channel cause permanent neonatal diabetes mellitus (PNDM). This results from a decrease in the ability of ATP to close the channel, which thereby suppresses insulin secretion. PNDM mutations that cause a severe reduction in ATP inhibition may produce additional symptoms such as developmental delay and epilepsy. We identified a heterozygous mutation (L164P) in the pore-forming (Kir6.2) subunit of the channel in three unrelated patients and examined its functional effects. METHODS: The patients (currently aged 2, 8 and 20 years) developed diabetes shortly after birth. The two younger patients attempted transfer to sulfonylurea therapy but were unsuccessful (up to 1.1 mg kg(-1) day(-1)). They remain insulin dependent. None of the patients displayed neurological symptoms. Functional properties of wild-type and mutant channels were examined by electrophysiology in Xenopus oocytes. RESULTS: Heterozygous (het) and homozygous L164P K(ATP) channels showed a marked reduction in channel inhibition by ATP. Consistent with its predicted location within the pore, L164P enhanced the channel open state, which explains the reduction in ATP sensitivity. HetL164P currents exhibited greatly increased whole-cell currents that were unaffected by sulfonylureas. This explains the inability of sulfonylureas to ameliorate the diabetes of affected patients. CONCLUSIONS/INTERPRETATION: Our results provide the first demonstration that mutations such as L164P, which produce a severe reduction in ATP sensitivity, do not inevitably cause developmental delay or neurological problems. However, the neonatal diabetes of these patients is unresponsive to sulfonylurea therapy. Functional analysis of PNDM mutations can predict the sulfonylurea response

Voltage-dependent inactivation gating at the selectivity filter of the MthK K+ channel

Voltage-dependent K+ channels can undergo a gating process known as C-type inactivation, which involves entry into a nonconducting state through conformational changes near the channel’s selectivity filter. C-type inactivation may involve movements of transmembrane voltage sensor domains, although the mechanisms underlying this form of inactivation may be heterogeneous and are often unclear. Here, we report on a form of voltage-dependent inactivation gating observed in MthK, a prokaryotic K+ channel that lacks a canonical voltage sensor and may thus provide a reduced system to inform on mechanism. In single-channel recordings, we observe that Po decreases with depolarization, with a half-maximal voltage of 96 ± 3 mV. This gating is kinetically distinct from blockade by internal Ca2+ or Ba2+, suggesting that it may arise from an intrinsic inactivation mechanism. Inactivation gating was shifted toward more positive voltages by increasing external [K+] (47 mV per 10-fold increase in [K+]), suggesting that K+ binding at the extracellular side of the channel stabilizes the open-conductive state. The open-conductive state was stabilized by other external cations, and selectivity of the stabilizing site followed the sequence: K+ ≈ Rb+ > Cs+ > Na+ > Li+ ≈ NMG+. Selectivity of the stabilizing site is weaker than that of sites that determine permeability of these ions, suggesting that the site may lie toward the external end of the MthK selectivity filter. We could describe MthK gating over a wide range of positive voltages and external [K+] using kinetic schemes in which the open-conductive state is stabilized by K+ binding to a site that is not deep within the electric field, with the voltage dependence of inactivation arising from both voltage-dependent K+ dissociation and transitions between nonconducting (inactivated) states. These results provide a quantitative working hypothesis for voltage-dependent, K+-sensitive inactivation gating, a property that may be common to other K+ channels

The Promise and Perils of Private Voluntary Regulation: Labor Standards and Work Organization in Two Mexican Garment Factories

This paper is part of a larger project on globalization and labor standards organized by Professor Richard Locke of M.I.T.. In addition to the results presented in this paper (some of which appear as well in Monica Romis, "Beneath Corporate Codes of Conduct: What Drives Compliance in Two Mexican Garment Factories," (Masters Thesis, Dept. of Urban Studies and Planning, M.I.T., 2005)), the project entailed field research in China, Turkey, Europe and the United States as well as systematic analysis of Nike’s factory audits of working conditions in over 800 factories in 51 countries.What role can private voluntary regulation play in improving labor standards and working conditions in global supply chain factories? How does this system relate to and interact with other systems of labor regulation and work organization? This paper seeks to address these questions through a structured comparison of two factories supplying Nike, the world’s largest athletic footwear and apparel company. These two factories have many similarities - both are in Mexico, both are in the apparel industry, both produce more or less the same products for Nike (and other brands) and both are subject to the same code of conduct. On the surface, both factories appear to have similar employment (i.e., recruitment, training, remuneration) practices and they receive comparable scores when audited by Nike’s compliance staff. However, underlying (and somewhat obscured by) these apparent similarities, significant differences in actual labor conditions exist between these two factories. What drives these differences in working conditions? What does this imply for traditional systems of monitoring and codes of conduct? Field research conducted at these two factories reveals that beneath the code of conduct and various monitoring efforts aimed at enforcing it, workplace conditions and labor standards are shaped by very different patterns of work organization and human resource management policies