Eliminating Obstacles to Freedom of Establishment: The Competitive Edge of UK Company Law

This article examines the implications of the E.C.J.'s decisions in Überseering and Inspire Art against the background of the principal competing theories relating to lex societatis. It considers the tension between freedom of establishment (EC Treaty, arts 43 and 48) and the protective objectives of national corporate law regimes aimed at defeating the so-called Delaware effect. It goes on to argue that significant issues remain unresolved. More particularly, it questions whether creditor protection mechanisms contained in national insolvency laws will, in future, be viewed as obstacles to freedom of establishment

Company Law: Chapter 14

In this chapter we consider the duties which a director owes to the company. In Chapter 13 we explained that directors are fiduciaries and so much of the case law on their duties is founded on principles originating from the law of trusts and agency. We also saw that the early part of the 20th century marked a significant shift in the way the judges viewed the office of director. In tandem with this development the courts adopted a stricter approach towards the standard of care and skill expected of directors in the performance of their management roles. A concern of both equity and common law courts was to develop a corpus of rules designed to prevent directors abusing their considerable powers. The policy objective is based on prophylaxis and the result is a formidable body of reported decisions in which the judges have been developing the contours of directors’ liabilities. In addition to the work of the courts, legislation has also imposed a range of duties, devised principally as reactive measures against specific abuses by directors, particularly in relation to fraudulent asset stripping. Confronted with this considerable body of law, it came as little surprise that the Company Law Review (CLR), in line with its objectives of maximising clarity and accessibility, recommended that the duties of directors should be codified by way of a statutory restatement. Thus, the ‘general duties of directors’ now appear in Part 10 of the 2006 Act

Effect of antiandrogen flutamide on measures of hepatic regeneration in rats

Male rat liver undergoes a process of demasculinization during hepatic regeneration following partial hepatectomy. The possibility that antiandrogens might potentiate this demasculinization process and in so doing augment the hepatic regenerative response was investigated. Adult male Wistar rats were treated with the antiandrogen flutamide (2 mg/rat/day or 5 mg/rat/day subcutaneously) or vehicle for three days prior to and daily after a 70% partial hepatectomy. At various times after hepatectomy, the liver remnants were removed and weighed. Rates of DNA and polyamine synthesis were assessed by measuring thymidine kinase and ornithine decarboxylase activities, respectively. Hepatic estrogen receptor status and the activity of alcohol dehydrogenase, an androgen-sensitive protein, were measured. Prior to surgery, the administration of 5 mg/day flutamide reduced the hepatic cytosolic androgen receptor activity by 98% and hepatic cytosolic estrogen receptor content by 92% compared to that present in vehicle-treated controls. After hepatectomy, however, all differences in sex hormone receptor activity between the treatment groups were abolished. The rate of liver growth after partial hepatectomy in the three groups was identical. Moreover, hepatectomy-induced increases in ornithine decarboxylase activity and thymidine kinase activity were comparable. These data demonstrate that, although flutamide administration initially alters the sex hormone receptor status of the liver, these affects have no effect on the hepatic regenerative response following a partial hepatectomy. © 1989 Plenum Publishing Corporation

A False Start in the Race Against Doping in Sport: Concerns With Cycling’s Biological Passport

Professional cycling has suffered from a number of doping scandals. The sport’s governing bodies have responded by implementing an aggressive new antidoping program known as the biological passport. Cycling’s biological passport marks a departure from traditional antidoping efforts, which have focused on directly detecting prohibited substances in a cyclist’s system. Instead, the biological passport tracks biological variables in a cyclist’s blood and urine over time, monitoring for fluctuations that are thought to indirectly reveal the effects of doping. Although this method of indirect detection is promising, it also raises serious legal and scientific concerns. Since its introduction, the cycling community has debated the reliability of indirect biological-passport evidence and the clarity, consistency, and transparency of its use in proving doping violations. Such uncertainty undermines the legitimacy of finding cyclists guilty of doping based on this indirect evidence alone. Antidoping authorities should address these important concerns before continuing to pursue doping sanctions against cyclists solely on the basis of their biological passports

The Importance of pH in Regulating the Function of the Fasciola hepatica Cathepsin L1 Cysteine Protease

The helminth parasite Fasciola hepatica secretes cathepsin L cysteine proteases to invade its host, migrate through tissues and digest haemoglobin, its main source of amino acids. Here we investigated the importance of pH in regulating the activity and functions of the major cathepsin L protease FheCL1. The slightly acidic pH of the parasite gut facilitates the auto-catalytic activation of FheCL1 from its inactive proFheCL1 zymogen; this process was ∼40-fold faster at pH 4.5 than at pH 7.0. Active mature FheCL1 is very stable at acidic and neutral conditions (the enzyme retained ∼45% activity when incubated at 37°C and pH 4.5 for 10 days) and displayed a broad pH range for activity peptide substrates and the protein ovalbumin, peaking between pH 5.5 and pH 7.0. This pH profile likely reflects the need for FheCL1 to function both in the parasite gut and in the host tissues. FheCL1, however, could not cleave its natural substrate Hb in the pH range pH 5.5 and pH 7.0; digestion occurred only at pH≤4.5, which coincided with pH-induced dissociation of the Hb tetramer. Our studies indicate that the acidic pH of the parasite relaxes the Hb structure, making it susceptible to proteolysis by FheCL1. This process is enhanced by glutathione (GSH), the main reducing agent contained in red blood cells. Using mass spectrometry, we show that FheCL1 can degrade Hb to small peptides, predominantly of 4–14 residues, but cannot release free amino acids. Therefore, we suggest that Hb degradation is not completed in the gut lumen but that the resulting peptides are absorbed by the gut epithelial cells for further processing by intracellular di- and amino-peptidases to free amino acids that are distributed through the parasite tissue for protein anabolism

γ-Glutamylcysteine detoxifies reactive oxygen species by acting as glutathione peroxidase-1 cofactor

Reactive oxygen species regulate redox-signaling processes, but in excess they can cause cell damage, hence underlying the aetiology of several neurological diseases. Through its ability to down modulate reactive oxygen species, glutathione is considered an essential thiol-antioxidant derivative, yet under certain circumstances it is dispensable for cell growth and redox control. Here we show, by directing the biosynthesis of γ-glutamylcysteine—the immediate glutathione precursor—to mitochondria, that it efficiently detoxifies hydrogen peroxide and superoxide anion, regardless of cellular glutathione concentrations. Knocking down glutathione peroxidase-1 drastically increases superoxide anion in cells synthesizing mitochondrial γ-glutamylcysteine. In vitro, γ-glutamylcysteine is as efficient as glutathione in disposing of hydrogen peroxide by glutathione peroxidase-1. In primary neurons, endogenously synthesized γ-glutamylcysteine fully prevents apoptotic death in several neurotoxic paradigms and, in an in vivo mouse model of neurodegeneration, γ-glutamylcysteine protects against neuronal loss and motor impairment. Thus, γ-glutamylcysteine takes over the antioxidant and neuroprotective functions of glutathione by acting as glutathione peroxidase-1 cofactor

Assessing bird exclusion effects in a wetland crossed by a railway (Sado estuary, Portugal)

L. Borda-de-Água et al. (eds.), Railway Ecology, Chapter 11, p. 179-195Linear transportation infrastructures may displace wildlife from nearby areas that otherwise would provide adequate habitat conditions. This exclusion effect has been documented in roads, but much less is known about railways. Here we evaluated the potential exclusion effect on birds of a railway crossing a wetland of international importance (Sado Estuary, Portugal). We selected 22 sectors representative of locally available wetland habitats (salt pans, rice paddy fields, and intertidal mudflats); of each, half were located either close to (0–500 m) or far from (500–1500 m) the railway line. Water birds were counted in each sector between December 2012 and October 2015, during two months per season (spring, summer, winter, and autumn) and year, at both low and high tide. We recorded 46 species, of which the most abundant (>70% of individuals) were black-headed gull, greater flamingo, northern shoveler, black-tailed godwit, and lesser black-backed gull. Peak abundances were found in autumn and winter. There was no significant variation between sectors close to and far from the railway in species richness, total abundance, and abundance of the most common species. Some species tended to be most abundant either close to or far from the railway albeit not significantly so but this often varied across the tidal and annual cycles. Overall, our study did not find noticeable exclusion effects of this railway on wetland birds, with spatial variation in abundances probably reflecting habitat selection and daily movement patterns. Information is needed on other study systems to assess the generality of our findingsinfo:eu-repo/semantics/publishedVersio