Wanted! Dead or alive: the tale of the Brown’s Grayling (Pseudochazara amymone)

The Brown’s Grayling (Pseudochazara amymone) is one of the most enigmatic and sought after species among European butterflies. Hiding its exact distribution for almost 40 years with the idea of protecting it, resulted in an increasing collector’s interest, with market prices reaching up to 1,000 euro for a single female after its discovery in Albania. Aiming to demystify this butterfly and enable entomologists and conservationists to see the species in its natural environment, we provide detailed information on its distribution in south-eastern Albania. In addition, we modelled the potential species distribution to facilitate further surveys within its potential range. The modelled range of P. amymone is highly fragmented stretching from the central part of eastern Albania to northern Greece and is strongly bound to ophiolite geological strata. The species was re-assessed as Endangered according to the IUCN criteria, with a predicted population decline due to construction of hydroelectric power plants in one of the locations. We argue that hiding valuable information regarding threatened insect species may have negative effects and we advocate publishing available distribution data so that conservation measures may be undertaken where and when necessary.     

VEGF-B: A survival,or an angiogenic factor?

Despite its early discovery and high sequence homology to the other VEGF family members, the biological function of VEGF-B remained debatable for a long time, and VEGF-B has received little attention from the field thus far. Recently, we and others have found that (1) VEGF-B is a potent survival factor for different types of cells by inhibiting apoptosis via suppressing the expression of BH3-only protein and other apoptotic/cell death-related genes. (2) VEGF-B has a negligible role in inducing blood vessel growth in most organs. Instead, it is critically required for blood vessel survival. VEGF-B targeting inhibited pathological angiogenesis by abolishing blood vessel survival in different animal models. (3) Using different types of neuro-injury and neurodegenerative disease models, VEGF-B treatment protected endangered neurons from apoptosis without inducing undesired blood vessel growth or permeability. Thus, VEGF-B is the first member of the VEGF family that has a potent survival/anti-apoptotic effect, while lacking a general angiogenic activity. Our work thus advocates that the major function of VEGF-B is to act as a “survival,” rather than an “angiogenic” factor and implicates a therapeutic potential of VEGF-B in treating different types of vascular and neurodegenerative diseases.Key words: VEGF-B, survival factor, angiogenesis, apoptosis, vascular biology     

Dead or Alive? Factors Affecting the Survival of Victims during Attacks by Saltwater Crocodiles (Crocodylus porosus) in Australia

Conflicts between humans and crocodilians are a widespread conservation challenge and the number of crocodile attacks is increasing worldwide. We identified the factors that most effectively decide whether a victim is injured or killed in a crocodile attack by fitting generalized linear models to a 42-year dataset of 87 attacks (27 fatal and 60 non-fatal) by saltwater crocodiles (Crocodylus porosus) in Australia. The models showed that the most influential factors were the difference in body mass between crocodile and victim, and the position of victim in relation to the water at the time of an attack. In-water position (for diving, swimming, and wading) had a higher risk than on-water (boating) or on-land (fishing, and hunting near the water''s edge) positions. In the in-water position a 75 kg person would have a relatively high probability of survival (0.81) if attacked by a 300 cm crocodile, but the probability becomes much lower (0.17) with a 400 cm crocodile. If attacked by a crocodile larger than 450 cm, the survival probability would be extremely low (<0.05) regardless of the victim’s size. These results indicate that the main cause of death during a crocodile attack is drowning and larger crocodiles can drag a victim more easily into deeper water. A higher risk associated with a larger crocodile in relation to victim’s size is highlighted by children’s vulnerability to fatal attacks. Since the first recently recorded fatal attack involving a child in 2006, six out of nine fatal attacks (66.7%) involved children, and the average body size of crocodiles responsible for these fatal attacks was considerably smaller (384 cm, 223 kg) than that of crocodiles that killed adults (450 cm, 324 kg) during the same period (2006–2014). These results suggest that culling programs targeting larger crocodiles may not be an effective management option to improve safety for children.     

Echinococcosis: an emerging or re-emerging zoonosis?

The aim of this review is a critical discussion of factors actually or potentially contributing to persistence or emergence of echinococcosis in humans. Alveolar echinococcosis (AE), a life-threatening infection of humans, is caused by a larval stage of Echinococcus multilocularis. The adult parasite inhabits the intestine of foxes and other carnivores and has a wide distribution in the northern hemisphere (North America and northern and central Eurasia). Recent surveys in central Europe have extended the known geographical occurrence of E. multilocularis in foxes from four countries at the end of the 1980s to at least 11 countries in 1999. Cases of human AE previously regularly reported from only four countries are now recorded from seven countries, but the annual incidences are low. Since adequate information from earlier surveys is not available, it is not possible to conclude if the new findings reflect a recent extension of the parasite's range or just the first identification of hitherto unnoticed endemic areas. Evidence of parasite spreading has been reported from North America and Japan. Factors with the potential of enhancing the infection risk for humans in the future include increasing fox populations and parasite prevalences, progressing invasion of cities by foxes, the establishment of urban cycles of the parasite, and the spill-over of the E. multilocularis infection from wild carnivores to domestic dogs and cats. In view of the potential severity and fatality of AE in humans health authorities should initiate internationally coordinated countermeasures. Although control programmes against human cystic echinococcosis (CE), caused by E. granulosus, have been established in some countries and effective control strategies are available, the parasite has still a wide geographical distribution affecting many countries of all continents. Thus, human CE is persisting in many parts of the world with high incidences, and in some areas it is a re-emerging problem. For example, alarming increases of the number of human cases have been reported from Bulgaria and Kazakhstan, and the People's Republic of China. Progress in control can only be expected if health authorities attribute a higher priority to this disease and if all modern diagnostic and control options (for example vaccination of intermediate host animals) can be used.     

Germline genome editing: Moratorium,hard law,or an informed adaptive consensus?

With the development of practical means of human germline genome editing (HGGE) in recent years, there have been calls for stricter regulation and oversight over HGGE interventions with potential for heritable changes in the germline. An international moratorium has been advocated. We examine the practicality of such a proposal, as well as of a regulation through the “traditional” mechanisms of international and municipal laws. We argue that these mechanisms are unlikely to achieve their intended objectives and that the better approach is to engage the international community of stakeholders, researchers, scientists, clinicians, and other workers directly involved in the field in working toward the development of an “informed adaptive consensus”. We offer suggestions as to how this may be achieved and how existing indirect levers of regulation may be harnessed toward this end.     

Non-canonical autophagy: an exception or an underestimated form of autophagy?

Macroautophagy (hereafter called autophagy) is a dynamic and evolutionarily conserved process used to sequester and degrade cytoplasm and entire organelles in a sequestering vesicle with a double membrane, known as the autophagosome, which ultimately fuses with a lysosome to degrade its autophagic cargo. Recently, we have unraveled two distinct forms of autophagy in cancer cells, which we term canonical and non-canonical autophagy. In contrast to classical or canonical autophagy, non-canonical autophagy is a process that does not require the entire set of autophagy-related (Atg) proteins in particular Beclin 1, to form the autophagosome. Non-canonical autophagy is therefore not blocked by the knockdown of Beclin 1 or of its binding partner hVps34. Moreover overexpression of Bcl-2, which is known to block canonical starvation-induced autophagy by binding to Beclin 1, is unable to reverse the non-canonical autophagy triggered by the polyphenol resveratrol in the breast cancer MCF-7 cell line. In MCF-7 cells, at least, non-canonical autophagy is involved in the caspase-independent cell death induced by resveratrol.     

The mast cell: an active participant or an innocent bystander?

Mast cells (MC) are phylogenetically old cells which are distributed throughout the human organism and, on the whole, occupy roughly the volume of the spleen. MC have long been recognized as key cells of type I hypersensitivity reactions. Several lines of evidence, however, indicate that they not only express critical effector functions in classic IgE-associated allergic disorders, but also play important roles in host defence against parasites, bacteria and perhaps even viruses. Indeed, it is now clear that MC can contribute to host defence in the context of either acquired or innate immune responses through the release of a myriad of pro-inflammatory and immunoregulatory molecules and the expression of a wide spectrum of surface receptors for cytokines and chemokines. Moreover, there is growing evidence that MC exert distinct non-immunological functions, playing a relevant role in tissue homeostasis, remodeling and fibrosis as well as in the processes of tissue angiogenesis. In this review, we provide a small insight into the biology of human MC and their potential implications in clinical pathology.     

Troponin-tropomyosin: an allosteric switch or a steric blocker?

The interaction of myosin subfragment 1 (S1) with actin-tropomyosin-troponin (regulated actin) is highly nucleotide dependent. The binding of S1 or S1-ADP (but not S1-ATP nor N,N'-rho-phenylenedimaleimide-modified S1-ATP) to regulated actin activates ATP hydrolysis even in the absence of Ca(2+). Investigations with S1 and S1-ADP have led to the idea that some actin sites are directly blocked toward the binding of S1 either by tropomyosin or troponin. The blocked state is thought to occur only at ionic strengths greater than 50 mM. The question is whether nonactivating S1 binding is blocked under the same conditions. We show that troponin inhibits binding of the nonactivating state, N,N'-rho-phenylenedimaleimide-S1-ATP, to actin but only when tropomyosin is absent. A lag in the rate of binding of activating S1 to actin (an indicator of the blocked state) occurs only in the presence of tropomyosin. Thus, tropomyosin inhibits binding of rigor S1 but not S1-ATP-like states. No evidence for an ionic strength-dependent change in the mechanism of regulation was observed either from measurements of the rate of activating S1 binding or from the equilibrium binding of nonactivating S1 to actin. At all conditions examined, N,N'-rho-phenylenedimaleimide-S1-ATP bound to regulated actin in the absence of Ca(2+). These results support the view of regulation in which tropomyosin movement is an allosteric switch that is modulated by activating myosin binding but that does not function solely by regulating myosin binding.     

Hypocretins: waking, arousal, or action?

The role of hypocretin (orexin) neurotransmission in waking and arousal, though of intense interest, is poorly understood. In this issue of Neuron, demonstrate that, in general, hypocretin neurons are minimally active during both sleep and quiet waking. In contrast, these neurons display robust activity during periods of alert and/or active waking.