Why do Neurons Enter the Cell Cycle?

Increasing evidence indicates that postmitotic, terminally differentiated neurons activate the cell cycle before death. The purpose of this cell cycle activation, however, remains elusive. In proliferating cells, cell cycle machinery is a major contributor to the DNA damage response, which is comprised of growth arrest. In quiescent cells such as terminally differentiated neurons, cell cycle-associated events may also be part of the DNA damage response. A link between DNA damage and repair, cell cycle regulation and cell death is becoming increasingly recognized for cycling cells but remains elusive for quiescent cells. Neurons are particularly susceptible to oxidative stress due to the high rate of oxidative metabolism in the brain and the low level of antioxidant enzymes compared to other somatic tissues. This is supported by fact that the intracellular end point of many neurotoxic stimuli is oxidative stress, which also represents a major cause of the neuropathology underlying a variety of neurodegenerative diseases. DNA is perhaps the major target of oxyradicals. Thus, oxidative stress may cause DNA damage, which is countered by a complex defense mechanism, the DNA damage response, which involves not only the elimination of DNA damage, but its coordination with other cellular processes such as cell-cycle progression, together directing to preserve genomic integrity. The function of such response is the removal of DNA damage by DNA repair pathways, or the elimination of damaged cells via apoptosis. The present review discusses the idea that the cell cycle machinery is a critical element of the DNA damage response not only in cycling, but also quiescent cells, and may bear the same function: to repair the damage or initiate apoptosis if the damage is too extensive to be repaired.     

When do objects become landmarks? A VR study of the effect of task relevance on spatial memory

We investigated how objects come to serve as landmarks in spatial memory, and more specifically how they form part of an allocentric cognitive map. Participants performing a virtual driving task incidentally learned the layout of a virtual town and locations of objects in that town. They were subsequently tested on their spatial and recognition memory for the objects. To assess whether the objects were encoded allocentrically we examined pointing consistency across tested viewpoints. In three experiments, we found that spatial memory for objects at navigationally relevant locations was more consistent across tested viewpoints, particularly when participants had more limited experience of the environment. When participants' attention was focused on the appearance of objects, the navigational relevance effect was eliminated, whereas when their attention was focused on objects' locations, this effect was enhanced, supporting the hypothesis that when objects are processed in the service of navigation, rather than merely being viewed as objects, they engage qualitatively distinct attentional systems and are incorporated into an allocentric spatial representation. The results are consistent with evidence from the neuroimaging literature that when objects are relevant to navigation, they not only engage the ventral "object processing stream", but also the dorsal stream and medial temporal lobe memory system classically associated with allocentric spatial memory.     

When do conservation planning methods deliver? Quantifying the consequences of uncertainty

The rapid global loss of biodiversity has led to a proliferation of systematic conservation planning methods. In spite of their utility and mathematical sophistication, these methods only provide approximate solutions to real-world problems where there is uncertainty and temporal change. The consequences of errors in these solutions are seldom characterized or addressed. We propose a conceptual structure for exploring the consequences of input uncertainty and oversimplified approximations to real-world processes for any conservation planning tool or strategy. We then present a computational framework based on this structure to quantitatively model species representation and persistence outcomes across a range of uncertainties. These include factors such as land costs, landscape structure, species composition and distribution, and temporal changes in habitat. We demonstrate the utility of the framework using several reserve selection methods including simple rules of thumb and more sophisticated tools such as Marxan and Zonation. We present new results showing how outcomes can be strongly affected by variation in problem characteristics that are seldom compared across multiple studies. These characteristics include number of species prioritized, distribution of species richness and rarity, and uncertainties in the amount and quality of habitat patches. We also demonstrate how the framework allows comparisons between conservation planning strategies and their response to error under a range of conditions. Using the approach presented here will improve conservation outcomes and resource allocation by making it easier to predict and quantify the consequences of many different uncertainties and assumptions simultaneously. Our results show that without more rigorously generalizable results, it is very difficult to predict the amount of error in any conservation plan. These results imply the need for standard practice to include evaluating the effects of multiple real-world complications on the behavior of any conservation planning method.     

Variational models of life-histories: When do solutions exist?

Techniques are presented for analyzing Euler-Lotka models in which age-specific birth and death rates depend on a collection v = (v₁,…, v_n) of trait parameters. Sufficient conditions are established for the existence of a v such that the growth rate r(v) is locally optimal. We analyze a general age-at-maturity model, and give criteria for the existence of such variational solutions within each of several sub-models.     

Where do we stand on the autoimmunity hypothesis of Chagas disease?

The question posed in the title elicits as much controversy today as it did when I wrote about this subject in the first issue of Parasitology Today 20 years ago. A consensus is now emerging that Trypanosoma cruzi, the etiological agent of Chagas disease, bears primary responsibility for producing chagasic pathology. Whether one or more of the autoimmune events described in human and experimental Chagas disease can contribute to, or aggravate, this pathology is the current question.     

When do sperm of the sea urchin,Pseudocentrotus depressus,undergo the acrosome reaction at fertilization?

Jelly coats of the sea urchin, Pseudocentrotus depressus, were stripped off the eggs, and the eggs were “inseminated.” After penetration through the isolated jelly hull, sperm swarmed in the cavity previously occupied by the egg. Electron microscopic examination could not detect any sperm with reacted acrosome. Observation was also made of the sperm penetrating through the intact jelly coat-egg complex. Although a number of sperm were examined in ultrathin sections, only those attached to the vitelline layer had undergone the acrosome reaction; those sperm embedded in jelly but not attached to the vitelline layer had not undergone the acrosome reaction. The sequence of events in fertilization of this species and of other echinoids is discussed.     

Remarks on the Nomenclature of“Dryopteris borreri Newman I854”

The nameDryopteris borreri Newman 1854 was not validly published in the specific rank. A new nameDryopteris pseudo-mas (Wollaston) Holub etPouzar 1967 is proposed as the correct name for this European species.