Oligodendrocyte is a highly specialized glial cell type in the vertebrate central nervous system, which guarantees the long-distance transmission of action potential by producing myelin sheath wrapping adjacent axons. Disrupted myelin and oligodendrocytes are hallmarks of some devastating neurological diseases, such as multiple sclerosis, although their contribution to neurodegeneration in a given disease is still controversial. However, accumulating evidence from clinical studies and genetic animal models implicates oligodendrocyte dysfunction as one of major events in the processes of initiation and progression of neurodegeneration. In this article, we will review recent progress in understanding non-traditional function of oligodendrocytes in neuronal support and protection independent of myelin sheath and its possible contribution to neurodegeneration. Oligodendrocytes play a pivotal role in neurodegenerative diseases among which special emphasis is given to multiple system atrophy and Alzheimer’s disease in this review.

This review discussed metabolism in poultry and wild birds with an emphasis on what remains to be elucidated. Circulating concentrations of glucose are much greater in both poultry and wild birds than in mammals which in turn are higher than in reptiles. The basis for this difference is unknown but does not appear to be related to the requirements of flight. Furthermore, birds exhibit a refractoriness to potential adverse effects of very high circulating concentrations of glucose. Again the basis of this is unclear. There is substantial information on the control of metabolism in poultry, although which hormones are exerting physiologic roles remains to be clarified. There is a tacit but unverified assumption that the control mechanisms are the same in wild birds and in poultry. Despite, significant research focus on metabolism in poultry and to a less extent wild birds, there is a dearth of studies determining metabolism in a quantitative manner.

The serine/threonine-specific protein kinase AKT is gaining recognition as a major crossroad in numerous cellular signaling pathways through its ability to regulate cell differentiation, proliferation, survival and metabolism. This review focuses on the recent advances in AKT signaling and downstream events in T cells, emphasizing its contrasting role in conventional and regulatory (Treg) T cell populations. Activation of AKT has been known for many years to be critical in the development and function of conventional T cells. However, it has just recently been uncovered that AKT exerts an inhibitory effect on Treg generation and suppressor function. These studies have placed AKT at the nexus of Treg development and function, thus opening novel avenues for therapeutic manipulation.

Recently, mounting evidence implicating reactive oxygen species (ROS) generated by NADPH oxidase (NOX) enzymes in the pathogenesis of several neurodegenerative diseases including Amyotrophic lateral sclerosis (ALS), Alzheimer’s (AD), Parkinson’s (PD) and polyglutamine disease, have arisen. NOX enzymes are transmembrane proteins and generate reactive oxygen species by transporting electrons across lipid membranes. Under normal healthy conditions, low levels of ROS produced by NOX enzymes have been shown to play a role in neuronal differentiation and synaptic plasticity. However, in chronic neurodegenerative diseases over-activation of NOX in neurons, as well as in astrocytes and microglia, has been linked to pathogenic processes such as oxidative stress, exitotoxicity and neuroinflammation. In this review, we summarize the current knowledge about NOX functions in the healthy central nervous system and especially the role of NOX enzymes in neurodegenerative disease processes.

Abiotic stresses such as drought, cold, and high salinity are among the most adverse factors that affect plant growth and yield in the field. MicroRNAs are small RNA molecules that regulate gene expression in a sequence-specific manner and play an important role in plant stress response. Identifying abiotic stress-associated microRNAs and understanding their function will help develop new strategies for improvement of plant stress tolerance. Here we highlight recent advances in our understanding of abiotic stress-associated miRNAs in various plants, with focus on their discovery, expression analysis, and evolution.

During hunting, bats of suborder Microchiropetra emit intense ultrasonic pulses and analyze the weak returning echoes with their highly developed auditory system to extract the information about insects or obstacles. These bats progressively shorten the duration, lower the frequency, decrease the intensity and increase the repetition rate of emitted pulses as they search, approach, and finally intercept insects or negotiate obstacles. This dynamic variation in multiple parameters of emitted pulses predicts that analysis of an echo parameter by the bat would be inevitably affected by other co-varying echo parameters. The progressive increase in the pulse repetition rate throughout the entire course of hunting would presumably enable the bat to extract maximal information from the increasing number of echoes about the rapid changes in the target or obstacle position for successful hunting. However, the increase in pulse repetition rate may make it difficult to produce intense short pulse at high repetition rate at the end of long-held breath. The increase in pulse repetition rate may also make it difficult to produce high frequency pulse due to the inability of the bat laryngeal muscles to reach its full extent of each contraction and relaxation cycle at a high repetition rate. In addition, the increase in pulse repetition rate increases the minimum threshold (i.e. decrease auditory sensitivity) and the response latency of auditory neurons. In spite of these seemingly physiological disadvantages in pulse emission and auditory sensitivity, these bats do progressively increase pulse repetition rate throughout a target approaching sequence. Then, what is the adaptive value of increasing pulse repetition rate during echolocation? What are the underlying mechanisms for obtaining maximal information about the target features during increasing pulse repetition rate? This article reviews the electrophysiological studies of the effect of pulse repetition rate on multiple-parametric selectivity of neurons in the central nucleus of the inferior colliculus of the big brown bat, Eptesicus fuscus using single repetitive sound pulses and temporally patterned trains of sound pulses. These studies show that increasing pulse repetition rate improves multiple-parametric selectivity of inferior collicular neurons. Conceivably, this improvement of multiple-parametric selectivity of collicular neurons with increasing pulse repetition rate may serve as the underlying mechanisms for obtaining maximal information about the prey features for successful hunting by bats.

Since the discovery of protein phosphorylation as an important modulator of many cellular processes, the involvement of protein kinases in diseases, such as cancer, diabetes, cardiovascular diseases, and central nervous system pathologies, has been extensively documented. Our understanding of many disease pathologies at the molecular level, therefore, requires the comprehensive identification of substrates targeted by protein kinases. In this review, we focus on recent techniques for kinase substrate identification in high throughput, in particular on genetic and proteomic approaches. Each method with its inherent advantages and limitations is discussed.

Epigenetic deregulation is intimately associated with the development of human diseases. Intensive studies are currently underway to clarify the mechanism for the sake of achieving ideal diagnostic and therapeutic goals. It has been demonstrated that enzymes with histone-modifying activities can also target non-histone proteins, with the underlying mechanism remaining obscure. In this review, we focus on a novel histone mimicry strategy that may be wildly adapted during the non-histone substrate recognition process. Its potential clinical implications are also discussed.

Biomineralization processes are frequently found in nature. Living organisms use various strategies to create highly ordered and hierarchical mineral structures under physiologic conditions in which the temperatures and pressures are much lower than those required to form the same mineralized structures by chemical synthesis. Although the mechanism of biomineralization remains elusive, proteins have been found responsible for the formation of such mineral structures in many cases. These proteins are active components in the process of biomineralization. The mechanisms by which their function can vary from providing active organic matrices that control the formation of specific mineral structures to being catalysts that facilitate the crystallization of certain metal ions. This review summarizes the current understanding of the functions of several representative biomineralization proteins from vertebrates to bacteria in the hopes of providing useful insight and guidance for further elucidation of mechanisms of biomineralization processes in living organisms.

Complex systems from different fields of knowledge often do not allow a mathematical description or modeling, because of their intricate structure composed of numerous interacting components. As an alternative approach, it is possible to study the way in which observables associated with the system fluctuate in time. These time series may provide valuable information about the underlying dynamics. It has been suggested that complex dynamic systems, ranging from ecosystems to financial markets and the climate, produce generic early-warning signals at the “tipping points,” where they announce a sudden shift toward a different dynamical regime, such as a population extinction, a systemic market crash, or abrupt shifts in the weather. On the other hand, the framework of Self-Organized Criticality (SOC), suggests that some complex systems, such as life itself, may spontaneously converge toward a critical point. As a particular example, the quasispecies model suggests that RNA viruses self-organize their mutation rate near the error-catastrophe threshold, where robustness and evolvability are balanced in such a way that survival is optimized. In this paper, we study the time series associated to a classical discrete quasispecies model for different mutation rates, and identify early-warning signals for critical mutation rates near the error-catastrophe threshold, such as irregularities in the kurtosis and a significant increase in the autocorrelation range, reminiscent of 1/f noise. In the present context, we find that the early-warning signals, rather than broadcasting the collapse of the system, are the fingerprint of survival optimization.