An Exploratory Study of Extreme Sport Athletes' Nature Interactions: From Well-Being to Pro-environmental Behavior.

Traditionally, perceptions about extreme sport athletes being disconnected from nature and a risk-taking population have permeated the research literature. Drawing upon theoretical perspectives from environmental, sport, organizational and positive psychology, this qualitative study attempts to explore the lived experiences of four male and four female extreme sport athletes. The purpose of this study was to gain insight and understanding into the individuals' attitudes toward the benefits of extreme sport activities for well-being, resilience and pro-environmental behavior. Eight participants (Mean age = 40.5 years; SD = ± 12.9) provided written informed consent to partake in semi-structured interviews. Each athlete provided written consented to allow the publication of their identifiable data and in order to facilitate sharing of their autobiographical account of their experiences. After conducting thematic analysis, meta-themes that emerged from the analyses were as follows: (a) early childhood experiences, (b) the challenge of the outdoors, (c) their emotional response to nature, (d) nature for coping, (e) restorative spaces, and (f) environmental concern. The findings convey great commonalities across the participants with regard to their mindset, their emotional well-being as well as their connectivity with nature and attitudes toward the natural environment. The cognitive-affective-social-behavioral linkage of the benefits of extreme sport participation for well-being, psychological recovery and pro-environmental behavior are highlighted. This study examining the lived experiences of extreme sportspeople provides a novel contribution to our contemporary understanding of extreme athletes' relationship to nature and its commensurate impact upon well-being and pro-environmental attitudes. The findings suggest that extreme sport participation, while inherently risky has psychological benefits ranging from evoking positive emotions, developing resilience and life coping skills to cultivating strong affinity to and connection with nature and the natural environment.

Cytochrome c oxidase deficiency accelerates mitochondrial apoptosis by activating ceramide synthase 6.

Although numerous pathogenic changes within the mitochondrial respiratory chain (RC) have been associated with an elevated occurrence of apoptosis within the affected tissues, the mechanistic insight into how mitochondrial dysfunction initiates apoptotic cell death is still unknown. In this study, we show that the specific alteration of the cytochrome c oxidase (COX), representing a common defect found in mitochondrial diseases, facilitates mitochondrial apoptosis in response to oxidative stress. Our data identified an increased ceramide synthase 6 (CerS6) activity as an important pro-apoptotic response to COX dysfunction induced either by chemical or genetic approaches. The elevated CerS6 activity resulted in accumulation of the pro-apoptotic C16 : 0 ceramide, which facilitates the mitochondrial apoptosis in response to oxidative stress. Accordingly, inhibition of CerS6 or its specific knockdown diminished the increased susceptibility of COX-deficient cells to oxidative stress. Our results provide new insights into how mitochondrial RC dysfunction mechanistically interferes with the apoptotic machinery. On the basis of its pivotal role in regulating cell death upon COX dysfunction, CerS6 might potentially represent a novel target for therapeutic intervention in mitochondrial diseases caused by COX dysfunction.

Hijacking the host proteasome for the temporal degradation of bacterial effectors.

To establish infection, intracellular pathogens need to modulate host cellular processes. Modulation of host processes is achieved by the action of various "effector proteins" which are delivered from the bacteria to the host cell cytosol. In order to orchestrate host cell reprogramming, the function of effectors inside host cells is regulated both temporally and spatially. In eukaryotes one of the most prominent processes used to degrade proteins is the ubiquitin-proteasome system. Recently it has emerged that the intracellular pathogen Legionella pneumophila is able to achieve temporal regulation of an effector using the ubiquitin-proteasome system. After establishing its replicative niche, the L. pneumophila effector SidH is degraded by the host proteasome. Most remarkably another effector protein LubX is able to mimic the function of an eukaryotic E3 ubiquitin ligase and polyubiquitinates SidH, targeting it for degradation. In this paper we describe a method to detect the polyubiquitin-modified forms of SidH in vitro and in vivo. Analyzing the temporal profile of polyubiquitination and degradation of bacterial effectors aids towards our understanding of how bacteria hijack host systems.

Legionella pneumophila subversion of host vesicular transport by SidC effector proteins.

Tethering proteins play a key role in vesicular transport, ensuring that cargo arrives at a specific destination. The bacterial effector protein SidC and its paralog SdcA have been described as tethering factors encoded by the intracellular pathogen Legionella pneumophila. Here, we demonstrate that SidC proteins are important for early events unique to maturation of vacuoles containing Legionella and discover monoubiquitination of Rab1 as a new SidC-dependent activity. The crystal structure of the SidC N-terminus revealed a novel fold that is important for function and could be involved in Legionella adaptations to evolutionarily divergent host cells it encounters in natural environments.

Theory of mind deficits in patients with mild symptoms of major depressive disorder.

The aim of this study was to investigate theory of mind (ToM) in a sample of depressed patients with mild symptom severity using a measure with varied cognitive processing demands. Patients demonstrated impaired performance on second-order, cognitively demanding ToM scenarios. Reduced ToM ability was associated with poor psychosocial functioning.

Psychological factors that may confer risk for bipolar disorder.

Several psychological domains may be dysfunctional in people with bipolar disorder (BD). When dysfunction occurs prior to onset of mood symptoms, it may signify risk for onset of the full syndrome of illness. Among these domains, cognitive dysfunction has received considerable attention as a possible endophenotype for BD, with some suggestion that changes in cognitive function may antedate onset of mood symptoms in individuals at risk for BD. Domains of social cognition, including emotion comprehension, theory of mind, and empathy, along with autobiographical memory, represent understudied aspects of psychological function that may be dysfunctional in people with BD. Temperament and personality factors, such as ruminative tendencies and neuroticism, may also leave some people vulnerable to mood instability. This review summarises the evidence for dysfunction in each of these domains for people with BD and examines whether there is any evidence that this dysfunction antedates the onset of mood symptoms or confers risk for illness.

Conditional requirement for exopolysaccharide in the Mesorhizobium-Lotus symbiosis.

Rhizobial surface polysaccharides are required for nodule formation on the roots of at least some legumes but the mechanisms by which they act are yet to be determined. As a first step to investigate the function of exopolysaccharide (EPS) in the formation of determinate nodules, we isolated Mesorhizobium loti mutants affected in various steps of EPS biosynthesis and characterized their symbiotic phenotypes on two Lotus spp. The wild-type M. loti R7A produced both high molecular weight EPS and lower molecular weight (LMW) polysaccharide fractions whereas most mutant strains produced only LMW fractions. Mutants affected in predicted early biosynthetic steps (e.g., exoB) formed nitrogen-fixing nodules on Lotus corniculatus and L. japonicus 'Gifu', whereas mutants affected in mid or late biosynthetic steps (e.g., exoU) induced uninfected nodule primordia and, occasionally, a few infected nodules following a lengthy delay. These mutants were disrupted at the stage of infection thread (IT) development. Symbiotically defective EPS and Nod factor mutants functionally complemented each other in co-inoculation experiments. The majority of full-length IT observed harbored only the EPS mutant strain and did not show bacterial release, whereas the nitrogen-fixing nodules contained both mutants. Examination of the symbiotic proficiency of the exoU mutant on various L. japonicus ecotypes revealed that both host and environmental factors were linked to the requirement for EPS. These results reveal a complex function for M. loti EPS in determinate nodule formation and suggest that EPS plays a signaling role at the stages of both IT initiation and bacterial release.

Patients with bipolar disorder show impaired performance on complex tests of social cognition.

The literature concerning social cognitive performance in people with bipolar disorder (BD) reveals a mixed pattern of findings. We compared performance between patients with BD and matched controls on two social cognitive tasks that involved: (i) the decoding of mental states from pictures of eyes (Reading the Mind in the Eyes Test), and (ii) a video-based test that requires participants to discriminate social cues to make interpersonal judgments (Interpersonal Perception Task-15; IPT-15). We also sought to evaluate the association between symptom severity, social functioning, and social cognitive ability in patients with BD. Relative to controls, patients with BD were impaired at discriminating mental states from pictures of eyes and in making complex social judgments. Impaired responding on the IPT-15 was also associated with reduced psychosocial functioning. These results provide evidence of impaired performance on complex tests of social cognition in patients with BD. Impairments in social cognition may be associated with well-documented declines in the frequency of social interactions and development of interpersonal relationships found in this patient population.

Systematic review of the neural basis of social cognition in patients with mood disorders.

BACKGROUND: This review integrates neuroimaging studies of 2 domains of social cognition--emotion comprehension and theory of mind (ToM)--in patients with major depressive disorder and bipolar disorder. The influence of key clinical and method variables on patterns of neural activation during social cognitive processing is also examined. METHODS: Studies were identified using PsycINFO and PubMed (January 1967 to May 2011). The search terms were "fMRI," "emotion comprehension," "emotion perception," "affect comprehension," "affect perception," "facial expression," "prosody," "theory of mind," "mentalizing" and "empathy" in combination with "major depressive disorder," "bipolar disorder," "major depression," "unipolar depression," "clinical depression" and "mania." RESULTS: Taken together, neuroimaging studies of social cognition in patients with mood disorders reveal enhanced activation in limbic and emotion-related structures and attenuated activity within frontal regions associated with emotion regulation and higher cognitive functions. These results reveal an overall lack of inhibition by higher-order cognitive structures on limbic and emotion-related structures during social cognitive processing in patients with mood disorders. Critically, key variables, including illness burden, symptom severity, comorbidity, medication status and cognitive load may moderate this pattern of neural activation. LIMITATIONS: Studies that did not include control tasks or a comparator group were included in this review. CONCLUSION: Further work is needed to examine the contribution of key moderator variables and to further elucidate the neural networks underlying altered social cognition in patients with mood disorders. The neural networks under lying higher-order social cognitive processes, including empathy, remain unexplored in patients with mood disorders.

An Overview of Psychological and Neurobiological Mechanisms by which Early Negative Experiences Increase Risk of Mood Disorders.

OBJECTIVE: Early life experiences are associated with severe and long-lasting effects on behavioural and emotional functioning, which in turn are thought to increase the risk for unipolar depression and other disorders of affect regulation. The neurobiological and psychological mechanisms through which adverse early life experiences confer risk are poorly understood. METHOD: Alterations in brain structure and function in limbic and prefrontal cortical regions have been linked to early negative experiences and to mood disorders. RESULTS: There are a number of psychological domains that may be dysfunctional in people with mood disorders, and which, if the dysfunction occurs prior to onset of mood symptoms, may signify a risk factor for depression. Cognitive dysfunction has been examined in patients with mood disorders, with some suggestion that changes in cognitive function may antedate the onset of mood symptoms, and may be exacerbated in those who experienced early negative trauma. Social cognition, including emotion comprehension, theory of mind and empathy, represent under-studied domains of psychological function that may be negatively influenced by early adverse experience. Temperament and personality factors may also leave people vulnerable to mood instability. CONCLUSION: This review summarizes the evidence for dysfunction in each of these domains for people with mood disorders.

Altered empathic responding in major depressive disorder: relation to symptom severity, illness burden, and psychosocial outcome.

Individuals with major depressive disorder (MDD) demonstrate deficits in multiple social cognitive domains; however, systematic investigations of empathic responding have not been performed. Twenty patients with MDD completed two measures of empathy, the Interpersonal Reactivity Index (IRI: Davis, 1980, 1983) and the Toronto Empathy Questionnaire (TEQ: Spreng et al., 2009). Relative to matched controls, patients with MDD reported significantly reduced levels of empathy measured broadly on the TEQ and specifically in cognitive ('Perspective Taking') and affective ('Empathic Concern') domains captured by the IRI. A higher illness burden (i.e., greater number of past depressive episodes) was associated with greater reductions in perspective taking ability. This study provides early evidence of impaired empathic abilities in patients with MDD that may worsen with illness progression. Alternatively, reductions in perspective taking ability may contribute to a more severe course of illness in this population. Further longitudinal work is needed to characterize the relation between social cognitive performance and social functioning in this population.

Impaired theory of mind performance in patients with recurrent bipolar disorder: Moderating effect of cognitive load.

The aim of this study was to investigate theory of mind (ToM) performance on tasks that varied in the demands they placed on cognitive processing resources in a sample of 14 bipolar patients with subsyndromal illness and 14 controls. Patients showed impaired performance on cognitively demanding second-order ToM tasks. Reduced ToM performance was associated with longer illness duration, and with increased symptom severity.

Subcellular forms and biochemical events triggered in human cells by HCV polyprotein expression from a viral vector.

To identify the subcellular forms and biochemical events induced in human cells after HCV polyprotein expression, we have used a robust cell culture system based on vaccinia virus (VACV) that efficiently expresses in infected cells the structural and nonstructural proteins of HCV from genotype 1b (VT7-HCV7.9). As determined by confocal microscopy, HCV proteins expressed from VT7-HCV7.9 localize largely in a globular-like distribution pattern in the cytoplasm, with some proteins co-localizing with the endoplasmic reticulum (ER) and mitochondria. As examined by electron microscopy, HCV proteins induced formation of large electron-dense cytoplasmic structures derived from the ER and containing HCV proteins. In the course of HCV protein production, there is disruption of the Golgi apparatus, loss of spatial organization of the ER, appearance of some "virus-like" structures and swelling of mitochondria. Biochemical analysis demonstrate that HCV proteins bring about the activation of initiator and effector caspases followed by severe apoptosis and mitochondria dysfunction, hallmarks of HCV cell injury. Microarray analysis revealed that HCV polyprotein expression modulated transcription of genes associated with lipid metabolism, oxidative stress, apoptosis, and cellular proliferation. Our findings demonstrate the uniqueness of the VT7-HCV7.9 system to characterize morphological and biochemical events related to HCV pathogenesis.

Symbiosis-induced cascade regulation of the Mesorhizobium loti R7A VirB/D4 type IV secretion system.

The Mesorhizobium loti R7A symbiosis island contains genes encoding a VirB/D4 type IV secretion system (T4SS) similar to that of Agrobacterium tumefaciens. This system has host-dependent effects on symbiosis that probably are due to translocation of two effector proteins, Msi059 and Msi061, into host cells. Here we report that, as in A. tumefaciens, the M. loti vir genes are transcriptionally regulated by a VirA/VirG two-component regulatory system. A virGN54D mutant gene of M. loti caused constitutive expression of lacZ reporter gene fusions to virB1, virD4, msi059, and msi061. Expression of these gene fusions also was activated by a NodD gene product from Rhizobium leguminosarum in the presence of the inducer naringenin, as was a virA::lacZ fusion. This activation was dependent on a nod box present 851 bp upstream of virA, and a mutant with the nod box deleted formed effective nodules on Leucaena leucocephala, the same symbiotic phenotype as other M. loti vir mutants. In contrast, the wild-type strain formed small, empty nodules whereas a nodD1 mutant was completely Nod-. These results indicate that the M. loti vir genes are induced in a symbiosis-specific manner that involves a two-tiered regulatory cascade, and that the vir effectors act after Nod factor during infection thread formation.

Effects of ciprofibrate on testicular and adrenal steroidogenic enzymes in the rat.

Testicular and adrenal steroidogenic enzymes were measured radiometrically following oral dosing of rats with ciprofibrate (2-[4-(2,2-dichlorocyclopropyl) phenoxyl]-2-methylpropinoic acid), a peroxisome proliferator. Six-week-old male Fisher 344 rats were fed a diet containing ciprofibrate (0.025%, w/w) for 3, 7, 14, 28, 56, 84, 112 or 140 days leading to a daily ciprofibrate intake of approximately 15 mg/kg body weight/day. Ciprofibrate caused a marked inhibition of testicular 3beta-hydroxysteroid dehydrogenase-isomerase (3beta-HSD) activity that was significant after 3 days and subsequently decreased to 40% of control level. Ciprofibrate treatment also reduced 17beta-hydroxysteroid dehydrogenase (17beta-HSD) activity to a lesser extent but had no effect on 17-hydroxylase (17-OHase) activity. Immunoblot analyses indicated that ciprofibrate treatment did not alter enzyme protein levels and semi-quantitative RT-PCR analysis also revealed no significant changes in testicular 3beta-HSD mRNA levels. Furthermore, in addition to the enzyme-specific effect of ciprofibrate on 3beta-HSD in the testes, a tissue-specific effect was also evident, since no significant effects of ciprofibrate were seen on the activities of 3beta-HSD or 21-OHase in the adrenal glands from the same animals.

Edaphic races and phylogenetic taxa in the Lasthenia californica complex (Asteraceae: Heliantheae): an hypothesis of parallel evolution.

Lasthenia californica sensu Ornduff consists of two races that differ in their flavonoid pigments and edaphic tolerances. Recent phylogenetic studies of Lasthenia have revealed that members of L. californica sensu Ornduff belong to two phylogenetic species. The relationship of the edaphic races to these new species and to each other is the focus of this study. Characterization of flavonoid profiles and phylogenetic placement of 33 populations demonstrates that races and phylogenetic taxa are not concordant, suggesting that one or both edaphic races evolved in parallel in the two clades. We hypothesize an edaphically linked ecological role for flavonoid differences that first revealed the existence of two races.

The post-natal heart contains a myocardial stem cell population.

The recent identification of stem cell pools in a variety of unexpected tissue sources has raised the possibility that a pluripotent stem cell population may reside in the myocardium and contribute to the post-natal growth of this tissue. Here, we demonstrate that the post-natal myocardium contains a resident verapamil-sensitive side population (SP), with stem cell-like activity. When growth of the post-natal heart was attenuated through over-expression of a dominant negative cardiac transcription factor (MEF2C), the resident SP cell population was subject to activation, followed by a consequent depletion. In addition, cardiac SP cells are capable of fusion with other cell types, but do not adopt the corresponding gene expression profile. These observations suggest that a responsive stem cell pool resides in the adult myocardium, and may influence adaptation of the post-natal heart.