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PubMed2006

Is love of nature in the US becoming love of electronic media? 16-year downtrend in national park visits explained by watching movies, playing video games, internet use, and oil prices.

After 50 years of steady increase, per capita visits to US national parks have declined since 1988. This decline, coincident with the rise in electronic entertainment media, may represent a shift in recreation choices with broader implications for the value placed on biodiversity conservation and environmentally responsible behavior. We compared the decline in per capita visits with a set of indicators representing alternate recreation choices and constraints. The Spearman correlation analyses found this decline in NPV to be significantly negatively correlated with several electronic entertainment indicators: hours of television, (rs=-0.743, P<0.001), video games (rs=-0.773, P<0.001), home movies (rs=-0.788, P<0.001), theatre attendance (rs=-0.587, P<0.025) and internet use (rs=-0.783, P<0.001). There were also significant negative correlations with oil prices (rs=-0.547, P<0.025), foreign travel (rs=-0.452, P<0.05), and Appalachian Trail hikers (rs=-0.785, P<0.001). Income was significantly positively correlated with foreign travel (rs=0.621, P<0.005) but negatively correlated with national park visits (rs=-0.697, P<0.005). There was no significant correlation of mean number of vacation days, indicating available vacation time is probably not a factor. Federal funding actually increased during this period, and so was rejected as a probable factor. Park capacity was rejected as limiting since both total overnight stays and visits at the seven most popular parks rose well into the mid-1990s. Aging of baby boomers was also rejected as they are only now reaching retirement age, and thus during the period of visitation decline were still of prime family vacation age. Multiple linear regression of four of the entertainment media variables as well as oil prices explains 97.5% of this recent decline (r=0.975, multiple r2=0.950, adjusted multiple r2=0.925, SE=0.015, F=37.800, P<0.0001). We may be seeing evidence of a fundamental shift away from people's appreciation of nature (biophilia, Wilson 1984) to 'videophilia,' which we here define as "the new human tendency to focus on sedentary activities involving electronic media." Such a shift would not bode well for the future of biodiversity conservation.

Ecology↗

PubMed2005

Presence of cholinergic and calcium channel blocking activities explains the traditional use of Hibiscus rosasinensis in constipation and diarrhoea.

The aqueous-ethanolic extract of the aerial parts of Hibiscus rosasinensis Linn. (Malvaceae) was studied for the possible presence of spasmogenic and spasmolytic constituents to rationalize its traditional use in gastrointestinal disorders. The crude extract (Hr.Cr) caused a concentration-dependent (1-10mg/mL) spasmogenic effect in isolated guinea-pig ileum, which was blocked in the presence of atropine (0.1 microM). In spontaneously contracting rabbit jejunum, the plant extract exhibited a weak stimulatory effect at lower doses (0.03-0.30 mg/mL) followed by an inhibitory effect at higher doses (1.0-3.0mg/mL). Pretreatment of the tissues with atropine blocked the stimulatory effect resulting in the potentiation of the spasmolytic effect. Hr.Cr (0.03-1.0mg/mL) also showed an inhibitory effect on K(+) (80 mM)-induced contractions. The calcium channel blocking activity was confirmed when Hr.Cr shifted the Ca(2+) concentration-response curves to the right, similar to verapamil. Activity-directed fractionation revealed that the spasmolytic component(s) was separated in the ethyl acetate, while the spasmogenic in the petroleum ether fraction. The aqueous fraction exhibited a combination of weak spasmogenic and spasmolytic effects. These data indicate that the crude extract contains spasmogenic and spasmolytic constituents mediating their effect through cholinergic receptors activation and blockade of Ca(2+) influx, respectively, which may explain its traditional use in constipation and diarrhoea.

Acetylcholine↗

PubMed2004

Age-associated changes in intestinal fructose uptake are not explained by alterations in the abundance of GLUT5 or GLUT2.

A reduction in nutrient absorption may contribute to malnourishment in the elderly. The objectives of this study were to determine the effects of aging on the absorption of fructose in rats, as well as the mechanisms of these adaptive changes. Male Fischer 344 rats aged 1, 9, and 24 months were fed standard Purina chow for 2 weeks (PMI #5001, PMI Nutritionals, Brentwood, MO). The uptake of (14)C-labeled D-fructose was determined in vitro using the intestinal sheet method. Intestinal samples were taken for RNA isolation and for brush border membrane (BBM) and basolateral membrane (BLM) preparation. Northern blotting, Western blotting, and immunohistochemistry were used to determine the effects of age and diet on GLUT5 and GLUT2. When expressed on the basis of intestinal or mucosal weights, aging was associated with a decline in jejunal and ileal fructose uptake, whereas jejunal fructose uptake was increased when expressed on the basis of serosal or mucosal surface area. The alterations in fructose uptake were not paralleled by changes in GLUT5 or GLUT2 abundance. These results indicate that 1) the effect of age on fructose uptake depends on the method used to express results, and 2) the age-associated changes in uptake are not explained by alterations in GLUT5 and GLUT2.

Aging↗

PubMed2006

Depressive symptoms may explain elevated plasma levels of homocysteine in females with eating disorders.

Elevated plasma homocysteine levels have been found in different psychiatric disorders, including major depression and eating disorders. The aim of the present study was to evaluate whether presence of depression or depressive symptoms is associated with elevated homocysteine levels in patients with eating disorders. Total plasma homocysteine levels were assessed in 44 females with anorexia nervosa (n = 21) or bulimia nervosa (n = 23). Comorbid major depressive disorder (MDD) was diagnosed according to DSM-IV criteria using a semi-structured interview (SCID-I). Furthermore, depressive symptoms were assessed using Beck's depression inventory (BDI). Presence of MDD was not associated with elevated homocysteine levels (t-test: T = 0.42; df = 42; P = 0.68). However, self-rated presence of clinically relevant depressive symptoms (BDI score18) was associated with elevated homocysteine (T = -2.8; df = 42; P = 0.008). Presence of depressive symptoms may explain elevated homocysteine levels previously reported in patients with eating disorders or vice versa. Longitudinal studies are needed to unravel this hen or egg problem.

Adolescent↗

PubMed2006

Explaining medically unexplained symptoms: toward a multidimensional, theory-based approach to somatization.

In spite of the apparent clinical importance of somatization, the concept does not have a single meaning. The focus of the present article is therefore not on scrutinizing existing diagnostic categories but rather on the different dimensions that relate to somatization and on the relevance of psychological models such as social learning theory, stress coping, illness cognition, and self-regulation models for explaining more carefully the predisposing, precipitating, and perpetuating factors of (different types of) somatization. This combined approach could lead to the definition of more homogeneous and, therefore, clinically more meaningful subgroups of somatization.

Humans↗

PubMed2004

Drastic growth effect may explain sympatric cannibalistic polymorphism.

Cannibalistic polyphenism is observed in many fishes and amphibians. In the case of amphibian larvae, cannibal morph and typical morph coexist. Benefits and costs of the cannibal morph have been studied empirically but the mechanism of the maintenance of polymorphism is not well known. Here, we construct a game model of typical and cannibal morph strategies to obtain the condition of stable coexistence. Generally, once an individual succeeds in cannibalism, it grows very quickly, which facilitates the next cannibalism. In a model without this 'drastic growth effect', stable coexistence cannot occur. To represent drastic growth effect, it is assumed that cannibal/typical morph stage is followed by giant/normal stage. A cannibal morph that performs cannibalism in the first stage can become a 'giant' in the next stage. This model allows stable coexistence of cannibal and typical morphs. The condition for coexistence is that payoff of a giant is two times larger than normal individuals. As long as direct consumption of victim's body is considered as reward for successful cannibalism, coexistence cannot be explained. When the reward is considered as social standing of being outstanding size in a population, sympatric cannibalistic polymorphism is possible, without regard to the initial size variation or resource shortage.

Amphibians↗

PubMed2004

A tiling approach to virus capsid assembly explaining a structural puzzle in virology.

A novel approach for the description of the protein stoichiometry of viral capsids, that is the protein shells protecting the viral genome, is introduced based on tiling theory. This approach generalizes Caspar-Klug theory of quasi-equivalence to account also for non-quasi-equivalent subunit arrangements in icosahedral virus capsids that have been observed experimentally but are not covered by the Caspar-Klug approach. In particular, the new approach is used to explain the structure of polyoma virus, Simian Virus 40 and L-A virus capsids, which are considered structural puzzles in view of Caspar-Klug theory.

Capsid↗

PubMed2005

Lifesaving explains mortality decline with time.

Mortality rates of human populations in developed countries are declining with time. We show that this effect can be explained via a 'lifesaving' methodology. Our approach is based on considering a non-homogeneous Poisson process of potentially harmful events. Each of these events can be 'cured' with a given probability or can result in a termination of the Poisson process (death) with a complementary probability. A lifesaving ratio, defining the corresponding relative increase in life expectancy for homogeneous and heterogeneous populations is analyzed. Some generalizations are discussed. Several simple examples are considered.

Humans↗

PubMed2005

Do vasoactive neuropeptide autoimmune disorders explain pyridostigmine's association with Gulf War syndrome?

Gulf War syndrome (GWS) is a perplexing multi-symptom condition comprising a constellation of signs and symptoms consistently described in the literature. These include muscle fatigue and tiredness, malaise, myalgia, impaired cognition, ataxia, diarrhoea, bladder dysfunction, sweating disturbances, headaches, fever, arthralgia, skin rashes, and gastrointestinal and sleep disturbances. Excessive chemical sensitivity and odour intolerance is reported. Epidemiological analysis suggests association with pyridostigmine bromide (PB) use as nerve gas prophylaxis, insect repellent, certain vaccination regimes, a variety of possible chemical exposures and physical and psychological stress. Pituitary adenylate cyclase-activating polypeptide (PACAP), calcitonin gene-related peptide (CGRP) and vasoactive intestinal peptide (VIP) are potent vasoactive (vasodilatory) neuropeptides (VNs) having pleiotropic functions as immunomodulators, neuroregulators and hormones. VNs also have neurotrophic and anti-apoptotic roles. VNs act on G protein-coupled receptors (GPCRs) to activate adenylate cyclase, an important step in cyclic AMP metabolism. Autoimmune dysfunction of these VNs or their receptors is postulated to give rise to fatigue-related conditions such as chronic fatigue syndrome (CFS). Complex mechanisms involving heat shock proteins (hsps) and cytosine-guanine dinucleotide (CpG) DNA fragments may also be associated with autoimmunity to VNs or their GPCRs in contributing to fatigue-related conditions. Dysfunction of certain VNs may be the missing link in explaining the nebulous nexus between PB and GWS. This paper explores a possible link between exposures to PB and other chemical, physical and psychological stressors in producing a fatigue-related illness possibly related to autoimmune dysfunction of certain VNs. Treatment options involving restoration of VN function are considered in the context of analogues with other neurotransmitter fatigue-related conditions such as myasthenia gravis (MG). While evidence associating these conditions is thin, vasoactive neuropeptide neurotransmitters of the VIP/PACAP family have acetylcholine co-transmission functions via specific GPCRs. Autoimmune reactions to these receptors may have parallels with muscarinic (e.g., Sjogren's syndrome) and nicotinic (e.g., MG) acetylcholine neurotransmission. Hence theoretically, treatment options such as thymectomy, corticosteroids, plasma exchange, anti-idiotype antibodies and receptor genomic expression reactivation/suppression may be considered. Paradoxically pyridostigmine may prove to have a role in therapy although VN treatment/replacement may be associated with tachyphylaxis.

Autoimmune Diseases↗

PubMed2005

Integrating the theories of Darwin and Bernoulli: maladaptive baroreceptor network dysfunction may explain the pathogenesis of aortic aneurysms.

Current treatment options for aortic aneurysms are suboptimal and their pathogenic mechanisms remain unclear. We propose the existence of a coordinated multi-node baroreceptor network that measures pressures at all vascular bifurcations and enables system-wide hemodynamic coordination and vasomotor regulation, in accordance with the principle of Bernoulli. While the presence of baroreceptors at bifurcations remains unknown, behavior at the level of systems predicts their existence, possibly as glomus cell derivatives. We propose that pressure misregistration among sensor nodes at different vascular bifurcations can precipitate feed-forward dysfunctions that promote thrombosis, inflammation, and vasomotor dysregulation resulting in aneurysm formation. One example of this phenomenon is aortic aneurysm, which is currently attributed to focal anatomic defects. As plaque builds in the infrarenal aorta, the increased blood velocity through this segment can widen the difference between pressures sensed at the iliac and the renal artery bifurcations. Due to the Bernoulli effect, this change creates an incorrect impression of reduced dynamic pressure at the kidneys. The erroneous perception of hypovolemia can induce a pernicious cycle of maladaptive adrenergia and associated coagulation and thrombosis, particularly in the infrarenal aortic segment as the body attempts to normalize renal perfusion. Atherosclerosis can further exacerbate baroreceptor dysfunction by interfering with sensor biology in feed-forward fashion. Hypertension may be a consequence as well as a source of atherosclerosis and aneurysm. The described system may have evolved when trauma-related hypovolemia was a far more prevalent driver of natural selection but may be rendered maladaptive in the setting of modern stressors. Failure to address these factors may explain the suboptimal long-term outcomes with current surgical and endovascular treatments for aneurysms. Implications for other potential sensor networks including chemoreceptors and lymphoid tissues at bifurcating biologic branch-points such as vessels, airways, nerves, lymphatics, and ducts are discussed. Our framework may also provide a new basis for understanding thoracic aneurysm, renovascular dysfunctions, coronary artery disease, carotid artery disease, pulmonary embolism, portal hypertension, venous thrombosis, biliary disease, pancreatic disease, and neurologic disease. Novel treatment paradigms based on drugs or interconnected networks of devices that modulate sensors are envisioned. Improving the interface between sensors and their substrate information by techniques such as minimally traumatic atherectomy or thrombectomy may also restore appropriate sensor function. Lessons learned from bifurcation sensors and their potential maladaptations may generalize to other types of branching systems including botany, civil engineering, and Pitot tube aeronautics.

Animals↗

PubMed2005

Intestinal involvement is not sufficient to explain hypertransaminasemia in celiac disease?

Chronic unexplained hypertransaminasemia is an isolated clinical manifestation of celiac disease (CD) and lacks of a clear physiopathological explanation. Since CD and tropical sprue (TS) have similar intestinal functional and histological pattern of injury and that an increased inflammatory response has been reported to occur in patients with irritable bowel syndrome (IBS), liver involvement might be expected to occur either in TS or IBS. However, according to author's prior observations, the frequency of hypertransaminasemia is significantly higher in CD than in TS and IBS-diarrhea predominant patients (IBS-D). Thus, based on current knowledge, intestinal mucosal damage, increased intestinal permeability and/or an active intestinal inflammatory response do not completely explain liver damage in CD. We hypothesize that other factors, unique to CD not present in TS or IBS-D, like gluten toxicity and the presence of tissular transglutaminase (tTG) an auto-antigen with pro-inflammatory and remodeling properties, act in addition to intestinal mucosal injury and account to hypertransaminasemia in CD. Further research focusing on the mechanisms of gluten and tTG hepatic toxicity, and/or the characterization of the expression, secretion and enteral-hepatic transport of certain pro-inflammatory cytokines is needed, to understand the possible links between intestinal and liver disorders seen in CD.

Animals↗

PubMed2005

Impaired neuronal glucose uptake in pathogenesis of schizophrenia - can GLUT 1 and GLUT 3 deficits explain imaging, post-mortem and pharmacological findings?

The largely empirical dopamine theory has limited value in clarifying the pathogenesis of schizophrenia, due to its inability to explain consistent imaging findings, such as cortical grey matter loss, reduced frontal and thalamic activity, and, reduced D1 receptor load. Furthermore, the most effective drug for treating positive and negative symptoms - clozapine - has minimal dopaminergic activity. We present an alternative hypothesis centring on presumed deficits in membrane bound glucose transporter proteins GLUT 1 and GLUT 3, either in absolute numbers or functional capacity. In situations of high demand, intracellular hypoglycaemia in neurones and astrocytes will produce acute symptoms of misperceptions, misinterpretations, anxiety and irritability - the usual features of prodromal and first onset schizophrenia. Furthermore, reduced glucose uptake will disrupt production of glutamate--functionally similar to the schizophrenia-like syndrome produced by PCP, a glutamate antagonist. In the longer term, reduced neuronal growth and poor synaptic contacts will produce chronic cognitive difficulties and perpetuate acute symptoms. A backlog effect due to reduced brain uptake of glucose would produce systemic hyperglycaemia observed in drug nai ve subjects. Rat studies have shown that clozapine and similar compounds block GLUT proteins in the brain and peripherally, more so than selective dopamine blockers. By blocking GLUT proteins, clozapine would break malfunctioning circuits, resulting in the disappearance of cognitive and perceptual symptoms. Unfortunately, these drugs would also raise systemic glucose levels, increasing the risk of diabetes, as observed in longer term studies of clozapine in particular. We summarise potentially useful research strategies, including studying the genotype of GLUT proteins with respect to schizophrenia phenotypes, activation studies involving fMRI using deoxyglucose as a substrate, and investigating clinical features of schizophrenic patients prior to and following treatment for co-existing diabetes.

Brain↗

PubMed2004

Cytochrome-c-oxidase redox changes during visual stimulation measured by near-infrared spectroscopy cannot be explained by a mere cross talk artefact.

The detection of redox changes in cytochrome-c-oxidase ([Cyt-ox]) in response to cerebral activation by non-invasive NIRS is hampered by methodological spectroscopic issues related to the modification of the Beer-Lambert law. Also, the question whether a change in the enzyme's redox-state is elicited by functional stimulation is unresolved. In a previous study, we found physiological evidence in favour of an activation-induced increase in oxidation of the enzyme [J. Cereb. Blood Flow Metab. 19 (1999) 592], while in a second study on spectroscopic cross talk, we found that the [Cyt-ox] changes to potentially be an artefact of the spectroscopic approach [J. Biomed. Opt. 7 (2002) 51]. Here, we use two different stimuli which differentially activate areas either rich or poor in [Cyt-ox] content (blob/interblob in visual cortex V1 and pale/thin stripes in V2) to further clarify this apparent discrepancy. In a first experiment, two stimuli were presented in an alternating fashion for 20 s and all stimulation periods were separated by resting periods of 40 s. We observed similar changes in [Cyt-ox] for both stimuli. To become more sensitive to the potentially very small optical changes related to changes in [Cyt-ox], we tried to minimise global haemodynamic and metabolic effects in a second experiment by omitting the resting periods. Our hypothesis was that [Cyt-ox] changes could be fully explained by cross talk as it is predicted from our last study [J. Biomed. Opt. 7 (2002) 51]. However, in more than half of the experiments, we were not able to model the changes in Cyt-ox calculated from measured attenuation spectra as a cross talk artefact. We interpret this finding as an argument in favour of the existence of [Cyt-ox] changes in response to functional stimulation. This finding, however, does not lessen the liability of the [Cyt-ox] changes to cross talk and calls for great caution when [Cyt-ox] changes are derived from NIRS measurements based on the modified Beer-Lambert approach. Further (invasive) validation studies are required.

Adult↗

PubMed2005

Determinants of dominance: is language laterality explained by physical or linguistic features of speech?

The nature of cerebral asymmetry of the language function is still not fully understood. Two main views are that laterality is best explained (1) by left cortical specialization for the processing of spectrally rich and rapidly changing sounds, and (2) by a predisposition of one hemisphere to develop a module for phonemes. We tested both of these views by investigating magnetic brain responses to the same brief acoustic stimulus, placed in contexts where it was perceived either as a noise burst with no resemblance of speech, or as a native language sound being part of a meaningless pseudoword. In further experiments, the same acoustic element was placed in the context of words. We found reliable left hemispheric dominance only when the sound was placed in word context. These results, obtained in a passive odd-ball paradigm, suggest that neither physical properties nor phoneme status of a sound are sufficient for laterality. In order to elicit left lateralized cortical activation in normal right-handed individuals, a rapidly changing spectrally rich sound with phoneme status needs to be placed in the context of frequently encountered larger language elements, such as words. This demonstrates that language laterality is bound to the processing of sounds as units of frequently occurring meaningful items and can thus be linked to the processes of learning and memory trace formation for such items rather than to their physical or phonological properties.

Adult↗

PubMed2006

Nonlinearities in rapid event-related fMRI explained by stimulus scaling.

Because of well-known nonlinearities in fMRI, responses measured with rapid event-related designs are smaller than responses measured with spaced designs. Surprisingly, no study to date has tested whether rapid designs also change the pattern of responses across different stimulus conditions. Here we report the results of such a test. We measured cortical responses to a flickering checkerboard at different contrasts using rapid and spaced event-related fMRI. The relative magnitude of responses across contrast conditions differed between rapid and spaced designs. Modeling the effect of the rapid design as a scaling of stimulus strength provided a good account of the data. The data were less well fit by a model that scaled the strength of responses. A similar stimulus scaling model has explained effects of neural adaptation, which suggests that adaptation may account for the observed difference between rapid and spaced designs. In a second experiment, we changed the stimulus in ways known to reduce neural adaptation and found much smaller differences between the two designs. Stimulus scaling provides a simple way to account for nonlinearities in event-related fMRI and relate data from rapid designs to data gathered using slower presentation rates.

Adaptation, Physiological↗

PubMed2005

DISCO! Dissociation of cone opsins: the fast and noisy life of cones explained.

Vertebrate retinas contain two types of photoreceptors. Rods are for vision in dim light, while cones provide high-speed color vision in bright light. In this issue of Neuron, Kefalov et al. present data to explain the reduced sensitivity and faster response kinetics of cones. They show that the chromophore dissociates from cone but not rod visual pigment, yielding apo-opsin. This apo-opsin activates the signaling cascade to desensitize cones and speed the photoresponse.

Ambystoma↗

PubMed2005

Visuomotor 'immunity' to perceptual illusion: a mismatch of attentional demands cannot explain the perception-action dissociation.

Recent findings of visuomotor immunity to perceptual illusions have been attributed to a perception-action division of labour within two anatomically segregated streams in the visual cortex. However, critics argue that such experimental findings are not valid and have suggested that the perception-action dissociations can be explained away by differential attentional/processing demands, rather than a functional dissociation in the neurologically intact brain: perceptual tasks require processing of the entire illusion display while visuomotor tasks only require processing the target that is acted upon. The present study examined whether grasping of the Müller-Lyer display would remain immune to the illusion when the task required the direction of attention or a related resource towards both Müller-Lyer shafts. Twelve participants were required to match and grasp two Müller-Lyer shafts bimanually (i.e. one with each hand). It was found that bimanual grasping was not significantly affected by the illusion, while there was a highly significant illusion effect on perceptual estimation by matching. Furthermore, it was established that this dissociation did not result from a differing baseline rate of change in manual estimation and grasping aperture to a change in physical object size. These findings provide further support for the postulated perception-action dissociation and fail to uphold the idea that grasping 'immunity' to the Müller-Lyer illusions merely represents an experimental artefact.

Adult↗

PubMed2005

A blend of polyphenolic compounds explains the stimulatory effect of red wine on human endothelial NO synthase.

A high intake of polyphenolic compounds is likely to have beneficial effects on the cardiovascular system. Especially red wine is a rich source of polyphenols, and we have previously shown that French red wine upregulates eNOS, a protective enzyme in the cardiovascular system. The current study tested (poly)phenolic constituents of red wine for their ability to enhance eNOS expression (and the activity of a 3.5-kb human eNOS promoter) in human EA.hy 926 endothelial cells. Of the compounds tested, we found 3,4',5-trihydroxy-trans-stilbene (trans-resveratrol) to be the most efficacious stimulator of eNOS expression (and eNOS transcription), but this compound alone could not explain the total stimulatory effect of red wine. The flavanols catechin and epicatechin, the flavonols fisetin, myricetin, isoquercitrin and hyperoside, the anthocyanins delphinidin, malvidin, and paeonidin, gallic acid, and the hydroxycinnamic acids ferulic acid and sinapinic acid did not change eNOS expression or eNOS promoter activity in any substantial way. The flavonol quercetin inhibited eNOS expression (with no effect on eNOS promoter activity). Cinnamic acid was a rather potent enhancer of eNOS expression, however with an efficacy of only 170%. Surprisingly, it reduced eNOS promoter activity. The anthocyanins cyanidin, the hydroxycinnamic acids p-coumaric acid and caffeic acid, and the phenolic acids benzoic acid and vanillic acid also enhanced eNOS expression moderately (with no effect on eNOS promoter activity). Thus, the increase in eNOS in response to red wine involves several polyphenolic compounds with a major contribution from trans-resveratrol and lesser contributions from cinnamic and hydroxycinnamic acids, cyanidin, and some phenolic acids.

Anthocyanins↗