Orientation integration in detection and discrimination of contrast-modulated patterns

Orientation detection and discrimination thresholds were measured for Gabor ‘envelopes’ formed from contrast-modulation of luminance ‘carriers’. Consistent with previous research differences between carrier and envelope orientation had no effect on sensitivity to envelopes. Using plaid carriers in which the proportion of contrast modulation ‘carried’ by each plaid component was systematically manipulated, it was shown that this tolerance to carrier-envelope orientation difference reflects linear summation across orientation indicative of a single second-stage channel coding for contrast-defined structure. That contrast envelopes did not exhibit linear summation across spatial-frequency, nor across combinations of orientation and spatial-frequency differences, suggests that these second-order channels operate only within certain spatial scales. Using arrays of Gabor micropatterns as carriers in which the orientation distribution of the carriers was manipulated independently of the difference between envelope orientation and mean carrier orientation, it was further demonstrated that the locus of orientation integration must occur prior to envelope detection. In the context of two-stage models that incorporate a non-linearity between the stages, the pattern of results obtained is consistent with the operation of an orientation pooling process between first-stage and second-stage channels, analogous to having all filters of the first-stage feed into all filters of the second-stage within the same spatial-frequency band.

Spatio-temporal selectivity of loss of colour and luminance contrast sensitivity with mutiple sclerosis and optic neuritis

Colour and luminance-contrast thresholds were measured in the presence of dynamic Random Luminance-contrast Masking (RLM) in individuals who had had past diagnoses of optic neuritis (ON) some of whom have progressed to a diagnosis of multiple sclerosis (MS). To explore the spatio-temporal selectivity of chromatic and luminance losses in MS/ON, thresholds were measured using three different sizes and modulation rates of the RLM displays: small checks modulating slowly, medium-sized checks with moderate modulation and large checks modulating rapidly. The colour of the chromatic stimuli used were specified in a cone-excitation space to measure relative impairments in red–green and blue–yellow chromatic channels. These observers showed chromatic thresholds along the L/(L + M) axis that were higher than those along the S-cone axis for all display sizes/modulation rates and both red-green and blue-yellow colour thresholds were higher than luminance-contrast thresholds. The principal change in thresholds with spatio-temporal changes in the display was a reduction in thresholds for L/(L + M) and S-cones with increasing check size and modulation rate. However, luminance contrast thresholds did not change with display size/rate. These results are consistent with MS/ON selectively affecting processing in colour pathways rather than in the magnocellular pathway, and that within the colour pathways neurones with opposed L- and M-cone inputs are more damaged than colour-opponent neurons with input from S-cones.

On the perceived location of global motion

We measured the effects of coherent motion of one set of dots on the perceived location of Gaussian envelopes formed by luminance modulation of a second set of dots. Perceived shifts in envelope location in the direction of coherent motion were obtained even when the dots forming the envelopes did not physically move in the direction of coherent motion. In such cases, perceived shifts coincided with stimulus configurations that permitted motion integration of the envelope dots with the coherently moving dots, for example, when envelope dots moved in random directions as opposed to being static. In subsequent experiments we explored the type of motion integration underlying the positional shifts obtained. We discounted the possibility that the visual system incorrectly attributes motion signals associated with coherently moving dots to envelope dots by demonstrating that positional shifts could be obtained even when the coherent dots were laterally displaced to either side of the envelope dots such that the regions occupied by the dots did not overlap. We also discounted spatio-temporal summation within the receptive fields of low-spatial-frequency motion-sensitive mechanisms by demonstrating that positional shifts persisted even when the dot displays were high-pass filtered. These results, coupled with the observation that the proportion of coherently moving dots required to produce positional shifts correlated well with global motion thresholds measured for the same dot configurations, suggests that visual processes which underlie motion-dependent positional shifts are based at least in part on cooperative interactions of the type implicated in global motion.

Chromatic and luminance losses with multiple sclerosis and optic neuritis measured using dynamic random luminance contrast noise

We measured thresholds for detecting changes in colour and in luminance contrast in observers with multiple sclerosis (MS) and/or optic neuritis (ON) to determine whether reduced sensitivity occurs principally in red-green or blue-yellow second-stage chromatic channels or in an achromatic channel. Colour thresholds for the observers with MS/ON were higher in the red-green direction than in the blue-yellow direction, indicating greater levels of red-green loss than blue-yellow loss. Achromatic thresholds were raised less than either red-green or blue-yellow thresholds, showing less luminance-contrast loss than chromatic loss. With the MS/ON observers, blue-yellow and red-green thresholds were positively correlated but increasing impairment was associated with more rapid changes in red-green thresholds than blue-yellow thresholds. These findings indicate that demyelinating disease selectively reduces sensitivity to colour vision over luminance vision and red-green colours over blue-yellow colours.

Modulation of tumor necrosis factor receptors 1 and 2 in chronic hepatitis B and C: The differences and implications in pathogenesis

Tumor necrosis factor (TNF) plays a role in the pathogenesis of chronic hepatitis B (CHB) and chronic hepatitis C (CHC). The difference in the cytokine responses between hepatitis B virus (HBV) and hepatitis C virus (HCV) infections may have implications in the pathogenesis of these diseases. We performed a comparative study to examine the possible differences in the TNF-TNF receptor (TNFR) response between CHB and CHC. We studied the cytokine levels of 38 patients with CHB, 40 patients with CHC and 9 patients with dual hepatitis B and C, and compared them with the baseline levels of 12 healthy controls. The plasma levels of TNF-, interferon-, interleukin (IL)-2, IL-4, IL-10 and soluble TNFR-1 and 2 (sTNFR-1 and 2) were quantified by enzyme-linked immunosorbent assays. The expression of TNFR-1 and 2 in liver tissues was examined in 30 cases of CHB and 15 cases of CHC by semiquantitative reverse transcription polymerase chain reaction. The results showed that sTNFR-1 levels correlated with liver inflammation in all patients, whereas this correlation was not found with sTNFR-2 or other cytokines. Liver inflammation indicators were higher in HCV RNA+ than in HCV RNA– CHC. Most significantly, sTNFR-1 levels correlated with liver inflammation in CHB, but not in CHC. However, the expression of TNFR-1 and 2 in liver was similar between CHB and CHC. These findings suggest that the TNFR signal transduction pathway is modulated differently in HBV and HCV infection.

Influencing health through intestinal microbiota modulation and probiotics

Science has progressed fast in providing answers to probiotic health benefits to the consumers. This symposium also proves that progress is fast. However, several challenges still need to be solved and more effective strains and strain combinations discovered. This will pave the way from good probiotics to specific products for clearly identified target populations. The intestinal microbiota and its interaction(s) with probiotics challenges researchers to turn to the next new page to discover new approaches and treatment modalities that utilize probiotics as means of providing good nutrition with clear health benefits to all consumers.

Vitamin D: status, supplementation and immuno-modulation

Numerous studies have shown suboptimal vitamin D status in populations at high geographical latitudes, owing to a reduced capacity to synthesise vitamin D, especially during wintertime. Vitamin D supplementation has been shown to be effective at maintaining adequate vitamin D status throughout the year in these countries. Classically reported to play a central role in bone health, vitamin D has more recently been shown to modulate immune function by promoting an anti-inflammatory response, which may be related to onset or progression of autoimmune inflammatory disorders. One such condition is multiple sclerosis (MS). There is an increasing incidence of MS with increasing latitude, with higher prevalence reported in countries further away from the equator, where vitamin D synthesis is inadequate. Vitamin D has been shown to have positive effects on the animal model of MS, experimental autoimmune encephalomyelitis. However, there have been few human intervention studies to investigate the effect of vitamin D supplementation on symptoms of MS or indeed of other autoimmune disorders. Further research is required to examine the potential beneficial role of vitamin D in MS to ultimately determine the optimal vitamin D status required to alleviate symptoms and possibly prevent this and other chronic diseases.

Polar luminance measurements : a direction in qualifying modelling

Through experimentation, it is revealed that the polar luminance method is capable of measuring the modelling of an object effectively in scenarios where the vector/scalar ratio is deficient. It is suggested that polar luminance measurement is a new direction for the measurement of modelling.

Differential modulation of spinal and corticospinal excitability during drop jumps

Previously it was shown that spinal excitability during hopping and drop jumping is high in the initial phase of ground contact when the muscle is stretched but decreases toward takeoff. To further understand motor control of stretch-shortening cycle, this study aimed to compare modulation of spinal and corticospinal excitability at distinct phases following ground contact in drop jump. Motor-evoked potentials (MEPs) induced by transcranial magnetic stimulation (TMS) and H-reflexes were elicited at the time of the short (SLR)-, medium (MLR)-, and long (LLR, LLR2)-latency responses of the soleus muscle (SOL) after jumps from 31 cm height. MEPs and H-reflexes were expressed relative to the background electromyographic (EMG) activity. H-reflexes were highly facilitated at SLR (172%) and then progressively decreased (MLR = 133%; LLR = 123%; LLR2 = 110%). TMS showed no effect at SLR, MLR, and LLR, whereas MEPs were significantly facilitated at the LLR2 (122%; P = 0.003). Background EMG was highest at LLR and lowest at LLR2. Strong H-reflex facilitation at the beginning of the stance phase indicated significant contribution of Ia-afferent input to the α-motoneurons during this phase that then progressively declined toward takeoff. Conversely, corticospinal excitability was exclusively increased at the phase of push off (LLR2, ∼120 ms). It is argued that corticomotoneurons increased their excitability at LLR2. At LLR (∼90 ms), Ia-afferent transmission as well as corticospinal excitability was low, whereas background EMG was high. Therefore it is speculated that other sources, presumably subcortical in origin, contributed to the EMG activity at LLR in drop jumps.

Effects of variation in modulator temperature during cryogenic modulation in comprehensive two-dimensional gas chromatography

Many modulation systems in comprehensive 2D GC (GC×GC) are based on cryogenic methods. High trapping temperatures in these systems can result in ineffective trapping of the more volatile compounds, whilst temperatures that are too low can prevent efficient remobilisation of some compounds. To better understand the trapping and release of compounds over a wide range of volatilities, we have investigated a number of different constant temperature modulator settings, and have also examined a constant temperature differential between the cryo-trap and the chromatographic oven. These investigations have led us to modify the temperature regulation capabilities of the longitudinally modulated cryogenic system (LMCS). In contrast to the current system, where the user sets a constant temperature for the cooling chamber, the user now sets the temperature difference between the cryo-trap and the chromatographic oven. In this configuration, the cooling chamber temperature increases during the chromatographic run, tracking the oven temperature ramp. This produces more efficient, volatility-dependent modulation, and increases the range of volatile compounds that can be analysed under optimal trap-and-release conditions within a single analytical run. This system also reduces cryogenic fluid consumption.

The central nucleus of the amygdala ; a conduit for modulation of HPA axis responses to an immune challenge?

Physical stressors such as infection, inflammation and tissue injury elicit activation of the hypofhalamic-pituitary-adrenal (HPA) axis. This response has significant implications for both immune and central nervous system function. Investigations in rats into the neural substrates responsible for HPA axis activation to an immune challenge have predominantly utilized an experimental paradigm involving the acute administration of the pro-inflammatory cytokine interleukin-1 β (IL-1β). It is well recognized that medial parvocellular corticotrophin-releasing factor cells of the paraventricular nucleus (mPVN CRF) are critical in generating HPA axis responses to an immune challenge but little is known about how peripheral immune signals can activate and/or modulate the mPVN CRF cells. Studies that have examined the afferent control of the mPVN CRF cell response to systemic IL-1β have centred largely on the inputs from brainstem catecholamine cells. However, other regulatory neuronal populations also merit attention and one such region is a component of the limbic system, the central nucleus of the amygdala (CeA). A large number of CeA cells are recruited following systemic IL-lβ administration and there is a significant body of work indicating that the CeA can influence HPA axis function. However, the contribution of the CeA to HPA axis responses to an immune challenge is only just beginning to be addressed. This review examines three aspects of HPA axis control by systemic IL-lβ; (i) whether the CeA has a role in generating HPA axis responses to systemic IL-1 β, (ii) the identity of the neural connections between the CeA and mPVN CRF cells that might be important to HPA axis responses and (iii) the mechanisms by which systemic IL-lβ triggers the recruitment of CeA cells.

Differential involvement of rat medial prefrontal cortex dopamine receptors in modulation of hypothalamic- pituitary-adrenal axis responses to different stressors

Recent investigations have implicated the medial prefrontal cortex (mPFC) in modulation of subcortical pathways that contribute to the generation of behavioural, autonomic and endocrine responses to stress. However, little is known of the mechanisms involved. One of the key neurotransmitters involved in mPFC function is dopamine, and we therefore aimed, in this investigation, to examine the role of mPFC dopamine in response to stress in Wistar rats. In this regard, we infused dopamine antagonists SCH23390 or sulpiride into the mPFC via retrodialysis. We then examined changes in numbers of cells expressing the c-fos immediate-early gene protein product, Fos, in subcortical neuronal populations associated with regulation of hypothalamic-pituitary-adrenal (HPA) axis stress responses in response to either of two stressors; systemic injection of interleukin-1β, or air puff. The D1 antagonist, SCH23390, and the D2 antagonist, sulpiride, both attenuated expression of Fos in the medial parvocellular hypothalamic paraventricular nucleus (mpPVN) corticotropin-releasing factor cells at the apex of the HPA axis, as well as in most extra-hypothalamic brain regions examined in response to interleukin-1β. By contrast, SCH23390 failed to affect Fos expression in response to air puff in any brain region examined, while sulpiride resulted in an attenuation of the air puff-induced response in only the mpPVN and the bed nucleus of the stria terminalis. These results indicate that the mPFC differentially processes the response to different stressors and that the two types of dopamine receptor may have different roles.

Evidence that the bed nucleus of the stria terminalis contributes to the modulation of hypophysiotropic corticotropin-releasing factor cell responses to systemic interleukin-1β

Systemic infection activates the hypothalamic-pituitary-adrenal (HPA) axis, and brainstem catecholamine cells have been shown to contribute to this response. However, recent work also suggests an important role for the central amygdala (CeA). Because direct connections between the CeA and the hypothalamic apex of the HPA axis are minimal, the present study investigated whether the bed nucleus of the stria terminalis (BNST) might act as a relay between them. This was done by using an animal model of acute systemic infection involving intravascular delivery of the proinflammatory cytokine interleukin-1β (IL-1β, 1 μg/kg). Unilateral ibotenic acid lesions encompassing the ventral BNST significantly reduced both IL-1β-induced increases in Fos immunoreactivity in corticotropin-releasing factor (CRF) cells of the hypothalamic paraventricular nucleus (PVN) and corresponding increases in adrenocorticotropic hormone (ACTH) secretion. Similar lesions had no effect on CRF cell responses to physical restraint, suggesting that the effects of BNST lesions were not due to a nonspecific effect on stress responses. In further studies, we examined the functional connections between PVN, BNST, and CeA by combining retrograde tracing with mapping of IL-1β-induced increases in Fos in BNST and CeA cells. In the case of the BNST, these studies showed that systemic IL-1β administration recruits ventral BNST cells that project directly to the PVN. In the case of the CeA, the results obtained were consistent with an arrangement whereby lateral CeA cells recruited by systemic IL-1β could regulate the activity of medial CeA cells projecting directly to the BNST. In conclusion, the present findings are consistent with the hypothesis that the BNST acts as a relay between the CeA and PVN, thereby contributing to CeA modulation of hypophysiotropic CRF cell responses to systemic administration of IL-1β.