The fMRI response of the LGN and V1 to cardinal red-green, blue-yellow, and achromatic visual stimuli

We compared the responsiveness of the LGN and the early retinotopic cortical areas to stimulation of the two cone-opponent systems (red - green and blue - yellow) and the achromatic system. This was done at two contrast levels to control for any effect of contrast. MR images were acquired on seven subjects with a 4T Bruker MedSpec scanner. The early visual cortical areas were localised by phase encoded retinotopic mapping with a volumetric analysis (Dumoulin et al, 2003 NeuroImage 18 576 - 587). We initially located the LGN in four subjects by using flickering stimuli in a separate scanning session, but subsequently identified it using the experimental stimuli. Experimental stimuli were sine-wave counterphasing rings (2 Hz, 0.5 cycle deg-1), cardinal for the selective activation of the L/M cone-opponent (RG), S cone-opponent (BY), and achromatic (Ach) systems. A region of interest analysis was performed. When presented at equivalent absolute contrasts (cone contrast = 5% - 6%), the BOLD response of the LGN is strongest to isoluminant red - green stimuli and weakest to blue - yellow stimuli, with the achromatic response falling in between. Area V1, on the other hand, responds best to both chromatic stimuli, with the achromatic response falling below. The key change from the LGN to V1 is a dramatic boost in the relative blue - yellow response, which occurred at both contrast levels used. This greatly enhanced cortical response to blue - yellow relative to the red - green and achromatic responses may be due to an increase in cell number and/or cell response between the LGN and V1. We speculate that the effect might reflect the operation of contrast constancy across colour mechanisms at the cortical level.

Parasitic isopod Anilocra apogonae, a drag for the cardinal fish Cheilodipterus quinquelineatus

Cymothoid isopods Anilocra apogonae are regular ectoparasites of the cardinal fish Cheilodipterus quinquelineatus on the Great Barrier Reef. To determine whether this large isopod, attached to the head of the fish, affects the physiology and behaviour of its host, we conducted morphological measurements to obtain a condition index and several laboratory experiments on fish with and without isopods. The condition index did not vary between parasitised and non-parasitised wild fish. However, we found that parasitised fish lost more weight than unparasitised fish when fed a low food ration. Parasitised fish also had a higher rate of oxygen consumption than non-parasitised fish. When maintaining body posture in calm water, parasitised fish had an elevated pectoral fin beat frequency, probably because the isopod attaches asymmetrically, causing an asymmetrical weight balance for which the fish needs to compensate. Moreover, the sustained aerobic swimming speed as well as the swimming endurance at high water speeds were reduced in parasitised fish, possibly because of the drag from the parasite. The results suggest that parasites can have significant effects on fish even if this is not revealed by their body condition index in the wild. The metabolic effects found imply that parasitised fish may have to spend more time foraging to compensate for their higher metabolism. This could expose them to a higher risk of being eaten, a situation made worse by an impaired swimming ability that may reduce their capacity to escape a predator.

Identification of MIMO Hammerstein systems using cardinal spline functions

A new approach to identify multivariable Hammerstein systems is proposed in this paper. By using cardinal cubic spline functions to model the static nonlinearities, the proposed method is effective in modelling processes with hard and/or coupled nonlinearities. With an appropriate transformation, the nonlinear models are parameterized such that the nonlinear identification problem is converted into a linear one. The persistently exciting condition for the transformed input is derived to ensure the estimates are consistent with the true system. A simulation study is performed to demonstrate the effectiveness of the proposed method compared with the existing approaches based on polynomials. (C) 2006 Elsevier Ltd. All rights reserved.

Defective NF-kappaB Activation in Response to LPS in Type 1 Diabetes Dendritic Cells

Dendritic cells (DC) are the potent antigen presenting cells which modulate T cell responses to self or non-self antigens. DC play a significant role in the pathogenesis of autoimmune diseases, inflammation and infection, but also in the maintenance of tolerance. NF-kappaB, particularly RelB is a crucial pathway for myeloid DC differentiation and functional maturation. While the current paradigm is that mature, nuclear RelB+ DC prime T cells for immunity/autoimmunity and immature DC for tolerance, RelB-deficient mice paradoxically develop generalised systemic autoimmune inflammatory disease with myelopoiesis and splenomegaly. Previous studies suggested abnormal DC differentiation in healthy relatives of type 1 diabetes (t1dm) patients. Therefore, we compared NF- kB activation in monocyte-derived DC from t1dm and non-t1dm controls in response to LPS. While resting DC appeared normal, DC from 6 out of 7 t1dm patients but no t2dm or rheumatoid arthritis patients failed to translocate NF- kB subunits to the nucleus in response to LPS, along with a failure to up-regulate expression of cell surface CD40 and MHC class I. NF- kB subunit mRNA increased normally in t1dm DC after LPS. Both the classical or non-canonical NF- kB pathways were affected as both TNF-a and CD40 stimulation led to a similarly abnormal NF- kB response. In contrast, expression of phosphorylated p38 MAPK and pro-inflammatory cytokine production was intact. These abnormalities in NF- kB activation appear to be generally and specifically applicable at a post-translational level in t1dm, and have the capacity to profoundly influence immunoregulation in affected individuals.

Parasites of ornamental fish imported into Australia

Five commonly imported freshwater ornamental fish: Poecilia reticulata (guppy); Xiphophorus maculatus (platy); Paracheirodon innesi (neon tetra); Paracheirodon axelrodi (cardinal tetra); and Gyrinocheilus aymonieri (sucking catfish), 361 individuals in total, were examined for parasites immediately after being released from quarantine in Australia. Ten parasites species were found: Camallanus cotti; Centrocestus formosanus; Bothriocephalus acheilognathi; Urocleidoides reticulatus; Tetrahymena corlissi; Chilodonella piscicola; Hexamita sp.; Cryptobia sp.; Chloromyxum sp.; and an unidentified larval nematode. Though shipments had come from up to five different exporting companies, parasite prevalence was uniformly high. We suggest that prior to release, fish transported internationally should be checked for high risk pathogens such as Camallanus cotti, B. acheilognathi and Centrocestus formosanus, and treated for common infections such as Hexamita sp., Cryptobia sp. T. corlissi and Chilodonella piscicola to inhibit the spread of disease and enhance the survival of the fish.

Increased susceptibility to streptozotocin-induced beta-cell apoptosis and delayed autoimmune diabetes in alkylpurine-DNA-N-glycosylase-deficient mice

Type I diabetes is thought to occur as a result of the loss of insulin-producing pancreatic beta cells by an environmentally triggered autoimmune reaction. In rodent models of diabetes, streptozotocin (STZ), a genotoxic methylating agent that is targeted to the beta cells, is used to trigger the initial cell death. High single doses of STZ cause extensive beta -cell necrosis, while multiple low doses induce limited apoptosis, which elicits an autoimmune reaction that eliminates the remaining cells. We now show that in mice lacking the DNA repair enzyme alkylpurine-DNA-N-glycosylase (APNG), beta -cell necrosis was markedly attenuated after a single dose of STZ. This is most probably due to the reduction in the frequency of base excision repair-induced strand breaks and the consequent activation of poly(ADP-ribose) polymerase (PARP), which results in catastrophic ATP depletion and cell necrosis. Indeed, PARP activity was not induced in A-PNG(-/-) islet cells following treatment with STZ in vitro. However, 48 h after STZ treatment, there was a peak of apoptosis in the beta cells of APNG(-/-) mice. Apoptosis was not observed in PARP-inhibited APNG(+/+) mice, suggesting that apoptotic pathways are activated in the absence of significant numbers of DNA strand breaks. Interestingly, STZ-treated APNG(-/-) mice succumbed to diabetes 8 months after treatment, in contrast to previous work with PARP inhibitors, where a high incidence of beta -cell tumors was observed. In the multiple-low-dose model, STZ induced diabetes in both APNG(-/-) and APNG(-/-) mice; however, the initial peak of apoptosis was 2.5-fold greater in the APNG(-/-) mice. We conclude that APNG substrates are diabetogenic but by different mechanisms according to the status of APNG activity.

EMG activity normalization for trunk muscles in subjects with and without back pain

Purpose: The aims of the present study were to examine electromyographic (EMG) activity of six bilateral trunk muscles during maximal contraction in three cardinal planes, and to determine the direction of contraction that gives maximal activation for each muscle. both for healthy subjects and back-pain patients. Methods: Twenty-eight healthy subjects and 15 back-pain patients performed maximum voluntary contractions in three cardinal planes, Surface EMG signals were recorded from rectus abdominis, external oblique, internal oblique, latissimus dorsi, iliocostalis lumborum, and multifidus bilaterally. Root mean square values of the EMG data were calculated to quantify I the amplitude of EMG signals. Results: For both healthy subjects and back-pain patients. one single direction of contraction was found to give the maximum EMG signals for most muscles. Rectus abdominis demonstrated maximal activity in trunk flexion, external oblique in lateral flexion. internal oblique in axial rotation, and multifidus in extension. For the latissimus dorsi and iliocostalis lumborum. maximal activity was demonstrated in more than one cardinal plane. Conclusion: This study has implications for future research involving normalization of muscle activity to maximal levels required in many trunk EMG studies. As the latissimus dorsi and iliocostalis lumborum demonstrate individual differences in the plane that gives maximal activity, these muscles may require testing in more than one plane.

Autosomal dominant hypocalcemia: A novel activating mutation (E604K) in the cysteine-rich domain of the calcium-sensing receptor

We report a novel activating mutation (E604K) of the calcium-sensing receptor in a family with autosomal dominant hypocalcemia. Whereas all affected individuals exhibited marked hypocalcemia, some cases with untreated hypocalcemia exhibited seizures in infancy, whereas others were largely asymptomatic from birth into adulthood. The missense mutation E604K (G2182A, GenBank accession no. U20759), which affects an amino acid residue in the C terminus of the cysteine-rich domain of the extracellular head, co-segregated with hypocalcemia in all seven individuals for whom DNA was available. Two unaffected, normocalcemic members of the family did not exhibit the mutation. The molecular impact of the mutation on two key components of the signaling response was assessed in HEK-293 cells transiently transfected with cDNA corresponding to either the wild-type calcium-sensing receptor or the E604K mutation derived by site-directed mutagenesis. There was a significant leftward shift in the concentration response curves for the effects of extracellular Ca2+ on both intracellular Ca2+ mobilization (determined by aequorin luminescence) and MAPK activity (determined by luciferase expression). The C terminus of the cysteine-rich domain of the extracellular head may normally act to suppress receptor activity in the presence of low extracellular Ca2+ concentrations.