A method for rapid in vivo measurement of blood T1

We present a technique to measure the longitudinal relaxation time constant of venous blood (T_1b) in vivo in a few seconds. The MRI sequence consists of a thick‐slab adiabatic inversion, followed by a series of slice‐selective excitations and single‐shot echo planar imaging readouts. The time intervals between excitations were chosen so that blood in macroscopic vessels is fully refreshed between excitations, making the blood signal follow an unperturbed inversion recovery curve. Static tissue, which experiences the inversion and all excitation pulses, quickly reaches a steady state at a low signal as a result of partial saturation. This allows blood‐filled voxels to be discriminated from those containing static tissue, and to be fitted voxel‐by‐voxel to a simple inversion recovery model. The sequence was tested on a flow phantom with the proposed method, yielding T₁ values consistent to within 3% of those obtained using a conventional inversion recovery sequence with a spin‐echo readout. The method was applied to seven adult volunteers and 18 neonates. The blood T₁ of the neonates (1799 ± 206 ms; range, 1393–2035 ms) was found to be more variable than that of adults (1717 ± 39 ms; range, 1662–1779 ms). A linear correlation between the inverse of T_1b and the haematocrit was established in 12 neonates (R² = 0.90). Copyright © 2010 John Wiley & Sons, Ltd.     

The prevalence of allergic diseases in an unselected group of 6-year-old children. The DARC birth cohort study

This study determines the prevalence of atopic dermatitis, asthma, rhinoconjunctivitis, food hypersensitivity and urticaria and the frequency of sensitization in children with and without clinical allergic disease. In an ongoing prospective non-interventional birth cohort study of 562 unselected children, 404 children were subjected to interview, clinical examination, lung function measurements and allergy testing at 6 yr of age. Sensitization measured by skin prick test (SPT) and specific immunoglobulin E (S-IgE) was determined for 24 different allergens. The 1-yr period prevalence of atopic dermatitis, asthma and rhinoconjunctivitis was 14.4%, 6.2% and 13.6%. 25.7% of the children suffered from at least one of the three diseases. The frequency of sensitization in children with no disease (controls), any allergic disease, atopic dermatitis, asthma and rhinoconjunctivitis was 17%, 45%, 47%, 56% and 55% (defined as SPT ≥3 mm and/or S-IgE ≥0.35 kU/l for at least one allergen). Symptoms were linked to sensitization for 44% in the asthma group and 42% in the rhinoconjunctivitis group, whereas sensitization could not be linked to worsening of the eczema in any cases of atopic dermatitis. Overlap between the three diseases was significantly more frequent in sensitized children than in non-sensitized (19/46 = 41% vs. 9/58 = 16%, p = 0.004). The prevalence of food hypersensitivity and urticaria was 1.2% and 5.4% respectively. In unselected 6 yr old children, approximately half of the children with atopic dermatitis, asthma or rhinoconjunctivitis are IgE-sensitized. Sensitization tends to link these diseases to each other.     

Comorbidity of schizophrenia and infection: a population-based cohort study

Purpose

In this paper, we investigate the hypothesis that there is an overlap between infection and schizophrenia. Infections have been identified as a risk factor for schizophrenia, but the possible overlap between schizophrenia and infections remains unidentified so far. Here, we describe the use of the comorbidity index, a method for objectively integrating associations into a single measure estimating overlap.

Methods

Data were drawn from three population-based registers, the Civil Registration Register, the Danish Psychiatric Central Research Register, and the Danish National Hospital Register. We selected a cohort of 1,403,183 persons born in Denmark 1977–2002.

Results

Our results indicate that persons who have had a hospital contact with an infection (IRR 1.53, CI 1.46–1.61) are more likely to develop schizophrenia than persons who have not had such a contact. Persons who have had a diagnosis with schizophrenia are more likely to have had a hospital contact with an infection (IRR 1.73, 95 % CI 1.57–1.91) than persons who have had no schizophrenia diagnosis. A comorbidity index of 1.40 (95 % CI 1.34–1.46) was found, indicating an overlap between schizophrenia and infection.

Conclusion

Our findings indicate that schizophrenia and infections overlap and that they share risk factors. The comorbidity index showed that the co-occurrence of schizophrenia and infection was 40 % higher than if the two disorders had occurred independently. Although the incidence of schizophrenia and infection was associated with each factor, the overlap could not be explained by urbanicity, parental history of psychiatric admission and infection.

     

Epilepsy and risk of suicide: a population-based case-control study

BACKGROUND: Studies have linked epilepsy with an increased suicide risk, but the association might be modified by psychiatric, demographic, and socioeconomic factors. METHODS: Suicide cases were identified in the Cause of Death Register in Denmark from 1981 to 1997. Up to 20 controls, matched by sex, birth year, and calendar date, were assigned to each suicide case. FINDINGS: We identified 21 169 cases of suicide and 423 128 controls. 492 (2.32%) individuals who committed suicide had epilepsy compared with 3140 (0.74%) controls, corresponding to a three times higher risk (rate ratio [RR] 3.17 [95% CI 2.88-3.50]; p<0.0001). The RR remained high after excluding those with a history of psychiatric disease and adjusting for socioeconomic factors (1.99, 1.71-2.32; p<0.0001). The highest risk of suicide was identified in patients with epilepsy and comorbid psychiatric disease, even after adjusting for socioeconomic factors (13.7, 11.8-16.0; p<0.0001). In individuals with epilepsy, the highest risk of suicide was found during the first half year after diagnosis was made (5.35, 3.43-8.33; p<0.0001), and was especially high in those with a history of comorbid psychiatric disease (29.2, 16.4-51.9; p<0.0001). INTERPRETATION: Individuals with epilepsy have a higher risk of suicide, even if coexisting psychiatric disease, demographic differences, and socioeconomic factors are taken into account. Our study identifies people with newly diagnosed epilepsy as a vulnerable group that require special attention.     

Characterization of osteopontin expression and function after status epilepticus

Purpose: Osteopontin is a cytokine found in many tissues and plays a role in tissue injury and repair. This study had two goals: to characterize osteopontin expression after status epilepticus (SE), and to test the hypotheses that osteopontin affects the susceptibility to seizures or alters cell death and inflammation after SE. Methods: Pilocarpine was used to induce SE in OPN^?/? and OPN^+/+ mice to compare seizure susceptibility, neuropathological markers including real time PCR for inflammatory genes, and osteopontin immunohistochemistry. The effect of added osteopontin on excitotoxicity by N‐methyl‐d ‐aspartate in neuronal cultures of ONP^?/? mice was determined. Results: Neurons undergoing degeneration showed osteopontin immunoreactivity 2–3  days after SE. After 10 to 31 days degenerating axons in the thalamus were osteopontin‐positive. The susceptibility to seizures of OPN^?/? and OPN^+/+ mice in the pilocarpine, fluorothyl, and maximal electroshock models was similar. There were no significant differences in the extent of neuronal damage after pilocarpine‐induced SE, the expression of several neuropathological markers or the RNA levels of selected inflammatory genes. Recombinant and natural bovine osteopontin did not affect the extent of NMDA‐induced cell death in OPN^?/? mouse neuronal cultures. Conclusion: We demonstrated that osteopontin is up‐regulated in response to SE in distinct temporal sequences in the hippocampus, specifically in dege‐nerating neurons and axons. However, osteopontin did not appear to regulate neurodegeneration or inflammation within the first 3  days after SE.