422 research outputs found
Parcellation Scheme for a Spatio-Temporal Atlas of Fetal Brain Lobe Development
Introduction
Fetal brain development is a complex and dynamic process. During the third trimester of pregnancy the brain’s surface landscape changes from a smooth layer into a complex canopy with convolutions called gyri. The emergence of quantitative magnetic resonance imaging (MRI) has allowed for in vivo acquisition of high-resolution images of the fetal brain. Although a timeline for the emergence of important gyri exists; we currently lack an in vivo MRI model—or atlas—of the developing brain. Therefore, our objective was to develop a scheme to parcelate the third trimester in vivo fetal brain into lobes, and apply this scheme onto scans in healthy fetal MRI brains to create a spatiotemporal atlas.
Methods
Based on a previous parcellation scheme of the neonatal brain, and conventional anatomical landmarks for classic brain lobe divisions, we devised a scheme to parcellate the fetal brain between 29-37 weeks into five lobes: frontal, parietal, temporal, occipital, and insular. We used an atlas of T2 weighted MRI images from 80 fetuses without any known pathological conditions.
Results
Fetal atlases at 31, 33, 35, and 37 gestational weeks were parcellated into five lobes. Gestational week 29, the youngest gestational age in our sample, could not be parcellated because the landmarks outlined in our parcelation scheme have not yet appeared in the brain at this gestational age.
Discussion
Taken together, our results show that available conventional anatomical landmarks for the division of the third trimester brain into classic lobes are only reliably applicable down to gestational weeks 30-31. A parcellation scheme for the fetal brain younger than 30 weeks will require different anatomical parameters from higher resolution MR images. Nevertheless, the fetal brain lobe parcellations presented here can be used in their current form as a tool to identify regional, lobular brain growth disturbances in third trimester high-risk fetal populations
Experimental Photoallergic Contact Dermatitis: A Mouse Model
We have induced photoallergic contact dermatitis in mice to 3,3',4',5 tetrachlorosalicylanilide (TCSA), chlorpromazine and 6-methylcoumarin. These compounds are known to produce photoallergic contact dermatitis in humans. The photoallergic contact dermatitis reaction in the mouse is immunologically specific viz. mice photosensitized to TCSA react, by photochallenge, to that compound and not to chlorpromazine, and conversely. The reaction requires UVA at both sensitization and challenge. It appears to be T-cell medicated in that it can be passively transferred to syngeneic mice by lymph node cells from actively sensitized mice, histology of the reactions resembles that of classic allergic contact dermatitis in mice, challenge reactions are seen at 24 but not at 4hr, and photoallergic contact dermatitis can be induced in B-cell deficient mice. The availability of a mouse model for the study of photo-ACD will facilitate the identification of pertinent control mechanisms and may aid in the management of the disease. It is likely that a bioassay for photoallergens of humans can be based on this mouse model
The Influence of UVA and Visible Radiation on Acute Damage by Short-Wave UVR (λ < 320 nm)
The influence of UVA and visible radiation on the acute damage by short-wave ultraviolet radiation (UVR) (λ < 320 nm) was investigated in human volunteers, using delayed erythema and sunburn cell production as markers of injury. It was found that subsequent exposure to UVA + visible radiation produced a significant reduction of the threshold erythema dose by short-wave UVR, in a dose-dependent manner. Subsequent exposures to varying doses of UVA + visible radiation, as well as to visible light alone failed to influence sunburn cell production. It is concluded that there is a positive interaction between short-wave UVR and UVA in the induction of delayed erythema, but this may not apply to epidermal cell injury. Photorecovery was not observed
Pseudoceramide-Containing Physiological Lipid Mixture Reduces Adverse Effects of Topical Steroids
PURPOSE: Various therapeutic approaches have been suggested for preventing or reducing the adverse effects of topical glucocorticoids, including skin barrier impairment. Previously, we have shown that impairment of skin barrier function by the highest potency topical glucocorticoid, clobetasol 17-propinate (CP), can be partially prevented by co-application of a physiological lipid mixture containing pseudoceramide, free fatty acids, and cholesterol (multi-lamellar emulsion [MLE]). Skin atrophic effects of CP were also partially reduced by MLE. In this study, the preventive effects of MLE on the lowest potency topical glucocorticoid, hydrocortisone (HC), were investigated using animal models.
METHODS: Anti-inflammatory activity of topical HC was evaluated using a 12-O-tetradecanoylphobol-13-acetate-induced skin edema model. Topical steroid induced adverse effects were evaluated using hairless mouse.
RESULTS: The results showed that the anti-inflammatory activity was not altered by co-application of either MLE or hydrobase. However, co-application of MLE and 1.0% HC showed less impairment in the epidermal permeability barrier function, skin hydration, and skin surface pH compared with hydrobase. Stratum corneum integrity, evaluated by measuring trans-epidermal water loss after repeated tape stripping, showed less damage with MLE co-application. Long-term application of topical HC induced skin atrophy, measured by a reduction in skinfold and epidermal thickness and in the number of epidermal proliferating cell nucleus antigen (PCNA)-positive keratinocytes. Co-application of MLE did not affect the skinfold or epidermal thickness, but the number of PCNA-positive keratinocytes was less decreased with MLE use.
CONCLUSIONS: These results suggest that co-application of MLE is effective in reducing the local adverse effects of low-potency topical glucocorticoids and supports the therapeutic efficacy of physiological lipid mixtures on skin barrier function.ope
Stop the Pop: A Mixed-Methods Study Examining Children’s Physical and Emotional Responses during Three Days of Sugary Drink Cessation
Despite public health efforts to reduce sugary drink consumption, children’s intake continues to exceed recommendations. While numerous barriers to lowering sugary drink consumption have been identified, aversive feelings during sugary drink cessation may further challenge sustained reduction in children’s sugary drink consumption. Herein, we describe “Stop the Pop”, an intervention to examine children’s physical and emotional responses during three days of sugary drink cessation. Children (n = 150) ages 8–14, who reported habitual consumption of ≥12 ounces of sugary drinks daily, were instructed to avoid sweetened beverages for three days. At baseline and on each day of cessation, children completed a daily feelings questionnaire, and a subset of children (n = 30) also completed a qualitative interview following cessation. During sugary drink cessation, children reported physical and emotional improvements, including being less tired, angry, and annoyed; having less trouble sleeping; and less frequently arguing with others, getting in trouble, and getting mad. However, unfavorable responses, such as mood disturbances and having less energy, were reported by some participants. Our results suggest that children who habitually consume sugary drinks may experience physical and emotional improvements during short-term sugary drink cessation, although longer-term examination is needed and inter-individual variability in responses to cessation warrants further study
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