Plantar warts on Tollund Man's feet (Denmark, fourth century BC). Limits of retrospective dermatological diagnosis

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Ichthyosis with confetti presenting as collodion baby: a novel mutation in KRT10

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Duration and exclusiveness of breastfeeding and school-age lung function and asthma

Publication date: Available online 26 May 2017
Source:Annals of Allergy, Asthma & Immunology
Author(s): Evelien R. van Meel, Mandy de Jong, Niels J. Elbert, Herman T. den Dekker, Irwin K. Reiss, Johan C. de Jongste, Vincent W.V. Jaddoe, Liesbeth Duijts
BackgroundBreastfeeding reduces the risk of asthma in early childhood, but it is not clear whether its effect on respiratory morbidity is still present in later childhood.ObjectivesTo examine the associations of any breastfeeding, breastfeeding duration, and breastfeeding exclusiveness with lung function and asthma in school-aged children and whether associations were influenced by respiratory tract infections and maternal or child's atopic status.MethodsThis study of 4,464 children was embedded in a population-based prospective cohort study. Information on breastfeeding was obtained by multiple questionnaires from birth until 1 year of age. At 10 years of age, lung function was measured by spirometry, and information on asthma was obtained by questionnaire. Adjusted linear and logistic regression models were used to examine the associations.ResultsShorter duration of breastfeeding was associated with a lower forced expiratory volume in 1 second (FEV1) only (z score change, −0.01; 95% confidence interval [CI], −0.02 to −0.00) per month shorter breastfeeding, but not asthma. When categorized, breastfeeding for 2 to 4 months was associated with a lower forced vital capacity (FVC) (z score change, −0.11; 95% CI, −0.20 to −0.03) compared with breastfeeding for 6 months or longer. Nonexclusive breastfeeding for 4 months was associated with a lower FVC (z score change, −0.08; 95% CI, −0.16 to −0.01) compared with exclusive breastfeeding for 4 months. Results did not materially change after additional adjustment for lower respiratory tract infections and were not modified by maternal history of asthma or atopy, child's eczema, or inhalant allergic sensitization.ConclusionShorter duration and nonexclusivity of breastfeeding were associated with a lower FEV1 and FVC but not asthma at school-age.



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Association of of IgE Can f 2 and dyspnea in pet allergic patients

Publication date: Available online 26 May 2017
Source:Annals of Allergy, Asthma & Immunology
Author(s): Natalia Ukleja-Sokołowska, Ewa Gawrońska-Ukleja, Magdalena Żbikowska-Gotz, Ewa Socha, Kinga Lis, Łukasz Sokołowski, Zbigniew Bartuzi




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Plantar warts on Tollund Man's feet (Denmark, fourth century BC). Limits of retrospective dermatological diagnosis

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Ichthyosis with confetti presenting as collodion baby: a novel mutation in KRT10

http://ift.tt/2s6iDou

Genomics of sex hormone receptor signaling in hepatic sexual dimorphism

Publication date: Available online 26 May 2017
Source:Molecular and Cellular Endocrinology
Author(s): Daoshan Zheng, Xiao Wang, Per Antonson, Jan-Åke Gustafsson, Zhaoyu Li
The liver plays a crucial role in a variety of physiological processes. Sexual dimorphism is markedly defined in liver disorders, such as fatty liver diseases and liver cancer, but barely addressed in the normal liver. Distinct sex hormone signaling between male and female livers is the major driving factor for hepatic sexual dimorphism. Over 6000 genes are differently expressed between male and female livers in mice. Here we address how sex hormone receptors, estrogen receptor alpha (ERα) and androgen receptor (AR), mediate sexually dimorphic gene expression in mouse livers. We identified 5192 ERα target genes and 4154 AR target genes using ChIP-Seq. Using liver-specific ERα or AR knockout mice, we further identified direct and functional target genes of ERα (123 genes) and AR (151 genes) that contribute to hepatic sexual dimorphism. We also found that the most significant sexually dimorphic gene expression was initiated at birth by comparing hepatic gene expression data from the embryonic stage E10.5 to the postnatal stage P60 during liver development. Overall, our study indicates that sex hormone receptor signaling drives sexual dimorphism of hepatic gene expression throughout liver development.



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