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Objectives The findings of a previous multigene study indicated that the expression of a panel of seven specific genes had strong differential power regarding inflammatory bowel disease ( IBD) versus non- IBD, as well as ulcerative colitis ( UC) versus Crohn's disease ( CD). This prospective confirmatory study based on an independent patient cohort from a national Danish IBD centre was conducted in an attempt to verify these earlier observations. Design, setting and participants A total of 119 patients were included in the study ( CD, UC and controls). Three mucosal biopsies were retrieved from the left side of the colon of each patient. RNA was extracted, and RT- PCR was performed to retain expression profiles from the seven selected genes. Expression data from the training set (18 CD, 20 UC and 20 controls) were used to build a classification model, using quadratic discriminant analysis, and data from the test set (20 CD, 21 UC and 20 controls) were used to test the validity of the model. Results The present investigation did not confirm the previous observation that a panel of seven specific genes is able to distinguish between patients with CD and UC, whereas the discriminative power for IBD versus control subjects was substantiated. Conclusion Our results fail to demonstrate that the previously identified seven-gene classification model is able to discriminate between CD and UC but suggest that the gene panel merely discriminates between inflamed and noninflamed colonic tissue. Thus, a reliable and simple diagnostic tool is still warranted for optimal diagnosis and treatment of patients with IBD, especially the subgroup with unclassified disease. [ABSTRACT FROM AUTHOR]

Aim: The aim of this study was to investigate whether the choice reforms in healthcare in Stockholm county in 2008 and 2013 changed the sociodemographic user patterns of outpatient healthcare services for children., Methods: The study used regional data on healthcare use linked to sociodemographic data from national registers in the total population of children 0-15 years in the Stockholm county. Change in use of healthcare services was analysed in multiple linear regression in a difference in differences approach of socio-economic indicators., Results: The choice reform of 2013 increased children's overall use of specialised care by around 30% until 2017 while primary care use decreased by the same degree. The mean number of physician visits in specialised care for children with severe asthma increased from 3.9 to 5.2 per year. Overall, children in families with low maternal education, low disposable income and a non-Western background increased their use of specialised care more than children from families with a more privileged socio-economic situation., Conclusion: There was no indication that the choice reform in Stockholm county increased the social disparities in use of primary and specialised outpatient care for children, rather the opposite., (© 2023 The Authors. Acta Paediatrica published by John Wiley & Sons Ltd on behalf of Foundation Acta Paediatrica.)

The ubiquity and consequences of childhood growth stunting (<-2 SD in height-for-age Z score, HAZ) in rural areas of low-income nations has galvanized research into the reversibility of stunting, but the shortage of panel data has hindered progress. Using panel data from a native Amazonian society of foragers-farmers in Bolivia (Tsimane'), we estimate rates of catch-up growth for stunted children. One hundred forty-six girls and 158 boys 2 < or = age < or = 7 were measured annually during 2002-2006. Annual Delta height in cm and in HAZ were regressed separately against baseline stunting and control variables related to attributes of the child, mother, household, and village. Children stunted at baseline had catch-up growth rates 0.11 SD/year higher than their nonstunted age and sex peers, with a higher rate among children farther from towns. The rate of catch up did not differ by the child's sex. A 10% rise in household income and an additional younger sibling lowered by 0.16 SD/year and 0.53 SD/year the rate of growth. Results were weaker when measuring Delta height in cm rather than in HAZ. Possible reasons for catch-up growth include (a) omitted variable bias, (b) parental reallocation of resources to redress growth faltering, particularly if parents perceive the benefits of redressing growth faltering for child school achievement, and (c) developmental plasticity during this period when growth rates are most rapid and linear growth trajectories have not yet canalized.

For several years, it has been well accepted that insulin-like growth factor 1 (IGF-1) plays a critical role in peripubertal growth. Recently, we have provided evidence to suggest that this peptide may also be involved in the sexual maturation process, via an action to stimulate hypothalamic luteinizing hormone releasing hormone release. Because ethanol (ETOH) delays puberty, an event that is associated with depressed growth rates and decreased growth hormone and luteinizing hormone (LH) secretion via actions at the hypothalamic level, we investigated whether this drug is capable of altering the expression of genes encoding IGF-1 in liver and brain, as well as the expression of the type 1 IGF receptor (IGF-1R) within the median eminence (ME). Also, we wanted to determine if any regional changes in the expression of these genes were associated with concomitant alterations in the serum levels of IGF-1 and LH. Rats were implanted with gastric cannulae on day 24 and began receiving specific control or ETOH diets on day 29. Rats were killed on day 34, determined to be in the late juvenile stage of development, and their tissues and blood were collected. Results indicate that the ETOH-fed rats showed a decrease (p < 0.01) in the expression of hepatic IGF-1 mRNA when compared with the controls, and this paralleled depressions in both serum IGF-1 (p < 0.01) and LH (p < 0.01). In contrast, no changes were detected in IGF-1 mRNA expression in the preoptic area and hypothalamus, as well as in IGF-1R mRNA expression within the ME. These results suggest that the well-known detrimental effects of ETOH on growth rates and the progression of the female pubertal process in the rat may be associated with the drug's ability to depress the hepatic synthesis of IGF-1 and the subsequent prepubertal circulating levels of the protein.