There have been several reports that individuals with Fragile X syndrome (FXS) and animal models of FXS have communication deficits. The present study utilized two different call classification taxonomies to examine the sex‐specificity of ultrasonic vocalization (USV) production on postnatal day (PD8) in the FVB strain of Fmr1 knockout (KO) mice. One classification protocol requires the investigator to score each call by hand, while the other protocol uses an automated algorithm. Results using the hand‐scoring protocol indicated that male Fmr1 KO mice exhibited longer calls (P = .03) than wild types on PD8. Male KOs also produced fewer complex, composite, downward, short and two‐syllable call‐types, as well as more frequency steps and chevron call‐types. Female heterozygotes exhibited no significant changes in acoustic or temporal aspects of calls, yet showed significant changes in call‐type production proportions across two different classification taxonomies (P < .001). They exhibited increased production of harmonic and frequency steps calls, as well as fewer chevron, downward and short calls. According to the second high‐throughput analysis, female heterozygotes produced significantly fewer single‐type and more multiple‐type syllables, unlike male KOs that showed no changes in these aspects of syllable production. Finally, we correlated both scoring methods and found a high level of correlation between the two methods. These results contribute further knowledge of sex differences in USV calling behavior for Fmr1 heterozygote and KO mice and provide a foundation for the use of high‐throughput analysis of neonatal USVs. 相似文献
Wnt/β-catenin signalling is central to development and its regulation is essential in preventing cancer. Using phosphorylation of Dishevelled as readout of pathway activation, we identified Drosophila Wnk kinase as a new regulator of canonical Wnt/β-catenin signalling. WNK kinases are known for regulating ion co-transporters associated with hypertension disorders. We demonstrate that wnk loss-of-function phenotypes resemble canonical Wnt pathway mutants, while Wnk overexpression causes gain-of-function canonical Wnt-signalling phenotypes. Importantly, knockdown of human WNK1 and WNK2 also results in decreased Wnt signalling in mammalian cell culture, suggesting that Wnk kinases have a conserved function in ensuring peak levels of canonical Wnt signalling. 相似文献
Toxic Shock Syndrome (TSS), a superantigen‐mediated illness, is characterized by rash, hypotension and multi‐organ dysfunction. Predictors of TSS and related morbidity and mortality are poorly defined. In this study, data on 61,959,084 hospitalizations from the 2003–2012 Nationwide Inpatient Sample, a 20% stratified sample of US hospitalizations, were analyzed and ICD‐9‐CM coding used to identify 4491 hospitalizations with a diagnosis of TSS. Incidence, in‐hospital mortality rate, comorbidities, length of stay and costs of care attributable to TSS were determined. In multivariate survey logistic regression models, TSS was associated with female sex (adjusted odds ratio [95% confidence interval], 1.54 [1.48–1.60]), younger age (0–17 years, 2.17 [2.06–2.29]; 40–59: 0.53 [0.50–0.56]; 60–79: 0.28 [0.26–0.30]; 80+: 0.13 [0.11–0.14] compared with 18–39) and race/ethnicity (black, 0.63 [0.59–0.67]; Hispanic: 0.60 [0.56–0.64]; Asian, 1.11 [1.00–1.11]; and other, 0.83 [0.75–0.92] compared with white). Patients with TSS had a three‐fold greater cost of care (mean: $36,656 ± 942) and length of stay (LOS) (mean: 10.65 ± 0.23 days) than patients without TSS. Shared predictors of increased LOS and costs in patients with TSS were male sex; age 40–79 years; Black, Hispanic, Asian and other race/ethnicity; and more than one chronic condition. Predictors of in‐hospital mortality included respiratory failure (13.66 [11.37–16.43]), liver disease/failure (3.36 [2.59–4.34]), chickenpox (91.26 [27.74–300.25]), coagulopathy (2.14 [1.85–2.48]), and higher age. In conclusion, there are significant racial/ethnic, socioeconomic, and comorbid disparities in the incidence and mortality of TSS in adults and children in the USA. 相似文献
Aims: Metabolic syndrome (MS) is composed of several metabolic abnormalities that increase the risk of cardiovascular diseases and diabetes. Although there are treatments for the components of MS, this pathology maintains a high mortality, suggesting that there are other mechanisms in which orphan receptors such as GPR26 and GPR39 may be involved. For this reason, the aim of this work was to evaluate the expression of GPR26 and GPR39 orphan receptors in two models of MS (diet and genetics).
Materials and methods: We used male Wistar rats, which received 70% fructose in drinking water for 9 weeks, and obese Zucker rats. We measured weight, blood pressure, glucose, triglycerides, total cholesterol, HDL cholesterol, LDL cholesterol to determine the MS and the expression of the orphan receptors GPR26 and GPR39 in brain, heart, aorta, liver, and kidney by RT-PCR.
Results: The analysis of the expression of the orphan receptors GPR26 and GPR39 showed that the receptors are expressed in some tissues, but the expression of the GPR26 tends to decrease in the heart and aorta, whereas in the brain, no changes were observed, this receptor is not expressed in the liver and kidney of both strains. The expression of GPR39 isoforms depends on the tissue and MS model.
Conclusions: We conclude that the orphan receptors GPR26, GPR39v1, and GPR39v2 are expressed in different tissues and their profile expression is dependent on the etiology of the MS. 相似文献
The hypothesis that the morphological, physiological, and behavioral traits comprising the migratory syndrome in insects are genetically correlated through pleiotropic effects of genes controlling the titre of a common hormonal determinant is explored. Evidence that juvenile hormone (JH) influences the component traits of the migratory syndrome is presented, and thus JH is assumed to be the underlying, common determinant. However, readers are cautioned that this does not imply that JH is solely responsible for these traits, nor is this necessary for the arguments presented. For wing dimorphic taxa, the “correlated traits hypothesis” predicts covariance within wing morphs between JH titre and the proportion winged. Four simple genetic models for wing-morph determination are considered: single-locus with short-winged (SW) dominant; single-locus with long-winged (LW) dominant; polygenic, fixed threshold, shifting distribution; and polygenic, shifting threshold, fixed distribution. In each case, wing morphology is assumed to be a threshold trait with the liability being JH titre at some critical stage of development. All models predict covariation between %LW and the mean JH titre of at least one of the wing morphs, but the form and direction of the relationship depends critically on the genetic model used. The results suggest that we should expect the traits associated with the migratory syndrome, and hence the trade-offs associated with the evolution of wing dimorphism, to be correlated with proportion winged and, in this sense, to be frequency-dependent. 相似文献