AIM Since GH stimulates lipolysis in vivo after a 2-hr lag phase, we studied whether this involves GH signaling and gene expression in adipose tissue (AT). METHODS Human subjects (n = 9) each underwent intravenous exposure to GH versus saline with measurement of serum FFA, and GH signaling, gene array, and protein in AT biopsies after 30-120 min. Human data were corroborated in adipose-specific GH receptor knockout (FaGHRKO) mice versus wild-type mice. Expression of candidate genes identified in the array were investigated in 3T3-L1 adipocytes. RESULTS GH increased serum FFA and AT phosphorylation of STAT5b in human subjects. This was replicated in wild-type mice, but not in FaGHRKO mice. The array identified 53 GH-regulated genes, and Ingenuity Pathway analysis showed downregulation of PDE3b, an insulin-dependent antilipolytic signal, upregulation of PTEN that inhibits insulin-dependent antilipolysis, and downregulation of G0S2 and RASD1, both encoding antilipolytic proteins. This was confirmed in 3T3-L1 adipocytes, except for PDE3B, including reciprocal effects of GH and insulin on mRNA expression of PTEN, RASD1, and G0S2. CONCLUSION (a) GH directly stimulates AT lipolysis in a GHR-dependent manner, (b) this involves suppression of antilipolytic signals at the level of gene expression, (c) the underlying GH signaling pathways remain to be defined. © 2020 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of The Physiological Society and the American Physiological Society.FOCUSED CLINICAL QUESTION How to simply and quickly perform a periodontal screening and make a proper periodontal diagnosis using the 2018 proposed new periodontal classification? SUMMARY The 2018 periodontal classification has been released, however, it is challenging for clinicians especially for the dental students to apply the published information in practice. A diagnostic flowchart was created for 3 mostly common periodontal conditions; health, gingivitis and periodontitis. Additionally, flowcharts were proposed for diagnosis for periodontitis severity and risk of progression by staging and grading. Probing depth was the first clinical parameter to categorize the type of diseases. Subsequently, bleeding on probing, radiographic bone loss/clinical attachment loss and history of periodontal treatment were further added for making a proper diagnosis. Three clinical cases were given to demonstrate the use of the simplified proposed flowcharts. CONCLUSIONS The proposed diagnostic flowcharts are the user-friendly tool to assist clinicians to perform an initial screening and diagnosis based upon the 2018 newly proposed periodontal disease classification. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.There are two forms of diabetes insipidus, central (neurohypophyseal), and nephrogenic, caused by pathogenic variants in the AVP gene and the AVPR2 or AQP2 genes, respectively. We report on a four-generation family, seven individuals had central diabetes insipidus (CDI) and the female index patient seen from age 16 to 26 years had (mild) nephrogenic diabetes insipidus. In her father with CDI, a known pathogenic heterozygous AVP variant c.232_234del p.(Glu78del) was identified, confirming the diagnosis of CDI in him and the other affected family members. In the proband, molecular analysis disclosed a novel heterozygous AVPR2 gene variant, c.962A > T p.(Asn321Ile) and an extremely skewed X-inactivation, confirming X-linked nephrogenic diabetes insipidus (XL-NDI). Whole exome sequencing showed no further causative mutation. This is the first report on the co-existence of CDI and NDI in one family. Our review of symptomatic female AVPR2 heterozygotes includes 23 families with at least one affected female (including this study). There were 21 different causative mutations. Mutation types in females did not differ from those in males. Both severe XL-NDI and mild forms were reported in females. All six females with severe XL-NDI had complete loss-of-function (null) mutations. The remaining 17 female probands had milder XL-NDI caused by 14 missense variants and three null variants of the AVPR2 gene. X-inactivation was studied in nine of these females; all showed extreme or slight skewing. The review underlines that XL-NDI in female AVPR2 heterozygotes is always accompanied by skewed X-inactivation, emphasizing a need for X-inactivation studies in these females. © 2020 The Authors. American Journal of Medical Genetics Part A published by Wiley Periodicals, Inc.INTRODUCTION Pulmonary embolism (PE)-related death is often part of the primary outcome in venous thromboembolism (VTE) studies. The Scientific and Standardization Committee (SSC) of the International Society on Thrombosis and Haemostasis developed a definition for PE-related death and classification of the cause of death. The present survey evaluated a preliminary version of this definition and classification. METHODS Sixty-nine VTE experts from 9 countries were invited for a cross-sectional online survey on January 15th , 2019, including multiple-choice and open-ended questions on a seven-subcategory classification of the cause of death. Descriptive statistics were used to describe the results; qualitative comments were summarized. RESULTS Forty of 69 (58%) invitees completed the survey. All respondents agreed that guidance on classification of the cause of death in VTE studies is required. There was high agreement on the proposal (median overall score, 6; interquartile range, 6-7; scale from 1 [poor] to 7 [excellent]). All respondents approved the wording and content of the seven subcategories, except for 1 disagreeing vote for 2 subcategories (A3 'PE is not objectively confirmed, but is most likely the main cause of death', and C1 'Another cause of death is more likely than PE but has not been objectively confirmed'). Suggestions for improvement mainly concerned the extensiveness of the criteria and clinical situations described to define the cause of death. CONCLUSION Acceptance of the proposal was excellent. https://www.selleckchem.com/products/wnt-agonist-1.html Suggestions for improvement were incorporated in the SSC communication on the definition of PE-related death and classification of the cause of death in VTE studies. This article is protected by copyright. All rights reserved.