Methodology and implementation of the WHO European Childhood Obesity Surveillance Initiative (COSI)

Establishment of the WHO European Childhood Obesity Surveillance Initiative (COSI)has resulted in a surveillance system which provides regular, reliable, timely, andaccurate data on children's weight status—through standardized measurement ofbodyweight and height—in the WHO European Region. Additional data on dietaryintake, physical activity, sedentary behavior, family background, and schoolenvironments are collected in several countries. In total, 45 countries in the EuropeanRegion have participated in COSI. The first five data collection rounds, between 2007and 2021, yielded measured anthropometric data on over 1.3 million children. In COSI,data are collected according to a common protocol, using standardized instrumentsand procedures. The systematic collection and analysis of these data enables inter-country comparisons and reveals differences in the prevalence of childhood thinness,overweight, normal weight, and obesity between and within populations. Furthermore,it facilitates investigation of the relationship between overweight, obesity, and poten-tial risk or protective factors and improves the understanding of the development ofoverweight and obesity in European primary-school children in order to supportappropriate and effective policy responses.The authors gratefully acknowledge support through a grant from the Russian Government in the context of the WHO European Office for the Prevention and Control of NCDs. The ministries of health of Austria, Croatia, Greece, Italy, Malta, Norway, and the Russian Federation provided financial support for the meetings at which the protocol, data collection procedures, and analyses were discussed. Data collection in countries was made possible through funding from the following: Albania: WHO through the Joint Programme on Children, Food Security and Nutrition “Reducing Malnutrition in Children,” funded by the Millennium Development Goals Achievement Fund, and the Institute of Public Health. Austria: Federal Ministry of Labor, Social Affairs, Health and Consumer Protection of Austria. Bulgaria: Ministry of Health, National Center of Public Health and Analyses, and WHO Regional Office for Europe. Bosnia and Herzegovina: WHO country office support for training and data management. Croatia: Ministry of Health, Croatian Institute of Public Health, and WHO Regional Office for Europe. Czechia: Ministry of Health of the Czech Republic, grant number 17-31670A and MZCR—RVO EU 00023761. Denmark: Danish Ministry of Health. Estonia: Ministry of Social Affairs, Ministry of Education and Research (IUT 42-2), WHO Country Office, and National Institute for Health Development. Finland: Finnish Institute for Health and Welfare. France: Santé publique France (the French Agency for Public Health). Georgia: WHO. Greece: International Hellenic University and Hellenic Medical Association for Obesity. Hungary: WHO Country Office for Hungary. Ireland: Health Service Executive. Italy: Ministry of Health. Kazakhstan: Ministry of Health of the Republic of Kazakhstan, WHO, and UNICEF. Kyrgyzstan: World Health Organization. Latvia: Ministry of Health and Centre for Disease Prevention and Control. Lithuania: Science Foundation of Lithuanian University of Health Sciences and Lithuanian Science Council and WHO. Malta: Ministry of Health. Montenegro: WHO and Institute of Public Health of Montenegro. North Macedonia: Government of North Macedonia through National Annual Program of Public Health and implemented by the Institute of Public Health and Centers of Public Health; WHO country office provides support for training and data management. Norway: the Norwegian Ministry of Health and Care Services, the Norwegian Directorate of Health, and the Norwegian Institute of Public Health. Poland: National Health Programme, Ministry of Health. Portugal: Ministry of Health Institutions, the National Institute of Health, Directorate General of Health, Regional Health Directorates, and the kind technical support from the Center for Studies and Research on Social Dynamics and Health (CEIDSS). Romania: Ministry of Health. Russian Federation: WHO. San Marino: Health Ministry, Educational Ministry, and Social Security Institute and Health Authority. Serbia: WHO and the WHO Country Office (2015-540940 and 2018/873491-0). Slovakia: Biennial Collaborative Agreement between WHO Regional Office for Europe and Ministry of Health SR. Slovenia: Ministry of Education, Science and Sport of the Republic of Slovenia within the SLOfit surveillance system. Spain: Spanish Agency for Food Safety and Nutrition. Sweden: Public Health Agency of Sweden. Tajikistan: WHO Country Office in Tajikistan and Ministry of Health and Social Protection. Turkmenistan: WHO Country Office in Turkmenistan and Ministry of Health. Turkey: Turkish Ministry of Health and World Bank.info:eu-repo/semantics/publishedVersio

Thinness, overweight, and obesity in 6‐ to 9‐year‐old children from 36 countries: The World Health Organization European Childhood Obesity Surveillance Initiative - COSI 2015-2017

In 2015-2017, the fourth round of the World Health Organization (WHO) European Childhood Obesity Surveillance Initiative (COSI) was conducted in 36 countries. National representative samples of children aged 6–9 (203,323) were measured by trained staff, with similar equipment and using a standardized protocol. This paper assesses the children's body weight status and compares the burden of childhood overweight, obesity, and thinness in Northern, Eastern, and Southern Europe and Central Asia. The results show great geographic variability in height, weight, and body mass index. On average, the children of Northern Europe were the tallest, those of Southern Europe the heaviest, and the children living in Central Asia the lightest and the shortest. Overall, 28.7% of boys and 26.5% of girls were overweight (including obesity) and 2.5% and 1.9%, respectively, were thin according to the WHO definitions. The prevalence of obesity varied from 1.8% of boys and 1.1% of girls in Tajikistan to 21.5% and 19.2%, respectively, in Cyprus, and tended to be higher for boys than for girls. Levels of thinness, stunting, and underweight were relatively low, except in Eastern Europe (for thinness) and in Central Asia. Despite the efforts to halt it, unhealthy weight status is still an important problem in the WHO European Region.The authors gratefully acknowledge support from a grant from the Russian Government in the context of the WHO European Office for the Prevention and Control of NCDs. Data collection in the countries was made possible through funding from the following: Albania: WHO through the Joint Programme on Children, Food Security and Nutrition “Reducing Malnutrition in Children,” funded by the Millennium Development Goals Achievement Fund, and the Institute of Public Health; Austria: Federal Ministry of Social Affairs, Health, Care and Consumer Protection, Republic of Austria; Bulgaria: Ministry of Health, National Center of Public Health and Analyses, WHO Regional Office for Europe; Croatia: Ministry of Health, Croatian Institute of Public Health and WHO Regional Office for Europe; Czechia: Ministry of Health of the Czech Republic, grants AZV MZČR 17-31670 A and MZČR – RVO EÚ 00023761; Cyprus: not available; Denmark: Danish Ministry of Health; Estonia: Ministry of Social Affairs, Ministry of Education and Research (IUT 42-2), WHO Country Office, and National Institute for Health Development; Finland: Finnish Institute for Health and Welfare; France: Santé publique France, the French Agency for Public Health; Georgia: WHO; Greece: International Hellenic University and Hellenic Medical Association for Obesity; Hungary: WHO Country Office for Hungary; Ireland: Health Service Executive; Italy: Ministry of Health and Italian National Institute of Health; Kazakhstan: Ministry of Health of the Republic of Kazakhstan and WHO Country Office; Kyrgyzstan: World Health Organization; Latvia: Ministry of Health, Centre for Disease Prevention and Control; Lithuania: Science Foundation of Lithuanian University of Health Sciences and Lithuanian Science Council and WHO; Malta: Ministry of Health; Montenegro: WHO and Institute of Public Health of Montenegro; North Macedonia: funded by the Government of North Macedonia through National Annual Program of Public Health and implemented by the Institute of Public Health and Centers of Public Health in the country. WHO country office provided support for training and data management; Norway: Ministry of Health and Norwegian Institute of Public Health; Poland: National Health Programme, Ministry of Health; Portugal: Ministry of Health Institutions, the National Institute of Health, Directorate General of Health, Regional Health Directorates and the kind technical support from the Center for Studies and Research on Social Dynamics and Health (CEIDSS); Romania: Ministry of Health; Russian Federation: WHO; San Marino: Health Ministry, Educational Ministry, Social Security Institute and Health Authority; Serbia: World Health Organization (Ref. File 2015-540940); Slovakia: Biennial Collaborative Agreement between WHO Regional Office for Europe and Ministry of Health SR; Slovenia: Ministry of Education, Science and Sport of the Republic of Slovenia within the SLOfit surveillance system; Spain: Spanish Agency for Food Safety and Nutrition (AESAN); Sweden: Public Health Agency of Sweden; Tajikistan: WHO Country Office in Tajikistan and Ministry of Health and Social Protection; Turkmenistan: WHO Country Office in Turkmenistan and Ministry of Health; Turkey: Turkish Ministry of Health and World Bank.info:eu-repo/semantics/publishedVersio

Epigenetic changes and PTCH1, SHh and IHh protein expression in serous ovarian carcinomas

Serozni karcinomi jajnika najčešći su oblik epitelnih tumora jajnika. Uglavnom se dijagnosticiraju u uznapredovalom stadiju bolesti i imaju visoku stopu smrtnosti. Kod raka jajnika primijećena je poremećena aktivacija više signalnih puteva među kojima je i signalni put Hedgehog (Hh). Uloga signalnog puta Hh u raku jajnika, kao i u pojedinim histološkim podtipovima raka jajnika, nije dovoljno istražena. U ovoj disertaciji istražili smo ulogu proteina PTCH1, SHh i IHh, kao i promjene u metilacijskom statusu promotora istoimenih gena, u seroznim karcinomima jajnika. Istraživanje je provedeno na uzorcima seroznih karcinoma jajnika niskog (LGSC) i visokog (HGSC) stupnja malignosti, dok su uzorci zdravih jajnika i jajovoda služili kao kontrole. U istraživanju su korištene i stanične linije HGSC-a, OVCAR5, OVCAR8 i OVSHAO, i kontrolna stanična linija normalnih epitelnih stanica jajovoda, FNE1. Ekspresija proteina PTCH1, SHh i IHh u tkivnim uzorcima analizirana je metodom imunohistokemije, dok je u staničnim linijama ispitana uz pomoć imunofluorescencije i Western blota. Metilacijski obrazac DNA u promotorima gena PTCH1, SHh i IHh analizirali smo koristeći PCR ovisan o metilaciji (MSP). Ekspresija proteina PTCH1, SHh i IHh bila je značajno veća u karcinomima HGSC i LGSC u odnosu na kontrolna tkiva, kao i u karcinomskim u odnosu na kontrolnu staničnu liniju. U tumorskom tkivu i tumorskim stanicama u kulturi bila je izražena nuklearna ekspresija proteina PTCH1 što navodi na zaključak da bi navedeni protein mogao igrati aktivnu, tumor-promotorsku ulogu u jezgri malignih stanica seroznih karcinoma jajnika. U staničnim linijama detektirani su fragmenti proteina PTCH1 različite molekularne mase što upućuje na mogućnost proteolitičkog cijepanja ovog proteina. Autokrina signalizacija ovisna o SHh-ligandu utvrđena je u karcinomima HGSC i LGSC, dok su autokrina i parakrina signalizacija ovisna o IHh-ligandu uočene u karcinomima HGSC. Metilacija DNA u promotorima gena PTCH1, SHh i IHh nije bila povezana s razinom ekspresije ovih proteina što navodi na zaključak da ovaj mehanizam nije uključen u patogenezu seroznih karcinoma jajnika. Dobiveni rezultati upućuju na aktivnu ulogu proteina PTCH1, SHh i IHh u patogenezi seroznih karcinoma jajnika te doprinose boljem razumijevanju molekularne patogeneze ovih karcinoma.Serous ovarian carcinomas are the most common type of epithelial ovarian cancers. They are mostly diagnosed in the advanced stage of the disease and have a high mortality rate. In ovarian cancer, aberrant activation of several signaling pathways, including the Hh signaling pathway, has been observed. The role of Hh signaling pathway in ovarian cancer, as well as in certain histological subtypes of ovarian cancer, has not been sufficiently investigated. In this dissertation, we investigated the role of PTCH1, SHh and IHh proteins, as well as changes in the promoter methylation status of the corresponding genes, in serous ovarian carcinomas. Low- (LGSC) and high-grade (HGSC) serous ovarian carcinoma tissue samples were used in this study, while normal ovarian and fallopian tube tissue samples served as controls. HGSC cell lines, OVCAR5, OVCAR8 and OVSHAO, and control cell line, normal fallopian tube non-ciliated epithelium cell line FNE1, were also used in the study. PTCH1, SHh and IHh protein expression levels were analyzed using immunohistochemistry in tissue samples, and by immunofluorescence and Western blot in cell lines. DNA methylation pattern of PTCH1, SHh and IHh genes were analyzed by methylation-specific PCR (MSP). PTCH1, SHh and IHh protein expression levels were significantly higher in HGSCs and LGSCs compared to control tissues, as well as in cancer cell lines compared to control cell line. Nuclear expression of the PTCH1 protein in tumor tissue and cultured tumor cells suggests that this protein could play an active, tumor-promoter role in the nuclei of serous ovarian cancer cells. PTCH1 protein fragments of different molecular weight were detected in the cell lines, indicating possible proteolytic cleavage of this protein. Autocrine SHh signaling was found in HGSCs and LGSCs, while autocrine and paracrine IHh signaling were observed in HGSCs. DNA methylation of PTCH1, SHh, and IHh gene promoters were not in line with the expression levels of these proteins, leading to the conclusion that this mechanism is not involved in the pathogenesis of serous ovarian carcinoma. Our results indicate that PTCH1, SHh and IHh proteins play an active role in pathogenesis of serous ovarian carcinoma, and contribute to a better understanding of the molecular pathogenesis of these cancers

Epigenetic changes and PTCH1, SHh and IHh protein expression in serous ovarian carcinomas

Serozni karcinomi jajnika najčešći su oblik epitelnih tumora jajnika. Uglavnom se dijagnosticiraju u uznapredovalom stadiju bolesti i imaju visoku stopu smrtnosti. Kod raka jajnika primijećena je poremećena aktivacija više signalnih puteva među kojima je i signalni put Hedgehog (Hh). Uloga signalnog puta Hh u raku jajnika, kao i u pojedinim histološkim podtipovima raka jajnika, nije dovoljno istražena. U ovoj disertaciji istražili smo ulogu proteina PTCH1, SHh i IHh, kao i promjene u metilacijskom statusu promotora istoimenih gena, u seroznim karcinomima jajnika. Istraživanje je provedeno na uzorcima seroznih karcinoma jajnika niskog (LGSC) i visokog (HGSC) stupnja malignosti, dok su uzorci zdravih jajnika i jajovoda služili kao kontrole. U istraživanju su korištene i stanične linije HGSC-a, OVCAR5, OVCAR8 i OVSHAO, i kontrolna stanična linija normalnih epitelnih stanica jajovoda, FNE1. Ekspresija proteina PTCH1, SHh i IHh u tkivnim uzorcima analizirana je metodom imunohistokemije, dok je u staničnim linijama ispitana uz pomoć imunofluorescencije i Western blota. Metilacijski obrazac DNA u promotorima gena PTCH1, SHh i IHh analizirali smo koristeći PCR ovisan o metilaciji (MSP). Ekspresija proteina PTCH1, SHh i IHh bila je značajno veća u karcinomima HGSC i LGSC u odnosu na kontrolna tkiva, kao i u karcinomskim u odnosu na kontrolnu staničnu liniju. U tumorskom tkivu i tumorskim stanicama u kulturi bila je izražena nuklearna ekspresija proteina PTCH1 što navodi na zaključak da bi navedeni protein mogao igrati aktivnu, tumor-promotorsku ulogu u jezgri malignih stanica seroznih karcinoma jajnika. U staničnim linijama detektirani su fragmenti proteina PTCH1 različite molekularne mase što upućuje na mogućnost proteolitičkog cijepanja ovog proteina. Autokrina signalizacija ovisna o SHh-ligandu utvrđena je u karcinomima HGSC i LGSC, dok su autokrina i parakrina signalizacija ovisna o IHh-ligandu uočene u karcinomima HGSC. Metilacija DNA u promotorima gena PTCH1, SHh i IHh nije bila povezana s razinom ekspresije ovih proteina što navodi na zaključak da ovaj mehanizam nije uključen u patogenezu seroznih karcinoma jajnika. Dobiveni rezultati upućuju na aktivnu ulogu proteina PTCH1, SHh i IHh u patogenezi seroznih karcinoma jajnika te doprinose boljem razumijevanju molekularne patogeneze ovih karcinoma.Serous ovarian carcinomas are the most common type of epithelial ovarian cancers. They are mostly diagnosed in the advanced stage of the disease and have a high mortality rate. In ovarian cancer, aberrant activation of several signaling pathways, including the Hh signaling pathway, has been observed. The role of Hh signaling pathway in ovarian cancer, as well as in certain histological subtypes of ovarian cancer, has not been sufficiently investigated. In this dissertation, we investigated the role of PTCH1, SHh and IHh proteins, as well as changes in the promoter methylation status of the corresponding genes, in serous ovarian carcinomas. Low- (LGSC) and high-grade (HGSC) serous ovarian carcinoma tissue samples were used in this study, while normal ovarian and fallopian tube tissue samples served as controls. HGSC cell lines, OVCAR5, OVCAR8 and OVSHAO, and control cell line, normal fallopian tube non-ciliated epithelium cell line FNE1, were also used in the study. PTCH1, SHh and IHh protein expression levels were analyzed using immunohistochemistry in tissue samples, and by immunofluorescence and Western blot in cell lines. DNA methylation pattern of PTCH1, SHh and IHh genes were analyzed by methylation-specific PCR (MSP). PTCH1, SHh and IHh protein expression levels were significantly higher in HGSCs and LGSCs compared to control tissues, as well as in cancer cell lines compared to control cell line. Nuclear expression of the PTCH1 protein in tumor tissue and cultured tumor cells suggests that this protein could play an active, tumor-promoter role in the nuclei of serous ovarian cancer cells. PTCH1 protein fragments of different molecular weight were detected in the cell lines, indicating possible proteolytic cleavage of this protein. Autocrine SHh signaling was found in HGSCs and LGSCs, while autocrine and paracrine IHh signaling were observed in HGSCs. DNA methylation of PTCH1, SHh, and IHh gene promoters were not in line with the expression levels of these proteins, leading to the conclusion that this mechanism is not involved in the pathogenesis of serous ovarian carcinoma. Our results indicate that PTCH1, SHh and IHh proteins play an active role in pathogenesis of serous ovarian carcinoma, and contribute to a better understanding of the molecular pathogenesis of these cancers

Epigenetic changes and PTCH1, SHh and IHh protein expression in serous ovarian carcinomas

Serozni karcinomi jajnika najčešći su oblik epitelnih tumora jajnika. Uglavnom se dijagnosticiraju u uznapredovalom stadiju bolesti i imaju visoku stopu smrtnosti. Kod raka jajnika primijećena je poremećena aktivacija više signalnih puteva među kojima je i signalni put Hedgehog (Hh). Uloga signalnog puta Hh u raku jajnika, kao i u pojedinim histološkim podtipovima raka jajnika, nije dovoljno istražena. U ovoj disertaciji istražili smo ulogu proteina PTCH1, SHh i IHh, kao i promjene u metilacijskom statusu promotora istoimenih gena, u seroznim karcinomima jajnika. Istraživanje je provedeno na uzorcima seroznih karcinoma jajnika niskog (LGSC) i visokog (HGSC) stupnja malignosti, dok su uzorci zdravih jajnika i jajovoda služili kao kontrole. U istraživanju su korištene i stanične linije HGSC-a, OVCAR5, OVCAR8 i OVSHAO, i kontrolna stanična linija normalnih epitelnih stanica jajovoda, FNE1. Ekspresija proteina PTCH1, SHh i IHh u tkivnim uzorcima analizirana je metodom imunohistokemije, dok je u staničnim linijama ispitana uz pomoć imunofluorescencije i Western blota. Metilacijski obrazac DNA u promotorima gena PTCH1, SHh i IHh analizirali smo koristeći PCR ovisan o metilaciji (MSP). Ekspresija proteina PTCH1, SHh i IHh bila je značajno veća u karcinomima HGSC i LGSC u odnosu na kontrolna tkiva, kao i u karcinomskim u odnosu na kontrolnu staničnu liniju. U tumorskom tkivu i tumorskim stanicama u kulturi bila je izražena nuklearna ekspresija proteina PTCH1 što navodi na zaključak da bi navedeni protein mogao igrati aktivnu, tumor-promotorsku ulogu u jezgri malignih stanica seroznih karcinoma jajnika. U staničnim linijama detektirani su fragmenti proteina PTCH1 različite molekularne mase što upućuje na mogućnost proteolitičkog cijepanja ovog proteina. Autokrina signalizacija ovisna o SHh-ligandu utvrđena je u karcinomima HGSC i LGSC, dok su autokrina i parakrina signalizacija ovisna o IHh-ligandu uočene u karcinomima HGSC. Metilacija DNA u promotorima gena PTCH1, SHh i IHh nije bila povezana s razinom ekspresije ovih proteina što navodi na zaključak da ovaj mehanizam nije uključen u patogenezu seroznih karcinoma jajnika. Dobiveni rezultati upućuju na aktivnu ulogu proteina PTCH1, SHh i IHh u patogenezi seroznih karcinoma jajnika te doprinose boljem razumijevanju molekularne patogeneze ovih karcinoma.Serous ovarian carcinomas are the most common type of epithelial ovarian cancers. They are mostly diagnosed in the advanced stage of the disease and have a high mortality rate. In ovarian cancer, aberrant activation of several signaling pathways, including the Hh signaling pathway, has been observed. The role of Hh signaling pathway in ovarian cancer, as well as in certain histological subtypes of ovarian cancer, has not been sufficiently investigated. In this dissertation, we investigated the role of PTCH1, SHh and IHh proteins, as well as changes in the promoter methylation status of the corresponding genes, in serous ovarian carcinomas. Low- (LGSC) and high-grade (HGSC) serous ovarian carcinoma tissue samples were used in this study, while normal ovarian and fallopian tube tissue samples served as controls. HGSC cell lines, OVCAR5, OVCAR8 and OVSHAO, and control cell line, normal fallopian tube non-ciliated epithelium cell line FNE1, were also used in the study. PTCH1, SHh and IHh protein expression levels were analyzed using immunohistochemistry in tissue samples, and by immunofluorescence and Western blot in cell lines. DNA methylation pattern of PTCH1, SHh and IHh genes were analyzed by methylation-specific PCR (MSP). PTCH1, SHh and IHh protein expression levels were significantly higher in HGSCs and LGSCs compared to control tissues, as well as in cancer cell lines compared to control cell line. Nuclear expression of the PTCH1 protein in tumor tissue and cultured tumor cells suggests that this protein could play an active, tumor-promoter role in the nuclei of serous ovarian cancer cells. PTCH1 protein fragments of different molecular weight were detected in the cell lines, indicating possible proteolytic cleavage of this protein. Autocrine SHh signaling was found in HGSCs and LGSCs, while autocrine and paracrine IHh signaling were observed in HGSCs. DNA methylation of PTCH1, SHh, and IHh gene promoters were not in line with the expression levels of these proteins, leading to the conclusion that this mechanism is not involved in the pathogenesis of serous ovarian carcinoma. Our results indicate that PTCH1, SHh and IHh proteins play an active role in pathogenesis of serous ovarian carcinoma, and contribute to a better understanding of the molecular pathogenesis of these cancers

Endometrial Glucose Transporters in Health and Disease

Pregnancy loss is a frequent occurrence during the peri-implantation period, when there is high glucose demand for embryonic development and endometrial decidualization. Glucose is among the most essential uterine fluid components required for those processes. Numerous studies associate abnormal glucose metabolism in the endometrium with a higher risk of adverse pregnancy outcomes. The endometrium is incapable of synthesizing glucose, which thus must be delivered into the uterine lumen by glucose transporters (GLUTs) and/or the sodium-dependent glucose transporter 1 (SGLT1). Among the 26 glucose transporters (14 GLUTs and 12 SGLTs) described, 10 (9 GLUTs and SGLT1) are expressed in rodents and 8 (7 GLUTs and SGLT1) in the human uterus. This review summarizes present knowledge on the most studied glucose transporters in the uterine endometrium (GLUT1, GLUT3, GLUT4, and GLUT8), whose data regarding function and regulation are still lacking. We present the recently discovered SGLT1 in the mouse and human endometrium, responsible for controlling glycogen accumulation essential for embryo implantation. Moreover, we describe the epigenetic regulation of endometrial GLUTs, as well as signaling pathways included in uterine GLUT's expression. Further investigation of the GLUTs function in different endometrial cells is of high importance, as numerous glucose transporters are associated with infertility, polycystic ovary syndrome, and gestational diabetes

Hypermethylation of Secreted Frizzled Related Protein 1 gene promoter in different astrocytoma grades

Aim: To identify the involvement of Secreted Frizzled Related Protein 1 (SFRP1) promoter hypermethylation in different malignancy grades of astrocytoma and assess its association with beta-catenin, lymphoid-enhancer factor 1, and T-cell factor 1. Methods: Twenty-six astrocytoma samples were collected from 2008-2015. Promoter hypermethylation was evaluated by methylation-specific polymerase-chain-reaction and protein expression by immunohistochemistry and stereological analysis. The staining intensity was scored by comparing immunoreactivity with normal tissue and by using 10% and 50% cut-offs. Results: SFRP1 promoter methylation was found in 32% of astrocytomas. The number of hypermethylated samples increased in higher astrocytoma grades and was the highest in glioblastoma (P = 0.042 compared to other astrocytoma grades). There was 45.8% of samples with the lack of or weak expression of SFRP1 protein and 29.2% with strong expression. Samples with methylated promoter expressed significantly less SFRP1 than samples with unmethylated promoter (P = 0.031). Beta-catenin expression levels were elevated. Yet, glioblastomas with unmethylated SFRP1 promoter had significantly less beta-catenin (P = 0.033). Strong expression of lymphoid-enhancer factor 1 was associated to higher astrocytoma grades (P = 0.006). Conclusion: SFRP1 gene was epigenetically silenced in glioblastomas when compared to low astrocytoma grades, which may suggest that the lack of its protein is involved in astrocytoma progression

Dishevelled family proteins (DVL1-3) expression in IUGR placentas

Dishevelled family proteins (DVL1, DVL2, and DVL3) are cytoplasmic mediators involved in canonical and non-canonical Wnt signaling that are important in embryonic development. The role of DVL proteins in the placental tissue remains mostly unknown. In the current study, we explored the role of Dishevelled proteins in naturally invasive tissue, trophoblast. Formalin-fixed paraffin-embedded samples of 15 term placentas from physiologic term pregnancies and 15 term placentas from pregnancies complicated with intrauterine growth restrictions (IUGR) were used for the study. Expression levels of mRNA for DVL1, DVL2, and DVL3 in placentas were analyzed by quantitative real-time PCR (qRT-PCR). DVL1, DVL2, and DVL3 protein expression were semi-quantitatively analyzed using immunohistochemistry. The expression of DVL2 and DVL3 proteins was significantly higher in trophoblasts in placental villi from IUGR pregnancies compared with the control group of term placentas. In contrast, DVL3 protein expression was significantly higher in endothelial cells in placental villi from IUGR pregnancies compared with normal term placentas. The observed differences at protein levels between normal and IUGR placentas were not confirmed at the mRNA levels of DVL genes. Our data indicate the active involvement of DVL proteins in IUGR-related placentas. No significant changes were observed in DVL mRNA levels between the two groups of placentas. Further studies are required to explore the clinical relevance of these observations

Methodology and implementation of the WHO European Childhood Obesity Surveillance Initiative (COSI)

Establishment of the WHO European Childhood Obesity Surveillance Initiative (COSI) has resulted in a surveillance system which provides regular, reliable, timely, and accurate data on children's weight status-through standardized measurement of bodyweight and height-in the WHO European Region. Additional data on dietary intake, physical activity, sedentary behavior, family background, and school environments are collected in several countries. In total, 45 countries in the European Region have participated in COSI. The first five data collection rounds, between 2007 and 2021, yielded measured anthropometric data on over 1.3 million children. In COSI, data are collected according to a common protocol, using standardized instruments and procedures. The systematic collection and analysis of these data enables intercountry comparisons and reveals differences in the prevalence of childhood thinness, overweight, normal weight, and obesity between and within populations. Furthermore, it facilitates investigation of the relationship between overweight, obesity, and potential risk or protective factors and improves the understanding of the development of overweight and obesity in European primary-school children in order to support appropriate and effective policy responses