Zung A.,Hebrew University of Jerusalem |
Blumenfeld O.,The Israel Center for Disease Control |
Shehadeh N.,Meyer Childrens Hospital |
Dally Gottfried O.,Rivka Ziv Hospital |
And 40 more authors.
Pediatric Diabetes | Year: 2012
Background: Type 1 diabetes is an autoimmune disease occurring in genetically susceptible individuals. The precipitating cause is unclear. Recently, the Second Lebanon War exposed a large civilian population in northern Israel to significant psychological stress in the form of repeated barrages of missile attacks. Hypothesis: We hypothesized that trends in regional incidence of type 1 diabetes before and after the war would reflect an association with stress. Methods: All type 1 diabetes patients aged 0-17 yr who were reported to the Israel Juvenile Diabetes Register (n = 1822) in the four pre-war (2002-2005) and two post-war years (2006-2007) were included in the study. The patients were stratified by gender, age, ethnicity, family history of type 1 diabetes, season at diagnosis, and region of residency, namely, those who lived in the northern regions that were attacked and those in other regions. Results: The post-war incidence of type 1 diabetes was increased in the northern regions (rate ratio, RR = 1.27; p = 0.037), with no change in the other regions. This change was more prominent in males (RR = 1.55; p = 0.005) but similar in summer and winter, in different ages, and in different ethnic groups. There was no change in the proportion of new patients with a family history of the disease. Conclusions: For the first time in a large population, we found a positive association between the trauma of war and an increase in the incidence of type 1 diabetes in children and adolescents. The increase in incidence was not associated with genetic susceptibility to the disease. © 2011 John Wiley & Sons A/S.
Zung A.,Hebrew University of Jerusalem |
Tenenbaum-Rakover Y.,Pediatric Endocrinology Unit |
Barkan S.,Hebrew University of Jerusalem |
Hanukoglu A.,lfson Medical Center |
And 4 more authors.
Clinical Endocrinology | Year: 2010
Introduction Neonatal hyperthyrotropinaemia (HT), defined by elevated TSH and normal T 4, is either transient or persistent. The eventual outcome of neonatal HT is unpredictable and the management of HT patients is controversial. We assessed perinatal parameters and diagnostic measures that may distinguish between transient and persistent HT, compared with congenital hypothyroidism (CH). We also aimed to recommend optimal treatment in these forms of thyroid impairment. Design and patients A multi-centre, retrospective study was conducted in six paediatric endocrinology units. Forty-three HT patients and 83 CH patients were included in the study. Measurements We evaluated differences in birth weight (BW), gestational age (GA), modes of diagnosis, screening and confirmatory T 4 and TSH levels, thyroid imaging results and optimal thyroxine doses between HT and CH and between the two forms of HT. Results Newborns with HT had lower BW and GA than those with CH. Transient (n = 18) and persistent HT (n = 25) patients were indistinguishable by most parameters, but those with persistent HT had a higher prevalence of abnormal thyroid imaging (69%vs 8%; P = 0·005). During treatment, 79% and 55% of transient and persistent HT patients respectively experienced elevated levels of free T 4. Although most HT patients were reevaluated after 2·5 years, six transient HT patients stopped therapy and showed full recovery within the first year of life. Conclusions We recommend obtaining thyroid imaging to distinguish between the two forms of HT. Adherence to recommended doses of thyroxine and probably early cessation of therapy in transient HT can prevent iatrogenic hyperthyroidism in these patients. © 2010 Blackwell Publishing Ltd.
Yardeni D.,Ben - Gurion University of the Negev |
Loewenthal N.,Soroka Medical University Center |
Limony Y.,Soroka Medical University Center |
Hershkovitz E.,Soroka Medical University Center
Hormone Research in Paediatrics | Year: 2011
Aims: To examine ethnicity and gender differences in the evaluation of referred children with short stature and to investigate adherence of the primary care evaluation to published guidelines. Methods: Cross-sectional study in a referral center. 371 short patients aged 2-18 years were included. Outcome measures were patient's growth characteristics, final diagnosis, and prevalence of pre-referral patient data. Results: The study population was composed of 239 Bedouin children and 132 Jewish children (p < 0.0001). More males (61%) than females were evaluated (p < 0.0001). There were no significant differences between males and females in age and growth parameters at the time of referral. Bedouins, males and females, were significantly shorter than their Jewish counterparts at the time of referral: height SD -2.44 ± 0.73 and -2.62 ± 1.05 versus -2.13 ± 0.55 and -2.21 ± 0.57, respectively (p < 0.05). There were no significant ethnic or gender differences in the final diagnosis. Significant deficiencies in the primary care evaluation of referred short children were found. Conclusions: We demonstrated novel ethnic- and gender-based inequities in the evaluation of referred short children. We found that the current evaluation of short stature in our area does not comply with existing guidelines. © 2011 S. Karger AG, Basel.
PubMed | Soroka Medical University Center
Type: Journal Article | Journal: Biochimica et biophysica acta | Year: 2012
Cytosolic phospholipase A(2) (cPLA(2)) up-regulation has been reported in human colorectal cancer cells, thus we aimed to elucidate its role in the proliferation of the human colorectal cancer cell line, HT-29. EGF caused a rapid activation of cPLA(2) which coincided with a significant increase in cell proliferation. The inhibition of cPLA(2) activity by pyrrophenone or by antisense oligonucleotide against cPLA(2) (AS) or inhibition of prostaglandin E(2) (PGE(2)) production by indomethacin resulted with inhibition of cell proliferation, that was restored by addition of PGE(2). The secreted PGE(2) activated both protein kinase A (PKA) and PKB/Akt pathways via the EP2 and EP4 receptors. Either, the PKA inhibitor (H-89) or the PKB/Akt inhibitor (Ly294002) caused a partial inhibition of cell proliferation which was restored by PGE(2). But, inhibited proliferation in the presence of both inhibitors could not be restored by addition of PGE(2). AS or H-89, but not Ly294002, inhibited CREB activation, suggesting that CREB activation is mediated by PKA. AS or Ly294002, but not H-89, decreased PKB/Akt activation as well as the nuclear localization of -catenin and cyclin D1 and increased the plasma membrane localization of -catenin with E-cadherin, suggesting that these processes are regulated by the PKB pathway. Similarly, Caco-2 cells exhibited cPLA(2) dependent proliferation via activation of both PKA and PKB/Akt pathways. In conclusion, our findings suggest that the regulation of HT-29 proliferation is mediated by cPLA(2)-dependent PGE(2) production. PGE(2)via EP induces CREB phosphorylation by the PKA pathway and regulates -catenin and cyclin D1 cellular localization by PKB/Akt pathway.