PURPOSE: To investigate the caustic ingestion in children among different continents according to demographic characteristics (core purpose), main symptoms, common caustic agents, signs and symptoms, management, treatment and complications. METHODS: This systematic review was performed by searching the databases Science Direct, ProQuest, Google Scholar, and PubMed, electronically and manually. We included studies that were published from 1980 to 2013, at University of Medical Sciences of Tabriz, Iran. A strategic search was performed with keywords including caustic, corrosive, ingestion and children, and was limited to articles in English and Persian. Statistical analysis was performed by SPSS ver. 18. RESULTS: Of 63 selected articles of caustic ingestion with 9,888 samples, the proportion of Africa was 3 articles (4.8%) and 95 samples (1%), America 9 articles (14.3%) and 305 sample (3%), Asia 29 articles (46%) and 2,780 samples (28.1%), Europe 17 articles (27%) and 3,002 samples (30.4%), and Oceania 5 articles (7.9%) and 3,706 samples (37.5%). The average age was in the Africa 3.07+/-2.02 years, America 3.17+/-1.83 years, Asia 3.34+/-1.58 years, Europe 3.58+/-2.09 years and Oceania 3.52+/-2.02 years. Sex distribution was in Africa 76 males (0.91%) and 19 females (0.23%), America 49 males (0.58%) and 41 females (0.49%), Asia 1,575 males (18.76%) and 1,087 females (12.95%), Europe 1,018 males (12.13%) and 823 females (9.8%), and Oceania 1,918 males (22.85%) and 1,788 females (21.3%). Statistical analysis of the data indicated higher consumption in Europe and Oceania in the boys with higher average age of years. CONCLUSION: The comparison of caustic ingestion indicated that the cause substances of caustic ingestion in children are different among continents, therefore prevention strategy and different treatment guidelines among continents will be needed.
Africa ; Americas ; Asia ; Child* ; Eating* ; Europe ; Female ; Humans ; Iran ; Male ; Oceania ; Sex Distribution

PURPOSE: Stearoyl-CoA desaturase 1 (SCD1) is a novel therapeutic target in various malignancies, including breast cancer. The present study was designed to investigate the effect of the pharmacologic inhibition of SCD1 on fatty acid composition in tissue explant cultures of human breast cancer and to compare these effects with those in adjacent nonneoplastic breast tissue. METHODS: Paired samples of tumor and adjacent noncancerous tissue were isolated from 12 patients with infiltrating ductal breast cancer. Samples were explant cultured in vitro, exposed to the highly selective SCD1 inhibitor CAY10566, and examined for fatty acid composition by gas liquid chromatography. The cytotoxic and antigrowth effects were evaluated by quantification of lactate dehydrogenase release and by sulforhodamine B (SRB) measurement, respectively. RESULTS: Breast cancer tissue samples were found to have higher levels of monounsaturated fatty acids (MUFA) (p<0.001) and arachidonic acid (20:4n-6, p<0.001) and a lower level of linoleic acid (18:2n-6, p=0.02) than the normal-appearing breast tissues. While exhibiting no evident cytotoxicity, treatment with the SCD1 inhibitor, CAY10566 (0.1-1 microM), for 48 hours significantly increased 18:2n-6 levels in both the tumor and adjacent normal-appearing tissue (approximately 1.2 fold, p<0.05). However, the breast cancer tissue samples showed significant increases in the levels of MUFA and 20:4n-6 compared to the normal-appearing breast tissues (p<0.05). The SRB growth assay revealed a higher rate of inhibition with the SCD1 inhibitor in breast cancer tissues than in normal-appearing tissues (p<0.01, 41% vs. 29%). The SCD1 inhibitor also elevated saturated fatty acid (1.46-fold, p=0.001) levels only in the tumor tissue explant. CONCLUSION: The fatty acid composition and response to SCD1 inhibition differed between the explant cultures from breast cancer and the adjacent normal-appearing tissue. Altered fatty acid composition induced by SCD1 inhibition may also, in addition to Delta9 desaturation, modulate other reactions in de novo fatty acid synthesis and lipogenesis, and subsequently affect the overall survival and progression of breast cancer.
Arachidonic Acid ; Breast ; Breast Neoplasms* ; Chromatography, Liquid ; Fatty Acid Desaturases ; Fatty Acids, Monounsaturated ; Humans ; L-Lactate Dehydrogenase ; Linoleic Acid ; Lipogenesis ; Stearoyl-CoA Desaturase* ; Tissue Culture Techniques