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Background: Type 1 diabetes mellitus (T1D), characterized by chronic hyperglycemia and insulin dependence, is caused by the autoimmune destruction of β-cells in the pancreas. Diabetes mellitus can potentially lead to excessive accumulation of fat in the liver, resulting in fatty liver. Changes in pancreatic tissue during the course of the disease can lead to decreased insulin secretion and increased insulin resistance. Objectives: This study aimed to investigate the size and fat content of the liver and pancreas in children with T1D using ultrasound and to explore their relationship with clinical and laboratory indicators. Patients and Methods: In this case-control research, 43 children without diabetes made up the control group, whereas 43 children with T1D (diagnosed based on American Diabetes Association criteria) between the ages of 3 and 18 years made up the case group, from March 2020 until July 2021. A checklist was used to collect data on age, the duration of diabetes, insulin dose, gastrointestinal or liver symptoms, and autoimmune diseases. Moreover, the height and weight of patients were measured. The results of blood tests, including hemoglobin A1C (HbA1c), liver function tests, and autoantibodies related to diabetes, were extracted from the flies. A transabdominal ultrasound study was performed by two pediatric radiologists, with 8 years and 5 years of experience, to evaluate the liver and pancreas regarding size and fat content. Correlation between laboratory test results and ultrasound findings was assessed by statistical analysis. Data were analyzed using SPSS v26 with a significance level considered less than 0.05. T-test, Fisher's exact test, and Partial correlation were the tests applied for data analysis. Results: The two groups had significant differences in aspartate aminotransferase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP), bilirubin, and HbA1c levels, with higher values observed in diabetic subjects. There was no statistical difference between the two groups in terms of liver size. The frequency of fatty liver was higher in patients with T1D (65.1% in diabetic subjects versus 233% in non-diabetic subjects). The size of the body and tail of the pancreas in the case group was significantly lower than in the control group (1033 ± 2.87 vs. 12.30 ± 2.1, P = 0.004 for the body, 9.47 ± 2.4 vs. 10.86 ± 2.2, P = 0.007 for the tail). Fatty pancreas was more prevalent in T1D compared to the control group (P = 0.03). The size and grade of fatty pancreas did not significantly correlate with the presence of autoantibodies. Liver size and body mass index were positively correlated (P=0.03). Conclusion: Patients with T1D are more susceptible to nonalcoholic fatty liver disease (NAFLD). Pancreatic morphological alterations, including increased echogenicity and a decrease in the size of the pancreas (particularly at the body and tail), can be detected in ultrasound studies of children with T1D. Furthermore, no significant association was found between T1D autoantibodies and pancreatic morphological changes, suggesting that autoantibodies cannot be used to predict future pancreatic morphological alterations. [ABSTRACT FROM AUTHOR]

Purpose: To investigate the effect of cisplatin on cell toxicity and metastasis through modulation of KAI1 gene expression. Methods: MCF-7cells were incubated with different concentrations of cisplatin for 24 h. RNA was extracted by trizol and cDNA synthesized. KAI1 and TBP were chosen as target and internal control genes, respectively. Specific primers were designed by primer express software, v.3.0. KAI1/TBP and gene expression ratio was calculated using the formula, 2 -ΔΔCt. Results: Cisplatin exerted a dose-dependent inhibitory effect on the viability of highly metastatic MCF-7 cells. KAI1/TBP gene expression ratios were 1.97 ± 0.19 (p < 0.05), 2.96 ± 0.55 (p < 0.05), 9.06 ± 0.27 (p < 0.001) and 12.38 ± 0.88 (p < 0.01) in 10, 20, 50 and 100 µM concentrations of cisplatin. Conclusion: These findings indicate that cisplatin can inhibit metastasis by up-regulating KAI1 gene in MCF-7cells. [ABSTRACT FROM AUTHOR]