Osobitosti hiperlipoproteinemija u inzulin neovisnom dijabetesu

An open prospective study including 200 newly detected patients with NIDDM and hyperlipoproteinemia was carried out. Sixty-four patients with NIDDM were excluded from the study for failing to comply with the instructions by the researchers: loss to follow-up, switch to insulin therapy, cessation of menstrual periods, taking oral contraceptive agents, hypolipemics, diuretics or beta blockers. The control group consisted of 200 subjects with hyperlipoproteinemia and normal glucose tolerance. Patients with NIDDM were divided in two groups. The first group consisted of men (N=86), and the other of women (N=52). These two groups were further divided into subgroups: subjects below and above 50 years of age. The study aimed to determine the type and extent of changes occuring in patients with NIDDM and hyperlipidemia at the moment of optimal glycemic control, lipoprotein, apolipoprotein and leptin levels, as well as the influence of fat tissue distribution on individual lipoprotein, apolipoprotein and leptin fractions. Possible sex-related differences in particular lipoprotein, apolipoprotein and leptin fractions and the fertile age of female patients as compared to postmenopausal one, respectively, were studied. The following changes occurred at the moment of optimal glycemic control (HbA1c≤6.30%) in patients with newly detected NIDDM and hyperlipidemia: statistically significant reduction in total, HDL2 and VLDL cholesterol and triglycerides, although lipoprotein level was not optimal. HDL3 cholesterol and apo B levels were increased. Patients taking glibenclamide for glycemic control had a statistically significant increase in Lp(a) (p<0.045), whereas patients on diet alone did not reveal such an increase. Glycemic control had no effect on serum leptin level. In women with NIDDM, at the moment of optimal diabetes control, HDL cholesterol level negatively correlated with waist circumference, while triglyceride level showed a trend of positive correlation with waist circumference. HDL3 cholesterol showed negative correlation with WHR.l Women with NIDDM younger than 50 yrs. revealed positive correlation between apo B level and waist circumference. Women with NIDDM older than 50 yrs. showed negative correlation of HDL and HDL3 cholesterol levels to waist circumference at the moment of good glycemic control, whereas their correlation with triglyceride and VLDL cholesterol was found to be positive. WHR showed negative correlation with HDL3 cholesterol level. In men with NIDDM younger than 50 yrs. at the moment of good glycemic control positive correlation was found between triglyceride level and WHR and waist circumference. Correlation of VLD cholesterol to WHR was also positive, whereas to HDL cholesterol it was found to be negative. HDL2 cholesterol correlated negatively with BMI, but positively with WHR. No statistically significant correlation of lipoproteins and apolipoproteins with fat tissue distribution as defined by waist circumference, and BMI and WHR was found in male patients older than 50 yrs.. Fasting and postprandial leptin levels in patients with NIDDM and hyperlipidemia showed positive correlation with waist circumference and WHR. No statistically significant sex-related difference in lipoprotein and apolipoprotein fractions was observed, the same holding true for women of fertile age as compared to those in postmenopause. Female subjects with NIDDM had three times higher fasting and postprandial leptin levels in comparison with male subjects with NIDDM. Leptin level in women and men older than 50 yrs. of age was observed to be statistically significantly higher as compared to younger women and men with NIDDM

Improved Performances of Polyacrylamide Gel by Addition of a New Type of Polymer: Detection of Allelic Losses

The aim of this study was to improve detection of heterozygous samples and loss of heterozygosity using a new type of gel polymer. A total of 60 samples of normal and tumor colon tissue were tested. Elctrophoresis of amplified loci was performed on a standard acrylamide / N,Nmethylenebisacrylamide gel, and the same gel containing Spreadex polymer, NAB (native acrylamide- bis). Standard gel displayed 36 samples of normal tissue as homozygous. Electrophoresis of the same samples on gel with addition of polymer revealed 12/36 heterozygous samples. Five of 12 matched tumor samples displayed loss of heterozygosity that could not be detected on standard gel, because of its lower resolving power. Electrophoresis on a new polymer presents a simple, inexpensive, reproducible and non-radioactive method for loss of heterozygosity detection, with improved performances such as increased sensitivity, decreased amount of a sample and improved separation of closely spaced bands. Application of the polymer may contribute to a vide variety of diagnostic procedures

K-Ras and Dpc4 Mutations in Chronic Pancreatitis: Case Series Clinical Science Clinical Science

Aim To assess whether alterations in the K-ras, p53, and DPC4 genes are present in pancreatitis, a potential precancerous condition that can progress to pancreatic adenocarcinoma. To investigate the alterations occurring at hot spots of K-ras (exon 1), p53 (exons 5 and 7), and DPC4 (exons 8, 10 and 11). Methods In 10 patients with acute and 22 with chronic pancreatitis, without pancreatic intraepithelial neoplasia (PanIN), DNA was isolated from paraffin embedded tissue samples. The extracted DNA was analyzed by polymerase chain reaction (PCR), restriction fragment length polymorphism (RFLP) analysis, single-strand conformation polymorphism (SSCP) analysis, and DNA sequencing. Results In acute pancreatitis samples no mutations were found in any of the investigated genes. In 7 out of 22 samples of chronic pancreatitis nucleotide substitution at exon 1 of K-ras (five at codon 12 and two at codon 13) were found. No mutations in p53 (exons 5 and 7) were detected. Two samples had nucleotide substitutions at exons 8 and 11 of DPC4, introducing STOP signal and change in the amino acid sequence, respectively. One chronic pancreatitis sample displayed simultaneous mutations in K-ras (exon 1, codon 12) and DPC4 (exon 8, codon 358). Conclusion Mutations of K-ras and Dpc4 genes can accumulate already in non-malignant, inflammatory pancreatic tissue, suggesting its applicability in monitoring of further destruction of pancreatic tissue and progression into malignancy

K-Ras and Dpc4 Mutations in Chronic Pancreatitis: Case Series

Aim: To assess whether alterations in the K-ras, p53, and DPC4 genes are present in pancreatitis, a potential precancerous condition that can progress to pancreatic adenocarcinoma. To investigate the alterations occurring at hot spots of K-ras (exon 1), p53 (exons 5 and 7), and DPC4 (exons 8, 10 and 11). Methods: In 10 patients with acute and 22 with chronic pancreatitis, without pancreatic intraepithelial neoplasia (PanIN), DNA was isolated from paraffin embedded tissue samples. The extracted DNA was analyzed by polymerase chain reaction (PCR), restriction fragment length polymorphism (RFLP) analysis, single-strand conformation polymorphism (SSCP) analysis, and DNA sequencing. Results: In acute pancreatitis samples no mutations were found in any of the investigated genes. In 7 out of 22 samples of chronic pancreatitis nucleotide substitution at exon 1 of K-ras (five at codon 12 and two at codon 13) were found. No mutations in p53 (exons 5 and 7) were detected. Two samples had nucleotide substitutions at exons 8 and 11 of DPC4, introducing STOP signal and change in the amino acid sequence, respectively. One chronic pancreatitis sample displayed simultaneous mutations in K-ras (exon 1, codon 12) and DPC4 (exon 8, codon 358). Conclusion: Mutations of K-ras and Dpc4 genes can accumulate already in non-malignant, inflammatory pancreatic tissue, suggesting its applicability in monitoring of further destruction of pancreatic tissue and progression into malignancy