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Israa Elgaily, Abdelkarim A. Abdrabo,
Volume 0, Issue 0 (7-2024)
Abstract

Background: Various analytes are used to assess glycemic control in laboratory medicine. Glucose measurements show current glucose levels, but sample stability can be influenced by diet and stress. Hemoglobin A1c (HbA1c) is the best marker for long-term control but can be affected by elevated urea levels. This study compared glycated albumin (GA) and HbA1c in diabetic patients undergoing hemodialysis.
Methods: A comparative cross-sectional study was conducted with a sample size of 280 volunteers. Among these, there were 115 diabetic patients with end-stage renal disease (ESRD), 95 diabetic patients without ESRD, and 75 non-diabetic patients with ESRD. Laboratory measurements included HbA1c, GA, urea, and creatinine, assessed using standard laboratory techniques. Data analysis was carried out using SPSS statistical software.
Results: Levels of HbA1c were lower in diabetic patients with ESRD compared to diabetic patients without ESRD. In contrast, GA levels were higher in diabetics with ESRD. A significant negative association was observed between HbA1c levels and urea levels. However, creatinine levels were not associated with either HbA1c or GA.
Conclusion: The estimation of glycated hemoglobin levels can be affected by high blood urea. Therefore, GA may be a better glycemic indicator for diabetic patients with ESRD.

Ms Shirakdehi, M Rezaei, E Nadi, H Mahjoub, Mt Goodarzi,
Volume 8, Issue 1 (4-2014)
Abstract

Abstract Background and Objective: Oxidant-antioxidant imbalance plays a key role in pathogenesis of chronic obstructive pulmonary disease (COPD). This study aimed to evaluate homocystiene and total antioxidant capacity in COPD patients, compared to smoker and non-smoker healthy people. Material and Methods: We measured total antioxidant capacity with Cayman Kit, uric acid with Pars Azmoon kit٫ homocysteine with ELISA Kit and inflammatory cells (leukocytes) in 29 COPD patients, 29 smokers and 29 non-smokers. Results: Uric acid was significantly higher in COPD patients compared to healthy smokers and healthy non-smokers (p<0.05). Total antioxidant capacity was significantly lower in COPD patients compared to healthy, non smokers (p=0. 003). In COPD patients, homocysteine and leukocytes levels were significantly higher than those in healthy smokers (P<0.05) and healthy non- smokers (p<0.001). Conclusion: According to high inflammatory cells and low antioxidant capacity in COPD, early administration of appropriate medication is recommended to reduce systemic and topical inflammation. Reduction in the exposure to oxidizing compounds can slow the process of degradation and damage to lungs. Keywords: Chronic Obstructive Pulmonary Disease Homocysteine Oxidative Stress
Farzane Salarneia , Sare Zhand , Behnaz Khodabakhshi , Alijan Tabarraei , Mohammad Ali Vakili , Naeme Javid , Masoud Bazori , Abdolvahab Moradi ,
Volume 10, Issue 1 (1-2016)
Abstract

Abstract

      Background and objective: Hepatitis B virus (HBV) is a DNA virus with high tendency toward hepatic tissue. There are currently about 3 million HBV-infected people and 350 to 400 million chronic carriers of this virus in the world. X protein plays a role in the over-expression of oncogenes, carcinogenicity of liver cells and overlaps with the basal core promoter of the virus. Mutations at specific nucleotides of this region increase viral replication and liver disease progression. The aim of this study was to investigate the frequency of mutations at nucleotides 1762, 1764 and 1766 of HBV X gene in patients with chronic hepatitis B and hepatitis B-related cirrhosis.

      Methods: In this study, 102 patients including 68 chronic hepatitis patients and 34 patients with hepatitis B-related cirrhosis were enrolled. After DNA extraction, HBV X gene was amplified and sequenced using Semi Nested-PCR. Obtained gene sequences were compared with the standard sequence of HBV virus X gene available in the gene bank (Okamoto AB033559). Then, the mutations in the gene X of HBV were identified.

      Results: Comparison of the standard sequence with sequences obtained from patients showed the presence of A1762T / G1764A mutation in 12 chronic (17.64%) and 13 cirrhotic (38.23%) patients. Also, C1766G / G1764T mutations were found in 8.23% of chronic patients and 17.64% of cirrhotic patients.

      Conclusion: A1762T / G1764A mutations in the overlapping region of the basal core promoter with gene X C-terminal may lead to liver disease progression from chronic hepatitis to cirrhosis, by changing the amino acid sequence of the X protein.

    


Mahshid Zandi , Mohammad Ebrahimifard, Abdolvahab Moradi,
Volume 11, Issue 3 (5-2017)
Abstract

ABSTRACT
       Background and Objective: MiRNAs are small RNAs that are expressed in most eukaryotes, and can regulate gene expression by attaching to the 3’ end of target mRNA. MicroRNA-101 (miR-101) post-transcriptional regulation is important for host-virus interactions. In addition, miR-101 has a tumor suppressive role in liver cancer and metastasis, and induces apoptosis in tumor cells. We examined miR-101 expression in patients with chronic hepatitis B, hepatitis B virus (HBV)-associated cirrhosis and healthy individuals.
       Methods: The study was performed on 108 whole blood samples (36 samples from each group) collected in EDTA tubes. RNA was extraction by RNX-plus kit according to the manufacturer’s protocol. Finally, miRNA expression was evaluated using relative real time PCR.
         Results: A 2.4-fold increase was observed in miR-101 expression in patients with chronic hepatitis B, while there was a 3.5-fold increase in miR-101 expression in patients with HBV-associated cirrhosis compared with healthy controls (P=0.003). MiR-101 overexpression in patients with HBV-associated cirrhosis was more notable that in patients with chronic hepatitis B.
         Conclusion: According to the results, evaluating miR-101 expression may predict disease progression from chronic hepatitis B to HBV-associated cirrhosis.
         Keywords: MicroRNAs, Chronic Hepatitis B, Liver Cirrhosis, MiR-101.


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