Search

Chronic liver disease (CLD) is a major health problem worldwide. Non-alcoholic fatty liver disease (NAFLD), chronic hepatitis C (CHC), chronic hepatitis B (CHB), and alcoholic liver disease (ALD) are the most common etiologies of CLD. Liver biopsy is the gold standard for assessment of liver fibrosis, however, it is an invasive method. This review attempts to evaluate the usefulness of serum adiponectin, serum leptin, serum ferritin, serum transforming growth factor-β1 (TGF-β1), and serum platelet derived growth factor-BB (PDGF-BB) as non-invasive markers in the diagnosis of liver fibrosis/cirrhosis. A systematic search in MEDLINE, Web of Science, Scopus, and local databases was performed to identify articles published in English or Persian as of November 2017. Studies conducted among CLD patients, with biopsy proven fibrosis/cirrhosis, and providing sufficient details of patients' clinicopathological characteristics were included. In the 95 studies included, there were a total of 15,548 CLD patients. More than 83% of studies were carried out in Asia and Europe. The relationship between liver fibrosis/cirrhosis and serum levels of ferritin, adiponectin, leptin, TGF-β1, and PDGF-BB was assessed in 42, 33, 27, nine, and three studies, respectively. Serum levels of the markers, particularly ferritin, could successfully predict liver fibrosis/cirrhosis, however, these data might not be clinically replicated and further studies are needed. [ABSTRACT FROM AUTHOR]

Background A number of complex and rare mutations in epidermal growth factor receptor (EGFR) gene have been identified and the clinical implication of serum EGFR ligands has also been reported. However, the prognostic significance of these mutations and also the serum EGFR and its ligands in Non-Small Cell Lung Carcinoma (NSCLC) has remained a challenging issue. This study is aimed at finding the prognostic importance of EGFR rare mutations and serum EGFR, amphiregulin (AR), and TGF-α (Transforming Growth Factor-alpha) in NSCLC. Materials and method NSCLC patients ( n = 98) with mean age of 59 ± 10.5 were enrolled (M/F: 75/23). DNA was extracted from formalin fixed paraffin embedded tissues. Exons 19 and 21 were amplified using polymerase chain reaction followed by direct sequencing for identification of mutations. Serum EGFR, AR, and TGF-α were measured by ELISA. Results EGFR mutation rate in patients was 37% (exon 19 deletions: 72.2%, exon 21 substitutions: 27.8%). The E872K in exon 21 mutation-positive cases was the most frequent rare mutation detected (90%; 9/10 samples). A significant relationship was found between EGFR exon 21mutations and serum EGFR and TGF-α ( P < 0.05). Increased serum AR (> 3 pg/ml) and TGF-α (> 10.5 pg/ml) were associated with shorter overall survival ( P < 0.05). Conclusions The data clearly show that elevation of serum TGF-α and AR are associated with poor prognosis of NSCLC. In addition to the close relationship between EGFR mutations and serum EGFR, serum TGF-α changes was associated with the gene mutations. These findings could be implicated in clinical decision making related to EGFR-TKIs. [ABSTRACT FROM AUTHOR]

Recent studies have been established high degree of genetic diversity in solid organ tumors among individuals and even between individual tumor cells. This intratumor and intertumor genetic diversity results in a heterogeneous tumor with unique characteristics which potentially allows effective drug therapy. The goal of pharmacogenomics is to elucidate the genetic network(s) that underlie drug efficacy and drug resistance. Advances in targeted and personalized therapy play an increasingly important role in many common cancers, notably lung cancer, due to the high incidence, prevalence, mortality and the greater tendency towards drug resistance seen in these patients. Non-small cell lung cancer (NSCLC) is characterized by mutations in the epidermal growth factor receptor (EGFR) and or downstream kinase pathways. This has led to the development of highly selective monoclonal antibodies and EGFR tyrosine kinase inhibitors (EGFR-TKIs) to prevent cancer initiation, proliferation, differentiation, angiogenesis, survival, and invasion. However, resistance to many of these new treatments is induced and further pharmacogenomic analysis has revealed mutations associated with increased or reduced drug efficacy. Combinations of kinase inhibitors or potentially the targeting of cancer stem cells may further increase the success of pharmacogenomics in treating patients with lung cancer. [ABSTRACT FROM AUTHOR]

Background: Urinary tract infections (UTI) are the most common infections in community and hospitalized patients. Irrational consumption of antibiotics and creation of drug resistance make the treatment of these infections more difficult. Hence, determination of antibiotic resistance pattern is necessary to manage the treatment correctly; this was the main purpose of the present survey. Methods: This was a retrospective and cross-sectional study with targeted community of 2566 hospitalized patients with heart diseases in Tabriz Shahid Madani Cardiovascular Hospital, Iran, during 2009-2010. Urine cultures were studied for type of microorganisms and their antibiotic susceptibility patterns. The gathered data were analyzed. Findings: Out of 2566 urine cultures, 479 cases (18.7%) were positive for pathogenic microorganisms (bacteria and yeasts). Three hundred and forty eight (72.3%) patients were women and 131 (27.7%) were men. Mean age was 61.0 ± 18.6 years. Enteric gram-negative rods were the most frequent agents of UTI in different units of the hospital. Among isolated microorganisms, the highest susceptibility [306 cases (64%)] was reported for amikacin. Three hundred and twenty four cases among of all bacterial UTI (79%) were community-acquired infections. In addition, the laboratory had not followed reference guideline in reporting antibiotic susceptibility test results and performing antibiogram test for Staphylococcus aureus. Conclusion: We suggest amikacin for treatment of UTI in this hospital. Also, disobeying laboratory guidelines may impact treatment outcome and prevalence of antibiotic resistance in this medical center. [ABSTRACT FROM AUTHOR]

Introduction: Growth, proliferation, survival, and differentiation are the prominent characteristics of cells, which are affected by cancer. Epidermal growth factor receptor (EGFR) plays a pivotal role in the effective control of these features. Given the significance of EGFR signaling pathway in nonsmall cell lung cancer (NSCLC), EGFR expression is influential on these cell characteristics. In this paper, we studied EGFR expression and its association with demographic factors, clinicopathological features, and prognosis of NSCLC patients. Materials and Methods: In this retrospective cohort study which was done during 2009-12 at Ghaem Hospital, Mashhad, Iran. EGFR expression was evaluated in 96 patients with formalin-fixed, paraffin-embedded NSCLC tissues (43 adenocarcinomas, 48 squamous-cell carcinomas, and 5 large-cell carcinomas) using immunohistochemistry (IHC). Data analysis was performed by SPSS version 20.0. Results: Out of 96 specimens, approximately 53% were classified as positive for EGFR expression. The study group consisted of 68% (N=65) male and 32% (N=31) female subjects, with the mean age of 61.1±9.03 years. There was no difference between EGFR-positive and EGFR-negative patients in terms of the overall survival rate (P=0.49). In addition, no association was observed between tumor histology and EGFR expression (P=0.08), while EGFR-positive adenocarcinoma (N=28, 29%) was more prevalent compared to other subtypes of NSCLC. Moreover, there were no differences between tumor subtypes and the overall survival rate of the patients (P=0.21), and no association was found between EGFR expression and the patients' demographic factors (e.g. age and gender). Conclusion: The results of this study indicated that EGFR expression could not be a prognostic marker in NSCLC patients; however, it seems that using standardized IHC scoring is likely to yield more reliable data in this regard. [ABSTRACT FROM AUTHOR]

Multiple sclerosis (MS) is a complicated autoimmune disease characterized by inflammatory and demyelinating events in the central nervous system. The exact etiology and pathogenesis of MS have not been elucidated. However, a set of metabolic changes and their effects on immune cells and neural functions have been explained. This review highlights the contribution of carbohydrates and lipids metabolism to the etiology and pathogenesis of MS. Then, we have proposed a hypothetical relationship between such metabolic changes and the immune system in patients with MS. Finally, the potential clinical implications of these metabolic changes in diagnosis, prognosis, and discovering therapeutic targets have been discussed. It is concluded that research on the pathophysiological alterations of carbohydrate and lipid metabolism may be a potential strategy for paving the way toward MS treatment. • Abnormalities in the metabolic pathway of carbohydrates such as glycolysis contribute to the etiology and pathogenesis of MS. • The same is true for lipid metabolic pathways such as FAO, KBs, eicosanoids, lipoproteins, and cholesterol. • These pathologic changes can be utilized for diagnosis, prognosis, and discovering the therapeutic targets in MS patients. [ABSTRACT FROM AUTHOR]