INTRODUCTION    Chronic obstructive pulmonary disease (COPD) is the most important lung disease leading to disability and even death. Recent studies have shown that the platelet indices are associated with several cardiovascular diseases; however, there is little data on COPD. OBJECTIVES    We aimed to explore the relationship between platelet indices, together with the platelet-to-lymphocyte ratio (PLR), white blood cell count to mean platelet volume ratio (WMR), and red cell distribution width (RDW) and the severity of COPD. PATIENTS AND METHODS    This retrospective study was based on data collected from a total of 153 COPD patients admitted to our outpatient clinic between March 2014 and March 2015. All of the participants underwent pulmonary function tests; FEV1, FVC, and FEV1/FVC were measured. The study population was divided into four according to the severity of COPD as group A (mild), group B (mild to moderate), group C (moderate to severe), and group D (severe).  RESULTS    A significant increase was found in platelet distribution width (PDW), MPV, plateletcrit, PLR, and RDW while WMR decreased as the COPD severity increases. In the multiple logistic regression analysis, we found that PDW and RDW were independently associated with the presence of severe COPD. ROC curve analysis showed that a PDW>14.85 was associated with severe COPD with 85% sensitivity and 86% specificity while RDW>14.45 was associated with severe COPD with 90% sensitivity and 87% specificity. CONCLUSIONS    The PDW and the RDW are independently associated with disease severity, which may indicate hypoxemia, underlying inflammation, and oxidative stress in COPD.

Our study indicated the relationship between tumor length and clinicopathologic characteristics as well as long-term survival in esophageal cancer. A total of 116 patients who underwent curative surgery for thoracic esophageal cancer with standard lymphadenectomy in 2 fields between 2000 and 2010 were included in the study. The medical records of these patients were retrospectively reviewed. The patients with tumor length 3 cm had a highly significant difference in the involvement of adventitia and lymph node stations. The patients with tumor length 3 cm had significantly lower rates of involvement of the adventitia and lymph node stations. Tumor length could have a significant impact on both the overall survival and disease-free survival of patients with resected esophageal carcinomas and may provide additional prognostic value to the current tumor, node, and metastasis staging system before patients receive any cancer-specific treatment.

IntroductionMethotrexate is a cytotoxic agent used in leukemia, and several other cancer types and at lower doses in auto-inflammatory diseases such as rheumatoid arthritis, ankylosing spondylitis and psoriasis. Macrolide antibiotics are effective against gram-positive and Gram-negative bacteria. They have anti-inflammatory activities as well. Clarithromycin is a macrolide with anti-inflammatory activity through blockage of the p38 MAPK signal cascade, which is involved in methotrexate-induced pulmonary toxicity.AimIn this study, the efficacy of clarithromycin in protecting against pulmonary fibrosis was investigated in the rat model for methotrexate-induced pulmonary fibrosis.Material and methodsA total of 30 female rats were divided into three groups. Group I was administered intraperitoneal and intragastric saline; group II was administered oral 3 mg/kg methotrexate; and group III was administered oral 3 mg/kg methotrexate + intraperitoneal 200 mg/kg clarithromycin for 28 days. Histopathological analyses of the lung tissues were performed under light microscopy.ResultsNormal histopathological changes were observed in the control group. Pulmonary fibrosis was significantly higher in the methotrexate group than in the other groups (p < 0.005).ConclusionsClarithromycin was shown to be effective in protecting against methotrexate-induced pulmonary fibrosis; further studies should be performed to determine the dosage and safety.

IntroductionChronic obstructive pulmonary disease (COPD) is an irreversible progressive chronic inflammatory disease that causes shortness of breath in consequence of a decrease in pulmonary functions. The pulmonary inflammatory pathogenesis is multifactorial. We have too little up-to-date information about the relation between COPD and genetics. In our study, the relation with the SIRT1 gene's mononucleotide polymorphisms (SNP) rs7895833, rs7069102 and rs2273773 was analyzed through various laboratory data.Material and methodsOne hundred COPD patients from the archive records of the Chest Diseases Department of Muğla Sitki Kocman University Medical Faculty were included in the study. A control group was constituted from 100 healthy individuals who live in the same geographical region. The SIRT1 genotypes for these patients were determined using polymerase chain reaction (PCR) and confronting two-pair primers (CTPP) methods. The SIRT1 gene polymorphisms rs7895833, rs7069102 and rs2273773 were analyzed. GG, AG, AA genotypes and G and A alleles of rs7895833, TT, TC, CC genotypes and T and C alleles of rs2273773, and CC, CG, GG genotypes and C and G alleles of rs7069102 were examined. The data in both groups were compared.ConclusionsA significant difference between GG, AG and AA genotypes of rs7895833 was found. Especially, the AG genotype was observed more in the group with COPD, with a significant difference. A significant difference between TT, TC and CC genotypes of rs2273773 was found. There was a significant difference between two groups with regards to C and G alleles of rs7069102. A significant difference was not found between the groups with regards to G and A alleles of rs7895833. A difference was not found for both groups between T and C alleles of rs2273773. It shows that these polymorphisms of the SIRT1 gene may be associated with COPD.

Background: We aimed at exploring biological functions of differentially expressed miRNAs during carcinogenesis, to identify miRNAs dysegulations involved in DNA repair mechanisms, and to evaluate potential of miRNAs as prognostic and diagnostic biomarkers for early lung adenocarcinomas (LAC). Methods: We obtained 21 LAC and paired adjacent normal formalin-fixed, paraffinembedded lung tissues from patients who underwent curative resection for stage I LAC. We compared expression levels of eight miRNAs involved in the DNA repair mechanism between LAC and adjacent tissues. Results: Expressions of Hsa-miR-9-5p, hsa-miR-24-3p, hsa-miR-125a-3p, hsa-miR- 125b-5p, hsa-miR-155-5p, and hsa-let-7a-5p were significantly up-regulated in stage I LAC tissues compared with those in the adjacent tissues. In addition, expressions of hsa-mir-9-5p, hsa-mir-24-3p, hsa-mir-125a-3p, hsa-mir-125b-5p, and hsa-mir-155-5p were significantly up-regulated in stage Ia LAC tissues, whereas expressions of hsa-mir- 125a-3p and hsa-mir-125b-5p were significantly up-regulated in stage Ib LAC tissues. Receiver operating characteristic (ROC) analysis revealed that AUROC of hsa-mir-125b- 5p was 0.875 (P < 0.001). Conclusion: Expression of hsa-mir-125b-5p could be used to distinguish LAC from adjacent tissues. Our result suggests that hsa-mir125b-5p can be a prognostic and diagnostic biomarker for LAC.