Explore the vast range of titles available.

BackgroundLung cancer is the most often event cancer around the world and the first leading cause of cancer death in human beings. Rab39a protein is implicated in vesicular trafficking and fusion of phagosomes with lysosomes. Rab39a is overexpressed in lung cancer, which converts normal cells to abnormal cells that reproduce quickly, and resists programmed cell death that usually kills aberrant cells.AimIn the present study, the structure-based drug discovery approach is applied to identify new lead structures as cancer drug candidates against Rab39a.MethodsA valid three-dimensional (3D) model of Rab39a generation, the prediction of protein–protein interactions (Rab39a/DENND5B) and active site identification were achieved by computational techniques.ResultsOur studies suggest that the amino acid residues from PHE28 to LYS63 are important for binding with the ligand molecules. Subsequently, the virtual screening study was carried out with ligand databases against the active site of Rab39a.ConclusionThe ligand molecules with hetero amine moieties and amide group (-CONH-) have shown good value of docking score and agreeable ADME properties, so they were prioritized as potential inhibitors of Rab39a protein. Hence, Rab39a has emerged as a therapeutic target for drug development towards lung cancer.

Gaucher disease (GD) is the most frequently encountered lysosomal storage disease caused by inborn defects of the membrane-bound lysosomal enzyme, acid β-glucosidase or glucocerebrosidase. This defective activity causes an accumulation of glucocerebroside (glucosylceramide) in the lysosomes of cells derived from the monocyte/macrophage lineage. Glucocerebroside-engorged cells, termed Gaucher cells, infiltrate various organs, leading to multisystemic abnormalities. The mechanisms by which systemic and organ-specific involvement is propagated or initiated remain unclear. Studies are increasingly recognizing the role of immune dysregulation and inflammation in the pathogenesis of Gaucher disease. Many cytokines have been reported as mediators of tissue damage in Gaucher disease. Bone and lung disease are serious causes of morbidity in non neuronopathic Gaucher disease. The progress in the understanding of the pathogenesis or relevant mechanism(s) of Gaucher disease is providing insights into additional therapeutic targets, enabling the potential for optimized patient outcomes with the use of adjunctive or supplemental agents.

Background : The exposure to noxious agwents such as lead my cause lung disorders. Objectives: In the present study, pulmonary function tests and self-reported respiratory symptoms in lead exposure workers were compared with matched control subjects. Materials and Methods : The frequency of respiratory symptoms were evaluated in a sample of 108 lead exposure workers and 100 control subjects with similar age using a questionnaire including questions on respiratory symptoms in the past year. Pulmonary function tests (PFT) were also measured in lead exposure workers and in controls. Results : Most lead exposure workers (63 %) reported work-related respiratory symptoms. Chest tightness (26 %), cough (17 %) and sputum (16 %) were the most common symptoms and only 6 % of lead exposure workers reported wheezing (P < 0.001 for all case except wheezing). Most PFT values were also significantly reduced among lead exposure workers (P < 0.05 to P < 0.001 except MEF75, MEF50, MEF25, and MMEF. The lead concentration in urine and serum of lead exposure workers were significantly higher than control (P < 0.001 for both cases). Conclusions : These results showed that c lead exposure workers have higher frequencies of respiratory symptoms higher serum and urine lead concentration but lower PFT values.

Background : The prevention of ventilator-associated pneumonia (VAP) can decrease the duration of mechanical ventilation, length of hospital stay, mortality, and healthcare costs. Objectives : the aim of this study was to compare the effect of the elevation of head of bed (HOB) to 30 and 45 degreess on the incidence of VAP. Methods: This study was a 3 group controlled randomized clinical trial. It consisted of 120 patients who were under mechanical ventilation and hospitalized in the intensive care unit (ICU) from February to July 2016 in the selected governmental hospitals of Iran University of Medical Sciences. The patients were allocated into 3 groups. The patients of intervention groups received interventions consisting of HOB elevation to 30 and 45 degreess for 3 consecutive days. The patients in the control group were in the routine position in the bed for 3 consecutive days. The HOB elevation was measured using the goniometer and recorded by nurses in perticular forms. At the end of the third day, VAP and pressure ulcers were evaluated using the clinical pulmonary infection score (CPIS) as well as Braden scales. The data were analyzed using descriptive and inferential statistics. Results: Statistically significant differences were reported in terms of VAP between the groups of the HOB evelation to 30 degrees (32.50%) and 45 degrees (20.00%) and control groups (52.50%) (P = 0.01). However, the mean scores of pressure ulcer showed no statistically significant differences between the groups (P = 0.625). The greatest change in position was performed by the staff nurses for nursing care in the group of 45 degrees elevation that reported as 6.125 ± 3.13 hours. Conclusions: The HOB elevation to 45 degrees helped with the prevention of VAP compared with the HOB elevation to 30 degrees as well as bed routine. Therefore, it is suggested that nurses elevate HOB to 45 degrees (more than 30 degrees) among mechanicallyventilated patients admitted to the ICU.

Pulmonary hyalinising granuloma (PHG) is a rare fibrosclerosing inflammatory lung condition of unknown aetiology. It is characterised by solitary or multiple pulmonary nodules that are usually found incidentally while imaging the chest for other reasons. We report two cases of histologically proven PHG diagnosed at the Royal Hospital, Muscat, Oman. The first case was a 71-year-old male patient who presented in 2010 with a dry cough, weight loss and bilateral pulmonary nodules. The second case was a 58-year-old male patient who presented in 2012 and was found to have incidental bilateral pulmonary nodules on chest X-ray. Both patients were started on prednisolone and on follow-up the PHG nodules remained stable. Although there is no definitive treatment, PHG generally has an excellent prognosis.

Background: Lung adenocarcinoma (LUAD) is the most common histological subtype of non-small cell lung cancer with very poor 5-year overall survival (OS) rate. It is histopathologically difficult to predict clinical outcome in early-stage LUAD. Identifying reliable prognostic biomarker is absolutely critical to benefit from early additional treatment for early-stage LUAD patients. Objectives: The purpose of the current study was to identify critical genes as prognostic biomarkers in early-stage LUAD using gene expression profiles based on the microarray. Methods: In this bioinformatics-based cross-study, gene expression profiles from early-stage LUAD, including GSE10072 and GSE19804 genes were integrated using bioinformatics methods, including differentially expressed gene analysis (DEGA), Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis, and protein-protein interaction (PPI) network construction. Subsequently, the survival analysis of key genes was performed using The Cancer Genome Atlas (TCGA) database and was validated using online Gene Expression Profiling Interactive Analysis (GEPIA) database. Results: A total of 89 up-regulated and 214 down-regulated genes were identified in early-stage LUAD, and the functional changes of 303 differentially expressed genes (DEGs) were mainly related to cell cycle. A PPI network was established by online STRING database with 207 nodes and 775 edges. Centrality analysis showed that CDKN3 and UBE2C genes were identified as key genes implicated in early-stage LUAD. Survival analysis revealed that low mRNA expressions of CDKN3 and UBE2C were significantly associated with longer OS of early-stage LUAD patients. Conclusions: This cross-study found key dysregulated genes involved in early-stage LUAD, which might provide insights into the pathogenesis of early-stage LUAD, and identified UBE2C and CDKN3 might serve as potential diagnostic and prognostic biomarkers and therapeutic targets for early-stage LUAD.