Background: Prostate cancer (PCa) is the second most frequent cause of cancer-related death in men worldwide. It is a heterogeneous disease at molecular and clinical levels which makes its prognosis and treatment outcome hard to predict. The epithelial-to-mesenchymal transition (EMT) marks a key step in the invasion and malignant progression of PCa. We sought to assess the co-expression of epithelial cytokeratin 8 (CK8) and mesenchymal vimentin (Vim) in locally-advanced PCa as indicators of EMT and consequently predictors of the progression status of the disease.Methods: Co-expression of CK8 and Vim was evaluated by immunofluorescence (IF) on paraffin-embedded tissue sections of 122 patients with PCa who underwent radical prostatectomies between 1998 and 2016 at the American University of Beirut Medical Center (AUBMC). EMT score was calculated accordingly and then correlated with the patients' clinicopathological parameters and PSA failure.Results: The co-expression of CK8/Vim (EMT score), was associated with increasing Gleason group. A highly significant linear association was detected wherein higher Gleason group was associated with higher mean EMT score. In addition, the median estimated biochemical recurrence-free survival for patients with < 25% EMT score was almost double that of patients with more than 25%. The validity of this score for prediction of prognosis was further demonstrated using cox regression model. Our data also confirmed that the EMT score can predict PSA failure irrespective of Gleason group, pathological stage, or surgical margins.Conclusion: This study suggests that assessment of molecular markers of EMT, particularly CK8 and Vim, in radical prostatectomy specimens, in addition to conventional clinicopathological prognostic parameters, can aid in the development of a novel system for predicting the prognosis of locally-advanced PCa.

Febrile seizures (FS) are a prevalent type of seizure occurs due to fever in children aged between six months and five years. This study aimed to explain the effect of electrolyte disturbance in FS and the role of procalcitonin (PCT) as an inflammatory biomarker in the diagnosis of FS. The case-control study was performed at the Children Welfare Hospital, Medical City, Baghdad, Iraq, included 90 children aged six months to five years divided into 40 children with FS, 30 children were admitted to emergency department with fever a count as a febrile control (FC) group and 20 healthy children free of infection. The study involved the measurement of serum electrolyte (Na, K, and Ca) and some inflammatory biomarkers (PCT, CRP, and ESR). The data revealed no significant difference in PRO and ESR between the FS and FC while there are significantly elevated PRO and ESR in patient groups as compared to that of the healthy control group at p <0.05. The data explain that the mean level of CRP was significantly higher in FS than FC while there was no significant difference between FC and healthy control groups. Lower serum sodium in FS as compared to FC and decrease serum potassium level in FS. In conclusion, Patients with FS have higher total WBC count, ANC and serum CRP levels than the febrile control group while significantly higher serum PCT and ESR levels in FS than healthy control. Also, lower serum sodium and potassium levels in FS patients could have a role in the development of FS.

Background and Objectives: Coronary artery disease (CAD) is a state of insufficient supply of oxygenated blood to a part of myocardium. The most common cause of myocardial ischemia is atherosclerosis. Inflammation plays an important role in atherosclerosis and hence CAD. The principle inflammatory markers that believed to have a key position in the pathogenesis of CAD include fetuin-A protein, high sensitive C-reactive protein (hs-CRP), tumor necrosis factor-alpha (TNF-α), and soluble intracellular adhesion molecule-one (sICAM-1). The aim of study was carried out to evaluate fetuin-A protein and some inflammatory biomarkers in patients with coronary artery disease. Subjects and Methods: Ninety subjects above forty year old; (45) patients with acute coronary syndrome (ACS); were divided in three groups: Unstable angina (UA), non-ST-elevation myocardial infarction (NSTEMI), and ST-elevation myocardial infarction (STEMI), all selected from Coronary Care Unit (CCU), and (45) apparently healthy age and sex matched subjects as controls. Five milliliters (5ml) of venous blood sample were drawn from each patient and healthy persons (controls), centrifuged to obtain serum, to be used for measuring the following variables: Fetuin-A protein, hs-CRP, TNF-α, sICAM-1. Results: Fetuin-A protein was significantly lower, while hs-CRP, TNFα, and sICAM-1 were higher in patients. A low Fetuin-A protein level was inversely associated with increasing age. A high TNFα level was associated with increased BMI. Conclusions: Lower serum Fetuin-A level, and higher serum levels of hs-CRP, TNFα, and sICAM-1 are associated with ACS. The future may be promising in rising of anew tests that use for evaluation of patients with suspected ACS.

Background: CCN1 is an extracellular matrix-associated protein thought to be implicated in tumor-stromal interaction in several solid tumors. The aim of our pilot study was to evaluate the correlation between CCN1 expression in stromal cells, pancreatic intraepithelial neoplasia (PanIN) and pancreatic ductal adenocarcinoma cells in resected pancreatic ductal adenocarcinoma (PDAC) specimens, and correlate that clinically. Methods: A total of 42 paraffin-embedded PDAC tumor specimens were stained for CCN1 and evaluated via immunohistochemical (IHC) analysis. Statistical analysis was performed to correlate between CCN1 expression profiles in tumor tissues and clinicopathological parameters of patients. Results: Our results showed CCN1 (CYR61) gene was highly expressed in PDAC tissues relative to other organ specific tumor tissues. Also, moderate and overexpression of CCN1 in PanIN was associated with PanIN grade 3 tissues. A statistically significant association was found between PanIN CCN1 scores on one hand and cancer stage, cancer grade, and CCN1 expression among ductal tumor cells and adjacent stromal cells on the other hand. Discussion: The associations demonstrated suggest that CCN1 might be contributing to a substantial role in the interaction between the pancreatic tumors on one hand and their surrounding microenvironment and their precursors on the other hand; hence, it might serve as a potential therapeutic target for PDAC.

Background Prostate cancer (PCa) is the most commonly diagnosed cancer and the second leading cause of cancer-related deaths among adult males globally. The poor prognosis of PCa is largely due to late diagnosis of the disease when it has already progressed to an advanced stage marked by androgen-independence, thus necessitating new strategies for early detection and treatment. We construe that these direly needed advances are limited by our poor understanding of early events in the progression of PCa and that would thus represent ideal targets for early intervention. To begin to fill this void, we interrogated molecular “oncophenotypes” that embody the transition of PCa from an androgen-dependent (AD) to–independent (AI) state. Methods To accomplish this aim, we used our previously established AD and AI murine PCa cell lines, PLum-AD and PLum-AI, respectively, which recapitulate primary and progressive PCa morphologically and molecularly. We statistically surveyed global gene expressions in these cell lines by microarray analysis. Differential profiles were functionally interrogated by pathways, gene set enrichment and topological gene network analyses. Results Gene expression analysis of PLum-AD and PLum-AI transcriptomes (n = 3 each), revealed 723 differentially expressed genes (392 upregulated and 331 downregulated) in PLum-AI compared to PLum-AD cells. Gene set analysis demonstrated enrichment of biological functions and pathways in PLum-AI cells that are central to tumor aggressiveness including cell migration and invasion facilitated by epithelial-to-mesenchymal transition (EMT). Further analysis demonstrated that the p38 mitogen-activated protein kinase (MAPK) was predicted to be significantly activated in the PLum-AI cells, whereas gene sets previously associated with favorable response to the p38 inhibitor SB203580 were attenuated (i.e., inversely enriched) in the PLum-AI cells, suggesting that these aggressive cells may be therapeutically vulnerable to p38 inhibition. Gene set and gene-network analysis also alluded to activation of other signaling networks particularly those associated with enhanced EMT, inflammation and immune function/response including, but not limited to Tnf , IL-6 , Mmp 2 , Ctgf , and Ptges . Accordingly, we chose SB203580 and IL-6 to validate their effect on PLum-AD and PLum-AI. Some of the common genes identified in the gene-network analysis were validated at the molecular and functional level. Additionally, the vulnerability to SB203580 and the effect of IL-6 were also validated on the stem/progenitor cell population using the sphere formation assay. Conclusions In summary, our study highlights pathways associated with an augmented malignant phenotype in AI cells and presents new high-potential targets to constrain the aggressive malignancy s...