Background: Liver-related death globally is caused mainly by cirrhosis. It is the final grade of extensive liver fibrosis, in which the hepatic architecture is modified. Cirrhosis is a common disease worldwide and can be the end stage for several reasons such as obesity, non-alcoholic fatty liver, alcoholism, viral infection such as viral hepatitis, immune disorders, bile duct obstruction, and metabolic diseases. Alpha-fetoprotein (AFP) is defined as a protein secreted by the germinal yolk sac and liver. AFP level is used as a marker to diagnose inherited disorders and chromosomal anomaly, whereas the high-sensitivity C-reactive protein (hs-CRP) has a separate correlation with NAFLD. Therefore, hs-CRP can be used as a beneficial marker for identifying liver defects. Subjects and Methods: Thirty participants with liver cirrhosis and 30 healthy participants as control (male and female) were enrolled. The participants from Baghdad, Iraq, were enrolled in this study. Blood and serum samples were obtained for the estimation of hemoglobin, serum AFP, and hs-CRP levels. Results:The pooled data of participants showed that hs-CRP and alpha-fetoprotein levels in the participants with cirrhosis were significantly higher than in the control group, P<0.0001. There were no significant differences in the sexes while considering alpha-fetoprotein, whereas hs-CRP levels were higher in males compared with females. Conclusion:This research shows a significantly high level of hs-CRP and alpha-fetoprotein in patients with liver cirrhosis compared with the control participants. There were non-significant gender differences concerning alpha-fetoprotein with significantly high level of hs-CRP in males compared with females.
Pulmonary fibrosis (PF) is an interstitial lung disease leading to scarring of the lung. There are several types of lung fibrosis as familial pulmonary fibrosis, idiopathic pulmonary fibrosis, and others associated with non-specific interstitial pneumonia. The most common type is idiopathic pulmonary fibrosis which is an unknown cause. Lung fibrosis causes changes in the histology of the lung by the disappearance of the lung parenchyma, replaced by an inflammatory infiltrate, and mild thickening of the pulmonary artery. The management of pulmonary fibrosis included Azathioprine, corticosteroid, and N-acetyl cysteinyl in 2011 but in 2014 this guideline was removed and replaced by nintedanib and pirfenidone. This study used Pirfenidone, as standard therapy for the treatment of pulmonary fibrosis, and montelukast is Cysteinyl leukotrienes (CysLT) antagonist which binds to its receptor (CysLTE4) located on smooth muscle cells of the respiratory airway causing anti-inflammatory effect by inhibition of inflammatory markers as TGFβ1. Sixty male rats were divided into five groups,12 rats for each group where the control group received distilled water by gastric gavage, the induction group received bleomycin intratracheally as a single dose, the pirfenidone group received pirfenidone 50mg/kg, montelukast group received montelukast 20mg/kg and the combination group received a half dose of pirfenidone and montelukast. After twenty-eight days after the treatment with montelukast or pirfenidone sacrifice rats and collect the organ (lungs) from each group were then placed in buffer formalin 10% for histopathological study. After 14 days from bleomycin dose, results show that bleomycin cause massive disappearance of pulmonary parenchyma that was replaced by an inflammatory infiltrate and medial thickening of the pulmonary artery in all groups, but montelukast and pirfenidone show normal lung paranchyma and pulmonary artery after 28 days of treatment in pirfenidone, montelukast, and combination groups. In conclusion, that bleomycin changes the histology of the lung causing induction of lung fibrosis in all groups after 14 days except control group but pirfenidone, montelukast, and combination of half dose of pirfenidone with a half dose of montelukast return the lung to normal architecture after 28 days of treatment.
This paper aims to find out if FOXP-3 was expressed in samples from Iraqi cervical cancer patients. Expression of FOXP-3 was detected in 55 cervical tissue samples by immunohistochemistry. Since thirty-five cases of aggressive cervical cancer were included, along with 20 normal samples used as controls. The nucleus and cytoplasm levels of FOXP-3 were counted, considering the ratio of positive cells and intensity. FOXP3 cytoplasmic staining was found in 27 out of 35 cases. Only 11 out of 35 samples displayed nuclear lymphocyte staining. Furthermore, four samples expressed this marker in both the nuclear and cytoplasm of the cervical cells. There is a highly significant difference in FOXP3 expression in the cytoplasm of malignant cells and lymphocytes compared to normal samples. Seven samples out of 11 cells correlated with lymph vascular invasion. These results show that tissue positive FOXP-3 possesses a possible diagnostic marker for Iraqi cervical cancer. FOXP3 is significantly expressed in cancer cells, and lymphocyte infiltrates [T-reg] compared to normal.
Objective: Metastatic spread of tumor cells to distant organs is the leading cause of mortality from cancer. Although metastatic tumor spread can occur via a different mechanism. lymphangiogenic factors recognized were vascular endothelial growth factor (VEGF)–C and –D, which bind to a tyrosine kinase receptor, VEGF receptor (R)–3. Binding affinities to VEGFR-2 receptor increase on the lymphatic and blood endothelium therefore enables both growth factors to also exert lymphangiogenic and angiogenic effects and increased incidence of lymph node metastasis. The aim of this study is to evaluate the VEGF-C protein expression in cervical cancer cells and lymph vessels and found the relationship of this marker with lymphangiogensis of Iraqi cervical cancer samples. Method: In this study, expression of VEGF-C was noticed in 55 cervical samples by Immuno- histochemistry. 35 cases diagnosed as invasive cervical cancer in addition to 20 normal samples consider as control. Immunohistochemistry was performed and the cytoplasm level of VEGF-C was scored by the percentage of positive cells and intensity. Results: The present data evaluated the prognostic significance of VEGF-C to cervical cancer, cytoplasm staining was seen in 29 cases (82.9 %) in cervical cancer tissues. Only 4 out of 35 cases (11.4 %) displayed cytoplasmic and nuclear tissue. There is significant difference of VEGF-C staining in lymphatic vessels and cancer cells (χ2= 5.04, p = 0.023*) regarding to positive expression (20/ 57.1%), (25/ 71.4 %) respectively and negative VEGF-C staining 15 (42.9%), 10 (28.6 %) respectively. High positive percentage of VEGF-C expression in cytoplasm of malignant cases in score 2& 3 (25.7%, 45.7 %, P-value= 0.0392 *, 0.029* respectively) as compared to normal cases (15%, 30% respectively). Demographic criteria of patients revealed association with VEGF-C expression patterns. Differentiation Well + moderately and histologic type Squamous carcinoma showed significantly associated with VEGF-C (P=0.0071** & 0.0071** respectively). Positive VEGF-C staining in cancer cells had more lymphatic vessel (17/68 %) as compared to negative cases (3/30 %) with Chi-Square 8.263, p value= 0.0061**. Also, positive VEGF-C staining had more lymph node associated (9/36%) compared to negative cases (1/10 %) with Chi-Square 13.503, p value= 0.0001**. Conclusion: In conclusion, high expression of vascular endothelial growth factor was noticed in cervical cancer cells and lymph vascular invasion indicating the important role of this marker as prognostic factor for Iraqi cervical cancer. Additionally, these results suggested that VEGF-C promoted cervical cancer metastasis using immunohistochemistry technique. Our findings offer new vision into the role of VEGF-C in cervical cancer development and give potential target for study the lymphangiogensis of tumor in Iraqi women.
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