Esraah Sattar Mahmood Alharris

Abstract Objective: To assess the diagnostic value of serum carcinoembryonic antigen in the detection and prognosis of colorectal malignant epithelial tumors. Study Design: Case-control study Place and Duration of Study: This study was conducted at the Department of Pathology & Forensic Medicine, College of Medicine, University of Al-Qadisiyah, Iraq from 1st June 2023 to 31st December 2023. Methods: Thirty-one patients with colorectal cancer and 36 controls. The serum level of carcinoembryonic antigens was collected from both groups. In addition, information about the age of the patients, sex of patients, tumor stage, and tumor grade was collected. Results: Serum carcinoembryonic antigen levels were higher significantly in patients who have colorectal cancer patients in comparison to control (2.70 (2.20) vs.1.85 (1.28) ng/ml, respectively). The cut-off value of serum carcinoembryonic antigen was >2.5 ng/ml with a sensitivity level of 58.1 %, a specificity level of 83.3 %, and an accuracy level of 73.1, with the area under the curve of 0.731 indicating a fair ability to differentiate.

ABSTRACT Background: It has been documented that the mortality rate in diabetic persons can reach 10%. In addition, it has been shown that the rate of mortality and the need for respiratory support are higher among newly diagnosed cases of diabetes mellitus compared with patients known to have diabetes mellitus for a relatively long duration. In the setting of the pandemic of COVID-19, glycemic control for the patients admitted to hospitals is critical, as is diabetes screening to uncover undiagnosed cases. Aim of the study: To explore the possible link between diabetes mellitus and COVID-19 in Iraq Patients and methods: The current research was carried out in Al-Diwaniyah Province, Iraq, in Al-Diwaniyah Teaching Hospital, including the word of medicine, respiratory unit, and intensive care unit. The study started on Sept 15, 2021 and ended on Apr 15, 2022. The study was cross-sectional and included 100 patients with a diagnosis of COVID-19 evidenced by polymerase chain reaction (PCR) test and CT-scan “computed tomography scan of the chest. Those patients were chosen randomly from the pool of patients visiting the teaching hospital. The age range of patients was between 18 and 94 years, with 45 males and 55 females. Laboratory investigation results were retrieved from patients’ records and included random blood sugar, lactate dehydrogenase, d-dimer, HbA1c%, and “C-reactive protein (CRP).” Results: The mean values of age, random blood sugar (RBS), lactate dehydrogenase (LDH), d-dimer, HbA1c, and HS-CRP were comparable between males and females (p >0.05). Patients with high HbA1c levels (HbA1c ≥ 6.5%) were older and had significantly higher levels of random blood sugar and d-dimer than patients with HbA1c < 6.5%. The d-dimer level showed a significant positive correlation to RBS, LDH, HbA1c, and HS-CRP (p <0.05). Conclusion: Higher levels of markers of inflammation were associated with HbA1c levels in the diabetic range, indicating a bi-directional relation between diabetes mellitus and the severity of COVID-19.

Asthma is a chronic respiratory disease highly prevalent worldwide. Recent studies have suggested a role for microbiome-associated gut–lung axis in asthma development. In the current study, we investigated if Resveratrol (RES), a plant-based polyphenol, can attenuate ovalbumin (OVA)-induced murine allergic asthma, and if so, the role of microbiome in the gut–lung axis in this process. We found that RES attenuated allergic asthma with significant improvements in pulmonary functions in OVA-exposed mice when tested using plethysmography for frequency (F), mean volume (MV), specific airway resistance (sRaw), and delay time(dT). RES treatment also suppressed inflammatory cytokines in the lungs. RES modulated lung microbiota and caused an abundance of Akkermansia muciniphila accompanied by a reduction of LPS biosynthesis in OVA-treated mice. Furthermore, RES also altered gut microbiota and induced enrichment of Bacteroides acidifaciens significantly in the colon accompanied by an increase in butyric acid concentration in the colonic contents from OVA-treated mice. Additionally, RES caused significant increases in tight junction proteins and decreased mucin (Muc5ac) in the pulmonary epithelium of OVA-treated mice. Our results demonstrated that RES may attenuate asthma by inducing beneficial microbiota in the gut-lung axis and through the promotion of normal barrier functions of the lung.

Neuroblastoma (NBL) is one of the most common childhood cancers that originate from the immature nerve cells of the sympathetic system. Studies with NBL cancers have also shown that miRNAs are dysregulated and may play a critical role in pathogenesis. Cannabidiol (CBD) is a non-psychoactive compound found in marijuana which has been previously shown by our laboratory and others to induce apoptosis in cancer cells. However, there are no studies reported to test if CBD mediates these effects through regulation of miRNA. In the current study, therefore, we investigated if CBD induces apoptosis in human NBL cell lines, SH SY5Y and IMR-32, and if it is regulated by miRNA. Our data demonstrated that CBD induces apoptosis in NBL cells through activation of serotonin and vanilloid receptors. We also found that caspase-2 and -3 played an important role in the induction of apoptosis. CBD also significantly reduced NBL cell migration and invasion in vitro. Furthermore, CBD blocked mitochondrial respiration and caused a shift in metabolism towards glycolysis. CBD altered the expression of miRNA specifically, down-regulating hsa-let-7a and upregulating hsa-mir-1972. Downregulation of let-7a increased expression of target caspase-3, and growth arrest specific-7 (GAS-7) genes. Upregulation of hsa-mir-1972 caused decreased expression of BCL2L1 and SIRT2 genes. Together, our studies suggest that CBD-mediated apoptosis in NBL cells is regulated by miRNA.

Asthma is a chronic inflammatory disease of airways mediated by T-helper 2 (Th2) cells involving complex signaling pathways. Although resveratrol has previously been shown to attenuate allergic asthma, the role of miRNA in this process has not been studied. We investigated the effect of resveratrol on ovalbumin-induced experimental allergic asthma in mice. To that end, BALB/c mice were immunized with ovalbumin (OVA) intraperitoneally followed by oral gavage of vehicle (OVA-veh) or resveratrol (100 mg/kg body) (OVA-res). On day 7, the experimental groups received intranasal challenge of OVA followed by 7 days of additional oral gavage of vehicle or resveratrol. At day 15, all mice were euthanized and bronchioalveolar fluid (BALF), serum and lung infiltrating cells were collected and analyzed. The data showed that resveratrol significantly reduced IL-5, IL-13, and TGF-β in the serum and BALF in mice with OVA-induced asthma. Also, we saw a decrease in CD3+CD4+, CD3+CD8+, and CD4+IL-4+ cells with increase in CD4+CD25+FOXP3+ cells in pulmonary inflammatory cell infiltrate in OVA-res group when compared to OVA-veh. miRNA expression arrays using lung infiltrating cells showed that resveratrol caused significant alterations in miRNA expression, specifically downregulating the expression of miR-34a. Additionally, miR-34a was found to target FOXP3, as evidenced by enhanced expression of FOXP3 in the lung tissue. Also, transfection studies showed that miR-34a inhibitor upregulated FOXP3 expression while miR-34a-mimic downregulated FOXP3 expression. The current study suggests that resveratrol attenuates allergic asthma by downregulating miR-34a that induces increased expression of FOXP3, a master regulator of Treg development and functions.

This study aimed to assess the significance of human epidermal growth factor (HER-2/neu) protein overexpression and its possible correlation with vascular endothelial growth factor (VEGF),grade and stage in human non otherwise specified breast cancer. The present investigation was performed over a period starting from November 2008 to January 2009 .Formalin fixed, paraffin-embedded blocks from 30 patients with breast cancer were included in this study. A group of 15 patients with benign breast lesions (fibroadenoma) was included as a comparative group and 15 normal breast tissue sections were included as control group. Labeled Streptavidin-Biotin Complex (LSAB) method was employed for immunohistochemical detection of HER-2/neu. Avidin-Biotin Complex (ABC) method was employed for immunohistochemical detection of VEGF . A total of 30 malignant cases were included.HER2/neu was considered as positive in(18 cases)60% of non otherwise specified invasive ductal carcinoma and VEGF was considered as positive in (21cases)70% with concomitant positivity of both markers in more than half (16 cases)53.3% out of 30 malignant cases . No overexpression of both markers have been noticed in normal or benign (fibroadenoma) breast tissue sections with significant difference from that of malignant cases(P<0.05).We did not find any significant difference between overexpression of both(HER-2/neu and VEGF) in relation to age ,tumor size ,tumor stage and positive or negative lymph node breast cancer cases (P>0.05). However there was positive relation between HER-2/neu overexpression and the grade of tumor (P<0.05) ,while there was no significant difference between VEGF overexpression and the tumor grade(P>0.05).HER-2/neu overexpression was positively correlated with VEGF immunostaining in relation to grade and stage (P<0.05). Based upon the findings of this study, it can be concluded that both HER-2/neu and VEGF play an important role in the pathogenesis of non other wised specified breast cancer and supports the evidence of its role in evolution ,angiogenesis and cell survival of this aggressive tumor . This study recommended that the blocking of both HER-2/neu and VEGF may be a target for blocking the evolution and angiogenesis and hence improving the efficacy of anti cancer therapy against this aggressive type of breast cancer.

Objective: To assess the significance of vascular endothelial growth factor (VEGF) protein over expression in human breast cancer, and its possible correlation with cell proliferation marker (Ki-67), grade and stage of breast cancer. Methods: We carried out this study at the Department of Pathology, Kufa University, between November 2006 and September 2007. A retrospective study was employed on paraffin-embedded blocks from 52 female patients with breast cancer. A group of 21 patients with benign breast lesions was included for comparison and 14 cases of normal breast tissue as a control group. This investigation designed to employ immunohistochemistry using Avidin-Biotin Complex (ABC) method for detection of both VEGF and Ki-67. Results: A total of 87 samples was included. Vascular endothelial growth factor immunoexpression was considered as positive in 61.5% of malignant and in 19% of benign breast lesions. No over expression sign has been noticed in normal breast tissue (p<0.005). No significant difference in VEGF over expression among different histological types of breast cancer (p>0.05). Vascular endothelial growth factor immunostaining was positively correlated with Ki-67, grade, stage, lymph node metastasis, and recurrence of breast cancer (p<0.05). No such correlation has been seen when the age of the patients has been considered. Conclusion: Vascular endothelial growth factor Vascular endothelial growth factor plays an important role in pathogenesis of breast cancer evolution, and supports the evidence of its role in angiogenesis and cell survival. This study recommended that the blocking of VEGF may be a target for blocking angiogenesis and hence improving the efficacy of anti-cancer therapy.