ابراهيم رحيم جاسم العادلي

Background: Asprosin, a novel adipokine primarily secreted by white adipose tissue during fasting. Circulating asprosin promotes hepatic glucose release and has been reported to be elevated in obesity, type 2 diabetes mellitus, and metabolic syndrome (MetS), correlating with markers of insulin resistance such as HOMA-IR.

Abstract: Background: Growing evidence suggests that angiotensin-converting enzyme 2 (ACE2) is involved in lipid metabolism as well as cardiovascular homeostasis. Genetic variations in ACE2 have been linked to metabolic disorders including dyslipidemia which is one of the most common features of type 2 diabetes mellitus. However there has been very limited study on association between ACE2 polymorphisms with dyslipidemia in patients with type 2 diabetes mellitus specifically Iraqi population.

Abstract: Background: Type 2 diabetes mellitus (T2DM) is a multifactorial disease often accompanied by dyslipidemia, a major cardiovascular risk factor. Genetic variations in the LDL receptor (LDLR) gene have been implicated in lipid metabolism abnormalities. This study investigates the association of LDLR polymorphisms with dyslipidemia in Iraqi T2DM patients

ABSTRACT : Gestational diabetes mellitus (GDM) was define the metabolic disorder in pregnancy majoring to acute plus chronic complications in mothers as well asnew-borns. Previous research has appeared to demonstrate an association between both secreted frizzled related protein 4 (SFRP4) plusirisin values on the one hand and the occurrence of Type2 Diabetes, although there is no comparable evidence in respect to GDM. Therefore, the aim of the study to conclude, if there is an connection between SFRP4 and GDM and likewise for irisin and if so to explore the connection between these markers and glycaemic parameters. The present case control study included a group of 60 women of GDM and a group of 30 healthy pregnant women (control group). Both groups were subjected to clinical examination encompassing fasting serum glucose (FSG), oral glucose tolerance test (OGTT), HbA1C plus lipid profile levels determined by spectrophotometric methods. Fasting serum insulin, SFRP4 and irisin concentrations were measured in sera by the ELISA technique. Body mass index (BMI) plus HOMAIR were also calculated. The data was analyzed and articulated in terms of (Mean±SD). Person correlation was undertaken in order to study the serum correlation of SFRP and irisin to glycaemic control and lipid profile in the studied groups. The present study show that the mean age value was identical in thetwo groups. Median BMI, fasting serum glucose, OGTT at 1 hour, OGTT at 2 hours, HbA1C and serum insulin values were elevatedof GDM patients when compared to healthy pregnant women, The median SFRP4 values were increased in the GDM patients group; while the median irisin values were increased in the control group. Serum SFRP4 values were elevated and irisin values reduced in GDM patients.Theseresults recommended that serum SFRP4 and irisin values could be introduced as predictor markers for GDM. Additional investigations are wanted to discover the “biological effects” of SFRP4 and irisin going on pregnant women.

Abstract Glioblastoma multiforme (GBM) is a malignant tumour of astrocytes in the brain which accounts for approximately one third of all tumours in the nervous system. Despite the availability of chemotherapy, the median survival rate for all patients is between 15 to 24 months. Temozolomide (TMZ) and carmustine (BCNU) are the most common chemotherapeutic agents used in combination with radiotherapy or surgery to treat GBM. The overexpression of PrPc in GBM has been reported and its involvement in the resistance to alkylating agents (TMZ and BCNU) was speculated. The exact role of PrPc in GBM, i.e. how it is affected by chemotherapeutic agents and small molecules, needs to be further investigated. In this work, the effect of TMZ and BCNU on PrPc was evaluated using U87 glioblastoma cell line. The results showed that 24 h treatment with TMZ or BCNU followed by 48 h resting gave the highest level of G2/M cells (about 84%) when compared with untreated cells. The upregulations of p53 and p21 are believed to be the key cause for this increment. PRNP gene is also upregulated in TMZ or BCNU treated U87 cells for 24 h treatment followed by 48 h resting and this may contribute to the resistance these cells towards the treatments due to the cytoprotective effect of this protein despite less PrPc is detected at protein level. Some of these findings are in agreement while others are opposite to those previously reported. The resistance to chemotherapy is considered as one of the main limitations for the effective treatment of cancer, especially for GBM. PRNP gene in U87 cell line was silenced to determine cell proliferation and chemoresistance. A decrease of 80% in PrPc level was obtained after 48 h of treatment with transfection reagents. Additionally, the level of the PrPc knockdown was retained 5 days post-knockdown. Silencing of the PRNP gene in glioblastoma cell line U87 reduces cell proliferation in a time-dependent manner. In addition, positive cells with proliferation marker ki67 were significantly decreased in knockdown cells after 5 days. This implies that PrPc contributes to the malignance of the cancer cells. It was also found that there was no significant reduction in cell proliferation in response to TMZ or BCNU in knockdown cells and p21 is upregulated in TMZ or BCNU knockdown cells. Therefore, silencing PRNP gene may impact the function of p21 which contributes to the resistance to alkylating agents TMZ and BCNU. In an attempt to sensitise U87 cells to TMZ, the combination treatment of MG132 with TMZ did not improve the apoptosis rate and no accumulative effect was observed. High concentration of MG132 increased the level of PrPc in U87 cells after a short incubation time. The level of PrPc was also evaluated in U87 cells treated with the compounds (FAPi) which inhibit the Fancony Anaemia (FA) pathway by reduction of FANCD2 using high content imaging by ImageXpress Micro. These compounds did not affect the level of PrPc in these cells with or without combination with TMZ or BCNU showing that these FAPi are target specific. Several novel families of heteroaromatic compounds (30 compounds) previous shown to be cytotoxic to embryonic carcinoma cells (NT2) were screened on U87 cells and eight of them were found to be inhibit the proliferation of the cells. The compound 175 that belongs to the acridine family induced apoptosis for U87 cells. It also arrests U87 cells in G2/M and upregulate p53 and p21 proteins which are regulatory for cell cycle. That may open the door to examine more acridine compounds as anti-glioblastoma agents.

Background Coronary artery disease (CAD) is a group of diseases caused by plaque formation in the wall of arteries supplying blood to the heart. Adiponectin (ADIPOQ) is an adipocytokine that controls carbohydrate and lipid metabolism, has anti-diabetic properties, and correlates well with cardio-metabolic risk. ADIPOQ gene polymorphism is reported to be associated with CAD in numerous populations. Objective To explore the impact of adiponectin gene polymorphism, rs2241766 T > G, rs1501299 G > T, rs17300539 G > A, rs266729 G > A, and rs822395 A > C SNPs, on the CAD in the Iraqi population.