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PURPOSE: Primary open-angle glaucoma (POAG) is a clinical progressive neuropathy which can lead to irreversible blindness if left untreated. A low level of serum Vitamin D3 is a major risk factor for glaucoma, and hence, represents a second target for glaucoma therapy following intraocular pressure (IOP). However, there is still controversy about whether there is a direct correlation between Vitamin D3 deficiency and the risk of increased IOP. This study aims to investigate the correlation between low serum levels of 1,24-dihydroxycholecalciferol and the development of open-angle glaucoma. METHODS: The study included a total of forty-one patients with POAG. Patients were classified into whether they have chronic illnesses such as type 2 diabetes and hypertension. Matching control subjects of 20 healthy controls were also included in the study. Anthropometric measures and venous blood samples were taken from all participants for serum analysis of various biochemical markers including serum 1,25-dihydroxycholecalciferol (1,25(OH)2D) levels. RESULTS: Overall, serum Vitamin D3 levels were 15% significantly lower in the patient's cohort with open-angle glaucoma as compared to the healthy participants (P < 0.05). Among those, 63% of type 2 diabetic participants had significantly low levels of Vitamin D3 (P < 0.01). There was also a significant 70% reduction in serum Vitamin D3 levels among the hypertensive participants, (P < 0.001). CONCLUSION: We concluded that lower serum 1,25(OH) 2D levels were significantly associated with an increased risk of open-angle glaucoma in patients with chronic illnesses. [ABSTRACT FROM AUTHOR]

Abstract Background The importance of doxorubicin (Dox), as a potent antitumor antibiotic, is limited by the development of life-threatening cardiomyopathy. It has been shown that free radicals are involved in acute doxorubicin-induced toxicity. The aim of this study was to determine the protective effect of vitamin E and telmisartan in acute doxorubicin induced cardiotoxicity. Methods Thirty two male Sprague - Dawly rats were involved in this study and were randomly separated into 4 groups, eight rats in each group, one group received normal saline I.P as control and second group received doxorubicin 20 mg/kg I.P, the other two groups also received doxorubicin 20 mg/kg I.P as single dose after seven cumulative doses (for seven days) of vitamin E (100 mg/kg) and telmisartan (1 mg/kg) respectively. Immunofluorescent staining for monocytes infiltration and analyses of plasma by (ELISAs) for MCP-1and troponin I. Western immunoblotting assay for ICAM-1, while left ventricular function was analyzed by microcatheter, also estimated the level of oxidative stress parameters (MDA and Catalase) and cardiac enzymes activities (CK-MB and LDH) before starting drugs treatment and after treatment period by 48 hours. Results The immunofluorescent staining showed that administration of vitamin E and telmisartan are attenuated of mononuclear cell infiltration; (p Conclusions Antioxidant effect (Vitamin E and telmisartan) have been shown to decrease doxorubicininduced cardiotoxicity.

Background: Compared with the general population, patients with diabetes mellitus (DM) usually show higher platelet reactivity, which increases their risk of atherothrombotic events, such as acute coronary syndrome, during the percutaneous coronary intervention (PCI). Endothelial nitric oxide synthase (eNOS) gene polymorphisms have been associated with many diseases, but their role as risk factors of coronary artery disease (CAD) in DM is yet unknown. Although acetylsalicylic acid and clopidogrel are prescribed individually or in combination for high-cardiovascular risk patients with overall improvements in outcomes, DM patients are still at greater risk of recurrent ischemic events. Objective: This study was conducted to determine the effect of DM on the association of e-NOS polymorphisms with clopidogrel resistance in patients with CAD undergoing PCI. Methods: Three-hundred twenty-four of CAD patients were recruited in this case-control study. All patients were subjected to platelets function test within at least two hours before PCI techniques to determine the clopidogrel resistance first then classified accordingly to clopidogrel resistance group (case group n=111) and non-clopidogrel resistance group (control group n=213). Each group was subdivided into a diabetic patient’s group and nondiabetic patients’ group. Blood samples were taken for genotyping analysis and phenotyping determination by measuring the level of nitric oxide in the plasma via colorimetric method. The genotype analysis was carried using allele-specific polymerase chain reaction based on the banding pattern on gel electrophoresis(GEP) to evaluate whether genetic e-NOS polymorphisms (T786C, exon 7 G894T and intron 4 (4a4b) affect NO formation in both groups. Odds ratios for these polymorphisms were then estimated for the clopidogrel and non-clopidogrel resistance groups. Results: Approximately 34.25% of the study population showed clopidogrel resistance. No significant difference in serum NO levels between the case and control groups (26.1 ± 1.52 µM vs. 25.41 ± 1.18 µM; P = 0.727) was observed. The effect of diabetes on clopidogrel resistance was significant in the case group (20.06 ± 1.82 µM) in diabetes patients when compared with 26.52 ± 2.40 µM in non- diabetes patients (P = 0.03), but within a control group, the effect diabetes on clopidogrel resistance was not significant (P = 0.07), while the effect of diabetes was not significant in diabetes patient (P = 0.09) and nondiabetes (P = 0.4) when the comparison between case and control. The study found that e-NOS intron 4 (4a4b) polymorphisms genotypes were significantly associated in the diabetic group as compared with non –diabetic group in patients' resistant to clopidogrel [ab genotype: OR = 2.4 (1.1–5.69), P=0.02; aa genotype: OR = 2.8 (0.89–8.7), P=0.03], while there was a negative association between diabetic group and non–diabetic group in patients' sensitive to clopidogrel. However, e-NOS polymorphisms of the T786C and exon 7 G894T genotypes showed no association between diabetic and nondiabetic patients of both resistant or sensitive patients except mutant homozygous CC of T786C showed a significant association between diabetic and non-diabetic patients in case and control groups (P = 0.02, 0.04) respectively. Conclusions: Our study indicates that e-NOS gene polymorphisms, specifically the 4a allele (4a/ab) and mutant homozygous CC (T786C), maybe determinants of clopidogrel resistance in diabetic CAD patients. [ABSTRACT FROM AUTHOR]

Autophagy is a self-energy supplier process response to stressful or fasting conditions where cell degrades and recycles intracellular constituents as an alternative way of energy source. Unfortunately Autophagy process play important role in tumor cell resistance to anticancer drugs. Osteosarcoma is the most commonly diagnosed primary malignant tumor of the bone. The present study evaluates the role of Autophagy inhibitor hydroxychloroquine (HCQ) on doxorubicin-induced cell death in Osteosarcoma cell line (MG-63). The results of current study found that doxorubicin induced Autophagy in Osteosarcoma (MG-63) cells, exhibiting an increased microtubule associated protein 1 light chain 3 (LC3)level, a decrease in SQSTM1 (p62) level, moreover using of Autophagy modulator increased in generation of reactive oxygen species (ROS) and decreased Autophagy activity and increased Osteosarcoma-cell death. Although doxorubicin-induced cell death was enhanced by combined with HCQ but at high concentration of doxorubicin the cytotoxicity was decreased with increased Autophagy activity. These finding suggest that Autophagy attenuate cytotoxicity effect of doxorubicin by decreasing level of ROS, while HCQ improved doxorubicincytotoxicity on Osteosarcoma by inhibiting of Autophagy process. [ABSTRACT FROM AUTHOR]

Background: Nephrotoxicity is a serious & common side effect of aminoglycoside and is induced by generation of reactive oxygen species. Emerging evidence reveals that curcumin possesses antioxidant activity, therefore, this research was undertaken to evaluate the potential protective effects of curcumin in amiloration of nephrotoxicity induced by gentamicin in male rats. Materials and Methods: Eighteen male Spraque-Dawley rats were included in this study. They were divided randomly into three equal groups (six rats each). Groups I (Control) received only normal saline i.p, Groups II (GN) received gentamicin (100 mg/kg/day), Group III (GN+CUR) received a combination treatment gentamicin (100 mg/kg/day, i.p) & curcumin (200 mg/kg/day p.o). The duration of treatment was eight days and at the end of the study, animals were sacrificed and the blood sample was collected for assessment of renal function, blood urea & serum creatinine. Both kidneys were removed and prepared for a histopathology examination. Results: blood urea and creatinine were significantly higher (P < .05) in gentamycin treated group (group II) as compared to the control group (group I). However, the levels of these parameters in group 3 (co-treatment of gentamicin and curcumin) were significantly lower than those in group 2 (P < .05). Further, the histological score of renal damage was higher in the gentamicin group than in the control group. Combination treatment of curcumin and gentamicin (groupIII) significantly attenuated the histopathological damage. Conclusion: Curcumin attenuated gentamicin-induced renal injury in rats' models. [ABSTRACT FROM AUTHOR]

Background: Methotrexate (MTX)-induced liver injury is a common problem that is described as increased level of hepatic biomarkers that is seen in 14%-25% of patients with inflammatory bowel disease and 49% of patients with rheumatoid arthritis or as idiosyncratic induced liver injury that is seen in 1% of patients with inflammatory bowel disease, or as fibrosis and cirrhosis in 17% of rheumatoid arthritis patients and 25% of psoriatic patients. This profile may rarely progress to acute liver failure. Aim: The aim is to study the effect of TAK-242 and GIT-27 on MTX-induced liver injury. Materials and Methods: Thirty-five Albino-Wistar rats were divided into five groups: the first group was maintained on distilled water, the second group was administered intraperitoneal (I.P.) dimethyl sulfoxide followed by oral MTX, the third group was administered oral MTX, the fourth group was administered I.P. TAK-242 followed by oral MTX, and the fifth group was administered I.P. GIT-27 followed by oral MTX. Results: The significant increase in markers of hepatic function, inflammatory and oxidative stress markers, as well as severe liver histopathologic change "steatosis" induced by methotrexate were alleviated in the animals pretreated with the drugs TAK-242 and GIT-27. With significant improvement in serum level of alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, bilirubin, interleukin-6, tumor necrosis factor-a, malondialdehyde and reduced glutathione; beside an improved histopathologic profile of moderate steatosis. Conclusion: This study suggests that both TAK-242 and GIT-27 protect against liver injury induced by MTX depending on their antagonism of the inflammatory Toll-like receptors 4 and 2/6. [ABSTRACT FROM AUTHOR]

Copyright of Al-Qadisiah Medical Journal is the property of Republic of Iraq Ministry of Higher Education & Scientific Research (MOHESR) and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Al-Qadisiah Medical Journal is the property of Republic of Iraq Ministry of Higher Education & Scientific Research (MOHESR) and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objectives: The objective of this study was to investigate the hepatoprotective effect of Omega 3 and selenium on Methotrexate (MTX) induced hepatotoxicity. Methods: A total of 28 New Zealand white rabbits were used in this study. The animals were equally divided in to four groups. All groups were maintained on standard chow diet throughout the experiment (8 weeks). Group 1 was treated with normal saline water (control), group 2 with methotrexate (MTX, hepatotoxic), group 3 with MTX plus Omega-3 and group 4 with MTX plus Selenium (Se). The hepatoprotective potential of Omega-3 and Se were evaluated in MTX induced hepatotoxic animals. Changes in the level of serum liver function (SGOT, SGPT, ALP, bilirubin, total serum protein and PT) and oxidation markers (MDA, GSH and SOD) were tested in both MTX treated and untreated groups. Histologic examination of liver tissues was also performed. Results: MTX produced a significant alteration serum liver function and oxidation markers. Concomitant use of Omega-3 and Se with MTX was found to restore significantly the altered liver function and oxidation markers. Further significant improvement in liver histopathological features was observed. Conclusion: our study suggested that the additive drugs (Omega-3 and Se) possess hepatoprotection against MTX induced hepatotoxicity. [ABSTRACT FROM AUTHOR]