إيناس حسين علي الدفاعي

Abstract Smoking destroys the vascular system, increases plaque deposits in atherosclerosis, and increases inflammation. The present study was performed to determine the effect of smoking on the levels of low-density lipoprotein and very low-density lipoprotein in smokers. A cross-control study was carried out in the outpatient clinic in Baghdad, Iraq. The study was carried out 60 by individuals from February 2021 to July 2021. Participants in this study included adult smokers and non-smokers of both genders, and the levels of LDL and VLDL were determined using an Automatic Chemistry Analyze. The results revealed that the total number of smokers was 60 individuals from both genders; there was a significant difference in mean low-density lipoprotein and very low-density lipoprotein levels. There is a significant difference in LDL Values between non-smokers and smokers (129.853±7.880; P<0.05). Non-smokers showed lower LDL values (104.460±7.950; P<0.05). Regarding VLDL values, results revealed that smokers were showing higher values than a non-smoker (49.641±4.02), (28.986±1.676) respectively, P<0.05). LDL and VLDL levels are more prevalent in current cigarette smokers than in non-smokers. Heavy smokers have higher LDL and VLDL values for a cigarette than non-smokers, which is consistent with observations in other populations. Keywords: Lipid profile, LDL, VLDL, Cigarette smoking

Abstract Type 2 diabetes mellitus (DM) is a persistent metabolic condition illness with a rapidly rising prevalence in the entire world. The management of T2DM varies greatly across the government and industry sectors in Iraq; Using this variant brought on by unequal access to treatment. The goal of this agreement is to present uniform advice about the process of treat patients with T2DM for the initial time. while taking into account regional challenges in Iraq. A group of Iraqi internists and diabetologists from throughout the nation gave their approval to these consensus statements. The recommendation was based entirely on the most recent and current level of evidence. T2DM makes up about 90% of all diabetes cases. As a result of the reduced insulin response in T2DM, This condition is referred to as insulin resistance. In this condition, To keep glycemic control, insulin is ineffectual, which is first countered by an elevation in the synthesis of insulin; however, over time, the secretion of insulin falls, which results in T2DM.

Abstract All substances used to eliminate or manage pests are collectively referred to as "pesticides," including insecticides (insecticides), fungicides (fungi), and herbicides (weedicides). One of the main supporters of the green revolution sought ways to improve and utilized suitable pesticides to control the wide range of insect and plant pests that have a detrimental impact on the quantity and quality of the world's food supply. This review looks at pesticide categories, toxicity, deciding variables, pesticides in water supplies, contaminated soils, impacts on human health, and techniques for detection, removal, and repair. Furthermore, this essay contrasts the analytical techniques used to measure the very low concentrations of pesticides, as well as gives a concise overview of the separation procedures utilized for pesticide examination. Finally, our research suggests that new technologies for detecting pesticide residues and other very harmful pollutants be developed. Both severe, or simple, and persistent, or hard, unfavorable health effects can arise from the use of pesticides, and they can manifest months or years after administration. The goal of this project is to demonstrate the detrimental effects of chemical pesticides, as well as their repercussions on the environment and people's health in Iraq. We could conclude that incorrect use of these substances might be harmful in the short- or long-term. Governmental agencies in charge of these materials should pursue alternate control strategies to decrease the danger and abuse of these compounds. Taking into account that educating the public about the dangers of pesticides is a crucial part of preserving improved both the environment and health in Iraq, that might be better and have no adverse effect on health and the environment. Keywords: Pesticide, contamination, human influence.

The milk thistle compound Silibinin (i.e., a 1:1 mixture of Silybin A and Silybin B) stimulates vasculogenesis of mouse embryonic stem (ES) cells. Because vasculogenesis and leukopoiesis are interrelated, the effect of Silibinin on leukopoiesis of ES cells was investigated. Treatment of differentiating ES cells with hydrosoluble Silibinin-C-2',3-dihydrogen succinate dose-dependent increased the number of CD18+ , CD45+ , and CD68+ cells, indicating leukocyte/macrophage differentiation. Silibinin treatment activated phosphoinositide 3-kinase (PI3K), AKT (protein kinase B), signal transducer and activator of transcription 3 (STAT3), stimulated hypoxia-induced factor-1α (HIF-1α), and vascular endothelial growth factor receptor 2 (VEGFR2) expression and raised intracellular nitric oxide (NO). Western blot experiments showed that upon coincubation with either the PI3K inhibitor LY294002, the STAT3 inhibitor Stattic, the AKT antagonist AKT inhibitor VIII, or the NO inhibitor L-NAME, the Silibinin-induced expression of CD18, CD45, and CD68 was abolished. Moreover, the stimulation of HIF-1α and VEGFR2 expression was blunted upon STAT3 and PI3K/AKT inhibition. Treatment of differentiating ES cells with L-NAME abolished the stimulation of VEGFR2 and VE-cadherin expression achieved with Silibinin, indicating that NO is involved in vasculogenesis and leukocyte differentiation pathways. In summary, the data of the present study demonstrate that Silibinin stimulates leukocyte differentiation of ES cells, which is associated to vasculogenesis and regulated by PI3K/AKT-, STAT3-, and NO-mediated signaling.

Abstract Silibinin, the bioactive compound of milk thistle (Silybum marianum), exerts tissue protective and regenerative effects that may include stem cell differentiation toward vascular cells. The purpose of the present study was to investigate whether silibinin stimulates blood vessel formation from mouse embryonic stem (ES) cells and to unravel the underlying signaling cascade. Vascular branching points were assessed by confocal laser scanning microscopy and computer-assisted image analysis of CD31-positive cell structures. Protein expression of vascular markers and activation of protein kinases were determined by western blot. Nitric oxide (NO) generation was investigated by use of the fluorescent dye 4-amino-5-methylamino-2',7'-difluorofluorescein diacetate. Silibinin dose-dependently increased CD31-positive vascular branching points in embryoid bodies cultivated from ES cells. This was paralleled by increase of protein expression levels for the endothelial-specific markers vascular endothelial cadherin (VE-cadherin), vascular endothelial growth factor receptor 2, and hypoxia-inducible factor-1α. Moreover, silibinin increased activation of endothelial nitric oxide synthase (eNOS), which boosted generation of NO in embryoid bodies and enhanced phosphorylation of signal transducer and activator of transcription 3 (STAT3) as well as phosphoinositide 3-kinase (PI3-K) and AKT. Vasculogenesis, VE-cadherin expression, STAT3 and AKT phosphorylation, NO generation, and eNOS phosphorylation were inhibited by the small molecule STAT3 inhibitor Stattic, AKT inhibitor VIII, the PI3-K inhibitor LY294002, or the NOS inhibitor Nω-Nitro-L-arginine methyl ester hydrochloride. In conclusion, our findings indicate that silibinin induces vasculogenesis of ES cells via activation of STAT3, PI3-K, and AKT, which regulate NO generation by eNOS.

Abstract The milk thistle (Silybum marianum (L.) Gaertn.) compound silibinin may be an inhibitor of the angiotensin II type 1 (AT1) receptor which is expressed in differentiating embryonic stem (ES) cells and is involved in the regulation of cardiomyogenesis. In the present study, it was demonstrated that silibinin treatment decreased the number of spontaneously contracting cardiac foci and cardiac cell areas differentiated from ES cells as well as contraction frequency and frequency of calcium (Ca2+) spiking. In contrast, angiotensin II (Ang II) treatment stimulated cardiomyogenesis as well as contraction and Ca2+ spiking frequency, which were abolished in the presence of silibinin. Intracellular Ca2+ transients elicited by Ang II in rat smooth muscle cells were not impaired upon silibinin treatment, excluding the possibility that the compound acted on the AT1 receptor. Ang II treatment activated extracellular signal-regulated kinase 1/2 (ERK1/2), c-Jun NH2-terminal kinase (JNK), and p38 mitogen-activated protein kinase (MAPK) pathways in embryoid bodies which were abolished upon silibinin pretreatment. In summary, our data suggest that silibinin inhibits cardiomyogenesis of ES cells by interfering with Ang II signaling downstream of the AT1 receptor.

An introductory lecture will be given on the latest developments in stem cell research

سلبنين يحقز ع تمايز الاوعيه الدمويه وخلايا كريات الدم البيضاء عن طريق اشارات معينه NO-mediated and PI3K/AKT-STAT3- ومن جهة اخرى يمنع تمايز الخلايا القلبية خلال تثبيط مسار الانجوتونسين خلال اشارات معينه (ERK1/2, p38 & JNK)