Blood and plasma viscosity are the major factors affecting blood flow and normal circulation. Whole blood viscosity is mainly affected by plasma viscosity, red blood cell deformability/aggregation and hematocrit, and other physiological factors. Thirty patients (twenty males + ten females) with age range 50–65 years, normotensive with history of cerebrovascular disorders, were selected according to the American Heart Stroke Association. Blood viscosity and other rheological parameters were measured after two-day abstinence from any medications. Dual effects of vinpocetine and pyritinol exhibit significant effects on all hemorheological parameters (P < 0.05), especially on low shear whole blood viscosity (P < 0.01), but they produced insignificant effects on total serum protein and high shear whole blood viscosity (P > 0.05). Therefore, joint effects of vinpocetine and pyritinol improve blood and plasma viscosity in patients with cerebrovascular disorders.

No abstract

Adipose tissue-derived serine protease inhibitor (vaspin), which has endocrine and local roles in atherosclerosis growth, is also synthesized by adipose tissue; it was found that vaspin was negatively correlated with blood pressure in obese patients, while vaspin levels were decreased in endothelial dysfunction. The aim of the present study was to determine rosuvastatin modulation effects on serum vaspin levels in acute coronary syndrome (ACS) with class I obesity. A total number of seventy patients with acute coronary syndrome previously and currently treated with rosuvastatin was compared to 40 patients with IHD not treated by rosuvastatin as a control. Vaspin serum levels were higher in rosuvastatin-treated patients with acute coronary syndrome compared to the patients with acute coronary syndrome not treated by rosuvastatin, p < 0.01. Additionally, in the rosuvastatin-treated group, patients with STEMI showed higher vaspin serum levels compared to NSTEMI p < 0.01. Conclusion: Rosuvastatin significantly increases vaspin serum levels in acute coronary syndrome.

Extracts of ginkgo biloba have been broadly prescribed toward advance symptoms of cognitive dysfunction ranging in severity from mild memory loss to dementia also; in delaying the development of dementia; ginkgo biloba has been encouraged commercially as a smart medicine to augment the brain function of healthy people. Piracetam is a no tropic remedy correlated to inhibitory γ-aminobutyric acid (GABA) neurotransmitter. Piracetam may be the initial agent acting on cognitive function without sedation. Thirty subjects (30 males) arbitrarily choose as of medical college students. The contributors were allowable to perform mutually on the psychomotor performance device tester and the computerized n-back test (working memory task) to obtain knowledge from those tests sooner than the commencing of the examination. All psychometric response time and working memory test parameters calculated previous to the experimental research, so the identical volunteers considered as control and through four days of receiving the ginkgo biloba 60mg/day (trunature GSL),piracetam 800 mg/day (neutrophil) or both drugs so the enrolled participants divided into three groups .Group A take ginkgo biloba, group B take piracetam and group C take piracetam and ginkgo biloba.Piracetam significantly improve cognitive and working memory at all levels P<0.05 while it showed insignificant effects on psychometric reaction time parameters except it ameliorate the total reaction time (TRT) P <0.05. The differential effects of ginkgo biloba showed significant effects on psychometric reaction time and cognitive central Integrity P<0.05 and insignificant effects on working memory accuracy except at level І-Back where it produced significant effects P<0.05. Combined effects of ginko biloba and piracetam on psychomotor performances, cognitive function and working memory produced significant effects P <0.05.Conclusion: Combined effects of piracetam and ginkgo biloba produced more significant effects than either ginkgo biloba or piracetam alone on cognitive function and working memory.

The p53 gene is also known as tumor suppressor p53. The main functions of the p53 gene are an anticancer effect and cellular genomic stability via various pathways including activation of DNA repair, induction of apoptosis, and arresting of cell growth at the G1/S phase. Normally, the p53 gene is inactivated by mouse double minute 2 proteins (mdm2), but it is activated in chronic myeloid leukemia (CML). Tyrosine kinase inhibitors are effective chemotherapeutic agents in the management of CML. The purpose of the present study was to evaluate the differential effect of imatinib and nilotinib on p53 gene serum levels in patients with CML. A total number of 60 patients with chronic myeloid leukemia with ages ranging from 47 to 59 years were recruited from the Iraqi Hematology Center. They started with tyrosine kinase inhibitors as first-line chemotherapy. They were divided into two groups—Group A, 29 patients treated with imatinib and Group B, 31 patients treated with nilotinib—and compared with 28 healthy subjects for evaluation p53 serum levels regarding the selective effect of either imatinib or nilotinib. There were significantly (p < 0.01) high p53 gene serum levels in patients with CML (2.135 ± 1.44 ng/mL) compared to the control (0.142 ± 0.11 ng/mL). Patients with CML that were treated with either imatinib or nilotinib showed insignificant differences in most of the hematological profile (p > 0.05) whereas, p53 serum levels were high (3.22 ± 1.99 ng/mL) in nilotinib-treated patients and relatively low (1.18 ± 0.19 ng/mL) in imatinib-treated patients (p = 0.0001). Conclusions: Nilotinib is more effective than imatinib in raising p53 serum levels in patients with chronic myeloid leukemia.