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    Hemoglobin A1c-related histologic characteristics of symptomatic carotid plaques
    (Wolters Kluwer Medknow Publications, 2019) Tecellioglu, M.; Alan, S.; Kamisli, S.; Tecellioglu, F. S.; Kamisli, O.; Ozcan, C.
    Background: The aims of our study were to compare the histomorphological characteristics of carotid plaques and glycosylated hemoglobin (HbA1c), which are risk factors for ischemic stroke, in patients who underwent carotid endarterectomy for carotid artery stenosis. Moreover, we aimed to identify the structures that were histologically affected by symptomatic carotid plaques in cases with elevated HbA1c. Materials and Methods: A total of 64 patients who presented with ischemic stroke and had not previously been diagnosed with diabetes were retrospectively evaluated. All stroke risk factors were reviewed. Carotid plaques were graded separately by two different pathologists through microscopic assessment of the following parameters: plaque rupture, lipid core, fibrous cup thickness, inflammation, intraplaque hemorrhage, thrombus, calcification, necrotic core, and neovascularization. An HbA1c value <6.3% was accepted as normal or indicative of prediabetes (group 1), whereas patients with values ranging between 6.3-7.4%, 7.5-8.4%, and 8.4% were categorized into the effectively controlled (group 2), less effectively controlled (group 3), and uncontrolled (group 4) groups, respectively. Results: The mean age of the patients was 73.0 4.5 years in group 1, 69.7 2.3 years in group 2, 66.0 8.5 years in group 3, and 62.7 7.1 years in group 4. A negative correlation was present between age and HbA1c. Smoking, hypertension, low-density lipoprotein cholesterol levels, and triglyceride levels were not significantly different among the four groups. According to the HbA1c classifications, the fibrous cup thickness was 2.64 0.3 mm in group 1, 1.85 0.4 mm in group 2, 1.68 0.5 mm in group 3, and 1.45 0.6 mm in group 4. The fibrous cup became thinner as the HbA1c value increased. Other parameters of unstable carotid plaques did not differ among the HbA1c groups. Conclusions: Increased HbA1c values seem to contribute to plaque instability through the formation of a thin fibrous cup. Thus, of the carotid artery plaque parameters including fibrous cup thickness, plaque rupture, lipid core, inflammation, intraplaque hemorrhage, thrombus, calcification, necrotic core, and neovascularization, fibrous cup thickness is the only histomorphological feature that affected by HbA1c.
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    The silencing of PDGF-B pathway by Chitosan/siRNA nanoplexes in therapy of the experimental mesangial proliferative glomerulonephritis
    (Mary Ann Liebert, Inc, 2016) Salva, E.; Alan, S.; Yilmaz, I.; Turan, S. O.; Akbuga, J.
    [Abstract Not Available]
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    Thalidomide attenuates learning and memory deficits induced by intracerebroventricular administration of streptozotocin in rats
    (Taylor & Francis Ltd, 2013) Elcioglu, H. K.; Kabasakal, L.; Alan, S.; Salva, E.; Tufan, F.; Karan, M. A.
    Neuroinflammatory responses caused by amyloid beta (A beta) peptide deposits are involved in the pathogenesis of Alzheimer's disease (AD). Thalidomide has a significant anti-inflammatory effect by inhibiting TNF-alpha, which plays role in A beta neurotoxicity. We investigated the effect of thalidomide on AD-like cognitive deficits caused by intracerebroventricular injection of streptozotocin (STZ). Intraperitoneal thalidomide was administered 1 h before the first dose of STZ and continued for 21 days. Learning and memory behavior was evaluated on days 17, 18 and 19, and the rats were sacrificed on day 21 to examine histopathological changes. STZ injection caused a significant decrease in the mean escape latency in passive avoidance and decreased improvement of performance in Morris water maze tests. Histopathological changes were examined using hematoxylineosin and Bielschowsky staining. Brain sections of STZ treated rats showed increased neurodegeneration and disturbed linear arrangement of cells in the cortical area compared to controls. Thalidomide treatment attenuated significantly STZ induced cognitive impairment and histopathological changes. Thalidomide appears to provide neuroprotection from the memory deficits and neuronal damage induced by STZ.