Factor V Leiden mutation and its relation to left atrial thrombus in chronic nonrheumatic atrial fibrillation

The genetic defect of coagulation factor V, known as factor V Leiden, produces a resistance to degradation by activated protein C and increased venous thrombosis. However, the role of factor V Leiden in the formation of left atrial thrombus with nonrheumatic atrial fibrillation has not been studied. We investigated whether factor V Leiden is a risk factor for left atrial thrombus in patients with nonrheumatic atrial fibrillation. We analyzed clinical, echocardiographic, and biochemical data in 105 consecutive patients with nonrheumatic atrial fibrillation. These patients were divided into two groups: group A (n = 37) with left atrial thrombus and group B (n = 68) without left atrial thrombus. The study also included 42 control subjects. Left atrial thrombus was investigated by using both transthoracic echocardiography and transesophageal echocardiography. Blood samples from the patients and controls were analyzed for the factor V Leiden mutation by DNA analysis, using the polymerase chain reaction. There was no significant difference in the prevalence of factor V Leiden between the patients and control subjects. The prevalence of factor V Leiden mutation was 8.1% (3/37) in patients with left atrial thrombus, and 8.8% (6/68) in patients without left atrial thrombus. The prevalence of factor V Leiden was 7.1% (3/42) in control subjects. The prevalance of factor V Leiden was 10% (2/20) in patients with spontaneous echo contrast and 8% (7/85) in patients without spontaneous echo contrast. Multivariate analyses showed that left ventricular ejection fraction was an independent predictor of left atrial thrombus. Factor V Leiden mutation is not a risk factor for left atrial thrombus formation and spontaneous echo contrast in patients with nonrheumatic atrial fibrillation.     

Cytotoxic and Antibacteriial Actiivity of the Mixture of Olive Oil and Lime Cream in Vitro Conditions

The mixture of olive oil and lime cream has been traditionally used to treat external burns in the region of Hatay/Antakya and middle Anatolia. Olive oil and lime cream have been employed by many physicians to treat many ailments in the past. A limited number of studies have shown the antibacterial effect of olive oil and that it does not have any toxic effect on the skin. But we did not find any reported studies on the mixture of olive oil and lime cream. The aim of this paper is to investigate the cytotoxic and antibacterial activity of olive oil and lime cream individually or/and in combination in vitro conditions, by using disk-diffusion method and in cell culture. The main purpose in using this mixture is usually to clear burns without a trace. Agar overlay, MTT (Cytotoxicity assay) and antibacterial susceptibility tests were used to investigate the cytotoxic and antibacterial activity of olive oil and lime cream. We found that lime cream has an antibacterial activity but also cytotoxic on the fibroblasts. On the other hand olive oil has limited or no antibacterial effect and it has little or no cytotoxic on the fibroblasts. When we combined lime cream and olive oil, olive oil reduced its cytotoxic impact. These results suggest that mixture of olive oil and lime cream is not cytotoxic and has antimicrobial activity.     

Does cigarette smoke exposure lead to histopathological alterations in the olfactory epithelium? An electron microscopic study on a rat model

Objective: This study was conducted to examine the influence of smoke exposure of variable duration on the ultrastructure of and histopathologic and morphologic alterations in the olfactory epithelium.

Methods: A total of 24 Wistar albino rats were randomly assigned to three groups and fed a standard rat chow and tap water. Experimental rats in groups I and II were exposed to cigarette smoke in a glass cabin over a period of 2 months for 5 or 15 min, respectively, four times daily; control rats (group III) were not exposed to cigarette smoke. After dissection, all tissue specimens were processed using routine procedures for TEM.

Results: Groups I and II exhibited the presence of intraepithelial inflammatory cells and especially deep invaginations in the nuclear membrane of supporting cells. Extended intercellular spaces, cytoplasmic protrusions on the apical surface of supporting cells, atrophy of microvilli and olfactory neuron cilia as well as numerous electron-dense granular structures and lysosome-like structures were observed to an increasing degree from group I to group II. Particularly in group II, both supporting cells and olfactory neurons exhibited a cytoplasmic edema, mitochondrial degeneration, and numerous vacuolar structures, as well as apoptotic and minimal necrotic changes. In this group, hyperplasia of basal cells was also observed.

Conclusion: Our electron microscopic findings show that cigarette smoke leads to toxic degenerative changes in the rat olfactory mucosa.     

Hyperbaric oxygen therapy improves angiogenesis and bone formation in critical sized diaphyseal defects

Besides the use of autologous bone grafting several osteoconductive and osteoinductive methods have been reported to improve bone healing. However, persistent non‐union occurs in a considerable number of cases and compromised angiogenesis is suspected to impede bone regeneration. Hyperbaric oxygen therapy (HBO) improves angiogenesis. This study evaluates the effects of HBO on bone defects treated with autologous bone grafting in a bone defect model in rabbits. Twenty‐four New‐Zealand White Rabbits were subjected to a unilateral critical sized diaphyseal radius bone defect and treated with autologous cancellous bone transplantation. The study groups were exposed to an additional HBO treatment regimen. Bone regeneration was evaluated radiologically and histologically at 3 and 6 weeks, angiogenesis was assessed by immunohistochemistry at three and six weeks. The additional administration of HBO resulted in a significantly increased new bone formation and angiogenesis compared to the sole treatment with autologous bone grafting. These results were apparent after three and six weeks of treatment. The addition of HBO therapy to autologous bone grafts leads to significantly improved bone regeneration. The increase in angiogenesis observed could play a crucial role for the results observed. © 2015 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 33:513–520, 2015.     

Proline at the P2 position in protein C is important for calcium- mediated regulation of protein C activation and secretion

Protein C is a vitamin K-dependent plasma serine protease zymogen, which upon activation, functions as an anticoagulant. Protein C activation is catalyzed by a complex of thrombin (T) with thrombomodulin (TM). This activation is Ca(2+)-dependent, but Ca2+ inhibits protein C activation by thrombin alone. In most proteases, specificity is determined primarily by the residues that lie near the scissile bond. In protein C, the P2 position is Pro, whereas in the fibrinogen A chain, P2 is Val. We have expressed a Pro-->Val mutant of protein C (P168V) in mammalian cells. At saturating Ca2+, the P168V and wild-type proteins were activated by the T-TM complex equivalently, but half maximal rates of activation were obtained at 50 mumol/L Ca2+ for wild type and approximately 5 mmol/L Ca2+ for the P168V mutant. In the absence of TM, Ca2+ no longer inhibited the activation of the P168V mutant. These results indicate that Pro168 influences the Ca(2+)- dependent conformational changes in protein C that control activation. Recently, a patient with thrombotic complications has been identified with a Pro168-->Leu substitution. Both the P168V and the P168L mutation lead to impaired secretion caused by retention within the cell.