Open Peer to Peer Technologies

Peer-to-peer applications allow us to separate out the concepts of authoring information and publishing that same information. It allows for decentralized application design, something that is both an opportunity and a challenge. All the peer-to-peer applications, in various ways, return the content, choice, and control to ordinary users. Tiny end points on the Internet, sometimes even without knowing each other, exchange information and form communities. In these applications there are no more clients and servers, instead the communication takes place between cooperating peers. There are many applications nowadays which are being labeled as peer-to-peer. A way to examine the distinction of whether an application is peer-to-peer or not is to check on the owner of the hardware that the service runs on. Like Napster, if the huge part of the hardware that Napster runs on is owned by the Napster users on millions of desktops then it is peer-to-peer. Peer-to-peer is a way of decentralizing not only features, but costs and administration also. By decentralizing data and therefore redirecting users so they download data directly from other user's computers, Napster reduced the load on its servers to the point where it could cheaply support tens of millions of users. The same principle is used in many commercial peer-to-peer systems. In short peer-to-peer cannot only distribute files. It can also distribute the burden of supporting network connections. The overall bandwidth remains the same as in centralized systems, but bottlenecks are eliminated at central sites and equally importantly, at their ISPs. Search techniques are important to making peer-to-peer systems useful. But there is a higher level of system design and system use. Topics like trust, accountability and metadata have to be handled before searching is viable

Evaluation of diastolic function in hypertensive using echocardiography

Background: Heart failure is one of the most common causes of cardiovascular morbidity along with mortality and hypertension is the most common cause of cardiac failure. Recent studies have shown that isolated diastolic dysfunction very often accompanies hypertensive heart disease. Aims: The present study was conducted to identify the risk of cardiac failure in hypertensive individuals by evaluating diastolic function using mitral inflow velocities of echocardiography.Methods: Subjects attending cardiology outpatient department for master health check up with age between 25 to 80 years were selected. The procedure was explained and consent was obtained from the subjects. All the subjects underwent a detailed clinical examination. Height, weight and blood pressure of the subjects was measured and BMI was calculated. Two-dimensional Doppler echocardiographic examinations were performed with an ultrasonographic system (Philips iE 133 Echo Doppler). The student t test, chi square test and logistic regression analysis were used to find the influence of ejection fraction and heart rate on diastolic function.Results: The trans-mitral inflow parameters on Doppler echocardiography such as E wave deceleration time (DT), isovolumetric relaxation time (IVRT) and early to late transmitral peak flow velocities ratio (E/A) were significantly different in hypertensive subjects on treatment having normal ejection fraction, when compared to normotensive subjects. We observed a decrease in E/A ratio and increase in DT, IVRT with hypertension.Conclusions: From the present study it can be concluded that hypertension is significantly associated with diastolic dysfunction of heart, even in subjects with normal systolic function.

Secoisolariciresinol Diglucoside: Relevance to Angiogenesis and Cardioprotection against Ischemia-Reperfusion Injury

ABSTRACT Therapeutic angiogenesis represents a novel approach for the prevention and treatment of ischemic heart disease. This study examined a novel method of stimulating myocardial angiogenesis using secoisolariciresinol diglucoside (SDG), a plant lignan isolated from flaxseed. SDG has been shown to decrease serum cholesterol and reduce the extent of atherosclerosis. In the present study, the angiogenic properties of SDG were investigated in three different models. First, in the in vitro model, human coronary arteriolar endothelial cells (HCAEC) treated with SDG (50 and 100 M) showed a significant increase in tubular morphogenesis compared with control. Western blot analysis indicated an increased expression of vascular endothelial growth factor (VEGF), kinase insert domain-containing receptor (KDR), Flt-1, angiopoietin-1 (Ang-1), Tie-1, and phosphorylated endothelial nitric oxide synthase (p-eNOS) in the SDG-treated cells. Second, in the ex vivo ischemia/reperfusion model, SDG-treated rats (20 mg/kg b.wt./day for 2 weeks orally) showed an increased level of aortic flow and functional recovery after 2 h of reperfusion following 30 min of ischemia compared with the control group [dP/dt (mm Hg/s) of 2110 Ϯ 35 versus 1752 Ϯ 62]. SDG reduced infarct size compared with the control group by 32% (38 versus 26%) and also decreased cardiomyocyte apoptosis. Increased protein expression of VEGF, Ang-1, and p-eNOS was also observed in the SDGtreated group. Third, in the in vivo myocardial infarction model, SDG increased capillary density and myocardial function as evidenced by increased fractional shortening and ejection fraction. In conclusion, these results suggest that SDG has potent angiogenic and antiapoptotic properties that may contribute to its cardioprotective effect in ischemic models. Ischemic heart disease develops as a consequence of coronary atherosclerotic lesion formation. Coronary collateral vessels and microvascular angiogenesis develop as adaptive responses to myocardial ischemia, which ameliorates the function of the damaged heart. Modulation of adaptive response to ischemic heart disease has become a major focus of current research. Therapeutic coronary angiogenesis (sprouting of new vessels at the capillary level) and collateralization (opening of pre-existing vessels) have tremendous therapeutic potential as strategies for treatment of patients with ischemic heart disease, along with traditional coronary interventional therapies such as coronary artery bypass graft (CABG) and percutaneous transluminal coronary intervention (PTCI). Angiogenesis is a complex process that requires growth factors such as vascular endothelial growth factor (VEGF) and the angiopoietin (Ang) systems that directly or indirectly affect the endothelial cells and produce proliferation and differentiation. VEGF is one of the critical factors involved in mobilization and induction of mitosis in endothelial progenitor cells Article, publication date, and citation information can be found a

Targeting inflammation after myocardial infarction

Purpose of review: Inflammation plays a key role in clearing cellular debris and recovery after acute myocardial infarction (AMI). Dysregulation of or prolonged inflammation may result in adverse cardiac remodeling and major adverse clinical events (MACE). Several pre-clinical studies and moderate sized clinical trials have investigated the role of immunomodulation in improving clinical outcomes in patients with AMI.Recent findings: Clinical data from the Canakinumab Atherothrombosis Outcome (CANTOS) and Colchicine Cardiovascular Outcomes Trial (COLCOT) have provided encouraging results among patients with AMI. Several other clinical and pre-clinical trials have brought about the prospect of modulating inflammation at various junctures of the inflammatory cascade including inhibition of complement cascade, interleukins, and matrix metalloproteinases. In patients with AMI, modulation of residual inflammation via various inflammatory pathways and mediators may hold promise for further reducing MACE. Learning from current data and understanding the nuances of immunomodulation in AMI are key for future trials and before widespread dissemination of such therapies

Resveratrol alleviates cardiac dysfunction in streptozotocin-induced diabetes: Role of nitric oxide, thioredoxin, and heme oxygenase

Excessive oxidative stress has been implicated in the pathology and complications of diabetes, which leads to myocardial ischemia reperfusion injury. The present study was designed to examine whether resveratrol (trans-3,5,4′-trihydroxystilbene), a polyphenolic compound present in red wine has a direct cardioprotective effect on diabetic myocardium. Resveratrol (2.5 mg/kg body wt/day) and L-NAME (25 mg/kg body wt/day) were administered orally for 15 days to streptozotocin (65 mg/kg)-induced diabetic rats. Sprague Dawley rats were divided into 5 groups: (i) control, (ii) diabetic, (iii) diabetic + resveratrol, (iv) diabetic + resveratrol + L-NAME (nitric oxide synthase inhibitor), and (v) diabetic + L-NAME. In our present study resveratrol demonstrated significant reduction in glucose level in diabetic rats. After the treatment, the hearts were excised and subjected to 30 min of global ischemia followed by 2 h of reperfusion. Resveratrol-treated diabetic rats demonstrated significant reduction in glucose levels as compared to the nontreated diabetic animals, and improved left ventricular function throughout reperfusion compared to the diabetic or L-NAME- treated animals (dp/dtmax 1457 ± 51 vs 999 ± 44 mm Hg/s at 120 min reperfusion). Cardioprotection from ischemic injury in resveratrol-treated diabetic rats showed decreased infarct size (42% vs 51%) and cardiomyocyte apoptosis (35% vs 40%) as compared with diabetic animals. Resveratrol produced significant induction of p-AKT, p-eNOS, Trx-1, HO-1, and VEGF in addition to increased activation of MnSOD activity in diabetic animals compared to nondiabetic animals. However treatment with L-NAME in resveratrol-treated and nontreated diabetic animals demonstrated significant downregulation of the above-noted protein expression profile and MnSOD activity. In the present study we found that the mechanism(s) responsible for the cardioprotective effect of resveratrol in the diabetic myocardium include upregulation of Trx-1, NO/HO-1, and VEGF in addition to increased MnSOD activity and reduced blood glucose level. Thus this study shows a novel mechanism of pharmacological preconditioning with resveratrol in the diabetic myocardium