Does LDL-C Estimation Using Anandaraja’s Formula Give a Better Agreement with Direct LDL-C Estimation than the Friedewald’s Formula?

Estimation of low density lipoprotein cholesterol (LDL-C) is crucial in management of coronary artery disease patients. Though a number of homogenous assays are available for estimation of LDL-C, use of calculated LDL-C by Friedewald’s formula (FF) is common in Indian laboratories for logistic reasons. Recently Anandaraja and colleagues have derived a new formula for calculating LDL-C. This formula needs to be evaluated before it is extensively applied in diagnosis. We measured LDL-C by homogenous method (D-LDL-C) in 515 fasting samples. Friedewald’s and Anandaraja’s formulas were used for calculation of LDL-C (F-LDL-C and A-LDL-C, respectively). The mean LDL-C levels were 123.3 ± 53.2, 112.4 ± 50.2 and 109.2 ± 49.8 mg/dl for D-LDL-C, F-LDL-C and A-LDL-C, respectively. There was a statistically significant difference between the results (P > 0.001) obtained by calculation formulas compared to the measured LDL-C. There was underestimation of LDL-C by 10.8 and 14 mg/dl by Friedewald’s and Anandaraja’s formulas respectively. The Pearson’s correlation between F-LDL-C and D-LDL-C was 0.931 and that between A-LDL-C and D-LDL-C was 0.930. Bland–Altman graphs showed a definite agreement between mean and differences of the calculation formulas and direct LDL-C with 95% of values lying with in ±2 SD limits. The mean percentage difference (calculated as {(Calculated LDL-C)-(D-LDL-C)}/D-LDL-C × 100) for F-LDL-C was maximum (−11.6%) at HDL-C ≥ 60 mg/dl and TG levels of 200–300 mg/dl (−10.4%) compared to D-LDL-C. A-LDL-C results gave highest mean percentage difference at total cholesterol concentrations <100 mg/dl (−37.3%) and HDL-C < 40 mg/dl (−17.1%), respectively. The results of our study showed that FF is better in agreement with D-LDL-C than Anandaraja’s formula for estimation of LDL-C by calculation though both lead to its underestimation.     

Nanotechnology: A Revolution in Cancer Diagnosis

Nanotechnology has brought revolution in cancer detection and treatment. It has capability to detect even a single cancerous cell in vivo and deliver the highly toxic drugs to the cancerous cells. Nanoshells, carbon nanotubes, quantum dots, supermagnetic nanoparticles, nano wires, nanodiamonds, dandrimers, and recently synthesized nanosponges are some of the materials used for cancer detection. Using specific cross linkers, such as specific antibodies against cancer cells individual cancer cells can be located. With the aid of a novel set of lipid-coated, targeted quantum dots a method for quantifying multiple specific biomarkers on the surfaces of individual cancer cells was also developed. This approach to quantitative biomarker detection stands to improve the histopathology methods used to diagnosis pancreatic and other cancers and enable the development of methods to spot cancer cells circulating in the blood stream. Certain nano materials can also deliver cancer drugs at the site so the drug toxicity can also be reduced.     

Silver Nano Particles Prevent Platelet Adhesion on Immobilized Fibrinogen

Vascular thrombotic disorders have emerged as a serious threat to our society. Platelet adhesion to fibrinogen, collagen and other platelet activators exposed over the atherosclerotic plaques can trigger platelet signaling events, activate platelets and lead to thrombotic events. Since anticoagulant and thrombolytic treatment strategies are usually associated with serious bleeding complications, preventing platelets adhesion may help to maintain platelets in an inactive state. In this study we tried to find out the effect of Silver nanoparticles, through their interaction with various platelet surface integrins on platelet adhesion on immobilized fibrinogen. Platelets, isolated from anti-coagulated human whole blood sample from healthy donors, were suspended in physiological buffer and each sample was divided into four tubes. In three of them 0.05, 0.5, and 5 μM concentrations of Silver nanoparticles were added, fourth tube served as control. Platelet adhesion on immobilized fibrinogen matrices and integrin mediated cell signaling events were studied in all the four samples. In the present study we show that nanosilver prevent platelet adhesion without conferring any lytic effect on them and effectively prevents integrin-mediated platelet responses in a concentration-dependent manner.     

Kinetic analysis of LDL oxidation in IHD and IHD risk subjects in Indian population

High plasma concentration of low-density lipoprotein (LDL) is associated with increased risk of atherosclerosis. Modified forms of LDL, especially oxidized LDL play a major role in its pathogenesis. This article gives detailed insight into the kinetics ofin vitro LDL oxidation by copper at different concentrations in normal and high-risk group subjects. Basal level of oxidatively modified LDL was significantly higher in ischaemic heart disease (IHD) and IHD hyperlipidemic subjects compared to normolipidemic and, hyperlipidemic control subjects, respectively. Derivatization of amino groups of apo-lipoprotein as monitored by estimating free amino groups concentration, was significantly higher in high-risk group and established IHD cases. Kinetics of oxidation was studied with two different concentrations of CuSO₄ (2.5 mM and 7.5 mM). thiobarbituric acid reactive substances (TBARS) level increases with time, and up to 95% oxidation was observed in 8 hr. About 60–65% less free amino groups were observed in native-LDL isolated from IHD patients compared to normal subjects. Study also showed an increase in two oxidative products studied, 20α-OH-cholesterol and 4-cholesten-3-one with oxidation time accompanied by corresponding decrease in LDL cholesterol. Increase in oxidative species was more evident in high-risk group and IHD patient. Basal level of oxidatively modified LDL measured in terms of TBARS was significantly higher in present study, strongly support that the extent of LDL oxidation monitored as TBARS and FAG level in circulating-LDL could be used as risk marker for high risk group.     

Pro-oxidant and anti-oxidant status in patients of sickle cell anaemia

The role of oxidant damage to red cells in sickle cell anaemia has been of interest in recent years. Although, available reports suggest that sickle cell erythrocytes are susceptible to endogenous free radical mediated oxidant damage there remains discrepancy in the status of antioxidant enzymes and antioxidant vitamins in these patients. In view of this, 107 cases of sickle cell anaemia (36 ‘SS’ and 71 ‘AS’ pattern—as confirmed by haemoglobin electrophoresis) were subjected to analysis of malondialdehyde, ascorbic acid, superoxide dismutase and albumin. The results were compared with 54 age and sex matched healthy controls. The results indicate a marked increase in lipid peroxidation and superoxide dismutase levels in both ‘SS’ and ‘AS’ types of sickle cell anaemia as compared to controls. Although no difference was observed in the levels of albumin in these groups the levels of ascorbic acid were significantly depleted in sickle cell anaemia patients. The results are indicative of enhanced lipid peroxidation along with imbalance in the pro-oxidant and antioxidant status in patients of sickle cell anaemia.     

Hypoxia-Induced Inflammatory Chemokines in Subjects with a History of High-Altitude Pulmonary Edema

High altitude hypoxia is known to induce an inflammatory response in immune cells. Hypoxia induced inflammatory chemokines may contribute to the development of high altitude pulmonary edema (HAPE) by causing damage to the lung endothelial cells and thereby capillary leakage. In the present study, we were interested to know whether chronic inflammation may contribute to HAPE susceptibility. We examined the serum levels of macrophage inflammatory protein-1α (MIP-1α), monocyte chemoattractant protein-1 (MCP-1) and interleukin-8 in group (1) HAPE Susceptible subjects (n = 20) who had past history of HAPE and group (2) Control (n = 18) consist of subjects who had stayed at high altitude for 2 years without any history of HAPE. The data obtained confirmed that circulating MCP-1, MIP-1α were significantly upregulated in HAPE-S individuals as compared to the controls suggestive of chronic inflammation. However, it is not certain whether chronic inflammation is cause or consequence of previous episode of HAPE. The moderate systemic increase of these inflammatory markers may reflect considerable local inflammation. The existence of enhanced level of inflammatory chemokines found in this study support the hypothesis that subjects with past history of HAPE have higher baseline chronic inflammation which may contribute to HAPE susceptibility.