Biomedical subjects

Angel K Markov

Publications and source records attributed to Angel K Markov.

5 recordsLinked to original sources

PubMed2005

Einthoven's triangle: lead errors and an algorithm for solution.

The three bipolar leads (I, II, and III) of the 12-lead electrocardiogram are subject to technical errors that not only confound interpretation but may lead to faulty clinical actions. While some errors are readily recognized, even experienced electrocardiographers overlook others. This paper reviews the nature of limb lead errors and offers what we think is a generally useful method to deduce the observed, but erroneous, lead configurations.

Algorithms↗

PubMed2004

Fructose-1,6-diphosphate suppresses T-lymphocyte proliferation, promotes apoptosis and inhibits interleukins-1, 6, beta-actin mRNAs, and transcription factors expression.

The overall objective of this study was to determine the role fructose 1,6-diphosphate (FDP), a naturally occurring glycolytic intermediate, plays in activated T-lymphocytes. The hypothesis is twofold. First, we propose that FDP inhibits T cell proliferation to a greater extent than fructose-1-phosphate (F1P), fructose-6-phosphate (F6P) and mannose-6-phosphate (M6P); second, we argue that FDP suppresses immune activation by inhibiting inflammatory cytokine expression, inhibiting expression of key transcription factors, and by inducing apoptosis in immune cells. Rat spleen cells were incubated with concanavalin A (ConA) and increasing concentrations of FDP. Proliferation was determined by tritiated thymidine uptake. FDP inhibited splenocyte proliferation in a dose-related manner while F1P, F6P, M6P demonstrated inhibition only at high concentrations (5000 microg/ml). RNA was harvested from FDP and ConA-treated cells and IL-1 and IL-6 gene expression was analyzed by RT-PCR. IL-1 and IL-6 mRNA expression was completely inhibited at 500-5000 microg/ml FDP. Apoptosis in FDP-treated lymphocytes was determined by DNA fragmentation and flow cytometry. Propidium iodide (PI) staining demonstrated a 39% rate of apoptosis in splenocytes treated with ConA and 5000 microg/ml FDP. Extensive DNA fragmentation was present at 250-5000 microg/ml FDP, and maximal inhibition occurred at 5 microg/ml. F1P, F6P and M6P showed maximal inhibition only at 5000 microg/ml. Nuclear extracts from FDP-treated splenocytes were analyzed by electrophoretic mobility shift assay. ConA activation of NF-kappaB and AP-1 was dramatically inhibited by FDP. Interestingly, beta-actin showed extensive inhibition with FDP and ConA, thus suggesting new possibilities of its being used as a therapeutic modality in arterial injury where the beta-actin, an important cytoskeleton element, plays a very important role. These data indicate that FDP may be a useful immunosuppressive agent. In conclusion, FDP is not only an immunosuppressant but also an anti-inflammatory agent.

Actins↗

PubMed2003

Fructose diphosphate attenuates the acetaminophen-induced liver injury in the rat evidence for involvement of nitric oxide.

We have previously shown that fructose-1,6-diphosphate (FDP) stimulates the synthesis of nitric oxide probably by stimulating the hepatic inducible nitric oxide synthase (iNOS). The aim of the present study was to evaluate the hepatoprotective role of FDP in acetaminophen-induced liver injury and whether this hepatoprotective effect is mediated by nitric oxide. Liver injury was induced in adult Sprague-Dawley rats by the administration of acetaminophen (1.6 g/kg by gavage) 10 min prior to the intraperitoneal injection of either FDP or normal saline. Liver injury was assessed by alanine aminotransferase (ALT) activity in the serum. iNOS and malondialdehyde (MDA) levels were determined in liver homogenates. Acetaminophen produced striking elevations of serum ALT, high MDA levels and a profound decrease in the liver iNOS. Administration of FDP attenuated the ALT and MDA elevations and prevented the liver iNOS depletion caused by acetaminophen. Pretreatment of the animals with the iNOS inhibitor L-NAME abolished this hepatoprotection. These findings suggest that FDP protects against acetaminophen-induced liver injury, at least partly, by stimulating production of nitric oxide.

Acetaminophen↗

PubMed2002

Fructose-1,6-diphosphate alone and in combination with cyclosporine potentiates rat cardiac allograft survival and inhibits lymphocyte proliferation and interleukin-2 expression.

BACKGROUND: Fructose-1,6-diphosphate (FDP) reduces postischemic reperfusion injury and is used alone and in combination with cyclosporine A (CsA) as an immunosuppressant. METHODS: Wistar-Furth rat hearts were grafted to Lewis rats. Activated T-cell proliferation, viability, and interleukin-2 expression were determined. RESULTS: Mean survival in days were: saline 7.12+/-0.64, FDP 350 mg/kg perioperatively 13.5+/-1.4, FDP 350 mg/kg twice daily 11.4+/-0.75, CsA 2.5 mg/kg daily 12+/-0.81, CsA 5.0 mg/kg daily 12.4+/-0.81, CsA 2.5 mg/kg + FDP 350 mg/kg twice daily 17.6+/-0.4, and CsA 5 mg/kg + FDP 350 mg/kg twice daily 28.2+/-0.97. FDP maximally inhibits T-cell proliferation and concomitantly increases cell viability at 5,000 to 500 microg/mL, whereas CsA inhibits at 500 ng/mL. FDP completely inhibited interleukin-2 expression at 5,000 to 500 microg/mL, whereas CsA partially inhibited at 50 to 500 ng/mL. CONCLUSION: FDP + CsA prolongs cardiac survival and FDP inhibits T-cell proliferation.

Animals↗

PubMed2002

Prevention of alpha-naphthylthiourea-induced pulmonary edema with fructose-1,6-diphosphate.

Neutrophil-derived oxygen free radicals have been implicated in the pathogenesis of noncardiogenic pulmonary edema. Fructose-1,6-diphosphate (FDP) has been shown to inhibit oxygen free radicals production by activated neutrophils. Thus, we investigated whether FDP would attenuate formation of pulmonary edema in anesthetized dogs injected with alpha-naphthylthiourea (ANTU). Hemodynamic studies involved measurements of left ventricular systolic and end-diasystolic pressures (LVSP and LVEDP), pulmonary artery pressure (PaP), heart rate (HR), and cardiac output (CO). Mean wet weight to dry weight ratios of lung tissue samples were calculated. Following baseline measurements, dogs were injected intravenously (IV) with ANTU 5 mg / kg (n = 16) and 10 mg / kg (n = 8) and half of the dogs were randomly selected to receive 75 mg / kg FDP (10%) and subsequent infusion of 7 mg / kg / min. The rest were given 0.9% NaCl in the same manner. Four hours after ANTU administration, the animals were euthanatized. Except for decline in the CO (nonsignificant), no significant changes in systemic hemodynamics within and between the groups were noted. In the FDP group, PaP and pulmonary arteriolar resistance (PaR) remained unchanged. In the saline group, PaP increased from 12.5 +/- 2.44 to 21.8 +/- 3.14 mm Hg (P < .001) and PaR from 166 +/- 29 to 468 +/- 74 dynes. cm / sec(5) (P < .005). During the study LVDEP, PaO(2), PaCO(2), and hematocrit did not change significantly within and between the groups. The lungs mean wet weight to dry weight ratios for the sham-operated dogs were 4.20 +/- 0.41, for the FDP group 4.32 +/- 0.59 and 6.22 +/- 1.37 for the saline group (P < .0005). These data indicate that FDP protected the lung from ANTU-induced injury.

Animals↗