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1.

001-es BibID:BIBFORM014426
Első szerző:Lekli István (gyógyszerész)
Cím:Functional recovery of diabetic mouse hearts by glutaredoxin-1 gene therapy: role of Akt-FoxO-signaling network / I. Lekli, S. Mukherjee, D. Ray, N. Gurusamy, Young-Ho Kim, A. Tosaki, R. M. Engelman, Y-S. Ho, D. K. Das
Dátum:2010
ISSN:0969-7128
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Gene Therapy. - 17 : 4 (2010), p. 478-485. -
További szerzők:Mukherjee, Subhendu Ray, Diptarka Gurusamy, Narasimman Kim, Young-Ho Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész) Engelman, Richard M. Ho, Ye-Shih Das, Dipak Kumar
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2.

001-es BibID:BIBFORM042332
035-os BibID:PMID:7799644
Első szerző:Maulik, Nilanjana
Cím:Myocardial salvage by 1-O-hexadecyl-Sn-glycerol : possible role of peroxisomal dysfunction in ischemia reperfusion injury / Nilanjana Maulik, Arpad Tosaki, Richard M. Engelman, Gerald A. Cordis, Dipak K. Das
Dátum:1994
ISSN:0160-2446
Megjegyzések:A recent study demonstrated biochemical and structural alterations of peroxisomes in rat kidney after ischemia/reperfusion. We examined whether peroxisomes play any role in the pathophysiology of myocardial ischemia/reperfusion injury. Isolated perfused rat heart was made ischemic for 30 min by terminating coronary flow (CF), followed by 30-min reperfusion. Experiments were divided into two groups; the experimental group received 1-O-hexadecyl-Sn-glycerol (chimyl alcohol) (25, 50, and 100 microM) before ischemia, and the control group received an equivalent amount of saline. Two of the experimental groups (50 and 100 microM) demonstrated improved postischemic myocardial performance, as demonstrated by accelerated recovery in left ventricular developed pressure (LVDP) and CF, as well as reduction in the incidence of ventricular fibrillation (VF). However, because the heart rate (HR) was significantly reduced in the 100-microM chimyl alcohol group, subsequent studies were performed with 50 microM chimyl alcohol as the optimal dose. Chimyl alcohol (50 microM) also reduced cellular injury, as evidenced by reduced creatine kinase (CK) release, and decreased development of oxidative stress, as evidenced by reduced formation of malonaldehyde (MDA). Peroxisomal catalase activity was decreased in the control group after ischemia/reperfusion, and chimyl alcohol treatment restored the activity of the enzyme. Our results indicate that chimyl alcohol, a precursor of ether-linked phosphoglyceride biosynthesis, can reduce myocardial ischemia/reperfusion injury, possibly by restoring catalase activity and reducing oxidative stress through synthesis of ether lipids, suggesting a possible role of peroxisomal disorder in ischemia/reperfusion injury.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:Journal of Cardiovascular Pharmacology. - 24 : 3 (1994), p. 486-492. -
További szerzők:Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész) Engelman, Richard M. Cordis, Gerald A. Das, Dipak Kumar
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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3.

001-es BibID:BIBFORM041701
Első szerző:Maulik, Nilanjana
Cím:Myocardial salvage by chimyl alcohol : possible role of peroxisomal dysfunction in reperfusion injury / Maulik N., Tosaki A., Engelman R. M., Cordis G. A., Das D. K.
Dátum:1994
Megjegyzések:The results of this study suggest that reperfusion of ischemic myocardium may lead to the peroxisomal disorder both functionally and biochemically. An alkyl glycerol such as chimyl alcohol can protect the ischemic heart from the reperfusion injury probably by enhancing the plasmalogen synthesis.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Annals of the New York Academy of Sciences. - 723 (1994), p. 380-384. -
További szerzők:Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész) Engelman, Richard M. Cordis, Gerald A. Das, Dipak Kumar
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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4.

001-es BibID:BIBFORM042055
Első szerző:Nilanjana, Maulik
Cím:Lanthanum Provides Cardioprotection by Modulating Na+-Ca2+ Exchange / Maulik Nilanjana, Arpad Tosaki, Engelman Richard M., Chatterjee Gorachand, Das Dipak K.
Dátum:1996
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
HEM
Megjelenés:Annals of the New York Academy of Sciences. - 779 (1996), p. 546-550. -
További szerzők:Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész) Engelman, Richard M. Chatterjee, Gorachand Das, Dipak Kumar
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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5.

001-es BibID:BIBFORM042024
Első szerző:Tósaki Árpád (kísérletes farmakológus, gyógyszerész)
Cím:The Role of Protein Kinase C in Ischemic/Reperfused Preconditioned Isolated Rat Hearts / Tósaki Árpád, Maulik Nilanjana, Engelman Daniel T., Engelman Richard M., Das K. Dipak
Dátum:1996
Megjegyzések:Protein kinase C (PKC) has been implicated in the preconditioning-induced cardiac protection in ischemic/reperfused myocardium. We studied the effect of PKC inhibition with calphostin C (25, 50, 100, 200, 400, and 800 nM), a potent and specific inhibitor of PKC, in isolated working nonpreconditioned and preconditioned ischemic/reperfused hearts. In the nonpreconditioned groups, all hearts underwent 30 min of normothermic global ischemia followed by 30 min of reperfusion. In the preconditioned groups, hearts were subjected to four cycles of ischemic preconditioning by using 5 min of ischemia followed by 10 min reperfusion, before the induction of 30 min ischemia and reperfusion. At low concentrations of calphostin C (25, 50, and 100 nM), the PKC inhibitor had no effect on the incidence or arrhythmias or postischemic cardiac function in the nonpreconditioned ischemic/reperfused groups. With 200 and 400 nM of calphostin C, a significant increase in postischemic function and a reduction in the incidence of arrhythmias were observed in the nonpreconditioned ischemic/reperfused groups. Increasing the concentration of calphostin C to 800 NM, the recovery of postischemic cardiac function was similar to that of the drug-free control group. In preconditioned hearts, lower concentrations (< 100 nM) of calphostin C did not change the response of the myocardium to ischemia and reperfusion in comparison to the preconditioned drug-free myocardium. Two hundred and 400 nM of the PKC inhibitor further reduced the incidence of ventricular fibrillation (VF) from the preconditioned drug-free value of 50% to 0 (p < 0.05) and 0 (p < 0.05), respectively, indicating that the combination of the two, preconditioning and calphostin C, affords significant additional protection. Increasing the concentration of calphostin C to 800 nM blocked the cardioprotective effect of preconditioning (100% incidence of VF). The recovery of cardiac function was similarly improved at calphostin C doses of 200 and 400 nM and was reduced at 800 nM (p < 0.05). With 200 and 400 nM of calphostin C, both cytosolic and particulate PKC activity were reduced by approximately 40 and 60%, respectively, in both preconditioned and preconditioned/ischemic/reperfused hearts. The highest concentration of calphostin C (800 nM) resulted in almost a complete inhibition of cytosolic (100%) and particulate (85%) PKC activity correlated with the abolition of preconditioning-induced cardiac protection. In conclusion, calphostin C protects the ischemic myocardium obtained from intact animals, provides significant additional protection to preconditioning at moderate doses, and blocks the protective effect of preconditioning at high concentrations. The dual effects of calphostin C appear to be strictly dose and "enzyme inhibition" related.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
MSH
Megjelenés:Journal of Cardiovascular Pharmacology. - 28 : 5 (1996), p. 723-731. -
További szerzők:Maulik, Nilanjana Engelman, Daniel T. Engelman, Richard M. Das, Dipak Kumar
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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6.

001-es BibID:BIBFORM041709
035-os BibID:PMID:8906193
Első szerző:Tósaki Árpád (kísérletes farmakológus, gyógyszerész)
Cím:Effects of cromakalim and glibenclamide in ischemic and reperfused hearts / Arpad Tosaki, Richard M. Engelman, Dipak K. Das
Dátum:1996
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:Annals of the New York Academy of Sciences. - 793 (1996), p. 460-465. -
További szerzők:Engelman, Richard M. Das, Dipak Kumar
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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7.

001-es BibID:BIBFORM041708
035-os BibID:PMID:7752071
Első szerző:Tósaki Árpád (kísérletes farmakológus, gyógyszerész)
Cím:Alpha-1 adrenergic receptor agonist-induced preconditioning in isolated working rat hearts / Arpad Tosaki, Nadeem S. Behjet, Daniel T. Engelman, Richard M. Engelman, Dipak K. Das
Dátum:1994
Megjegyzések:The aim of this study was to determine whether pharmacologic preconditioning, without a short episode of myocardial hypoxia or ischemia, could improve myocardial function after a prolonged period of ischemia. Isolated rat hearts were perfused with .01, .1 or 1 mg/L of phenylephrine for 5 min followed by a 10-min washout period (preconditioning) before the induction of 30 min of normothermic global ischemia and 30 min of reperfusion. Hearts preconditioned with increasing concentrations of phenylephrine (an alpha-1 adrenergic receptor agonist) produced a reduction in the incidence of reperfusion-induced ventricular fibrillation (VF) and ventricular tachycardia (VT). Preconditioning of the hearts with the highest dose of phenylephrine (1.0 mg/L), after 30 min of ischemia, reduced the incidence of reperfusion-induced VF and VT from their nonpreconditioned control values of 87% and 100% to 33% (P < .05) and 50% (P < .05), respectively. After 30 min of ischemia, the recovery of myocardial function was significantly improved in phenylephrine-preconditioned groups. Thus, .1 and 1.0 mg/L of phenylephrine increased aortic flow from its nonpreconditioned control value of 10.8 +/- .9 ml/min to 22.4 +/- 2.4 ml/min (P < .05) and 26.5 +/- 1.5 ml/min (P < .05), respectively. Phenylephrine (1.0 mg/L) preconditioning significantly reduced ischemia/reperfusion-induced tissue Na+ and Ca2+ gains and prevented K+ and Mg2+ loss measured by an atomic absorption spectro-photometer. Our results show that alpha-1 adrenergic stimulation (preconditioning) can prevent postischemic abnormalities in intracellular ions, reperfusion arrhythmias, and contractile function without the inhibition of O2 delivery.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:The Journal of Pharmacology and Experimental Therapeutics. - 273 : 2 (1994), p. 689-694. -
További szerzők:Behjet, Nadeem S. Engelman, Daniel T. Engelman, Richard M. Das, Dipak Kumar
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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8.

001-es BibID:BIBFORM041707
035-os BibID:PMID:8531071
Első szerző:Tósaki Árpád (kísérletes farmakológus, gyógyszerész)
Cím:Diabetes and ATP-sensitive potassium channel openers and blockers in isolated ischemic/reperfused hearts / Arpad Tosaki, Daniel T. Engelman, Richard M. Engelman, Dipak K. Das
Dátum:1995
Megjegyzések:The incidence of reperfusion ventricular fibrillation (VF) and tachycardia (VT), heart function and the maldistribution of cardiac cations were studied in isolated ischemic/reperfused hearts obtained from streptozotocin-induced diabetic rats. Effects of an ATP-sensitive potassium (KATP) channel opener, cromakalim, and a KATP channel blocker, glibenclamide, also were studied. After 2 and 8 weeks of diabetes, hearts were isolated and subjected to 30 min of ischemia followed by reperfusion. After 2 weeks of diabetes, the incidence of VF and VT was reduced from their nondiabetic control values of 100 and 100 to 42% (P < .05) and 50% (P < .05), respectively. The reduction in VF and VT was not observed with progressive diabetes and after 8 weeks cardiac failure developed. In the 8-week diabetics, the development of cardiac failure was reflected in the aggravation of heart function (26, 16 and 17% reductions in aortic flow, left ventricular developed pressure and first derivative of developed pressure, respectively), and ion shifts (56 and 71% accumulation in cellular Na+ and Ca++, respectively, and 15% loss in cell K+) before the induction of ischemia. After ischemia/reperfusion, these changes were pronounced in diabetic groups. Cromakalim aggravated and glibenclamide attenuated the incidence of arrhythmias, contractile function and ion shifts induced by ischemia/reperfusion in diabetic hearts. The data show that the use of KATP channel openers as anti-ischemic agents may be of particular concern in the population of postinfarction diabetic patients who are known to be at high risk of sudden coronary death.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:The Journal of Pharmacology and Experimental Therapeutics. - 275 : 3 (1995), p. 1115-1123. -
További szerzők:Engelman, Daniel T. Engelman, Richard M. Das, Dipak Kumar
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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9.

001-es BibID:BIBFORM041704
035-os BibID:PMID:7921376
Első szerző:Tósaki Árpád (kísérletes farmakológus, gyógyszerész)
Cím:Ginkgo biloba extract (EGb 761) improves postischemic function in isolated preconditioned working rat hearts / Arpad Tosaki, Daniel T. Engelman, Tibor Pali, Richard M. Engelman, Marie-Therese Droy-Lefaix
Dátum:1994
ISSN:0954-6928
Megjegyzések:We studied the effect of preconditioning and Gikgo biloba extract (EGb 761) in relation to the recovery of contractile function after global ischemia in the isolated working rat heart. METHODS: Hearts (n = 12 in each group) were randomly divided into five groups: In group I, hearts were subjected to 30 min of normothermic global ischemia followed by 30 min of reperfusion; in group II, they were subjected to one cycle of preconditioning consisting of 5 min ischemia and 10 min reperfusion before the induction of 30 min of ischemia and 30 min of reperfusion; group III hearts underwent two cycles of preconditioning; group IV hearts underwent three cycles of preconditioning; and group hearts underwent four cycles of preconditioning before the onset of 30 min ischemia followed by 30 min of reperfusion. RESULTS: Ventricular fibrillation (total) and ventricular tachycardia (no preconditioning) both fell from 100% to 50% (P < 0.05) after four cycles of preconditioning. In relation to ventricular fibrillation, preconditioning significantly reduced the formation of oxygen free radicals, measured by electron spin resonance spectroscopy (ESR), but recovery of cardiac function was low in all preconditioned groups. Because of the relatively low incidence of arrhythmias (50% ventricular fibrillation and 50% ventricular tachycardia) and relatively low cardiac function in Group V, EGb 761, a free-radical scavenger, was chosen to improve myocardial contractile function in preconditioned hearts. Fifty and 100 mg/kg of EGb 761 (per os) significantly improved coronary flow, aortic flow, left ventricular developed pressure (LVDP), and the first derivative of LVDP (LVDdP/dtmax) in the four-cycle preconditioned group. Thus, after 30 min of reperfusion, aortic flow was improved from 11.6 +/- 0.9 ml/min to 19.7 +/- 1.2 ml/min (P < 0.05) with a dose of 50 mg/kg of EGb 761 and to 22.0 +/- 1.5 ml/min (P < 0.05) with a dose 100 mg/kg of EGb 761, in the four-cycle preconditioned group. During reperfusion, the formation of free radicals was reduced by approximately 50 and 60% using 50 mg/kg and 100 mg/kg of EGb 761, respectively, when compared with the four-cycle preconditioned drug-free control group. CONCLUSION: We have demonstrated that EGb 761 can improve contractile function after global ischemia in the isolated working rat heart by reducing the formation of oxygen free radicals, and we have shown that this protection is additive to that of ischemia-induced preconditioning.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:Coronary Artery Disease 5 : 5 (1994), p. 443-450. -
További szerzők:Engelman, Daniel T. Pali Tibor Engelman, Richard M. Droy-Lefaix, Marie-Thérèse
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10.

001-es BibID:BIBFORM041702
Első szerző:Tósaki Árpád (kísérletes farmakológus, gyógyszerész)
Cím:Extracellular Magnesium Manipulation Reduces Reperfusion Arrhythmias and Ion Shifts in Isolated Rat Hearts / Tosaki A., Engelman R. M., Das D. K.
Dátum:1994
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Annals of the New York Academy of Sciences. - 723 (1994), p. 385-388. -
További szerzők:Engelman, Richard M. Das, Dipak Kumar
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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11.

001-es BibID:BIBFORM041700
Első szerző:Tósaki Árpád (kísérletes farmakológus, gyógyszerész)
Cím:Effects of preconditioning on reperfusion arrhythmias, myocardial functions, formation of free radicals, and ion shifts in isolated ischemic/reperfused rat hearts / Tosaki A., Cordis G. A., Szerdahelyi P., Engelman R. M., Das D. K.
Dátum:1994
ISSN:0160-2446
Megjegyzések:The effects of preconditioning on development of reperfusion-induced ventricular fibrillation (VF), ventricular tachycardia (VT), free radical formation, and ion shifts, particularly those of Na, K, Ca, and Mg, were studied in isolated rat heart. Hearts were randomly divided into four groups: group I, aerobically perfused time-matched controls with no preconditioning or ischemia; group II, hearts subjected to 30-min global ischemia followed by 30-min reperfusion; group III, hearts subjected to one cycle of preconditioning, consisting of 5-min global ischemia plus 10-min reperfusion, followed by 30-min global ischemia plus 30-min reperfusion; and group IV, hearts subjected to four cycles of preconditioning (5-min ischemia plus 10-min reperfusion) followed by 30-min ischemia plus 30-min reperfusion. The incidences of VF and VT were reduced from their nonpreconditioned ischemic values of 100 and 100% in group II to 83 and 92% in group III and to 33% (p < 0.05) and 41% (p < 0.05) in group IV, respectively. Maximum malondialdehyde formation, as an indirect marker of free radicals, was observed after 30-min ischemia followed by 10-min reperfusion (0.72 +/- 0.1 nmol/ml) in the nonpreconditioned ischemic group (protocol II). One and four cycles of preconditioning reduced formation of malondialdehyde from the nonpreconditioned ischemic value of 0.72 +/- 0.1 to 0.35 +/- 0.02 and 0.26 +/- 0.02 nmol/ml (p < 0.05), respectively. The same trend was observed when free radical formation was directly detected by salicylic acid
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Journal Of Cardiovascular Pharmacology. - 23 : 3 (1994), p. 365-373. -
További szerzők:Cordis, Gerald A. Szerdahelyi Péter Engelman, Richard M. Das, Dipak Kumar
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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12.

001-es BibID:BIBFORM041692
Első szerző:Tósaki Árpád (kísérletes farmakológus, gyógyszerész)
Cím:Effects of extracellular magnesium manipulation on reperfusion-induced arrhythmias and myocardial ion shifts in isolated ischemic reperfused rat hearts / Tosaki A., Szerdahelyi P., Engelman R. M., Das D. K.
Dátum:1993
ISSN:0022-3565
Megjegyzések:Isolated rat hearts were subjected to global ischemia followed by reperfusion, and a reduction in the incidence of reperfusion-induced ventricular fibrillation and ventricular tachycardia was brought about by increasing the extracellular Mg concentration in the perfusion buffer. Thus the incidence of ventricular fibrillation was reduced from its control value of 100% in 1.2 mM Mg to 83% by 2.4 mM Mg (P = N.S.), to 42% by 3.6 mM Mg (P < .05), to 17% by 4.8 mM Mg (P < .001) and to 17% by 9.6 mM Mg (P < .001). The corresponding values for ventricular tachycardia were 100% (control, 1.2 mM Mg) vs. 92% (P = N.S.), 50% (P < .05), 25% (P < .01) and 25% (P < .01), respectively. In further studies, extracellular Ca was reduced by 50% (1.2 mM) in the perfusion buffer just before ischemia and during reperfusion. The incidence of ventricular fibrillation was reduced from its control value of 83% in 1.2 mM Mg to 75% by 1.8 mM Mg (P = N.S.), to 33% by 2.4 mM Mg (P < .05), to 17% by 3.6 mM Mg (P < .01) and to 8% by 4.8 mM Mg (P < .01). The incidence of ventricular tachycardia followed the same pattern. Myocardial Na, K, Ca and Mg were measured by atomic absorption spectrophotometer after the removal of ions from the extracellular space. In controls, 30 min of ischemia resulted in 3- and 4-fold accumulation of myocardial Na and Ca, respectively, and during reperfusion these values were similar to the values for 30-min ischemia.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Journal Of Pharmacology And Experimental Therapeutics. - 267 : 3 (1993), p. 1045-1053. -
További szerzők:Szerdahelyi Péter Engelman, Richard M. Das, Dipak Kumar
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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