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1.

001-es BibID:BIBFORM041168
035-os BibID:PMID:12409985
Első szerző:Cui, Jianhua
Cím:Cardioprotection with grapes / Jianhua Cui, Bela Juhasz, Arpad Tosaki, Nilanjana Maulik, Dipak K. Das
Dátum:2002
Megjegyzések:Epidemiologic studies suggest that mild-to-moderate wine consumption is associated with a reduced incidence of mortality and morbidity from coronary heart disease. Because wines are produced from grapes, this study was done to determine whether the grapes were equally cardioprotective. Sprague-Dawley male rats were given (orally) standardized grape extract (SGE) (obtained from the California Table Grape Commission, Fresno, CA, U.S.A.) (50, 100, or 200 mg/kg body weight per day) for 3 weeks. Time-matched control experiments were performed by feeding the animals 45 microg/100 g of glucose plus 45 microg/100 g of fructose per day for 3 weeks. After 21 days, rats were killed and the hearts excised and perfused via working mode. Hearts were made ischemic for 30 min followed by 2 h of reperfusion. At 100 mg/kg and at 200 mg/kg, grapes provided significant cardioprotection as evidenced by improved postischemic ventricular recovery (aortic flow, developed pressure, the maximum first derivative of the developed pressure) and reduced amount of myocardial infarction. There were no differences in results between the two groups (100 mg/kg versus 200 mg/kg). No cardioprotection was apparent when rats were given grape samples at a dose of 50 mg/100 g/d. SGE reduced the malonaldehyde content of the heart, indicating reduction of oxidative stress during ischemia and reperfusion. In vitro studies demonstrated that the SGE could directly scavenge superoxide and hydroxyl radicals that are formed in the ischemic reperfused myocardium. The results demonstrate that the hearts of the rats fed SGE are resistant to myocardial ischemia reperfusion injury, suggesting a cardioprotective role of grapes.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:Journal of Cardiovascular Pharmacology 40 : 5 (2002), p. 762-769. -
További szerzők:Juhász Béla (1978-) (kísérletes farmakológus) Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész) Maulik, Nilanjana Das, Dipak Kumar
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2.

001-es BibID:BIBFORM041167
035-os BibID:PMID:12074987
Első szerző:Cui, Jianhua
Cím:Cardioprotective abilities of white wine / Jianhua Cui, Arpad Tosaki, Gerald A. Cordis, Alberto A. E. Bertelli, Aldo Bertelli, Nilanjana Maulik, Dipak K. Das
Dátum:2002
ISSN:0077-8923
Megjegyzések:To study if white wines, like red wine, can also protect the heart from ischemia reperfusion injury, ethanol-free extracts of three different white wines (WW1, WW2 and WW3) (100 mg/100 g body weight) were given orally to Sprague Dawley rats (200 g body weight) for three weeks. Control rats were given water only for the same period of time. After three weeks, rats were anesthetized and sacrificed, and the hearts excised for the preparation of isolated working rat heart. All hearts were subjected to 30 min global ischemia followed by two hours of reperfusion. The results demonstrated that among the three different white wines, only WW2 showed cardioprotection as evidenced by improved post-ischemic ventricular recovery compared to control. The amount of malonaldehyde production in white wine-fed rat hearts were lower compared to that found in control hearts indicating reduced formation of the reactive oxygen species. In vitro studies using chemiluminescence technique revealed that these white wines scavenged both superoxide anions and hydroxyl radicals. The results of our study demonstrated that only WW2 white wine provided cardioprotection as evidenced by the improved the post-ischemic contractile recovery and reduced myocardial infarct size. The cardioprotective effect of this white wine may be attributed, at least in part, from its ability to function as an in vivo antioxidant.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:Annals of The New York Academy of Sciences 957 (2002), p. 308-316. -
További szerzők:Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész) Cordis, Gerald A. Bertelli, Alberto A. A. Bertelli, Aldo Maulik, Nilanjana Das, Dipak Kumar
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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3.

001-es BibID:BIBFORM041166
035-os BibID:PMID:12074986
Első szerző:Cui, Jianhua
Cím:Reduction of myocardial ischemia reperfusion injury with regular consumption of grapes / Jianhua Cui, Gerald A. Cordis, Arpad Tosaki, Nilanjana Maulik, Dipak K. Das
Dátum:2002
ISSN:0077-8923
Megjegyzések:Recently several polyphenolic antioxidants derived from grape seeds and skins have been implicated in cardioprotection. This study was undertaken to determine if the grapes were equally cardioprotective. Sprague Dawley male rats were given (orally) standardized grape extract (SGE) for a period of three weeks. Time-matched control experiments were performed by feeding the animals 45 microg/100 of glucose plus 45 microg/100 g fructose per day for three weeks. After 30 days, rats were sacrificed, hearts excised and perfused via working-mode. Hearts were made ischemic for 30 min followed by two hours of reperfusion. At 100 mg/kg and at 200 mg/kg, SGE provided significant cardioprotection as evidenced by improved post-ischemic ventricular recovery and reduced amount of myocardial infarction. No cardioprotection was apparent when rats were given grape samples at a dose of 50 mg/100 g/day. In vitro studies demonstrated that the SGE could directly scavenge superoxide and hydroxyl radicals which are formed in the ischemic reperfused myocardium. The results demonstrate that the heats of the rats fed SGE reduced myocardial ischemia reperfusion injury by functioning as in vivo antioxidant.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:Annals of The New York Academy of Sciences. - 957 (2002), p. 302-307. -
További szerzők:Cordis, Gerald A. Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész) Maulik, Nilanjana Das, Dipak Kumar
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
DOI
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4.

001-es BibID:BIBFORM042017
Első szerző:Das, Samarjit
Cím:Potentiation of a survival signal in the ischemic heart by resveratrol through p38 mitogen-activated protein kinase/mitogen- and stress-activated protein kinase 1/cAMP response element-binding protein signaling / Das Samarjit, Tosaki Arpad, Bagchi Debasis, Maulik Nilanjana, Das K. Dipak
Dátum:2006
ISSN:0022-3565
Megjegyzések:Resveratrol (3,4',5-trihydroxy-trans-stilbene), a naturally occurring polyphenolic compound found abundantly in grape skins and red wines, has been found to pharmacologically precondition the heart against ischemia reperfusion injury through the potentiation of a survival signal involving cAMP response element-binding protein-dependent phosphatidylinositol 3-kinase-Akt-BclII pathway. The present study was designed to determine whether, similar to ischemic preconditioning, resveratrol uses mitogen-activated protein kinases (MAPKs) as upstream signaling targets. The isolated rat hearts were preperfused for 15 min with Krebs-Henseleit bicarbonate buffer in the absence (control) or presence of extracellular signal-regulated kinase (ERK) 1/2 inhibitor 2'-amino-3'-methoxyflavone (PD98059), p38 MAPK inhibitor 4-(4-fluorophenyl)-2-(4-hydroxyphenyl)-5-(4-pyridyl)-1H-imidazole (SB-202190), mitogen- and stress-activated protein kinase 1 (MSK-1) inhibitor N-[2-(4-bromocinnamylamino)ethyl]-5-isoquinoline (H89), protein kinase A inhibitor (9S,10S,12R)-2,3,9,10,11,12-hexahydro-10hydroxy-9-methyl-1-oxo-9,12-epoxy-1H-diindolo[1,2,3fg: 3',2',1'-kl]-pyrrolo[3,4-i][1,6]benzodiazocine-10-carboxylic acid hexyl ester (KT5720), resveratrol only, resveratrol plus PD98059, resveratrol plus SB-202190, resveratrol plus H89, or resveratrol plus KT5720. Consistent with previous reports, resveratrol provided cardioprotection as evidenced by its ability to improve postischemic ventricular function, reduction of myocardial infarct size, and cardiomyocyte apoptosis. The cardioprotection afforded by resveratrol was partially abolished with PD98059 or SB-202190, suggesting that ERK1/2 and p38 MAPK play roles in resveratrol-mediated preconditioning. An MSK-1 inhibitor, H89, abolished resveratrol-mediated preconditioning, indicating MSK-1 to be the downstream target molecule for both ERK1/2 and p38 MAPK. KT5720 had no effect on resveratrol-mediated cardioprotection. Corroborating these results, Western blot analysis revealed phosphorylation of ERK1/2, p38 MAPK, MAPK-activated protein (MAPKAP) kinase 2, and MSK-1 with resveratrol and inhibition of phosphorylation with corresponding inhibitors. These results showed for the first time that resveratrol triggers an MAPK signaling pathway involving ERK1/2 and p38 MAPK, the former using MSK-1 as the downstream target and the latter, using both MAPKAP kinase 2 and MSK-1 as downstream targets.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
MSH
Megjelenés:Journal Of Pharmacology And Experimental Therapeutics. - 317 : 3 (2006), p. 980-988. -
További szerzők:Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész) Bagchi, Debasis Maulik, Nilanjana Das, Dipak Kumar
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DOI
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5.

001-es BibID:BIBFORM042016
Első szerző:Das, Samarjit
Cím:Resveratrol-Mediated Activation of cAMP Response Element-Binding Protein through Adenosine A3 Receptor by Akt-Dependent and -Independent Pathways / Das Samarjit, Tosaki Arpad, Bagchi Debasis, Maulik Nilanjana, Das K. Dipak
Dátum:2005
ISSN:0022-3565
Megjegyzések:A recent study documented a role of adenosine A(3)-Akt-cAMP response element-binding protein (CREB) survival signaling in resveratrol preconditioning of the heart. In this study, we demonstrate that resveratrol-mediated CREB activation can also occur through an Akt-independent pathway. Isolated rat hearts were perfused for 15 min with Krebs-Henseleit bicarbonate (KHB) buffer containing resveratrol in the absence or presence of adenosine A(3) receptor blocker MRS-1191 [3-ethyl-5-benzyl-2-methyl-4-phenylethynyl-6-phenyl-1,4-(+/-)-dihydropyridine-3,5-dicar-boxylate], phosphatidylinositol 3 (PI3)-kinase inhibitor LY294002 [2-(4-morpholinyl)-8-phenyl-1(4H)-benzopyran-4-one hydrochloride], mitogen-activated extracellular signal-regulated protein kinase inhibitor PD098059 [2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one], or a combination of LY294002 and PD098059. All hearts were subsequently subjected to 30-min ischemia followed by 2-h reperfusion. Cardioprotection was examined by determining infarct size, cardiomyocyte apoptosis, and ventricular recovery. Resveratrol phosphorylated both Akt and CREB that was blocked by MRS-1191, which also abolished cardioprotective abilities of resveratrol. LY294002 completely inhibited Akt phosphorylation but partially blocked the phosphorylation of CREB. Inhibition of PI3-kinase also partially blocked resveratrol's ability to precondition the heart. PD098059 partially blocked the phosphorylation of CREB and resveratrol-mediated cardioprotection. Preperfusing the hearts with LY294002 and PD098059 together completely abolished the phosphorylation of CREB, simultaneously inhibiting resveratrol-mediated cardioprotection. The results indicate that resveratrol preconditions the hearts through adenosine A(3) receptor signaling that triggers the phosphorylation of CREB through both Akt-dependent and -independent pathways, leading to cardioprotection.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
MSH
Megjelenés:Journal Of Pharmacology And Experimental Therapeutics. - 314 : 2 (2005), p. 762-769. -
További szerzők:Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész) Bagchi, Debasis Maulik, Nilanjana Das, Dipak Kumar
Internet cím:Szerző által megadott URL
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Intézményi repozitóriumban (DEA) tárolt változat
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6.

001-es BibID:BIBFORM001465
Első szerző:Juhász Béla (kísérletes farmakológus)
Cím:Adrenocorticotrope hormone fragment (4-l0) attenuates the ischemia/reperfusion-induced cardiac injury in isolated rat hearts / Juhász B., Dér P., Szodoray P., Gesztelyi R., Lekli I., Bak I., Antal M., Maulik N., Tósaki Á., Vecsernyés M.
Dátum:2007
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:Antioxidants and Redox Signaling. - 9 : 11 (2007), p. 1851-1861. -
További szerzők:Dér Péter Szodoray Péter (1973-) (belgyógyász, orvos) Gesztelyi Rudolf (1969-) (kísérletes farmakológus) Lekli István (1981-) (gyógyszerész) Bak István (1975-) (vegyész, analitikus, farmakológus) Antal Miklós (1951-) (orvos, anatómus) Maulik, Nilanjana Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész) Vecsernyés Miklós (1959-) (gyógyszertechnológus, endokrinológus)
Internet cím:elektronikus változat
DOI
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7.

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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8.

001-es BibID:BIBFORM042056
Első szerző:Maulik, Nilanjana
Cím:Induction of iNOS gene expression by monophosphoryl lipid A : a pharmacological approach for myocardial adaptation to ischemia / Maulik N., Tosaki A., Elliott G. T., Maulik G., Das D. K.
Dátum:1998
Megjegyzések:Using the concept that exposing a cell to an adverse environment (stress) results in the stimulation of its endogenous defense system, hearts have been adapted to ischemia by exposing them to diverse stresses. Recently, 24-h pretreatment of monophosphoryl lipid A (MLA), a chemically modified derivative of endotoxin, was found to render the hearts more tolerant to ischemic reperfusion injury. Since nitric oxide has recently been implicated in myocardial preservation and since inducible nitric oxide synthetase (iNOS) was originally characterized in macrophages and shown to be maximally induced by bacterial lipopolysaccharides (endotoxin), we sought to determine whether MLA mediates its cardioprotective effects through the iNOS expression. For this, rats were injected with MLA (300 micrograms/kg) or vehicle (control), and after 24 h the animals were sacrificed and the isolated working hearts were made ischemic for 30 min followed by 30 min of reperfusion. MLA-treated hearts were found to be tolerant to ischemic reperfusion injury as evidenced by improved postischemic ventricular recovery. After 30 min of reperfusion, left ventricular developed pressure (LVDP) and its maximum first derivative (LVmaxdp/dt) were 13.3 +/- 0.3 kPa and 537 +/- 13 kPa/s, respectively, in the MLA-treated group, as compared with 10.2 +/- 0.4 kPa (p < 0.05) and 447 +/- 11 kPa/s (p < 0.05), respectively, for the control group. Aortic flow and coronary flow were 20.1 +/- 1.4 ml/min and 19.1 +/- 0.8 ml/min, respectively, in the MLA group, as compared with 9.5 +/- 0.8 ml/min (p < 0.05) and 15.9 +/- 0.7 ml/min (p < 0.05), respectively, for the untreated group. To examine the induction of the iNOS expression, RNAs were extracted from the control and MLA-treated hearts (after 2, 4, 6, 8, 12 and 24 h of treatment) and Northern blot analysis was performed using specific cDNA probe for iNOS. A single band of approximately 4.6 kb corresponding to iNOS mRNA was detected after 4 h of MLA treatment, while the maximal iNOS expression was found between 6-8 h of MLA treatment. The results of this study demonstrate that MLA induces the expression of iNOS and protects the myocardium from ischemic reperfusion injury.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
HEM
Megjelenés:Drugs under Experimental and Clinical Research. - 24 : 3 (1998), p. 117-124. -
További szerzők:Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész) Elliott, Gary T. Maulik, Gautam Das, Dipak Kumar
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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9.

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
DOI
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10.

001-es BibID:BIBFORM005161
Első szerző:Nagy Norbert (kísérletes farmakológus)
Cím:Overexpression of glutaredoxin-2 reduces myocardial cell death by preventing both apoptosis and necrosis / Norbert Nagy, Gautam Malik, Arpad Tosaki, Ye-Shih Ho, Nilanjana Maulik, Dipak K. Das
Dátum:2008
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Journal of Molecular and Cellular Cardiology. - 44 : 2 (2008), p. 252-260. -
További szerzők:Malik, Gautam Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész) Ho, Ye-Shih Maulik, Nilanjana Das, Dipak Kumar
Internet cím:elektronikus változat
DOI
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11.

001-es BibID:BIBFORM002214
035-os BibID:PMID:17397860
Első szerző:Nagy Norbert (kísérletes farmakológus)
Cím:Ischemic preconditioning involves dual cardio-protective axes with p38MAPK as upstream target / Norbert Nagy, Keisuke Shiroto, Gautam Malik, Chi-Kuang Huang, Mathias Gaestel, Maha Abdellatif, Arpad Tosaki, Nilanjana Maulik, Dipak K. Das
Dátum:2007
Megjegyzések:The existing literature indicates a crucial role of p38 MAP (mitogen-activated protein) kinase (p38MAPK) and its downstream target MAPKAP kinase 2 (MK2) in ischemic preconditioning (IPC). Accordingly, deletion of MK2 gene should abolish the cardioprotective ability of IPC. Interestingly, we were able to partially precondition the hearts from MK2(-/-) knockout mice suggesting the existence of an as yet unknown alternative downstream target of p38MAPK. A recent study from our laboratory also determined a crucial role of CREB (cyclic AMP response element binding protein) in IPC. Since CREB is a downstream target of MSK-1 (mitogen- and stress-activated protein kinase-1) situated at the crossroad of ERK (extracellular receptor kinase) and p38MAPK signaling pathways, we reasoned that MSK-1 could be a downstream molecular target for p38MAPK and ERK signaling in the IPC hearts. To test this hypothesis, the rat hearts were subjected to IPC by four cyclic episodes of 5 min ischemia and 10 min reperfusion. As expected, IPC induced the activation of ERK1/2, p38MAPK, MK2 and HSP (heat shock protein) 27 as evidenced by their increased phosphorylation; and the inhibition of p38MAPK with SB203580 almost completely, and the inhibition of ERK1/2 with PD098059 partially, abolished cardioprotective effects of IPC. Inhibition of MSK-1 with short hairpin RNA (shRNA) also abolished the IPC-induced cardioprotection. SB203580 partially blocked the effects of MSK-1 suggesting that MSK-1 sits downstream of p38MAPK. shRNA-MSK-1 blocked the contribution of both p38MAPK and ERK1/2 as it is uniquely situated at the downstream crossroad of both of these MAP kinases. Although MSK-1 sits downstream of both ERK1/2 and p38MAPK, ERK1/2 activation appears to play less significant role compared to p38MAPK, since its inhibition blocked MSK activation only partially. Consistent with these results, shRNA-MSK-1 blocked the partial PC in MK2(-/-) hearts, and in combination with SB203580, completely abolished the PC effects in the wild-type hearts. The IPC-induced survival signaling was almost completely inhibited with SB203580, and only partially with PD 098059 as evidenced from the inhibition patterns of IPC induced activation of CREB, Akt and Bcl-2. Again SB203580 alone or in combination with shRNA-MSK-1 inhibited IPC induced survival signal comparatively, suggesting that MSK-1 exists downstream of p38MAPK. Taken together, these results indicate for the first time MSK-1 as an alternative (other than MK2) downstream target for p38MAPK, which also transmits survival signal through the activation of CREB.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:Journal of Molecular and Cellular Cardiology 42 : 5 (2007), p. 981-990. -
További szerzők:Shiroto, Keisuke Malik, Gautam Huang, Chi-Kuang Gaestel, Mathias Abdellatif, Maha Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész) Maulik, Nilanjana Das, Dipak Kumar
Internet cím:elektronikus változat
DOI
Borító:

12.

001-es BibID:BIBFORM002216
Első szerző:Thirunavukkarasu, Mahesh
Cím:VEGFR1 (Flt-1+/-) gene knockout leads to the disruption of VEGF-mediated signaling through the nitric oxide/heme oxygenase pathway in ischemic preconditioned myocardium / Mahesh Thirunavukkarasu, Bela Juhasz, Lijun Zhan, Venugopal P. Menon, Arpad Tosaki, Hajime Otani, Nilanjana Maulik
Dátum:2007
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Free Radical Biology and Medicine 42 : 10 (2007), p. 1487-1495. -
További szerzők:Juhász Béla (1978-) (kísérletes farmakológus) Zhan, Lijun Menon, Venugopal P. Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész) Otani, Hajime Maulik, Nilanjana
Internet cím:elektronikus változat
DOI
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