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001-es BibID:	BIBFORM065227
Első szerző:	Szabó Gábor (budapesti orvos)
Cím:	Letter to the Editor : corrections to the natriuretic peptide article in Journal of Cardiology / Szabó Gabor, Nagy Balint
Dátum:	2012
ISSN:	0914-5087
Megjegyzések:	We read the article of Nishikimi et al. with great interest [1] on "Current biochemistry, molecular biology, and clinical relevance of natriuretic peptides." The content of the article is very interesting and nicely collected, but we found a few mistakes and we would like to call your attention to these.1. Page 132. BNP section, line 14. "Exon 3 encodes the terminal tyrosine and the 3· untranslated region," correctly it is histidine as the authors show correctly in Fig. 1.2. Page 133. Fig. 2. It says corin cuts the proANP 26?151 (proANP 1?126) to Nt proANP and ?ANP. This takes place at Arg?Arg bond (98?99). If we use what the authors state (26?124 and 125?151) this Arg?Arg is located at 99?100, so the ?ANP has only 27 amino acids. While the correct numbering is 26?123 and 124?151 so the ?ANP has the correct 28 amino acids with the cutting place at 98?99 [2].3. Page 134. Fig. 4. According to the figure by cutting the proCNP to CNP (cleaving enzymes PC2 and/or PC1/3) we are receiving the active CNP which consists of 22 amino acids, while based on the figure we are having the molecule which consists only of 21 amino acids, so the correct numbers are not 106?126 (21), rather 105?126 (22).These are small details but we should use the correct data to give exact information to the readers.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok levél natriuretec peptid B type
Megjelenés:	Journal of Cardiology 59 : 1 (2012), p. 97-97. -
További szerzők:	Nagy Bálint (1956-) (molekuláris genetikus)
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM065211
Első szerző:	Szelényi Zsuzsanna
Cím:	Inflammation and oxidative stress caused by nitric oxide synthase uncoupling might lead to left ventricular diastolic and systolic dysfunction in patients with hypertension / Zsuzsanna Szelényi, Ádám Fazakas, Gábor Szénási, Melinda Kiss, Narcis Tegze, Bertalan Csaba Fekete, Eszter Nagy, Imre Bodó, Bálint Nagy, Attila Molvarec, Attila Patócs, Lilla Pepó, Zoltán Prohászka, András Vereckei
Dátum:	2015
ISSN:	1671-5411
Megjegyzések:	OBJECTIVE:To investigate the role of oxidative stress, inflammation, hypercoagulability and neuroendocrine activation in the transition of hypertensive heart disease to heart failure with preserved ejection fraction (HFPEF).METHODS:We performed echocardiography for 112 patients (? 60 years old) with normal EF (18 controls and 94 with hypertension), and determined protein carbonylation (PC), and tetrahydrobiopterin (BH4), C-reactive protein (CRP), interleukin-6 (IL-6), tumor necrosis factor-? (TNF-?), fibrinogen, plasminogen activator inhibitor type-I (PAI-I), von Willebrand factor, chromogranin A (cGA) and B-type natriuretic peptide (BNP) levels from their blood samples.RESULTS:We found that 40% (38/94) of the patients with hypertension (HT) had no diastolic dysfunction (HTDD-), and 60% (56/94) had diastolic dysfunction (HTDD+). Compared to the controls, both patient groups had increased PC and BH4, TNF-?, PAI-I and BNP levels, while the HTDD+ group had elevated cGA and CRP levels. Decreased atrial and longitudinal left ventricular (LV) systolic and diastolic myocardial deformation (strain and strain rate) was demonstrated in both patient groups versus the control. Patients whose LV diastolic function deteriorated during the follow-up had elevated PC and IL-6 level compared to their own baseline values, and to the respective values of patients whose LV diastolic function remained unchanged. Oxidative stress, inflammation, BNP and PAI-I levels inversely correlated with LV systolic, diastolic and atrial function.CONCLUSIONS:In patients with HT and normal EF, the most common HFPEF precursor condition, oxidative stress and inflammation may be responsible for LV systolic, diastolic and atrial dysfunction, which are important determinants of the transition of HT to HFPEF.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban heart failure hypertension Inflammation oxidative stress
Megjelenés:	Journal of Geriatric Cardiology 12 (2015), p. 1-10. -
További szerzők:	Fazakas Ádám Szénási Gábor Kiss Melinda Tegze, Narcis Fekete Bertalan C. Nagy Eszter (Budapest) Bodó Imre Nagy Bálint (1956-) (molekuláris genetikus) Molvarec Attila (szülész-nőgyógyász) Patócs Attila Pepó Lilla Prohászka Zoltán Vereckei András
Internet cím:	DOI Intézményi repozitóriumban (DEA) tárolt változat
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