Spin-Isospin Excitations and Muon Capture by Nuclei

By analyzing the energy-weighted moments of the strength function calculated in RPA and beyond it is shown that the explanation of the effect of missing strength of Gamow-Teller transitions requires that residual interaction produce high-excited $1^{+}$ particle-hole collective states. The example of this interaction is presented. The manifestations of spin-isospin nuclear response in nuclear muon capture are discussed.Comment: 16 pages, 5 figures, 2 tables. The talk at the XVI International School on Nuclear Physics, Neutron Physics and Nuclear Energy, September 19-26, Varna, Bulgari

Comparative analysis of involvement of UGT1 and UGT2 splice variants of UDP-galactose transporter in glycosylation of macromolecules in MDCK and CHO cell lines

Nucleotide sugar transporters deliver nucleotide sugars into the Golgi apparatus and endoplasmic reticulum. This study aimed to further characterize mammalian UDP-galactose transporter (UGT) in MDCK and CHO cell lines. MDCK-RCAr and CHO-Lec8 mutant cell lines are defective in UGT transporter, although they exhibit some level of galactosylation. Previously, only single forms of UGT were identified in both cell lines, UGT1 in MDCK cells and UGT2 in CHO cells. We have identified the second UGT splice variants in CHO (UGT1) and MDCK (UGT2) cells. Compared to UGT1, UGT2 is more abundant in nearly all examined mammalian tissues and cell lines, but MDCK cells exhibit different relative distribution of both splice variants. Complementation analysis demonstrated that both UGT splice variants are necessary for N- and O-glycosylation of proteins. Both mutant cell lines produce chondroitin-4-sulfate at only a slightly lower level compared to wild-type cells. This defect is corrected by overexpression of both UGT splice variants. MDCK-RCAr mutant cells do not produce keratan sulfate and this effect is not corrected by either UGT splice variant, overexpressed either singly or in combination. Here we demonstrate that both UGT splice variants are important for glycosylation of proteins. In contrast to MDCK cells, MDCK-RCAr mutant cells may possess an additional defect within the keratan sulfate biosynthesis pathway

Chronic vasopeptidase inhibition restores endothelin‐converting enzyme activity and normalizes endothelin levels in salt‐induced hypertension

Background. Vasopeptidase inhibition (VPI) represents a new therapeutic principle including both inhibition of angiotensin‐converting enzyme (ACE) and neutral endopeptidase (NEP). The present study investigated the effect of the vasopeptidase inhibitor omapatrilat on endothelin‐1 (ET‐1)‐mediated vascular function in salt‐induced hypertension. Methods. Dahl salt‐sensitive rats (n=6/group) on standard or salt‐enriched (4% NaCl) chow were treated for 8 weeks with either omapatrilat (36±4 mg/kg/day), captopril (94±2 mg/kg/day) or placebo. Aortic and renal artery segments were isolated and suspended in organ chambers for isometric tension recording. Functional endothelin‐converting enzyme (ECE) activity was assessed in native segments and after preincubation with omapatrilat. Furthermore, vascular ECE protein levels as well as plasma and tissue ET‐1 levels were determined. Results. The increase in systolic blood pressure of salt‐fed rats was prevented by omapatrilat and captopril to a comparable degree. In salt‐induced hypertension, functional ECE activity (calculated as the ratio of the contraction to big ET‐1 divided by the contraction to ET‐1) in renal arteries (0.46±0.05) and in aorta (0.68±0.05) was reduced as compared with control animals (0.9±0.05 and 0.99±0.04, respectively; P<0.05). While omapatrilat in vitro blunted the response to big endothelin‐1 (big ET‐1) and diminished ECE activity further (P<0.01 vs native segments), chronic treatment with omapatrilat in vivo restored contractions to ET‐1 (120±6%) and big ET‐1 (98±9%) in renal arteries, and therefore normalized renovascular ECE activity. In addition, omapatrilat normalized plasma ET‐1 concentrations (12.9±1.2 vs 16.6±1.4 pg/ml on high salt diet; P<0.05) and renovascular ECE protein levels. Conclusions. In salt‐induced hypertension, vasopeptidase inhibition restores alterations in the endothelin system, such as renovascular ECE activity and responsiveness to ET‐1 and big ET‐1 with chronic but not acute in vitro application. Thus, the beneficial effects of vasopeptidase inhibition may reflect a resetting of cardiovascular control systems and therefore may be particularly suited to treat hypertension and heart failur

Chronic vasopeptidase inhibition restores endothelin‐converting enzyme activity and normalizes endothelin levels in salt‐induced hypertension

Background. Vasopeptidase inhibition (VPI) represents a new therapeutic principle including both inhibition of angiotensin‐converting enzyme (ACE) and neutral endopeptidase (NEP). The present study investigated the effect of the vasopeptidase inhibitor omapatrilat on endothelin‐1 (ET‐1)‐mediated vascular function in salt‐induced hypertension. Methods. Dahl salt‐sensitive rats (n=6/group) on standard or salt‐enriched (4% NaCl) chow were treated for 8 weeks with either omapatrilat (36±4 mg/kg/day), captopril (94±2 mg/kg/day) or placebo. Aortic and renal artery segments were isolated and suspended in organ chambers for isometric tension recording. Functional endothelin‐converting enzyme (ECE) activity was assessed in native segments and after preincubation with omapatrilat. Furthermore, vascular ECE protein levels as well as plasma and tissue ET‐1 levels were determined. Results. The increase in systolic blood pressure of salt‐fed rats was prevented by omapatrilat and captopril to a comparable degree. In salt‐induced hypertension, functional ECE activity (calculated as the ratio of the contraction to big ET‐1 divided by the contraction to ET‐1) in renal arteries (0.46±0.05) and in aorta (0.68±0.05) was reduced as compared with control animals (0.9±0.05 and 0.99±0.04, respectively; P<0.05). While omapatrilat in vitro blunted the response to big endothelin‐1 (big ET‐1) and diminished ECE activity further (P<0.01 vs native segments), chronic treatment with omapatrilat in vivo restored contractions to ET‐1 (120±6%) and big ET‐1 (98±9%) in renal arteries, and therefore normalized renovascular ECE activity. In addition, omapatrilat normalized plasma ET‐1 concentrations (12.9±1.2 vs 16.6±1.4 pg/ml on high salt diet; P<0.05) and renovascular ECE protein levels. Conclusions. In salt‐induced hypertension, vasopeptidase inhibition restores alterations in the endothelin system, such as renovascular ECE activity and responsiveness to ET‐1 and big ET‐1 with chronic but not acute in vitro application. Thus, the beneficial effects of vasopeptidase inhibition may reflect a resetting of cardiovascular control systems and therefore may be particularly suited to treat hypertension and heart failur