Search Results - (Author, Cooperation:R. Kleta)

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  1. 1
    C. Rotimi ; A. Abayomi ; A. Abimiku ; V. M. Adabayeri ; C. Adebamowo ; E. Adebiyi ; A. D. Ademola ; A. Adeyemo ; D. Adu ; D. Affolabi ; G. Agongo ; S. Ajayi ; S. Akarolo-Anthony ; R. Akinyemi ; A. Akpalu ; M. Alberts ; O. Alonso Betancourt ; A. M. Alzohairy ; G. Ameni ; O. Amodu ; G. Anabwani ; K. Andersen ; F. Arogundade ; O. Arulogun ; D. Asogun ; R. Bakare ; N. Balde ; M. L. Baniecki ; C. Beiswanger ; A. Benkahla ; L. Bethke ; M. Boehnke ; V. Boima ; J. Brandful ; A. I. Brooks ; F. C. Brosius ; C. Brown ; B. Bucheton ; D. T. Burke ; B. G. Burnett ; S. Carrington-Lawrence ; N. Carstens ; J. Chisi ; A. Christoffels ; R. Cooper ; H. Cordell ; N. Crowther ; T. Croxton ; J. de Vries ; L. Derr ; P. Donkor ; S. Doumbia ; A. Duncanson ; I. Ekem ; A. El Sayed ; M. E. Engel ; J. C. Enyaru ; D. Everett ; F. M. Fadlelmola ; E. Fakunle ; K. H. Fischbeck ; A. Fischer ; O. Folarin ; J. Gamieldien ; R. F. Garry ; S. Gaseitsiwe ; R. Gbadegesin ; A. Ghansah ; M. Giovanni ; P. Goesbeck ; F. X. Gomez-Olive ; D. S. Grant ; R. Grewal ; M. Guyer ; N. A. Hanchard ; C. T. Happi ; S. Hazelhurst ; B. J. Hennig ; C. Hertz ; Fowler ; W. Hide ; F. Hilderbrandt ; C. Hugo-Hamman ; M. E. Ibrahim ; R. James ; Y. Jaufeerally-Fakim ; C. Jenkins ; U. Jentsch ; P. P. Jiang ; M. Joloba ; V. Jongeneel ; F. Joubert ; M. Kader ; K. Kahn ; P. Kaleebu ; S. H. Kapiga ; S. K. Kassim ; I. Kasvosve ; J. Kayondo ; B. Keavney ; A. Kekitiinwa ; S. H. Khan ; P. Kimmel ; M. C. King ; R. Kleta ; M. Koffi ; J. Kopp ; M. Kretzler ; J. Kumuthini ; S. Kyobe ; C. Kyobutungi ; D. T. Lackland ; K. A. Lacourciere ; G. Landoure ; R. Lawlor ; T. Lehner ; M. Lesosky ; N. Levitt ; K. Littler ; Z. Lombard ; J. F. Loring ; S. Lyantagaye ; A. Macleod ; E. B. Madden ; C. R. Mahomva ; J. Makani ; M. Mamven ; M. Marape ; G. Mardon ; P. Marshall ; D. P. Martin ; D. Masiga ; R. Mason ; M. Mate-Kole ; E. Matovu ; M. Mayige ; B. M. Mayosi ; J. C. Mbanya ; S. A. McCurdy ; M. I. McCarthy ; H. McIlleron ; S. O. Mc'Ligeyo ; C. Merle ; A. O. Mocumbi ; C. Mondo ; J. V. Moran ; A. Motala ; M. Moxey-Mims ; W. S. Mpoloka ; C. L. Msefula ; T. Mthiyane ; N. Mulder ; G. Mulugeta ; D. Mumba ; J. Musuku ; M. Nagdee ; O. Nash ; D. Ndiaye ; A. Q. Nguyen ; M. Nicol ; O. Nkomazana ; S. Norris ; B. Nsangi ; A. Nyarko ; M. Nyirenda ; E. Obe ; R. Obiakor ; A. Oduro ; S. F. Ofori-Acquah ; O. Ogah ; S. Ogendo ; K. Ohene-Frempong ; A. Ojo ; T. Olanrewaju ; J. Oli ; C. Osafo ; O. Ouwe Missi Oukem-Boyer ; B. Ovbiagele ; A. Owen ; M. O. Owolabi ; L. Owolabi ; E. Owusu-Dabo ; G. Pare ; R. Parekh ; H. G. Patterton ; M. B. Penno ; J. Peterson ; R. Pieper ; J. Plange-Rhule ; M. Pollak ; J. Puzak ; R. S. Ramesar ; M. Ramsay ; R. Rasooly ; S. Reddy ; P. C. Sabeti ; K. Sagoe ; T. Salako ; O. Samassekou ; M. S. Sandhu ; O. Sankoh ; F. S. Sarfo ; M. Sarr ; G. Shaboodien ; I. Sidibe ; G. Simo ; M. Simuunza ; L. Smeeth ; E. Sobngwi ; H. Soodyall ; H. Sorgho ; O. Sow Bah ; S. Srinivasan ; D. J. Stein ; E. S. Susser ; C. Swanepoel ; G. Tangwa ; A. Tareila ; O. Tastan Bishop ; B. Tayo ; N. Tiffin ; H. Tinto ; E. Tobin ; S. M. Tollman ; M. Traore ; M. J. Treadwell ; J. Troyer ; M. Tsimako-Johnstone ; V. Tukei ; I. Ulasi ; N. Ulenga ; B. van Rooyen ; A. P. Wachinou ; S. P. Waddy ; A. Wade ; M. Wayengera ; J. Whitworth ; L. Wideroff ; C. A. Winkler ; S. Winnicki ; A. Wonkam ; M. Yewondwos ; T. sen ; N. Yozwiak ; H. Zar
    American Association for the Advancement of Science (AAAS)
    Published 2014
    Staff View
    Publication Date:
    2014-06-21
    Publisher:
    American Association for the Advancement of Science (AAAS)
    Print ISSN:
    0036-8075
    Electronic ISSN:
    1095-9203
    Topics:
    Biology
    Chemistry and Pharmacology
    Computer Science
    Medicine
    Natural Sciences in General
    Physics
    Keywords:
    Africa ; Disease/*genetics ; England ; Genetics, Medical/trends ; Genome-Wide Association Study/*trends ; Genomics/*trends ; Health ; Humans ; National Institutes of Health (U.S.) ; United States
    Published by:
    Latest Papers from Table of Contents or Articles in Press
  2. 2
    Staff View
    ISSN:
    1437-9813
    Keywords:
    Key words Ovarian tumor ; Children ; Hypercalcemia ; Small-Cell carcinoma
    Source:
    Springer Online Journal Archives 1860-2000
    Topics:
    Medicine
    Notes:
    Abstract Tumors of the ovary in girls represent about 80% of pediatric genital tumors; approximately 30% of these tumors are malignant. The risk of malignancy increases with decreasing age. The most frequent finding is a teratoma; other tumors are rare. Small-cell carcinoma (SCCO) of the ovary is extremely rare, occurring mostly in young women. We present an 8-year-old girl with a SCCO of the hypercalcemic type. The findings and treatment are discussed with emphasis on the poor prognosis in these patients, even in stage 1 disease. The current literature is reviewed.
    Type of Medium:
    Electronic Resource
    URL:
    Articles: DFG German National Licenses
  3. 3
    Schlatter, E. ; Ankorina, I. ; Haxelmans, S. ; Kleta, R.
    Springer
    Published 1995
    Staff View
    ISSN:
    1432-2013
    Keywords:
    Adenosine ; Fura-2 ; SHR rats ; WKY rats ; Diadenosine triphosphate ; Diadenosine tetraphosphate ; Diadenosine pentaphosphate ; Diadenosine hexaphosphate
    Source:
    Springer Online Journal Archives 1860-2000
    Topics:
    Medicine
    Notes:
    Abstract Diadenosine polyphosphates (Ap n A) are known to influence cellular Ca2+ activity ([Ca2+]i) in several cells. Their vasoactive potency has been described in various systems including the kidney. We examined the effects of diadenosine polyphosphates, adenosine 5′-triphosphate (ATP) and angiotensin II (Ang II) on cytosolic Ca2+ activity of mesangial cells (MC) in culture obtained from normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive (SHR) rats. [Ca2+]i was measured as a fluorescence ratio F 340/F 380 with the fura-2 technique using three excitation wavelengths (340 nm, 360 nm and 380 nm) and a photon counting tube. Resting [Ca2+]i was not significantly different in MC from WKY and SHR rats and was measured as 132±9 nmol/l (n=65) and 114±12 nmol/l (n=36), respectively. Diadenosine polyphosphates (Ap3A–Ap6A) increased [Ca2+]i transiently with an initial peak and a secondary plateau phase comparable to the effects of ATP or Ang II. Increases in [Ca2+]i induced by all these agonists were not significantly different between MC of WKY and SHR rats. ATP, Ap3A, Ap4A, Ap5A, Ap6A (each 5 μmol/l) increased the fura-2 fluorescence ratio initially by 0.66±0.09 (n=33), 0.52±0.08 (n=18), 0.25±0.05 (n=16), 0.09±0.06 (n=7), 0.09±0.04 (n=11), respectively. A half-maximal initial increase in the fura-2 fluorescence ratio was reached at 22 nmol/l, 0.9 μmol/l, 2.0 μmol/l and 4.0 μmol/l with Ang II, Ap3A, ATP and Ap4A, respectively. Ap4A (100 μmol/l, n=18) led to a reversible contraction of MC. Diadenosine polyphosphates increase [Ca2+]i in rat MC, in a similar manner to ATP or Ang II and lead to a contraction of MC, suggesting that these nucleotides are also involved in the control of glomerular haemodynamics.
    Type of Medium:
    Electronic Resource
    URL:
    Articles: DFG German National Licenses
  4. 4
    Cermak, R. ; Kleta, R. ; Forssmann, W. G. ; Schlatter, E.
    Springer
    Published 1996
    Staff View
    ISSN:
    1432-2013
    Keywords:
    Key words Patch clamp ; Adenosine ; 293 B ; Cromakalim ; Angiotensin II ; Atrial natriuretic peptide (ANP) ; Brain natriuretic peptide (BNP) ; Urodilatin
    Source:
    Springer Online Journal Archives 1860-2000
    Topics:
    Medicine
    Notes:
    Abstract Mesangial cells (MC) are a main target of natriuretic peptides in the kidney and are thought to play a role in regulating glomerular filtration rate. We examined the influence of cGMP-generating (i.e. guanosine 3′,5′-cyclicmonophosphate) peptides on membrane voltages (V m) of rat MC by using the fast whole-cell patch-clamp technique. The cGMP-generating peptides were tested at maximal concentrations ranging from 140 to 300 nmol/l. Whereas human CNP (C natriuretic peptide), rat guanylin and human uroguanylin had no significant effect on V m of these cells, human BNP (brain natriuretic peptide), rat CDD/ANP-99-126 (cardiodilatin/atrial natriuretic peptide) and rat CDD/ ANP-95-126 (urodilatin) hyperpolarized V m significantly by 1.6 ± 0.4 mV (BNP, n = 8), 3.7 ± 0.3 mV (CDD/ANP-99-126, n = 25) and 2.8 ± 0.4 mV (urodilatin, n = 9), respectively. The half-maximally effective concentration (EC50) for the latter two was around 400 pmol/l each. This hyperpolarization could be mimicked with 0.5 mmol/l 8-bromo-guanosine 3′,5′-cyclic monophosphate (8-Br-cGMP) and was blocked by 5 mmol/l Ba2+. The K+ channel blocker 293 B (100 μmol/l) depolarized basal V m by 4.3 ± 0.4 mV (n = 8), but failed to inhibit the hyperpolarization induced by CDD/ANP-99-126 (160 nmol/l) (n = 8). The K+ channel opener cromakalim (10 μmol/l) neither influenced basal V m nor altered the hyperpolarization induced by 160 nmol/l CDD/ANP-99-126 (n = 8). Adenosine (100 μmol/l) hyperpolarized V m by 13.4 ± 1.3 mV (n = 16). At 100 μmol/l, 293 B did not inhibit the adenosine-induced hyperpolarization (n = 6). At 160 nmol/l, CDD/ANP-99-126 enhanced the adenosine-induced hyperpolarization significantly by 1.5 ± 0.6 mV (n = 10). CDD/ANP-99-126 (160 nmol/l) failed to modulate the value to which V m depolarized in the presence of 1 nmol/l angiotensin II (n = 10), but accelerated the repolarization to basal V m by 49 ± 20% (n = 8). These results indicate that the natriuretic peptides CDD/ANP-99-126, CDD/ANP-95-126 and BNP hyperpolarize rat MC probably due to an increase of a K+ conductance. This effect modulates the voltage response induced by angiotensin II. The natriuretic-peptide-activated conductance can be blocked by Ba2+, but not by 293 B and cannot be activated by cromakalim. This increase in the K+ conductance seems to be additive to that inducable by adenosine, indicating that different K+ channels are activated by these hormones.
    Type of Medium:
    Electronic Resource
    URL:
    Articles: DFG German National Licenses
  5. 5
    Staff View
    ISSN:
    1432-2013
    Keywords:
    Fast whole-cell ; Patch-clamp ; K+ conductance ; Non-selective cation conductance ; Cl− conductance ; SHR ; WKY ; Adenosine
    Source:
    Springer Online Journal Archives 1860-2000
    Topics:
    Medicine
    Notes:
    Abstract Diadenosine polyphosphates have been shown to influence renal perfusion pressure. As mesangial cells may contribute to these effects we investigated the effects of diadenosine triphosphate (Ap3A), diadenosine tetraphosphate (Ap4A), diadenosine pentaphosphate (Ap5A) and diadenosine hexaphosphate (Ap6A) on membrane voltage (V m) and membrane conductance (g m) in mesangial cells (MC) of normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive (SHR) rats in primary and long-term culture. We applied the patch-clamp technique in the fast-whole-cell configuration to measure V m and g m. To compare the effects of diadenosine polyphosphates with hitherto known agonists we also tested adenosine 5′-triphosphate (ATP) and angiotensin II (Ang II). As there was no significant difference in the V m values in MC of WKY (−42±1 mV, n=70) and SHR rats (−45±2 mV, n=99) as well as in the agonist-induced changes of V m, all data were pooled. The V m of all the cells was −44±1 mV (n=169) and g m was 15.9±1.8 nS (n=141). Ion-exchange experiments showed the presence of a K+ and a non-selective cation conductance in resting MC whereas a Cl− conductance or a Na+selective conductance could not be observed. Ap3A, Ap4A, Ap5A, AP6A and ATP each at a concentration of 5 μmol/l, led to a significant depolarization of V m by 5±2 mV (n=14), 7±1 mV (n=25), 3±1 mV (n=23), 2±1 mV (n=16), and 14±2 mV (n=23), respectively. For Ap4A, the most potent diadenosine polyphosphate, we determined the half-maximally effective concentration (EC 50) as 6 μmol/l (n=5–25), for ATP as 2 μmol/l (n=9–37), and for Ang II as 8 nmol/l (n=6–18). Ap4A 100 μmol/l increased g m significantly by 55±20% (n=16), 100 μmol/l ATP by 135±60% (n=18). The diadenosine polyphosphates examined were able to depolarize V m (Ang II 〉ATP〉 Ap4A〉Ap3A〉Ap5A〉Ap6A) by activation of a Cl− conductance and a non-selective cation conductance, as do ATP or Ang II.
    Type of Medium:
    Electronic Resource
    URL:
    Articles: DFG German National Licenses
  6. 6
    Cermak, R. ; Kleta, R. ; Forssmann, W. G. ; Schlatter, E.
    Springer
    Published 1996
    Staff View
    ISSN:
    1432-2013
    Keywords:
    Patch clamp ; Adenosine ; 293 B Cromakalim ; Angiotensin II ; Atrial natriuretic peptide (ANP) ; Brain natriuretic peptide (BNP) ; Urodilatin
    Source:
    Springer Online Journal Archives 1860-2000
    Topics:
    Medicine
    Notes:
    Abstract Mesangial cells (MC) are a main target of natriuretic peptides in the kidney and are thought to play a role in regulating glomerular filtration rate. We examined the influence of cGMP-generating (i.e. guanosine 3′,5′-cyclicmonophosphate) peptides on membrane voltages (Vm) of rat MC by using the fast whole-cell patch-clamp technique. The cGMP-generating peptides were tested at maximal concentrations ranging from 140 to 300 nmol/1. Whereas human CNP (C natriuretic peptide), rat guanylin and human uroguanylin had no significant effect on Vm of these cells, human BNP (brain natriuretic peptide), rat CDD/ANP-99-126 (cardiodilatin/atrial natriuretic peptide) and rat CDD/ANP-95-126 (urodilatin) hyperpolarized Vm significantly by 1.6 ± 0.4 mV (BNP,n = 8), 3.7 ± 0.3 mV (CDD/ANP-99-126,n = 25) and 2.8 ± 0.4 mV (urodilatin,n = 9), respectively. The half-maximally effective concentration (EC50) for the latter two was around 400 pmol/l each. This hyperpolarization could be mimicked with 0.5 mmol/1 8-bromo-guanosine 3′,5′-cyclic monophosphate (8-Br-cGMP) and was blocked by 5 mmol/1 Ba2+. The K+ channel blocker 293 B (1O)) μmol/l) depolarized basal Vm by 4.3 ± 0.4 mV (n = 8), but failed to inhibit the hyperpolarization induced by CDD/ANP-99-126 (160 nmol/1) (n = 8). The K+ channel opener cromakalim (10 μmol/1) neither influenced basal Vm nor altered the hyperpolarization induced by 160 nmol/1 CDD/ANP-99-126 (n = 8). Adenosine (100 μmol/1) hyperpolarized Vm by 13.4 ± 1.3 mV (n = 16). At 100 μmol/1, 293 B did not inhibit the adenosine-induced hyperpolarization (n = 6). At 160 nmol/l, CDD/ANP-99-126 enhanced the adenosine-induced hyperpolarization significantly by 1.5 ± 0.6 mV (n = 10). CDD/ANP-99-126 (160 nmol/1) failed to modulate the value to which Vm depolarized in the presence of 1 nmol/l angiotensin II (n = 10), but accelerated the repolarization to basal Vm, by 49 ± 20% (n = 8). These results indicate that the natriuretic peptides CDD/ANP-99-126, CDD/ANP-95-126 and BNP hyperpolarize rat MC probably due to an increase of a K+ conductance. This effect modulates the voltage response induced by angiotensin II. The natriuretic-peptide-activated conductance can be blocked by Ba2+, but not by 293 B and cannot be activated by cromakalim. This increase in the K+ conductance seems to be additive to that inducable by adenosine, indicating that different K+ channels are activated by these hormones.
    Type of Medium:
    Electronic Resource
    URL:
    Articles: DFG German National Licenses
  7. 7
    Kleta, R. ; Mohrmann, M. ; Schlatter, E.
    Springer
    Published 1995
    Staff View
    ISSN:
    1432-2013
    Keywords:
    Renal proximal tubule ; Slow-whole cell ; Patch-clamp ; K+ conductance ; Non-selective cation conductance ; Cell culture
    Source:
    Springer Online Journal Archives 1860-2000
    Topics:
    Medicine
    Notes:
    Abstract LLC-PK1 cells serve as a widely used model for the renal proximal tubule. Until now, little has been found out about their membrane voltage (V m) and ionic conductances (g). Several studies have shown changes in cell properties during differentiation and ageing. The aim of this study was to examine the relationship between V m or g and the age of these cells. Therefore, we investigated single cells, subconfluent and confluent monolayers of LLC-PK1 cells aged 1–8 days with the slow-whole-cell patch-clamp technique. The V m of all cells was-34±2 mV (n=75) and the membrane conductance (g m) was 2.3±0.3 nS (n=30). V m in cells aged up to 2 days was-24±3 mV (n=22) whereas V m in cells aged 5–8 days was -50±3 mV (n=15). An increase of extracellular K+ from 3.6 to 18.6 mmol/l led to a depolarization in all cells of 4±1 mV (n=31) and an increase of g m by 17±13% (n=15). Complete replacement of extracellular Na+ by N-methyl-D-glucamine (NMDG) led to a hyperpolarization of 19±2 mV (n=38) and gm was lowered by 27±14% (n=17). A reduction in extracellular Cl− from 147 to 32 mmol/l showed no significant effect on V m (n=16) or g m (n=11). Amiloride (10 μmol/l) had no significant effect on V m (n=13) or g m (n=7). The reduction of the extracellular osmolarity from 290 to 160 mosmol/l led to a hyperpolarization of 11±1 mV (n=18) and an increase in g m by 326±117% (n=12). There was no significant correlation between g m and cell age. LLC-PK1 cells used in this study have a K+ conductance and a non-selective cation conductance in parallel. With increasing age, LLC-PK1 cells became more and more conductive for K+ and lost their nonselective cation conductance. There is no evidence for a significant amiloride-sensitive Na+ or Cl− conductance in these cells. The K+ conductance could be activated by osmotically induced cell swelling.
    Type of Medium:
    Electronic Resource
    URL:
    Articles: DFG German National Licenses