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Your search keyword '"Varga, Gábor"' showing total 25 results
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25 results on '"Varga, Gábor"'

5. Maternal overnutrition elevates offspring’s blood pressure—A systematic review and meta‐analysis

Author

Eitmann, Szimonetta, primary, Mátrai, Péter, additional, Németh, Dávid, additional, Hegyi, Péter, additional, Lukács, Anita, additional, Bérczi, Bálint, additional, Czumbel, László Márk, additional, Kiss, István, additional, Gyöngyi, Zoltán, additional, Varga, Gábor, additional, Balaskó, Márta, additional, and Pétervári, Erika, additional

Published
2022
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6. Endoscopic versus microscopic stapes surgery outcomes: A meta‐analysis and systematic review

Author

Koukkoullis, Alexandros, primary, Tóth, István, additional, Gede, Noémi, additional, Szakács, Zsolt, additional, Hegyi, Péter, additional, Varga, Gábor, additional, Pap, István, additional, Harmat, Kinga, additional, Németh, Adrienn, additional, Szanyi, István, additional, Lujber, László, additional, Gerlinger, Imre, additional, and Révész, Péter, additional

Published
2019
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7. Endoscopic type I tympanoplasty is as effective as microscopic type I tympanoplasty but less invasive—A meta‐analysis

Author

Pap, István, primary, Tóth, István, additional, Gede, Noémi, additional, Hegyi, Péter, additional, Szakács, Zsolt, additional, Koukkoullis, Alexandros, additional, Révész, Péter, additional, Harmat, Kinga, additional, Németh, Adrienne, additional, Lujber, László, additional, Gerlinger, Imre, additional, Bocskai, Tímea, additional, Varga, Gábor, additional, and Szanyi, István, additional

Published
2019
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13. CFTR gene transfer to human cystic fibrosis pancreatic duct cells using a Sendai virus vector

Author

Rakonczay, Zoltán, primary, Hegyi, Péter, additional, Hasegawa, Mamoru, additional, Inoue, Makoto, additional, You, Jun, additional, Iida, Akihiro, additional, Ignáth, Imre, additional, Alton, Eric W.F.W., additional, Griesenbach, Uta, additional, Óvári, Gabriella, additional, Vág, János, additional, Da Paula, Ana C., additional, Crawford, Russell M., additional, Varga, Gábor, additional, Amaral, Margarida D., additional, Mehta, Anil, additional, Lonovics, János, additional, Argent, Barry E., additional, and Gray, Michael A., additional

Published
2007
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23. Inhibition of quorum-sensing signals by essential oils.

Author

Szabó MA, Varga GZ, Hohmann J, Schelz Z, Szegedi E, Amaral L, and Molnár J

Subjects
Acyl-Butyrolactones metabolism, Chromobacterium drug effects, Chromobacterium growth & development, Escherichia coli drug effects, Escherichia coli growth & development, Magnoliopsida chemistry, Rosmarinus, Anti-Bacterial Agents pharmacology, Oils, Volatile pharmacology, Plant Oils pharmacology, Quorum Sensing drug effects
Abstract

The role of quorum sensing (QS) is well known in microbial pathogenicity and antibiotic resistance. QS is responsible for motility, swarming, and biofilm production based on the signal molecules, e.g., acylated homoserine lactones (AHLs) produced by micro-organisms above certain population density. The inhibition of QS may reduce pathogenicity, antibiotic resistance and biofilm formation in systemic and local infections. The homoserine lactones and other transmitters contribute to antibiotic resistance and pathogenicity of several bacteria; consequently the inhibition of QS signals reduces the problem of resistance and virulence. Due to the increasing number of persistent non-treatable infections, there is an urgent need to develop new strategies to combat infections that destabilize bacterial communities in the host. The effect of essential oils on bacterial growth and QS were evaluated using the sensor strain Chromobacterium violaceum CV026 and N-acyl homoserine lactone (AHL) producing Escherichia coli ATTC 31298 and the grapevine colonizing Ezf 10-17 strains. Of the tested oils, rose, geranium, lavender and rosemary oils were the most potent QS inhibitors. Eucalyptus and citrus oils moderately reduced pigment production by CV026, whereas the chamomile, orange and juniper oils were ineffective., (Copyright (c) 2009 John Wiley & Sons, Ltd.)

Published
2010
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24. SLC26 transporters and the inhibitory control of pancreatic ductal bicarbonate secretion.

Author

Hegyi P, Rakonczay Z Jr, Tiszlavicz L, Varró A, Tóth A, Rácz G, Varga G, Gray MA, and Argent BE

Subjects
4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid analogs & derivatives, 4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid pharmacology, Animals, Cell Membrane drug effects, Cell Membrane metabolism, Enzyme Activation drug effects, Guinea Pigs, Pancreatic Ducts drug effects, Protein Kinase C metabolism, Secretin metabolism, Substance P metabolism, Antiporters metabolism, Bicarbonates metabolism, Pancreatic Ducts metabolism
Abstract

SLC26 anion exchangers (probably SLC26A3 and SLC26A6) are expressed on the apical membrane of pancreatic duct cells and play a key role in HCO3- secretion; a process that is inhibited by the neuropeptide, substance P (SP). SP had no effect on basolateral HCO3- transporters in the duct cell or on CFTR Cl- channels, but inhibited a Cl- -dependent HCO3- efflux step on the apical membrane. In microperfused ducts, luminal H2DIDS (0.5mM) caused intracellular pH to alkalinize (consistent with inhibition of HCO3- efflux) and, like SP, inhibited HCO3- secretion. SP did not reduce HCO3- secretion further when H2DIDS was applied to the duct lumen, suggesting that SP and H2DIDS inhibit the same transporter on the apical membrane. As SLC26A6 is DIDS-sensitive, this isoform is the likely target for SP. The inhibitory effect of SP was mimicked by phorbol 12,13-dibutyrate (PDBu), an activator of protein kinase C (PKC). Moreover, bisindolylmaleimide, a blocker of PKC, relieved the inhibitory effect of both SP and PDBu on HCO3- secretion. Western blot analysis revealed that guinea pig pancreatic ducts express the alpha, beta1, delta, epsilon, eta, theta, zeta and mu isoforms o f PKC. We conclude that PKC is a negative regulator of SLC26 activity in pancreatic duct cells.

Published
2006

25. Involvement of endogenous CCK and CCK1 receptors in colonic motor function.

Author

Varga G, Bálint A, Burghardt B, and D'Amato M

Subjects
Animals, Cholecystokinin antagonists & inhibitors, Cholecystokinin genetics, Gastrointestinal Motility drug effects, Humans, Receptor, Cholecystokinin A antagonists & inhibitors, Receptor, Cholecystokinin A genetics, Cholecystokinin physiology, Colon physiology, Gastrointestinal Motility physiology, Receptor, Cholecystokinin A physiology
Abstract

Cholecystokinin (CCK) is a brain-gut peptide; it functions both as a neuropeptide and as a gut hormone. Although the pancreas and the gallbladder were long thought to be the principal peripheral targets of CCK, CCK receptors are found throughout the gut. It is likely that CCK has a physiological role not only in the stimulation of pancreatic and biliary secretions but also in the regulation of gastrointestinal motility. The motor effects of CCK include postprandial inhibition of gastric emptying and inhibition of colonic transit. It is now evident that at least two different receptors, CCK(1) and CCK(2) (formerly CCK-A and CCK-B, respectively), mediate the actions of CCK. Both localization and functional studies suggest that the motor effects of CCK are mediated by CCK(1) receptors in humans. Since CCK is involved in sensory and motor responses to distension in the intestinal tract, it may contribute to the symptoms of constipation, bloating and abdominal pain that are often characteristic of functional gastrointestinal disorders in general and irritable bowel syndrome (IBS), in particular. CCK(1) receptor antagonists are therefore currently under development for the treatment of constipation-predominant IBS. Clinical studies suggest that CCK(1) receptor antagonists are effective facilitators of gastric emptying and inhibitors of gallbladder contraction and can accelerate colonic transit time in healthy volunteers and patients with IBS. These drugs are therefore potentially of great value in the treatment of motility disorders such as constipation and constipation-predominant IBS.

Published
2004
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