SINTESIS DAN OPTIMASI MEMBRAN SELULOSA ASETAT PADA PROSES MIKROFILTRASI BAKTERI

Tujuan dari penelitian ini adalah mensintesis membran selulosa asetat yang dapat dipakai untuk sterilisasi larutan media pertumbuhan bakteri. Dalam penelitian ini, diupayakan modifikasi ukuran pori membran yang sesuai untuk proses sterilisasi, yaitu mempunyai permeabilitas dan selektivitas tinggi terhadap bakteri tetapi rendah terhadap komponen media lain yang lolos melalui membran. Pembuatan membran dilakukan dengan sistem tiga komponen selulosa asetat, aseton, dan aditif formamida. Struktur pori membran diupayakan asimetris. Karakteristik membran dilakukan terhadap uji permselektivitas (rejeksi), permeabilitas (fluks), struktur dan morfologi membran.Uji dilakukan terhadap larutan umpan media tumbuh bakteri yang dikontaminasi dengan bakteri E-coli. Dari hasil penelitian diperoleh bahwa membran selulosa asetat dapat digunakan untuk menyaring bakteri. Komposisi larutan cetak berpengaruh pada nilai fluks dan nilai rejeksi.Makin tinggi komposisi larutan selulosa asetat, rejeksi makin tinggi dan fluks makin rendah. Proses gelasi (pemberian waktu untuk penguapan pelarut) dapat meningkatkan rejeksi dari 62,94% menjadi 67,83% pada waktu gelasi 1 menit. Kondisi terbaik dari percobaan komposisi selulosa asetat 16%, aseton 50% dan formamida 34%, waktu gelasi 1 menit dengan nilai rejeksi 67,83% dan nilai fluks 16,25 lt.m-2.jam-1. Pengamatan Scanning Electron Microscope (SEM) menunjukkan struktur pori membran asimetris

Endothelial overexpression of endothelin-1 modulates aortic, carotid, iliac and renal arterial responses in obese mice

Endothelin-1 (ET-1) is essential for mammalian development and life, but it has also been implicated in increased cardiovascular risk under pathophysiological conditions. The aim of this study was to determine the impact of endothelial overexpression of the prepro-endothelin-1 gene on endothelium-dependent and endothelium-independent responses in the conduit and renal arteries of lean and obese mice. Obesity was induced by high-fat-diet (HFD) consumption in mice with Tie-1 promoter-driven, endothelium-specific overexpression of the prepro-endothelin-1 gene (TET(het)) and in wild-type (WT) littermates on a C57BL/6N background. Isometric tension was measured in rings (with endothelium) of the aorta (A), carotid (CA) and iliac (IA) arteries as well as the main (MRA) and segmental renal (SRA) arteries; all experiments were conducted in the absence or presence of L-NAME and/or the COX inhibitor meclofenamate. The release of prostacyclin and thromboxane A2 was measured by ELISA. In the MRA, TET(het) per se increased contractions to endothelin-1, but the response was decreased in SRA in response to serotonin; there were also improved relaxations to acetylcholine but not insulin in the SRA in the presence of L-NAME. HFD per se augmented the contractions to endothelin-1 (MRA) and to the thromboxane prostanoid (TP) receptor agonist U46619 (CA, MRA) as well as facilitated relaxations to isoproterenol (A). The combination of HFD and TET(het) overexpression increased the contractions of MRA and SRA to vasoconstrictors but not in the presence of meclofenamate; this combination also augmented further relaxations to isoproterenol in the A. Contractions to endothelin-1 in the IA were prevented by endothelin-A receptor antagonist BQ-123 but only attenuated in obese mice by BQ-788. The COX-1 inhibitor FR122047 abolished the contractions of CA to acetylcholine. The release of prostacyclin during the latter condition was augmented in samples from obese TET(het) mice and abolished by FR122047. These findings suggest that endothelial TET(het) overexpression in lean animals has minimal effects on vascular responsiveness. However, if comorbid with obesity, endothelin-1-modulated, prostanoid-mediated renal arterial dysfunction becomes apparent