15,857 research outputs found
No change in amount of HGF protein or hepatocyte proliferation in HGF KO mice after PH.
No full text<p>(<b>A</b>) Genomic recombination is present in cre-inducible HGF<sup>ex.5 flox</sup> KO mice at all time points after PH, as assessed by PCR. (<b>B</b>) RT-PCR shows a significant amount of full-length HGF mRNA remaining in KOs even after PH. (<b>C</b>) The amount of unrecombined HGF is slightly decreased in HGF KO as compared to controls before and after PH, as assessed by real-time PCR. (<b>D</b>) Comparable amounts of HGF protein in control and HGF KO livers after PH. Ponceau represents loading control. (<b>E</b>) Proliferation is unaffected in HGF KO mice after PH, as shown by representative images of Ki67 IHC (100X).</p
PENGARUH pH TERHADAP DEGRADASI HIDROLITIK BENANG BEDAH SINTETIS BERBASIS POLI(GLIKOLAT-KO-LAKTAT)
Full text linkPENGARUH pH TERHADAP DEGRADASI HIDROLITIK BENANG BEDAH SINTETIS BERBASIS POLI(GLIKOLAT-KO-LAKTAT). Telah dilakukan studi in vitro tentang pengaruh pH terhadap proses degradasi hidrolitik benang bedah sintesis berbasis kopolimer poli(glikolat-ko-laktat). Pengujian dilakukan dengan cara inkubasi dalamlarutan penyangga dengan nilai pH 4, pH 7 dan pH 10 selama beberapaminggu pada suhu 37 oC. Perubahan strukturmikro dan morfologi diamati dengan peralatan Scanning Electron Microscope (SEM), dan X-Ray Diffraction (XRD). Hasil penelitian menunjukkan bahwa kecepatan degradasi hidrolitik benang bedah dipengaruhi oleh kondisi pH lingkungan, yang mana semakin tinggi pH semakin cepat proses degradasi. Pada pH 4 proses degradasi benang bedah tampak nyata setelah inkubasi selama 9 minggu sedangkan pada pada pH 10 setelah 4 minggu. Proses degradasi diiringi dengan kenaikan kristalinitas benang yang tampak nyata terutama pada pH 4
Lipid accumulation in wild-type (WT) and PPARβ-null (KO) mice after PH.
No full text<p>(A) Hematoxylin and eosin staining shows lipid accumulation in WT mice, but not in KO mice, 36 hr after PH. Sham tissue used as negative control. (B) Hepatic gene expression levels of (B) PPARα and (C) PPARγ in WT and KO mice over a time course from 0 to 72 hours after PH (n = 3). Means ± SD are graphed. * <i>p</i><0.05.</p
Experiments and simulations of pH in tumors with wild-type, HIF-1<i>α</i>-, and HIF-2<i>α</i>-deficient macrophages (WT, HIF-1<i>α</i> KO, and HIF-2<i>α</i> KO).
No full text<p>Horizontal axis represents time (in days) and vertical axis shows the pH value. (a): Experimental data of pH against time with error bars. Red: WT; Blue: HIF-1<i>α</i> KO; Green: HIF-2<i>α</i> KO. (b) – (d): Comparison of experiments (dots with error bars) and numerical simulations (dash curves) of pH in tumor with WT, HIF1-<i>α</i>, and HIF-2<i>α</i> KO macrophages, respectively.</p
Met expression and activation is altered in HGF KO mice after CCl4 and PH.
No full text<p>(<b>A</b>) WB for total Met shows increased expression in HGF KO animals at D2 after CCl4/PH. GAPDH represents loading control. (<b>B</b>) IP shows that Met is phosphorylated and active in controls but not in HGF KOs at D2 after CCl4/PH. Successful pulldown of Met is verified, and a non-specific band is used as normalizing control.</p
Liver regeneration is compromised in HGF KO mice after CCl4 and PH due to a decrease in HGF.
No full text<p>(<b>A</b>) Real-time PCR demonstrates decreased HGF mRNA in HGF<sup>ex.5 flox</sup>; Cre-ER<sup>T</sup> KO mice treated with both CCl4 and PH as compared to control at D1 after PH. (<b>B</b>) Graph of liver weight to body weight ratios after CCl4/PH shows a significant decrease in HGF KOs at D2. (*P<0.05) (<b>C</b>) Representative images of PCNA IHC on livers harvested at D2 after PH in control and HGF KO animals treated with CCl4 (200X) (<b>D</b>) Quantification of PCNA staining shown in (C). A total of 5 fields per liver (n = 3 per condition) were counted. (**P<0.01) (<b>E</b>) WB for HGF and PCNA shows a dramatic decrease in both proteins in HGF KO animals at D2 after CCl4/PH. Ponceau represents loading control. (<b>F</b>) HGF IHC in control and HGF KO livers harvested at D2 after PH demonstrates sparse and irregular distribution of HGF protein.</p
Depressed E2f downstream target gene expression in PPARβ-null (KO) mice after PH.
No full text<p>(A) qPCR analysis of E2f target gene involved in cell cycle, DNA synthesis and replication, and DNA repair. (B) Real time qPCR analysis of Cyclin D over a time course from 0 to 72 hours after PH. (C) Western blot analysis of Cyclin D at 36–48 hr after PH. Real time qPCR analysis of (D-E) Cyclin E/Cdk2, and (G-H) Cyclin A, B/Cdk1 in wild-type (WT) and KO mice over a time course from 0 to 72 hours after PH. (I) Western blot analysis of Cyclin E at 36–48 hr after PH (n = 3). Means ± SD are graphed. * <i>p</i><0.05.</p
TRβ is transiently downregulated after PH and liver regeneration is delayed in TRα1/TRβ double KO mice.
No full text<p>(A,B) WT and TRα1/TRβ KO mice (‘KO’) were submitted to 70% PH, and the protein levels of TRα1 (55 kDa) and TRβ (47 kDa) were determined by Western blot, and expressed as percentage of the normalized band intensities (using β-actin as control) <i>vs.</i> sham operated animals at 0 h. (C) mRNA levels of TRα1 and TRβ were determined by quantitative real time RT-PCR. (D) The serum levels of T3 and T4 after PH were measured and expressed as percentage <i>vs.</i> sham operated animals at 0 h. The basal values were 7.4±0.5 and 36.5±4.2 µg/dl for T4 in WT and KO, respectively; 78±5 and 2965±307 ng/dl for T3 in WT and KO, respectively. (E) Liver mass recovery after PH was determined in these animals and in WT mice treated with MMI to pharmacologically induce hypothyroidism, and in one group of animals thyroid hormone was restituted by administration of T4. (F) Acute liver injury after PH was evaluated by measuring serum AST levels. Results show means ± SD of 6 to 8 animals per condition (B,C,E,F), 4 animals (D) or a representative blot of three (A). #P<0.01 <i>vs.</i> the corresponding condition at 0h (B,D); *P<0.05, **P<0.01 <i>vs.</i> WT condition or T4-untreated WT animals (E,F).</p
Normal liver regeneration in CPEB4-knockout (KO) mice after partial hepatectomy (PH).
No full text(A) The body weight of 2-month-old CPEB4 wild-type (WT) and -KO male littermates was measured, then mice underwent 70% PH. At the designated time after the surgery, livers were isolated for measuring liver weight/body weight. Date are mean ± standard deviation from 2 WT or KO mice per time point. (B) Western blot analysis of CPEB4, cyclin B1 (CCNB1), proliferating cell nuclear antigen (PCNA) and β-actin in liver tissues. The liver tissues at the time-zero-point were collected from sham-operated mice.</p
An intracellular pH gradient in the anammox bacterium Kuenenia stuttgartiensis as evaluated by (31)P NMR
Full text linkThe cytoplasm of anaerobic ammonium oxidizing (anammox) bacteria consists of three compartments separated by membranes. It has been suggested that a proton motive force may be generated over the membrane of the innermost compartment, the “anammoxosome”. 31P nuclear magnetic resonance (NMR) spectroscopy was employed to investigate intracellular pH differences in the anammox bacterium Kuenenia stuttgartiensis. With in vivo NMR, spectra were recorded of active, highly concentrated suspensions of K. stuttgartiensis in a wide-bore NMR tube. At different external pH values, two stable and distinct phosphate peaks were apparent in the recorded spectra. These peaks were equivalent with pH values of 7.3 and 6.3 and suggested the presence of a proton motive force over an intracytoplasmic membrane in K.stuttgartiensis. This study provides for the second time—after discovery of acidocalcisome-like compartments in Agrobacterium tumefaciens—evidence for an intracytoplasmic pH gradient in a chemotrophic prokaryotic cell.BiotechnologyApplied Science
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