Mesophase Formation during in vitro Cholesterol Gallstone Dissolution: A Specific Effect of Ursodeoxycholic Acid

1981 ◽  
Vol 70 (6) ◽  
pp. 713-715 ◽  
Author(s):  
C.C. Su ◽  
J.Y. Park ◽  
W.I. Higuchi ◽  
M.H. Alkan ◽  
O.I. Corrigan ◽  
...  
Keyword(s):  
Ursodeoxycholic Acid ◽  
Cholesterol Gallstone ◽  
Specific Effect ◽  
Gallstone Dissolution ◽  
Mesophase Formation

In vitro Cholesterol Gallstone Dissolution after Fragmentation with Shock Waves

Digestion ◽  
1986 ◽  
Vol 34 (1) ◽  
pp. 51-59 ◽  
Author(s):  
M. Neubrand ◽  
T. Sauerbruch ◽  
F. Stellaard ◽  
G. Paumgartner
Keyword(s):  
Shock Waves ◽  
Cholesterol Gallstone ◽  
Gallstone Dissolution

Mesophase Formation During Cholesterol Gallstone Dissolution in Human Bile: Effect of Bile Acid Composition

1984 ◽  
Vol 73 (8) ◽  
pp. 1160-1161 ◽  
Author(s):  
C.C. Su ◽  
W.I. Higuchix ◽  
I.T. Gilmore ◽  
R.G. Danzinger ◽  
A.F. Hofmann
Keyword(s):  
Bile Acid ◽  
Acid Composition ◽  
Cholesterol Gallstone ◽  
Human Bile ◽  
Gallstone Dissolution ◽  
Mesophase Formation

Abstract 153: IL-10 Accelerates Re-Endothelialization and Inhibits Post-injury Intimal Hyperplasia following Carotid Artery Denudation by Attenuating TNF-alpha-induced Endothelial Cell Dysfunction

2014 ◽  
Vol 115 (suppl_1) ◽  
Author(s):  
Suresh K Verma ◽  
Prasanna Krishnamurthy ◽  
Alexander R Mackie ◽  
Erin E Vaughan ◽  
Mohsin Khan ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Inflammatory Responses ◽  
Thrombus Formation ◽  
Specific Effect ◽  
Mononuclear Phagocytes ◽  
Tnf Alpha ◽  
Post Injury ◽  
Knock Out ◽  
Cytokines And Chemokines

The association of inflammation with atherosclerosis and restenosis is now fairly well established. Restenosis, a persistent complication of percutaneous vascular interventions, is thought to be a complex response to injury, which includes early thrombus formation, neointimal growth and acute inflammation. Mononuclear phagocytes are likely participants in the host response to vascular injury, via the secretion of cytokines and chemokines, including TNF-alpha (TNF). Others and we have previously shown that IL-10 inhibits TNF and other inflammatory mediators produced in response to cardiovascular injuries. The specific effect of IL-10 on endothelial cell (EC) biology is not well elucidated. Here we report that in a mouse model of carotid denudation, IL-10 knock-out mice (IL10KO) displayed significantly delayed ReEndothelialization and enhanced neointimal growth compared to their WT counterparts. Exogenous treatment of recombinant IL-10 dramatically blunted the inflammatory cell infiltration and neointimal thickening while significantly accelerating the recovery of the injured endothelium both WT and IL10KO mice. In vitro, IL10 co-treatment reversed TNF-mediated growth arrest, EC cell cycle inhibition, EC-monocyte adhesion and EC apoptosis. At signaling level, IL-10 reduced TNF-induced activation of JNK MAP kinase while simultaneously activating PI3K/Akt pathway. Because IL-10 function and signaling are important components for control of inflammatory responses, these results may provide insights necessary to develop strategies for modulating vascular repair and other accelerated arteriopathies, including transplant vasculopathy and vein graft hyperplasia.

THE INFLUENCE OF AND PEPTIDES ON MITOCHONDRIES STAIN AND L7A RIBOSOMES PROTEIN EXPRESSION DURING HUMAN PINEAL GLAND AND THYMUS CELL SENESCENCE

2020 ◽  
pp. 741-747
Author(s):  
О. М. Ивко ◽  
А. О. Дробинцева ◽  
Д. О. Леонтьева ◽  
И. М. Кветной ◽  
В. О. Полякова ◽  
...  
Keyword(s):  
Pineal Gland ◽  
Ribosomal Protein ◽  
Laser Scanning ◽  
Specific Effect ◽  
Cell Senescence ◽  
Laser Scanning Microscopy ◽  
Confocal Laser ◽  
Protein L ◽  
Mitotracker Red

Методом конфокальной лазерной сканирующей микроскопии верифицированы новые молекулярные мишени действия геропротекторных пептидов AEDG (эпиталона) и KE (вилона). Показано, что при старении клеток эпифиза и тимуса in vitro окраска митохондрий MitoTracker Red снижается, а синтез рибосомального белка L 7 A компенсаторно возрастает. Пептид AEDG в 1,5 раза повышал площадь окрашивания митохондрий MitoTracker Red и на 22 % снижал экспрессию белка рибосом L 7 A в культурах клеток эпифиза человека при их репликативном старении. Пептид KE в 1,5 раза повышал площадь окрашивания митохондрий MitoTracker Red и на 15 % снижал экспрессию белка рибосом L 7 A в культурах клеток тимуса человека при их репликативном старении. Можно предположить, что пептиды AEDG и KE обладают тканеспецифическим свойством, нормализующим функции митохондрий и рибосом пинеалоцитов и тимоцитов. It was verified new molecular targets of geroprotective activity of AEDG (epitalon) and KE (vilon) peptides by the method of confocal laser scanning microscopy. It was shown that the MitoTracker Red mitochondries staining decreased and L 7 A ribosomal protein synthesis compensatory increased during pineal and thymic cell senescence in vitro . AEDG peptide increases in 1,5 times the square of MitoTracker Red mitochondries staining and decreases on 22% the expression of ribosomal protein L 7 A in cultures of human pineal gland cells during its senescence. KE peptide increases in 1,5 times the square of MitoTracker Red mitochondries staining and decreases on 15% the expression of ribosomal protein L 7 A in cultures of human thymic cells during its senescence. The square of MitoTracker Red mitochondries staining decreases and the expression of L 7 A ribosomal protein compensatory increases during pineal gland and thymic cells senescence. We can suppose that AEDG and KE peptides have a tissue-specific effect that normalizes the functions of mitochondria and ribosomes of pinealocytes and thymocytes.

Correction to: “Evaluation of Lincomycin as a Cholesterol Gallstone Dissolution Rate Accelerator”

1985 ◽  
Vol 74 (12) ◽  
pp. 1344
Author(s):  
Bob D. Rush ◽  
Mary J. Ruwart ◽  
Bradley D. Anderson ◽  
William I. Higuchi
Keyword(s):  
Dissolution Rate ◽  
Cholesterol Gallstone ◽  
Gallstone Dissolution

scholarly journals KBE009: A Bestatin-Like Inhibitor of the Trypanosoma cruzi Acidic M17 Aminopeptidase With In Vitro Anti-Trypanosomal Activity

Life ◽  
2021 ◽  
Vol 11 (10) ◽  
pp. 1037
Author(s):  
Jorge González-Bacerio ◽  
Irina Arocha ◽  
Mirtha Elisa Aguado ◽  
Yanira Méndez ◽  
Sabrina Marsiccobetre ◽  
...  
Keyword(s):  
Trypanosoma Cruzi ◽  
Rational Design ◽  
Specific Effect ◽  
Dermal Fibroblasts ◽  
Aminopeptidase Activity ◽  
Geometrical Shape ◽  
Starting Point ◽  
Insight Into ◽  
Leucyl Aminopeptidase

Chagas disease, caused by the kinetoplastid parasite Trypanosoma cruzi, is a human tropical illness mainly present in Latin America. The therapies available against this disease are far from ideal. Proteases from pathogenic protozoan have been considered as good drug target candidates. T. cruzi acidic M17 leucyl-aminopeptidase (TcLAP) mediates the major parasite’s leucyl-aminopeptidase activity and is expressed in all parasite stages. Here, we report the inhibition of TcLAP (IC50 = 66.0 ± 13.5 µM) by the bestatin-like peptidomimetic KBE009. This molecule also inhibited the proliferation of T. cruzi epimastigotes in vitro (EC50 = 28.1 ± 1.9 µM) and showed selectivity for the parasite over human dermal fibroblasts (selectivity index: 4.9). Further insight into the specific effect of KBE009 on T. cruzi was provided by docking simulation using the crystal structure of TcLAP and a modeled human orthologous, hLAP3. The TcLAP-KBE009 complex is more stable than its hLAP3 counterpart. KBE009 adopted a better geometrical shape to fit into the active site of TcLAP than that of hLAP3. The drug-likeness and lead-likeness in silico parameters of KBE009 are satisfactory. Altogether, our results provide an initial insight into KBE009 as a promising starting point compound for the rational design of drugs through further optimization.

Sign in / Sign up

Export Citation Format

Share Document