Hepatobiliary Kinetics of 113mIn-Phenolphthalexon

1981 ◽  
Vol 20 (02) ◽  
pp. 90-93
Author(s):  
P.B. Parab ◽  
U.R. Raikar ◽  
R.D. Ganatra ◽  
M. C. Patel
Keyword(s):  
Biliary Excretion ◽  
Iminodiacetic Acid ◽  
Organ Distribution ◽  
Liver Uptake ◽  
On Line ◽  
Rapid Clearance ◽  
Chemical Purity ◽  
Kinetics Of ◽  
High Liver

Phenolphthalexon, a compound with iminodiacetic acid as a functional group, has been labelled with 113mIn to high chemical purity and its usefulness in studies of biliary excretion patency has been studied. Organ distribution of 113mIn-phenolphthalexon in mice was characterized by high liver uptake (50.8% of the administered dose after 5 min) and rapid clearance through the gall bladder. An animal model for studying obstruction of biliary excretion has been developed. Data on the kinetics of the radiopharmaceutical were obtained by collecting in-vivo data through an on-line computer.

scholarly journals Kinetics of biliary excretion of the main two bilirubin photoproducts after injection into Gunn rats

1981 ◽  
Vol 198 (1) ◽  
pp. 107-112 ◽  
Author(s):  
S Onishi ◽  
N Kawade ◽  
S Itoh ◽  
K Isobe ◽  
S Sugiyama ◽  
...  
Keyword(s):  
Biliary Excretion ◽  
Half Life ◽  
Gunn Rats ◽  
Kinetics Of

The kinetics of biliary excretion of the main two photoproducts after injection into Gunn rats were examined. The photoproducts that are obtained from experiments in vitro consist of unknown pigment, photobilirubin IXa and a small amount of (ZZ)-bilirubin IXa. It was confirmed previously that the first two photoproducts are identical with the main two photoproducts obtained in vivo. In experiments on four animals, the average of total biliary recoveries of unknown pigment was 81.4%, and that of photobilirubin IXa in the bile estimated by the Sigma-minus method was 29.8 min and that for unknown pigment was 4.3 min. The rate of thermal reversion of photobilirubin IXa to (ZZ)-bilirubin IXa in the bile at 37 degrees C was very rapid, i.e. its half-life was 6.2 min.

Effect of pH and inhibitors on beta-amyloid fibril assembly

1996 ◽  
Vol 54 ◽  
pp. 752-753
Author(s):  
Beverly E. Maleeff ◽  
Timothy K. Hart ◽  
Stephen J. Wood ◽  
Ronald Wetzel
Keyword(s):  
Amyloid Fibril ◽  
Peptide Fragment ◽  
Hydrophobic Peptides ◽  
Amyloid Fibril Formation ◽  
Effects Of Ph ◽  
Severity Of The Disease ◽  
Kinetics Of ◽  
The Brain

Alzheimer's disease is characterized post-mortem in part by abnormal extracellular neuritic plaques found in brain tissue. There appears to be a correlation between the severity of Alzheimer's dementia in vivo and the number of plaques found in particular areas of the brain. These plaques are known to be the deposition sites of fibrils of the protein β-amyloid. It is thought that if the assembly of these plaques could be inhibited, the severity of the disease would be decreased. The peptide fragment Aβ, a precursor of the p-amyloid protein, has a 40 amino acid sequence, and has been shown to be toxic to neuronal cells in culture after an aging process of several days. This toxicity corresponds to the kinetics of in vitro amyloid fibril formation. In this study, we report the biochemical and ultrastructural effects of pH and the inhibitory agent hexadecyl-N-methylpiperidinium (HMP) bromide, one of a class of ionic micellar detergents known to be capable of solubilizing hydrophobic peptides, on the in vitro assembly of the peptide fragment Aβ.

Kinetics of Various 99mTc-Sn-Pyrophosphate Compounds in the Rat

1977 ◽  
Vol 16 (04) ◽  
pp. 157-162 ◽  
Author(s):  
C. Schümichen ◽  
B. Mackenbrock ◽  
G. Hoffmann
Keyword(s):  
Normal Saline ◽  
Half Life ◽  
Compound A ◽  
Short Half Life ◽  
Low Concentrations ◽  
The Stability ◽  
Kinetics Of ◽  
In Vitro Stability

SummaryThe bone-seeking 99mTc-Sn-pyrophosphate compound (compound A) was diluted both in vitro and in vivo and proved to be unstable both in vitro and in vivo. However, stability was much better in vivo than in vitro and thus the in vitro stability of compound A after dilution in various mediums could be followed up by a consecutive evaluation of the in vivo distribution in the rat. After dilution in neutral normal saline compound A is metastable and after a short half-life it is transformed into the other 99mTc-Sn-pyrophosphate compound A is metastable and after a short half-life in bone but in the kidneys. After dilution in normal saline of low pH and in buffering solutions the stability of compound A is increased. In human plasma compound A is relatively stable but not in plasma water. When compound B is formed in a buffering solution, uptake in the kidneys and excretion in urine is lowered and blood concentration increased.It is assumed that the association of protons to compound A will increase its stability at low concentrations while that to compound B will lead to a strong protein bond in plasma. It is concluded that compound A will not be stable in vivo because of a lack of stability in the extravascular space, and that the protein bond in plasma will be a measure of its in vivo stability.

Continuous Quantitative Monitoring of Mural, Platelet-Dependent, Thrombus Kinetics in the Crushed Rat Femoral Vein

1991 ◽  
Vol 65 (04) ◽  
pp. 425-431 ◽  
Author(s):  
F Stockmans ◽  
H Deckmyn ◽  
J Gruwez ◽  
J Vermylen ◽  
R Acland
Keyword(s):  
Thrombus Formation ◽  
Femoral Vein ◽  
Maximum Size ◽  
Digital Analysis ◽  
Video Recordings ◽  
Quantitative Monitoring ◽  
Set Up ◽  
Kinetics Of ◽  
Quantitative Nature

SummaryA new in vivo method to study the size and dynamics of a growing mural thrombus was set up in the rat femoral vein. The method uses a standardized crush injury to induce a thrombus, and a newly developed transilluminator combined with digital analysis of video recordings. Thrombi in this model formed rapidly, reaching a maximum size 391 ± 35 sec following injury, after which they degraded with a half-life of 197 ± 31 sec. Histological examination indicated that the thrombi consisted mainly of platelets. The quantitative nature of the transillumination technique was demonstrated by simultaneous measurement of the incorporation of 111In labeled platelets into the thrombus. Thrombus formation, studied at 30 min interval in both femoral veins, showed satisfactory reproducibility overall and within a given animalWith this method we were able to induce a thrombus using a clinically relevant injury and to monitor continuously and reproducibly the kinetics of thrombus formation in a vessel of clinically and surgically relevant size

Acquired Haemophilia: Functional Study of Antibodies to Factor VIII

1981 ◽  
Vol 45 (03) ◽  
pp. 285-289 ◽  
Author(s):  
J P Allain ◽  
A Gaillandre ◽  
D Frommel
Keyword(s):  
Factor Viii ◽  
Functional Study ◽  
Factor Viii Inhibitor ◽  
Acquired Haemophilia ◽  
Viii Inhibitor ◽  
Kinetics Of ◽  
Antibody Function ◽  
Native Plasma

SummaryFactor VIII complex and its interaction with antibodies to factor VIII have been studied in 17 non-haemophilic patients with factor VIII inhibitor. Low VIII:C and high VIIIR.Ag levels were found in all patients. VIII:WF levels were 50% of those of VTIIRrAg, possibly related to an increase of poorly aggregated and electrophoretically fast moving VIIIR:Ag oligomers.Antibody function has been characterized by kinetics of VIII :C inactivation, saturability by normal plasma and the slope of the affinity curve. Two major patterns were observed:1) Antibodies from 6 patients behaved similarly to those from haemophiliacs by showing second order inhibition kinetics, easy saturability and steep affinity slope (> 1).2) Antibodies from other patients, usually with lower titres, inactivated VIII :C according to complex order kinetics, were not saturable, and had a less steep affinity slope (< 0.7). In native plasma, or after mixing with factor VIII concentrate, antibodies of the second group did not form immune complexes with the whole factor VIII molecular complex. However, dissociation procedures did release some antibodies from apparently low molecular weight complexes formed in vivo or in vitro. For appropriate management of non-haemophilic patients with factor VIII inhibitor, it is important to determine the functional properties of their antibodies to factor VIII.

Uptake, Internalization and Degradation of the Novel Plasminogen Activator Reteplase (BM 06.022) in the Rat

1995 ◽  
Vol 74 (06) ◽  
pp. 1501-1510 ◽  
Author(s):  
J Kuiper ◽  
H van de Bilt ◽  
U Martin ◽  
Th J C van Berkel
Keyword(s):  
Plasminogen Activator ◽  
Liver Cells ◽  
The Novel ◽  
Uptake Mechanism ◽  
Liver Uptake ◽  
Lysosomal Compartment ◽  
Β Phase ◽  
Α Phase ◽  
Parenchymal Liver

SummaryThe catabolism of the novel plasminogen activator reteplase (BM 06.022) was described. For this purpose BM 06.022 was radiolabelled with l25I or with the accumulating label l25I-tyramine cellobiose (l25I-TC).BM 06.022 was injected at a pharmacological dose of 380 μg/kg b.w. and it was cleared from the plasma in a biphasic manner with a half-life of about 1 min in the α-phase and t1/2of 20-28 min in the β-phase. 28% and 72% of the injected dose was cleared in the α-phase and β-phase, respectively. Initially liver, kidneys, skin, bones, lungs, spleen, and muscles contributed mainly to the plasma clearance. Only liver and the kidneys, however, were responsible for the uptake and subsequent degradation of BM 06.022 and contributed for 75% to the catabolism of BM 06.022. BM 06.022 was degraded in the lysosomal compartment of both organs. Parenchymal liver cells were responsible for 70% of the liver uptake of BM 06.022. BM 06.022 associated rapidly to isolated rat parenchymal liver cells and was subsequently degraded in the lysosomal compartment of these cells. BM 06.022 bound with low-affinity to the parenchymal liver cells (550 nM) and the binding of BM 06.022 could be displaced by t-PA (IC50 5.6 nM), indicating that the low-density lipoprotein receptor-related protein (LRP) could be involved in the binding of BM 06.022. GST-RAP, which is an inhibitor of LRP, could in vivo significantly inhibit the uptake of BM 06.022 in the liver.It is concluded that BM 06.022 is metabolized primarily in the liver and the kidneys. These organs take up and degrade BM 06.022 in the lysosomes. The uptake mechanism of BM 06.022 in the kidneys is unknown, while LRP is responsible for a low-affinity binding and uptake of BM 06.022 in parenchymal liver cells.

Turnover of Human Extrinsic (Tissue-Type) Plasminogen Activator in Rabbits

1981 ◽  
Vol 46 (03) ◽  
pp. 658-661 ◽  
Author(s):  
C Korninger ◽  
J M Stassen ◽  
D Collen
Keyword(s):  
Plasminogen Activator ◽  
Intravenous Injection ◽  
Active Site ◽  
Half Life ◽  
Degradation Products ◽  
Gel Filtration ◽  
Tissue Type ◽  
Organ Distribution ◽  
Small Rise

SummaryThe turnover of highly purified human extrinsic plasminogen activator (EPA) (one- and two-chain form) was studied in rabbits. Following intravenous injection, EPA-activity declined rapidly. The disappearance rate of EPA from the plasma could adequately be described by a single exponential term with a t ½ of approximately 2 min for both the one-chain and two-chain forms of EPA.The clearance and organ distribution of EPA was studied by using 125I-labeled preparations. Following intravenous injection of 125I-1abeled EPA the radioactivity disappeared rapidly from the plasma also with a t ½ of approximately 2 min down to a level of 15 to 20 percent, followed by a small rise of blood radioactivity. Gel filtration of serial samples revealed that the secondary increase of the radioactivity was due to the reappearance of radioactive breakdown products in the blood. Measurement of the organ distribution of 125I at different time intervals revealed that EPA was rapidly accumulated in the liver, followed by a release of degradation products in the blood.Experimental hepatectomy markedly prolonged the half-life of EPA in the blood. Blocking the active site histidine of EPA had no effect on the half-life of EPA in blood nor on the gel filtration patterns of 125I in serial plasma samples.It is concluded that human EPA is rapidly removed from the blood of rabbits by clearance and degradation in the liver. Recognition by the liver does not require a functional active site in the enzyme. Neutralization in plasma by protease inhibitors does not represent a significant pathway of EPA inactivation in vivo.

Binding kinetics of fluorescent bisphosphonates as a tool for monitoring bone dynamics in vivo

2013 ◽  
Author(s):  
Robert Tower ◽  
Graeme Campbell ◽  
Marc Muller ◽  
Olga Will ◽  
Frederieka Grundmann ◽  
...  
Keyword(s):  
Binding Kinetics ◽  
Kinetics Of ◽  
Bone Dynamics

n. 178 (15): Dor On Line

Dor on line ◽  
2015 ◽  
Author(s):  
Paulo Barboni
Keyword(s):  
On Line

Edição de Maio de 2015 - Ano 15 - Número 178 Leitores de nosso boletim Dor On Line, a edição de maio de 2015 traz um editorial sobre a homeopatia e a dor. Na seção Divulgação Científica, trazemos alertas sobre a dor em bebês com diagnóstico por imagem; a dor e demência em pacientes internados; estudos sobre um produto natural derivado de fungos e a dor na osteoartrite; e o uso de opioides na dor crônica e uma nova tecnologia para o tratamento da dor por estimulação elétrica. Na seção Ciência e Tecnologia, trazemos alertas sobre o veneno da aranha armadeira, o placeboloma, a analgesia da N-acetil cisteína, evidencias de que a estimulação in vivo de queratinócitos basta para induzir nocicepção, e o tratamento da neuropatia por estreptozotocina por células mesenquimais. Boa leitura! EDITORIAL DO MÊS Homeopatia, Dor e o Conselho de Pesquisa Médica e Saúde Nacional da Austrália Paulo Gustavo Barboni Dantas Nascimento, Camila Alves Areda Divulgação Científica 1. Estudo com ressonância magnética revela que os bebês sentem dores como os adultos. Pesquisadores destacam a importância do tratamento adequado para o alívio da dor em bebês Andressa Daiane de Carvalho Zaparolli 2. Dor, agitação e comportamentos problemas em pessoas com demência internados em leitos hospitalares gerais: um estudo de coorte longitudinal. Dor e sintomas da demência: uma melhor perspectiva de avaliação e controle da dor Thatiane Sandielen Lima Soares 3. Cordycepin usado como mediadores inflamatórios na osteoartrite. Fungo conhecido como de outro planeta para tratar inflamação e dor Ieda Regina dos Santos 4. As taxas de uso indevido de opioides, abuso e dependência em dor crônica. Uma revisão sistemática e síntese de dados Sarah Lima Carneiro de Sousa 5. Empresa brasileira desenvolve equipamentos portáteis para tratamento da dor. Estimulação elétrica nervosa transcutânea para a dismenorreia/dor abdominal e recuperação de atletas Maria Clotilde Rossetti-Ferreira, Paulo Gustavo Barboni Dantas Nascimento Ciência e Tecnologia 6. Uso de fração de veneno de aranha possui efeito antinociceptivo. Veneno da aranha armadeira pode ser útil no alívio de sintomas de dores neuropáticas Anne Karoline Schreiber 7. Genética e o efeito placebo: o placeboma. Evidências revelam que variações genéticas nas vias de neurotransmissores do cérebro modificam o efeito placebo Andressa Daiane de Carvalho Zaparolli 8. N-acetil cisteína pode promover analgesia em humanos. Uma nova perspectiva clínica Rangel Leal Silva 9. Estimulação de queratinócitos selecionados é o suficiente para nocicepção. Queratinócitos com TRPV1 ativos, ao serem estimulados provocam nocicepção Ana Carolina Alves M de Moura 10. Células-tronco mesenquimais e a neuropatia periférica diabética. Avaliação do efeito do transplante de células-tronco no tratamento da neuropatia Amanda de Araujo Fonseca 

n. 192 (16): Dor On Line

Dor on line ◽  
2016 ◽  
Author(s):  
Paulo Barboni
Keyword(s):  
On Line ◽  
Óxido Nítrico

Edição de Julho de 2016 - Ano 16 - Número 192   Esta é uma edição especial: uma homenagem ao idealizador deste projeto! Aqui nos despedimos do Prof. Dr. Sérgio Henrique Ferreira, que nos deixou neste mês de julho, depois de uma vida dedicada ao desenvolvimento da Ciência Brasileira, à sua divulgação e difusão. Este “jornal eletrônico” (como ele sempre chamava o DOL), agora com 16 anos de existência, é uma evidência disso. Por esse motivo, a Equipe DOL tomou para si uma árdua tarefa neste momento de seu passamento: honrar nosso Editor-Chefe com uma edição que pudesse traduzir um pouco do que foi a somatória de suas contribuições como cientista, pesquisador, educador e amigo... Esperamos que nosso objetivo tenha sido alcançado... Boa leitura!   Editorial (especial) Sérgio Henrique Ferreira: quando a curiosidade é a força motriz... Ieda Regina dos Santos, José Waldik Ramon, Mani Indiana Funez e Paulo Gustavo Barboni Dantas Nascimento Nossa ideia ao escrever este editorial foi contar resumidamente (e “bem resumidamente”) um pouco da história dessa figura ímpar chamada Sérgio Henrique Ferreira. Além da parte textual, procuramos fazer algo um pouco diferente, criando um mural de fotos que ilustra momentos da vida do idealizador do DOL – Dor On Line, mostrando um pouco mais de suas facetas...   Alertas (especial) 1. Toxina isolada do veneno da jararaca potencializa ação da Bradicinina. Um novo mecanismo in vivo para o desenvolvimento de novas drogas. Paulo Gustavo Barboni Dantas Nascimento 2. Isolamento de peptídeos potencializadores da ação da bradicinina presentes no veneno da jararaca Bothrops. Um passo a mais para o desenvolvimento dos inibidores da ECA Cássia Regina da Silva 3. Efeitos da indometacina e da aspirina sobre a liberação de prostaglandinas. Um passo a mais em direção ao Nobel. Andreza Urba de Quadros 4. Prostaglandinas e a analgesia da aspirina. No caminho de desvendar a sensibilização de aferentes periféricos. Mani Indiana Funez 5. O bloqueio da geração local de prostaglandinas esclarece o efeito analgésico da aspirina.  A via clássica de ação das aspirinas. Alexandre Hashimoto Pereira Lopes 6. A hiperalgesia das prostaglandinas. O envolvimento de íons cálcio e o cAMP. Paulo Gustavo Barboni Dantas Nascimento 7. Bloqueio pelo soro anti-macrófagos da migração de neutrófilos polimorfonucleares para a cavidade peritoneal inflamada. Neutrófilos e sua atuação como células de alarme durante o processo inflamatório Jozi Godoy Figueiredo 8. Interleucina-1 beta como potente agente hiperalgésico. A Interleucina IL-1β, potente agente hiperalgésico, é antagonizada por um tripeptídeo análogo. Miriam das Dores Fonseca 9. Mecanismo de ação da analgesia periférica da morfina - estimulação do sistema do L-arg/NO/GMPc. A morfina promove analgesia através do óxido nítrico em neurônios periféricos. Anne Karoline Schreiber 10. A analgesia periférica da morfina depende da ativação da via de sinalização. Mecanismo molecular de opioides. Erika Ivanna Araya Pallarés

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