In vivo natural-abundance17O/1H MRI of rhesus monkey body in a whole-body scanner

2003 ◽  
Vol 24 (3-4) ◽  
pp. 423-427 ◽  
Author(s):  
J. Hankiewicz ◽  
S. U. Brint ◽  
A. Guidotti ◽  
E. Costa ◽  
D. Fiat
2012 ◽  
Vol 61 (1) ◽  
pp. 129-139 ◽  
Author(s):  
Bobo Hu ◽  
Gopal Varma ◽  
Chris Randell ◽  
Stephen F. Keevil ◽  
Tobias Schaeffter ◽  
...  

2008 ◽  
Vol 60 (4) ◽  
pp. 917-927 ◽  
Author(s):  
Marie Poirier-Quinot ◽  
Jean-Christophe Ginefri ◽  
Olivier Girard ◽  
Philippe Robert ◽  
Luc Darrasse

Blood ◽  
1964 ◽  
Vol 24 (4) ◽  
pp. 356-371 ◽  
Author(s):  
DONALD VAN DYKE ◽  
HAL ANGER ◽  
MYRON POLLYCOVE

Abstract Distribution of marrow within the skeleton has been determined in man, rabbits, and rats by in vivo labeling of the marrow compartment with radioiron and either assaying each bone separately for radioactivity or obtaining a gamma-ray image of the distribution of the marrow by whole body scanner or positron scintillation camera. In man, extension of marrow into unusual sites was demonstrated after prolonged and severe stimulation, excessive blood loss, or hemolysis for a long period. A rabbit made severely anemic by administration of phenylhydrazine for 7 days showed extension of marrow into the distal portion of the humeri and femora. In rats in which erythropoiesis was stimulated by erythropoietin administration there was no significant increase in total marrow volume and no change in distribution of marrow within the skeleton. The positron scintillation camera provides an excellent method for qualitative evaluation of the marrow distribution. It has sufficient resolving power to give a good picture of the distribution of marrow with Fe52 in a skeleton as small as that of the rat. The distribution apparent from the positron pictures has been confirmed by complete skeletal analysis of individual bones.


1989 ◽  
Vol 30 (4) ◽  
pp. 365-368 ◽  
Author(s):  
K. E. Jensen ◽  
H. Nielsen ◽  
C. Thomsen ◽  
P. G. Sørensen ◽  
H. Karle ◽  
...  

Nine patients with myelodysplastic syndrome (MDS) were examined with magnetic resonance imaging and in vivo T1 relaxation time measurements of the vertebral bone marrow in a 1.5 tesla whole body scanner. Two patients underwent transformation to acute myeloid leukemia and were evaluated at follow-up examinations. At the time of diagnosis the T1 relaxation times of the vertebral bone marrow were significantly prolonged compared with normal values. The T1 relaxation times of the vertebral bone marrow in patients with MDS showed significantly lower values compared with patients with acute leukemia and did not differ from patients with polycythemia vera.


1993 ◽  
Vol 21 (2) ◽  
pp. 173-180
Author(s):  
Gunnar Johanson

This presentation addresses some aspects of the methodology, advantages and problems associated with toxicokinetic modelling based on in vitro data. By using toxicokinetic models, particularly physiologically-based ones, it is possible, in principle, to describe whole body toxicokinetics, target doses and toxic effects from in vitro data. Modelling can be divided into three major steps: 1) to relate external exposure (applied dose) of xenobiotic to target dose; 2) to establish the relationship between target dose and effect (in vitro data, e.g. metabolism in microsomes, partitioning in tissue homogenates, and toxicity in cell cultures, are useful in both steps); and 3) to relate external exposure to toxic effect by combining the first two steps. Extrapolations from in vitro to in vivo, between animal and man, and between high and low doses, can easily be carried out by toxicokinetic simulations. In addition, several factors that may affect the toxic response by changing the target dose, such as route of exposure and physical activity, can be studied. New insights concerning the processes involved in toxicity often emerge during the design, refinement and validation of the model. The modelling approach is illustrated by two examples: 1) the carcinogenicity of 1,3-butadiene; and 2) the haematotoxicity of 2-butoxyethanol. Toxicokinetic modelling is an important tool in toxicological risk assessment based on in vitro data. Many factors, some of which can, and should be, studied in vitro, are involved in the expression of toxicity. Successful modelling depends on the identification and quantification of these factors.


2021 ◽  
Vol 12 (1) ◽  
Author(s):  
KyeongJin Kim ◽  
Jin Ku Kang ◽  
Young Hoon Jung ◽  
Sang Bae Lee ◽  
Raffaela Rametta ◽  
...  

AbstractIncreased adiposity confers risk for systemic insulin resistance and type 2 diabetes (T2D), but mechanisms underlying this pathogenic inter-organ crosstalk are incompletely understood. We find PHLPP2 (PH domain and leucine rich repeat protein phosphatase 2), recently identified as the Akt Ser473 phosphatase, to be increased in adipocytes from obese mice. To identify the functional consequence of increased adipocyte PHLPP2 in obese mice, we generated adipocyte-specific PHLPP2 knockout (A-PHLPP2) mice. A-PHLPP2 mice show normal adiposity and glucose metabolism when fed a normal chow diet, but reduced adiposity and improved whole-body glucose tolerance as compared to Cre- controls with high-fat diet (HFD) feeding. Notably, HFD-fed A-PHLPP2 mice show increased HSL phosphorylation, leading to increased lipolysis in vitro and in vivo. Mobilized adipocyte fatty acids are oxidized, leading to increased peroxisome proliferator-activated receptor alpha (PPARα)-dependent adiponectin secretion, which in turn increases hepatic fatty acid oxidation to ameliorate obesity-induced fatty liver. Consistently, adipose PHLPP2 expression is negatively correlated with serum adiponectin levels in obese humans. Overall, these data implicate an adipocyte PHLPP2-HSL-PPARα signaling axis to regulate systemic glucose and lipid homeostasis, and suggest that excess adipocyte PHLPP2 explains decreased adiponectin secretion and downstream metabolic consequence in obesity.


1975 ◽  
Author(s):  
J. Björnson ◽  
I. Aursnes

In the interpretation of data obtained with 51Cr-labelled platelets it is vital to know whether they are functionally normal. Although survival of 51Cr-labelled platelets in vivo appears to be normal, platelet aggregability- has recently been shown to be reduced after the labelling procedure (Björnson, J., Sc and. J. Haemat. 13, 252–259).The aim of the present study was to examine the hemostatic effect of labelled platelets. Rabbits were made thrombocytopenic (< 35,000/μ1) by whole body irradiation. Bleeding times were recorded after standardized cuts on the inner side of the ear, a method showing an acceptable reproducibility (< 3 min in normals). The animals were then transfused with labelled platelet concentrates, increasing the platelet levels to about 200,000/μ) blood. Bleeding times of more than 15 min before transfusion were almost normalized 1 and 4 hours after transfusion. In controls transfusion of PRP led to similar shortening of bleeing time.It is concluded that platelets subjected to the 51Cr-labelling procedure to a large extent retain their hemostatic ability.


2020 ◽  
Vol 22 (Supplement_2) ◽  
pp. ii111-ii111
Author(s):  
Lan Hoang-Minh ◽  
Angelie Rivera-Rodriguez ◽  
Fernanda Pohl-Guimarães ◽  
Seth Currlin ◽  
Christina Von Roemeling ◽  
...  

Abstract SIGNIFICANCE Adoptive T cell therapy (ACT) has emerged as the most effective treatment against advanced malignant melanoma, eliciting remarkable objective clinical responses in up to 75% of patients with refractory metastatic disease, including within the central nervous system. Immunologic surrogate endpoints correlating with treatment outcome have been identified in these patients, with clinical responses being dependent on the migration of transferred T cells to sites of tumor growth. OBJECTIVE We investigated the biodistribution of intravenously or intraventricularly administered T cells in a murine model of glioblastoma at whole body, organ, and cellular levels. METHODS gp100-specific T cells were isolated from the spleens of pmel DsRed transgenic C57BL/6 mice and injected intravenously or intraventricularly, after in vitro expansion and activation, in murine KR158B-Luc-gp100 glioma-bearing mice. To determine transferred T cell spatial distribution, the brain, lymph nodes, heart, lungs, spleen, liver, and kidneys of mice were processed for 3D imaging using light-sheet and multiphoton imaging. ACT T cell quantification in various organs was performed ex vivo using flow cytometry, 2D optical imaging (IVIS), and magnetic particle imaging (MPI) after ferucarbotran nanoparticle transfection of T cells. T cell biodistribution was also assessed in vivo using MPI. RESULTS Following T cell intravenous injection, the spleen, liver, and lungs accounted for more than 90% of transferred T cells; the proportion of DsRed T cells in the brains was found to be very low, hovering below 1%. In contrast, most ACT T cells persisted in the tumor-bearing brains following intraventricular injections. ACT T cells mostly concentrated at the periphery of tumor masses and in proximity to blood vessels. CONCLUSIONS The success of ACT immunotherapy for brain tumors requires optimization of delivery route, dosing regimen, and enhancement of tumor-specific lymphocyte trafficking and effector functions to achieve maximal penetration and persistence at sites of invasive tumor growth.


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