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Biomedical subjects

Noriko Sato

Publications and source records attributed to Noriko Sato.

61 records · Page 4Linked to original sources
PubMed2002

Rapid accumulation and internalization of radiolabeled herceptin in an inflammatory breast cancer xenograft with vasculogenic mimicry predicted by the contrast-enhanced dynamic MRI with the macromolecular contrast agent G6-(1B4M-Gd)(256).

The rapid blood flow and perfusion of macromolecules in the inflammatory breast cancer xenograft (WIBC-9), which exhibits a "vasculogenic mimicry" type of angiogenesis without the participation of endothelial cells and expresses high levels of the HER-2/neu antigen, was evaluated in mice using 3D-micro-MR angiography using a novel macromolecular MR contrast agent [G6-(1B4M-Gd)(256)]. Herceptin, which recognizes the HER-2/neu antigen and has similar size (10 nm) to G6-(1B4M-Gd)(256), accumulated and internalized in the WIBC-9 tumors more quickly than in the control MC-5 tumors that progress with normal angiogenesis. Three dimensional micro-MRI with the G6-(1B4M-Gd)(256) macromolecular MRI contrast agent distinguishes between the different types of angiogenesis and is predictive of the rapid accumulation and internalization of Herceptin in the WIBC-9 inflammatory breast cancer xenograft.

Animals↗
PubMed2002

Induction of nephrotoxic serum nephritis in inbred mice and suppressive effect of colchicine on the development of this nephritis.

Accelerated nephrotoxic serum (NTS) nephritis is successfully produced in C57BL/6 mice, using anti-murine glomerular basement membrane (GBM) rabbit antiserum. Anti-murine GBM rabbits antiserum was obtained by immunization of New Zealand white rabbit with trypsinized GBM antigen from normal C57BL/6 mice. Preimmunization with normal rabbit IgG and injection with 150 microl of NTS induced typical NTS nephritis with cellular proliferation in glomeruli, occlusion of glomerular loops, crescents, tubulointerstitial changes and hyperazotemia within 14 days. Polymorphonuclear leucocytes (PMN) have an important role in induction and development of NTS nephritis. Furthermore, clinically used colchicine is thought to suppress functions of PMN. Therefore, the therapeutic effect of colchicine on NTS nephritis was examined. The histological score (HS) of the group treated with 60 microg kg (-1) of colchicine (2.8 +/- 0.5) was significantly lower than that of positive control group (4.03 +/- 0.3).The direct immunofluorescent microscopic study revealed that there is no quantitative difference in the deposition of rabbit IgG, mouse IgG and C3 in GBM between these two groups. Urinary protein excretion and hyperazotemia were significantly suppressed by treatment with 60 microg kg (-1) of colchicine. A NTS nephritis model was established, it was found that colchicine may have a suppressive effect on the development of glomerular nephritis.

Animals↗
PubMed2002

Renal tubular damage detected by dynamic micro-MRI with a dendrimer-based magnetic resonance contrast agent.

BACKGROUND: A noninvasive technique to evaluate the structure and function of the kidney would be useful to investigate renal diseases, especially acute renal failure. We have developed a novel technique to visualize functional micro-magnetic resonance (MR) images of the mouse kidney with a dendrimer-based macromolecular renal MR contrast agent. METHOD: Mice were injected with cisplatin or vehicle, then examined three days later by contrast-enhanced, dynamic high-resolution micro-MRI with 160 microm spatial resolution using a 1.5 T clinical MRI unit, a surface coil, and the renal contrast agent G4D-(1B4M-Gd)64. RESULTS: The cortex and outer stripe of the outer medulla of the mouse kidney were clearly visualized in the normal mice. In animals treated with cisplatin, the gradation of tubular damage as assessed by contrast enhanced dynamic MRI correlated with renal function. CONCLUSION: Contrast-enhanced, dynamic high-resolution micro-MRI with a novel dendrimer-based macromolecular renal MR contrast agent can be a powerful tool for in vivo observation of renal structural and functional damage.

Animals↗
PubMed2002

Increased (18)F-FDG uptake in a model of inflammation: concanavalin A-mediated lymphocyte activation.

UNLABELLED: The aim of this project was to study a mechanism that might explain the increased uptake of (18)F-labeled FDG seen in inflammation. The approach chosen was to examine the effect on (18)F-FDG uptake of acute activation of murine lymphocytes by concanavalin A (Con A). METHODS: Immunocompetent BALB/c mice and nude mice received an intravenous injection of 10 mg/kg Con A. Twenty-four hours later, the mice received an intravenous injection of 0.74 MBq (20 microCi) (18)F-FDG. One hour later, biodistribution was determined. The distribution of the radiolabel in the liver was also evaluated by autoradiography. In vitro (18)F-FDG uptake to splenocytes from BALB/c mice with and without Con A pretreatment were determined 30, 60, and 120 min after the splenocytes were mixed with (18)F-FDG (0.74 MBq [20 microCi]/200 microL). RESULTS: In immunocompetent BALB/c mice, pretreatment with Con A significantly increased (18)F-FDG uptake in the spleen and liver. Autoradiographs of the liver showed that pretreatment with Con A produced a specific localization of (18)F-FDG at periportal areas, where numerous sites of cellular infiltration were observed. In vitro binding of (18)F-FDG to the splenocytes was significantly higher for Con A-pretreated BALB/c mice than for control mice. CONCLUSION: This study showed that Con A increased (18)F-FDG uptake. Con A-activated lymphocytes actively took up (18)F-FDG both in vitro and in vivo, and (18)F-FDG specifically accumulated in Con A-mediated acute inflammatory tissues.

Animals↗
PubMed1999

Image Fusion System Using PACS for MRI, CT, and PET Images.

This paper presents and evaluates Picture Archiving and Communication System (PACS) and its interaction with the image fusion applications using positron emission tomography (PET), CT, and MRI, as well as some clinical applications of fusion images. A network connections between medium-sized PACS involving CT, MRI, SPECT, and PET were developed. Image registration and fusion was achieved in the PET's workstation by Advanced Visual System (AVS) software. Reconstructed datasets of CT, MRI, SPECT, and PET were transferred and archived in PACS servers. Series of anatomical images of CT and MRI were fused with metabolical images of PET with (18)F labeled fluoro-2-deoxy-D-glucose (FDG). Throughput rate of image data, as well as clinical applications of fusion images were evaluated and correlated with phantom studies. The average throughput rate of archiving and processing steps was 0.45 Mbps, 0.77 Mbps, respectively. Image fusion experiment using phantom and patients' data showed high accuracy in all directions. The combination of PACS and image fusion provided very useful clinical tools and made it quite easy to maximize the benefit from the diagnostic imaging.

Journal Article↗
PubMedDate not supplied

Differential uptake of (18)F-fluorodeoxyglucose by experimental tumors xenografted into immunocompetent and immunodeficient mice and the effect of immunomodification.

PURPOSE: To study the contribution of immunologic background to the uptake of fluorine-18-fluorodeoxyglucose ((18)F-FDG) by the tumor tissues. METHODS: The uptakes of (18)F-FDG to the same experimental tumor model (SCCVII) xenografted into immunocompetent and immunodeficient (athymic) mice were compared. In addition, the immunomodifying effect of steroid on the uptake of (18)F-FDG by these tumors was investigated. RESULTS: The uptake of (18)F-FDG by the tumors in immunocompetent mice was significantly higher than that in immunodeficient (athymic) mice. Although steroid pretreatment had no effect on the tumor uptake in immunodeficient mice, it significantly decreased the tumor uptake in immunocompetent mice. CONCLUSION: The higher tumor uptake of (18)F-FDG observed in immunocompetent mice, modulated by steroid pretreatment, was contributed by the host immune reaction, probably cellular immunity employed by T-lymphocytes. These findings can clinically conclude that the intense accumulation of (18)F-FDG in the metastatic lymph nodes, which contain only a small number of cancer cells, was caused by the enhanced uptake of (18)F-FDG by activated T-lymphocytes due to host immunity against cancer cells present in metastatic lymph nodes.

Animals↗