| 401. |
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| 402. |
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| 403. |
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| 404. |
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| 406. |
- Strand, S. E., et al.
(författare)
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Quantitative lymphoscintigraphy. I. Basic concepts for optimal uptake of radiocolloids in the parasternal lymph nodes of rabbits
- 1979
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Ingår i: Journal of Nuclear Medicine. - 0161-5505. ; 20:10, s. 1038-1046
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Tidskriftsartikel (refereegranskat)abstract
- The activity-size distribution of radiocolloids has been studied using gel-chromatography scanning (GCS) of columns filled with Sepharose 4B gel. Rabbits were injected subcutaneously with the colloid of interest, laid supine beneath a gamma camera, and imaged every 15 sec for 2 to 4 hr. From the stored data, the uptakes in the parasternal lymph nodes were analyzed in terms of a two-compartment model, and the rate constants measured. The substances tested were Au-198 colloid, Tc-99m antimony sulfide colloid, Tc-99m tin colloid, Tc-99m phytate, and Tc99m sulfur colloid. It was shown that the optimal particle size for the colloid is in the range 1-10 nm. The largest and most rapid uptake was found for Au-198 colloid, with a particle size of 5 nm, which appeared as a single peak in the GCS spectrum. The percentage uptake after 2 hr for Au-198 colloid was 8%, while it was 5% for antimony sulfide colloid, which was the best of the Tc-99m-labeled colloids. The GCS spectrum for the antimony product showed a single-peaked size distribution with a somewhat broader range: 5-15 nm. The particles of the other colloids were either too large to pass into the lymphatic system, or too small to be trapped.
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| 407. |
- Stuparu, Andreea D., et al.
(författare)
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Mechanisms of Resistance to Prostate-Specific Membrane Antigen-Targeted Radioligand Therapy in a Mouse Model of Prostate Cancer
- 2021
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Ingår i: Journal of nuclear medicine : official publication, Society of Nuclear Medicine. - : Society of Nuclear Medicine. - 0161-5505. ; 62:7, s. 989-995
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Tidskriftsartikel (refereegranskat)abstract
- Prostate-specific membrane antigen (PSMA)-targeted radioligand therapy (RLT) is effective against prostate cancer (PCa), but all patients relapse eventually. Poor understanding of the underlying resistance mechanisms represents a key barrier to development of more effective RLT. We investigate the proteome and phosphoproteome in a mouse model of PCa to identify signaling adaptations triggered by PSMA RLT. Methods: Therapeutic efficacy of PSMA RLT was assessed by tumor volume measurements, time to progression, and survival in C4-2 or C4-2 TP53-/- tumor-bearing nonobese diabetic scid γ-mice. Two days after RLT, the proteome and phosphoproteome were analyzed by mass spectrometry. Results: PSMA RLT significantly improved disease control in a dose-dependent manner. Proteome and phosphoproteome datasets revealed activation of genotoxic stress response pathways, including deregulation of DNA damage/replication stress response, TP53, androgen receptor, phosphatidylinositol-3-kinase/AKT, and MYC signaling. C4-2 TP53-/- tumors were less sensitive to PSMA RLT than were parental counterparts, supporting a role for TP53 in mediating RLT responsiveness. Conclusion: We identified signaling alterations that may mediate resistance to PSMA RLT in a PCa mouse model. Our data enable the development of rational synergistic RLT-combination therapies to improve outcomes for PCa patients.
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| 408. |
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| 409. |
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| 410. |
- Teipel, Stefan, et al.
(författare)
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Alzheimer Disease : Standard of Diagnosis, Treatment, Care, and Prevention
- 2022
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Ingår i: Journal of Nuclear Medicine. - : Society of Nuclear Medicine. - 0161-5505 .- 2159-662X. ; 63:7, s. 981-985
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Tidskriftsartikel (refereegranskat)abstract
- Alzheimer disease (AD) is the most frequent cause of dementia in people 60 y old or older. This white paper summarizes the current standards of AD diagnosis, treatment, care, and prevention. Cerebrospinal fluid and PET measures of cerebral amyloidosis and tauopathy allow the diagnosis of AD even before dementia (prodromal stage) and provide endpoints for treatments aimed at slowing the AD course. Licensed pharmacologic symptomatic drugs enhance cholinergic pathways and moderate excess of glutamatergic transmission to stabilize cognition. Disease-modifying experimental drugs moderate or remove brain amyloidosis, but so far with modest clinical effects. Nonpharmacologic interventions and a healthy lifestyle (diet, socioaffective inclusion, cognitive stimulation, physical exercise, and others) provide some beneficial effects. Prevention targets mainly modifiable dementia risk factors such as unhealthy lifestyle, cardiovascular–metabolic and sleep–wake cycle abnormalities, and mental disorders. A major challenge for the future is telemonitoring in the real world of these modifiable risk factors.
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