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This article provides a biographic and scientific profile of prof. Hrayr Terzian (Addis Abeba 1925-Verona 1988). In 1966, Terzian was appointed professor of the clinic of nervous and mental diseases in Cagliari, and in 1970 moved to Verona, where until his death he led the Neurology Clinic serving as the first rector of the local university. As a close friend of the psychiatrist Franco Basaglia (1924-1980), Terzian contributed to the reform of the Italian mental health system. His interests and scientific contributions were extremely broad. He was the first to describe the electroencephalographic changes induced by the antipsychotic chlorpromazine and, together with Henri Gastaut (1915-1995) and his wife Yvette, to describe the rolandic arched ("mu") rhythm. He contributed to elucidate the inhibitory mechanisms of the cerebellum on the antigravity postural tone and provided the first description of Klüver-Bucy syndrome in humans. Always attentive to the social and political aspects of medical practice, prof. Terzian achieved outstanding results both in experimental neurophysiology and in clinical neurology. Besides offering a tribute to Hrayr Terzian, this article provides a brief historical overview of the different clinical pictures caused by bilateral temporal lesions from the first animal observations by Sanger Brown (1852-1928) and sir Edward Albert Sharpey-Schäfer (1850-1935), later confirmed and expanded upon by Heinrich Klüver (1897-1979) and Paul C. Bucy (1904-1992), to the first cases of bitemporal lesions in humans, including that of the famous patient H.M. (Henry Gustav Molaison, 1926-2008).

Previous studies have shown that Aβ-amyloid (Aβ) likely promotes tau to spread beyond the medial temporal lobe. selleck inhibitor However, the Aβ levels necessary for tau to spread in the neocortex is still unclear.

Four hundred sixty-six participants underwent tau imaging with [18F]MK6420 and Aβ imaging with [

F]NAV4694. Aβ scans were quantified on the Centiloid (CL) scale with a cut-off of 25 CL for abnormal levels of Aβ (A+). Tau scans were quantified in three regions of interest (ROI) (mesial temporal (Me); temporoparietal neocortex (Te); and rest of neocortex (R)) and four mesial temporal region (entorhinal cortex, amygdala, hippocampus, and parahippocampus). Regional tau thresholds were established as the 95%ile of the cognitively unimpaired A- subjects. The prevalence of abnormal tau levels (T+) along the Centiloid continuum was determined.

The plots of prevalence of T+ show earlier and greater increase along the Centiloid continuum in the medial temporal area compared to neocortex. Prevalence of T+ was low but associated with Aβ level between 10 and 40 CL reaching 23% in Me, 15% in Te, and 11% in R. Between 40 and 70 CL, the prevalence of T+ subjects per CL increased fourfold faster and at 70 CL was 64% in Me, 51% in Te, and 37% in R. In cognitively unimpaired, there were no T+ in R below 50 CL. The highest prevalence of T+were found in the entorhinal cortex, reaching 40% at 40 CL and 80% at 60 CL.

Outside the entorhinal cortex, abnormal levels of cortical tau on PET are rarely found with Aβ below 40 CL. Above 40 CL prevalence of T+ accelerates in all areas. Moderate Aβ levels are required before abnormal neocortical tau becomes detectable.

Outside the entorhinal cortex, abnormal levels of cortical tau on PET are rarely found with Aβ below 40 CL. Above 40 CL prevalence of T+ accelerates in all areas. Moderate Aβ levels are required before abnormal neocortical tau becomes detectable.

Tendency is to moderate the injected activity and/or reduce acquisition time in PET examinations to minimize potential radiation hazards and increase patient comfort. This work aims to assess the performance of regular full-dose (FD) synthesis from fast/low-dose (LD) whole-body (WB) PET images using deep learning techniques.

Instead of using synthetic LD scans, two separate clinical WB

F-Fluorodeoxyglucose (

F-FDG) PET/CT studies of 100 patients were acquired one regular FD (~ 27 min) and one fast or LD (~ 3 min) consisting of 1/8

of the standard acquisition time. A modified cycle-consistent generative adversarial network (CycleGAN) and residual neural network (ResNET) models, denoted as CGAN and RNET, respectively, were implemented to predict FD PET images. The quality of the predicted PET images was assessed by two nuclear medicine physicians. Moreover, the diagnostic quality of the predicted PET images was evaluated using a pass/fail scheme for lesion detectability task. Quantitative analysis usinges present almost similar performance in terms of lesion detectability, qualitative scores, and quantification bias and variance.

Peptide-based prostate-specific membrane antigen (PSMA) targeted radionuclide therapy (TRT) agent [

Lu]-PSMA-617 has emerged as leading TRT candidate for treatment of castration-resistant prostate cancer (mCRPC). [

Lu]-PSMA-617 and other small molecule-based PSMA ligands have shown efficacy in reducing the tumor burden in mCRPC patients but irradiation to the salivary gland and kidneys is a concern and dose-limiting factor. Therefore, methods to reduce non-target organ toxicity are needed to safely treat patients and preserve their quality of life. Herein, we report that addition of cold PSMA ligand PSMA-11 can aid in reducing the uptake of [

Lu]-PSMA-617 in the salivary glands and kidneys.

Groups of athymic nude mice (n = 4) bearing PC3-PIP (PSMA+) tumor xenografts were administered with [

Lu]-PSMA-617 along with 0, 5, 100, 500, 1000, and 2000 pmoles of PSMA-11 and biodistribution studies were performed at 1 h.

Biodistribution studies at 1 h post-administration revealed that [

Lu]-PSMA-617 uptake in PC3-PIP tumors was 21.71 ± 6.13, 18.7 ± 2.03, 26.44 ± 2.94, 16.21 ± 3.5, 13.52 ± 3.68, and 12.03 ± 1.96 %ID/g when 0, 5, 100, 500, 1000, and 2000 pmoles of PSMA-11 were added, respectively. Corresponding uptake valuesin kidney were 123.14 ± 52.52, 132.31 ± 47.4, 84.29 ± 78.25, 2.12 ± 1.88, 1.16 ± 0.36, and 0.64 ± 0.23 %ID/g, respectively. Corresponding salivary gland uptake values were 0.48 ± 0.11, 0.45 ± 0.15, 0.38 ± 0.3, 0.08 ± 0.03, 0.09 ± 0.07, and 0.05 ± 0.02 % ID/g, respectively.

The uptake of [

Lu]-PSMA-617 in the salivary gland and kidney can be substantially reduced without significantly impacting tumor uptake by adding cold PSMA-11.

The uptake of [177Lu]-PSMA-617 in the salivary gland and kidney can be substantially reduced without significantly impacting tumor uptake by adding cold PSMA-11.