The RAYCAN Discoverist 180 (RAYCAN D180) is a novel preclinical positron emission tomography (PET) and computed tomography (CT) integrated system for the imaging of small-and medium-sized animals and plants. We measured a system resolution of (2.56±0.04) mm (radial), (2.46±0.05) mm (transverse), (1.67±0.03) mm (axial) at the center of the field of view using a filtered backprojection reconstruction algorithm. A OSEM-PSF-3D reconstruction algorithm improves the spatial resolution to (1.34±0.04) mm (radial), (1.35±0.05) mm (transverse) and (1.64±0.04) mm (axial). The peak noise equivalent count rate of the system is (713±2) kcps, (207±2) kcps and (47±1) kcps reached at approximately 97 MBq for the mouse-, rat-and monkey-like phantoms respectively. This result is approximately 2× higher and is reached at approximately 3× higher activity in comparison with most of the existing commercial and research scanners. The peak absolute system sensitivity is (4.00±0.02)% and is competitive with state-of-the-art preclinical PET scanners. We found a image uniformity of (4.86±0.04)%. Finally, we report the static PET/CT scan of a mouse and of a leaf of Epipremnum aureum, and the time-activity curves of the 18F-FDG metabolism in mouse left myocardial ventricle and kidneys obtained with a PET/CT scan in dynamic modality.

Alzheimer’s disease (AD) is a neurodegenerative disease characterized by decreased glucose metabolism and increased neuroinflammation. Hexokinase (HK) is the key enzyme of glucose metabolism and is associated with mitochondria to exert its function. Recent studies have demonstrated that the dissociation of HK from mitochondria is enough to activate the NOD-like receptor protein 3 (NLRP3) inflammasome and leads to the release of interleukin-1β (IL-1β). However, the effect of increased IL-1β on the expression of HK is still unclear in AD. In this paper, we used positron emission tomography (PET), Western blotting and immunofluorescence to study the glucose metabolism, and the expression and distribution of HK in AD. Furthermore, we used lipopolysaccharide (LPS), nigericin (Nig), CY-09 and lonidamine (LND) to treat N2a and N2a-sw cells to investigate the link between IL-1β and HK in AD. The results show decreased expression of HK and the dissociation of HK from mitochondria in AD. Furthermore, a reduction of the expression of IL-1β could increase the expression of HK in AD. These results suggest that inhibiting inflammation may help to restore glucose metabolism in AD.

One of the most challenging areas of sensor development for nuclear medicine is the design of proton therapy monitoring systems. Sensors are operated in a high detection rate regime in beam-on conditions. We realized a prototype of a monitoring system for proton therapy based on the technique of positron emission tomography. We used the Plug and Imaging (P&I) technology in this application. This sensing system includes LYSO/silicon photomultiplier (SiPM) detection elements, fast digital multi voltage threshold (MVT) readout electronics and dedicated image reconstruction algorithms. In this paper, we show that the P&I sensor system has a uniform response and is controllable in the experimental conditions of the proton therapy room. The prototype of PET monitoring device based on the P&I sensor system has an intrinsic experimental spatial resolution of approximately 3 mm (FWHM), obtained operating the prototype both during the beam irradiation and right after it. The count-rate performance of the P&I sensor approaches 5 Mcps and allows the collection of relevant statistics for the nuclide analysis. The measurement of both the half life and the relative abundance of the positron emitters generated in the target volume through irradiation of ${10}^{10}$ protons in approximately 15 s is performed with 0.5% and $5\%$ accuracy, respectively.

Chronic sleep insufficiency is becoming a common issue in the young population nowadays, mostly due to life habits and work stress. Studies in animal models of neurological diseases reported that it would accelerate neurodegeneration progression and exacerbate interstitial metabolic waste accumulation in the brain. In this paper, we study whether chronic sleep insufficiency leads to neurodegenerative diseases in young wild-type animals without a genetic pre-disposition. To this aim, we modeled chronic sleep fragmentation (SF) in young wild-type mice. We detected pathological hyperphosphorylated-tau (Ser396/Tau5) and gliosis in the SF hippocampus. ¹⁸F-labeled fluorodeoxyglucose positron emission tomography scan (¹⁸F-FDG-PET) further revealed a significant increase in brain glucose metabolism, especially in the hypothalamus, hippocampus and amygdala. Hippocampal RNAseq indicated that immunological and inflammatory pathways were significantly altered in 1.5-month SF mice. More interestingly, differential expression gene lists from stress mouse models showed differential expression patterns between 1.5-month SF and control mice, while Alzheimer's disease, normal aging, and APOEε4 mutation mouse models did not exhibit any significant pattern. In summary, 1.5-month sleep fragmentation could generate AD-like pathological changes including tauopathy and gliosis, mainly linked to stress, as the incremented glucose metabolism observed with PET imaging suggested. Further investigation will show whether SF could eventually lead to chronic neurodegeneration if the stress condition is prolonged in time.

Background: Parkinson’s Disease (PD) is the second most frequent degenerative disorder, the risk of which increases with age. A preclinical PD diagnostic test does not exist. We identify PD blood metabolites and metabolic pathways significantly correlated with age to develop personalized age-dependent PD blood biomarkers. Results: We found 33 metabolites producing a receiver operating characteristic (ROC) area under the curve (AUC) value of 97%. PCA revealed that they belong to three pathways with distinct age-dependent behavior: glycine, threonine and serine metabolism correlates with age only in PD patients; unsaturated fatty acids biosynthesis correlates with age only in a healthy control group; and, finally, tryptophan metabolism characterizes PD but does not correlate with age. Conclusions: The targeted analysis of the blood metabolome proposed in this paper allowed to find specific age-related metabolites and metabolic pathways. The model offers a promising set of blood biomarkers for a personalized age-dependent approach to the early PD diagnosis.

The present-day rapid growth of computer power, in particular, parallel computing systems of ultrahigh performance requires a new approach to the creation of models and solution algorithms for major problems. An algorithm for solving parabolic and elliptic equations is proposed. The capabilities of the method are demonstrated by solving astrophysical problems on high-performance computer systems with massive parallelism.