Plant stress detection is considered one of the most critical areas for the improvement of crop yield in the compelling worldwide scenario, dictated by both the climate change and the geopolitical consequences of the Covid-19 epidemics. A complicated interconnection of biotic and abiotic stressors affect plant growth, including water, salt, temperature, light exposure, nutrients availability, agrochemicals, air and soil pollutants, pests and diseases. In facing this extended panorama, the technology choice is manifold. On the one hand, quantitative methods, such as metabolomics, provide very sensitive indicators of most of the stressors, with the drawback of a disruptive approach, which prevents follow up and dynamical studies. On the other hand qualitative methods, such as fluorescence, thermography and VIS/NIR reflectance, provide a non-disruptive view of the action of the stressors in plants, even across large fields, with the drawback of a poor accuracy. When looking at the spatial scale, the effect of stress may imply modifications from DNA level (nanometers) up to cell (micrometers), full plant (millimeters to meters), and entire field (kilometers). While quantitative techniques are sensitive to the smallest scales, only qualitative approaches can be used for the larger ones. Emerging technologies from nuclear and medical physics, such as computed tomography, magnetic resonance imaging and positron emission tomography, are expected to bridge the gap of quantitative non-disruptive morphologic and functional measurements at larger scale. In this review we analyze the landscape of the different technologies nowadays available, showing the benefits of each approach in plant stress detection, with a particular focus on the gaps, which will be filled in the nearby future by the emerging nuclear physics approaches to agriculture.

There is an increasing risk of mental disorders, such as acute stress disorder (ASD), post-traumatic stress disorder (PTSD) and depression among survivors who were trapped in rubble during earthquake. Such long-term impaction of a single acute restraint stress has not been extensively explored. In this study, we subjected mice to 24-hour-restraint to simulate the trapping episode, and investigated the acute (2 days after the restraint) and long-term (35 days after the restraint) impacts. Surprisingly, we found that the mice displayed depression-like behaviors, decreased glucose uptake in brain and reduced adult hippocampal neurogenesis 35 days after the restraint. Differential expression profiling based on microarrays suggested that genes and pathways related to depression and other mental disorders were differentially expressed in both PFC and hippocampus. Furthermore, the depression-like phenotypes induced by 24-hour-restraint could be reversed by fluoxetine, a type of antidepressant drug. These findings demonstrated that a single severe stressful event could produce long-term depressive-like phenotypes. Moreover, the 24-hour-restraint stress mice could also be used for further studies on mood disorders.

The reduction of the cerebral glucose metabolism is closely related to the activation of the NOD-like receptor protein 3 (NLRP3) inflammasome in Alzheimer’s disease (AD); however, its underlying mechanism remains unclear. In this paper, ¹⁸F-flurodeoxyglucose positron emission tomography was used to trace cerebral glucose metabolism in vivo, along with Western blotting and immunofluorescence assays to examine the expression and distribution of associated proteins. Glucose and insulin tolerance tests were carried out to detect insulin resistance, and the Morris water maze was used to test the spatial learning and memory ability of the mice. The results show increased NLRP3 inflammasome activation, elevated insulin resistance, and decreased glucose metabolism in 3×Tg-AD mice. Inhibiting NLRP3 inflammasome activation using CY-09, a specific inhibitor for NLRP3, may restore cerebral glucose metabolism by increasing the expression and distribution of glucose transporters and enzymes and attenuating insulin resistance in AD mice. Moreover, CY-09 helps to improve AD pathology and relieve cognitive impairment in these mice. Although CY-09 has no significant effect on ferroptosis, it can effectively reduce fatty acid synthesis and lipid peroxidation. These findings provide new evidence for NLRP3 inflammasome as a therapeutic target for AD, suggesting that CY-09 may be a potential drug for the treatment of this disease.

An x-ray energy spectrum plays an essential role in computed tomography (CT) imaging and related tasks. Because of the high photon flux of clinical CT scanners, most of the spectrum estimation methods are indirect and usually suffer from various limitations. In this study, we aim to provide a segmentation-free, indirect transmission measurement–based energy spectrum estimation method using dual-energy material decomposition. The general principle of this method is to minimize the quadratic error between the polychromatic forward projection and the raw projection to calibrate a set of unknown weights, which are used to express the unknown spectrum together with a set of model spectra. The polychromatic forward projection is performed using material-specific images, which are obtained using dual-energy material decomposition. The algorithm was evaluated using numerical simulations, experimental phantom data, and realistic patient data. The results show that the estimated spectrum matches the reference spectrum quite well and the method is robust. Extensive studies suggest that the method provides an accurate estimate of the CT spectrum without dedicated physical phantom and prolonged workflow. This paper may be attractive for CT dose calculation, artifacts reduction, polychromatic image reconstruction, and other spectrum-involved CT applications.

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.