Improving maize’s N uptake and N use efficiency by strengthening roots’ absorption capacity when intercropped with legumes

Maize’s nitrogen (N) uptake can be improved through maize-legume intercropping. N uptake mechanisms require further study to better understand how legumes affect root growth and to determine maize’s absorptive capacity in maize-legume intercropping. We conducted a two-year field experiment with two N treatments (zero N (N0) and conventional N (N1)) and three planting patterns (monoculture maize (Zea mays L.) (MM), maize-soybean (Glycine max L. Merr.) strip intercropping (IMS), and maize-peanut (Arachis hypogaea L.) strip intercropping (IMP)). We sought to understand maize’s N uptake mechanisms by investigating root growth and distribution, root uptake capacity, antioxidant enzyme activity, and the antioxidant content in different maize-legume strip intercropping systems. Our results showed that on average, the N uptake of maize was significantly greater by 52.5% in IMS and by 62.4% in IMP than that in MM. The average agronomic efficiency (AE) of maize was increased by 110.5 % in IMS and by 163.4 % in IMP, compared to MM. The apparent recovery efficiency (RE) of maize was increased by 22.3% in IMS. The roots of intercropped maize were extended into soybean and peanut stands underneath the space and even between the inter-rows of legume, resulting in significantly increased root surface area density (RSAD) and total root biomass. The root-bleeding sap intensity of maize was significantly increased by 22.7–49.3% in IMS and 37.9–66.7% in IMP, compared with the MM. The nitrate-N content of maize bleeding sap was significantly greater in IMS and IMP than in MM during the 2018 crop season. The glutathione (GSH) content, superoxide dismutase (SOD), and catalase (CAT) activities in the root significantly increased in IMS and IMP compared to MM. Strip intercropping using legumes increases maize’s aboveground N uptake by promoting root growth and spatial distribution, delaying root senescence, and strengthening root uptake capacity.

Radiotracers for Bone Marrow Infection Imaging

Introduction: Radiotracers are widely used in medical imaging, using techniques of gamma-camera imaging (scintigraphy and SPECT) or positron emission tomography (PET). In bone marrow infection, there is no single routine test available that can detect infection with sufficiently high diagnostic accuracy. Here, we review radiotracers used for imaging of bone marrow infection, also known as osteomyelitis, with a focus on why these molecules are relevant for the task, based on their physiological uptake mechanisms. The review comprises [67Ga]Ga-citrate, radiolabelled leukocytes, radiolabelled nanocolloids (bone marrow) and radiolabelled phosphonates (bone structure), and [18F]FDG as established radiotracers for bone marrow infection imaging. Tracers that are under development or testing for this purpose include [68Ga]Ga-citrate, [18F]FDG, [18F]FDS and other non-glucose sugar analogues, [15O]water, [11C]methionine, [11C]donepezil, [99mTc]Tc-IL-8, [68Ga]Ga-Siglec-9, phage-display selected peptides, and the antimicrobial peptide [99mTc]Tc-UBI29-41 or [68Ga]Ga-NOTA-UBI29-41. Conclusion: Molecular radiotracers allow studies of physiological processes such as infection. None of the reviewed molecules are ideal for the imaging of infections, whether bone marrow or otherwise, but each can give information about a separate aspect such as physiology or biochemistry. Knowledge of uptake mechanisms, pitfalls, and challenges is useful in both the use and development of medically relevant radioactive tracers.

Melanocore uptake by keratinocytes occurs through phagocytosis and involves Protease-activated receptor-2 activation

In the skin epidermis, melanin is produced and stored within melanosomes in melanocytes and then transferred to keratinocytes. Different models have been proposed to explain the melanin transfer mechanism, which differ essentially in how melanin is transferred – either in a membrane-bound melanosome or as a melanosome core, i.e. melanocore. Here we investigated the endocytic route followed by melanocores and melanosomes during internalization by keratinocytes, by comparing the uptake of melanocores isolated from the supernatant of melanocyte cultures with melanosomes isolated from melanocytes. We show that inhibition of actin dynamics impairs the uptake of both melanocores and melanosomes. Moreover, depletion of critical proteins involved in actin-dependent uptake mechanisms, namely Rac1 and CtBP1/BARS, together with inhibition of Rac1-dependent signaling pathways or macropinocytosis suggest that melanocores are internalized by phagocytosis, whereas melanosomes are internalized by macropinocytosis. Furthermore, we confirmed that melanocore, but not melanosome uptake is dependent on the Protease-activated receptor-2 (PAR-2) and found that PAR-2 can be specifically activated by melanocores. As skin pigmentation was shown to be regulated by PAR-2 activation, our results further support the melanocore mechanism of melanin transfer and further refine this model, which can now be described as coupled melanocore exo/phagocytosis.

Potential involvement of extracellular citrate in brain tumor progression.

: Brain tissue is known to have elevated citrate levels necessary to regulate ion chelation, neuron excitability, and the supply of necessary energy substrates to neurons. Importantly, citrate also acts as a central substrate in cancer metabolism. Recent studies have shown that extracellular citrate levels in the brain undergo significant changes during tumor development, and may play a dual role in tumor progression, as well as cancer cell aggressiveness. In the present article, we review available literature describing changes of citrate levels in brain tissue, blood, and cerebrospinal fluid, as well as intracellular alterations during tumor development before and after metastatic progression. Based on the available literature and our recent findings, we hypothesize that changes in extracellular citrate levels may be related to the increased consumption of this metabolite by cancer cells; interestingly, cancer-associated cells, including reactive astrocytes, might be a source of citrate. Extracellular citrate uptake mechanisms, as well as potential citrate synthesis and releasing by surrounding stroma, could provide novel targets for anti-cancer treatments of primary brain tumors and brain metastases.