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Neutron depth profiling (NDP) is a non-destructive analysis method which is widely used in lithium batteries, semiconductors, and other complex and high-precision industries. The NDP spectrum is the second particles of the interaction between neutrons and target nuclides, and then the content and spatial information of the target nuclides in the measured samples are obtained by unfolding the NDP spectrum. At present, the common NDP spectrum unfolding algorithm is the maximum likelihood expectation maximization (MLEM) algorithm. But in some case, the MLEM algorithm falls into the local optimal solution. In this paper, a hybrid PSO-MLEM algorithm by taking advantages of the wide search range of PSO (particle swarm optimization) and the fast convergence speed of MLEM was proposed. In the PSO-MLEM algorithm, the dynamic acceleration factor was used to balance the local optimal and the global optimal on the particle displacement in each iteration, which improved the convergence speed and the accuracy of the algorithm. The PSO-MLEM algorithm was applied to unfold the NDP spectra of lithium batteries with 0, 5, and 10 hours of charging and discharging, which were simulated by Geant4 tool. The unfolding results of PSO-MLEM algorithm were compared to the results of PSO algorithm, MLEM algorithm and singular value decomposition solving least squares (SVDLS) algorithm. The correlation coefficients of the unfolding result by PSO-MLEM algorithm and the reference distributions are 0.993, 0.984, and 0.946, respectively, and the relative average errors are 14.46%, 9.84%, and 9.41%. Compared with PSO algorithm, the convergence speed of PSO-MLEM algorithm is improved from 800 times to 100 times, and the relative error is reduced from about 50% to about 10%. To the MLEM algorithm, the PSO-MLEM algorithm improves the global optimization capability and avoids the problem of local optimal solution caused by the influence of the initial value of the MLEM algorithm, especially with the result of 0 hour. The SVDLS algorithm is worked well in unfolding NDP spectra except the NDP spectrum of lithium battery at 0 hour. Compared to result of SVDLS algorithm, the PSO-MLEM algorithm has better convergence properties and is numerically stable.

Waste printed circuit boards (WPCBs) contain valuable material resources and hazardous substances, thereby posing a challenge for sustainable resource recovery and environmental protection initiatives. Overcoming this challenge will require mapping the toxic footprint of WPCBs to specific materials and substances used in manufacturing electronic components (ECs). Therefore, this work collected 50 EC specimens from WPCBs in five ubiquitous consumer products, such as television, refrigerator, air conditioner, washing machine and computer. The work extracted and analyzed metal contents and used leachability assessments based on tests adopted by the regulatory policies from China and the United States. The work found that copper and iron are the most abundant constituents in ECs, with concentrations ranging 5.90-796.62 g/kg and 0-831.53 g/kg, respectively; whereas abundance of precious metal content is in the order of silver > gold > palladium > platinum, with silver concentration ranging 15-5290 mg/kg. The content of marginally-regulated toxic substance arsenic ranged 0-9700 mg/kg; whereas fully regulated toxic metals such as chromium, lead and mercury did not exceed the thresholds set by China and US standards. The work found new toxic threats from arsenic and selenium leached from 20 of 50 ECs exceeding regulatory standards. These results will aid manufacturers and recyclers in protecting workers' health and environmental quality from arsenic and selenium pollution, and should initiate discussion about regulating these toxic components as part of a comprehensive program to reduce the toxic footprint of electronic products.

The parathyroid hormone (PTH) type 1 receptor (PTHR) is a class B G protein–coupled receptor (GPCR) that regulates mineral ion, vitamin D, and bone homeostasis. Activation of the PTHR by PTH induces both transient cell surface and sustained endosomal cAMP production. To address whether the spatial (location) or temporal (duration) dimension of PTHR-induced cAMP encodes distinct biological outcomes, we engineered a biased PTHR ligand (PTH7d) that elicits cAMP production at the plasma membrane but not at endosomes. PTH7d stabilized a unique active PTHR conformation that mediated sustained cAMP signaling at the plasma membrane due to impaired β-arrestin coupling to the receptor. Experiments in cells and mice revealed that sustained cAMP production by cell surface PTHR failed to mimic the pharmacological effects of sustained endosomal cAMP production on the abundance of the rate-limiting hydroxylase catalyzing the formation of active vitamin D, as well as increases in circulating active vitamin D and Ca2+ and in bone formation in mice. Thus, similar amounts of cAMP generated by PTHR for similar lengths of time in different cellular locations, plasma membrane and endosomes, mediate distinct physiological responses. These results unveil subcellular signaling location as a means to achieve specificity in PTHR-mediated biological outcomes and raise the prospect of rational drug design based upon spatiotemporal manipulation of GPCR signaling.

Calcium and its putative receptor (CaSR) control skeletal development by pacing chondrocyte differentiation and mediating osteoblast (OB) function during endochondral bone formation-an essential process recapitulated during fracture repair. Here, we delineated the role of the CaSR in mediating transition of callus chondrocytes into the OB lineage and subsequent bone formation at fracture sites and explored targeting CaSRs pharmacologically to enhance fracture repair. In chondrocytes cultured from soft calluses at a closed, unfixed fracture site, extracellular [Ca2+ ] and the allosteric CaSR agonist (NPS-R568) promoted terminal differentiation of resident cells and the attainment of an osteoblastic phenotype. Knockout (KO) of the Casr gene in chondrocytes lengthened the chondrogenic phase of fracture repair by increasing cell proliferation in soft calluses but retarded subsequent osteogenic activity in hard calluses. Tracing growth plate (GP) and callus chondrocytes that express Rosa26-tdTomato showed reduced chondrocyte transition into OBs (by >80%) in the spongiosa of the metaphysis and in hard calluses. In addition, KO of the Casr gene specifically in mature OBs suppressed osteogenic activity and mineralizing function in bony calluses. Importantly, in experiments using PTH (1-34) to enhance fracture healing, co-injection of NPS-R568 not only normalized the hypercalcemic side effects of intermittent PTH (1-34) treatment in mice but also produced synergistic osteoanabolic effects in calluses. These data indicate a functional role of CaSR in mediating chondrogenesis and osteogenesis in the fracture callus and the potential of CaSR agonism to facilitate fracture repair. © 2019 American Society for Bone and Mineral Research.