Stateless Two-Stage Multiple Criteria Scheduling in Nuclear Medicine

Examination in nuclear medicine exhibits scheduling difficulties due to its intricate clinical issues, such as varied radiopharmaceuticals for different diseases, machine preparation and length of scan, and patients’ and hospital’s criteria and/or limitations. Many scheduling methods exist but are limited for nuclear medicine. In this paper, we present stateless two-stage scheduling to cope with multiple criteria decision making. The first stage mostly deals with patients’ conditions. The second stage concerns more the clinical condition and its correlations with patients’ preference which presents more complicated intertwined configurations. A greedy algorithm is proposed in the second stage to determine the (time slot and patient) pair in linear time. The result shows practical and efficient scheduling for nuclear medicine

Energy-Efficient Joint Resource Allocation Algorithms for MEC-Enabled Emotional Computing in Urban Communities

This paper considers a mobile edge computing (MEC) system, where the MEC server first collects data from emotion sensors and then computes the emotion of each user. We give the formula of the emotional prediction accuracy. In order to improve the energy efficiency of the system, we propose resources allocation algorithms. We aim to minimize the total energy consumption of the MEC server and sensors by jointly optimizing the computing resources allocation and the data transmitting time. The formulated problem is a non-convex problem, which is very difficult to solve in general. However, we transform it into convex problems and apply convex optimization techniques to address it. The optimal solution is given in closed form. Simulation results show that the total energy consumption of our system can be effectively reduced by the proposed scheme compared with the benchmark

Fabrication of multianalyte CeO2 nanograin electrolyte–insulator–semiconductor biosensors by using CF4 plasma treatment

Multianalyte CeO2 biosensors have been demonstrated to detect pH, glucose, and urine concentrations. To enhance the multianalyte sensing capability of these biosensors, CF4 plasma treatment was applied to create nanograin structures on the CeO2 membrane surface and thereby increase the contact surface area. Multiple material analyses indicated that crystallization or grainization caused by the incorporation of flourine atoms during plasma treatment might be related to the formation of the nanograins. Because of the changes in surface morphology and crystalline structures, the multianalyte sensing performance was considerably enhanced. Multianalyte CeO2 nanograin electrolyte–insulator–semiconductor biosensors exhibit potential for use in future biomedical sensing device applications

TNF-α Mediates Eosinophil Cationic Protein-induced Apoptosis in BEAS-2B Cells

<p>Abstract</p> <p>Background</p> <p>Eosinophilic granulocytes are important for the human immune system. Many cationic proteins with cytotoxic activities, such as eosinophil cationic protein (ECP) and eosinophil-derived neurotoxin (EDN), are released from activated eosinophils. ECP, with low RNase activity, is widely used as a biomarker for asthma. ECP inhibits cell viability and induces apoptosis to cells. However, the specific pathway underlying the mechanisms of ECP-induced cytotoxicity remains unclear. This study investigated ECP-induced apoptosis in bronchial epithelial BEAS-2B cells and elucidated the specific pathway during apoptosis.</p> <p>Results</p> <p>To address the mechanisms involved in ECP-induced apoptosis in human BEAS-2B cells, investigation was carried out using chromatin condensation, cleavage of poly (ADP-ribose) polymerase (PARP), sub-G1 distribution in cell cycle, annexin V labeling, and general or specific caspase inhibitors. Caspase-8-dependent apoptosis was demonstrated by cleavage of caspase-8 after recombinant ECP treatment, accompanied with elevated level of tumor necrosis factor alpha (TNF-α). Moreover, ECP-induced apoptosis was effectively inhibited in the presence of neutralizing anti-TNF-α antibody.</p> <p>Conclusion</p> <p>In conclusion, our results have demonstrated that ECP increased TNF-α production in BEAS-2B cells and triggered apoptosis by caspase-8 activation through mitochondria-independent pathway.</p

Finite-temperature phase transitions in ν=2\nu=2 bilayer quantum Hall systems

In this paper, the influence of an in-plane magnetic field B_\parallel on the finite-temperature phase transitions in nu=2 bilayer quantum Hall systems are examined. It is found that there can exist two types of finite-temperature phase transitions. The first is the Kosterlitz-Thouless (KT) transitions, which can have an unusual non-monotonic dependence on B_\parallel; the second type originates from the crossing of energy levels and always increases with B_\parallel. Based on these results, we point out that the threshold temperature observed in the inelastic light scattering experiments cannot be the KT transition temperature, because the latter shows a totally different B_\parallel-dependence as compared with the experimental observation. Instead, it should be the level-crossing temperature, which we found agrees with the B_\parallel-dependence observed. Moreover, combining the knowledge of these two transition temperatures, a complete finite-temperature phase diagram is presented.Comment: RevTeX, 5 pages with 3 EPS figures include

The dimer interface of the SARS coronavirus nucleocapsid protein adapts a porcine respiratory and reproductive syndrome virus-like structure

AbstractWe have employed NMR to investigate the structure of SARS coronavirus nucleocapsid protein dimer. We found that the secondary structure of the dimerization domain consists of five α helices and a β-hairpin. The dimer interface consists of a continuous four-stranded β-sheet superposed by two long α helices, reminiscent of that found in the nucleocapsid protein of porcine respiratory and reproductive syndrome virus. Extensive hydrogen bond formation between the two hairpins and hydrophobic interactions between the β-sheet and the α helices render the interface highly stable. Sequence alignment suggests that other coronavirus may share the same structural topology

Defective INPP5E distribution in NPHP1‐related Senior–Loken syndrome

Background: Senior-Loken syndrome is a rare genetic disorder that presents with nephronophthisis and retinal degeneration, leading to end-stage renal disease and progressive blindness. The most frequent cause of juvenile nephronophthisis is a mutation in the nephronophthisis type 1 (NPHP1) gene. NPHP1 encodes the protein nephrocystin-1, which functions at the transition zone (TZ) of primary cilia. Methods: We report a 9-year-old Senior-Loken syndrome boy with NPHP1 deletion, who presents with bilateral vision decrease and cystic renal disease. Renal function deteriorated to require bilateral nephrectomy and renal transplant. We performed immunohistochemistry, H&E staining, and electron microscopy on the renal sample to determine the subcellular distribution of ciliary proteins in the absence of NPHP1. Results: Immunohistochemistry and electron microscopy of the resected kidney showed disorganized cystic structures with loss of cilia in renal tubules. Phosphoinositides have been recently recognized as critical components of the ciliary membrane and immunostaining of kidney sections for phosphoinositide 5-phosphatase, INPP5E, showed loss of staining compared to healthy control. Ophthalmic examination showed decreased electroretinogram consistent with early retinal degeneration. Conclusion: The decreased expression of INPP5E specifically in the primary cilium, coupled with disorganized cilia morphology, suggests a novel role of NPHP1 that it is involved in regulating ciliary phosphoinositide composition in the ciliary membrane of renal tubular cells

Mouse γ-Synuclein Promoter-Mediated Gene Expression and Editing in Mammalian Retinal Ganglion Cells

Optic neuropathies are a group of optic nerve (ON) diseases caused by various insults including glaucoma, inflammation, ischemia, trauma, and genetic deficits, which are characterized by retinal ganglion cell (RGC) death and ON degeneration. An increasing number of genes involved in RGC intrinsic signaling have been found to be promising neural repair targets that can potentially be modulated directly by gene therapy, if we can achieve RGC specific gene targeting. To address this challenge, we first used adeno-associated virus (AAV)-mediated gene transfer to perform a low-throughput in vivo screening in both male and female mouse eyes and identified the mouse γ-synuclein (mSncg) promoter, which specifically and potently sustained transgene expression in mouse RGCs and also works in human RGCs. We further demonstrated that gene therapy that combines AAV-mSncg promoter with clustered regularly interspaced short palindromic repeats (CRISPR)/Cas9 gene editing can knock down pro-degenerative genes in RGCs and provide effective neuroprotection in optic neuropathies.SIGNIFICANCE STATEMENT Here, we present an RGC-specific promoter, mouse γ-synuclein (mSncg) promoter, and perform extensive characterization and proof-of-concept studies of mSncg promoter-mediated gene expression and clustered regularly interspaced short palindromic repeats (CRISPR)/Cas9 gene editing in RGCs in vivo To our knowledge, this is the first report demonstrating in vivo neuroprotection of injured RGCs and optic nerve (ON) by AAV-mediated CRISPR/Cas9 inhibition of genes that are critical for neurodegeneration. It represents a powerful tool to achieve RGC-specific gene modulation, and also opens up a promising gene therapy strategy for optic neuropathies, the most common form of eye diseases that cause irreversible blindness