Optimum Design of Quenching Capacitor Integrated Silicon Photomultipliers for TOF-PET Application

AbstractThe prototype SiPM was designed and fabricated for MRI compatible PET using the customized CMOS process at National Nanofab Center in KAIST. The SiPM was designed to have a size of 3x3 mm2 composed of micro-cells of 65x65μm2 with a fill factor of 68%. The size of a micro-cell was determined by optimization between the photon detection efficiency (PDE) and the dynamic range for the photons of 511 keV from LYSO crystal. In the micro-cell structure, a specially designed quenching capacitor (QC) is added parallel to quenching resistor using the Metal-Insulator-Metal (MIM) process. This QC integrated SiPMs (QC-SiPM) was devised to realize rapid response of output pulses and to enhance the timing resolution of SiPM. Coincidence timing resolution of PET detectors depends on the output pulse shapes which are the convolution of the intrinsic pulse shape of scintillation crystals and the single photon pulse shape at the micro-cell in a SiPM. A quenching capacitor parallel to a quenching resistor provides a fast current path at the beginning stage of avalanche process, than reduces rising time of single photon pulse shape. In this study the rise time of the QC-SiPM signal was analyzed to be 22.5ns while that for the regular SiPM was 34.3ns

Methano­ldinitrato[N-(2-pyridylmethyl­ene)aniline]copper(II)

The Cu atom in the title compound, [Cu(NO3)2(C12H10N2)(CH3OH)], adopts a square-pyramidal geometry, being ligated by two N atoms of the bidentate N-(2-pyridylmethyl­ene)­aniline (ppma) ligand, two O atoms of NO3 ligands and one O atom of a methanol molecule, which occupies the apical position. The phenyl ring on the ppma ligand is twisted out of the pyridine plane, forming a dihedral angle of 42.9 (1)°. In the crystal, inter­molecular O—H⋯O hydrogen bonds between methanol and NO3 ligands form an extensive one-dimensional network extending parallel to [100]

Properties of Central Caustics in Planetary Microlensing

To maximize the number of planet detections, current microlensing follow-up observations are focusing on high-magnification events which have a higher chance of being perturbed by central caustics. In this paper, we investigate the properties of central caustics and the perturbations induced by them. We derive analytic expressions of the location, size, and shape of the central caustic as a function of the star-planet separation, $s$, and the planet/star mass ratio, $q$, under the planetary perturbative approximation and compare the results with those based on numerical computations. While it has been known that the size of the planetary caustic is \propto \sqrt{q}, we find from this work that the dependence of the size of the central caustic on $q$ is linear, i.e., \propto q, implying that the central caustic shrinks much more rapidly with the decrease of $q$ compared to the planetary caustic. The central-caustic size depends also on the star-planet separation. If the size of the caustic is defined as the separation between the two cusps on the star-planet axis (horizontal width), we find that the dependence of the central-caustic size on the separation is \propto (s+1/s). While the size of the central caustic depends both on $s$ and q, its shape defined as the vertical/horizontal width ratio, R_c, is solely dependent on the planetary separation and we derive an analytic relation between R_c and s. Due to the smaller size of the central caustic combined with much more rapid decrease of its size with the decrease of q, the effect of finite source size on the perturbation induced by the central caustic is much more severe than the effect on the perturbation induced by the planetary caustic. Abridged.Comment: 5 pages, 4 figures, ApJ accepte

Transcriptional Regulator TonEBP Mediates Oxidative Damages in Ischemic Kidney Injury

TonEBP (tonicity-responsive enhancer binding protein) is a transcriptional regulator whose expression is elevated in response to various forms of stress including hyperglycemia, inflammation, and hypoxia. Here we investigated the role of TonEBP in acute kidney injury (AKI) using a line of TonEBP haplo-deficient mice subjected to bilateral renal ischemia followed by reperfusion (I/R). In the TonEBP haplo-deficient animals, induction of TonEBP, oxidative stress, inflammation, cell death, and functional injury in the kidney in response to I/R were all reduced. Analyses of renal transcriptome revealed that genes in several cellular pathways including peroxisome and mitochondrial inner membrane were suppressed in response to I/R, and the suppression was relieved in the TonEBP deficiency. Production of reactive oxygen species (ROS) and the cellular injury was reproduced in a renal epithelial cell line in response to hypoxia, ATP depletion, or hydrogen peroxide. The knockdown of TonEBP reduced ROS production and cellular injury in correlation with increased expression of the suppressed genes. The cellular injury was also blocked by inhibitors of necrosis. These results demonstrate that ischemic insult suppresses many genes involved in cellular metabolism leading to local oxidative stress by way of TonEBP induction. Thus, TonEBP is a promising target to prevent AKI

The farnesoid X receptor negatively regulates osteoclastogenesis in bone remodeling and pathological bone loss

Farnesoid X receptor (FXR, NR1H4) is a member of the nuclear receptor superfamily of ligand-activated transcription factors. Since the role of FXR in osteoclast differentiation remains ill-defined, we investigated the biological function of FXR on osteoclastogenesis, using FXR-deficient mice. We demonstrated that FXR deficiency increases osteoclast formation in vitro and in vivo. First, FXR deficiency was found to accelerate osteoclast formation via down-regulation of c-Jun N-terminal kinase (JNK) 1/2 expression. Increased expression of peroxisome proliferator-activated receptor (PPAR)γ and peroxisome proliferator-activated receptor gamma coactivator 1 (PGC- 1)β seems to mediate the pro-osteoclastogenic effect of FXR deficiency via the JNK pathway. In addition, we found that FXR deficiency downregulated the expression of interferon-β (IFN-β), a strong inhibitor of osteoclastogenesis, via receptor activator of nuclear factor-kappaB ligand (RANKL). We further suggested that interference of IFN-β expression by FXR deficiency impaired the downstream JAK3-STAT1 signaling pathways, which in turn increased osteoclast formation. Finally, FXR deficiency accelerated unloading- or ovariectomy-induced bone loss in vivo. Thus, our findings demonstrate that FXR is a negative modulator in osteoclast differentiation and identify FXR as a potential therapeutic target for postmenopausal osteoporosis and unloadinginduced bone loss

Accidental intradural injection during attempted epidural block -A case report-

Several cases of accidental subdural injection have been reported, but only few of them are known to be accidental intradural injection during epidural block. Therefore we would like to report our experience of accidental intradural injection. A 68-year-old female was referred to our pain clinic due to severe metastatic spinal pain. We performed a diagnostic epidural injection at T9/10 interspace under the C-arm guided X-ray view. Unlike the usual process of block, onset was delayed and sensory dermatomes were irregular range. We found out a dense collection of localized radio-opaque contrast media on the reviewed X-ray findings. These are characteristic of intradural injection and clearly different from the narrow wispy bands of contrast in the subdural space

Effect of GCSB-5, a Herbal Formulation, on Monosodium Iodoacetate-Induced Osteoarthritis in Rats

Therapeutic effects of GCSB-5 on osteoarthritis were measured by the amount of glycosaminoglycan in rabbit articular cartilage explants in vitro, in experimental osteoarthritis induced by intra-articular injection of monoiodoacetate in rats in vivo. GCSB-5 was orally administered for 28 days. In vitro, GCSB-5 inhibited proteoglycan degradation. GCSB-5 significantly suppressed the histological changes in monoiodoacetate-induced osteoarthritis. Matrix metalloproteinase (MMP) activity, as well as, the levels of serum tumor necrosis factor-α, cyclooxygenase-2, inducible nitric oxide synthase protein, and mRNA expressions were attenuated by GCSB-5, whereas the level of interleukin-10 was potentiated. By GCSB-5, the level of nuclear factor-κB p65 protein expression was significantly attenuated but, on the other hand, the level of inhibitor of κB-α protein expression was increased. These results indicate that GCSB-5 is a potential therapeutic agent for the protection of articular cartilage against progression of osteoarthritis through inhibition of MMPs activity, inflammatory mediators, and NF-κB activation