Enhancement of phase separation in the InGaN layer for self-assembled In-rich quantum dots

The enhancement of phase separation in the InGaN layer grown on a GaN layer with a rough surface was investigated for the formation of self-assembled In-rich quantum dots(QDs) in the InGaN layer. Transmission electron microscopy images showed that In-rich QDs with a size of 2–5 nm were formed even in an InGaN layer with a low indium content, and a layer thickness less than the critical thickness. The room-temperature photoluminescence(PL) spectrum of this layer showed emission peaks corresponding to In-rich QDs. The temperature-dependent PL spectra showed dominant peak shifts to the lower energy side, indicating that the self-assembled In-rich QDs are formed in the InGaN layer grown on a rough GaNsurface and that the carriers are localized in In-rich QDs

Sequences of the Cytochrome C Oxidase Subunit I (COI) Gene are Suitable for Species Identification of Korean Calliphorinae Flies of Forensic Importance (Diptera: Calliphoridae)

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/75068/1/j.1556-4029.2009.01126.x.pd

NF-κB/STAT3/PI3K signaling crosstalk in iMycEμ B lymphoma

<p>Abstract</p> <p>Background</p> <p>Myc is a well known driver of lymphomagenesis, and Myc-activating chromosomal translocation is the recognized hallmark of Burkitt lymphoma, an aggressive form of non-Hodgkin's lymphoma. We developed a model that mimics this translocation event by inserting a mouse <it>Myc </it>cDNA gene into the immunoglobulin heavy chain locus, just upstream of the intronic Eμ enhancer. These mice, designated iMyc^Eμ, readily develop B-cell lymphoma. To study the mechanism of Myc-induced lymphoma, we analyzed signaling pathways in lymphoblastic B-cell lymphomas (LBLs) from iMyc^Eμmice, and an LBL-derived cell line, iMyc^Eμ-1.</p> <p>Results</p> <p>Nuclear factor-κB (NF-κB) and signal transducer and activator of transcription 3 (STAT3) were constitutively activated in iMyc^Eμmice, not only in LBLs but also in the splenic B-lymphocytes of young animals months before tumors developed. Moreover, inhibition of either transcription factor in iMyc^Eμ-1 cells suppressed growth and caused apoptosis, and the abrogation of NF-κB activity reduced DNA binding by both STAT3 and Myc, as well as Myc expression. Inhibition of STAT3 signaling eliminated the activity of both NF-κB and Myc, and resulted in a corresponding decrease in the level of Myc. Thus, in iMyc^Eμ-1 cells NF-κB and STAT3 are co-dependent and can both regulate Myc. Consistent with this, NF-κB and phosphorylated STAT3 were physically associated with one another. In addition, LBLs and iMyc^Eμ-1 cells also showed constitutive AKT phosphorylation. Blocking AKT activation by inhibiting PI3K reduced iMyc^Eμ-1 cell proliferation and caused apoptosis, via downregulation of NF-κB and STAT3 activity and a reduction of Myc levels. Co-treatment with NF-κB, STAT3 or/and PI3K inhibitors led to additive inhibition of iMyc^Eμ-1 cell proliferation, suggesting that these signaling pathways converge.</p> <p>Conclusions</p> <p>Our findings support the notion that constitutive activation of NF-κB and STAT3 depends on upstream signaling through PI3K, and that this activation is important for cell survival and proliferation, as well as for maintaining the level of Myc. Together, these data implicate crosstalk among NF-κB, STAT3 and PI3K in the development of iMyc^EμB-cell lymphomas.</p

THE EFFECTS OF WEARING SPANDEX GARMENT WITH COMPRESSION BAND ON KINEMATIC VARIABLES DURING A GOLF SWING

The purpose of this study was to investigate how spandex garment with compressive band affects kinematic variables during a golf swing. The X-factor and angular velocity of the club in EG were increased during the down swing phase, whereas the significant changes of other kinematic variables were not found in this study. Thus, the effects of wearing spandex garment with compression band cannot be explained as a function of the kinematic variables of interest. It is clear that wearing spandex garment with compressive band may enhance joint stability, which in turn may affect joint kinetics and muscle activation. This has led to suggestions of the need for further kinetic and EMG analyses to evaluate its function

Detection of Bartonella henselae DNA by Polymerase Chain Reaction in a Patient with Cat Scratch Disease : A Case Report

We report a case of cat scratch disease caused by Bartonella henselae in Korea. A 25-yr-old woman developed left cervical lymphadenopathy with history of contact with a dog. The cervical lymphadenopathy persisted for 1 month and resolved gradually and spontaneously. Serologic test was not done during the acute stage of the disease. Immunofluorescent antibody test performed during the convalescent stage was positive for B. henselae. To confirm B. henselae infection, polymerase chain reaction (PCR) analysis using aspirates of cervical lymph node was performed and the presence of B. henselae DNA was demonstrated. This is the first reported case of cat scratch disease in Korea confirmed by PCR for B. henselae DNA

Lipid emulsion inhibits the cardiac toxicity caused by chloroquine via inhibition of reactive oxygen species production

Background Lipid emulsion (LE) is effective in treating intractable cardiac depression induced by the toxicity of highly lipid-soluble drugs including local anesthetics. However, the effect of LE on chloroquine (CQ)-evoked cardiac toxicity remains unclear. This study aimed to examine the effect of Lipofundin MCT/LCT, an LE, on the cardiotoxicity caused by CQ in H9c2 rat cardiomyoblasts and elucidate the underlying cellular mechanism. Methods The effects of CQ (1 × 10-4 M), LE, and the reactive oxygen species (ROS) scavengers mitotempo and N-acetyl-L-cysteine (NAC), alone or combined, on cell viability and migration, apoptosis, ROS production, calcium levels, mitochondrial membrane potential, and adenosine triphosphate (ATP) were examined. Additionally, the effects of LE on the activities of catalase (CAT), malondialdehyde (MDA), and superoxide dismutase (SOD) induced by CQ were assessed. Results Pretreatment with LE, mitotempo, or NAC reversed the reduction in cell migration and viability, mitochondrial membrane potential, and ATP levels evoked by CQ, and inhibited the increase in cleaved caspase-3, ROS, and calcium concentration induced by CQ. LE inhibited the increase in Bax expression, terminal deoxynucleotidyl transferase dUTP nick end labeling-positive cells, MDA activity, and late apoptosis, and reversed the reduction in SOD and CAT activity induced by CQ. CQ did not significantly affect cleaved caspase-8 expression, and LE did not significantly affect CQ concentration. Conclusions Collectively, these results suggest that LE (Lipofundin MCT/LCT) inhibits the cardiotoxicity and late apoptosis induced by CQ toxicity via the intrinsic mitochondrial apoptotic pathway that is associated with direct inhibition of ROS production

Acute respiratory alkalosis occurring after endoscopic third ventriculostomy -A case report-

An endoscopic third ventriculostomy was performed in a 55-year-old man with an obstructive hydrocephalus due to aqueductal stenosis. The vital signs and laboratory studies upon admission were within the normal limits. Anesthesia was maintained with nitrous oxide in oxygen and 6% desflurane. The patient received irrigation with approximately 3,000 ml normal saline during the procedure. Anesthesia and operation were uneventful. However, he developed postoperative hyperventilation in the recovery room, and arterial blood gas analysis revealed acute respiratory alkalosis. We report a rare respiratory alkalosis that occurred after an endoscopic third ventriculostomy