http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Shawl Assefa,Beza Shewangizaw,Kenzemed Kassie Yassin,Lisanu Getaneh 한국작물학회 2021 Journal of crop science and biotechnology Vol.24 No.4
Defciency of sulfur (S) is increasingly being reported in the soils of Ethiopia. While some studies have shown signifcant response of barley to S application, information on the response of barley to S application is conspicuously lacking. The average yield of barley in Ethiopia is lower compared to the world and potential yield. It is mostly constrained by the depletion of soil fertility, caused by imbalanced fertilization, limited application of organic manure, intensive cropping. A feld experiment was conducted at two locations for three consecutive years (2014–2016) to determine the efect of S on growth, yield components, and yield of food barley. An experiment consisting of six levels S (0, 10, 20,30,40, and 50 kg ha−1) laid out in RCB design with three replications. The study results revealed that growth and yield components of barley were not afected by various levels of S. In the case of barley grain and straw yield was signifcantly afected by S levels compared to control treatment. Application of S at 20 kg ha−1 increased grain and straw yield of food barley by 16.8 and 20.2% compared to control, respectively. Application of 20 kg S ha−1 produced the highest marginal rate of return (MMR) (3493.2%). The present result revealed that barley yield has been improved by the application of S fertilizer. Therefore, the application of 20 kg S ha−1 is initiate to be the further most economically feasible treatment for food barley production in the Basona woreba district.
Shawl, Asif Iqbal,Park, Kwang-Hyun,Kim, Uh-Hyun Landes Bioscience 2009 Islets Vol.1 No.3
<P>Insulin has an autocrine/paracrine role through insulin receptors in pancreatic 관-cells. Herein, we show the insulin receptor signaling pathway underlying CD38/ADPR-cyclase activation for NAADP/cADPR formation to induce Ca2+ rise, ultimately resulting in 관-cell proliferation. Binding of insulin on insulin receptors leads to the activation of IRS/Akt/PI3K/PLC. Activation of PLC generates IP3 and DAG; the former induces Ca (2+) release, resulting in activation of CD38/ADPR-cyclase for cADPR production via cGMP-dependent mechanism and the latter activates PKC, resulting in activation of ADPR-cyclase for NAADP synthesis. The NAADP-induced Ca (2+) signal is required for IP3-induced Ca (2+) release from the ER. CD38 plays an important role in insulin receptor signaling in 관-cells by reflecting a declined sustained Ca (2+) signal, cADPR levels, and 관-cell proliferation in response to insulin in CD38 (-/-) islets. However, evidence indicates that a hitherto-unidentified ADPR cyclase in addition to CD38 participates in insulin-induced signaling through cADPR and NAADP synthesis. In conclusion, insulin receptor signaling in 관-cells employs three Ca (2+) signaling messengers, IP3, NAADP, and cADPR through a complex but concerted action of signaling molecules for Ca2+ signaling, which is involved in the proliferation of the islets.</P>
Gul, Rukhsana,Shawl, Asif Iqbal,Kim, Suhn-Hee,Kim, Uh-Hyun American Physiological Society 2012 American journal of physiology, Heart and circulat Vol.302 No.4
<P> Reactive oxygen species (ROS) and Ca<SUP>2+</SUP> signals are closely associated with the pathogenesis of cardiac hypertrophy. However, the cause and effect of the two signals in cardiac hypertrophy remain to be clarified. We extend our recent report by investigating a potential interaction between ROS and Ca<SUP>2+</SUP> signals utilizing in vitro and in vivo angiotensin II (ANG II)-induced cardiac hypertrophy models. ANG II-induced initial Ca<SUP>2+</SUP> transients mediated by inositol trisphosphate (IP3) triggered initial ROS production in adult rat cardiomyocytes. The ROS generated by activation of the NAD(P)H oxidase complex via Rac1 in concert with Ca<SUP>2+</SUP> activates ADP-ribosyl cyclase to generate cyclic ADP-ribose (cADPR). This messenger-mediated Ca<SUP>2+</SUP> signal further augments ROS production, since 2,2′-dihydroxyazobenzene, an ADP-ribosyl cyclase inhibitor, or 8-Br-cADPR, an antagonistic analog of cADPR, abolished further ROS production. Data from short hairpin RNA (shRNA)-mediated knockdown of Akt1 and p47<SUP>phox</SUP> demonstrated that Akt1 is the upstream key molecule responsible for the initiation of Ca<SUP>2+</SUP> signal that activates p47<SUP>phox</SUP> to generate ROS in cardiomyocytes. Nuclear translocation of nuclear factor of activated T-cell in cardiomyocytes was significantly suppressed by treatment with NAD(P)H oxidase inhibitors as well as by shRNA against Akt1 and p47<SUP>phox</SUP>. Our results suggest that in cardiomyocytes Ca<SUP>2+</SUP> and ROS messengers generated by ANG II amplify the initial signals in a cooperative manner, thereby leading to cardiac hypertrophy. </P>
Sultan, Phalisteen,Shawl, A.S.,Jan, Arif,Hamid, B.,Irshad, H. 한국작물학회 2009 Journal of crop science and biotechnology Vol.12 No.4
We have done comparative morphological and chemotaxonomic studies to investigate the phylogenetic relationship of different accessions within the Podophyllum species. HPLC profiles revealed that all Podophyllum hexandrum accessions collected from different geographical locations are chemically highly diverse. Also, we have observed that chemotaxonomic studies clearly demonstrated that chemical characters of the Podophyllum hexandrum are suitable to generate essentially the same relationship as revealed by RAPD analysis.
Nam, Tae-Sik,Park, Kwang-Hyun,Shawl, Asif Iqbal,Kim, Byung-Ju,Han, Myung-Kwan,Kim, Youngho,Moss, Joel,Kim, Uh-Hyun American Society for Biochemistry and Molecular Bi 2014 The Journal of biological chemistry Vol.289 No.23
<P>NAD glycohydrolases (NADases) catalyze the hydrolysis of NAD to ADP-ribose and nicotinamide. Although many members of the NADase family, including ADP-ribosyltransferases, have been cloned and characterized, the structure and function of NADases with pure hydrolytic activity remain to be elucidated. Here, we report the structural and functional characterization of a novel NADase from rabbit reticulocytes. The novel NADase is a glycosylated, glycosylphosphatidylinositol-anchored cell surface protein exclusively expressed in reticulocytes. shRNA-mediated knockdown of the NADase in bone marrow cells resulted in a reduction of erythroid colony formation and an increase in NAD level. Furthermore, treatment of bone marrow cells with NAD, nicotinamide, or nicotinamide riboside, which induce an increase in NAD content, resulted in a significant decrease in erythroid progenitors. These results indicate that the novel NADase may play a critical role in regulating erythropoiesis of hematopoietic stem cells by modulating intracellular NAD.</P>