Rubisco activity and gene expression of tropical tree species under light stress

Tropical rain forests contain an ecologically and physiologically diverse range of vegetation and habitats. Sun-acclimated plants can be divided into two groups, shade-tolerant and shade-intolerant, according to the plant’s physiological and genetic responses. Some tropical species have potential capacity for light damage in a shaded environment as well as shade-tolerance to compensate for the impaired light harvesting complex. In particular, ribulose‐1,5‐bisphosphate carboxylase/oxygenase (Rubisco) is regulated by the Calvin cycle, which participated in protein synthesis. Rubisco plays a role in CO2 fixation, which helps supply the energy to regulate Rubisco for ribulose 1,5-bisphosphate (RuBP) reduction. Light intensity is associated with the photosynthetic rate and genetic response to moderate growth environments.Keywords: Gene expression, growth, light intensity, Rubisco activityAfrican Journal of Biotechnology Vol. 12(20), pp. 2764-276

Scientific Evidence for Korean Medicine and Its Integrative Medical Research 2017

In 2016, the total medical fee for Korea Medicine (KM) in South Korea was over 4 billion dollars and the National Health Insurance of South Korea paid about 2.09 billion dollars for medical services provided by 19, 737 KM doctors in 302 KM hospitals and 14, 150 KM local clinics. Actually, 12.9 million Korean patients received 105 million outpatient services provided by KM doctors in 2016. The older the Korean society is, the more important the role of KM becomes, because Korea is anticipated to be a hyperaged society in 2028. As well as the Donguibogam, which was enlisted on the Memory of the Word by UNESCO in 2009, Sasang typology, Sasang Constitutional Medicine, Sa-am acupuncture, Chuna therapy, Pharmacopuncture, Korean physical therapy, Korean psychotherapy, and so on characterize KM. But more integrative researches and scientific evidences for KM might strengthen both clinical efficacy and applicability of KM. In this respect, it seems to be unavoidable that KM utilizes cutting-edge techniques of modern science. The more accurate and efficient practice of KM innovated with the modern bioscientific technology would help people live healthy lives. Our special issue, which had opened for 6 months in the first half of 2017, focused on scientific evidence for KM and its integrative medical research

The effect of various design codes and dynamic magnification on buildings with torsional irregularity

Seismic provisions have utilized design eccentricities to reduce planar irregularities in lateral stiffness of buildings. In calculating a design eccentricity, the torsional amplification factor may be applied either to accidental eccentricity or to both inherent and accidental eccentricities according to design codes. In this paper, different code provisions and their impact on torsional responses of buildings are investigated using example buildings with various aspect ratios and inherent eccentricities. It was found that the design eccentricity in KBC-2009 using torsional amplification factor for only accidental eccentricity reflects the dynamic magnification more accurately than that in KBC-2006 using this factor for both inherent and accidental eccentricity. And dynamic magnification of a torsionally imbalanced building is affected by the size of seismic design force of response spectrum analysis than design eccentricity of equivalent static analysis in KBC-2009. In other words, design eccentricity including torsional amplification factor in KBC-2009 do not reflect the dynamic magnification accurately

Role of \u3cem\u3eEgr-1\u3c/em\u3e Gene Expression in B Cell Receptor-Induced Apoptosis in an Immature B Cell Lymphoma

Ligation of B cell receptor (BCR) on BKS-2, an immature B cell lymphoma by anti-IgM antibodies (Ab) caused apoptosis. Here we report that signaling through B cell receptor in wild type BKS-2 cells down-regulated the expression of Egr-1, a zinc finger-containing transcription factor. A reduction in the level ofEgr-1 mRNA could be demonstrated as early as 30 min after the ligation of BCR on BKS-2 cells. Immunocytochemical and Western blot analysis revealed that the expression of EGR-1 protein was also inhibited by anti-IgM treatment. Antisense oligonucleotides to Egr-1 caused growth inhibition and apoptosis in BKS-2 cells, suggesting that expression of Egr-1 is important for the survival of these B lymphoma cells. In contrast to wild type BKS-2 cells, the mutant 1.B5 cell line, which is refractory to B cell receptor-mediated growth-inhibitory signals, showed an increased expression of Egr-1 upon treatment with anti-IgM. These results implicate a role for Egr-1 in blocking B cell receptor-mediated apoptosis in immature B cells

Xanthogranulomatous Cystitis Arising from the Posterior Wall of the Bladder

Xanthogranulomatous cystitis is a rare, benign chronic inflammatory disease of unknown etiology. Herein we report a case of a 41-year-old man who presented with painless hematuria and a bladder mass on imaging studies

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

Molecular and cytological features of the mouse B-cell lymphoma line iMyc(Eμ)-1

BACKGROUND: Myc-induced lymphoblastic B-cell lymphoma (LBL) in iMyc(Eμ )mice may provide a model system for the study of the mechanism by which human MYC facilitates the initiation and progression of B cell and plasma cell neoplasms in human beings. We have recently shown that gene-targeted iMyc(Eμ )mice that carry a His(6)-tagged mouse Myc cDNA, Myc(His), just 5' of the immunoglobulin heavy-chain enhancer, Eμ, are prone to B cell and plasma cell tumors. The predominant tumor (~50%) that arose in the iMyc(Eμ )mice on the mixed genetic background of segregating C57BL/6 and 129/SvJ alleles was LBL. The purpose of this study was to establish and characterize a cell line, designated iMyc(Eμ)-1, for the in-depth evaluation of LBL in vitro. METHODS: The morphological features and the surface marker expression profile of the iMyc(Eμ)-1 cells were evaluated using cytological methods and FACS, respectively. The cytogenetic make-up of the iMyc(Eμ)-1 cells was assessed by spectral karyotyping (SKY). The expression of the inserted Myc(His )gene was determined using RT-PCR and qPCR. Clonotypic immunoglobulin gene arrangements were detected by Southern blotting. The global gene expression program of the iMyc(Eμ)-1 cells and the expression of 768 "pathway" genes were determined with the help of the Mouse Lymphochip(© )and Superarray(© )cDNA micro- and macroarrays, respectively. Array results were verified, in part, by RT-PCR and qPCR. RESULTS: Consistent with their derivation from LBL, the iMyc(Eμ)-1 cells were found to be neoplastic IgM(high)IgD(low )lymphoblasts that expressed typical B-cell surface markers including CD40, CD54 (ICAM-1), CD80 (B7-1) and CD86 (B7-2). The iMyc(Eμ)-1 cells harbored a reciprocal T(9;11) and three non-reciprocal chromosomal translocations, over-expressed Myc(His )at the expense of normal Myc, and exhibited gene expression changes on Mouse Lymphochip(© )microarrays that were consistent with Myc(His)-driven B-cell neoplasia. Upon comparison to normal B cells using eight different Superarray(© )cDNA macroarrays, the iMyc(Eμ)-1 cells showed the highest number of changes on the NFκB array. CONCLUSION: The iMyc(Eμ)-1 cells may provide a uniquely useful model system to study the growth and survival requirements of Myc-driven mouse LBL in vitro