Defect review in the photonics revolution: the critical role of near-field optics in the characterization of waveguides, optical interconnects, optical and electro-optical switches, lasers, and their intergrated emulations

2001 ◽  
Author(s):  
Aaron Lewis
Keyword(s):  
Optical Interconnects ◽  
Near Field ◽  
Critical Role ◽  
Optical Switches ◽  
Near Field Optics

scholarly journals The Effect of Octapeptide Repeats on Prion Folding and Misfolding

2021 ◽  
Vol 22 (4) ◽  
pp. 1800
Author(s):  
Kun-Hua Yu ◽  
Mei-Yu Huang ◽  
Yi-Ru Lee ◽  
Yu-Kie Lin ◽  
Hau-Ren Chen ◽  
...  
Keyword(s):  
Amyloid Fibrils ◽  
Age Of Onset ◽  
Prion Diseases ◽  
Critical Role ◽  
Threshold Effect ◽  
Central Feature ◽  
Terminal Domain ◽  
Amyloid Aggregates

Misfolding of prion protein (PrP) into amyloid aggregates is the central feature of prion diseases. PrP has an amyloidogenic C-terminal domain with three α-helices and a flexible tail in the N-terminal domain in which multiple octapeptide repeats are present in most mammals. The role of the octapeptides in prion diseases has previously been underestimated because the octapeptides are not located in the amyloidogenic domain. Correlation between the number of octapeptide repeats and age of onset suggests the critical role of octapeptide repeats in prion diseases. In this study, we have investigated four PrP variants without any octapeptides and with 1, 5 and 8 octapeptide repeats. From the comparison of the protein structure and the thermal stability of these proteins, as well as the characterization of amyloids converted from these PrP variants, we found that octapeptide repeats affect both folding and misfolding of PrP creating amyloid fibrils with distinct structures. Deletion of octapeptides forms fewer twisted fibrils and weakens the cytotoxicity. Insertion of octapeptides enhances the formation of typical silk-like fibrils but it does not increase the cytotoxicity. There might be some threshold effect and increasing the number of peptides beyond a certain limit has no further effect on the cell viability, though the reasons are unclear at this stage. Overall, the results of this study elucidate the molecular mechanism of octapeptides at the onset of prion diseases.

scholarly journals Expression, Purification, and Characterization of (R)-Sulfolactate Dehydrogenase (ComC) from the Rumen MethanogenMethanobrevibacter milleraeSM9

Archaea ◽  
2017 ◽  
Vol 2017 ◽  
pp. 1-6
Author(s):  
Yanli Zhang ◽  
Linley R. Schofield ◽  
Carrie Sang ◽  
Debjit Dey ◽  
Ron S. Ronimus
Keyword(s):  
Biosynthetic Pathway ◽  
Critical Role ◽  
Reduction Reaction ◽  
Coenzyme M ◽  
Purification And Characterization ◽  
The Third ◽  
Optimal Activity ◽  
Methyl Coenzyme M Reductase

(R)-Sulfolactate dehydrogenase (EC 1.1.1.337), termed ComC, is a member of an NADH/NADPH-dependent oxidoreductase family of enzymes that catalyze the interconversion of 2-hydroxyacids into their corresponding 2-oxoacids. The ComC reaction is reversible and in the biosynthetic direction causes the conversion of (R)-sulfolactate to sulfopyruvate in the production of coenzyme M (2-mercaptoethanesulfonic acid). Coenzyme M is an essential cofactor required for the production of methane by the methyl-coenzyme M reductase complex. ComC catalyzes the third step in the first established biosynthetic pathway of coenzyme M and is also involved in methanopterin biosynthesis. In this study, ComC fromMethanobrevibacter milleraeSM9 was cloned and expressed inEscherichia coliand biochemically characterized. Sulfopyruvate was the preferred substrate using the reduction reaction, with 31% activity seen for oxaloacetate and 0.2% seen forα-ketoglutarate. Optimal activity was observed at pH 6.5. The apparentKMfor coenzyme (NADH) was 55.1 μM, and for sulfopyruvate, it was 196 μM (for sulfopyruvate theVmaxwas 93.9 μmol min−1 mg−1andkcatwas 62.8 s−1). The critical role of ComC in two separate cofactor pathways makes this enzyme a potential means of developing methanogen-specific inhibitors for controlling ruminant methane emissions which are increasingly being recognized as contributing to climate change.

scholarly journals The Chlamydia-Secreted Protease CPAF Promotes Chlamydial Survival in the Mouse Lower Genital Tract

2016 ◽  
Vol 84 (9) ◽  
pp. 2697-2702 ◽  
Author(s):  
Zhangsheng Yang ◽  
Lingli Tang ◽  
Lili Shao ◽  
Yuyang Zhang ◽  
Tianyuan Zhang ◽  
...  
Keyword(s):  
Genital Tract ◽  
Chlamydial Infection ◽  
Critical Role ◽  
Content Type ◽  
Lower Genital Tract ◽  
Successful Infection ◽  
Multiple Strains

Despite the extensivein vitrocharacterization of CPAF (chlamydialprotease/proteasome-likeactivityfactor), its role in chlamydial infection and pathogenesis remains unclear. We now report that aChlamydia trachomatisstrain deficient in expression of CPAF (L2-17) is no longer able to establish a successful infection in the mouse lower genital tract following an intravaginal inoculation. The L2-17 organisms were cleared from the mouse lower genital tract within a few days, while a CPAF-sufficientC. trachomatisstrain (L2-5) survived in the lower genital tract for more than 3 weeks. However, both the L2-17 and L2-5 organisms maintained robust infection courses that lasted up to 4 weeks when they were directly delivered into the mouse upper genital tract. The CPAF-dependent chlamydial survival in the lower genital tract was confirmed in multiple strains of mice. Thus, we have demonstrated a critical role of CPAF in promotingC. trachomatissurvival in the mouse lower genital tracts. It will be interesting to further investigate the mechanisms of the CPAF-dependent chlamydial pathogenicity.

scholarly journals Molecular insights into regulation of JAK2 in myeloproliferative neoplasms

Blood ◽  
2015 ◽  
Vol 125 (22) ◽  
pp. 3388-3392 ◽  
Author(s):  
Olli Silvennoinen ◽  
Stevan R. Hubbard
Keyword(s):  
Molecular Characterization ◽  
Human Disease ◽  
Molecular Mechanisms ◽  
Myeloproliferative Neoplasms ◽  
Critical Role ◽  
Hematologic Malignancies ◽  
Janus Kinase ◽  
Constitutive Activation

Abstract The critical role of Janus kinase-2 (JAK2) in regulation of myelopoiesis was established 2 decades ago, but identification of mutations in the pseudokinase domain of JAK2 in myeloproliferative neoplasms (MPNs) and in other hematologic malignancies highlighted the role of JAK2 in human disease. These findings have revolutionized the diagnostics of MPNs and led to development of novel JAK2 therapeutics. However, the molecular mechanisms by which mutations in the pseudokinase domain lead to hyperactivation of JAK2 and clinical disease have been unclear. Here, we describe recent advances in the molecular characterization of the JAK2 pseudokinase domain and how pathogenic mutations lead to constitutive activation of JAK2.

scholarly journals Isolation and Characterization of Cryptococcus neoformans Spores Reveal a Critical Role for Capsule Biosynthesis Genes in Spore Biogenesis

2009 ◽  
Vol 8 (4) ◽  
pp. 595-605 ◽  
Author(s):  
Michael R. Botts ◽  
Steven S. Giles ◽  
Marcellene A. Gates ◽  
Thomas R. Kozel ◽  
Christina M. Hull
Keyword(s):  
Cryptococcus Neoformans ◽  
Fungal Pathogens ◽  
Critical Role ◽  
Spore Formation ◽  
Yeast Cells ◽  
Isolation And Characterization ◽  
Specific Configuration ◽  
First Time

ABSTRACT Spores are essential particles for the survival of many organisms, both prokaryotic and eukaryotic. Among the eukaryotes, fungi have developed spores with superior resistance and dispersal properties. For the human fungal pathogens, however, relatively little is known about the role that spores play in dispersal and infection. Here we present the purification and characterization of spores from the environmental fungus Cryptococcus neoformans. For the first time, we purified spores to homogeneity and assessed their morphological, stress resistance, and surface properties. We found that spores are morphologically distinct from yeast cells and are covered with a thick spore coat. Spores are also more resistant to environmental stresses than yeast cells and display a spore-specific configuration of polysaccharides on their surfaces. Surprisingly, we found that the surface of the spore reacts with antibodies to the polysaccharide glucuronoxylomannan, the most abundant component of the polysaccharide capsule required for C. neoformans virulence. We explored the role of capsule polysaccharide in spore development by assessing spore formation in a series of acapsular strains and determined that capsule biosynthesis genes are required for proper sexual development and normal spore formation. Our findings suggest that C. neoformans spores may have an adapted cell surface that facilitates persistence in harsh environments and ultimately allows them to infect mammalian hosts.

scholarly journals Full in vivo characterization of carbonate chemistry at the site of calcification in corals

2019 ◽  
Vol 5 (1) ◽  
pp. eaau7447 ◽  
Author(s):  
Duygu S. Sevilgen ◽  
Alexander A. Venn ◽  
Marian Y. Hu ◽  
Eric Tambutté ◽  
Dirk de Beer ◽  
...  
Keyword(s):  
Critical Role ◽  
Carbonate Chemistry ◽  
Saturation State ◽  
Stylophora Pistillata ◽  
Coral Calcification ◽  
Carbon Concentrating Mechanisms ◽  
In Vivo Characterization

Reef-building corals form their calcium carbonate skeletons within an extracellular calcifying medium (ECM). Despite the critical role of the ECM in coral calcification, ECM carbonate chemistry is poorly constrained in vivo, and full ECM carbonate chemistry has never been characterized based solely on direct in vivo measurements. Here, we measure pHECMin the growing edge ofStylophora pistillataby simultaneously using microsensors and the fluorescent dye SNARF-1, showing that, when measured at the same time and place, the results agree. We then conduct microscope-guided microsensor measurements of pH, [Ca2+], and [CO32−] in the ECM and, from this, determine [DIC]ECMand aragonite saturation state (Ωarag), showing that all parameters are elevated with respect to the surrounding seawater. Our study provides the most complete in vivo characterization of ECM carbonate chemistry parameters in a coral species to date, pointing to the key role of calcium- and carbon-concentrating mechanisms in coral calcification.

Characterization of pathogenic CD8 + T cells in Chlamydia - infected OT1 mice

2021 ◽  
Author(s):  
Zengzi Zhou ◽  
Qi Tian ◽  
Luying Wang ◽  
Xin Sun ◽  
Nu Zhang ◽  
...  
Keyword(s):  
T Cells ◽  
Chlamydia Trachomatis ◽  
Cd8 T Cells ◽  
Chlamydial Infection ◽  
Critical Role ◽  
Wild Type ◽  
Chlamydia Muridarum ◽  
Time Of Infection

Chlamydia trachomatis is a leading infectious cause of infertility in women due to its induction of lasting pathology such as hydrosalpinx. Chlamydia muridarum induces mouse hydrosalpinx because C. muridarum can both invade tubal epithelia directly (as a 1 st hit) and induce lymphocytes to promote hydrosalpinx indirectly (as a 2 nd hit). In the current study, a critical role of CD8 + T cells in chlamydial induction of hydrosalpinx was validated in both wild type C57BL/6J and OT1 transgenic mice. OT1 mice failed to develop hydrosalpinx partially due to the failure of their lymphocytes to recognize chlamydial antigens. CD8 + T cells from naïve C57BL/6J rescued the recipient OT1 mice to develop hydrosalpinx when naïve CD8 + T cells were transferred at the time of infection with Chlamydia . However, when the transfer was delayed for 2 weeks or longer after the chlamydial infection, naïve CD8 + T cells no longer promoted hydrosalpinx. Nevertheless, Chlamydia -immunized CD8 + T cells still promoted significant hydrosalpinx in the recipient OT1 mice even when the transfer was delayed for 3 weeks. Thus, CD8 + T cells must be primed within 2 weeks after chlamydial infection to be pathogenic but once primed, they can promote hydrosalpinx for >3 weeks. However, Chlamydia -primed CD4 + T cells failed to promote chlamydial induction of pathology in OT1 mice. This study has optimized an OT1 mouse-based model for revealing the pathogenic mechanisms of Chlamydia -specific CD8 + T cells.

scholarly journals Interplay between Cellular and Molecular Inflammatory Mediators in Lung Cancer

2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Mario Orozco-Morales ◽  
Giovanny Soca-Chafre ◽  
Pedro Barrios-Bernal ◽  
Norma Hernández-Pedro ◽  
Oscar Arrieta
Keyword(s):  
Lung Cancer ◽  
Immune Suppression ◽  
Critical Role ◽  
Inflammatory Cells ◽  
T Cell Response ◽  
Invasion And Metastasis ◽  
Remodeling Of Extracellular Matrix ◽  
Tumor Associated Neutrophils

Inflammation is a component of the tumor microenvironment and represents the 7th hallmark of cancer. Chronic inflammation plays a critical role in tumorigenesis. Tumor infiltrating inflammatory cells mediate processes associated with progression, immune suppression, promotion of neoangiogenesis and lymphangiogenesis, remodeling of extracellular matrix, invasion and metastasis, and, lastly, the inhibition of vaccine-induced antitumor T cell response. Accumulating evidence indicates a critical role of myeloid cells in the pathophysiology of human cancers. In contrast to the well-characterized tumor-associated macrophages (TAMs), the significance of granulocytes in cancer has only recently begun to emerge with the characterization of tumor-associated neutrophils (TANs). Recent studies show the importance of CD47 in the interaction with macrophages inhibiting phagocytosis and promoting the migration of neutrophils, increasing inflammation which can lead to recurrence and progression in lung cancer. Currently, therapies are targeted towards blocking CD47 and enhancing macrophage-mediated phagocytosis. However, antibody-based therapies may have adverse effects that limit its use.

scholarly journals A peek into Epac physiology in the kidney

2019 ◽  
Vol 317 (5) ◽  
pp. F1094-F1097 ◽  
Author(s):  
Viktor N. Tomilin ◽  
Oleh Pochynyuk
Keyword(s):  
Current Knowledge ◽  
Collecting Duct ◽  
Critical Role ◽  
Second Messenger ◽  
Electrolyte Transport ◽  
Urinary Concentration ◽  
Renal Epithelium ◽  
Downstream Effector

cAMP is a critical second messenger of numerous endocrine signals affecting water-electrolyte transport in the renal tubule. Exchange protein directly activated by cAMP (Epac) is a relatively recently discovered downstream effector of cAMP, having the same affinity to the second messenger as protein kinase A, the classical cAMP target. Two Epac isoforms, Epac1 and Epac2, are abundantly expressed in the renal epithelium, where they are thought to regulate water and electrolyte transport, particularly in the proximal tubule and collecting duct. Recent characterization of renal phenotype in mice lacking Epac1 and Epac2 revealed a critical role of the Epac signaling cascade in urinary concentration as well as in Na+ and urea excretion. In this review, we aim to critically summarize current knowledge of Epac relevance for renal function and to discuss the applicability of Epac-based strategies in the regulation of systemic water-electrolyte homeostasis.

scholarly journals Phospholipase C in mouse oocytes: characterization of β and γ isoforms and their possible involvement in sperm-induced Ca2+ spiking

1996 ◽  
Vol 316 (2) ◽  
pp. 583-591 ◽  
Author(s):  
Genevieve DUPONT ◽  
Orla M. McGUINNESS ◽  
Martin H. JOHNSON ◽  
Michael J. BERRIDGE ◽  
Franck BORGESE
Keyword(s):  
Monoclonal Antibodies ◽  
Phospholipase C ◽  
Kinase Inhibitors ◽  
Critical Role ◽  
Inhibitory Effect ◽  
Functional Studies ◽  
Mouse Oocytes ◽  
Mature Mouse

This study involved an investigation of the role of phospholipase C (PLC) in generating repetitive Ca2+ spikes at fertilization. Using a PCR-based strategy we have demonstrated that mouse oocytes have mRNA coding for PLCβ1, PLCβ3 and PLCγ isoenzymes. Furthermore, immunodetection of PLCγ1 using monoclonal antibodies reveals that PLCγ1 protein is present in mature mouse oocytes, ruling out the possibility that mRNA was being transcribed but not expressed. We were unsuccessful at detecting the presence of PLCβ protein, but the presence of this isoform can be inferred from functional studies. The PLC inhibitor, U73122, exerted an inhibitory effect on oocytes activated by spermatozoa or acetylcholine at concentrations of 10 and 30 μM respectively, while its inactive analogue had no effect. The soluble tyrosine kinase inhibitors, genistein (100 μM), herbimycin (10 μM) and geldanamycin (0.6 μM) which could affect signalling through PLCγ hindered but never completely inhibited Ca2+ spiking in response to fertilization. We conclude that the activation of PLC to generate InsP3 may play a critical role in fertilization.

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