bluuebunny/crossref_metadata_2025_split huggingface dataset:
The Membrane-Associated Methane Monooxygenase (pMMO) and pMMO-NADH:Quinone Oxidoreductase Complex from
Methylococcus capsulatus
Bath
Authors: Choi Dong-W. , Kunz Ryan C. , Boyd Eric S. , Semrau Jeremy D. , Antholine William E. , Han J.-I. , Zahn James A. , Boyd Jeffrey M. , de la Mora Arlene M. , DiSpirito Alan A. 
Published: September 2003

ABSTRACT

Improvements in purification of membrane-associated methane monooxygenase (pMMO) have resulted in preparations of pMMO with activities more representative of physiological rates: i.e., >130 nmol · min
−1
· mg of protein
−1
. Altered culture and assay conditions, optimization of the detergent/protein ratio, and simplification of the purification procedure were responsible for the higher-activity preparations. Changes in the culture conditions focused on the rate of copper addition. To document the physiological events that occur during copper addition, cultures were initiated in medium with cells expressing soluble methane monooxygenase (sMMO) and then monitored for morphological changes, copper acquisition, fatty acid concentration, and pMMO and sMMO expression as the amended copper concentration was increased from 0 (approximately 0.3 μM) to 95 μM. The results demonstrate that copper not only regulates the metabolic switch between the two methane monooxygenases but also regulates the level of expression of the pMMO and the development of internal membranes. With respect to stabilization of cell-free pMMO activity, the highest cell-free pMMO activity was observed when copper addition exceeded maximal pMMO expression. Optimization of detergent/protein ratios and simplification of the purification procedure also contributed to the higher activity levels in purified pMMO preparations. Finally, the addition of the type 2 NADH:quinone oxidoreductase complex (NADH dehydrogenase [NDH]) from
M. capsulatus
Bath, along with NADH and duroquinol, to enzyme assays increased the activity of purified preparations. The NDH and NADH were added to maintain a high duroquinol/duroquinone ratio.
The
Geobacillus stearothermophilus
V
iscS
Gene, Encoding Cysteine Desulfurase, Confers Resistance to Potassium Tellurite in
Escherichia coli
K-12
Authors: Tantaleán Juan C. , Araya Manuel A. , Saavedra Claudia P. , Fuentes Derie E. , Pérez José M. , Calderón Iván L. , Youderian Philip , Vásquez Claudio C. 
Published: September 2003

ABSTRACT

Many eubacteria are resistant to the toxic oxidizing agent potassium tellurite, and tellurite resistance involves diverse biochemical mechanisms. Expression of the
iscS
gene from
Geobacillus stearothermophilus
V, which is naturally resistant to tellurite, confers tellurite resistance in
Escherichia coli
K-12, which is naturally sensitive to tellurite. The
G. stearothermophilus iscS
gene encodes a cysteine desulfurase. A site-directed mutation in
iscS
that prevents binding of its pyridoxal phosphate cofactor abolishes both enzyme activity and its ability to confer tellurite resistance in
E. coli
. Expression of the
G. stearothermophilus iscS
gene confers tellurite resistance in tellurite-hypersensitive
E. coli iscS
and
sodA sodB
mutants (deficient in superoxide dismutase) and complements the auxotrophic requirement of an
E. coli iscS
mutant for thiamine but not for nicotinic acid. These and other results support the hypothesis that the reduction of tellurite generates superoxide anions and that the primary targets of superoxide damage in
E. coli
are enzymes with iron-sulfur clusters.
Identification of Three Genes Encoding P
II
-Like Proteins in
Gluconacetobacter diazotrophicus
: Studies of Their Role(s) in the Control of Nitrogen Fixation
Authors: Perlova Olena , Ureta Alejandro , Nordlund Stefan , Meletzus Dietmar 
Published: September 2003

ABSTRACT

In our studies on the regulation of nitrogen metabolism in
Gluconacetobacter diazotrophicus
, an endophytic diazotroph of sugarcane, three
glnB
-like genes were identified and their role(s) in the control of nitrogen fixation was studied. Sequence analysis revealed that one P
II
protein-encoding gene,
glnB
, was adjacent to a
glnA
gene (encoding glutamine synthetase) and that two other P
II
protein-encoding genes, identified as
glnK1
and
glnK2
, were located upstream of
amtB1
and
amtB2
, respectively, genes which in other organisms encode ammonium (or methylammonium) transporters. Single and double mutants and a triple mutant with respect to the three P
II
protein-encoding genes were constructed, and the effects of the mutations on nitrogenase expression and activity in the presence of either ammonium starvation or ammonium sufficiency were studied. Based on the results presented here, it is suggested that none of the three P
II
homologs is required for
nif
gene expression, that the GlnK2 protein acts primarily as an inhibitor of
nif
gene expression, and that GlnB and GlnK1 control the expression of
nif
genes in response to ammonium availability, both directly and by relieving the inhibition by GlnK2. This model includes novel regulatory features of P
II
proteins.
Tethering of the
Bacillus subtilis
σ
E
Proprotein to the Cell Membrane Is Necessary for Its Processing but Insufficient for Its Stabilization
Authors: Ju Jingliang , Haldenwang W. G. 
Published: September 2003

ABSTRACT

σ
E
, a sporulation-specific transcription factor of
Bacillus subtilis
, is synthesized as an inactive proprotein with a 27-amino acid extension at its amino terminus. This “pro” sequence is removed by a developmentally regulated protease, but when present, it blocks σ
E
activity, tethers σ
E
to the bacterium's cytoplasmic membrane, and promotes σ
E
stability. To investigate whether pro-σ
E
processing and/or stabilization are tied to membrane sequestration, we used fluorescent protein fusions to examine the membrane binding of SigE variants. The results are consistent with membrane association as a prerequisite for pro-σ
E
processing but not as a sufficient cause for the proprotein's stability.
Percolation in Random Cantor Sets
Authors: Orzechowski Mark E. 
Published: September 2003

The d-dimensional random Cantor set is a generalization of the classical "middle-thirds" Cantor set. Starting with the unit cube [0, 1]d, at every stage of the construction we divide each cube remaining into Nd equal subcubes, and select each of these at random with probability p. The resulting limit set is a random fractal C. We present some of the main probabilistic properties of C, with an emphasis on the existence of large connected components ("percolation") and (d-1)-dimensional surfaces ("sheet-percolation"). We also look at some closely related models. Rigorous proofs are not attempted, but we give some heuristic explanations and further references. These notes formed the basis for a talk at the NATO Advanced Study Institute on Fractal Image Encoding and Analysis in Trondheim, Norway on July 8–17, 1995.
Fractals in Transition Processes
Authors: Mintz R. I. , Berg D. B. 
Published: September 2003

The present work is devoted to the design of model physical and computer systems with competitive interactions and analysis of structures, generated by their various metastable states. As it was marked at the NATO Advanced Study Institute "Fractal image encoding and analysis" (Norway, 1995), that description and quantitative analysis of fractals forming in such systems at the self-organizing, transition processes is an unsolved problem, so called "terra incognita", which is requiring future investigations.
Deletion of alanine 2201 in the FVIII C2 domain results in mild hemophilia A by impairing FVIII binding to VWF and phospholipids and destroys a major FVIII antigenic determinant involved in inhibitor development
Authors: d'Oiron Roseline , Lavergne Jean-Maurice , Lavend'homme Renaud , Benhida Abdellah , Bordet Jean-Claude , Negrier Claude , Peerlinck Kathelijne , Vermylen Jos , Saint-Remy Jean-Marie , Jacquemin Marc 
Published: September 2003

AbstractThe C2 domain of factor VIII (FVIII) mediates FVIII binding to von Willebrand factor (VWF) and phospholipids (PLs), thereby determining the stability and the activity of FVIII. A deletion of Ala2201 (Del2201) was identified in the FVIII C2 domain of 2 unrelated patients with mild hemophilia A (FVIII:C 11%-33%). This mutation prevents FVIII binding to a human monoclonal antibody recognizing the C2 domain and inhibiting FVIII binding to VWF and phospholipids. By comparison to healthy FVIII, Del2201 FVIII had a significantly reduced binding to VWF, which likely contributes to reduced FVIII levels in plasma. Del2201 FVIII interaction with phospholipids was evaluated in an FXa generation assay, using various concentrations of synthetic phospholipid vesicles mimicking an activated platelet surface. At the lowest phospholipid concentration allowing FXa generation, Del2201 FVIII activity was reduced 3-fold. This is the first report of a mutation altering FVIII binding to phospholipids and occurring in patients with hemophilia A.
Platelet ADP receptors contribute to the initiation of intravascular coagulation
Authors: Leon Catherine , Alex Meike , Klocke Antje , Morgenstern Eberhard , Moosbauer Christine , Eckly Anita , Spannagl Michael , Gachet Christian , Engelmann Bernd 
Published: September 2003

AbstractWhile the adenosine 5′-diphosphate (ADP) pathway is known to enhance thrombus formation by recruiting platelets and leukocytes to the primary layer of collagen-adhering platelets, its role for the initiation of coagulation has not been revealed. Ex vivo inhibition of the P2Y12 ADP receptor by clopidogrel administration diminished the rapid exposure of tissue factor (TF), the major initiator of coagulation, in conjugates of platelets with leukocytes established by the contact of whole blood with fibrillar collagen. Under in vitro conditions, the P2Y12 and P2Y1 ADP receptors were both found to be implicated in the exposure of TF in collagen-activated whole blood. Immunoelectron-microscopy revealed that collagen elicited the release of TF from its storage pools within the platelets. Functional activation of the intravascular TF was reduced by inhibition of the ADP receptors, partially due to the disruption of the platelet-neutrophil adhesions. Injection of collagen into the venous system of mice increased the number of thrombin-antithrombin complexes, indicative for the formation of thrombin in vivo. In P2Y1-deficient mice, the ability of collagen to enhance the generation of thrombin was impaired. In conclusion, the platelet ADP pathway supports the initiation of intravascular coagulation, which is likely to contribute to the concomitant formation of fibrin at the site of the growing thrombus.
Clinical course of patients with WASP gene mutations
Authors: Imai Kohsuke , Morio Tomohiro , Zhu Yi , Jin Yinzhu , Itoh Sukeyuki , Kajiwara Michiko , Yata Jun-ichi , Mizutani Shuki , Ochs Hans D. , Nonoyama Shigeaki 
Published: September 2003

AbstractMutations of the Wiskott-Aldrich syndrome protein (WASP) gene result either in the classic Wiskott-Aldrich syndrome (WAS) or in a less severe form, X-linked thrombocytopenia (XLT). A phenotype-genotype correlation has been reported by some but not by other investigators. In this study, we characterized WASP gene mutations in 50 Japanese patients and analyzed the clinical phenotype and course of each. All patients with missense mutations were WASP-positive. In contrast, patients with nonsense mutations, large deletions, small deletions, and small insertions were WASP-negative. Patients with splice anomalies were either WASP-positive or WASP-negative. The clinical phenotype of each patient was correlated with the presence or absence of WASP. Lack of WASP expression was associated with susceptibility to bacterial, viral, fungal, and Pneumocystis carinii infections and with severe eczema, intestinal hemorrhage, death from intracranial bleeding, and malignancies. Rates for overall survival and survival without intracranial hemorrhage or other serious complications were significantly lower in WASP-negative patients. This analysis provides evidence for a strong phenotype-genotype correlation and demonstrates that WAS protein expression is a useful tool for predicting long-term prognosis for patients with WAS/XLT. Based on data presented here, hematopoietic stem cell transplantation should be considered, especially for WASP-negative patients, while the patients are young to improve prognosis.
Marked elevation of the chemokine CCL18/PARC in Gaucher disease: a novel surrogate marker for assessing therapeutic intervention
Authors: Boot Rolf G. , Verhoek Marri , de Fost Maaike , Hollak Carla E. M. , Maas Mario , Bleijlevens Boris , van Breemen Marielle J. , van Meurs Marjan , Boven Leonie A. , Laman Jon D. , Moran Mary Teresa , Cox Timothy M. , Aerts Johannes M. F. G. 
Published: September 2003

AbstractGaucher disease is characterized by storage of glucosylceramide in lysosomes of tissue macrophages as the result of an autosomal recessively inherited deficiency in glucocerebrosidase. Progressive accumulation of these glycolipid-laden Gaucher cells causes a variety of debilitating symptoms. The disease can be effectively treated by costly intravenous infusions with recombinant glucocerebrosidase. Chitotriosidase is massively secreted by Gaucher cells and its plasma levels are used to monitor efficacy of enzyme therapy. Broad-scale application is hampered by the common genetic defect in this surrogate marker. We report that in plasma of symptomatic patients with Gaucher disease the chemokine CCL18 is on average 29-fold elevated, without overlap between patient and control values (median control plasma level is 33 ng/mL, range, 10-72 ng/mL; median Gaucher plasma level is 948 ng/mL, range, 237-2285 ng/mL). Plasma CCL18 concentrations decrease during therapy, comparably to chitotriosidase levels. Immunohistochemistry demonstrates that Gaucher cells are the prominent source of CCL18. Plasma CCL18 levels can serve as alternative surrogate marker for storage cells in patients with Gaucher disease and monitoring of plasma CCL18 levels proves to be useful in determination of therapeutic efficacy, especially in patients who are deficient in chitotriosidase activity. The potential physiologic consequences of chronically elevated CCL18 in patients with Gaucher disease are discussed.
FLT3 ligand causes autocrine signaling in acute myeloid leukemia cells
Authors: Zheng Rui , Levis Mark , Piloto Obdulio , Brown Patrick , Baldwin Brenda R. , Gorin Norbert C. , Beran Miloslav , Zhu Zhenping , Ludwig Dale , Hicklin Dan , Witte Larry , Li Yiwen , Small Donald 
Published: September 2003

AbstractThe FLT3 receptor tyrosine kinase is highly expressed in most acute leukemias and frequently mutated in acute myeloid leukemia (AML). The mutated form of the receptor is constitutively activated and known to play an important role in AML, but the activation state of the overexpressed wild-type (wt) receptor is, at present, unknown. In this study, we examined the activation state of the wild-type receptor in AML. We found that the wild-type receptor was constitutively phosphorylated/activated in 8 of 12 primary AML samples and 4 of 13 leukemia cell lines. To explain why wtFLT3 is often activated, we investigated the expression of its ligand, FL, by these same cells. Coexpression of FL with FLT3 was a universal finding in both primary AML samples and leukemic-derived cell lines. To further prove that autocrine signaling was accounting for the activation, we showed that conditioned media but not fresh media was able to activate FLT3. In addition, an antibody that blocks binding of ligand to the receptor blocks FLT3 activation. Finally, depletion of FL from conditioned media is able to block the activation of FLT3. Taken together, these findings represent strong evidence that wtFLT3 is often constitutively activated in AML and thus, like its mutated form, might contribute to the altered signaling that characterizes leukemogenesis.
Neonatal gene transfer with a retroviral vector results in tolerance to human factor IX in mice and dogs
Authors: Zhang Jun , Xu Lingfei , Haskins Mark E. , Parker Ponder Katherine 
Published: September 2003

AbstractThe effect of neonatal gene transfer on antibody formation was determined using a retroviral vector (RV) expressing human factor IX (hFIX). Normal mice from different strains injected intravenously with RV as newborns achieved therapeutic levels of hFIX without antibody production and were tolerant as adults to challenge with hFIX. Neonatal hemophilia B mice that received different amounts of RV achieved stable and dose-related expression of hFIX without anti-hFIX antibody formation. After protein challenge, antibody formation was markedly reduced for animals that expressed hFIX at levels higher than 14 ng/mL (0.3% of normal). However, antibodies developed for animals that received the lowest dose of RV and expressed hFIX at approximately 2 ng/mL before protein challenge. In dogs, neonatal injection of a high dose of RV resulted in 500 ng/mL hFIX in plasma without antibody formation. We conclude that neonatal gene transfer with RV does not induce antibody responses to hFIX in mice or dogs and that mice achieving levels greater than 3 × 10–10 M hFIX are usually tolerant to protein injection as adults. Low-dose gene therapy or frequent protein injections in the neonatal period might induce tolerance to subsequent injections of protein with a low risk for adverse effects.
Selective inactivation of CCR5 and decreased infectivity of R5 HIV-1 strains mediated by opioid-induced heterologous desensitization
Authors: Szabo Imre , Wetzel Michele A , Zhang Ning , Steele Amber D , Kaminsky David E , Chen Chongguang , Liu-Chen Lee-Yuan , Bednar Filip , Henderson Earl E , Howard O M Zack , Oppenheim Joost J , Rogers Thomas J 
Published: September 2003

AbstractThe opiates are well-established immunomodulatory factors, and recent evidence suggests that μ- and δ-opioid receptor ligands alter chemokine-driven chemotactic responses through the process of heterologous desensitization. In the present report, we sought to examine the capacity of μ- and δ-opioids to modulate the function of chemokine receptors CCR5 and CXCR4, the two major human immunodeficiency virus (HIV) coreceptors. We found that the chemotactic responses to the CCR1/5 ligand CCL5/regulated on activation, normal T expressed and secreted, but not the CXCR4 ligand stromal cell-derived factor-1α/CXCL12 were inhibited following opioid pretreatment. Studies were performed with primary monocytes and Chinese hamster ovary cells transfected with CCR5 and the μ-opioid receptor to determine whether cross-desensitization of CCR5 was a result of receptor internalization. Using radiolabeled-binding analysis, flow cytometry, and confocal microscopy, we found that the heterologous desensitization of CCR5 was not associated with a significant degree of receptor internalization. Despite this, we found that the cross-desensitization of CCR5 by opioids was associated with a decrease in susceptibility to R5 but not X4 strains of HIV-1. Our findings are consistent with the notion that impairment of the normal signaling activity of CCR5 inhibits HIV-1 coreceptor function. These results have significant implications for our understanding of the effect of opioids on the regulation of leukocyte trafficking in inflammatory disease states and the process of coreceptor-dependent HIV-1 infection. The interference with HIV-1 uptake by heterologous desensitization of CCR5 suggests that HIV-1 interaction with this receptor is not passive but involves a signal transduction process.
A Self‐Powered Reconfigurable Intelligent Metasurface
Authors: Mu Yajie , Chang Mingyang , Wang Xin , Han Jiaqi , Xia Dexiao , Ma Xiangjin , Liu Haixia , Li Long 
Published: January 2024

AbstractIn recent years, reconfigurable intelligent metasurface (RIS) has gained much attention due to its flexibility in modulating the phase, amplitude, and polarization of electromagnetic waves. It is widely used for wireless power and information transmission. However, RIS requires an external wired power supply or batteries to activate their modulation capabilities, as they do not generate the required energy themselves. This paper presents a self‐powered RIS that does not require an external wired power supply or batteries. The modulation capability is activated by harvesting radio frequency (RF) energy. The self‐powered RIS consists of an energy‐metatom, which is loaded with a PIN diode for flexible phase modulation. The inclusion of an absorber/energy port on the energy‐metatom allows for independent RF energy harvesting. The RIS consisting of energy‐metatoms can cut out all wired power supplies and batteries so that it can dynamically regulate electromagnetic waves by self‐powered means. As a proof‐of‐concept, a prototype composed of 10 × 10 energy‐metatoms is fabricated. The measured results are in good agreement with the simulated. This self‐powered RIS can be used as an “infinite‐lifetime” power supply for dynamic electromagnetic modulation in the RIS.
Ferrocene Appended Porphyrin‐Based Bipolar Electrode Material for High‐Performance Energy Storage
Authors: Chowdhury Shagor , Jana Saibal , Panguluri Sai. P. K. , Wenzel Wolfgang , Klayatskaya Svetlana , Ruben Mario 
Published: January 2024

AbstractThe versatile properties of bipolar organic electrode materials have attracted considerable attention in the field of electrochemical energy storage (EES). However, their practical application is hindered by their inherent limitations including low intrinsic electrical conductivity, low specific capacity, and high solubility. Herein, a bipolar organic molecule combining both porphyrin and ferrocene moieties (CuDEFcP) [5,15‐bis(ethynyl)‐10,20‐di ferrocenyl porphinato]copper(II)) has been developed. It is proposed as a new organic electrode material with multifunctional application for rechargeable organic lithium‐based batteries (ROLBs) and dual‐ion organic symmetric batteries (SDIBs). Superior performance was delivered as cathode material in lithium based dual‐ion batteries (LDIBs), with a high initial discharge capacity of 300 mAh. g−1 at 0.2 A. g−1 and a reversible capacity of 58 mAh. g−1 after 5000 cycles at 1 A. g−1. However, employing it as an anode material in lithium‐ion batteries (LIBs), a reversible capacity of 295 mAh. g−1 at 0.2 A. g−1 was delivered. In SDIBs, in which CuDEFcP is used as both anode and cathode, an average discharge voltage of 2.4 V and an energy density of 261 Wh.kg−1 were achieved.
The detection of PD‐L1 expression on liquid‐based cytology in pleural effusion of lung adenocarcinoma and its prognostic evaluation: Between paired liquid‐based cytology and cell block samples
Authors: Ma Haiyue , Jia Jia , Sun Zihan , Xiao Xiaoyue , Liang Shuo , Zhao Linlin , Zhang Zhihui 
Published: January 2024

AbstractBackgroundProgrammed death‐ligand 1 (PD‐L1) expression levels measured by immunohistochemistry have been proven to predict the outcome of immunotherapy in lung adenocarcinoma (LUAD). However, data on PD‐L1 expression on liquid‐based cytology (LBC) in malignant pleural effusion (MPE) is scarce.MethodsThis study cohort included 60 cases with MPE suffering from LUAD. PD‐L1 SP263 assay was used for immunocytochemistry (ICC) on LBC and matched cell block (CB) to validate ICC protocols on LBC slides. Clinical outcomes were analyzed based on immunotherapy and PD‐L1 tumor proportion scores (TPS) on LBC slides and CBs.ResultsPD‐L1 expression with TPS ≥1% was lower in LBCs than in CBs (33 of 60 [55.0%] vs. 35 of 60 [58.3%]; p = .687). Even with the TPS ≥50% threshold, PD‐L1 expression was lower in LBCs (10 of 60 [16.7%] vs. 15 of 60 [25%]; p = .125). Epidermal growth factor receptor (EGFR) exon 20 mutation, tumor cell proportion, and pleural fluid neutrophil‐to‐lymphocyte ratio were related to PD‐L1 expression on CBs (p = .013, p = 0.022, and p = .011), respectively. Patients with subsequent immune checkpoint inhibitor therapy remained a better prognostic in subgroups of PD‐L1 positive expression on LBC slides (TPS ≥1%, p = .041).ConclusionsLBC specimens had comparable performance to CBs in PD‐L1 assessment and predicting treatment response to PD‐L1‐defined therapy.