bluuebunny/crossref_metadata_2025_split huggingface dataset:
Carbon isotope ratios and nitrogen abundances in relation to
cathodoluminescence characteristics for some diamonds from the Kaapvaal Province,
S. Africa
Authors: Harte B. , Fitzsimons I. C. W. , Harris J. W. , Otter M. L. 
Published: July 2002

Abstract
Secondary ion mass spectrometry (SIMS) techniques have been used to study the
variation of C isotope ratio and N abundance within selected diamonds in relation
to their crystal growth zones. The growth zones are seen in cathodoluminescence
(CL), and include both octahedral and cuboid zones within typical diamonds of
external octahedral morphology. Compositions were determined by use of a primary
133Cs+ ion beam and measurement of
12C−, 13C, and
12C14N−
secondary ions at high mass resolution on a Cameca ims-4f ion microprobe at
Edinburgh University.
In each of the diamonds, different growth zones have marked differences in N
abundance, which are as great as 0–1400 ppm within one diamond. Changes of several
hundred ppm N are common across both octahedral and cuboid growth zones, and
appear sharp and abrupt at the boundaries of the growth zones. In general for the
common blue CL, luminescence increases with N abundance. The changes in N
abundance across fine scale (∼100 µm) growth zones show that the total N contents
determined by IR spectroscopy may show great variations of abundance. In contrast,
within detection limits, δ13C appears constant across many
growth zone boundaries. Thus the factors controlling uptake of N from the
fluid/melt reservoir in which natural diamonds grow often do not influence
δ13C. No evidence of progressive variation or
fractionation of C isotopes during growth was found.
Some original variation in C isotope composition may have been eliminated by
diffusion of C atoms subsequent to growth, because of the storage of natural
diamonds over millions of years in the Earth's mantle at temperatures of
950–1250°C. Such atomic mobility does not homogenize N distribution because of the
proven tendency of N to form aggregates of atoms. A survey of experimental
estimates of single atom (C) diffusion parameters, suggests that diffusion
distances of ∼100 µm are likely at high temperatures (∼1100°C) over long time
periods (∼1.0 Ga). Therefore, with refinement of the diffusion parameters and
measurements, the extent of C isotope homogenization in natural diamonds, as well
as N aggregation state, might provide quantitative evidence of their
time-temperature history under mantle conditions.
Phosphoinositide 3-kinase modulation of β3-integrin represents an endogenous “braking” mechanism during neutrophil transmatrix migration
Authors: Bruyninckx Walter J. , Comerford Katrina M. , Lawrence Donald W. , Colgan Sean P. 
Published: July 2002

AbstractDuring episodes of inflammation, neutrophils (polymorphonuclear leukocytes [PMNs]) encounter subendothelial matrix substrates that may require additional signaling pathways as directives for movement through the extracellular space. Using an in vitro endothelial and epithelial model, inhibitors of phosphoinositide 3-kinase (PI3K) were observed to promote chemoattractant-stimulated migration by as much as 8 ± 0.3-fold. Subsequent studies indicated that PMNs respond in a similar manner to RGD-containing matrix substrates and that PMN-matrix interactions are potently inhibited by antibodies directed against β3- but not β1-integrin antibodies, and that PI3K inhibitors block β3-integrin dependence. Biochemical analysis of intracellular β3-integrin uncoupling by PI3K inhibitors revealed diminished β3-integrin tyrosine phosphorylation and decreased association with p72syk. Similarly, the p72sykinhibitor piceatannol promoted PMN transmatrix migration, whereas HIV-tat peptide-facilitated loading of peptides corresponding to the β3-integrin cytoplasmic tail identified the functional tyrosine residues for this activity. These data indicate that PI3K-regulated β3-integrin represents a natural “braking” mechanism for PMNs during transit through the extracellular matrix.
Modifications in the CD36 binding domain of the Plasmodium falciparum variant antigen are responsible for the inability of chondroitin sulfate A adherent parasites to bind CD36
Authors: Gamain Benoit , Smith Joseph D. , Miller Louis H. , Baruch Dror I. 
Published: July 2002

Abstract
Adhesion of mature Plasmodium falciparum parasitized erythrocytes to microvascular endothelial cells or to placenta contributes directly to the virulence and severe pathology of P falciparum malaria. Whereas CD36 is the major endothelial receptor for microvasculature sequestration, infected erythrocytes adhering in the placenta bind chondroitin sulfate A (CSA) but not CD36. Binding to both receptors is mediated by different members of the large and diverse protein family P falciparum erythrocyte membrane protein-1 (PfEMP-1) and involves different regions of the molecule. The PfEMP-1–binding domain for CD36 resides in the cysteine-rich interdomain region 1 (CIDR-1). To explore why CSA-binding parasites do not bind CD36, CIDR-1 domains from CD36- or CSA-binding parasites were expressed in mammalian cells and tested for adhesion. Although CIDR-1 domains from CD36-adherent strains strongly bound CD36, those from CSA-adherent parasites did not. The CIDR-1 domain has also been reported to bind CSA. However, none of the CIDR-1 domains tested bound CSA. Chimeric proteins between CIDR-1 domains that bind or do not bind CD36 and mutagenesis experiments revealed that modifications in the minimal CD36-binding region (M2 region) are responsible for the inability of CSA-selected parasites to bind CD36. One of these modifications, mapped to a 3–amino acid substitution in the M2 region, ablated binding in one variant and largely reduced binding of another. These findings provide a molecular explanation for the inability of placental sequestered parasites to bind CD36 and provide additional insight into critical residues for the CIDR-1/CD36 interaction.
Ordered recombination of immunoglobulin light chain genes occurs at the IGK locus but seems less strict at theIGL locus
Authors: van der Burg Mirjam , Tümkaya Talip , Boerma Marjan , de Bruin-Versteeg Sandra , Langerak Anton W. , van Dongen Jacques J. M. 
Published: July 2002

AbstractRegulation of allelic and isotypic exclusion of human immunoglobulin (Ig) light-chain genes was studied in 113 chronic B-cell leukemias as a “single-cell” model that allowed complete analysis of each light chain allele. Our data show that monospecific Ig light chain expression is in about 90% of cases determined by ordered recombination: Igκ gene (IGK) rearrangements, followed byIGK deletions and Igλ gene (IGL) rearrangements, resulting in the presence of only one functional Ig light chain rearrangement. In about 10% (10 cases), 2 functional Ig light chain rearrangements (IGK/IGL or IGL/IGL, but not IGK/IGK) were identified. This might be explained by the fact that regulation of the ordered recombination process is not fully strict, particularly when the IGL locus is involved. Unfavorable somatic mutations followed by receptor editing might have contributed to this finding. Eight of these 10 cases indeed contained somatic mutations. In cases with 2 functional Ig light chain rearrangements, both alleles were transcribed, but monospecific Ig expression was still maintained. This suggests that in these cases allelelic exclusion is not regulated at the messenger RNA level but either at the level of translation or protein stability or via preferential pairing of Ig light and Ig heavy chains. Nevertheless, ordered rearrangement processes are the main determinant for monospecific Ig light chain expression.
Coexpression of band 3 mutants and Rh polypeptides: differential effects of band 3 on the expression of the Rh complex containing D polypeptide and the Rh complex containing CcEe polypeptide
Authors: Beckmann Roland , Smythe Jonathan S. , Anstee David J. , Tanner Michael J. A. 
Published: July 2002

AbstractK562 cells were stably transfected with cDNAs encoding the band 3 found in Southeast Asian ovalocytosis (B3SAO, deletion of residues 400-408), band 3 with a transport-inactivating E681Q point mutation (B3EQ), or normal band 3 (B3). Flow cytometric analysis and quantitative immunoblotting revealed that B3SAO expressed alone was translocated to the plasma membrane, at levels similar to B3 or B3EQ. Nine monoclonal antibodies that reacted with extracellular loops of B3 also reacted with B3SAO, although the affinity of most antibodies for the mutant protein was reduced. Both known Wrb epitopes were expressed on K562/B3SAO cells, demonstrating that B3SAO interacts with glycophorin A. The growth rates of K562 clones expressing equivalent amounts of B3 and B3EQ were the same, suggesting that the potentially toxic transport function of band 3 may be regulated in K562 cells. The band 3–mediated enhancement of Rh antigen reactivity and the depression of Rh epitopes on SAO erythrocytes were investigated by comparing the coexpression of B3, B3SAO, or B3EQ in K562 clones expressing exogenous RhcE or RhD polypeptides. The results are consistent with an interaction between band 3 and the Rh polypeptide–Rh glycoprotein (RhAG) complex, which may enhance translocation of the complex or affect its conformation in the plasma membrane. The data suggest that the interaction between band 3 and the RhD–RhAG complex is weaker than it is between band 3 and the RhCcEe–RhAG complex.
Proliferation of primitive myeloid progenitors can be reversibly induced by HOXA10
Authors: Björnsson Jon Mar , Andersson Elisabet , Lundström Patrik , Larsson Nina , Xu Xiufeng , Repetowska Ewa , Humphries R. Keith , Karlsson Stefan 
Published: July 2002

AbstractRecent studies show that several Hox transcription factors are important for regulation of proliferation and differentiation in hematopoiesis. Among these is H0XA10, which is selectively expressed at high levels in the most primitive subpopulation of human CD34+ bone marrow cells. When overexpressed, H0XA10 increases the proliferation of early progenitor cells and can lead to the development of myeloid leukemia. To study the effects of H0XA10 on primitive hematopoietic progenitors in more detail, transgenic mice were generated with regulatable H0XA10 expression. The transgenic mouse model, referred to as tetO-HOXA10, contains theH0XA10 gene controlled by a tetracycline-responsive element and a minimal promoter. Thus, the expression of H0XA10 is inducible and reversible depending on the absence or presence of tetracycline or its analog, doxycycline. A retroviral vector containing the tetracycline transactivator gene (tTA) was used to induce expression of the H0XA10 gene in bone marrow cells from the transgenic mice. Reverse transcription–polymerase chain reaction analysis confirmed regulatable H0XA10 expression in several transgenic lines. H0XA10 induction led to the formation of hematopoietic colonies containing blastlike cells and megakaryocytes. Moreover, the induction of H0XA10 resulted in significant proliferative advantage of primitive hematopoietic progenitors (spleen colony-forming units [CFU-S12]), which was reversible on withdrawal of induction. Activation of H0XA10 expression intet0-H0XA10 mice will therefore govern proliferation of primitive myeloid progenitors in a regulated fashion. This novel animal model can be used to identify the target genes of HOXA10 and better clarify the specific role of HOXA10 in normal and malignant hematopoiesis.
p53 dysfunction in B-cell chronic lymphocytic leukemia: inactivation of ATM as an alternative toTP53 mutation
Authors: Pettitt Andrew R. , Sherrington Paul D. , Stewart Grant , Cawley John C. , Taylor A. Malcolm R. , Stankovic Tatjana 
Published: July 2002

Abstract
The well-established association between TP53 mutations and adverse clinical outcome in a range of human cancers reflects the importance of p53 protein in regulating tumor-cell growth and survival. Although it is theoretically possible for p53 dysfunction to arise through mechanisms that do not involve TP53 mutation, such a phenomenon has not previously been demonstrated in a sporadic tumor. Here, we show that p53 dysfunction in B-cell chronic lymphocytic leukemia (CLL) can occur in the absence of TP53 mutation and that such dysfunction is associated with mutation of the gene encoding ATM, a kinase implicated in p53 activation. Forty-three patients with CLL were examined for p53 dysfunction, as detected by impaired up-regulation of p53 and of the p53-dependent protein p21CIP1/WAF1 after exposure to ionizing radiation (IR). Thirty (70%) patients had normal p53 responses and underwent progressive IR-induced apoptosis. In 13 (30%) patients, p21 up-regulation was markedly impaired, indicating p53 dysfunction. Six (14%) of these patients with p53 dysfunction had increased baseline levels of p53, were found to have TP53 mutations, and were completely resistant to IR-induced apoptosis. In the other 7 (16%) patients with p53 dysfunction, IR-induced p53 up-regulation and apoptosis were markedly impaired, but baseline levels of p53 were not increased, and no TP53 mutations were detected. Each of these patients was found to have at least one ATM mutation, and a variable reduction in ATM protein was detected in all 4 patients examined. This is the first study to provide a direct demonstration that p53 dysfunction can arise in a sporadic tumor by a mechanism that does not involve TP53 mutation.
Dynamic molecular modeling of pathogenic mutations in the spectrin self-association domain
Authors: Zhang Zhushan , Weed Scott A. , Gallagher Patrick G. , Morrow Jon S. 
Published: July 2002

AbstractDisruption of spectrin self-association underlies many inherited hemolytic disorders. Using dynamic modeling and energy minimization, the 3-dimensional structure of the self-association domain has been estimated in human erythrocyte spectrin and the structural consequences of 17 elliptogenic mutations determined. The predicted structure of the normal self-association domain was remarkably similar to the crystal structure of the Drosophila α-spectrin 14th repeat unit, despite replacement in the human sequence of over 70% of the amino acids relative to fly spectrin, including 2 prolines in the human sequence that appear in helical regions of the fly structure. The predicted structure placed all hydrophilic residues at the surface and identified 4 salt bridges, 9 hydrophobic interactions, and 4 H-bonds that stabilize the native self-association unit. Remarkably, every pathologic point mutation, including seemingly conservative substitutions such as G for A, A for V, or K for R (single-letter amino acid codes), led to conformational rearrangements in the predicted structure. The degree of structural disruption, as measured by root-mean-square deviation of the predicted backbone structure from theDrosophila structure, correlated strongly with the severity of clinical disease associated with each mutation. This approach thus enables an accurate prediction, from the primary sequence, of the clinical consequences of specific point mutations in spectrin. The 3-dimensional structure of the self-association domain derived here is likely to be accurate. It provides a powerful heuristic model for understanding how point mutations disrupt cytoskeletal function in a variety of hemolytic disorders.
HIV gp120 receptors on human dendritic cells
Authors: Turville Stuart G. , Arthos Jim , Mac Donald Kelli , Lynch Garry , Naif Hassan , Clark Georgina , Hart Derek , Cunningham Anthony L. 
Published: July 2002

AbstractDendritic cells (DCs) are important targets for human immunodeficiency virus (HIV) because of their roles during transmission and also maintenance of immune competence. Furthermore, DCs are a key cell in the development of HIV vaccines. In both these settings the mechanism of binding of the HIV envelope protein gp120 to DCs is of importance. Recently a single C-type lectin receptor (CLR), DC-SIGN, has been reported to be the predominant receptor on monocyte-derived DCs (MDDCs) rather than CD4. In this study a novel biotinylated gp120 assay was used to determine whether CLR or CD4 were predominant receptors on MDDCs and ex vivo blood DCs. CLR bound more than 80% of gp120 on MDDCs, with residual binding attributable to CD4, reconfirming that CLRs were the major receptors for gp120 on MDDCs. However, in contrast to recent reports, gp120 binding to at least 3 CLRs was observed: DC-SIGN, mannose receptor, and unidentified trypsin resistant CLR(s). In marked contrast, freshly isolated and cultured CD11c+ve and CD11c−ve blood DCs only bound gp120 via CD4. In view of these marked differences between MDDCs and blood DCs, HIV capture by DCs and transfer mechanisms to T cells as well as potential antigenic processing pathways will need to be determined for each DC phenotype.
Erythropoietin expression in primary rat Sertoli and peritubular myoid cells
Authors: Magnanti Massimo , Gandini Orietta , Giuliani Laura , Gazzaniga Paola , Marti Hugo H. , Gradilone Angela , Frati Luigi , Aglianò Anna Maria , Gassmann Max 
Published: July 2002

AbstractKidney and liver are the major organs of erythropoietin (Epo) synthesis. However, Epo messenger RNA (mRNA) has been detected in several organs, such as brain, lung, and testis. Furthermore, functional Epo receptors have been demonstrated on different cell types, including rat Leydig cells. The aim of the study was to identify testicular cells expressing Epo mRNA and to quantitate its levels by competitive reverse transcriptase–polymerase chain reaction (RT-PCR). Besides whole testis, Epo transcripts were found in Sertoli and peritubular myoid cells, while no signal was detected in Leydig cells. Exposure of Sertoli cells to CoCl2 led to an increase of Epo mRNA level. Semiquantitative competitive RT-PCR presented an increase in the level of Epo mRNA in Sertoli cells stimulated by follicle-stimulating hormone, while exposure of peritubular myoid cells cultures to testosterone reduced Epo mRNA expression. Due to the blood-testis barrier, basal expression of Epo suggests a not yet defined function of this hormone in testis.
Race and Ethnicity and Diagnostic Testing for Common Conditions in the Acute Care Setting
Authors: Ellenbogen Michael I. , Weygandt P. Logan , Newman-Toker David E. , Anderson Andrew , Rim Nayoung , Brotman Daniel J. 
Published: August 2024

ImportanceOveruse of diagnostic testing is pervasive, but the extent to which it varies by race and ethnicity in the acute care setting is poorly understood.ObjectiveTo use a previously validated diagnostic intensity index to evaluate differences in diagnostic testing rates by race and ethnicity in the acute care setting, which may serve as a surrogate for diagnostic test overuse.Design, Setting, and ParticipantsThis was a cross-sectional study of emergency department (ED) discharges, hospital observation stays, and hospital admissions using administrative claims among EDs and acute care hospitals in Kentucky, Maryland, North Carolina, and New Jersey, from 2016 through 2018. The diagnostic intensity index pairs nonspecific principal discharge diagnoses (nausea and vomiting, abdominal pain, chest pain, and syncope) with related diagnostic tests to estimate rates of nondiagnostic testing. Adults with an acute care encounter with a principal discharge diagnosis of interest were included. Data were analyzed from January to February 2024.ExposureRace and ethnicity (Asian, Black, Hispanic, White, other [including American Indian, multiracial, and multiethnic], and missing).Main Outcomes and MeasuresReceipt of a diagnostic test. Generalized linear models with a hospital-specific indicator variable were estimated to calculate the adjusted odds ratio of receiving a test related to the principal discharge diagnosis by race and ethnicity, controlling for primary payer and zip code income quartile.ResultsOf 3 683 055 encounters (1 055 575 encounters [28.7%] for Black, 300 333 encounters [8.2%] for Hispanic, and 2 140 335 encounters [58.1%] for White patients; mean [SD] age of patients with encounters, 47.3 [18.8] years; 2 233 024 encounters among females [60.6%]), most (2 969 974 encounters [80.6%]) were ED discharges. Black compared with White patients discharged from the ED with a diagnosis of interest had an adjusted odds ratio of 0.74 (95% CI, 0.72-0.75) of having related diagnostic testing. No other racial or ethnic disparities of a similar magnitude were observed in any acute care settings.Conclusions and RelevanceIn this study, White patients discharged from the ED with a nonspecific diagnosis of interest were significantly more likely than Black patients to receive related diagnostic testing. The extent to which this represents diagnostic test overuse in White patients vs undertesting and missed diagnoses in Black patients deserves further study.
Commissioning and validation of a single photon beam model in RayStation for multiple matched Elekta Linacs
Authors: Su Lin , Huang Ellen , Miles Devin A. , Farjam Reza , Marsh Ian R. , Li Qiongge , Moore Joseph A. , McNutt Todd R. , Ding Kai , Wang Ken Kang‐Hsin , Robinson Adam , Kuri Gregory , Seabrease Richard , Adam David P. , Oglesby Ryan , Shen Bin , Wu Binbin , Lee Junghoon , Jia Xun , Han‐Oh Sarah 
Published: August 2024

AbstractPurposeA single treatment planning system (TPS) model for matched linacs provides flexible clinical workflows from patient treatment to intensity‐modulated radiation therapy (IMRT) quality assurance (QA) measurement. Since general guidelines for building a single TPS model and its validation for matched linacs are not well established, we present our RayStation photon TPS modeling strategy for matched Elekta VersaHD linacs.MethodThe four linacs installed from 2013 to 2020 were matched in terms of Percent Depth Dose (PDD), profile, output factor and wedge factors for 6‐MV, 10‐MV, 15‐MV, and 6‐MV‐FFF, and maintained following TG‐142 recommendations until RayStation commissioning. The RayStation single model was built to represent all four linacs within the tolerance limits recommended by MPPG‐5.a. The comprehensive validation tests were performed for one linac following MPPG‐5.a and TG‐119 guidelines, and spot checks for the other three. Our TPS modeling/validation method was evaluated by re‐analyzing the previous 103 patient‐specific IMRT/volumetric modulated arc therapy (VMAT) QA measurements with the calculated planar doses by the single model in comparison with the analysis results using four individual Pinnacle TPS models.ResultsFor all energies, our single model PDDs were within 1% agreement of the four‐linac commissioning measurements. The MPPG‐5.a validation tests from 5.1 through 7.5 and all TG‐119 measurements passed within the recommended tolerance limits. The IMRT QA results (mean ± standard deviation) for RayStation single model versus Pinnacle individual models were 98.9% ± 1.3% and 98.0% ± 1.4% for 6‐MV, 99.9% ± 0.1% and 99.1% ± 1.9% for 10‐MV, and 98.2% ± 1.3% and 97.9% ± 1.8% for 6‐MV‐FFF, respectively.ConclusionWe successfully built and validated a single photon beam model in RayStation for four Elekta Linacs. The proposed new validation methods were proven to be both efficient and effective.