bluuebunny/crossref_metadata_2025_split huggingface dataset:
Sixteenth century tubular glass beads: non‐destructive chemical characterization using synchrotron radiation XRF
Authors: Veiga J. P. , Figueiredo M. O. 
Published: September 2002

AbstractThe results of a photon microprobe (synchrotron radiation XRF) study of tubular blue glass beads of the Nueva Cadiz type uncovered by recent excavations in the center of Lisbon are reported as a contribution to the non‐destructive chemical characterization of these cultural artifacts, aiming ultimately at ascertaining their provenance and manufacturing location. Either twisted or plain, with round or square cross‐sections, the beads are clearly formed by two blue vitreous layers separated by an opaque white stratum, but a fourth inner transparent bluish layer is visible in the cross‐section of most beads studied. These strata differ essentially in the content of colorant ions (Cu, and occasionally Co traces), fuser metals (essentially Pb) and white layer opacifier (Sn oxide). Other minor and trace elements were determined: K, Ca, Ti, Mn, Fe, Ni, Zn, Ga, As, Br, Rb, Sr, Y, Zr, Nb, Ba, Sb, Hg and Bi. The bromine increase in the outer layers was attributed to burial. Some minor elements are tentatively related to the fuser carrier compound and other chemical components are discussed in terms of raw materials and glass typology. Copyright © 2002 John Wiley & Sons, Ltd.
Post‐translational modifications of the AFET3 gene product—a component of the iron transport system in budding cells and mycelia of the yeast Arxula adeninivorans
Authors: Wartmann Thomas , Stephan Udo W. , Bube Ines , Böer Erik , Melzer Michael , Manteuffel Renate , Stoltenburg Regina , Guengerich Laura , Gellissen Gerd , Kunze Gotthard 
Published: September 2002

AbstractThe yeast Arxula adeninivorans is characterized by a temperature‐dependent dimorphism. A. adeninivorans grows as budding cells at temperatures up to 42°C, but forms mycelia at higher temperatures. A strong correlation exists between morphological status and iron uptake, achieved by two transport systems that differ in iron affinity. In the presence of high Fe(II) concentrations (>2 µm), budding cells accumulate iron concentrations up to seven‐fold higher than those observed in mycelia, while at low Fe(II) concentrations (<2 µm), both cell types accumulate similar amounts of iron. The copper‐dependent Fe(II) oxidase Afet3p, composed of 615 amino acids, is a component of the high‐affinity iron transport system. This protein shares a high degree of homology with other yeast iron transport proteins, namely Fet3p of Saccharomyces cerevisiae, Cafet3p of Candida albicans and Pfet3p of Pichia pastoris. Expression of the AFET3 gene is found to be strongly dependent on iron concentration but independent of the morphological stage; however, cell morphology was found to influence post‐translational modifications of the gene product. O‐glycosylation was observed in budding cells only, whereas N‐glycosylation occurred in both cell types. The N‐glycosylated 103 kDa glycoprotein matures into the 108.5 kDa form, further characterized by serine phosphorylation. Both N‐glycosylation and phosphorylation occur at low iron concentrations (≤5 µm). The mature Afet3p of 108.5 kDa is uniformly distributed within the plasma membrane in cells of both morphological stages. Copyright © 2002 John Wiley & Sons, Ltd.
Dehydroepiandrosterone (DHEA) metabolism in Saccharomyces cerevisiae expressing mammalian steroid hydroxylase CYP7B: Ayr1p and Fox2p display 17β‐hydroxysteroid dehydrogenase activity
Authors: Vico Pedro , Cauet Gilles , Rose Ken , Lathe Richard , Degryse Eric 
Published: September 2002

AbstractWe have engineered recombinant yeast to perform stereospecific hydroxylation of dehydroepiandrosterone (DHEA). This mammalian pro‐hormone promotes brain and immune function; hydroxylation at the 7α position by P450 CYP7B is the major pathway of metabolic activation. We have sought to activate DHEA via yeast expression of rat CYP7B enzyme. Saccharomyces cerevisiae was found to metabolize DHEA by 3β‐acetylation; this was abolished by mutation at atf2. DHEA was also toxic, blocking tryptophan (trp) uptake: prototrophic strains were DHEA‐resistant. In TRP+ atf2 strains DHEA was then converted to androstene‐3β,17β‐diol (A/enediol) by an endogenous 17β‐hydroxysteroid dehydrogenase (17βHSD). Seven yeast polypeptides similar to human 17βHSDs were identified: when expressed in yeast, only AYR1 (1‐acyl dihydroxyacetone phosphate reductase) increased A/enediol accumulation, while the hydroxyacyl‐CoA dehydrogenase Fox2p, highly homologous to human 17βHSD4, oxidized A/enediol to DHEA. The presence of endogenous yeast enzymes metabolizing steroids may relate to fungal pathogenesis. Disruption of AYR1 eliminated reductive 17βHSD activity, and expression of CYP7B on the combination background (atf2, ayr1, TRP+) permitted efficient (>98%) bioconversion of DHEA to 7α‐hydroxyDHEA, a product of potential medical utility. Copyright © 2002 John Wiley & Sons, Ltd.
Characterization of a chaperone ClpB homologue ofParacoccidioides brasiliensis
Authors: Jesuino Rosália S. A. , Azevedo Maristela O. , Felipe M. Sueli S. , Pereira Maristela , de Almeida Soares Célia M. 
Published: September 2002

AbstractWe report the cloning and sequence analysis of a genomic clone encoding aParacoccidioides brasiliensisClpB chaperone homologue (PbClpB). Theclpbgene was identified in a λ Dash II library. Sequencing ofPbclpbrevealed a long open reading frame capable of encoding a 792 amino acid, 87.9 kDa protein, pI of 5.34. The predicted polypeptide contains several consensus motifs of the ClpB proteins. Canonical sequences such as two putative nucleotide‐binding sites, chaperonins ClpA/B signatures and highly conserved casein kinase phosphorylation domains are present. ClpB is 69% to 49% identical to members of the ClpB family from several organisms from prokaryotes to eukaryotes. The transcript ofPbclpB was detected as a mRNA species of 3.0 kb, preferentially expressed in the yeast parasitic phase of the fungus. A 89 kDa protein was also detected in yeast cells ofP. brasiliensis. The sequence of theclpbgene and the deduced ClpB protein have been submitted to GenBank under Accession No. AF449501. Copyright © 2002 John Wiley & Sons, Ltd.
Genomic differences between Candida glabrata and Saccharomyces cerevisiae around the MRPL28 and GCN3 loci
Authors: Walsh David W. , Wolfe Kenneth H. , Butler Geraldine 
Published: September 2002

AbstractWe report the sequences of two genomic regions from the pathogenic yeast Candida glabrata and their comparison to Saccharomyces cerevisiae. A 3 kb region from C. glabrata was sequenced that contains homologues of the S. cerevisiae genes TFB3, MRPL28 and STP1. The equivalent region in S. cerevisiae includes a fourth gene, MFA1, coding for mating factor a. The absence of MFA1 is consistent with C. glabrata's asexual life cycle, although we cannot exclude the possibility that a‐factor gene(s) are located somewhere else in its genome. We also report the sequence of a 16 kb region from C. glabrata that contains a five‐gene cluster similar to S. cerevisiae chromosome XI (including GCN3) followed by a four‐gene cluster similar to chromosome XV (including HIS3). A small‐scale rearrangement of gene order has occurred in the chromosome XI‐like section. The sequences have been deposited in the GenBank database with Accession Nos AY083606 and AY083607. Copyright © 2002 John Wiley & Sons, Ltd.
PCR‐based identification of pathogenic Candida species using primer mixes specific to Candida DNA topoisomerase II genes
Authors: Kanbe Toshio , Horii Toshinobu , Arishima Takuo , Ozeki Munetaka , Kikuchi Akihiko 
Published: September 2002

AbstractFor rapid identification of Candida to the species level, degenerated primers and specific primers based on the genomic sequences of DNA topoisomerase II of C. albicans, C. dubliniensis, C. tropicalis (genotypes I and II), C. parapsilosis (genotypes I and II), C. krusei, C. kefyr, C. guilliermondii, C. glabrata, C. lusitaniae and Y. lipolytica were designed and their specificities tested in PCR‐based identifications. Each of the specific primers selectively and exclusively amplified its own DNA fragment, not only from the corresponding genomic DNA of the Candida sp. but also from DNA mixtures containing other DNAs from several fungal species. For a simpler PCR‐based identification, the specific primers were divided into three groups (PsI, PsII and PsIII), each of which contained four specific primer pairs. PCR with the primer mixes yielded four different sizes of PCR product, corresponding to each Candida sp. in the sample DNA. To obtain higher sensitivity of PCR amplification, sample DNAs were preamplified by the degenerated primer pair (CDF28/CDR148), followed by the main amplification using the primer mixes. By including this nested PCR step, 40 fg yeast genomic DNA was detected in the sample. Furthermore, we applied this nested PCR to a clinical diagnosis, using splenic tissues from experimentally infected mice and several clinical materials from patients. In all cases, the nested PCR amplifications detected proper DNA fragments of Candida spp., which were also identified by the standard identification tests. These results suggest that nested PCR, using primer mixes of the Candida DNA topoisomerase II genes, is simple and feasible for the rapid detection/identification of Candida to species level in clinical materials. Copyright © 2002 John Wiley & Sons, Ltd.
Outbreak of Mycobacterium marinum infection among captive snakes and bullfrogs
Authors: Maslow Joel N. , Wallace Roberta , Michaels Margaret , Foskett Holly , Maslow Elizabeth A. , Kiehlbauch Julia A. 
Published: September 2002

AbstractSince 1985 mycobacterial infection has been observed occasionally among snakes and bullfrogs housed in the Wisconsin exhibit at the Milwaukee Zoo. Prospective screening of animals was initiated in September 1990, after two cases occurred in March and June 1990. Overall, of 47 animals that were housed in the exhibit from 1981 through its closure in 1995, 15 (31.9%) were diagnosed with mycobacterial infection. That includes 10 cases (of 24 animals; 40% prevalence) that occurred during the final 5 years, when all animals were actively being screened for infection. Infection was documented by culture for seven animals, histology for four animals, and both histology and culture for four animals. Species determination of nine of the 10 isolates revealed Mycobacterium marinum. Genetic fingerprinting of the eight available isolates using pulsed field gel electrophoresis (PFGE) showed that six animals (five snakes and one bullfrog) were infected with the same strain of M. marinum (strain A) and two snakes were infected with a second strain (strain B). Deaths of animals infected with strain A spanned 1992–1995, and for strain B 1990–1992. It is postulated that possible routes of transmission were inhalation of infected aerosols or ingestion of contaminated food, water, or fomites. These data suggest that in closed systems the presence of mycobacterial infection in one animal significantly increases the risk of infection for all animals. Moreover, individual pathogenic strains may persist for prolonged periods of time. Zoo Biol 21:233–241, 2002. © 2002 Wiley‐Liss, Inc.
Comparison of different drying and storage methods on quantifiable concentrations of fecal steroids in the cheetah
Authors: Terio Karen A. , Brown Janine L. , Moreland Rachel , Munson Linda 
Published: September 2002

AbstractFecal steroid analysis is a powerful tool that can provide important information on the health, physiology, and reproductive status of nondomestic species. However, studying free‐ranging animals requires that feces be stored and transported from the collection site to the laboratory in a manner that prevents degradation or alteration of steroid metabolites. To determine the effects of different handling and storage methods on fecal steroids, 30 fresh fecal samples from five captive cheetahs were collected, thoroughly mixed, separated into aliquots, and processed (stored or dried) under different conditions. Concentrations of gonadal and adrenal steroid hormones were analyzed in feces stored frozen at –20°C or at room temperature in 95% ethanol. Both frozen and ethanol‐stored aliquots were desiccated using a lyophilizer, solar oven, or conventional oven. The steroid values from aliquots stored and desiccated using the different methods were compared to those obtained using the optimal storage method of freezing at –20°C and desiccating in a lyophilizer (control). Concentrations of corticoid, estrogen, progestagen, and androgen metabolites in fecal extracts were quantified by radioimmunoassay. Androgen metabolite concentrations were not significantly affected (P > 0.05) by storage or drying methods. Fecal samples stored at room temperature in ethanol and lyophilized also had steroid concentrations that did not differ (P > 0.05) from controls. However, the concentrations of corticoid and estrogen metabolites were significantly lower (P < 0.05), and progestagen metabolites were significantly higher (P < 0.05) in samples desiccated in solar and conventional ovens without regard to storage method. These results suggest that storage of fecal samples at room temperature in ethanol is the best alternative to freezing for subsequent analysis of steroid hormone concentrations. Differences in measured concentrations of hormones in oven‐desiccated samples could be due to hormone degradation or shifts in the immunodominant metabolite. Therefore, validation of storage and processing techniques should be included in the development of any new fecal steroid analysis methodology. Zoo Biol 21:215–222, 2002. © 2002 Wiley‐Liss, Inc.
Carotenoids, vitamin A, and vitamin E concentrations during egg development in panther chameleons (Furcifer pardalis)
Authors: Dierenfeld Ellen S. , Norkus Edward B. , Carroll Kathryn , Ferguson Gary W. 
Published: September 2002

AbstractInsects are known to be poor sources of preformed vitamin A, leading to the speculation that insectivorous species, including reptiles, may be able to convert carotenoid precursors to meet dietary requirements for this nutrient. This study was conducted to indirectly evaluate carotenoid and vitamin A metabolism in the panther chameleon (Furcifer pardalis). Eggs were obtained from females in Madagascar that were yolked either early or later in the breeding season, and carotenoid (α‐ and β‐carotene, cryptoxanthin, lutein/zeaxanthin, and lycopene), vitamin A, and vitamin E concentrations were measured in egg contents in early, middle, or late embryonic development. An overall trend of decreased nutrient concentration as eggs matured (from egg period 1 (yolks) to egg period 3 (embryos)) was seen within both clutch groups. The season of clutch deposition was a significant influence on egg weight, α‐carotene, and lutein/zeaxanthin concentrations, but on no other nutrients. Chameleon yolks contained considerably higher levels of carotenoids than levels previously reported from two viviparous lizard species, and β‐carotene concentrations were of the same magnitude as reported in grazing tortoises. β‐Carotene and β‐cryptoxanthin were the predominant carotenoids in yolk and embryos, comprising about 95% of total carotenoids detected. Measurable concentrations of retinol at all stages of egg development in the chameleons suggests effective conversion from carotenoid precursors, with concentrations similar to those measured in other lizard eggs. Information from eggs obtained in native habitats may provide baseline data on nutrient interactions to improve and optimize captive dietary management; preliminary data suggest that micronutrient environments may vary over the protracted breeding season, with possible implications for embryo health and survival. Zoo Biol 21:295–303, 2002. © 2002 Wiley‐Liss, Inc.
Motor and associative deficits in D2 dopamine receptor knockout mice
Authors: Fowler S.C. , Zarcone T.J. , Vorontsova E. , Chen R. 
Published: September 2002

AbstractBehavioral abnormalities produced by D2 dopamine receptor gene deletion in mice have been attributed either to resulting Parkinson‐like features (i.e. response slowing and response initiation difficulties) or to behavioral deficits contributed by alleles of the originating 129Sv strain. Three strategies were used to address these conflicting hypotheses: (1) we used mice congenic at n10 backcross into the C57BL/6 line to minimize the 129Sv contribution; (2) we compared mice that were wild‐type (+/+), heterozygous (+/−), or homozygous (−/−) for the D2 gene with the two most relevant inbred lines (129Sv and C57BL/6) and (3) we used both conventional and novel behavioral assessment methods. Behavioral attributes were expressed in terms of locomotor activity, wall rearing, rotarod performance, operant response acquisition, operant response performance, lick dynamics (force, rhythm), grip strength, and tremor in response to harmaline challenge. Results showed that, compared to controls, the −/− mice exhibited longer duration wall rears, retarded operant response acquisition, increased latencies to move from the operandum to the reward well, and exaggerated response to harmaline. Age was investigated as a variable (10–11 weeks versus 41–44 weeks of age) in the locomotor activity and wall rear assessments. A gene dosage effect (deficits in the +/− mice) on these two variables became apparent in the older mice. Taken together, the results showed that mice without the D2 gene exhibited Parkinson‐like behavioral features that were not easily attributed to alleles contributed by the 129Sv strain, but were consistent with basal ganglia dysfunction.
The role of glutamate receptor maturation in perinatal seizures and brain injury
Authors: Jensen Frances E. 
Published: September 2002

AbstractThe perinatal age window is characterized by vulnerability to age‐specific patterns of injury. Hypoxia/ischemia occurs in a number of settings both in term and preterm neonates, yet the patterns of response appear dependent upon the age of the infant. In the preterm neonate, hypoxic/ischemic insults result in selective white matter injury, termed periventricular leukomalacia (PVL), with little or no cortical pathology. However, in term babies, hypoxic encephalopathy is the most common cause of seizures, and also can result in cortical infarction. Extracellular glutamate accumulates in the setting of hypoxia/ischemia, and excess activation of glutamate receptors has been implicated in hypoxic/ischemic cellular death. Glutamate receptors are developmentally regulated in both neuronal and glial cells within the brain. Using rodent models, we have shown that hypoxia/ischemia results in selective white matter injury in postnatal day (P) seven rat pups, while hypoxia causes seizures in P10–12 rats, but not at younger or older ages. We have further demonstrated that antagonists of the α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazole propionic acid (AMPA) glutamate receptor subtype block white matter injury at P7 and seizures at P10. We have shown that AMPA receptors are relatively overexpressed in oligodendrocytes (OLs) within white matter at P7 and in neurons in cortex and hippocampus at P10. Hence maturational patterns of glutamate receptor expression correlate with age‐specific regional susceptibility to injury to hypoxia/ischemia. While glutamate receptor blockade represents a rational strategy in the treatment of perinatal hypoxic/ischemic brain injury, it is unclear what role variations in their expression play in normal development and plasticity. Further investigation of patterns of glutamate receptor subunit expression in human brain and in experimental animal models is necessary to determine potential age specific strategies as well as adverse effects.
GFAP mutations in Alexander disease
Authors: Li Rong , Messing Albee , Goldman James E. , Brenner Michael 
Published: September 2002

AbstractAlexander disease is a rare but often fatal disease of the central nervous system. Infantile, juvenile and adult forms have been described that present with different clinical signs, but are unified by the characteristic presence in astrocytes of Rosenthal fibers–protein aggregates that contain glial fibrillary acidic protein (GFAP) and small stress proteins. The chance discovery that mice expressing a human GFAP transgene formed abundant Rosenthal fibers suggested that mutations in the GFAP gene are a cause of Alexander disease. Sequencing results from several laboratories have indeed now identified GFAP coding mutations in most cases of the disease, including both the infantile and juvenile forms. These mutations have been found in the 1A, 2A and 2B segments of the conserved central rod domain of GFAP, and also in the variable tail region. All changes detected are heterozygous missense mutations, and none has been found in any parent of a patient that has been tested. This indicates that most cases of Alexander disease arise through de novo, dominant, GFAP mutations. Many of these mutations are homologous to ones described in other intermediate filament diseases. These other diseases have been attributed to a dominant loss of function, as the intermediate filament network is usually disrupted and a similar phenotype is observed in mice in which the corresponding intermediate filament gene has been inactivated. However, astrocytes of Alexander disease patients have normal appearing intermediate filaments, and GFAP null mice do not display the symptoms or pathology of Alexander disease. Thus, Alexander disease likely results from a dominant gain of function. Drawing upon the homology of many of the Alexander disease mutations to those found in other intermediate filament diseases, it is suggested that the gain of function is due to a partial block of filament assembly that leads to accumulation of an intermediate that participates in toxic interactions.
Role of syntaxin 1A on serotonin transporter expression in developing thalamocortical neurons
Authors: Quick Michael W. 
Published: September 2002

AbstractNeurotransmitter transporters are regulated through a variety of signal transduction mechanisms which may operate in order to maintain appropriate levels of transmitter in the synaptic cleft. GABA and glycine transporters both interact with components of the neurotransmitter release, such as the SNARE protein syntaxin 1A, suggesting that protein–protein interactions are a common method for regulating members of the neurotransmitter transporter family, and thus, linking the release of transmitter to its subsequent re‐uptake. In the present report, the interaction of syntaxin 1A with endogenous serotonin transporters (SERT) expressed in developing thalamocortical neurons is examined. Incubation of thalamocortical cultures with botulinum toxin C1, which specifically cleaves syntaxin 1A, decreased SERT function. Serotonin (5HT) saturation analysis showed that the effect of the toxin was to decrease maximum transport capacity with little change to the affinity of the transporter for 5HT. The 5HT uptake data were consistent with biotinylation experiments showing a decrease in the surface expression of SERT following toxin treatment. In addition, co‐immunoprecipitation experiments showed that SERT and syntaxin 1A form a protein complex in these neurons. These data show that components of the transmitter release machinery interact with endogenously expressed amine transporters, and suggest a mechanism for the control of transmitter levels in disorders related to aminergic signaling.