bluuebunny/crossref_metadata_2025_split huggingface dataset:
Thiol compounds inhibit mercury-induced immunological and immunopathological alterations in susceptible mice
Authors: Hu H , Moöller G , Abedi-Valugerdi M 
Published: November 2003

Abstract
In vitro mercury induces a high proliferative response in splenic lymphocytes and in vivo it induces a systemic autoimmune disease in susceptible mouse strains. This disease is characterized by increased serum levels of IgE and IgG1 antibodies, by the production of anti-nucleolar antibodies and by the formation of renal immune complex deposits. We have previously found that the presence of 2-mercaptoethanol (2-ME) inhibited mercury-induced cell proliferation in vitro. In this study, we tested the effects of four other thiol compounds, namely dithiothreitol (DTT), L-cysteine, meso-2,3-dimercaptosuccinic acid (meso-DMSA) and 2,3-dimercapto-1-propanesulfonic acid, Na salt (DMPS) on mercury-induced immunological changes both in vitro and in vivo. We found that in vitro, the addition of all thiol compounds abrogated mercury-induced cell aggregation and proliferation. In vivo, injection of meso-DMSA and/or DMPS (s.c. or i.p.) immediately following exposure to mercury markedly decreased IgG1 synthesis in spleen cells and serum IgE levels in mercury-susceptible SJL mice. Treatment with DMPS also prevented mercury-induced IgG1 anti-nucleolar antibody synthesis and the development of mesangial IgG1 immune complex deposits in SJL mice.
Serum concentrations of free and total insulin‐like growth factor‐I, IGF binding proteins ‐1 and‐3 and IGFBP‐3 protease activity in boys with normal or precocious puberty
Authors: Juul Anders , Flyvbjerg Allan , Frystyk Jan , Müller Jørn , Skakkebæk Niels E. 
Published: November 2003

OBJECTIVE Circulating IGF‐I and IGF binding protein‐3 (IGFBP‐3) levels both increase in puberty where growth velocity is high. The amount of free IGF‐I is dependent on the IGF‐I level and on the concentrations of the specific IGFBPs. Furthermore, IGFBP‐3 proteolysis regulates the bioavailability of IGF‐I. However, the concentration of free IGF‐I and possible IGFBP‐3 proteolytic activity in puberty has not previously been studied.SUBJECTS AND MEASUREMENTS We investigated serum levels of easily dissociable IGF‐I concentrations and ultrafiltrated free IGF‐I levels by specific assays in 60 healthy boys and in 5 boys with precocious puberty before and during GnRH agonist treatment. In addition, total serum IGF‐I, IGFBP‐1 and IGFBP‐3 levels as well as IGFBP‐3 protease activity were determined.RESULTS Free (dissociable and ultrafiltrated) IGF‐I concentrations were significantly higher in pubertal boys than in prepubertal children and correlated significantly with the molar ratio between IGF‐I and IGFBP‐3 (r=0.69, P<0.0001 and r=0.54, P=0.0008, respectively) and inversely with IGFBP‐1 (r=−0.47, P<0.0001 and r=−0.43, P=0.0003, respectively). Multiple regression analysis suggested that IGFBP‐3 level, and not IGFBP‐1, was the major determinant of the free IGF‐I serum level in normal boys. Free IGF‐I levels were elevated in boys with precocious puberty and decreased during GnRH treatment. IGFBP‐3 proteolysis was constant throughout puberty (mean 20%).CONCLUSIONS We conclude that easily dissociable and ultrafiltrated free IGF‐I serum levels are increased in boys with normal and precocious puberty and suggest that the increased free IGF‐I serum concentration in puberty primarily reflects changes in total concentrations of IGF‐I and IGFBPs secondary to increased GH secretion, but that it is not influenced by changes in IGFBP‐3 proteolysis.
CO2 flux estimates tend to overestimate ecosystem C sequestration at elevated CO2
Authors: Niklaus P. A. , Stocker R. , Körner CH. , Leadley P. W. 
Published: November 2003

Abstract1. Instantaneous leaf photosynthesis and land area‐based net ecosystem CO2 exchange (NEC) are almost universally increased at elevated CO2 concentrations, at least in the short term and under high light conditions. This raises the possibility that terrestrial ecosystems sequester extra C in response to elevated CO2, and it has been hypothesized that part of this extra C is stored in soils.2. Attempts to quantify ecosystem C sequestration experimentally are based on (i) ecosystem CO2 exchange measurements; (ii) C isotope tracking; and (iii) direct C stock measurements.3. Because direct C stock measurements are insensitive to increases in ecosystem C storage in the range expected, and C isotope tracking is methodologically difficult because of the need to account for new and old soil C pools, NEC measurements were considered to be a more direct and unbiased method to estimate net ecosystem production and C sequestration at elevated CO2.4. Here we present a case study in calcareous grassland under long‐term CO2 enrichment in which we demonstrate that calculated C balances are extremely sensitive to systematic experimental biases inherent in any CO2 flux‐based study at elevated CO2. A sensitivity analysis demonstrates that these systematic errors tend to result in severe overestimation of ecosystem C accretion under elevated CO2.5. Carbon isotope data and soil pool C and N measurements from the same study add to the evidence that the C balance derived from CO2 flux measurements at elevated CO2 is overestimated.6. Based on this evidence, and the wide attention given to C sequestration at elevated CO2, we suggest a critical reconsideration of the appropriateness of NEC measurement in CO2‐enriched ecosystems as a basis for calculating ecosystem C balances at elevated CO2.
Seasonal field metabolic rate and dietary intake in Arabian Babblers (Turdoides squamiceps) inhabiting extreme deserts
Authors: Anava A. , Kam M. , Shkolnik A. , Degen A. A. 
Published: November 2003

Abstract1. Arabian Babblers (Turdoides squamiceps Cretzsch.; mean adult body mass = 72·5 g) inhabit extreme deserts of Israel. They consume invertebrates and fruits and, at least at our study site, do not drink. It was hypothesized that babblers (1) in general, use relatively less energy and water than other birds of its body mass; and (2) consume a more water‐rich diet (mainly fruits) in summer and more energy‐rich diet (mainly invertebrates) in winter. Doubly labelled water was used to determine seasonal field metabolic rate (FMR) and water influx rate (WIR) and to estimate dietary selection in free‐living Arabian Babblers.2. Babblers in winter weighed significantly more than in summer, and males weighed more than females in both seasons. Tritiated water (TOH) space, as a proportion of body mass, was higher in males than in females in summer but no difference between sexes was found in winter. Males in summer had a higher TOH space, proportionally, than males in winter but there was no difference between seasons in females. Mass‐specific WIR did not differ between sexes in any season and averaged 0·475 ml g−1 d−1 in winter which was significantly higher than the 0·283 ml g−1 d−1 in summer.3. The mean daily energy expenditure of the babblers did not differ either between seasons or between sexes within seasons and averaged 1·61 kJ g−1 d−1 in winter and 1·68 kJ g−1 d−1 in summer. It was calculated that each babbler consumed an average of 5·09 g dry matter invertebrates and 1·83 g dry matter fruits in summer (for a 68·2‐g bird; mean adult body mass in summer) and 3·49 g dry matter invertebrates and 6·61 g dry matter fruits in winter (for a 76·9‐g bird; mean adult body mass in winter).4. When compared with other avian species, FMR and WIR of babblers were lower than bird species in general, but were similar to those of other desert birds. It was calculated that proportional dietary intake, on a dry matter basis, included 0·79 insects and 0·21 fruits in summer and 0·35 insects and 0·65 fruits in winter. Therefore, the babblers consumed a relatively energy‐rich diet in summer and water‐rich diet in winter which refuted our hypothesis. Most of the metabolizable energy was provided by invertebrates in both seasons; invertebrates provided more water in summer but fruits provided more in winter.
Dynamics of chromosomes and microtubules visualized by multiple‐wavelength fluorescence imaging in living mammalian cells: effects of mitotic inhibitors on cell cycle progression
Authors: Haraguchi Tokuko , Kaneda Toru , Hiraoka Yasushi 
Published: November 2003

Background:Mitotic events are accomplished by a coordinated interaction of molecular components within a cell. The continuous observation of specific molecular components in individual living cells provides a unique opportunity to examine the temporal and spatial coordination of these components. In order to be able to observe dynamic events in living mammalian cells, we have developed a computerized fluorescence microscope system.Results:Using this fluorescence microscope system, we observed the dynamic behaviour of chromosomes and microtubules in living HeLa cells throughout an entire cell cycle. Chromosomes and microtubules were stained with Hoechst 33342 and rhodamine‐conjugated tubulin, respectively. Microinjected rhodamine‐tubulin was incorporated into microtubules at all stages of the cell cycle. In addition, rhodamine‐tubulin stained the centrosomes during the G2 phase of the cell cycle and allowed us to observe centrosome movement. We also examined the effects of mitotic inhibitors on cell cycle progression. In a living cell treated with an inhibitor of type II DNA topoisomerase (ICRF‐193) chromosomes formed an aberrant metaphase plate and failed to segregate. However, following mitotic spindle disassembly, the chromosomes decondensed normally. While the cell began to divide into two portions, cell division was eventually aborted and the daughter cells, still connected by a cytoplasmic bridge, rejoined into a single cell. These results demonstrate how a polyploid nucleus is generated in the presence of ICRF‐193. On the other hand, microtubule polymerization inhibitors, such as colchicine, nocodazole and vinblastine, arrested the cell in the metaphase with condensed chromosomes; cytochalasin D did not affect the mitotic behaviour of either chromosomes or microtubules.Conclusions:Our observations of living cells demonstrate that the failure of chromosome segregation in and of itself does not prevent an exit from the metaphase, whereas the inhibition of microtubule assembly arrests cells at metaphase. Thus, a metaphase checkpoint is monitored by functional spindle microtubules but not by the completion of chromosome segregation.
Alteration of telomeric sequences and senescence caused by mutations in RAD50 of Saccharomyces cerevisiae
Authors: Mary Kironmai K. , Muniyappa K. 
Published: November 2003

Background:Vegetatively dividing cells of Saccharomyces cerevisiae carrying a mutation in RAD50 grow significantly more slowly in rich medium and are sensitive to DNA damage inflicted by X‐ray or chemical mutagens. RAD50 function is essential for the formation and repair of meiosis‐specific double‐strand breaks and chromosome stability.Results:We present evidence for two new phenotypes associated with the rad50Δ mutant; shortened telomeres and cell senescence. Comparison of TG1–3 telomeric sequences in an isogenic pair of RAD50 and rad50Δ haploid strains showed that they were considerably shortened in the latter. Although rad50Δ mutation conferred cell enlargement and slow growth, cell doubling was faster but caused an increase in the frequency of cell death. Telomeres were restored to the wild‐type size in hemizygous RAD50/rad50Δ and rad50S/rad50Δ strains; however, they showed a significant increase in rad50S/rad50S diploid with a concomitant rise in cell viability. Telomeres were stabilized in hemizygous RAD50/rad50Δ and rad50S/rad50Δ diploids during prolonged growth, suggesting that even a half‐dosage of RAD50 is sufficient to conserve the telomere size during successive cell divisions. Furthermore, cells bearing the rad50Δ mutation revealed abnormalities in nuclear segregation and, in the presence of hydroxyurea, displayed phenotypes consistent with defects in S‐phase checkpoint control.Conclusion:This report presents evidence of the involvement of a gene relevant to recombinational repair in the maintenance of telomeres.We conclude that the phenotypes displayed by yeast rad50Δ cells have intriguing similarities among the human cell lines representing DNA repair‐deficient chromosome instability syndromes.
Characterization of the mouse prostaglandin F receptor gene: a transgenic mouse study of a regulatory region that controls its expression in the stomach and kidney but not in the ovary
Authors: Hasumoto Ken‐yuh , Sugimoto Yukihiko , Gotoh Megumi , Segi Eri , Yamasaki Atsushi , Yamaguchi Masahiro , Honda Hiroaki , Hirai Hisamaru , Negishi Manabu , Kakizuka Akira , Ichikawa Atsushi 
Published: November 2003

Background:The actions of prostaglandin F2α are mediated by a cell‐surface receptor (FP), but little is known about the regulation of FP gene expression. To clarify the mechanisms underlying tissue specific transcription of the mouse FP gene, we isolated and characterized mouse genomic DNA clones encoding FP.Results:Structural analysis revealed that the mouse FP gene is composed of three exons and two introns, and spans more than 11 kilobases. By primer extension and PCR analyses, the major transcription start site was identified as a cytosine nucleotide, but additional sites of transcription initiation were found in the ovary. There was no apparent difference in the FP gene transcription initiation site between the ovary, kidney and stomach. Sequence analysis of the putative promoter region showed only two potential SP‐1 binding sites, but no other typical well‐known consensus sequences. We generated transgenic mice with the potential promoter region of the FP gene connected to the lacZ reporter gene. Northern blot analysis showed that the pattern of expression of the transgene corresponded to that of FP expression, except in the ovary. Upon analysis by in situ hybridization, the lacZ gene transcripts were found to be expressed in the fundic glands in the stomach, and the cortical tubules in the kidney, in which endogenous FP transcripts were also expressed. On the contrary, expression of lacZ transcripts was not detected in the corpora lutea, where the highest expression of FP mRNA was observed.Conclusions:These studies suggest that a separate control mechanism exists for FP expression in the ovary, distinct from the expression in the stomach and kidney.
Inhibition of transpositional recombination by OrfA and OrfB proteins encoded by insertion sequence IS3
Authors: Sekine Yasuhiko , Izumi Ken‐ichiro , Mizuno Takaaki , Ohtsubo Eiichi 
Published: November 2003

Background:An insertion element IS3 is flanked by terminal inverted repeat (IR) sequences. IS3 encodes two, out‐of‐phase, overlapping open reading frames, orfA and orfB, from which three proteins are produced. OrfAB is a transframe protein produced by −1 translational frameshifting between orfA and orfB, and it is known to be IS3 transposase. OrfA and OrfB are the proteins produced without frameshifting, but their functions have not been elucidated.Results:A plasmid carrying an IS3 mutant that produces only transposase generates miniplasmids—which are the IS3‐mediated intramolecular transposition products—as well as characteristic IS3 circles and linear IS3 molecules. OrfA inhibited the generation of these small molecules to a lesser degree, but OrfB did not. OrfB, together with OrfA, however, inhibited the generation more strongly than OrfA alone. OrfA also inhibited the intermolecular transposition of mini‐IS3 with the chloramphenicol‐resistance gene flanked by IRs to a reduced frequency, and OrfB together with OrfA inhibited it almost completely. OrfA and/or OrfB did not, however, repress transcription from the promoter in the left‐terminal region preceding orfA.Conclusions:The results obtained above show that OrfA and OrfB are not repressors but are inhibitors of transpositional recombination promoted by transposase. OrfA with an α helix‐turn‐α helix DNA‐binding motif may compete with transposase to bind to terminal IRs. OrfA, together with OrfB that has a DDE motif conserved in retroviral integrases, may inhibit the formation of an active transpososome consisting of transposase, two terminal IRs and target DNA for the strand transfer reaction. IS3 with a limited size, 1258 bp in length, uses strategies of translational frameshifting and coupling to produce transposase as well as negative regulators to make its copies at a low level, which minimizes a deleterious effect of transposition on bacterial hosts.
How representative are Pipelle endometrial biopsies? A retrospective analysis of 324 biopsies followed by transcervical resection of the endometrium or hysterectomy
Authors: Krampl E. , Søby B. , Istre O. 
Published: November 2003

ObjectiveTo evaluate the diagnostic accuracy of Pipelle endometrial biopsies before surgical treatment of uterine bleeding disorders.DesignRetrospective analysis.SettingCounty Hospital unit specializing in operative hysteroscopy.InterventionsRoutine outpatient endometrium biopsies were taken from 628 patients because of uterine bleeding disorders. Of these patients, 249 underwent transcervical resection of the endometrium (TCRE) and 75 had a hysterectomy within 6 months.ResultsComparing the two subgroups ‘malignant’ and ‘benign’, the positive predictive value for endometrial malignancy was 100% (95% CI, 73.5–100). Insufficient tissue was obtained in five cases (1.5%); in three there were submucous fibroids, in one sampling took place after TCRE, and one patient had atrophic endometrium.ConclusionAdequate preoperative histological assessment of the endometrium is feasible with Pipelle biopsies, and they are highly accurate in detecting endometrial malignancy.
Sources of resistance to Pseudomonas syringae pv. phaseolicola races in Phaseolus vulgaris
Authors: TAYLOR J. D. , TEVERSON D. M. , DAVIS J. H. C. 
Published: November 2003

One thousand and forty‐eight Phaseolus bean accessions were evaluated for resistance to six races of Pseudomonas syringae pv. phaseolicola. The accessions originated from regions of the Americas and Africa where the disease is important and included wild type accessions and some known resistance sources. Resistance, graded on a five‐point scale, was of two types: qualitative, which was shown to be race‐specific, and quantitative. Race specific resistance genes (R‐genes) were detected in 49.4% of accessions with the following gene frequencies: R1 (10.3%), R2 (0.3%), R3 (25.0%), R4 (35.0%) and R5 (0.2%).Evidence for quantitative variation in resistance, in the absence of specific R‐genes, was shown by the distribution of infection scores, 76% of accessions showing maximum susceptibility (grades 4–5), 23% showing intermediate resistance (grades 2–4), and 1% showing high levels of quantitative resistance (grades 1–2). The last 1% of accessions showed interactions which were not race‐specific and it is suggested that they may possess race non‐specific resistance. It is possible that several of the accessions in this category carry the recessive gene derived from PI 150414. Other accessions were of unknown parentage and may represent new sources of quantitative, potentially race non‐specific, resistance. It is suggested that the combination of race specific and race non‐specific resistance could provide an effective strategy for establishing durable resistance.
Provider‐sponsored virtual communities for chronic patients: improving health outcomes through organizational patient‐centred knowledge management
Authors: Winkelman Warren J. , Choo Chun Wei 
Published: November 2003

AbstractPatients with long‐term chronic disease experience numerous illness patterns and disease trends over time, resulting in different sets of knowledge needs than patients who intermittently seek medical care for acute or short‐term problems. Health‐care organizations can promote knowledge creation and utilization by chronic patients through the introduction of a virtual, private, disease‐specific patient community. This virtual socialization alters the role of chronic disease patients from external consumers of health‐care services to a ‘community of practice’ of internal customers so that, with the tacit support of their health‐care organization, they have a forum supporting the integration of knowledge gained from the experiences of living with chronic disease in their self‐management. Patient‐centred health‐care organizations can employ the virtual community to direct and support the empowerment of chronic patients in their care.
Giant keratoacanthoma arising in hypertrophic lichen planus
Authors: Giesecke Leah M , Reid Catherine M , James Craig L , Huilgol Shyamala C 
Published: November 2003

SUMMARYA 45‐year‐old man presented with a rapidly enlarging tumour in an area of long‐standing hypertrophic lichen planus of the lower leg. Histological examination of the resected specimen showed it to be a giant keratoacanthoma measuring 37 × 57 mm. Neoplastic change is a rarely reported complication of chronic variants of cutaneous lichen planus. To date there have been only two reports of keratoacanthoma development in association with lichen planus.
Allergic contact dermatitis to an expired moisturiser
Authors: Lim Adrian C , Freeman Susanne 
Published: November 2003

SUMMARYA 64‐year‐old man developed an allergic contact dermatitis while using an expired sorbolene cream. Patch tests to the product ingredients were all negative. Repeated open application test to the expired product produced a strong reaction while an identical‐brand non‐expired product did not elicit a reaction, suggesting the presence of an unidentified degradation product or compound, acting as an allergen in the expired product. This case is intriguing in that it contrasts the ubiquitous use of over‐the‐counter topical agents with the exceedingly low incidence of contact dermatitis to expired topical products.
Nicotine‐induced neuroprotection against N‐methyl‐d‐aspartic acid or β‐amyloid peptide occur through independent mechanisms distinguished by pro‐inflammatory cytokines
Authors: Gahring Lorise C. , Meyer Erin L. , Rogers Scott W. 
Published: November 2003

AbstractNicotine, the causative agent of addiction to tobacco, can also be a neuroprotectant. Nicotine‐induced neuroprotection against different toxins is imparted through pharmacologically distinct neuronal nicotinic acetylcholine receptors (nAChR) where protection against chronic N‐methyl‐d‐aspartic acid (NMDA) exposure is through nAChRα7 but protection against the toxic peptide of amyloid precursor protein, Aβ25−35, is through nAChRα4β2. The inflammatory cytokine tumor necrosis factor alpha (TNFα) is also neuroprotective, however, in the presence of nicotine, neuroprotection against NMDA is abolished. The specificity of nicotine–TNFα antagonism was further refined using a mouse transgenic dominant negative of nAChRα7 in which nicotine failed to induce neuroprotection against NMDA and antagonism of TNFα was absent. However, nicotine‐mediated neuroprotection against Aβ25−35 was unaffected and, therefore, did not require the expression of functional nAChRα7s. The mechanism of TNFα‐mediated neuroprotection and antagonism by nicotine was independent of caspase 8 activation or nuclear factor kappa B translocation in neurons but C6‐ceramide addition to neuronal cultures subsequently exposed to NMDA mimicked the neuroprotective effect of TNFα and, like TNFα, it was antagonized by cotreatment with nicotine. Therefore, the neuroprotective effects of nicotine against differing toxic assaults requires distinct nAChR subtypes and proceeds through intracellular pathways that overlap with similarly different mechanisms initiated by pro‐inflammatory cytokines. These results provide insight into how nicotine imparts neuroprotection and modulates inflammatory responses.