bluuebunny/crossref_metadata_2025_split huggingface dataset:
Feedbacks of Vegetation on Summertime Climate Variability over the North American Grasslands. Part II: A Coupled Stochastic Model
Authors: Wang Weile , Anderson Bruce T. , Entekhabi Dara , Huang Dong , Kaufmann Robert K. , Potter Christopher , Myneni Ranga B. 
Published: October 2006

AbstractA coupled linear model is derived to describe interactions between anomalous precipitation and vegetation over the North American Grasslands. The model is based on biohydrological characteristics in the semiarid environment and has components to describe the water-related vegetation variability, the long-term balance of soil moisture, and the local soil–moisture–precipitation feedbacks. Analyses show that the model captures the observed vegetation dynamics and characteristics of precipitation variability during summer over the region of interest. It demonstrates that vegetation has a preferred frequency response to precipitation forcing and has intrinsic oscillatory variability at time scales of about 8 months. When coupled to the atmospheric fields, such vegetation signals tend to enhance the magnitudes of precipitation variability at interannual or longer time scales but damp them at time scales shorter than 4 months; the oscillatory variability of precipitation at the growing season time scale (i.e., the 8-month period) is also enhanced. Similar resonance and oscillation characteristics are identified in the power spectra of observed precipitation datasets. The model results are also verified using Monte Carlo experiments.
Atmospheric Forcing on the Barents Sea Winter Ice Extent
Authors: Sorteberg Asgeir , Kvingedal Børge 
Published: October 2006

Abstract
The atmospheric forcing on the Barents Sea ice extent during winter [December–February (DJF)] has been investigated for the period 1967–2002. The time series for the sea ice extent is updated and includes the winter of 2005, which marks a new record low in the wintertime Barents Sea ice extent, and a linear trend of −3.5% decade−1 in the ice extent was found. Covariability between the Barents Sea ice extent and the atmospheric mean seasonal flow and the synoptic cyclones has been discussed separately. For the mean flow, linear correlations and regression analysis reveal that anomalous northerly (southerly) winds prevail in the Nordic Seas during winters with extensive (sparse) Barents Sea ice extent. Some of the variability in the mean flow is captured by the North Atlantic Oscillation (NAO); however, the wintertime link between the Barents Sea ice extent and the NAO is moderate. By studying the cyclone activity in the high-latitude Northern Hemisphere using a dataset of individual cyclones, two regions that influence the wintertime Barents Sea ice extent were identified. The variability in the northward-moving cyclones traveling into the Arctic over East Siberia was found to covary strongly with the Barents Sea ice extent. The main mechanism is believed to be the change in the Arctic winds and in ice advection connected to the cyclones. In addition, cyclone activity of northward-moving cyclones over the western Nordic Seas was identified to strongly influence the Barents Sea ice extent. This relationship was particularly strong on decadal time scales and when the ice extent lagged the cyclone variability by 1–2 yr. The lag indicates that the mechanism is related to the cyclones’ ability to modulate the inflow of Atlantic water into the Nordic Seas and the transport time of oceanic heat anomalies from the Nordic Seas into the Barents Sea. Multiple regression indicates that the two mechanisms may explain (or at least covary with) 46% of the wintertime Barents Sea variance over the 1967–2002 period and that 79% of the decadal part of the ice variability may be predicted 2 yr ahead using information about the decadal cyclone variability in the Nordic Seas.
Detection of prokaryotic promoters from the genomic distribution of hexanucleotide pairs
Authors: Jacques Pierre-Étienne , Rodrigue Sébastien , Gaudreau Luc , Goulet Jean , Brzezinski Ryszard 
Published: October 2006

Abstract

Background
In bacteria, sigma factors and other transcriptional regulatory proteins recognize DNA patterns upstream of their target genes and interact with RNA polymerase to control transcription. As a consequence of evolution, DNA sequences recognized by transcription factors are thought to be enriched in intergenic regions (IRs) and depleted from coding regions of prokaryotic genomes.

Results
In this work, we report that genomic distribution of transcription factors binding sites is biased towards IRs, and that this bias is conserved amongst bacterial species. We further take advantage of this observation to develop an algorithm that can efficiently identify promoter boxes by a distribution-dependent approach rather than a direct sequence comparison approach. This strategy, which can easily be combined with other methodologies, allowed the identification of promoter sequences in ten species and can be used with any annotated bacterial genome, with results that rival with current methodologies. Experimental validations of predicted promoters also support our approach.

Conclusion
Considering that complete genomic sequences of over 1000 bacteria will soon be available and that little transcriptional information is available for most of them, our algorithm constitutes a promising tool for the prediction of promoter sequences. Importantly, our methodology could also be adapted to identify DNA sequences recognized by other regulatory proteins.
Differential expression of WNT4 in testicular and ovarian development in a marsupial
Authors: Yu Hongshi , Pask Andrew J , Shaw Geoffrey , Renfree Marilyn B 
Published: October 2006

AbstractBackgroundWNT4 is a key regulator of gonadal differentiation in humans and mice, playing a pivotal role in early embryogenesis. Using a marsupial, the tammar wallaby, in which most gonadal differentiation occurs after birth whilst the young is in the pouch, we show by quantitative PCR during early testicular and ovarian development that WNT4 is differentially expressed ingonads.ResultsBefore birth, WNT4 mRNA expression was similar in indifferent gonads of both sexes. After birth, in females WNT4 mRNA dramatically increased during ovarian differentiation, reaching a peak by day 9–13 post partum (pp) when the ovarian cortex and medulla are first distinguishable. WNT4 protein was localised in the ovarian cortex and at the medullary boundary. WNT4 mRNA then steadily decreased to day 49, by which time all the female germ cells have entered meiotic arrest. In males, WNT4 mRNA was down-regulated in testes immediately after birth, coincident with the time that seminiferous cords normally form, and rose gradually after day 8. By day 49, when testicular androgen production normally declines, WNT4 protein was restricted to the Leydig cells.ConclusionThis is the first localisation of WNT4 protein in developing gonads and is consistent with a role for WNT4 in steroidogenesis. Our data provide strong support for the suggestion that WNT4 not only functions as an anti-testis gene during early development, but is also necessary for later ovarian and testicular function.
Stem-loop structures in prokaryotic genomes
Authors: Petrillo Mauro , Silvestro Giustina , Di Nocera Pier Paolo , Boccia Angelo , Paolella Giovanni 
Published: October 2006

Abstract

Background
Prediction of secondary structures in the expressed sequences of bacterial genomes allows to investigate spontaneous folding of the corresponding RNA. This is particularly relevant in untranslated mRNA regions, where base pairing is less affected by interactions with the translation machinery. Relatively large stem-loops significantly contribute to the formation of more complex secondary structures, often important for the activity of sequence elements controlling gene expression.

Results
Systematic analysis of the distribution of stem-loop structures (SLSs) in 40 wholly-sequenced bacterial genomes is presented. SLSs were searched as stems measuring at least 12 bp, bordering loops 5 to 100 nt in length. G-U pairing in the stems was allowed. SLSs found in natural genomes are constantly more numerous and stable than those expected to randomly form in sequences of comparable size and composition. The large majority of SLSs fall within protein-coding regions but enrichment of specific, non random, SLS sub-populations of higher stability was observed within the intergenic regions of the chromosomes of several species. In low-GC firmicutes, most higher stability intergenic SLSs resemble canonical rho-independent transcriptional terminators, but very frequently feature at the 5'-end an additional A-rich stretch complementary to the 3' uridines. In all species, a clearly biased SLS distribution was observed within the intergenic space, with most concentrating at the 3'-end side of flanking CDSs. Some intergenic SLS regions are members of novel repeated sequence families.

Conclusion
In depth analysis of SLS features and distribution in 40 different bacterial genomes showed the presence of non random populations of such structures in all species. Many of these structures are plausibly transcribed, and might be involved in the control of transcription termination, or might serve as RNA elements which can enhance either the stability or the turnover of cotranscribed mRNAs. Three previously undescribed families of repeated sequences were found in Yersiniae, Bordetellae and Enterococci.
Progressive ganglion cell loss and optic nerve degeneration in DBA/2J mice is variable and asymmetric
Authors: Schlamp Cassandra L , Li Yan , Dietz Joel A , Janssen Katherine T , Nickells Robert W 
Published: October 2006

Abstract

Background
Glaucoma is a chronic neurodegenerative disease of the retina, characterized by the degeneration of axons in the optic nerve and retinal ganglion cell apoptosis. DBA/2J inbred mice develop chronic hereditary glaucoma and are an important model system to study the molecular mechanisms underlying this disease and novel therapeutic interventions designed to attenuate the loss of retinal ganglion cells. Although the genetics of this disease in these mice are well characterized, the etiology of its progression, particularly with respect to retinal degeneration, is not. We have used two separate labeling techniques, post-mortem DiI labeling of axons and ganglion cell-specific expression of the βGeo reporter gene, to evaluate the time course of optic nerve degeneration and ganglion cell loss, respectively, in aging mice.

Results
Optic nerve degeneration, characterized by axon loss and gliosis is first apparent in mice between 8 and 9 months of age. Degeneration appears to follow a retrograde course with axons dying from their proximal ends toward the globe. Although nerve damage is typically bilateral, the progression of disease is asymmetric between the eyes of individual mice. Some nerves also exhibit focal preservation of tracts of axons generally in the nasal peripheral region. Ganglion cell loss, as a function of the loss of βGeo expression, is evident in some mice between 8 and 10 months of age and is prevalent in the majority of mice older than 10.5 months. Most eyes display a uniform loss of ganglion cells throughout the retina, but many younger mice exhibit focal loss of cells in sectors extending from the optic nerve head to the retinal periphery. Similar to what we observe in the optic nerves, ganglion cell loss is often asymmetric between the eyes of the same animal.

Conclusion
A comparison of the data collected from the two cohorts of mice used for this study suggests that the initial site of damage in this disease is to the axons in the optic nerve, followed by the subsequent death of the ganglion cell soma.
Employment status and differences in the one-year coverage of physician visits: different needs or unequal access to services?
Authors: Virtanen Pekka , Kivimäki Mika , Vahtera Jussi , Koskenvuo Markku 
Published: October 2006

Abstract
Background
The dichotomy employed vs. unemployed is still a relevant, but rather crude measure of status in current labour markets. Also, studies concerning the association of employment status with health have to specify the type of the employment as well as the characteristics of the unemployment. This study aims to reveal differences and potential inequalities in physician visits among seven groups in the core-periphery structures of the labour markets.

Methods
A total of 16 000 Finns responded to a postal survey in 2003. Their visits to physicians in public primary health care, occupational health care, private health services, hospital outpatient clinics and dental care services during previous year were measured as indicators of service utilisation. Participants were classified as employees having a permanent or fixed-term and full-time or part-time contract and as those experiencing short-term, prolonged or long-term unemployment. Differences in the one-year coverage of physician visits between these groups of employees were analysed using logistic regression analyses where differences in the need for services were controlled for by including demographics and self-rated health assessments in the models.

Results
Permanently employed respondents had visited a physician most often, and the need-adjusted regression models showed significantly lower odds ratios for a visit among fixed-term employees (OR 0.65, 95% CI 0.53–0.81) and in particular among the long-term unemployed (OR 0.21, 95% CI 0.14–0.31). A stratified analysis according to health care sector showed the lowest odds ratios in occupational health care and private physicians (ORs between 0.05 and 0.73) and also low odds ratios for dentists (ORs between 0.45 and 0.91), whereas visits to public primary health care were more common among non-permanent employees and the unemployed (ORs between 1.46 and 2.39).

Conclusion
The use of physician services varies according to labour market status, being relatively low among the non-permanently employed and the unemployed. This underuse is emphasised when clinical need is taken into account. The main reasons for the variance evidently lie in the structures of the Finnish health service system. The result may indicate non-optimal health care of the population on the periphery of the labour market, but it may also reflect the importance of employment status as a context for need and the decision to visit a physician.
In vitro susceptibilities of Brucella melitensis isolates to eleven antibiotics
Authors: Turkmani Aun , Ioannidis Alexandros , Christidou Athanasia , Psaroulaki Anna , Loukaides Feidias , Tselentis Yiannis 
Published: October 2006

Abstract

Background
Brucellosis is an endemic disease present in many countries worldwide, but it is rare in Europe and North America. Nevertheless brucella is included in the bacteria potentially used for bioterrorism. The aim of this study was the investigation of the antibiotic susceptibility profile of brucella isolates from areas of the eastern Mediterranean where it has been endemic.

Methods
The susceptibilities of 74 Brucella melitensis isolates derived from clinical samples (57) and animal products (17) were tested in vitro. The strains originate from Crete (59), Cyprus (10), and Syria (5). MICs of tetracycline, rifampicin, streptomycin, gentamicin, norfloxacin, ciprofloxacin, levofloxacin, trimethoprim/sulfamethoxazole, ampicillin, amoxicillin/clavulanic acid, and erythromycin were detected by E-test method. The NCCLS criteria for slow growing bacteria were considered to interpret the results.

Results
All the isolates were susceptible to tetracycline, streptomycin, gentamicin, ciprofloxacin, norfloxacin, and levofloxacin. Two isolates presented reduced susceptibility to rifampicin (MIC value: 1.5 mg/l) and eight to SXT (MIC values: 0.75–1.5 mg/l). Erythromycin had the highest (4 mg/l) MIC90value and both norfloxacin and erythromycin the highest (1.5 mg/l) MIC50 value.

Conclusion
Brucella isolates remain susceptible in vitro to most antibiotics used for treatment of brucellosis. The establishment of a standardized antibiotic susceptibility method for Brucella spp would be useful for resistance determination in these bacteria and possible evaluation of bioterorism risks.
Co-activator p120 is increased by gonadotropins in the rat ovary and enhances progesterone receptor activity
Authors: Yoshino Miki , Mizutani Tetsuya , Yamada Kazuya , Yazawa Takashi , Ogata-Kawata Hiroko , Sekiguchi Toshio , Kajitani Takashi , Miyamoto Kaoru 
Published: October 2006

Abstract

Background
Ovarian follicular development is primarily dependent on pituitary gonadotropins. Identification of gonadotropin-inducible genes in the ovary is one of the effective approaches for the study of follicular development. In this study we identify rat homologue of p120, a nuclear transcription co-activator, as one of the FSH inducible genes in the rat granulosa cells.

Methods
A full-length cDNA encoding rat p120 was cloned, and expression of the gene in the ovary was examined by Northern blotting. Tissue localization of p120 was examined by in situ hybridization. Cellular functions of p120 were studied by co-transfection of rat p120 gene together with estrogen receptor (ER)-alpha, ER-beta, androgen receptor (AR), or progesterone receptor (PR) genes.

Results
A full-length cDNA encoding rat p120 was characterized as a protein with 957 amino acid residues. Rat p120 was expressed ubiquitously, but strongly in the ovary and the testis. Expression of p120 mRNA was also induced in vivo by PMSG or PMSG/hCG treatment. Strong expression of p120 mRNA was observed in the granulosa cells of pre-ovulatory large antral follicles. Progesterone receptor was co-localized with p120 in the large antral follicles. Co-transfection experiments revealed that rat p120 activated AR, ER-alpha, ER-beta, and PR in the presence of their respective ligands.

Conclusion
These observations suggest that rat p120 is strongly induced in the ovarian granulosa cells, and may work together with PR in the granulosa cells of ovulatory follicles to promote the ovulation process.
Multiple endocrine neoplasia type 1
Authors: Marini Francesca , Falchetti Alberto , Monte Francesca Del , Sala Silvia Carbonell , Gozzini Alessia , Luzi Ettore , Brandi Maria Luisa 
Published: October 2006

Abstract
Multiple Endocrine Neoplasia type 1 (MEN1) is a rare autosomal dominant hereditary cancer syndrome presented mostly by tumours of the parathyroids, endocrine pancreas and anterior pituitary, and characterised by a very high penetrance and an equal sex distribution. It occurs in approximately one in 30,000 individuals. Two different forms, sporadic and familial, have been described. The sporadic form presents with two of the three principal MEN1-related endocrine tumours (parathyroid adenomas, entero-pancreatic tumours and pituitary tumours) within a single patient, while the familial form consists of a MEN1 case with at least one first degree relative showing one of the endocrine characterising tumours. Other endocrine and non-endocrine lesions, such as adrenal cortical tumours, carcinoids of the bronchi, gastrointestinal tract and thymus, lipomas, angiofibromas, collagenomas have been described. The responsible gene, MEN1, maps on chromosome 11q13 and encodes a 610 aminoacid nuclear protein, menin, with no sequence homology to other known human proteins. MEN1 syndrome is caused by inactivating mutations of the MEN1 tumour suppressor gene. This gene is probably involved in the regulation of several cell functions such as DNA replication and repair and transcriptional machinery. The combination of clinical and genetic investigations, together with the improving of molecular genetics knowledge of the syndrome, helps in the clinical management of patients. Treatment consists of surgery and/or drug therapy, often in association with radiotherapy or chemotherapy. Currently, DNA testing allows the early identification of germline mutations in asymptomatic gene carriers, to whom routine surveillance (regular biochemical and/or radiological screenings to detect the development of MEN1-associated tumours and lesions) is recommended.
Steroidogenic Acute Regulatory Protein (StAR): Evidence of Gonadotropin-Induced Steroidogenesis in Alzheimer Disease
Authors: Webber Kate M , Stocco Douglas M , Casadesus Gemma , Bowen Richard L , Atwood Craig S , Previll Laura A , Harris Peggy LR , Zhu Xiongwei , Perry George , Smith Mark A 
Published: October 2006

Abstract

Background
Alzheimer disease (AD) is clinically characterized by progressive memory loss, impairments in behavior, language and visual-spatial skills and ultimately, death. Epidemiological data reporting the predisposition of women to AD has led to a number of lines of evidence suggesting that age-related changes in hormones of the hypothalamic-pituitary-gonadal (HPG) axis following reproductive senescence, may contribute to the etiology of AD. Recent studies from our group and others have reported not only increases in circulating gonadotropins, namely luteinizing hormone (LH) in individuals with AD compared with control individuals, but also significant elevations of LH in vulnerable neuronal populations in individuals with AD compared to control cases as well as the highest density of gonadotropin receptors in the brain are found within the hippocampus, a region devastated in AD. However, while LH is higher in AD patients, the downstream consequences of this are incompletely understood. To begin to examine this issue, here, we examined the expression levels of steroidogenic acute regulatory (StAR) protein, which regulates the first key event in steroidogenesis, namely, the transport of cholesterol into the mitochondria, and is regulated by LH through the cyclic AMP second messenger pathway, in AD and control brain tissue.

Results
Our data revealed that StAR protein was markedly increased in both the cytoplasm of hippocampal pyramidal neurons as well as in the cytoplasm of other non-neuronal cell types from AD brains when compared with age-matched controls. Importantly, and suggestive of a direct mechanistic link, StAR protein expression in AD brains colocalized with LH receptor expression.

Conclusion
Therefore, our findings suggest that LH is not only able to bind to its receptor and induce potentially pathogenic signaling in AD, but also that steroidogenic pathways regulated by LH may play a role in AD.