bluuebunny/crossref_metadata_2025_split huggingface dataset:
Future Perspectives on Employee Selection: Key Directions for Future Research and Practice
Authors: Anderson Neil , Lievens Filip , Van Dam Karen , Ryan Ann Marie 
Published: September 2004

Les recherches sur la sélection et l’évaluation sont abordées d’un point de vue tourné vers l’avenir. On recense quatre grand thèmes d’importance majeure dans le développement des futures recherches: la prédiction bimodale, l’adaptation polyvalente, les réactions et décisions pertinentes et les tensions entre la recherche et la pratique dans la sélection professionnelle. Pour chacun de ces thèmes, nous soulevons certains problèmes qui restent à traiter. On discute enfin des conséquences sur la patique et les avancées actuelles dans le domaine de la sélection, traditionnellement l’une des plus actives des disciplines centrales de la psychologie internationales du travail.A future‐oriented perspective for selection and assessment research is presented. Four superordinate themes of critical import to the development of future research are identified: (i) bimodal prediction, (ii) multilevel fit, (iii) applicant reactions and decision making, and (iv) tensions between research and practice in employee selection. Under each theme we pose a number of outstanding questions for research. Implications for practice and the ongoing advancement of the sub‐field of selection, traditionally one of the most robust core disciplines in international IWO psychology, are discussed.
Soluble factors elaborated by human brain endothelial cells induce the concomitant expansion of purified human BM CD34+CD38– cells and SCID-repopulating cells
Authors: Chute John P. , Muramoto Garrett G. , Fung Jennifer , Oxford Carol 
Published: September 2004

AbstractThe CD34+CD38– phenotype identifies a population in the bone marrow that is enriched in the steady state for hematopoietic stem cells (HSCs). Following ex vivo culture of CD34+ cells, HSC content is difficult to measure since committed CD34+CD38+ progenitors down-regulate CD38 surface expression during culture. In this study, we sought to define the phenotype of human HSCs following ex vivo culture under conditions that support the expansion of human cells capable of repopulating non-obese diabetic/severe combined immunodeficiency (SCID)–repopulating cells (SRCs). Contact coculture of fluorescence-activated cell sorter (FACS)–sorted bone marrow (BM) CD34+CD38– cells with human brain endothelial cells (HUBECs) supported a 4.4-fold increase in CD34+CD38– cells with a concordant 3.6-fold increase in SRCs over 7 days. Noncontact HUBEC cultures and the addition of thrombopoietin, stem cell factor (SCF), and macrophage colony stimulating factor I receptor (Fms)–like tyrosine kinase 3 (Flt-3) ligand supported further increases in CD34+CD38– cells (6.4-fold and 13.1-fold), which correlated with significant increases in SRC activity. Moreover, cell-sorting studies performed on HUBEC-cultured populations demonstrated that SRCs were significantly enriched within the CD34+CD38– subset compared with the CD34–CD38– population after culture. These results indicate that human HSCs can be identified and characterized by phenotype following expansion culture. These studies also demonstrate that HUBEC-elaborated soluble factors mediate a unique and potent expansion of human HSCs.
A stochastic model for retinocollicular map development
Authors: Koulakov Alexei A , Tsigankov Dmitry N 
Published: September 2004

Abstract
Background
We examine results of gain-of-function experiments on retinocollicular maps in knock-in mice [Brown et al. (2000) Cell 102:77]. In wild-type mice the temporal-nasal axis of retina is mapped to the rostral-caudal axis of superior colliculus. The established map is single-valued, which implies that each point in retina maps to a unique termination zone in superior colliculus. In homozygous Isl2/EphA3 knock-in mice the map is double-valued, which means that each point on retina maps to two termination zones in superior colliculus. This is because about 50 percent of cells in retina express Isl2, and two types of projections, wild-type and Isl2/EphA3 positive, form two branches of the map. In heterozygous Isl2/EphA3 knock-ins the map is intermediate between the homozygous and wild-type: it is single-valued in temporal and double-valued in the nasal parts of retina. In this study we address possible reasons for such a bifurcation of the map.

Results
We study the map formation using stochastic model based on Markov chains. In our model the map undergoes a series of reconstructions with probabilities dependent upon a set of chemical cues. Our model suggests that the map in heterozygotes is single-valued in temporal region of retina for two reasons. First, the inhomogeneous gradient of endogenous receptor in retina makes the impact of exogenous receptor less significant in temporal retina. Second, the gradient of ephrin in the corresponding region of superior colliculus is smaller, which reduces the chemical signal-to-noise ratio. We predict that if gradient of ephrin is reduced by a genetic manipulation, the single-valued region of the map should extend to a larger portion of temporal retina, i.e. the point of transition between single-and doulble-valued maps should move to a more nasal position in Isl2-EphA3 heterozygotes.

Conclusions
We present a theoretical model for retinocollicular map development, which can account for intriguing behaviors observed in gain-of-function experiments by Brown et al., including bifurcation in heterozygous Isl2/EphA3 knock-ins. The model is based on known chemical labels, axonal repulsion/competition, and stochasticity. Possible mapping in Isl2/EphB knock-ins is also discussed.
Hepatitis B virus variants in an HIV-HBV co-infected patient at different periods of antiretroviral treatment with and without lamivudine
Authors: Santos Eneida A , Sucupira Michel VF , Arabe Juçara , Gomes Selma A 
Published: September 2004

Abstract
Background
Lamivudine inhibits replication of both human immunodeficiency virus (HIV) and hepatitis B virus (HBV) and is commonly used as part of antiretroviral therapy. The main limitation in the use of lamivudine is resistant mutation selection. Most of these mutations affect the YMDD motif of the HBV DNA polymerase. The resistance occurs through M550V or M550I aminoacid replacements. The M550V variation may be accompanied by L526M mutation, notably in HIV-HBV co-infected patients. The aim of this study was to investigate mutations associated with lamivudine resistance in a hemodialysis patient chronically co-infected with HIV-1 and HBV, who was submitted to several antiretroviral treatments.

Methods
HBV isolates derived from three blood samples collected at different times of antiretroviral therapies with and without lamivudine, were titred and submitted to nucleotide sequencing.

Results
HBV isolate derived from a sample collected in 1999 during an antiretroviral treatment with lamivudine showed the lamivudine resistant double mutation (L526M, M550V). However, no mutation associated with lamivudine resistance was observed in the HBV genome derived from the sample collected during a period of treatment without lamivudine (2001). After reinstitution of lamivudine (2002), the predominant HBV population exhibited a rare triple mutation (V519L, L526M, M550V), which has previously been associated with an in vitro reduction of virus antigenicity (escape mutant). HBV DNA was detected at high levels (108–109 copies/ml) in the three blood samples.

Conclusions
Reintroduction of lamivudine as part of antiretroviral treatment in a patient who had developed lamivudine resistant HBV strains favored the predominance of an HBV isolate with reduced antigenicity. The absence of hepatitis acute exacerbation in this patient may be correlated to the absence of significant variations of the viral load, which was independent of the presence of mutations in the HBV DNA polymerase.
A rational treatment of Mendelian genetics
Authors: Porteous John W 
Published: September 2004

Abstract
Background
The key to a rational treatment of elementary Mendelian genetics, specifically to an understanding of the origin of dominant and recessive traits, lies in the facts that: (1) alleles of genes encode polypeptides; (2) most polypeptides are catalysts, i.e. enzymes or translocators; (3) the molecular components of all traits in all cells are the products of systems of enzymes, i.e. of fluxing metabolic pathways; (4) any flux to the molecular components of a trait responds non-linearly (non-additively) to graded mutations in the activity of any one of the enzymes at a catalytic locus in a metabolic system; (5) as the flux responds to graded changes in the activity of an enzyme, the concentrations of the molecular components of a trait also change.

Conclusions
It is then possible to account rationally, and without misrepresenting Mendel, for: the origin of dominant and recessive traits; the occurrence of Mendel's 3(dominant):1(recessive) trait ratio; deviations from this ratio; the absence of dominant and recessive traits in some circumstances, the occurrence of a blending of traits in others; the frequent occurrence of pleiotropy and epistasis.
Mild hypothermia after near drowning in twin toddlers
Authors: Hein Ortrud Vargas , Triltsch Andreas , von Buch Christoph , Kox Wolfgang J , Spies Claudia 
Published: September 2004

Abstract
Introduction
We report a case of twin toddlers who both suffered near drowning but with different post-trauma treatment and course, and different neurological outcomes.

Methods and results
Two twin toddlers (a boy and girl, aged 2 years and 3 months) suffered hypothermic near drowning with protracted cardiac arrest and aspiration. The girl was treated with mild hypothermia for 72 hours and developed acute respiratory dysfunction syndrome and sepsis. She recovered without neurological deficit. The boy's treatment was conducted under normothermia without further complications. He developed an apallic syndrome.

Conclusion
Although the twin toddlers experienced the same near drowning accident together, the outcomes with respect to neurological status and postinjury complications were completely different. One of the factors that possibly influenced the different postinjury course might have been prolonged mild hypothermia.
G-CSF-mobilized CD34+ cells cultured in interleukin-2 and stem cell factor generate a phenotypically novel monocyte
Authors: Sconocchia Giuseppe , Fujiwara Hiroshi , Rezvani Katayoun , Keyvanfar Keyvan , El Ouriaghli Frank , Grube Matthias , Melenhorst Jos , Hensel Nancy , Barrett A John 
Published: September 2004

AbstractTo study the early stages of development from stem cells of the CD56+ cell population [which includes natural killer (NK) cells], granulocyte-colony stimulating factor-mobilized peripheral blood CD34+ cells from healthy donors were sorted to &gt;99% purity and cultured in the presence of stem cell factor and interleukin (IL)-2. After 3 weeks in culture, the majority of cells acquired CD33, with or without human leukocyte antigen-DR and CD14. In 20 stem cell donors tested, 8.7 ± 8.8% of cells were CD56+. Two major CD56+ subsets were identified: CD56bright, mainly CD33− cells (7±10%, n=11) with large, granular lymphocyte morphology, and CD56dim, mainly CD33+ (2.5±2, n=11) cells with macrophage morphology. The CD56bright population had cytoplasmic granzyme A but lacked killer inhibitory receptor, suggesting they were immature NK cells. The CD56dim, CD33+, population lacked NK markers. They may represent a minor subset of normal monocytes at a developmental stage comparable with the rare CD56+ CD33+ hybrid myeloid/NK cell leukemia. Consistent with a monocyte nature, CD56dimCD33+ proliferated and produced a variety of cytokines upon lipopolysaccharide stimulation, including IL-8, IL-6, monocyte chemoattractant protein-1, and macrophage-derived chemokine but not interferon-γ. In a short-term cytotoxicity assay, they failed to kill but powerfully inhibited the proliferation of the NK-resistant cell line P815. The generation of CD56+ cells was negatively regulated by hyaluronic acid and IL-4, indicating that extracellular matrix may play an important role in the commitment of CD34+ cells into CD56 myeloid and lymphoid lineages.
Insulin-Like Growth Factor-I Regulation of Hepatic Scavenger Receptor Class BI
Authors: Cao Wen M. , Murao Koji , Imachi Hitomi , Yu Xiao , Dobashi Hiroaki , Yoshida Kazuya , Muraoka Tomie , Kotsuna Noriko , Nagao Sachi , Wong Norman C. W. , Ishida Toshihiko 
Published: September 2004

AbstractHigh-density lipoprotein mediates a normal physiological process called reverse cholesterol transport. This process enables the transfer of cholesterol from peripheral tissues to the liver for further metabolism and eventual secretion in the form of bile. The scavenger receptor of the B class (SR-BI), human homolog of SR-BI, and CD36 and LIMPII analogous-1 (CLA-1) are different names for the same receptor that facilitates hepatocellular uptake of cholesterol from high-density lipoprotein. The pivotal role of this receptor in enterohepatic circulation of cholesterol and bile salts underlies our interest to study the regulation of hepatic SR-BI gene in response to the actions of IGF-I. The results of our studies showed that endogenous expression of SR-BI/CLA-1 was suppressed by exposure to GH or IGF-I in cultured HepG2 cells. This observation extended to a whole animal model of rats continuously infused with IGF-I. IGF-I decreased transcriptional activity of the SR-BI promoter. However, the inhibitory effect of IGF-I on SR-BI/CLA-1 promoter activity was abrogated by wortmannin, a specific inhibitor of phosphoinositide 3-kinase (PI3-K). Exposure of HepG2 cells to IGF-I elicited a rapid phosphorylation of Akt. We also demonstrated that the constitutively active form of both p110, a subunit of PI3-K, and Akt inhibited activity of the human SR-BI/CLA-1 promoter. Furthermore, the dominant-negative mutant of Akt abolished the ability of IGF-I to suppress activity of the SR-BI/CLA-1 promoter. In conclusion, PI3-K/Akt pathways participate in IGF-I-suppression of SR-BI/CLA-1 expression, which suggests that the activation of Akt plays an important role in cholesterol metabolism in liver.
Connective Tissue Growth Factor Mediates High Glucose Effects on Matrix Degradation through Tissue Inhibitor of Matrix Metalloproteinase Type 1: Implications for Diabetic Nephropathy
Authors: McLennan S. V. , Wang X. Y. , Moreno V. , Yue D. K. , Twigg S. M. 
Published: September 2004

AbstractHigh glucose concentration inhibits matrix degradation and affects the activities of the enzymes responsible, the matrix metalloproteinases (MMPs) and their tissue inhibitors (TIMPs). Connective tissue growth factor (CTGF) expression is increased in diabetic nephropathy and is a downstream mediator of TGF-β actions. However, whether CTGF regulates matrix degradation and the mechanism of effect in diabetes has not been reported. Human mesangial cells were cultured in media containing 5 or 25 mm glucose and, in some experiments, with recombinant human (rh)CTGF (0–1000 ng/ml) and/or appropriate neutralizing antibodies. Matrix degradation was inhibited by rhCTGF in a dose-dependent manner, and the decrease in matrix degradation caused by high glucose and by TGF-β was significantly attenuated by addition of CTGF-neutralizing antibody (by 40.2 and 69.1%, respectively). Similar to 25 mm glucose, addition of rhCTGF increased MMP-2, TIMP-1, and TIMP-3 mRNA by 2.5-, 2.1-, and 1.6-fold, respectively (P &lt; 0.05) but had no effect on membrane-type (MT)1-MMP or TIMP-2. Addition of TIMP-1 antibody to conditioned medium abolished the decrease in degradation caused by rhCTGF and partially prevented (by 79%) the glucose-induced inhibition of matrix degradation. In vivo studies of glomeruli from diabetic and control rats showed that intensive insulin treatment prevented the increase in expression of CTGF and TIMP-1 and attenuated the decreased matrix degradation seen in diabetes. In summary, CTGF inhibits matrix degradation by increasing TIMP-1 expression, and by this action it contributes to the inhibition of matrix breakdown by high glucose, implying that CTGF has a role in the reduced matrix degradation observed in diabetic nephropathy.
Ataxia-Telangiectasia Mutated Gene Controls Insulin-Like Growth Factor I Receptor Gene Expression in a Deoxyribonucleic Acid Damage Response Pathway via Mechanisms Involving Zinc-Finger Transcription Factors Sp1 and WT1
Authors: Shahrabani-Gargir Limor , Pandita Tej K. , Werner Haim 
Published: September 2004

AbstractThe IGF-I receptor (IGF-IR) has a central role in cell cycle progression as well as in the establishment of the transformed phenotype. Increased expression of the IGF-IR gene, in addition, is correlated with acquisition of radioresistance for cell killing. The ataxia-telangiectasia mutated (ATM) gene product has a pivotal role in coordinating the cellular response to DNA damage. The present study was aimed at testing the hypothesis that the ability of ATM to coordinate the DNA damage response that will lead to cell survival or, alternatively, to apoptosis depends, to a significant extent, on its capacity to control IGF-IR gene expression. The potential involvement of ATM in regulation of IGF-IR expression and function was investigated in isogenic cells with and without ATM function [AT22IJE-T/pEBS7 (ATM −/−) and ATM-corrected AT22IJE-T/YZ5 (ATM +/+) cells and 293 human embryonic kidney cells transfected with small interfering RNAs targeted to ATM]. In addition, the effect of ATM on IGF-IR expression was assessed in nonisogenic cells with ATM function (HFF + human telomerase reverse transcriptase) and without ATM function (GM5823 + human telomerase reverse transcriptase). Results obtained showed that IGF-IR gene expression and IGF-IR promoter activity were largely reduced in ATM −/− cells. Addition of the radiomimetic agent neocarzinostatin for 4 h, however, induced a significant increase in IGF-IR levels in cells without ATM function. In addition, IGF-I-induced IGF-IR and insulin receptor substrate-1 phosphorylation were greatly impaired in ATM-deficient cells. Furthermore, we identified zinc-finger transcription factors Sp1 and WT1 as potential mediators of the effect of ATM on IGF-IR gene expression. The present data suggests that the IGF-IR gene is a novel downstream target in an ATM-mediated DNA damage response pathway. Deregulated expression of the IGF-IR gene after ionizing radiation may be linked to genomic instability and enhanced transforming capacity.
Developmental Expression of Estrogen Receptor (ER) α and ERβ in the Hamster Ovary: Regulation by Follicle-Stimulating Hormone
Authors: Yang Peixin , Wang Jinrong , Shen Yulei , Roy Shyamal K. 
Published: September 2004

AbstractPerinatal expression of estrogen receptor (ER) protein and mRNA and the influence of FSH on this process were examined by immunofluorescence and RT-PCR using ovaries from fetal (d 13–15 of gestation) and postnatal [postnatal d 1–15 (P1–P15)] hamsters and from 8-d-old hamsters exposed in utero to an anti-FSH serum on d 12 of gestation and saline or equine chorionic gonadotropin (eCG) on P1. A few somatic cells expressing ERα immunoreactivity appeared first on d 14 of gestation and increased markedly by P8–P15 in the interstitial cells and granulosa cells of primordial follicles. In contrast, appreciable ERβ immunoreactivity was localized on d 13 of gestation, and more cells expressed ERβ immunoreactivity by P1–P8. By P7, ERβ immunoreactivity was present in cells adjacent to the oocytes, and by P8, ERβ was preferentially localized in the granulosa cells. Receptor immunoreactivities decreased markedly in P8 ovaries exposed in utero to the FSH antiserum but were reversed with postnatal eCG replacement. Oocytes and somatic cells expressed ERα and ERβ mRNA, and levels of ER mRNA in the ovary increased by P7–P8, corresponding to the appearance of primordial follicles. Thereafter, only ERβ mRNA levels increased progressively with postnatal ovary development. Similar to ER protein, mRNA levels decreased significantly in FSH antiserum-treated ovaries but were restored by eCG. These results indicate that both ER subtypes are expressed in undifferentiated somatic cells and the oocytes during perinatal ovary development in the hamster; however, ERβ expression segregates with the differentiation of granulosa cells. Furthermore, ER expression and differentiation of somatic cells to granulosa cells depend on perinatal FSH action.
Postnatal Regression of Hypothalamic Dopaminergic Neurons in Prolactin-Deficient Snell Dwarf Mice
Authors: Phelps C. J. 
Published: September 2004

AbstractBoth Snell (Pit-1dw or dwj, dw/dw) and Ames (Prophet of Pit-1df, df/df) dwarf mice fail to produce prolactin (PRL) as well as GH due to deficient transcription factor Pit-1 activity and have reduced numbers of hypothalamic PRL-inhibiting area A12 tuberoinfundibular dopaminergic (TIDA) neurons. It has been reported that the TIDA deficit in Ames dwarf mice develops postnatally as a reduction in number after an initial increase that is comparable to that of normal siblings. The present study was designed to characterize A12 TIDA neuronal development in the Snell dwarf (dw/dw) compared with littermate normal mice. Brains of normal (DW/?) and dwj/dwj mice were examined at 7, 14, 21, 30, and ≥ 60 postnatal days (d) by catecholamine fluorescence and quantification of neuron number after tyrosine hydroxylase immunostaining in dopaminergic (DA) areas A12, A13 (medial zona incerta), and A14 (periventricular nucleus). Fluorescence was less in dw/dw than in DW/? A12 perikarya and median eminence but was not reduced in other DA areas, such as substantia nigra, at all ages; A12 fluorescence was virtually absent in Snell dwarf adults. Numbers of TIDA neurons were comparable in normal and Snell dwarf mice at 7 d. In normal (DW/?) mice, A12 neurons increased in number to adult levels at 14 d and were significantly higher than in Snell dwarf (dw/dw) mice at 14 d (P &lt; 0.05) and at subsequent ages (P &lt; 0.01). In Snell dwarf mice, numbers of A12 neurons did not differ at 7, 14, and 21 d, decreased at 30 d (P &lt; 0.05), and reached, at 60 d, 23% of the population in normal sibling mice (P &lt; 0.01 compared with earlier ages). Neuron numbers in nonhypophysiotropic DA area A13 did not vary with age or phenotype. In A14, cell number was higher in both phenotypes at 14 d (P &lt; 0.05 for DW/?; P &lt; 0.01 for dw/dw); neuron number was lower in dw/dw than in DW/? mice at 30 d (P &lt; 0.05) and 60 d (P &lt; 0.01). Thus, compared with normal mice of the same strain, the A12 deficit is more severe in Snell (dw/dw) than in Ames (df/df) dwarf hypothalamus (48% of DF/?), as previously reported, and develops as a decline from the population present at 7 d rather than first increasing. A reduction in A14 neuron number also occurs in the Snell dwarf. Treatment of DW/dw- and dw/dw-containing litters with ovine PRL (50 μg/d, ip), beginning at 12 or 7 d and continuing until 42 d, resulted in TIDA neuron numbers in Snell dwarfs that were lower than those in normal siblings (P &lt; 0.01 for both) but were higher than in untreated adult dwarfs and comparable to the TIDA population size in dwarfs at 7 d, indicating that PRL maintained this maximal number and prevented TIDA neuron dedifferentiation, which occurs in dwarf postnatal development.