bluuebunny/crossref_metadata_2025_split huggingface dataset:
Expression of innate immune complement regulators on brain epithelial cells during human bacterial meningitis
Authors: Canova Cecile , Neal Jim W , Gasque Philippe 
Published: September 2006

Abstract

Background
In meningitis, the cerebrospinal fluid contains high levels of innate immune molecules (e.g. complement) which are essential to ward off the infectious challenge and to promote the infiltration of phagocytes (neutrophils, monocytes). However, epithelial cells of either the ependymal layer, one of the established niche for adult neural stem cells, or of the choroid plexus may be extremely vulnerable to bystander attack by cytotoxic and cytolytic complement components.

Methods
In this study, we assessed the capacity of brain epithelial cells to express membrane-bound complement regulators (ie, CD35, CD46, CD55 and CD59) in vitro and in situ by immunostaining of control and meningitis human brain tissue sections.

Results
Double immunofluorescence experiments for ependymal cell markers (GFAP, S100, ZO-1, E-cadherin) and complement regulators indicated that the human ependymal cell line model was strongly positive for CD55, CD59 compared to weak stainings for CD46 and CD35. In tissues, we found that CD55 was weakly expressed in control choroid plexus and ependyma but was abundantly expressed in meningitis. Anti-CD59 stained both epithelia in apical location while increased CD59 staining was solely demonstrated in inflamed choroid plexus. CD46 and CD35 were not detected in control tissue sections. Conversely, in meningitis, the ependyma, subependyma and choroid plexus epithelia were strongly stained for CD46 and CD35.

Conclusion
This study delineates for the first time the capacity of brain ependymal and epithelial cells to respond to and possibly sustain the innate complement-mediated inflammatory insult.
Short-term arginine deprivation results in large-scale modulation of hepatic gene expression in both normal and tumor cells: microarray bioinformatic analysis
Authors: Leong Hwei Xian , Simkevich Carl , Lesieur-Brooks Anne , Lau Bonnie W , Fugere Celine , Sabo Edmond , Thompson Nancy L 
Published: September 2006

Abstract

Background
We have reported arginine-sensitive regulation of LAT1 amino acid transporter (SLC 7A5) in normal rodent hepatic cells with loss of arginine sensitivity and high level constitutive expression in tumor cells. We hypothesized that liver cell gene expression is highly sensitive to alterations in the amino acid microenvironment and that tumor cells may differ substantially in gene sets sensitive to amino acid availability. To assess the potential number and classes of hepatic genes sensitive to arginine availability at the RNA level and compare these between normal and tumor cells, we used an Affymetrix microarray approach, a paired in vitro model of normal rat hepatic cells and a tumorigenic derivative with triplicate independent replicates. Cells were exposed to arginine-deficient or control conditions for 18 hours in medium formulated to maintain differentiated function.

Results
Initial two-way analysis with a p-value of 0.05 identified 1419 genes in normal cells versus 2175 in tumor cells whose expression was altered in arginine-deficient conditions relative to controls, representing 9–14% of the rat genome. More stringent bioinformatic analysis with 9-way comparisons and a minimum of 2-fold variation narrowed this set to 56 arginine-responsive genes in normal liver cells and 162 in tumor cells. Approximately half the arginine-responsive genes in normal cells overlap with those in tumor cells. Of these, the majority was increased in expression and included multiple growth, survival, and stress-related genes. GADD45, TA1/LAT1, and caspases 11 and 12 were among this group. Previously known amino acid regulated genes were among the pool in both cell types. Available cDNA probes allowed independent validation of microarray data for multiple genes. Among genes downregulated under arginine-deficient conditions were multiple genes involved in cholesterol and fatty acid metabolism. Expression of low-density lipoprotein receptor was decreased in both normal and tumor cells.

Conclusion
Arginine-sensitive regulation appears to be an important homeostatic mechanism to coordinate cell response and nutrient availability in hepatic cells. Genes predicted as arginine-responsive in stringent microarray data analysis were confirmed by Northern blot and RT-PCR. Although the profile of arginine-responsive genes is altered and increased, a considerable portion of the "arginome" is maintained upon neoplastic transformation.
Matrix metalloproteinases, their production by monocytes and macrophages and their potential role in HIV-related diseases
Authors: Webster Nicole L , Crowe Suzanne M 
Published: September 2006

Abstract
Matrix metalloproteinases (MMPs) are zinc-dependent endopeptidases that are a subfamily of metzincins. Matrix metalloproteinases are responsible for much of the turnover of extra-cellular matrix components and are key to a wide range of processes including tissue remodeling and release of biological factors. Imbalance between the MMPs and endogenous tissue inhibitors of metalloproteinases (TIMPs) can result in dysregulation of many biologic processes and lead to the development of malignancy, cardiovascular disease, and autoimmune and inflammatory disorders. MMP production by monocyte/macrophages is dependent on the cell type, state of differentiation, and/or level of activation and whether they are infected, e.g., by HIV-1. MMP expression by HIV-1 infected monocytes and macrophages may alter cellular trafficking and contribute to HIV-associated pathology such as HIV-associated dementia (HAD). This review will provide a classification of the MMP super-family with particular reference to those produced by monocyte/macrophages, describe their regulation and function within the immune system, and indicate their possible roles in the pathogenesis of disease, including HIV-associated dementia.
Roles of neutrophil-mediated inflammatory response in the bony repair of injured growth plate cartilage in young rats
Authors: Chung Rosa , Cool Johanna C , Scherer Michaela A , Foster Bruce K , Xian Cory J 
Published: September 2006

Abstract
Injured growth plate cartilage is often repaired by bony tissue, resulting in impaired bone growth in children. Previously, injury-induced, initial inflammatory response was shown to be an acute inflammatory event containing predominantly neutrophils. To examine potential roles of neutrophils in the bony repair, a neutrophil-neutralizing antiserum or control normal serum was administered systemically in rats with growth plate injury. The inflammatory response was found temporally associated with increased expression of neutrophil chemotactic chemokine cytokine-induced neutrophil chemoattractant-1 and cytokines TNF-α and IL-1β. Following the inflammatory response, mesenchymal infiltration, chondrogenic and osteogenic responses, and bony repair were observed at the injury site. Neutrophil reduction did not significantly affect infiltration of other inflammatory cells and expression of TNF-α and IL-1β and growth factors, platelet-derived growth factor-B and TGF-β1, at the injured growth plate on Day 1 and had no effects on mesenchymal infiltration on Day 4. By Day 10, however, there was a significant reduction in proportion of mesenchymal repair tissue but an increase (although statistically insignificant) in bony trabeculae and a decrease in cartilaginous tissue within the injury site. Consistently, in antiserum-treated rats, there was an increase in expression of osteoblastic differentiation transcription factor cbf-α1 and bone matrix protein osteocalcin and a decrease in chondrogenic transcription factor Sox-9 and cartilage matrix collagen-II in the injured growth plate. These results suggest that injury-induced, neutrophil-mediated inflammatory response appears to suppress mesenchymal cell osteoblastic differentiation but enhance chondrogenic differentiation, and thus, it may be involved in regulating downstream chondrogenic and osteogenic events for growth plate bony repair.
Surgical Mortality in Patients With Esophageal Cancer: Development and Validation of a Simple Risk Score
Authors: Steyerberg Ewout W. , Neville Bridget A. , Koppert Linetta B. , Lemmens Valery E.P.P. , Tilanus Hugo W. , Coebergh Jan-Willem W. , Weeks Jane C. , Earle Craig C. 
Published: September 2006

Purpose Surgery has curative potential in a proportion of patients with esophageal cancer, but is associated with considerable perioperative risks. We aimed to develop and validate a simple risk score for surgical mortality that could be applied to administrative data. Patients and Methods We analyzed 3,592 esophagectomy patients from four cohorts. We applied logistic regression analysis to predict mortality occurring within 30 days after esophagectomy for 1,327 esophageal cancer patients older than 65 years of age, diagnosed between 1991 and 1996 in the linked Surveillance, Epidemiology and End Results (SEER) - Medicare database. A simple score chart for preoperative risk assessment of surgical mortality was developed and validated on three other cohorts, including 714 SEER-Medicare patients diagnosed between 1997 and 1999, 349 patients from a population-based registry in the Netherlands diagnosed between 1993 and 2001, and 1,202 patients from a referral hospital in the Netherlands diagnosed between 1980 and 2002. Results Surgical mortality in the four cohorts was 11% (147 of 1,327), 10% (74 of 714), 7% (25 of 349), and 4% (45 of 1,202), respectively. Predictive patient characteristics included age, comorbidity (cardiac, pulmonary, renal, hepatic, and diabetes), preoperative radiotherapy or combined chemoradiotherapy, and a relatively low hospital volume. At validation, the simple score showed good agreement of predicted risks with observed mortality rates (calibration), but low discrimination (area under the receiver operating characteristic curve 0.58 to 0.66). Conclusion A simple risk score combining clinical characteristics along with hospital volume to predict surgical mortality after esophagectomy from administrative data may form a basis for risk adjustment in quality of care assessment.
Apnetic anesthesia for microlaryngeal surgery
Authors: Nelson Ralph A. , Miller Tom 
Published: September 2006

AbstractAn apneic anesthesia state can be induced and maintained with intravenous thiopental, succinylcholine, and 100 percent oxygen at 6L/min. by catheter. This technique allows an unobstructed view of the endolarynx, avoids trauma of the larynx by an endotracheal tube prior to diagnostic procedures, and precludes seeding the larynx and trachea with malignant cells. The rise in PnCO2 is 3 mm Hg/min. Arrhythmias that occur with laryngeal manipulation bear no relation to the level of arterial carbon dioxide. Patients can tolerate this technique for a minimum of 10 minutes, but eight of 31 patients could not tolerate the condition beyond that time. The subjects with apneic intolerance were found to have relatively low functional residual capacities and were relatively obese. An FRC/WT. above 17 was considered an indicator of high apneic tolerance, and an FRC/WT. below 15 an indicator of a patient who should be monitored closely. WT/IPPB should always be administered postoperatively.
Delayed post‐stapedectomy facial paralysis: A report of five cases
Authors: Althaus Sean R. , House Howard P. 
Published: September 2006

AbstractReview of a series of 2,307 stapedectomy procedures revealed five cases of delayed facial paralysis. The paralysis was clinically complete in three and incomplete in two cases. Onset of weakness occurred from five to 13 days postoperatively. Complete recovery occurred in all cases within eight weeks and surgical intervention was unnecessary.The cause of this uncommon complication is felt to be retrograde edema of the chorda tympani nerve into the facial trunk, or edema of a dehiscent facial nerve in the postoperative period. This phenomenon has not been stressed in the otologic literature to date.Careful evaluation of the patient, close follow‐up with nerve excitability testing in cases of complete paralysis, and steroid and vasodilator therapy is the recommended mode of management. Exploration and decompression of the facial nerve should be strongly considered if the nerve excitability threshold exceeds that of the normal side by 3.5 ma. or more, or should the stimulus threshold be lost altogether.With preservation of nerve excitability thresholds, the outlook for return of function is good, according to this small series.
Angiofibroma: A treatment approach
Authors: Biller Hugh F. , Sessions Donald G. , Ogura Joseph H. 
Published: September 2006

AbstractA systematic treatment approach for nasopharyngeal angiofibromas is presented. Surgery, as the primary treatment modality is advocated. Routine pre‐operative angiography is utilized for diagnosis and delineation of tumor extent. The surgical approach or approaches is dependent upon the tumor extent.
Recognition of Natural Expressions of Emotion by CVA Patients with Damage to the Left or Right Hemisphere
Authors: Bowen Rebecca , McDonald Skye 
Published: September 2006

AbstractThe present study investigated the ability of cerebrovascular accident (CVA) patients to perceive emotions portrayed by realistic stimuli. Statistical analyses demonstrated that CVA patients with damage to either the right or left cerebral hemisphere performed, on average, as well as controls did in perceiving emotions. However, a case study of one patient suggested that there may be a subset of CVA patients with right parieto-occipital damage who have deficits in the perception of negative emotions. The performance of this participant also indicated that deficits in emotion perception are ameliorated to some extent when patients are provided with realistic, complex stimuli that include a range of auditory and visual cues.
The methylenetetrahydrofolate reductase C677T gene mutation is associated with hyperhomocysteinemia, cardiovascular disease and plasma B-type natriuretic peptide levels in Korea
Authors: Cho Sung Eun , Sook Hong Ki , Shin Gil Ja , Chung Wha Soon 
Published: September 2006

AbstractClin Chem Lab Med 2006;44:1070–5.
Rheumatoid factor interference in the determination of carbohydrate antigen 19-9 (CA 19-9)
Authors: Berth Mario , Bosmans Eugene , Everaert Jacques , Dierick Jan , Schiettecatte Johan , Anckaert Ellen , Delanghe Joris 
Published: September 2006

AbstractClin Chem Lab Med 2006;44:1137–9.
Widespread Adaptive Evolution of Drosophila Genes With Sex-Biased Expression
Authors: Pröschel Matthias , Zhang Zhi , Parsch John 
Published: September 2006

AbstractMany genes in higher eukaryotes show sexually dimorphic expression, and these genes tend to be among the most divergent between species. In most cases, however, it is not known whether this rapid divergence is caused by positive selection or if it is due to a relaxation of selective constraint. To distinguish between these two possibilities, we surveyed DNA sequence polymorphism in 91 Drosophila melanogaster genes with male-, female-, or nonsex-biased expression and determined their divergence from the sister species D. simulans. Using several single- and multilocus statistical tests, we estimated the type and strength of selection influencing the evolution of the proteins encoded by genes of each expression class. Adaptive evolution, as indicated by a relative excess of nonsynonymous divergence between species, was common among the sex-biased genes (both male and female). Male-biased genes, in particular, showed a strong and consistent signal of positive selection, while female-biased genes showed more variation in the type of selection they experience. Genes expressed equally in the two sexes, in contrast, showed no evidence for adaptive evolution between D. melanogaster and D. simulans. This suggests that sexual selection and intersexual coevolution are the major forces driving genetic differentiation between species.
History and Structure of Sub-Saharan Populations ofDrosophila melanogaster
Authors: Pool John E , Aquadro Charles F 
Published: September 2006

AbstractDrosophila melanogaster is an important model organism in evolutionary genetics, yet little is known about the population structure and the demographic history of this species within sub-Saharan Africa, which is thought to contain its ancestral range. We surveyed nucleotide variation at four 1-kb fragments in 240 individual lines representing 21 sub-Saharan and 4 Palearctic population samples of D. melanogaster. In agreement with recent studies, we find a small but significant level of genetic differentiation within sub-Saharan Africa. A clear geographic pattern is observed, with eastern and western African populations composing two genetically distinct groups. This pattern may have resulted from a relatively recent establishment of D. melanogaster in western Africa. Eastern populations show greater evidence for long-term stability, consistent with the hypothesis that eastern Africa contains the ancestral range of the species. Three sub-Saharan populations show evidence for cosmopolitan introgression. Apart from those cases, the closest relationships between Palearctic and sub-Saharan populations involve a sample from the rift zone (Uganda), suggesting that the progenitors of Palearctic D. melanogaster might have come from this region. Finally, we find a large excess of singleton polymorphisms in the full data set, which is best explained by a combination of population growth and purifying selection.
Mutator Phenotype ofCaenorhabditis elegansDNA Damage Checkpoint Mutants
Authors: Harris Jasper , Lowden Mia , Clejan Iuval , Tzoneva Monika , Thomas James H , Hodgkin Jonathan , Ahmed Shawn 
Published: September 2006

AbstractDNA damage response proteins identify sites of DNA damage and signal to downstream effectors that orchestrate either apoptosis or arrest of the cell cycle and DNA repair. The C. elegans DNA damage response mutants mrt-2, hus-1, and clk-2(mn159) displayed 8- to 15-fold increases in the frequency of spontaneous mutation in their germlines. Many of these mutations were small- to medium-sized deletions, some of which had unusual sequences at their breakpoints such as purine-rich tracts or direct or inverted repeats. Although DNA-damage-induced apoptosis is abrogated in the mrt-2, hus-1, and clk-2 mutant backgrounds, lack of the apoptotic branch of the DNA damage response pathway in cep-1/p53, ced-3, and ced-4 mutants did not result in a Mutator phenotype. Thus, DNA damage checkpoint proteins suppress the frequency of mutation by ensuring that spontaneous DNA damage is accurately repaired in C. elegans germ cells. Although DNA damage response defects that predispose humans to cancer are known to result in large-scale chromosome aberrations, our results suggest that small- to medium-sized deletions may also play roles in the development of cancer.
A Genetic Linkage Map of the Hermaphrodite Teleost Fish Sparus aurata L.
Authors: Franch Rafaella , Louro Bruno , Tsalavouta Matina , Chatziplis Dimitris , Tsigenopoulos Costas S , Sarropoulou Elena , Antonello Jenny , Magoulas Andonis , Mylonas Constantinos C , Babbucci Massimiliano , Patarnello Tomaso , Power Deborah M , Kotoulas Giorgos , Bargelloni Luca 
Published: September 2006

Abstract
The gilthead sea bream (Sparus aurata L.) is a marine fish of great importance for fisheries and aquaculture. It has also a peculiar sex-determination system, being a protandrous hermaphrodite. Here we report the construction of a first-generation genetic linkage map for S. aurata, based on 204 microsatellite markers. Twenty-six linkage groups (LG) were found. The total map length was 1241.9 cM. The ratio between sex-specific map lengths was 1:1.2 (male:female). Comparison with a preliminary radiation hybrid (RH) map reveals a good concordance, as all markers located in a single LG are located in a single RH group, except for Ad-25 and CId-31. Comparison with the Tetraodon nigroviridis genome revealed a considerable number of evolutionary conserved regions (ECRs) between the two species. The mean size of ECRs was 182 bp (sequence identity 60–90%). Forty-one ECRs have a known chromosomal location in the pufferfish genome. Despite the limited number of anchoring points, significant syntenic relationships were found. The linkage map presented here provides a robust comparative framework for QTL analysis in S. aurata and is a step toward the identification of genetic loci involved both in the determination of economically important traits and in the individual timing of sex reversal.
Amh and Dmrta2 Genes Map to Tilapia (Oreochromis spp.) Linkage Group 23 Within Quantitative Trait Locus Regions for Sex Determination
Authors: Shirak Andrey , Seroussi Eyal , Cnaani Avner , Howe Aimee E , Domokhovsky Raisa , Zilberman Noam , Kocher Thomas D , Hulata Gideon , Ron Micha 
Published: September 2006

Abstract
Recent studies have revealed that the major genes of the mammalian sex determination pathway are also involved in sex determination of fish. Several studies have reported QTL in various species and strains of tilapia, regions contributing to sex determination have been identified on linkage groups 1, 3, and 23. Genes contributing to sex-specific mortality have been detected on linkage groups 2, 6, and 23. To test whether the same genes might control sex determination in mammals and fishes, we mapped 11 genes that are considered putative master key regulators of sex determination: Amh, Cyp19, Dax1, Dmrt2, Dmrta2, Fhl3l, Foxl2, Ixl, Lhx9, Sf1, and Sox8. We identified polymorphisms in noncoding regions of these genes and genotyped these sites for 90 individuals of an F2 mapping family. Mapping of Dax1 joined LG16 and LG21 into a single linkage group. The Amh and Dmrta2 genes were mapped to two distinct regions of LG23. The Amh gene was mapped 5 cM from UNH879 within a QTL region for sex determination and 2 cM from UNH216 within a QTL region for sex-specific mortality. Dmrta2 was mapped 4 cM from UNH848 within another QTL region for sex determination. Cyp19 was mapped to LG1 far from a previously reported QTL region for sex determination on this chromosome. Seven other candidate genes mapped to LG4, -11, -12, -14, and -17.
Genetic Dissection of Intermated Recombinant Inbred Lines Using a New Genetic Map of Maize
Authors: Fu Yan , Wen Tsui-Jung , Ronin Yefim I , Chen Hsin D , Guo Ling , Mester David I , Yang Yongjie , Lee Michael , Korol Abraham B , Ashlock Daniel A , Schnable Patrick S 
Published: September 2006

Abstract
A new genetic map of maize, ISU–IBM Map4, that integrates 2029 existing markers with 1329 new indel polymorphism (IDP) markers has been developed using intermated recombinant inbred lines (IRILs) from the intermated B73 × Mo17 (IBM) population. The website http://magi.plantgenomics.iastate.edu provides access to IDP primer sequences, sequences from which IDP primers were designed, optimized marker-specific PCR conditions, and polymorphism data for all IDP markers. This new gene-based genetic map will facilitate a wide variety of genetic and genomic research projects, including map-based genome sequencing and gene cloning. The mosaic structures of the genomes of 91 IRILs, an important resource for identifying and mapping QTL and eQTL, were defined. Analyses of segregation data associated with markers genotyped in three B73/Mo17-derived mapping populations (F2, Syn5, and IBM) demonstrate that allele frequencies were significantly altered during the development of the IBM IRILs. The observations that two segregation distortion regions overlap with maize flowering-time QTL suggest that the altered allele frequencies were a consequence of inadvertent selection. Detection of two-locus gamete disequilibrium provides another means to extract functional genomic data from well-characterized plant RILs.