bluuebunny/crossref_metadata_2025_split huggingface dataset:
Temporary Balloon Occlusion of the Cavernous Carotid Artery for Removal of an Orbital and Intracranial Foreign Body: Case Report
Authors: Cunningham Edwin J. , Albani Barbara , Masaryk Thomas J. , Rasmussen Peter A. 
Published: October 2004

AbstractOBJECTIVE AND IMPORTANCE:We describe the first reported use of temporary balloon occlusion of the cavernous internal carotid artery for controlled removal of a foreign object from the cavernous sinus. This endovascular approach may be an alternative to craniotomy in highly selected cases.CLINICAL PRESENTATION:A 34-year-old incarcerated male attempted suicide by stabbing the earpiece of his glasses through his right orbit into the intracranial compartment. He presented with complete ophthalmoplegia. The earpiece traversed the cavernous sinus, penetrating its posterior wall to enter the perimesencephalic cistern and cerebellum. Angiography demonstrated a small direct carotid-cavernous fistula.INTERVENTION:Removal of the foreign body was performed under general anesthesia in the angiography suite with the operating room on standby. Nondetachable and detachable balloons were inflated in the cavernous carotid artery to provide vascular control while the foreign body was withdrawn from the cranium at the orbit. Follow-up angiographic runs with the balloons deflated revealed minimal arteriovenous shunting, which disappeared on subsequent studies. The balloons were removed. The patient remained neurologically stable with his baseline right ophthalmoplegia and V1–V2 hemianesthesia. At the 6-week follow-up, the patient remained clinically stable with no evidence of carotid-cavernous fistula or interval abscess formation.CONCLUSION:Endovascular temporary balloon occlusion of the cavernous carotid artery provides immediate control of the vessel (with an option of permanent carotid sacrifice), allowing removal of a foreign body without craniotomy in appropriate cases.
Linear Accelerator Radiosurgery in the Treatment of Brain Metastases
Authors: Ulm Arthur J. , Friedman William A. , Bova Frank J. , Bradshaw Patrick , Amdur Robert J. , Mendenhall William M. 
Published: October 2004

Abstract

OBJECTIVE:
To review a 12-year experience treating metastatic brain disease with linear accelerator-based stereotactic radiosurgery (SRS).

METHODS:
We performed a retrospective analysis of all patients treated between 1989 and 2001 with linear accelerator radiosurgery for brain metastases. Patients were followed up both clinically and with imaging studies to document local control, regional control, and survival. Demographic data, dosing parameters, number of lesions, histology, history of whole-brain radiation therapy, and other factors were obtained prospectively. Cox proportional-hazards regression with multivariate and univariate analysis was performed with Stata 8.0 software.

RESULTS:
A total of 383 patients received SRS for brain metastases during the study interval. Median survival was 9 months. Patients with tumor-type melanoma or multiple metastatic lesions had decreased survival. Actuarial 1-year local control was 75%. Differences in regional control rates were not statistically significant between patients treated with SRS and whole-brain radiation therapy versus SRS alone.

CONCLUSION:
Radiosurgery is an effective and safe method for treating selected patients with brain metastases.
Preoperative Localization of the Carotid Bifurcation for Carotid Endarterectomy Using Magnetic Resonance Angiography without Tomography: Technical Note
Authors: Weaver Kyle D. , Huang Judy , Tamargo Rafael J. , Bernard Estrada J. 
Published: October 2004

Abstract

OBJECTIVE:
Carotid endarterectomy without angiography is becoming increasingly common. Magnetic resonance imaging accurately demonstrates vascular anatomy and the degree of stenosis but may not localize the cervical carotid bifurcation for incision planning without tomography. We report a method for preoperative localization of the bifurcation using the relatively constant axial coplanar relationship between the horizontal petrous (C2) segment of the internal carotid artery and the external auditory canal (EAC).

METHODS:
The vertical distance between the midpoint of the C2 segment and the cervical carotid bifurcation was measured on magnetic resonance angiography images in five patients. Before surgery, a transverse incision was planned the same distance below the EAC. After exposure, the distance from the EAC to the bifurcation was measured with calipers. The distances from the anterior, posterior, superior, and inferior wound margins during retraction were also measured.

RESULTS:
The mean vertical distance between the C2 segment and the bifurcation was 7.2 cm on preoperative imaging and 7.6 cm between the EAC and bifurcation using intraoperative measurement (difference, 0.4 cm). The average distances between the midportion of the bifurcation and the wound margins after retractor placement were 2.9, 2.4, 2.8, and 3.5 cm for anterior, posterior, superior, and inferior measurements, respectively.

CONCLUSION:
The C2 segment-cervical carotid bifurcation distance may be used to estimate accurately the vertical distance from the EAC to the bifurcation. When coupled with a transverse incision for carotid endarterectomy, the use of this preoperative measurement produces a target well centered within the operative field.
Embryonic signaling centers expressing BMP, WNT and FGF proteins interact to pattern the cerebral cortex
Authors: Shimogori Tomomi , Banuchi Victoria , Ng Hanyann Y. , Strauss Jonathan B. , Grove Elizabeth A. 
Published: October 2004

Recent findings implicate embryonic signaling centers in patterning the mammalian cerebral cortex. We used mouse in utero electroporation and mutant analysis to test whether cortical signaling sources interact to regulate one another. We identified interactions between the cortical hem, rich in Wingless-Int (WNT) proteins and bone morphogenetic proteins (BMPs), and an anterior telencephalic source of fibroblast growth factors (FGFs).Expanding the FGF8 domain suppressed Wnt2b, Wnt3a and Wnt5a expression in the hem. Next to the hem, the hippocampus was shrunken, consistent with its dependence for growth on a hem-derived WNT signal. Maintenance of hem WNT signaling and hippocampal development thus require a constraint on the FGF8 source, which is likely to be supplied by BMP activity. When endogenous BMP signaling is inhibited by noggin, robust Fgf8 expression appears ectopically in the cortical primordium.Abnormal signaling centers were further investigated in mice lacking the transcription factor EMX2, in which FGF8 activity is increased, WNT expression reduced, and the hippocampus defective. Suggesting that these defects are causally related, sequestering FGF8 in Emx2 homozygous mutants substantially recovered WNT expression in the hem and partially rescued hippocampal development.Because noggin can induce Fgf8 expression, we examined noggin and BMP signaling in the Emx2 mutant. As the telencephalic vesicle closed, Nog expression was expanded and BMP activity reduced,potentially leading to FGF8 upregulation. Our findings point to a cross-regulation of BMP, FGF, and WNT signaling in the early telencephalon,integrated by EMX2, and required for normal cortical development.
Three Novel Mutations in the Apolipoprotein E Gene in a Sample of Individuals with Type 2 Diabetes Mellitus
Authors: Stephens Jeffrey W , Sozen M Mert , Whittall Ros A , Caslake Muriel J , Bedford Dorothy , Acharya Jayshree , Hurel Steven J , Humphries Steve E 
Published: October 2004

AbstractBackground: Apolipoprotein E (apoE) is found in association with triglyceride-rich lipoproteins and is the ligand for the removal of these particles from the plasma. Genetic variations in exon 4 lead to three common gene variants: E2, E3, and E4.Methods: We performed apoE genotyping in 765 individuals with type 2 diabetes.Results: We identified three new variant heteroduplex patterns. Sequencing of these variants revealed three novel mutations that were related to biochemical and clinical characteristics. One mutation produced a frameshift at amino acid position 166, which predicted termination of protein synthesis. This individual had a heteroduplex pattern and sequence of E3E3, which was associated with a change in the plasma isoelectric focusing pattern and a 70% lower plasma concentration of apoE compared with healthy individuals. The other mutations were both single base changes. A CGC&gt;CAC change at amino acid position 150 predicted a substitution of Arg&gt;His. This individual had a heteroduplex pattern and sequence of E2E2, which was not associated with major changes in plasma lipids or apoE concentration. The third individual had a CGC&gt;CCC base change at amino acid position 114, which predicted an Arg&gt;Pro change. This person had a heteroduplex pattern and sequence of E3E3, higher plasma total cholesterol, and moderately decreased plasma apoE.Conclusions: The frequency of new mutations in this sample (1 in 255) is higher than that of a healthy population (1 in 7900). Further screening for common apoE gene variants in individuals at risk for dyslipidemia may reveal abnormal heteroduplex patterns and uncover further mutations in this important lipid-regulating gene.
Fibroblast Growth Factor Receptor Signaling Promotes Radial Glial Identity and Interacts with Notch1 Signaling in Telencephalic Progenitors
Authors: Yoon Keejung , Nery Susana , Rutlin Michael L. , Radtke Freddy , Fishell Gord , Gaiano Nicholas 
Published: October 2004

The Notch and fibroblast growth factor (FGF) pathways both regulate cell fate specification during mammalian neural development. We have shown previously that Notch1 activation in the murine forebrain promotes radial glial identity. This result, together with recent evidence that radial glia can be progenitors, suggested that Notch1 signaling might promote progenitor and radial glial character simultaneously. Consistent with this idea, we found that in addition to promoting radial glial characterin vivo, activated Notch1 (ActN1) increased the frequency of embryonic day 14.5 (E14.5) ganglionic eminence (GE) progenitors that grew into neurospheres in FGF2. Constitutive activation of C-promoter binding factor (CBF1), a Notch pathway effector, also increased neurosphere frequency in FGF2, suggesting that the effect of Notch1 on FGF responsiveness is mediated by CBF1.The observation that ActN1 promoted FGF responsiveness in telencephalic progenitors prompted us to examine the effect of FGF pathway activationin vivo. We focused on FGFR2 because it is expressed in radial glia in the GEs where ActN1 increases FGF2 neurosphere frequency, but not in the septum where it does not. Like ActN1, activated FGFR2 (ActFGFR2) promoted radial glial characterin vivo. However, unlike ActN1, ActFGFR2 did not enhance neurosphere frequency at E14.5. Additional analysis demonstrated that, unexpectedly, neither ActFGFR2 nor ActFGFR1 could replace the need for ligand in promoting neurosphere proliferation. This study suggests that telencephalic progenitors with radial glial morphology are maintained by interactions between the Notch and FGF pathways, and that the mechanisms by which FGF signaling promotes radial glial characterin vivoand progenitor proliferationin vitrocan be uncoupled.
Geometrische Normale zur Prüfung von Konturmessgeräten (Geometrical Standards for Testing of Contour Measuring Devices)
Authors: Neugebauer Michael , Jusko Otto , Wäldele Franz , Kedziora Heinz-Joachim , Meyer Maik , Volk Raimund 
Published: October 2004

Abstract
Es wird ein neu entwickeltes geometrisches Normal zur Prüfung von Konturmessgeräten im Tastschnittverfahren beschrieben. Dieses Arbeitsnormal vereint konvexe und konkave Geometrieelemente und verkörpert über 25 Radien, Winkel, laterale und vertikale Abstände. Die Kalibrierung erfolgt derzeit mit Koordinatenmessgeräten in der PTB. Die Kalibrierunsicherheiten betragen dabei 1 bis 1,5 μm für Abstände und Radien sowie 0,02° für Winkel. Für geplante Kalibrierungen mit Konturmessgeräten wurde zur Rückverfolgbarkeit der Messungen zusätzlich ein Transfernormal entwickelt.
Online-Analyse mit Lab-on-Chip-Systemen (Online Analysis with Lab-on-Chip Systems)
Authors: Herrmann Sigrun , Vonau Winfried 
Published: October 2004

Abstract
Es werden Ergebnisse der Entwicklung und Erprobung unterschiedlicher Lab-on-Chip-Systeme auf der Basis von elektrochemischen Sensoren vorgestellt. Das Design und der technologisch anspruchsvolle Herstellungsprozess von Sensorchips, aber auch Möglichkeiten der Verkapselung werden beschrieben. Die Entwicklung planarer Mikrosensorsysteme eröffnet beispielsweise die Möglichkeit zur Online-Analyse von Körperflüssigkeiten und zur Charakterisierung von Vitalitätskriterien. Anhand der ausgewählten Analysenbeispiele werden das breite Spektrum prinzipieller Einsatzmöglichkeiten für Lab-on-Chip-Systeme, gleichzeitig jedoch auch die Bedeutung der Materialauswahl für die Realisierung sensorspezifischer Anforderungen und applikationsbezogener Erfordernisse, wie z.B. Bio- oder Zellkompatibilität, deutlich.
Lrg1p Is a Rho1 GTPase-Activating Protein Required for Efficient Cell Fusion in Yeast
Authors: Fitch Pamela G , Gammie Alison E , Lee Debbie J , de Candal Valeria Brizzio , Rose Mark D 
Published: October 2004

Abstract
To identify additional cell fusion genes in Saccharomyces cerevisiae, we performed a high-copy suppressor screen of fus2Δ. Higher dosage of three genes, BEM1, LRG1, and FUS1, partially suppressed the fus2Δ cell fusion defect. BEM1 and FUS1 were high-copy suppressors of many cell-fusion-defective mutations, whereas LRG1 suppressed only fus2Δ and rvs161Δ. Lrg1p contains a Rho-GAP homologous region. Complete deletion of LRG1, as well as deletion of the Rho-GAP coding region, caused decreased rates of cell fusion and diploid formation comparable to that of fus2Δ. Furthermore, lrg1Δ caused a more severe mating defect in combination with other cell fusion mutations. Consistent with an involvement in cell fusion, Lrg1p localized to the tip of the mating projection. Lrg1p-GAP domain strongly and specifically stimulated the GTPase activity of Rho1p, a regulator of β(1-3)-glucan synthase in vitro. β(1-3)-glucan deposition was increased in lrg1Δ strains and mislocalized to the tip of the mating projection in fus2Δ strains. High-copy LRG1 suppressed the mislocalization of β(1-3) glucan in fus2Δ strains. We conclude that Lrg1p is a Rho1p-GAP involved in cell fusion and speculate that it acts to locally inhibit cell wall synthesis to aid in the close apposition of the plasma membranes of mating cells.
Meiotic Chromosome Synapsis in Yeast Can Occur Without Spo11-Induced DNA Double-Strand Breaks
Authors: Bhuiyan Hasanuzzaman , Schmekel Karin 
Published: October 2004

Abstract
Proper chromosome segregation and formation of viable gametes depend on synapsis and recombination between homologous chromosomes during meiosis. Previous reports have shown that the synaptic structures, the synaptonemal complexes (SCs), do not occur in yeast cells with the SPO11 gene removed. The Spo11 enzyme makes double-strand breaks (DSBs) in the DNA and thereby initiates recombination. The view has thus developed that synapsis in yeast strictly depends on the initiation of recombination. Synapsis in some other species (Drosophila melanogaster and Caenorhabditis elegans) is independent of recombination events, and SCs are found in spo11 mutants. This difference between species led us to reexamine spo11 deletion mutants of yeast. Using antibodies against Zip1, a SC component, we found that a small fraction (1%) of the spo11 null mutant cells can indeed form wild-type-like SCs. We further looked for synapsis in a spo11 mutant strain that accumulates pachytene cells (spo11Δ ndt80Δ), and found that the frequency of cells with apparently complete SC formation was 10%. Other phenotypic criteria, such as spore viability and homologous chromosome juxtaposition measured by FISH labeling of chromosomal markers, agree with several previous reports of the spo11 mutant. Our results demonstrate that although the Spo11-induced DSBs obviously promote synapsis in yeast, the presence of Spo11 is not an absolute requirement for synapsis.
Genetic Dissection of Nutritional Copper Signaling in Chlamydomonas Distinguishes Regulatory and Target Genes
Authors: Eriksson Mats , Moseley Jeffrey L , Tottey Stephen , del Campo Jose A , Quinn Jeanette , Kim Youngbae , Merchant Sabeeha 
Published: October 2004

Abstract
A genetic screen for Chlamydomonas reinhardtii mutants with copper-dependent growth or nonphotosynthetic phenotypes revealed three loci, COPPER RESPONSE REGULATOR 1 (CRR1), COPPER RESPONSE DEFECT 1 (CRD1), and COPPER RESPONSE DEFECT 2 (CRD2), distinguished as regulatory or target genes on the basis of phenotype. CRR1 was shown previously to be required for transcriptional activation of target genes like CYC6, CPX1, and CRD1, encoding, respectively, cytochrome c6 (which is a heme-containing substitute for copper-containing plastocyanin), coproporphyrinogen III oxidase, and Mg-protoporphyrin IX monomethylester cyclase. We show here that CRR1 is required also for normal accumulation of copper proteins like plastocyanin and ferroxidase in copper-replete medium and for apoplastocyanin degradation in copper-deficient medium, indicating that a single pathway controls nutritional copper homeostasis at multiple levels. CRR1 is linked to the SUPPRESSOR OF PCY1-AC208 13 (SOP13) locus, which corresponds to a gain-of-function mutation resulting in copper-independent expression of CYC6. CRR1 is required also for hypoxic growth, pointing to a physiologically meaningful regulatory connection between copper deficiency and hypoxia. The growth phenotype of crr1 strains results primarily from secondary iron deficiency owing to reduced ferroxidase abundance, suggesting a role for CRR1 in copper distribution to a multicopper ferroxidase involved in iron assimilation. Mutations at the CRD2 locus also result in copper-conditional iron deficiency, which is consistent with a function for CRD2 in a pathway for copper delivery to the ferroxidase. Taken together, the observations argue for a specialized copper-deficiency adaptation for iron uptake in Chlamydomonas.
Resistance to Volatile Anesthetics by Mutations Enhancing Excitatory Neurotransmitter Release in Caenorhabditis elegans
Authors: Hawasli Ammar H , Saifee Owais , Liu Christine , Nonet Michael L , Crowder C Michael 
Published: October 2004

AbstractThe molecular mechanisms whereby volatile general anesthetics (VAs) disrupt behavior remain undefined. In Caenorhabditis elegans mutations in the gene unc-64, which encodes the presynaptic protein syntaxin 1A, produce large allele-specific differences in VA sensitivity. UNC-64 syntaxin normally functions to mediate fusion of neurotransmitter vesicles with the presynaptic membrane. The precise role of syntaxin in the VA mechanism is as yet unclear, but a variety of results suggests that a protein interacting with syntaxin to regulate neurotransmitter release is essential for VA action in C. elegans. To identify additional proteins that function with syntaxin to control neurotransmitter release and VA action, we screened for suppressors of the phenotypes produced by unc-64 reduction of function. Loss-of-function mutations in slo-1, which encodes a Ca2+-activated K+ channel, and in unc-43, which encodes CaM-kinase II, and a gain-of-function mutation in egl-30, which encodes Gqα, were isolated as syntaxin suppressors. The slo-1 and egl-30 mutations conferred resistance to VAs, but unc-43 mutations did not. The effects of slo-1 and egl-30 on VA sensitivity can be explained by their actions upstream or parallel to syntaxin to increase the level of excitatory neurotransmitter release. These results strengthen the link between transmitter release and VA action.
Role of a Nonselective de Novo DNA Methyltransferase in Maternal Inheritance of Chloroplast Genes in the Green Alga, Chlamydomonas reinhardtii
Authors: Nishiyama Rie , Wada Yuko , Mibu Momoka , Yamaguchi Yube , Shimogawara Kosuke , Sano Hiroshi 
Published: October 2004

Abstract
In the green alga, Chlamydomonas, chloroplast DNA is maternally transmitted to the offspring. We previously hypothesized that the underlying molecular mechanism involves specific methylation of maternal gamete DNA before mating, protecting against degradation. To obtain direct evidence for this, we focused on a DNA methyltransferase, DMT1, which was previously shown to be localized in chloroplasts. The full-length DMT1 protein with a molecular mass of 150 kD was expressed in insect cells, and its catalytic activity was determined. In vitro assays using synthetic DNA indicated methylation of all cytosine residues, with no clear selectivity in terms of the neighboring nucleotides. Subsequently, transgenic paternal cells constitutively expressing DMT1 were constructed and direct methylation mapping assays of their DNA showed a clear nonselective methylation of chloroplast DNA. When transgenic paternal cells were crossed with wild-type maternal cells, the frequency of biparental and paternal offspring of chloroplasts increased up to 23% while between wild-type strains it was ∼3%. The results indicate that DMT1 is a novel type of DNA methyltransferase with a nonselective cytosine methylation activity, and that chloroplast DNA methylation by DMT1 is one of factors influencing maternal inheritance of chloroplast genes.
Accuracy and Power of Statistical Methods for Detecting Adaptive Evolution in Protein Coding Sequences and for Identifying Positively Selected Sites
Authors: Wong Wendy S W , Yang Ziheng , Goldman Nick , Nielsen Rasmus 
Published: October 2004

Abstract
The parsimony method of Suzuki and Gojobori (1999) and the maximum likelihood method developed from the work of Nielsen and Yang (1998) are two widely used methods for detecting positive selection in homologous protein coding sequences. Both methods consider an excess of nonsynonymous (replacement) substitutions as evidence for positive selection. Previously published simulation studies comparing the performance of the two methods show contradictory results. Here we conduct a more thorough simulation study to cover and extend the parameter space used in previous studies. We also reanalyzed an HLA data set that was previously proposed to cause problems when analyzed using the maximum likelihood method. Our new simulations and a reanalysis of the HLA data demonstrate that the maximum likelihood method has good power and accuracy in detecting positive selection over a wide range of parameter values. Previous studies reporting poor performance of the method appear to be due to numerical problems in the optimization algorithms and did not reflect the true performance of the method. The parsimony method has a very low rate of false positives but very little power for detecting positive selection or identifying positively selected sites.