bluuebunny/crossref_metadata_2025_split huggingface dataset:
Joins of projective varieties and multisecant spaces
Authors: Ballico E. 
Published: September 2004

Let

X
1

,
…
,

X
s

⊂

P

N

X_1,\dots ,X_s \subset {\mathbf {P}}^N

,

s
≥
1

s \ge 1

, be integral varieties. For any integers

k
i

>
0

k_i>0

,

1
≤
i
≤
s

1 \le i \le s

, and

t
≥
0

t \ge 0

set

k
→

:=
(

k
1

,
…
,

k
s

)

\vec {k}:= (k_1,\dots ,k_s)

and

X
→

:=
(

X
1

,
…
,

X
s

)

\vec {X}:= (X_1,\dots ,X_s)

. Let

Sec

(

X
→

;
t
,

k
→

)

\mbox {Sec}(\vec {X} ;t,\vec {k} )

be the set of all linear

t
t

-spaces contained in a linear

(

k
1

+
⋯
+

k
s

−
1
)

(k_1+\cdots +k_s-1)

-space spanned by

k
1

k_1

points of

X
1

X_1

,

k
2

k_2

points of

X
2

X_2

, …,

k
s

k_s

points of

X
s

X_s

. Here we study some cases where

Sec

(

X
→

;
t
,

k
→

)

\mbox {Sec}(\vec {X} ;t,\vec {k} )

has the expected dimension. The case

s
=
1

s=1

was recently considered by Chiantini and Coppens and we follow their ideas. The two main results of the paper consider cases where each

X
i

X_i

is a surface, more particularly:

s
=
3
,

k
1

=

k
2

=

k
3

=
1

and

t
=
1

\begin{equation*} s=3, k_1=k_2=k_3=1 \ \mbox {and} \ t=1 \end{equation*}

or

s
=
2
,

k
1

=
2
,

k
2

=
1

and

t
=
1
.

\begin{equation*} s=2, k_1=2, k_2 = 1 \ \mbox {and} \ t=1 . \end{equation*}
Filling analytic sets by the derivatives of 𝐶¹-smooth bumps
Authors: Fabian Marián , Kalenda Ondřej , Kolář Jan 
Published: September 2004

If

X
X

is an infinite-dimensional Banach space, with separable dual, and

M
⊂

X
∗

M\subset X^*

is an analytic set such that any point

x
∗

∈
M

x^*\in M

can be reached from

0
0

by a continuous path contained (except for the point

x
∗

x^*

) in the interior of

M
M

, then

M
M

is the range of the derivative of a

C
1

C^1

-smooth function on

X
X

with bounded nonempty support.
Analysis of array CGH data: from signal ratio to gain and loss of DNA regions
Authors: Hupé Philippe , Stransky Nicolas , Thiery Jean-Paul , Radvanyi François , Barillot Emmanuel 
Published: September 2004

Abstract
Motivation: Genomic DNA regions are frequently lost or gained during tumor progression. Array Comparative Genomic Hybridization (array CGH) technology makes it possible to assess these changes in DNA in cancers, by comparison with a normal reference. The identification of systematically deleted or amplified genomic regions in a set of tumors enables biologists to identify genes involved in cancer progression because tumor suppressor genes are thought to be located in lost genomic regions and oncogenes, in gained regions. Array CGH profiles should also improve the classification of tumors. The achievement of these goals requires a methodology for detecting the breakpoints delimiting altered regions in genomic patterns and assigning a status (normal, gained or lost) to each chromosomal region.
Results: We have developed a methodology for the automatic detection of breakpoints from array CGH profile, and the assignment of a status to each chromosomal region. The breakpoint detection step is based on the Adaptive Weights Smoothing (AWS) procedure and provides highly convincing results: our algorithm detects 97, 100 and 94% of breakpoints in simulated data, karyotyping results and manually analyzed profiles, respectively. The percentage of correctly assigned statuses ranges from 98.9 to 99.8% for simulated data and is 100% for karyotyping results. Our algorithm also outperforms other solutions on a public reference dataset.
Availability: The R package GLAD (Gain and Loss Analysis of DNA) is available upon request
Malignant Hyperthermia in North America
Authors: Sei Yoshitatsu , Sambuughin Nyamkhishig N. , Davis Edward J. , Sachs Daniel , Cuenca Phil B. , Brandom Barbara W. , Tautz Timothy , Rosenberg Henry , Nelson Thomas E. , Muldoon Sheila M. 
Published: September 2004

Background
Malignant hyperthermia (MH) is a pharmacogenetic disorder of skeletal muscle, manifested as a life-threatening hypermetabolic crisis after exposure to anesthetics. Type I ryanodine receptor 1 is the primary gene responsible for susceptibility to MH as well as central core disease, a congenital myopathy that predisposes susceptibility to MH. More than 40 mutations in the RyR1 gene cluster in three coding regions: the N-terminus, central, and C-terminus regions. However, the frequency of mutations in each region has not been studied in the North American MH-susceptible population.

Methods
The authors tested 124 unrelated patients with MH susceptibility for the presence of mutations in the N-terminus (exons 2, 6, 9, 11, 12, and 17), central (exons 39, 40, 44, 45, and 46), and C-terminus (exons 95, 100, 101, and 102) regions.

Results
Fourteen mutations have been identified in 29 of 124 MH-susceptible patients (23%). Approximately 70% of the mutations, which include a novel mutation, Ala 2437Val, were in the central region. In 8 patients (28%), mutations were identified in the N-terminus region. Screening the C-terminus region yielded a novel mutation, Leu4824Pro, in a single patient with a diagnosis of central core disease.

Conclusions
The detection rate for mutations is only 23% by screening mutations (or exons) listed in the 2002 North American consensus panel. The implications from this study suggest that testing the central region first is currently the most effective screening strategy for the North American population. Screening more exons in the three hot spots may be needed to find an accurate frequency of mutations in the RyR1 gene.
Teaching Residents Pediatric Fiberoptic Intubation of the Trachea
Authors: Wheeler Melissa , Roth Andrew G. , Dsida Richard M. , Rae Bronwyn , Seshadri Roopa , Sullivan Christine L. , Heffner Corri L. , Coté Charles J. 
Published: September 2004

Background
The authors' hypothesis was that a video-assisted technique should speed resident skill acquisition for flexible fiberoptic oral tracheal intubation (FI) of pediatric patients because the attending anesthesiologist can provide targeted instruction when sharing the view of the airway as the resident attempts intubation.

Methods
Twenty Clinical Anesthesia year 2 residents, novices in pediatric FI, were randomly assigned to either the traditional group (traditional eyepiece FI) or the video group (video-assisted FI). One of two attending anesthesiologists supervised each resident during FI of 15 healthy children, aged 1-6 yr. The time from mask removal to confirmation of endotracheal tube placement by end-tidal carbon dioxide detection was recorded. Intubation attempts were limited to 3 min; up to three attempts were allowed. The primary outcome measure, time to success or failure, was compared between groups. Failure rate and number of attempts were also compared between groups.

Results
Three hundred patient intubations were attempted; eight failed. On average, the residents in the video group were faster, were three times more likely to successfully intubate at any given time during an attempt, and required fewer attempts per patient compared to those in the traditional group.

Conclusions
The video system seems to be superior for teaching residents fiberoptic intubation in children.
Apolipoprotein E Genotype and Cognitive Dysfunction after Noncardiac Surgery
Authors: Abildstrom Hanne , Christiansen Michael , Siersma Volkert D. , Rasmussen Lars S. 
Published: September 2004

Background
Apolipoprotein E is important in recovery after neuronal damage. The epsilon4 allele of the apolipoprotein E gene has been shown as a risk factor for Alzheimer disease, poor outcome after cerebral injury, and accelerated cognitive decline with normal aging. The authors hypothesized that patients with the epsilon4 allele would have an increased risk of postoperative cognitive dysfunction (POCD) after noncardiac surgery.

Methods
In a multicenter study, a total of 976 patients aged 40 yr and older undergoing noncardiac surgery were tested preoperatively and 1 week and 3 months after surgery with a neuropsychological test battery comprising seven subtests. POCD was defined as a decline in test performance of more than 2 SD from the expected. Apolipoprotein E genotypes were determined by blood sample analysis at a central laboratory. Multivariate logistic regression analysis with POCD as the dependent variable assessed presence of the epsilon4 allele (yes/no) and other possible risk factors.

Results
The epsilon4 allele was found in 272 patients. One week after surgery, the incidence of POCD was 11.7% in patients with the epsilon4 allele and 9.9% in patients without the epsilon4 allele (P = 0.41). Three months later, POCD was found in 10.3% of patients with the epsilon4 allele and in 8.4% of patients without the epsilon4 allele (P = 0.40). Multivariate logistic regression analysis did not identify the epsilon4 allele as a risk factor at 1 week (P = 0.33) or 3 months (P = 0.57).

Conclusions
The authors were unable to show a significant association between apolipoprotein E genotype and POCD, but statistical power was limited because of a lower incidence of POCD than expected.
Effects of Cardiopulmonary Bypass on Sufentanil Pharmacokinetics in Patients Undergoing Coronary Artery Bypass Surgery
Authors: Hudson Robert J. , Thomson Ian R. , Jassal Rajive 
Published: September 2004

Background
Complete pharmacokinetic modeling, including assessment of the effect of cardiopulmonary bypass (CPB) on sufentanil disposition, has not been reported. The aims of this investigation were to define a model that accurately predicted sufentanil concentrations during and after cardiac surgery and to determine if CPB had a clinically significant impact on sufentanil pharmacokinetics.

Methods
Population pharmacokinetic modeling was applied to data from 21 patients undergoing coronary artery bypass grafting. The predictive ability of models was assessed by calculating bias, accuracy, and measured:predicted concentration ratios versus time. A simple three-compartment model, without covariates, was initially compared with models having weight or gender as covariates and was subsequently used as the foundation for multiple CPB-adjusted models (allowing step-changes of parameters at the start or end of CPB). The primary criterion for choosing more complex models was a significant improvement in log-likelihood; secondary criteria were significant improvement in bias or accuracy.

Results
Neither covariate (weight or gender) models improved bias or accuracy compared with the simple three-compartment model. A final CPB-adjusted model with V2 and Cl3 changing at the start of CPB and V1, Cl2, and Cl3 changing at the end of CPB had significantly greater log-likelihood values when compared with the simple three-compartment model and with less elaborate CPB-adjusted models. However, bias and accuracy for this final model were not significantly different from the simple three-compartment model.

Conclusions
When sufentanil is infused at a constant rate, with initiation of CPB, a pharmacokinetic model adjusted for CPB predicts that the sufentanil concentration will decrease approximately 17% and that it will begin to return to the prebypass concentration 12 min after initiation of CPB. At the end of CPB, this model also predicts a brief spike of the sufentanil concentration. These predictions reflect changes in the measured sufentanil concentrations. However, compared with a simple, three-compartment model, incorporating step-changes of pharmacokinetic parameters at the start or end of cardiopulmonary bypass (or both) did not significantly improve overall perioperative prediction of measured sufentanil concentrations. This suggests that CPB has clinically insignificant effects on sufentanil kinetics in adults.
A Brief Regional Ischemic-reperfusion Enhances Propofol-induced Depression in Left Ventricular Function of in situ Rat Hearts
Authors: Kuzumoto Naoya , Kitagawa Yutaka , Uemura Koichi , Ueyama Takashi , Yoshida Ken-ichi , Furuya Hitoshi , Takaki Miyako 
Published: September 2004

Background
Propofol is short-acting intravenous general anesthetics that reduces cardiovascular hemodynamics. The effects of propofol on intrinsic myocardial contractility, however, remain debatable. The aim of the current study was to test the hypothesis that inhibitory effects of propofol on left ventricular (LV) contractility and mechanical work capability of in situ ejecting rat hearts are attenuated after a brief regional ischemia and reperfusion.

Methods
The authors obtained steady-state LV pressure-volume loops and intermittently obtained LV end-systolic pressure-volume relation and evaluated effects of propofol on LV function by end-systolic pressure (ESPmLVV), systolic pressure-volume area (PVAmLVV) at midrange LV volume (mLVV).

Results
Propofol (5.2 +/- 0.3 approximately 11.1 +/- 3.7 microg.ml) significantly decreased ESP0.08 to 78 +/- 12% approximately 64 +/- 13% of prepropofol and PVA0.08 to 76 +/- 13%approximately 63 +/- 16% of prepropofol in normal hearts, whereas propofol at a lower concentration (4.1 +/- 1.0 microg/ml) did not. Although brief ischemic-reperfusion per se did not affect LV function, propofol after that, even at a lower concentration (4.1 +/- 1.0 microg/ml), significantly decreased ESP0.08 to 70 +/- 27% of prepropofol and PVA0.08 to 68 +/- 33% of prepropofol. Pretreatment with a protein kinase C (PKC) inhibitor, bisindolylmaleimide reduced the propofol (4.1 +/- 1.0 microg/ml)-induced greater decreases in ESP0.08 and PVA0.08 after brief ischemic-reperfusion to 94 +/- 33% and 92 +/- 39% of prepropofol. In the propofol-infused hearts after brief ischemic-reperfusion, protein kinase C-epsilon translocation to the nucleus-myofibril fraction was found.

Conclusion
In contrast to the study hypothesis, brief ischemic-reperfusion enhanced the inhibitory effects of propofol on LV systolic function; this enhancement is attributable to activation of protein kinase C.
Isoflurane Reduces the Carbachol-evoked Ca2+Influx in Neuronal Cells
Authors: Corrales Alexandra , Xu Fang , Garavito-Aguilar Zayra V. , Blanck Thomas J. J. , Recio-Pinto Esperanza 
Published: September 2004

Background
The authors previously reported that the isoflurane-caused reduction of the carbachol-evoked cytoplasmic Ca transient increase ([Ca]cyt) was eliminated by K or caffeine-pretreatment. In this study the authors investigated whether the isoflurane-sensitive component of the carbachol-evoked [Ca]cyt transient involved Ca influx through the plasma membrane.

Methods
Perfused attached human neuroblastoma SH-SY5Y cells were exposed to carbachol (1 mm, 2 min) in the absence and presence of isoflurane (1 mm) and in the absence and presence of extracellular Ca (1.5 mm). The authors studied the effect of the nonspecific cationic channel blocker La (100 microm), of the L-type Ca channel blocker nitrendipine (10 microm), and of the N-type Ca channel blocker omega-conotoxin GVIA (0.1 microm) on isoflurane modulation of the carbachol-evoked [Ca]cyt transient. [Ca]cyt was detected with fura-2 and experiments were carried out at 37 degrees C.

Results
Isoflurane reduced the peak and area of the carbachol-evoked [Ca]cyt transient in the presence but not in the absence of extracellular Ca. La had a similar effect as the removal of extracellular Ca. Omega-conotoxin GVIA and nitrendipine did not affect the isoflurane sensitivity of the carbachol response although nitrendipine reduced the magnitude of the carbachol response.

Conclusions
The current data are consistent with previous observations in that the carbachol-evoked [Ca]cyt transient involves both Ca release from intracellular Ca stores and Ca entry through the plasma membrane. It was found that isoflurane attenuates the carbachol-evoked Ca entry. The isoflurane sensitive Ca entry involves a cationic channel different from the L- or N- type voltage-dependent Ca channels. These results indicate that isoflurane attenuates the carbachol-evoked [Ca]cyt transient at a site at the plasma membrane that is distal to the muscarinic receptor.
Influence of Propofol on Neuronal Damage and Apoptotic Factors after Incomplete Cerebral Ischemia and Reperfusion in Rats
Authors: Engelhard Kristin , Werner Christian , Eberspächer Eva , Pape Monika , Stegemann Uta , Kellermann Kristine , Hollweck Regina , Hutzler Peter , Kochs Eberhard 
Published: September 2004

Background
Propofol reduces neuronal damage from cerebral ischemia when investigated for less than 8 postischemic days. This study investigates the long-term effects of propofol on neuronal damage and apoptosis-related proteins after cerebral ischemia and reperfusion.

Methods
Male Sprague-Dawley rats were randomly assigned as follows: group 1 (n = 32, control): fentanyl and nitrous oxide-oxygen; group 2 (n = 32, propofol): propofol and oxygen-air. Ischemia (45 min) was induced by carotid artery occlusion and hemorrhagic hypotension. Pericranial temperature and arterial blood gases were maintained constant. After 1, 3, 7, and 28 postischemic days, brains were removed, frozen, and sliced. Hippocampal eosinophilic cells were counted. The amount of apoptosis-related proteins Bax, p53, Bcl-2, and Mdm-2 and neurons positive for activated caspase-3 were analyzed.

Results
In propofol-anesthetized rats, no eosinophilic neurons were detected, whereas in control animals, 16-54% of hippocampal neurons were eosinophilic (days 1-28). In control animals, the concentration of Bax was 70-200% higher after cerebral ischemia compared with that in animals receiving propofol over time. Bcl-2 was 50% lower in control animals compared with propofol-anesthetized rats during the first 3 days. In both groups, a maximal 3% of the hippocampal neurons were positive for activated caspase-3.

Conclusions
These data show sustained neuroprotection with propofol. This relates to reduced eosinophilic and apoptotic injury. Activated caspase-3-dependent apoptotic pathways were not affected by propofol. This suggests the presence of activated caspase-3-independent apoptotic pathways.
Remifentanil Preconditioning Protects against Ischemic Injury in the Intact Rat Heart
Authors: Zhang Ye , Irwin Michael G. , Wong Tak Ming 
Published: September 2004

Background
Opioid receptors mediate cardiac ischemic preconditioning. Remifentanil is a new, potent ultra-short-acting phenylpiperidine opioid used in high doses for anesthesia. The authors hypothesize that pretreatment with this drug confers cardioprotection.

Methods
Male Sprague-Dawley rats were anesthetized and the chest was opened. All animals were subjected to 30 min of occlusion of the left coronary artery and 2 h of reperfusion. Before the 30-min occlusion, rats received either preconditioning by ischemia (ischemic preconditioning, 5-min occlusion, 5-min reperfusion x 3) or pretreatment with remifentanil, performed with the same regime (3 x 5-min infusions) using 0.2, 0.6, 2, 6, or 20 microg.kg.min intravenously. The experiment was repeated with naltrindole (a selective Delta-opioid receptor antagonist, 5 mg/kg), norbinaltorphimine (a selective kappa-OR antagonist, 5 mg/kg), or CTOP (a selective mu-opioid receptor antagonist, 1 mg/kg) administered before remifentanil-induced preconditioning or ischemic preconditioning, respectively. Infarct size, as a percentage of the area at risk, was determined by 2,3,5-triphenyltetrazolium staining.

Results
There was a dose-related reduction in infarct size/area at risk after treatment with remifentanil that was similar to that seen with ischemic preconditioning. This effect was prevented or significantly attenuated by coadministration of a mu, kappa, or Delta-opioid antagonist. The infarct-sparing effect of ischemic preconditioning was abolished by blockade of kappa-opioid receptors or Delta-opioid receptors but not by mu-opioid receptors.

Conclusion
Remifentanil mimics cardioprotection via all three opioid receptors. This differs from ischemic preconditioning, which confers cardioprotection via kappa- and Delta-, but not mu-opioid receptors. Part of the protective effect of remifentanil may be produced by mu-agonist activity outside the heart.
Influence of GABAAReceptor γ2Splice Variants on Receptor Kinetics and Isoflurane Modulation
Authors: Benkwitz Claudia , Banks Matthew I. , Pearce Robert A. 
Published: September 2004

Background
Gamma-aminobutyric acid type A (GABAA) receptors, the major inhibitory receptors in the brain, are important targets of many drugs, including general anesthetics. These compounds exert multiple effects on GABAA receptors, including direct activation, prolongation of deactivation kinetics, and reduction of inhibitory postsynaptic current amplitudes. However, the degree to which these actions occur differs for different agents and synapses, possibly because of subunit-specific effects on postsynaptic receptors. In contrast to benzodiazepines and intravenous anesthetics, there is little information available about the subunit dependency of actions of volatile anesthetics. Therefore, the authors studied in detail the effects of isoflurane on recombinant GABAA receptors composed of several different subunit combinations.

Methods
Human embryonic kidney 293 cells were transiently transfected with rat complementary DNAs of alpha1beta2, alpha1beta2gamma2L, alpha1beta2gamma2S, alpha5beta3, or alpha5beta3gamma2S subunits. Using rapid application and whole cell patch clamp techniques, cells were exposed to 10- and 2,000-ms pulses of gamma-aminobutyric acid (1 mm) in the presence or absence of isoflurane (0.25, 0.5, 1.0 mm). Anesthetic effects on decay kinetics, peak amplitude, net charge transfer and rise time were measured. Statistical significance was assessed using the Student t test or one-way analysis of variance followed by the Tukey post hoc test.

Results
Under control conditions, incorporation of a gamma2 subunit conferred faster deactivation kinetics and reduced desensitization. Isoflurane slowed deactivation, enhanced desensitization, and reduced peak current amplitude in alphabeta receptors. Coexpression with a gamma2 subunit caused these effects of isoflurane to be substantially reduced or abolished. Although the two gamma2 splice variants imparted qualitatively similar macroscopic kinetic properties, there were significant quantitative differences between effects of isoflurane on deactivation and peak current amplitude in gamma2S- versus gamma2L-containing receptors. The net charge transfer resulting from brief pulses of gamma-aminobutyric acid was decreased by isoflurane in alphabeta but increased in alphabetagamma receptors.

Conclusions
The results indicate that subunit composition does substantially influence modulation of GABAA receptors by isoflurane. Specifically, the presence of a gamma2 subunit and the identity of its splice variant are important factors in determining physiologic and pharmacologic properties. These results may have functional implications in understanding how anesthetic effects on specific types of GABAA receptors in the brain contribute to changes in brain function and behavior.