bluuebunny/crossref_metadata_2025_split huggingface dataset:
Human replication-dependent histone H3 genes are activated by a tandemly arranged pair of two CCAAT boxes
Authors: KOESSLER Heiner , KAHLE Joerg , BODE Christa , DOENECKE Detlef , ALBIG Werner 
Published: November 2004

We have analysed the transcriptional regulation of the human histone H3 genes using promoter deletion series, scanning mutagenesis, specific mutagenesis and electrophoretic mobility-shift assay experiments. The promoters of five of the six examined histone H3 genes showed near-maximal activity at lengths of 133–227 bp: H3/d 198 bp, H3/h 147 bp, H3/k 133 bp, H3/m 227 bp, H3/n 140 bp (exception H3/i). To search for functional cis-elements within these regions, we performed scanning mutagenesis of the two histone H3 promoters H3/k and H3/m. Mutagenesis revealed that the functional framework of the histone H3 promoters consists of a TATA box and two tandemly arranged CCAAT boxes in relatively fixed positions. Alterations of the distance between the CCAAT boxes and of the distance between the CCAAT boxes and the TATA box resulted in significant loss of activity. In electrophoretic mobility-shift assay experiments, the factor CBF (CCAAT-binding factor)/NF-Y (nuclear factor-Y) bound to isolated CCAAT boxes of the H3/k promoter. This suggests that an initiation complex is formed on the histone H3 promoter that has a defined structure and limited flexibility, consisting of two molecules of CBF/NF-Y and further (general or specific) transcription factors.
Interactions among p22, glyceraldehyde-3-phosphate dehydrogenase and microtubules
Authors: ANDRADE Josefa , PEARCE Sandy Timm , ZHAO Hu , BARROSO Margarida 
Published: November 2004

Previously, we have shown that p22, an EF-hand Ca2+-binding protein, interacts indirectly with microtubules in an N-myristoylation-dependent and Ca2+-independent manner. In the present study, we report that N-myristoylated p22 interacts with several microtubule-associated proteins within the 30–100 kDa range using overlay blots of microtubule pellets containing cytosolic proteins. One of those p22-binding partners, a 35–40 kDa microtubule-binding protein, has been identified by MS as GAPDH (glyceraldehyde-3-phosphate dehydrogenase). Several lines of evidence suggest a functional relationship between GAPDH and p22. First, endogenous p22 interacts with GAPDH by immunoprecipitation. Secondly, p22 and GAPDH align along microtubule tracks in analogous punctate structures in BHK cells. Thirdly, GAPDH facilitates the p22-dependent interactions between microtubules and microsomal membranes, by increasing the ability of p22 to bind microtubules but not membranes. We have also shown a direct interaction between N-myristoylated p22 and GAPDH in vitro with a KD of ∼0.5 μM. The removal of either the N-myristoyl group or the last six C-terminal amino acids abolishes the binding of p22 to GAPDH and reduces the ability of p22 to associate with microtubules. In summary, we report that GAPDH is involved in the ability of p22 to facilitate microtubule–membrane interactions by affecting the p22–microtubule, but not the p22–membrane, association.
Cryptococcal phospholipases: a novel lysophospholipase discovered in the pathogenic fungus Cryptococcus gattii
Authors: WRIGHT Lesley C. , PAYNE Jackie , SANTANGELO Rosemary T. , SIMPANYA Mukoma F. , CHEN Sharon C. A. , WIDMER Fred , SORRELL Tania C. 
Published: November 2004

The pathogenic fungus Cryptococcus neoformans produces an extracellular PLB1 (phospholipase B1), shown previously to be a virulence factor. A novel phospholipase (LPL1) with only LPL (lysophospholipase) and LPTA (transacylase) activities has now been characterized in C. gattii, and found to be a 66-kDa glycoprotein (by SDS/PAGE), with a native molecular mass of 670 kDa. The pI was 6.3, and it was active at high temperatures (to 70 °C), as well as at both acidic and neutral pH values. It was stimulated by calcium and palmitoyl carnitine at pH 7.0, but not at pH 5.0, and palmitoyl lysophosphatidylcholine was the preferred substrate. Sequencing indicated that LPL1 is a novel cryptococcal lysophospholipase, and not the gene product of CnLYSO1 or PLB1. A protein with only LPL and LPTA activities was subsequently isolated from two strains of C. neoformans var. grubii. A PLB1 enzyme was isolated from both C. gattii and a highly virulent strain of C. neoformans var. grubii (H99). In both cases, all three enzyme activities (PLB, LPL and LPTA) were present in one 95–120 kDa glycoprotein (by SDS/PAGE) with pI 3.9–4.3. Characterization of PLB1 from C. gattii showed that it differed from that of C. neoformans in its larger native mass (275 kDa), high PLB activity relative to LPL and LPTA, and preference for saturated lipid substrates. Differences in the properties between the secreted phospholipases of the two cryptococcal species could contribute to phenotypic differences that determine their respective environmental niches and different clinical manifestations.
Elevated temporal QT variability index in patients with chronic renal failure
Authors: JOHANSSON Mats , GAO Sinsia A. , FRIBERG Peter , ANNERSTEDT Marita , BERGSTRÖM Göran , CARLSTRÖM Jan , IVARSSON Ted , JENSEN Gert , LJUNGMAN Susanne , MATHILLAS Öivind , NIELSEN Finn-David , STRÖMBOM Ulf 
Published: November 2004

Patients with CRF (chronic renal failure) are at increased risk of cardiovascular diseases, and 60% of cardiovascular mortality in CRF is attributed to sudden death. Various abnormalities in myocardial repolarization are associated with the risk of ventricular arrhythmia. The aim of this study was to evaluate an index of temporal myocardial repolarization lability, the temporal QTVI (QT variability index), in patients with CRF. ECGs were recorded in 153 patients with CRF on haemodialysis (n=67), continuous ambulatory peritoneal dialysis (n=43) or conservative treatment (n=43) during 30 min of rest. QTVI was calculated as the logarithm of the ratio between the variances of the normalized QT and RR intervals. Age-matched healthy subjects (n=39) were examined for comparison. QTVI was increased by 47% in CRF patients compared with healthy subjects (−0.82±0.56 compared with −1.54±0.27 respectively; P&lt;0.01). QTVI did not differ among patients on dialysis or conservative treatment, whereas QTVI was elevated further in patients with diabetes compared with non-diabetic CRF patients (−0.56±0.54 compared with −0.94±0.52 respectively; P&lt;0.01). In a multiple linear regression analysis, diabetes and a history of coronary artery disease were the only independent predictors of QTVI in the CRF population. The present study demonstrates that elevated QTVI in patients with CRF is associated with diabetes and coronary disease. The present findings are important given that repolarization instability may predispose to ventricular arrhythmia and sudden death, events that occur frequently in CRF patients.
Superhigh strength and good soft-magnetic properties of (Fe,Co)–B–Si–Nb bulk glassy alloys with high glass-forming ability
Authors: Shen Baolong , Inoue Akihisa , Chang Chuntao 
Published: November 2004

Fe -based bulk ferromagnetic glassy alloys with diameters up to 5mm were formed in [(Fe1−xCox)0.75B0.2Si0.05]96Nb4 system by the copper mold casting method. The substitution of Co for Fe caused an increase of glass-forming ability as well as an improvement of mechanical and magnetic properties. The bulk glassy alloys exhibited superhigh fracture strength of 3900–4250MPa, Young’s modulus of 190–210GPa, elastic strain of 0.02, and plastic strain of 0.0025. The bulk glassy alloys also exhibited good soft magnetic properties, i.e., saturation magnetization of 0.84–1.13T, low coercive force of 1.5–2.7A∕m, high permeability exceeding 1.2×104, and Curie temperature of 600–690K.
At the request of the authors, this article is being retracted effective 29 March 2011.
Acute vascular occlusion in horses: effects on skeletal muscle size and blood flow
Authors: Abe T , Kearns CF , Filho HC Manso , Sato Y , Sleeper M , McKeever KH 
Published: November 2004

AbstractThe purpose of this study was to demonstrate whether acute vascular occlusion was safe and if it would result in changes to limb muscle size in horses. Six healthy, unfit Standardbred mares were used. Horses (standing at rest) wore an occlusion cuff at the most proximal position of the left forelimb. The right forelimb was used as control. An occlusion pressure of 200 mmHg was set for 5 min followed by a 2 min recovery. Three sets of occlusions were given to each horse. Muscle thickness was measured using B-mode ultrasound. The circumference of the forelimb and first phalanx was measured using a flexible tape measure. Pulsed-wave Doppler was performed on the radialis artery with a 5–10 MHz mechanical transducer at baseline and at each occlusion. Peak flow velocity (PFV) and the flow velocity integral (FVI) were measured each time. Mid-forelimb, but not first phalanx, girth was increased (P<0.05) in the occluded but not in the control leg following occlusion. Extensor and flexor muscle thickness was increased (P<0.05) in the occluded but not in the control leg. There were no changes (P>0.05) in PFV or FVI at any measurement time point. Acute vascular occlusion may be a suitable and safe model for studying muscle hypertrophy in horses.
African athletic aptitude and the social sciences
Authors: Hoberman John 
Published: November 2004

AbstractScientific investigation of racial athletic aptitude has been preceded by a century of pseudo- and quasi-scientific speculations on this topic. For this reason, physiological and anatomical research on African runners is performed in a social context that is still permeated by folkloric ideas about racial differences, some of which pertain to athletic performance. A powerful stereotype of ‘tropical nature’ and its ‘superabundant’ vitality has influenced non-African thinking about African athletic potential. The idea that evolutionary adaptation in Africa is a particularly severe version of natural selection has had a similar effect on Western thinking about African runners. Romantic ideas about African athletic aptitude may, therefore, be understood as modern versions of the doctrine of black ‘hardiness’ that survives in contemporary biomedicine in various forms.
Angiotensin-converting enzyme and human physical performance
Authors: Payne John , Montgomery Hugh 
Published: November 2004

AbstractGenes undoubtedly play a role in the development of a successful athlete. This view has flourished on anecdotes such as the observation of a child who displays the same aptitude for a particular sport as one of their parents, or a pair of sisters who both excel in the same discipline. However, the conclusions made from this type of observation have an obvious limitation: that similar environmental factors may be just as responsible as genetic inheritance in explaining the passage and sharing of talent between family members. Here, we review briefly the salient data showing that genes do play a role in athletic performance, and although the data examining the effect of specific genes are limited, we present data examining the role of the angiotensin-converting enzyme gene in human physical performance.
Estimation of the Plasma Effect Site Equilibration Rate Constant (ke0) of Propofol in Children Using the Time to Peak Effect
Authors: Muñoz Hernán R. , Cortínez Luis I. , Ibacache Mauricio E. , Altermatt Fernando R. 
Published: November 2004

Background
Targeting the effect site concentration may offer advantages over the traditional forms of administrating intravenous anesthetics. Because the lack of the plasma effect site equilibration rate constant (ke0) for propofol in children precludes the use of this technique in this population, the authors estimated the value of ke0 for propofol in children using the time to peak effect (tpeak) method and two pharmacokinetic models of propofol for children.

Methods
: The tpeak after a submaximal bolus dose of propofol was measured by means of the Alaris A-Line auditory evoked potential monitor (Danmeter A/S, Odense, Denmark) in 25 children (aged 3-11 yr) and 25 adults (aged 35-48 yr). Using tpeak and two previously validated sets of pharmacokinetic parameters for propofol in children, Kataria's and that used in the Paedfusor (Graseby Medical Ltd., Hertfordshire, United Kingdom), the ke0 was estimated according to a method recently published.

Results
The mean tpeak was 80 +/- 20 s in adults and 132 +/- 49 s in children (P < 0.001). The median ke0 in children was 0.41 min(-1) with the model of Kataria and 0.91 min(-1) with the Paedfusor model (P < 0.01). The corresponding t1/2 ke0 values, in minutes, were 1.7 and 0.8, respectively (P < 0.01).

Conclusions
: Children have a significantly longer tpeak of propofol than adults. The values of ke0 of propofol calculated for children depend on the pharmacokinetic model used and also can only be used with the appropriate set of pharmacokinetic parameters to target effect site in this population.
Platelet Gene Polymorphisms and Cardiac Risk Assessment in Vascular Surgical Patients
Authors: Faraday Nauder , Martinez Elizabeth A. , Scharpf Robert B. , Kasch-Semenza Laura , Dorman Todd , Pronovost Peter J. , Perler Bruce , Gerstenblith Gary , Bray Paul F. , Fleisher Lee A. 
Published: November 2004

Background
Current perioperative cardiac risk assessment tools use historic and surgical factors to stratify patient risk. Polymorphisms in platelet glycoprotein (GP) IIIa and GPIbalpha are associated with myocardial ischemic risk in nonsurgical settings, but their relation to perioperative ischemia is unclear. The authors hypothesized that platelet genotype would be an independent predictor of postoperative myocardial ischemia and would improve risk assessment when added to clinical factors.

Methods
One hundred ninety-six patients who underwent infrainguinal, abdominal aortic, or thoracoabdominal vascular surgery were evaluated for clinical and genetic factors that might predict the development of postoperative myocardial ischemia. Genomic DNA was genotyped for the Leu33Pro polymorphism of GPIIIa and the Thr145Met polymorphism of GPIbalpha. Myocardial ischemic outcome was determined by review of the medical record for cardiac death or myocardial infarction and by surveillance troponin I and automated continuous 12-lead electrocardiographic analysis.

Results
Sixty-five patients (33%) experienced one or more ischemic endpoints (2% death, 5% myocardial infarction, 20% troponin+, 22% electrocardiogram+). The Pro33 (adjusted odds ratio [OR], 2.4 [95% confidence interval, 1.2-6.2]) and Met145 (OR 3.4 [1.4-9.3]) genotypes were independent predictors of composite ischemic outcome by multivariate regression, as were diabetes mellitus (OR 4.0 [1.7-12.5]), abdominal aortic surgery (OR 4.1 [1.7-14.4]), and thoracoabdominal aortic surgery (OR 6.4 [2.7-23.8]). The addition of platelet gene polymorphisms to clinical factors improved fit (likelihood ratio testing chi-square = 13.5, P < 0.001) of an ischemia prediction model. The derived risk assessment tool had a receiver operator characteristic curve of 0.73 (0.65-0.81) compared with 0.64 (0.57-0.74) for a model excluding genetic factors (P = 0.04). A significant relation between the GPIbalpha polymorphism and ischemic outcome remained after excluding electrocardiographic ischemia from the composite endpoint.

Conclusions
Platelet polymorphisms are independent risk factors for postoperative myocardial ischemia and improve a risk prediction model when added to historic and surgical risk factors.
Differential Protective Effects of Volatile Anesthetics against Renal Ischemia–Reperfusion Injury In Vivo
Authors: Lee H Thomas , Ota-Setlik Ayuko , Fu Yulei , Nasr Samih H. , Emala Charles W. 
Published: November 2004

Background
Volatile anesthetics protect against cardiac ischemia-reperfusion injury via adenosine triphosphate-dependent potassium channel activation. The authors questioned whether volatile anesthetics can also protect against renal ischemia-reperfusion injury and, if so, whether cellular adenosine triphosphate-dependent potassium channels, antiinflammatory effects of volatile anesthetics, or both are involved.

Methods
Rats were anesthetized with equipotent doses of volatile anesthetics (desflurane, halothane, isoflurane, or sevoflurane) or injectable anesthetics (pentobarbital or ketamine) and subjected to 45 min of renal ischemia and 3 h of reperfusion during anesthesia.

Results
Rats treated with volatile anesthetics had lower plasma creatinine and reduced renal necrosis 24-72 h after injury compared with rats anesthetized with pentobarbital or ketamine. Twenty-four hours after injury, sevoflurane-, isoflurane-, or halothane-treated rats had creatinine (+/- SD) of 2.3 +/- 0.7 mg/dl (n = 12), 1.8 +/- 0.5 mg/dl (n = 6), and 2.4 +/- 1.2 mg/dl (n = 6), respectively, compared with rats treated with pentobarbital (5.8 +/- 1.2 mg/dl, n = 9) or ketamine (4.6 +/- 1.2 mg/dl, n = 8). Among the volatile anesthetics, desflurane demonstrated the least reduction in plasma creatinine after 24 h (4.1 +/- 0.8 mg/dl, n = 12). Renal cortices from volatile anesthetic-treated rats demonstrated reduced expression of intercellular adhesion molecule 1 protein and messenger RNA as well as messenger RNAs encoding proinflammatory cytokines and chemokines. Volatile anesthetic treatment reduced renal cortex myeloperoxidase activity and reduced nuclear translocation of proinflammatory nuclear factor kappaB. Adenosine triphosphate-dependent potassium channels are not involved in sevoflurane-mediated renal protection because glibenclamide did not block renal protection (creatinine: 2.4 +/- 0.4 mg/dl, n = 3).

Conclusion
Some volatile anesthetics confer profound protection against renal ischemia-reperfusion injury compared with pentobarbital or ketamine anesthesia by attenuating inflammation. These findings may have significant clinical implications for anesthesiologists regarding the choice of volatile anesthetic agents in patients subjected to perioperative renal ischemia.
Propofol Attenuates Peroxynitrite-mediated DNA Damage and Apoptosis in Cultured Astrocytes
Authors: Acquaviva Rosaria , Campisi Agata , Murabito Paolo , Raciti Giuseppina , Avola Roberto , Mangiameli Salvatore , Musumeci Ilenia , Barcellona Maria Luisa , Vanella Angelo , Li Volti Giovanni 
Published: November 2004

Background
The concentration of peroxynitrite in the brain increases after central nervous system injuries. The authors hypothesized that propofol, because of its particular chemical structure, mitigates the effects of peroxynitrite-mediated oxidative stress and apoptosis by the induction of heme oxygenase (HO)-1 in primary cultured astroglial cells.

Methods
Primary cultured astroglial cells were incubated for 18 h with a known peroxynitrite donor (3 mm SIN-1) in the presence or absence of propofol (40 microm, 80 microm, 160 microm, and 1 mm). The protective effects of propofol were evaluated by 3(4,5-dimethyl-thiazol-2-yl)2,5-diphenyl-tetrazolium bromide cytotoxicity assay, lactic dehydrogenase release, DNA ladderization by Comet assay, and caspase-3 activation by Western blot analysis.

Results
Appropriate propofol concentrations (ranging from 40 microm to 1 mm) significantly increased HO-1 expression and attenuated SIN-1-mediated DNA ladderization and caspase-3 activation. The protective effects of propofol were mitigated by the addition of tin mesoporphyrin, a potent inhibitor of HO activity. The addition of a specific synthetic inhibitor of nuclear factor kappaB abolished propofol-mediated HO-1 induction, suggesting a possible role of this nuclear transcriptional factor in our experimental conditions.

Conclusions
The antioxidant properties of propofol can be partially attributed to its scavenging effect on peroxynitrite as well as to its ability to increase HO-1 expression at higher concentrations, a property that might be relevant to neuroprotection during anesthesia.
Desflurane Preconditioning Induces Time-dependent Activation of Protein Kinase C Epsilon and Extracellular Signal-regulated Kinase 1 and 2 in the Rat Heart In Vivo
Authors: Toma Octavian , Weber Nina C. , Wolter Jessica I. , Obal Detlef , Preckel Benedikt , Schlack Wolfgang 
Published: November 2004

Background
Activation of protein kinase C epsilon (PKC-epsilon) and extracellular signal-regulated kinase 1 and 2 (ERK1/2) are important for cardioprotection by preconditioning. The present study investigated the time dependency of PKC-epsilon and ERK1/2 activation during desflurane-induced preconditioning in the rat heart.

Methods
Anesthetized rats were subjected to regional myocardial ischemia and reperfusion, and infarct size was measured by triphenyltetrazoliumchloride staining (percentage of area at risk). In three groups, desflurane-induced preconditioning was induced by two 5-min periods of desflurane inhalation (1 minimal alveolar concentration), interspersed with two 10-min periods of washout. Three groups did not undergo desflurane-induced preconditioning. The rats received 0.9% saline, the PKC blocker calphostin C, or the ERK1/2 inhibitor PD98059 with or without desflurane preconditioning (each group, n = 7). Additional hearts were excised at four different time points with or without PKC or ERK1/2 blockade: without further treatment, after the first or the second period of desflurane-induced preconditioning, or at the end of the last washout phase (each time point, n = 4). Phosphorylated cytosolic PKC-epsilon and ERK1/2, and membrane translocation of PKC-epsilon were determined by Western blot analysis (average light intensity).

Results
Desflurane significantly reduced infarct size from 57.2 +/- 4.7% in controls to 35.2 +/- 16.7% (desflurane-induced preconditioning, mean +/- SD, P < 0.05). Both calphostin C and PD98059 abolished this effect (58.8 +/- 13.2% and 64.2 +/- 15.4% respectively, both P < 0.05 versus desflurane-induced preconditioning). Cytosolic phosphorylated PKC-epsilon reached its maximum after the second desflurane-induced preconditioning and returned to baseline after the last washout period. Both calphostin C and PD98059 inhibited PKC-epsilon activation. ERK1/2 phosphorylation reached its maximum after the first desflurane-induced preconditioning and returned to baseline after the last washout period. Calphostin C had no effect on ERK1/2 phosphorylation.

Conclusions
Both, PKC and ERK1/2 mediate desflurane-induced preconditioning. PKC-epsilon and ERK1/2 are both activated in a time dependent manner during desflurane-induced preconditioning, but ERK1/2 activation during desflurane-induced preconditioning is not PKC dependent. Moreover, ERK1/2 blockade abolished PKC-epsilon activation, suggesting ERK-dependent activation of PKC-epsilon during desflurane-induced preconditioning.