bluuebunny/crossref_metadata_2025 huggingface dataset:
OBSERVATIONAL CONSTRAINTS ON DARK ENERGY MODEL
Authors: GONG YUNGUI
Published: June 2005

The recent observations support that our Universe is flat and expanding with acceleration. We analyze a general class of quintessence models by using the recent type Ia supernova and the first year Wilkinson Microwave Anisotropy Probe (WMAP) observations. For a flat universe dominated by a dark energy with constant ω which is a special case of the general model, we find that [Formula: see text] and ωQ≤-0.82, and the turnaround redshift zTwhen the universe switched from the deceleration phase to the acceleration phase is zT= 0.65. For the general model, we find that Ωm0~0.3, ωQ0~-1.0, β~0.5 and zT~0.67. A model independent polynomial parametrization of dark energy is also considered, the best fit model gives Ωm0= 0.40±0.14, ωQ0= -1.4 and zT= 0.37.
RADIATING COLLAPSE WITH VANISHING WEYL STRESSES
Authors: MAHARAJ S. D. , GOVENDER M.
Published: June 2005

In a recent approach in modeling a radiating relativistic star undergoing gravitational collapse the role of the Weyl stresses was emphasized. It is possible to generate a model which is physically reasonable by approximately solving the junction conditions at the boundary of the star. In this paper we demonstrate that it is possible to solve the Einstein field equations and the junction conditions exactly. This exact solution contains the Friedmann dust solution as a limiting case. We briefly consider the radiative transfer within the framework of extended irreversible thermodynamics and show that relaxational effects significantly alter the temperature profiles.
Δα/α FROM QSO ABSORPTION LINES DRIVEN BY AN OSCILLATING SCALAR FIELD
Authors: FUJII YASUNORI , MIZUNO SHUNTARO
Published: June 2005

The new result on the QSO absorption lines from the VLT–UVES sample is compared with the past reports on the time-variability of the fine-structure "constant" derived from the Keck/HIRES observation, on the basis of an oscillatory behavior of the scalar field supposed to be responsible for the cosmological acceleration.
MONOTONIC INDEPENDENCE ON THE WEAKLY MONOTONE FOCK SPACE AND RELATED POISSON TYPE THEOREM
Authors: WYSOCZAŃSKI JANUSZ
Published: June 2005

We show how the construction of t-transformation can be applied to the construction of a sequence of monotonically independent noncommutative random variables. We introduce the weakly monotone Fock space, on which these operators act. This space can be derived in a natural way from the papers by Pusz and Woronowicz on twisted second quantization. It was observed by Bożejko that, by taking μ = 0, for the μ-CAR relations one obtains the Muraki's monotone Fock space, while for the μ-CCR relations one obtains the weakly monotone Fock space. We show that the direct proof of the central limit theorem for these operators provides an interesting recurrence for the highest binomial coefficients. Moreover, we show the Poisson type theorem for these noncommutative random variables.
A review of the Mesoproterozoic to early Palaeozoic magmatic and tectonothermal history of south–central Africa: implications for Rodinia and Gondwana
Authors: Johnson Simon P. , Rivers Toby , De Waele Bert
Published: June 2005

This paper provides a review of the tectonic evolution of central–southern Africa from Mesoproterozoic to earliest Palaeozoic times, using available geological information and a robust U–Pb zircon database. During the late Mesoproterozoic, the southern margin of the Congo–Tanzania–Bangweulu Craton was characterized by suprasubduction-zone magmatism and the accretion of arc and microcontinental fragments. Magmatism within the adjacent Irumide Belt formed by recycling of older continental crust. Ophiolite blocks, possibly part of an olistostromal mélange, are present in a Neoproterozoic sequence overlying the Irumide Belt, and the occurrence of high-pressure/low-temperature subduction-zone metamorphism and protracted Neoproterozoic suprasubduction-zone magmatism demonstrates that there was an ocean to the south (present-day coordinates) of the Congo–Tanzania–Bangweulu Craton until the amalgamation of Gondwana at 550–520 Ma, indicating that the Congo–Tanzania–Bangweulu Craton was not part of Rodinia. On the basis of their different ages and styles of magmatism, the Mesoproterozoic Kibaran Belt, Choma–Kalomo Block and Irumide Belt are not components of the same orogen, therefore precluding a sub-Saharan-wide, linked ‘Kibaran’ (
sensu lato
) orogenic event. Evidence is presented to illustrate that the Congo–Tanzania–Bangweulu and Kalahari Cratons developed independently until their final collision during the Pan-African Orogeny along the Damara–Lufilian–Zambezi Orogen at
c
. 550–520 Ma.
150 million years of climatic stability: evidence from the Atacama Desert, northern Chile
Authors: HARTLEY ADRIAN J. , CHONG GUILLERMO , HOUSTON JOHN , MATHER ANNE E.
Published: June 2005

The sedimentary succession in the Atacama Desert records deposition under an arid to semiarid climate from the late Jurassic (150 Ma) to the present day. Palaeomagnetic data indicate no significant latitudinal movement of this area since the late Jurassic. The present-day location of the Atacama within the dry subtropical climate belt is the principal cause of aridity. This situation is likely to have prevailed since the late Jurassic, supplemented by (1) the continentality effect (enhanced by the Gondwanan landmass), and (2) the presence offshore of a cold, upwelling current (from at least the early Cenozoic onwards and possibly earlier), resulting in conditions promoting climatic stability and desert development. Rapid and extreme climatic fluctuations during the Plio-Pleistocene were not sufficient to destabilize the climate within the Atacama. Comparison with other long-lived deserts (e.g. SW USA, Namib, Sahara and Australia) suggests that the Atacama is the oldest extant desert on Earth.
Normal faulting and crustal deformation, Alkyonides Gulf and Perachora peninsula, eastern Gulf of Corinth rift, Greece
Authors: Leeder M.R. , Portman C. , Andrews J.E. , Collier R.E.Ll. , Finch E. , Gawthorpe R.L. , McNeill L.C. , Pérez-Arlucea M. , Rowe P.
Published: June 2005

Geophysical, structural, geochronological and geomorphological data indicate that the Psatha, East Alkyonides, Skinos and Pisia faults are Holocene-active structures whereas the status of the West Alkyonides, Strava, Perachora and Loutraki faults is less certain. We see no evidence for significant lateral surface fault growth. New data for late Pleistocene footwall uplift of the Psatha fault are comparable with previously estimated Holocene rates. Pre-Holocene stratigraphic sequences in the Alkyonides Gulf allow calculation of vertical displacement on the Skinos fault of 1.42–1.60 km over a period of >0.6 Ma. Previous palaeoseismological studies indicate comparable displacement rates extrapolated to 0.61–2.20 Ma, whereas extrapolation of previous geodetic data indicate a range of 0.17–0.46 Ma. The latter is too short given the evidence of the stratigraphic record, signifying either that these data may not be representative of longer-term rates, or that significant deformation has taken place elsewhere, for example, on offshore antithetic faults. A case is established for uniform late Quaternary (post-MIS 7) uplift of the Perachora peninsula at rates of
c
. 0.2–0.3 mm a
−1
. The lack of regional tilting over Perachora–Corinth–Isthmia is in marked contrast to the situation in the Alkyonides–Megara basins to the east.
470 Ma granitoid magmatism associated with the Grampian Orogeny in the Slishwood Division, NW Ireland
Authors: Flowerdew MichaelJ. , Daly J.Stephen , Whitehouse MartinJ.
Published: June 2005

Ion-microprobe U–Pb zircon geochronology demonstrates that magmatic rocks that cut the Slishwood Division are early Ordovician in age and relate to the earliest stages of the Grampian Orogeny. These tonalite and granite intrusions yield ages of 474 ± 5 Ma, 472 ± 6 Ma, 471 ± 5 Ma and 467 ± 6 Ma. A Sm–Nd mineral isochron of 457 ± 36 Ma confirms an Ordovician age for one of the tonalite bodies and demonstrates that they were affected by Ordovician metamorphism whereas biotite Rb–Sr mineral ages from two of the tonalite bodies show that the Slishwood Division had cooled below c. 350 °C at 449 ± 7 Ma. The early orogenic tonalite and granite intrusions are mylonitized in structures that overthrust the Dalradian Supergroup onto the Slishwood Division during major nappe formation and, thus, date the onset of such deformation at or before 471 ± 5 Ma, the age of the youngest intrusion where such field relations can be demonstrated.
Dual action of prostaglandin E2 on gastric acid secretion through different EP-receptor subtypes in the rat
Authors: Kato Shinichi , Aihara Eitaro , Yoshii Katsuhide , Takeuchi Koji
Published: June 2005

We examined the role of prostaglandin E (EP) receptor subtypes in the regulation of gastric acid secretion in the rat. Under urethane anesthesia, the stomach was superfused with saline, and the acid secretion was determined at pH 7.0 by adding 50 mM NaOH. The acid secretion was stimulated by intravenous infusion of histamine or pentagastrin. Various EP agonists were administered intravenously, whereas EP antagonists were given subcutaneously 30 min or intravenously 10 min before EP agonists. PGE2 suppressed the acid secretion stimulated by either histamine or pentagastrin in a dose-dependent manner. The acid inhibitory effect of PGE2 was mimicked by sulprostone (EP1/EP3 agonist) but not butaprost (EP2 agonist) or AE1–329 (EP4 agonist). The inhibitory effect of sulprostone, which was not affected by ONO-8711 (EP1 antagonist), was more potent against pentagastrin- (50% inhibition dose: 3.6 μg/kg) than histamine-stimulated acid secretion (50% inhibition dose: 18.0 μg/kg). Pentagastrin increased the luminal release of histamine, and this response was also inhibited by sulprostone. On the other hand, AE1–329 (EP4 agonist) stimulated the acid secretion in vagotomized animals with a significant increase in luminal histamine. This effect of AE1–329 was totally abolished by cimetidine as well as AE3–208 (EP4 antagonist). These results suggest that PGE2 has a dual effect on acid secretion: inhibition mediated by EP3 receptors and stimulation through EP4 receptors. The former effect may be brought about by suppression at both parietal and enterochromaffin-like cells, whereas the latter effect may be mediated by histamine released from enterochromaffin-like cells.
Increased corpus cavernosum smooth muscle tone associated with partial bladder outlet obstruction is mediated via Rho-kinase
Authors: Chang Shaohua , Hypolite Joseph A. , Zderic Stephen A. , Wein Alan J. , Chacko Samuel , DiSanto Michael E.
Published: June 2005

Numerous studies have now demonstrated that lower urinary tract symptoms (LUTS) are associated with erectile dysfunction (ED) in men independent of age or general health. Because one-third of men over the age of 50 will develop LUTS and a recent study showed ED in 62% of patients presenting for LUTS, the importance of determining the mechanistic link between these two pathologies is clear. Using a rabbit model of partial bladder outlet obstruction (PBOO), a primary cause of LUTS, we have identified an increased basal corpus cavernosum smooth muscle (CCSM) tone associated with an elevated level of smooth muscle myosin (SMM) phosphorylation in PBOO compared with sham-operated control rabbits (sham). Results from in vitro kinase and phosphatase assays using purified smooth muscle myosin showed increased kinase and decreased phosphatase activities in cellular extracts from corpora cavernosa isolated from PBOO compared with sham rabbits. Increased Rho-kinase expression in the CCSM of PBOO rabbits was suggested by the observations that Rho-kinase inhibitors attenuated the increased kinase activity and were less effective in relaxing CCSM strips from PBOO vs. sham rabbits. This hypothesis was then confirmed by RT-PCR and Western blotting, which demonstrated increased expression of both isoforms of Rho-kinase (ROKα and ROKβ). Increased SMM basal phosphorylation (necessary for SM contraction) in the CCSM of PBOO rabbits, mediated via an increase in Rho-kinase expression/activity, would be expected to make the CCSM more difficult to relax (necessary for erection), which suggests that the RhoA/Rho-kinase pathway as being involved in the mechanism for LUTS-associated ED.
Preterm birth makes the immature intestine sensitive to feeding-induced intestinal atrophy
Authors: Bjornvad Charlotte Reinhard , Schmidt Mette , Petersen Yvette Miata , Jensen Søren Krogh , Offenberg Hanne , Elnif Jan , Sangild Per Torp
Published: June 2005

Preterm birth and formula feeding predispose to small intestinal dysfunction, which may lead to necrotizing enterocolitis (NEC). In piglets, we tested whether the physiological and environmental transitions occurring at birth affect the response of the immature intestine to enteral feeding. Pig fetuses (106 days gestation, term = 115 days) were prepared with esophageal feeding tubes and fed either sow's colostrum ( n = 8) or infant formula ( n = 7) in utero. After 24 h of oral feeding, the pig fetuses were delivered by cesarean section and their gastrointestinal morphology and function were compared with those of preterm newborn (NB) littermates that were not fed ( n = 8) or fed colostrum ( n = 7) or formula ( n = 13) for 24 h after birth. Before birth, both colostrum and formula feeding resulted in marked increases in intestinal mass, brush-border enzyme activities, and plasma glucagon-like peptide 2 concentrations, to levels similar to those in NB colostrum-fed piglets. In contrast, NB formula-fed piglets showed reduced intestinal growth, decreased brush-border enzyme activities, and intestinal lesions, reflecting NEC. NB formula-fed pigs also showed impaired enterocyte endocytotic function and decreased antioxidative capacity, whereas brush-border enzyme mRNA levels were unaltered, relative to NB colostrum-fed pigs. Our results indicate that the feeding-induced growth and enzyme maturation of the immature intestine are not birth dependent. However, with a suboptimal diet (milk formula), factors related to preterm birth (e.g., microbial colonization and metabolic and endocrine changes) make the immature intestine sensitive to atrophy and development of NEC.
Sympathetic nervous activity decreases during head-down bed rest but not during microgravity
Authors: Christensen Niels J. , Heer Martina , Ivanova Krassimira , Norsk Peter
Published: June 2005

We tested the hypothesis that sympathoadrenal activity in humans is low during spaceflight and that this effect can be simulated by head-down bed rest (HDBR). Platelet norepinephrine and epinephrine were measured as indexes of long-term changes in sympathoadrenal activity. Ten normal healthy subjects were studied before and during HDBR of 2-wk duration, as well as during an ambulatory study period of a similar length. Platelet norepinephrine concentrations (half-life = 2 days) were studied in five cosmonauts, 2 wk before launch, within 12 h after landing after 11–12 days of flight, and at least 2 wk after return to Earth. Because of the long half-life of platelet norepinephrine, data obtained early after landing would still reflect the microgravity state. Platelet norepinephrine decreased markedly during HDBR ( P < 0.001), whereas there were no significant changes when subjects were ambulatory. Platelet epinephrine did not change during HDBR. During microgravity, platelet norepinephrine and epinephrine increased in four of the five cosmonauts. Platelet norepinephrine concentrations expressed in percentage of preflight and pre-HDBR values, respectively, were significantly different during microgravity compared with HDBR [153 ± 28% (mean ± SE) vs. 60 ± 6%, P < 0.004]. Corresponding values for platelet epinephrine were also significant (293 ± 85 vs. 90 ± 12%, P < 0.01). The mechanism of the platelet norepinephrine and epinephrine response during spaceflight flight is most likely related to the concomitant decrease in plasma volume. HDBR cannot be applied to simulate changes in sympathoadrenal activity during microgravity.
Early time course of myocardial electrical impedance during acute coronary artery occlusion in pigs, dogs, and humans
Authors: del Rio Carlos L. , McConnell Patrick I. , Clymer Bradley D. , Dzwonczyk Roger , Michler Robert E. , Billman George E. , Howie Michael B.
Published: June 2005

Changes in myocardial electrical impedance (MEI) and physiological end points have been correlated during acute ischemia. However, the importance of MEI's early time course is not clear. This study evaluates such significance, by comparing the temporal behavior of MEI during acute total occlusion of the left anterior descending coronary artery in anesthetized humans, dogs, and pigs. Here, interspecies differences in three MEI parameters (baseline, time to plateau onset, and plateau value normalized by baseline) were evaluated using Kruskal-Wallis ANOVA and post hoc tests ( P < 0.05). Noteworthy differences in the MEI time to plateau onset were observed: In dogs, MEI ischemic plateau was reached after 46.3 min (SD 12.9) min of occlusion, a significantly longer period compared with that of pigs and humans [4.7 (SD 1.2) and 4.1 min (SD 1.9), respectively]. However, no differences could be observed between both animal species regarding the normalized MEI ischemic plateau value (15.3% (SD 4.7) in pigs, vs. 19.6% (SD 2.6) in dogs). For all studied MEI parameters, only swine values resembled those of humans. The severity of myocardial supply ischemia, resulting from coronary artery occlusion, is known to be dependent on collateral flow. Thus, because dogs possess a well-developed collateral system (unlike humans or pigs), they have shown superior resistance to occlusion of a coronary artery. Here, the early MEI time course after left anterior descending coronary artery occlusion, represented by the time required to reach ischemic plateau, was proven to reflect such interspecies differences.
Histological Analysis of Vascular Patterns and Connections in the Ganglionic Eminence of Premature Neonates
Authors: Anstrom John A. , Thore Clara R. , Moody Dixon M. , Challa Venkata R. , Block Steven M. , Brown William R.
Published: June 2005

Capillaries of the ganglionic eminence (GE) are reported to display structural features, such as an unusually large diameter and thin walls that support the widely held notion that these vessels are immature, and an important factor in the pathogenesis of germinal matrix hemorrhage. In this study, structural characteristics of vessels in the GE of preterm neonates were studied with either collagen IV immunohistochemistry, which labels all vessels, or alkaline phosphatase enzyme histochemistry, a marker of arterioles and capillaries but not venules. Brains from 17 preterm neonates ranging in age from 24 to 38.5 weeks postconception were used to test the hypothesis that GE arterioles connect to a peculiar capillary bed that includes large sinusoidal vessels. Clearly identifiable arterioles were traced to their terminal branch points. We found that arterioles connected directly to alkaline phosphatase-positive capillaries with a diameter of approximately 5 µm, and not to large-diameter thin-walled sinusoids. The average diameter of GE capillaries measured only 0.30 µm, greater than that of capillaries in the cortex of the same specimen. Although it is commonly held that GE capillaries are structurally immature, our results indicate that arterial blood reaching the GE is delivered to a typical capillary bed.
Dysregulation of Non-Heme Iron Metabolism in Glial Brain Tumors
Authors: Mykhaylyk Olga , Dudchenko Nataly , Cherchenko Ada , Rozumenko Volodymir , Zozulya Yuriy
Published: June 2005

Objective: To study iron exchange irregularities in experimental animals and patients with glial brain tumors to ascertain the role of the ‘iron component’ in glial brain tumor pathogenesis. Subject and Methods: A suspension of A.101.08 tumor cells was implanted in the cortex of the left-brain hemisphere of rats to model experimentally induced glial brain tumor. At 7 or 14 days after implantation, blood and tissue samples from the tumor, peritumoral tissue, and brain regions were taken for analysis. Blood and plasma samples were obtained from 23 patients as well as biopsy samples taken during tumor removal surgery. Electron resonance spectroscopy was used to determine the concentrations of transferrin iron, transferrin in whole blood and in blood cells, and chelatable and stored iron in the tissues of experimental animals and patients. Results: Hypoferremia was found in rats with both small and large glial brain tumors, whereas hyperferremia was found to be a characteristic of malignant glial brain tumors in humans. We identified statistically significant increases in stored and chelatable iron concentrations in the tumor and peritumoral brain tissue compared to the blood and the adjacent brain tissue (probably normal) in both human malignant glial brain tumors and in rat experimental glial brain tumors. Conclusions: These findings suggest that iron misregulation plays a part in glial brain tumor pathogenesis and this may provide a basis for understanding the association between glial brain tumors and epilepsy.
Prevalence of Allergy Symptoms and Total IgE in a New York City Cohort and Their Association with Birth Order
Authors: Goldstein Inge F. , Perzanowski Matthew S. , Lendor Cynthia , Garfinkel Robin S. , Hoepner Lori A. , Chew Ginger L. , Perera Frederica P. , Miller Rachel L.
Published: June 2005

Background: An inverse association between birth order and allergic disease has been widely observed, but has not been examined in the high asthma prevalence, inner-city populations of the United States. As part of an ongoing prospective birth cohort study, the prevalence of early phenotypes of asthma and/or allergy was compared with those reported in other studies, and the association with birth order was evaluated. Methods: Children of Dominican and African-American mothers living in Northern Manhattan underwent detailed periodic questionnaires. Total IgE from the mothers (n = 321) and the children at birth (n = 291) and at ages 24 (n = 244) and 36 (n = 155) months was measured. The association between birth order and allergy symptoms was evaluated at 12 (n = 350), 24 (n = 290) and 36 (n = 247) months. Results: Total serum IgE was detectable (>0.5 IU/ml) in 35% of the children’s cord blood and averaged 15 and 21 IU/ml at ages 24 and 36 months, respectively. They were not significantly different at any age between children with and without older siblings. Additionally, at these ages, there were no consistent associations between birth order and either wheeze, itchy eyes or eczema. Conclusions: Despite a substantially higher prevalence of asthma in the Northern Manhattan community compared with other areas, total IgE levels at ages 24 and 36 months, but not cord blood, are similar to those reported in other areas of the world. In this community, results at this age do not support a protective effect of higher birth order.
International Registry for Primary Hyperoxaluria
Authors: Lieske John C. , Monico Carla G. , Holmes W. Scott , Bergstralh Erik J. , Slezak Jeffrey M. , Rohlinger Audrey L. , Olson Julie B. , Milliner Dawn S.
Published: June 2005

Background/Aims: Primary hyperoxaluria (PH) is an inherited disorder that causes calcium urolithiasis and renal failure. Due to its rarity, experience at most centers with this disease is limited. Methods: A secure, web-based, institutional review board/ethics committee and American Health Insurance Portability and Accountability Act (HIPAA)-compliant registry was developed to facilitate international contributions to a data base. To date 95 PH patients have been entered. Results: PH type was confirmed in 84/95 (PH1 79%, PH2 9%). Mean age ± SD at symptom onset was 9.5 ± 10.2 (median 5.5) years whereas age at diagnosis was 15.0 ± 15.2 (median 10.0) years. Urolithiasis was present at diagnosis in 90% (mean 7, median 1, stones prior to diagnosis) and nephrocalcinosis in 48%. Surprisingly 15% of the patients were asymptomatic at the time of diagnosis. Nineteen of the 95 patients were first recognized to have PH after they had reached end-stage renal disease, with the diagnosis made only after kidney transplantation in 7 patients. Patients were followed for 12.1 ± 10.6 (median 9.4) years. Thirty-four of 95 progressed to end-stage renal failure, before (19 patients) or after (15 patients) diagnosis. In the PH1 cohort actuarial renal survival was 64% at 30 years of age, 47% at 40 years, and 29% at 50 years. Conclusion: We have developed a PH registry, and demonstrated the feasibility of this secure, web-based approach for data entry. By facilitating accumulation of an increasing cohort of patients, this registry should allow more complete characterization of clinical expression of PH, an appreciation of geographic variability, and identification of treatment outcomes.
Survey of medication administration policies within schools in Sheffield
Authors: Chakraborty Rashmi N. , Hamer David J.
Published: June 2005

National guidelines exist to help schools in supporting pupils with medical needs. However, school staff are not contractually bound to help with the administration of medication and policies differ across schools, depending on local needs and views. A postal survey was conducted in Sheffield to elicit schools’ views regarding medication administration. Over 80 percent of the responding schools were willing to administer long-term medication and 67 percent would help with short-term needs as well. Written information from professionals is valued by most schools and many would prefer that dosages of medication are adjusted to avoid school hours. Of the schools, 17 percent did not want to take any responsibility for medication administration. Reluctance seems to arise from perceived lack of training and fear of litigation. These issues need to be addressed in order to improve school staff’s confidence with the administration of medication.
Consulting on feeding and sleeping problems in child health care: what is at the bottom of advice to parents?
Authors: Funkquist Eva-Lotta , Carlsson Marianne , Nyqvist Kerstin Hedberg
Published: June 2005

The aim of this study was to investigate and interpret ideas inherent in sleep and diet consultations concerning infants in Swedish child health services. Data were obtained through semi-structured interviews of professionals employed in these services. A qualitative method with a phenomenological approach was applied to analyse the data. The results indicate that professionals have underlying conceptions. They considered that when parents force food on their child, this is a violation of the child’s integrity. This view is based on the idea that such actions restrict the child’s right to self-determination. In the participants’ opinions, when the child is forced to sleep well, this is not regarded as a violation of the child’s integrity, but is perceived as support of the child’s autonomy. An underlying theoretical view may be that parents’ time can be saved if the child becomes independent of the parents at as early an age as possible.
Carvacrol and p-cymene inactivate Escherichia coli O157:H7 in apple juice
Authors: Kiskó Gabriella , Roller Sibel
Published: June 2005

Background

Outbreaks of food poisoning associated with drinking un-pasteurised apple juice contaminated with enterohaemorrhagic Escherichia coli O157:H7 are a cause of serious illness and occasionally death. Whilst a well-established heat process (pasteurisation) will readily eliminate the pathogen, some consumers are demanding more fresh-like foods that have not been subjected to processing methods that are perceived as severe and may lead to loss of flavour and vitamins. Therefore, alternative methods are being investigated to replace pasteurisation and improve the safety of minimally-processed juices. The addition of natural antimicrobial substances such as the phenolic substances carvacrol and p- cymene (derived from the essential oils of herbs and spices) provides a potential new route to assure safety and extend the shelf-life of raw fruit juices.

The aim of this study was to evaluate the addition of very low concentrations (0.25–1.25 mM) of carvacrol and p- cymene both individually and in combination as a novel means of controlling Escherichia coli O157:H7 in un-pasteurised apple juice.

Results

When inoculated at a level of 4 log CFU/ml into un-pasteurised apple juice (pH 3.20 ± 0.06), Escherichia coli O157:H7 survived for up to 3 and 19 days at 25° and 4°C, respectively. Treatment of the juice with 1.25 mM carvacrol or p- cymene reduced the numbers of E. coli O157:H7 to undetectable levels within 1–2 days at both storage temperatures. The effective concentrations of carvacrol could be reduced even further by combining it at 0.5 mM with cymene at 0.25 mM. The phenolic compounds were biocidal against both spoilage yeasts and E. coli O157:H7 thereby increasing the shelf-life and improving the safety of un-pasteurised apple juice, particularly when stored at chill temperatures.

Conclusion

The results showed that the natural antimicrobial compounds carvacrol and p-cymene could potentially be used to extend the shelf life and improve the safety margins in un-pasteurised chilled fruit juices.
Zinc-finger domains of the transcriptional repressor KLF15 bind multiple sites in rhodopsin and IRBP promoters including the CRS-1 and G-rich repressor elements
Authors: Otteson Deborah C , Lai Hong , Liu Yuhui , Zack Donald J
Published: June 2005

Background

In the retina, many of the genes that encode components of the visual transduction cascade and retinoid recycling are exclusively expressed in photoreceptor cells and show highly stereotyped temporal and spatial expression patterns. Multiple transcriptional activators of photoreceptor-specific genes have been identified, but little is known about negative regulation of gene expression in the retina. We recently identified KLF15, a member of the Sp/Krüppel-like Factor family of zinc-finger containing transcription factors, as an in vitro repressor of the promoters of the photoreceptor-specific genes rhodopsin and IRBP/Rbp3. To gain further insight into the mechanism of KLF15-mediated regulation of gene expression, we have characterized the binding characteristics and specificity of KLF15's DNA binding domains and defined the KLF15 binding sites in the rhodopsin and IRBP promoters.

Results

In EMSA and DNAseI footprinting assays, a KLF15-GST fusion protein containing the C-terminal zinc-finger domains (123 amino acids) showed zinc-dependent and sequence-specific binding to a 9 bp consensus sequence containing a core CG/TCCCC. Both the bovine rhodopsin and IRBP promoters contained multiple KLF15 binding sites that included the previously identified CRS-1 and G-rich repressor elements. KLF15 binding sites were highly conserved between the bovine, human, chimp and dog rhodopsin promoters, but less conserved in rodents. KLF15 reduced luciferase expression by bRho130-luc (containing 4 KLF15 sites) and repressed promoter activation by CRX (cone rod homeobox) and/or NRL (neural retina leucine zipper), although the magnitude of the reduction was smaller than previously reported for a longer bRho225-luc (containing 6 KFL15 sites).

Conclusion

KLF15 binds to multiple 9 bp consensus sites in the Rhodospin and IRBP promoters including the CRS-1 and G-rich repressor elements. Based on the known expression pattern of KLF15 in non-photoreceptor cells, we hypothesize an in vivo role for KLF15 in repressing photoreceptor-specific gene expression in the inner retina.
The placental RCAS1 expression during stillbirth
Authors: Wicherek Lukasz , Klimek Marek , Czekierdowski Artur , Popiela Tadeusz J , Galazka Krystyna , Tetlak Tomasz , Gilowski Andrzej , Dutsch-Wicherek Magdalena
Published: June 2005

Background

Independently of the fetal death cause the beginning and course of stillbirth is closely related with the growing cytotoxic activity at the maternal-fetal interface. RCAS1 participates in the inhibition of maternal immune response during pregnancy. The alterations of RCAS1 protein expression in placental cells seem to determine the beginning of the labor and participate in the placental abruption. The aim of the present study was to investigate RCAS1 expression in placentas obtained following stillbirths or normal term births. Methods: RCAS1 expression was evaluated by Western blot method with the use of monoclonal anti-RCAS1 antibody in 67 placental tissue samples. Pregnant women were divided into four groups according to the mode of labor onset – spontaneous or induced, and the type of labor, stillbirth or labor at term. Placental beta-Actin expression was chosen as a control protein. Relative amounts of placental RCAS1 were compared with the use of Student's t-test, whereas beta-Actin control data were compared with the use of Mann-Whitney U test. Results: The average relative amount of RCAS1 was significantly lower in women with induced stillbirths than in women with induced labor at term. Similarly, significantly lower RCAS1 placental levels were observed in patients with spontaneous stillbirths than in women with spontaneous labor at term. Significant differences in RCAS1 expression were also observed with the respect to the beginning of the stillbirth: spontaneous and induced. Lowest RCAS1 placental levels were observed in women with spontaneous stillbirth. Conclusions: These preliminary results indicate that the alterations of RCAS1 expression in the human placenta may be involved in the changes of maternal immune system that take place during stillbirth.
DNA Damage‐Induced Programmed Cell Death: Potential Roles in Germ Cell Development
Authors: YAMADA YUKIKO , COFFMAN CLARK R.
Published: June 2005

Abstract: The detection of DNA damage is necessary to protect against proliferation of potentially harmful cells and often results in cell cycle arrest and programmed cell death. Key components of DNA damage signaling networks include ATM, CHK2, p53, and Bax. Mutations in these damage signaling systems are linked to tumorigenesis and developmental abnormalities. Expression of some of these genes in primordial germ cells (PGCs) argues that PGCs may utilize DNA damage‐induced signaling mechanisms to select against germ cells that are genetically defective, thus maintaining the integrity of the germline. This paper summarizes the roles of these DNA damage signaling molecules and addresses their potential involvement in germ cell development.
The Function of the Neuronal Proteins Shc and Huntingtin in Stem Cells and Neurons: Pharmacologic Exploitation for Human Brain Diseases
Authors: ZUCCATO CHIARA , CONTI LUCIANO , REITANO ERIKA , TARTARI MARZIA , CATTANEO ELENA
Published: June 2005

Abstract: The identification of intracellular molecules and soluble factors that are important for neuronal differentiation and survival are of critical importance for development of therapeutic strategies for brain diseases. First, the activity of these factors/molecules may be enhanced in vivo in the attempt to induce proper neuronal differentiation and integration of the resident stem cells. Second, these factors may be applied ex vivo to increase the recovery of neurons from stem cells. Third, for those intracellular molecules that play crucial roles in neuronal survival, identification of their downstream targets may give us the chance to develop drug screening assays that use these targets for therapeutic purposes. In recent years, it has become evident that intracellular signaling processes are critical mediators of the responses of neural stem cells and neurons to growth factors. Analysis of the mechanisms of signal transduction has led to the striking finding that a handful of conserved signaling pathways appear to be used in different combinations to specify a wide variety of tissues or cells. This review will focus on the mechanisms by which specific molecules control the transition from proliferation to differentiation of neural progenitor cells and the subsequent survival of postmitotic neurons; it also discusses how this knowledge may be exploited to increase the potential efficacy of stem cell replacement in the damaged brain.
Stem Cells for Retinal Degenerative Disorders
Authors: MEYER JASON S. , KATZ MARTIN L. , KIRK MARK D.
Published: June 2005

Abstract: Many systemic and eye‐specific genetic disorders are accompanied by retinal degenerations that lead to blindness. In some of these diseases retinal degeneration occurs early in life and is quite rapid, whereas in other disorders, retinal degeneration starts later and progresses very slowly. At present, no therapies are available to patients for preventing or reversing the retinal degeneration that occurs in these diseases. Implantation of neural progenitor cells into the eye may be a means by which to retard or even reverse degeneration of the retina. To evaluate the potential of neural precursor cell implantation for treating retinal degenerative disorders, neuralized mouse embryonic stem cells from green fluorescent protein (GFP) transgenic mice were administered intravitreally to normal mice, mice with early retinal degeneration, and mice with slowly progressing retinal degeneration. In normal mice, the donor cells remained in the vitreous cavity and did not associate with the host retina. In mice with early retinal degeneration, implantation of the neural precursors was performed after the degeneration was almost complete. In these animals, the donor cells primarily associated closely with the inner surface of the retina, although a small fraction of donor cells did integrate into the host retina. Donor cells implanted in mice with slowly progressing retinal degeneration also associated with the inner retinal surface, but many more of the cells integrated into the retina. These findings indicate the importance of host tissue‐donor cell interactions in determining the fate of implanted neural precursor cells. These interactions will be a major consideration when devising strategies for using cell implantation therapies for neurodegenerative disorders.
Increased Oxidative Damage with Altered Antioxidative Status in Type 2 Diabetic Patients Harboring the 16189 T to C Variant of Mitochondrial DNA
Authors: LIN TSU‐KUNG , CHEN SHANG‐DER , WANG PEI‐WEN , WEI YAU‐HUEI , LEE CHENG‐FENG , CHEN TZU‐LING , CHUANG YAO‐CHUNG , TAN TENG‐YEOW , CHANG KU‐CHOU , LIOU CHIA‐WEI
Published: June 2005

Abstract: A transition of T to C at nucleotide position 16189 in mitochondrial DNA (mtDNA) has attracted biomedical researchers for its probable correlation with the development of diabetes mellitus in adult life. In diabetes, persistent hyperglycemia may cause high production of free radicals. Reactive oxygen species are thought to play a role in a variety of physiologic and pathophysiologic processes in which increased oxidative stress may play an important role in disease mechanisms. The aim of the present study was to clarify the degree of oxidative damage and plasma antioxidant status in diabetic patients and to see the potential influence of the 16189 variant of mtDNA on the oxidative status in these patients. An indicative parameter of lipid peroxidation, malondialdehyde (MDA), and total free thiols were measured from plasma samples of 165 type 2 diabetic patients with or without this variant and 168 normal subjects. Here we report an increase in the plasma levels of MDA and total thiols in type 2 diabetic patients compared with control subjects. The levels of plasma thiols in diabetic patients with the 16189 variant of mtDNA were not different from those in controls. These results suggest an increase in the oxidative damage and a compensatory higher antioxidative status in patients with type 2 diabetes. Harboring the 16189 mtDNA variant may impair the ability of a cell to respond properly to oxidative stress and oxidative damage.
Mitochondrial Transcription Factor A in the Maintenance of Mitochondrial DNA
Authors: KANG DONGCHON , HAMASAKI NAOTAKA
Published: June 2005

Abstract: Mitochondria have their own genome, which is essential for proper oxidative phosphorylation needed for a large part of ATP production in a cell. Although mitochondrial DNA‐less (rho0) cells can survive under special conditions, the integrity of the mitochondrial genome is critical for survival of multicellular organisms. Mitochondrial transcription factor A (TFAM), originally cloned as transcription factor, is essential for the maintenance of mtDNA. Recently, it has become known that TFAM plays critical roles in multiple aspects to maintain the integrity of mitochondrial DNA: transcription, replication, nucleoid formation, damage sensing, and DNA repair. The effects of TFAM in these aspects are intimately related to each other and to function as a whole for the purpose of maintenance of mtDNA.
Frequent Occurrence of Mitochondrial Microsatellite Instability in the D‐Loop Region of Human Cancers
Authors: WANG YUE , LIU VINCENT W.S. , NGAN HEXTAN Y.S. , NAGLEY PHILLIP
Published: June 2005

Abstract: We analyzed the occurrence of mitochondrial microsatellite instability (mtMSI) in 262 pairs of female cancer tissues with the matched normal controls. mtMSI was detected in only 4 of 12 microsatellites found in the mitochondrial genome (3 in the D‐loop and 1 in the 12S rRNA gene). Interestingly, 95.6% (87/91) of mtMSI was detected in the D‐loop, namely, at nucleotide positions 303‐315, 514‐523, and 16184‐16193. This demonstrates that the D‐loop is a hotspot for mtMSI. Different incidences of mtMSI at these three microsatellites were found in the four cancer types (including cervical, endometrial, ovarian, and breast). Together with those mtMSI reported in other studies, the differential occurrence of mtMSI at each of the markers in the D‐loop region was observed, indicating that the extent of mtMSI varies from one cancer to another. Although the mechanisms of generation and functional impact of mtMSI are still not clear, the high incidence of mtMSI in the D‐loop and its broad distribution in human cancers render it a potential marker for cancer detection.
Repeated Ovarian Stimulations Induce Oxidative Damage and Mitochondrial DNA Mutations in Mouse Ovaries
Authors: CHAO HSIANG‐TAI , LEE SHU‐YU , LEE HORNG‐MO , LIAO TIEN‐LING , WEI YAU‐HUEI , KAO SHU‐HUEI
Published: June 2005

Abstract: Superovulation by injection of exogenous gonadotropin is the elementary method to produce in vivo‐derived embryos for embryo transfer in women. Increased oocyte aneuploidy, embryo mortality, fetal growth retardation, and congenital abnormalities have been studied at higher‐dose stimulations. Ovarian and oocyte biological aging possibly may have adverse implications for human oocyte competence with repeated hyperstimulation. In this study, we found that reduced competence for the human oocyte has been associated with degenerative embryo upsurge during embryo culture and failure to develop into the blastocyst stage in the three, four, five, and six stimulation cycles. On the other hand, the numbers of ovulated oocytes were decreased in the groups with more ovarian stimulation. More aggregated mitochondria were found in the cytoplasm of the repetitively stimulated embryos. Higher amounts of oxidative damage including 8‐OH‐dG, lipoperoxides, and carbonyl proteins were also revealed in the ovaries with more cycle numbers of ovarian stimulation. Higher proportions of mtDNA mutations were also found. The detected molecular size of the mutated band was approximately 675 bp. Increased amounts of carbonyl proteins were also revealed after repeated stimulation. An understanding of the relationship between oocyte competence and ovarian responses to stimulation in the mouse may provide insights into the origin of oocyte defects and the biology of ooplasmic aging that could be of clinical relevance in the diagnosis and treatment of human infertility.
Dynamics of Mitochondria and Mitochondrial Ca2+ near the Plasma Membrane of PC12 Cells: A Study by Multimode Microscopy
Authors: YANG DE‐MING , LIN CHUNG‐CHIH , LIN HSIA YU , HUANG CHIEN‐CHANG , TSAI DIN PING , CHI CHIN‐WEN , KAO LUNG‐SEN
Published: June 2005

Abstract: The goal of this study is to examine whether there is a difference in the regulation of Ca2+ between mitochondria near the cell surface and mitochondria in the cytosol. Total internal reflection fluorescence and epifluorescence microscopy were used to monitor changes in the mitochondrial Ca2+ ([Ca2+]mt) between the mitochondria near the plasma membrane and those in the cytosol. The results show that [Ca2+]mt near the plasma membrane increased earlier and decayed slower after high K+ stimulation than average mitochondria in the cytosol. In addition, the changes in [Ca2+]mt in the mitochondria near the cell surface after a second stimulation were larger than those induced by the first stimulation. The results provide direct evidence to support the hypothesis that mitochondria in different subcellular localization show differential responses to the influx of extracellular Ca2+.
Propofol Specifically Inhibits Mitochondrial Membrane Potential but Not Complex I NADH Dehydrogenase Activity, Thus Reducing Cellular ATP Biosynthesis and Migration of Macrophages
Authors: WU GONG‐JHE , TAI YU‐TING , CHEN TA‐LIANG , LIN LI‐LING , UENG YUNE‐FANG , CHEN RUEI‐MING
Published: June 2005

Abstract: Propofol is a widely used intravenous anesthetic agent. Our previous study showed that a therapeutic concentration of propofol can modulate macrophage functions. Mitochondria play critical roles in the maintenance of macrophage activities. This study attempted to evaluate further the effects of mitochondria on the propofol‐induced suppression of macrophage functions using mouse macrophage‐like Raw 264.7 cells as the experimental model. Macrophages were exposed to a clinically relevant concentration of propofol for 1, 6, and 24 h. Analysis by the Trypan blue exclusion method revealed that propofol was not cytotoxic to macrophages. Exposure of macrophages to propofol did not affect mitochondrial NADH dehydrogenase activity of complex I. However, analysis of flow cytometry showed that propofol significantly decreased the mitochondrial membrane potential of macrophages. Cellular levels of ATP in macrophages were significantly reduced after propofol administration. In parallel with the dysfunction of mitochondria, the chemotactic analysis showed that exposure to propofol significantly inhibited the migration of macrophages. This study shows that a therapeutic concentration of propofol can specifically reduce the mitochondrial membrane potential, but there is no such effect on complex I NADH dehydrogenase activity. Modulation of the mitochondrial membrane potential may decrease the biosynthesis of cellular ATP and thus reduce the chemotactic activity of macrophages. This study provides in vitro data to validate mitochondrial dysfunction as a possible critical cause for propofol‐induced immunosuppression of macrophage functions.