bluuebunny/crossref_metadata_2025_split huggingface dataset:
ECT studies of the choking phenomenon in a gas–solid circulating fluidized bed
Authors: Du Bing , Warsito W. , Fan Liang‐Shih 
Published: June 2004

AbstractChoking is commonly defined as a phenomenon where a sudden change in the solids holdup occurs in a gas–solid fluidization system. In this study, the electrical capacitance tomography (ECT) based on the neural network multicriteria optimization image reconstruction technique (NNMOIRT), developed by this research group, is used to probe the mechanism of choking formation by examining a real‐time, quasi‐3D cross‐sectional flow structure of a circulating fluidized bed riser. The particles used are FCC catalysts. The ECT with NN‐MOIRT reveals a double solids‐ring flow structure and the presence of particle blobs at the center of the bed in the circulating fluidized bed (CFB) riser. This flow structure, when it is present at the entrance region of the riser, undergoes a distinct variation during the choking transition when the gas velocity is below the transport velocity Utr, but does not undergo a distinct variation when the gas velocity is above Utr. This flow structure, when it is present at the upper region of the riser, however, does not vary distinctly at any gas velocity. Such flow structure variations are not appreciably affected by the solids feeding patterns with or without a gas or solids distributor, or by the gas humidity. For the low gas velocities (<Utr), the borescope measurement indicates that the solids concentration in the particle blob and the blob size all increase as the solids circulation rate increases. The disintegration of the enlarged blobs or blob jets and the collapse of the solids suspension characterize the mechanics of the initiation of the choking transition to the dense‐phase fluidization regime attributed to solids suspension instability. © 2004 American Institute of Chemical Engineers AIChE J, 50: 1386–1406, 2004
Increased prevalence of unprovoked seizures in patients with a 22q11.2 deletion
Authors: Kao Amy , Mariani Juliana , McDonald‐McGinn Donna M. , Maisenbacher Melissa K. , Brooks‐Kayal Amy R. , Zackai Elaine H. , Lynch David R. 
Published: June 2004

AbstractMany neurologic abnormalities have been identified in patients with a deletion of chromosome region 22q11.2, including recurrent, apparently unprovoked seizures. We reviewed the database of patients with a 22q11.2 deletion at the Children's Hospital of Philadelphia to assess the prevalence of idiopathic epilepsy in this population. The records of 383 patients with a confirmed 22q11.2 deletion were reviewed for documentation of seizures; precipitating events such as hypocalcemia, fever, and recent surgery; MRI and EEG findings (to aid in seizure classification); and potential risk factors for epilepsy. Of 348 patients with adequately detailed histories, 27 patients had apparently unprovoked seizures (7% of the total population). A disproportionate number of these patients met criteria for generalized epilepsy. Cardiac disease and prematurity were not risk factors for the development of unprovoked seizures in this population. The prevalence of unprovoked seizures in individuals meeting criteria for epilepsy in patients with a 22q11.2 deletion evaluated at our institution is much greater than in the general population. The association with generalized epilepsy suggests that this increased risk is a primary manifestation of the genetic syndrome, not a secondary result of the other manifestations of 22q11.2 deletions. These results suggest that diagnostic screening for the 22q11.2 deletion syndrome should be considered in patients with epilepsy and other signs suggestive of this interstitial deletion syndrome, and have implications for the identification of potential genetic loci for idiopathic epilepsy. © 2004 Wiley‐Liss, Inc.
parkin mutation analysis in clinic patients with early‐onset Parkinson's disease
Authors: Poorkaj P. , Nutt J. G. , James D. , Gancher S. , Bird T. D. , Steinbart E. , Schellenberg G. D. , Payami Haydeh 
Published: June 2004

Abstractparkin mutations are the most common identified cause of Parkinson's disease (PD). It has been suggested that patients with young‐onset PD be screened for parkin mutations as a part of their clinical work‐up. The aim of this study was to assess parkin mutation frequency in a clinical setting, correlate genotype with phenotype, and evaluate the current justification for clinical parkin testing. Patients were selected from a movement disorder clinic based on diagnosis of PD and onset age ≤40 years. parkin was genotyped by sequence and dosage analysis for all 12 exons. Key relatives and controls were screened for identified mutations. Mutations were found in 7/39 patients. Two patients were compound heterozygous; five were heterozygous. Mutations included deletions in exons 2, 3, and 8, duplications in exons 2–4, and 9, and P437L substitution. Seventy‐eight percent of mutations were deletions/multiplications. A novel substitution (R402W) was found in one patient and in one control. None of the point mutations found in patients were detected in 96 controls. parkin phenotypes were consistent with idiopathic PD. In conclusion, parkin mutations are common in the clinic setting: 10% of PD patients had early‐onset and 18% of them had parkin mutations. However, if parkin is recessive, only 5% of early‐onset cases who had compound mutations could be attributed to this locus. Mutation frequency was 0.12 (95% CI 0.04–0.19). parkin cases can present as typical idiopathic PD, distinguishable only by molecular testing. Seventy percent of parkin cases were heterozygous. It is unclear whether heterozygous mutations are pathogenic. parkin‐based diagnosis and counseling require a better understanding of the mode of inheritance, penetrance, and carrier frequencies. © 2004 Wiley‐Liss, Inc.
Association of the dopamine transporter gene (DAT1) core promoter polymorphism −67T variant with schizophrenia
Authors: Khodayari N. , Garshasbi M. , Fadai F. , Rahimi A. , Hafizi L. , Ebrahimi A. , Najmabadi H. , Ohadi Mina 
Published: June 2004

AbstractDysfunction of the central dopaminergic neurotransmission has been suggested to play an important role in the etiology of schizophrenia. The dopamine transporter (DAT1) mediates the active reuptake of dopamine from the synapses and thereby plays a key role in the regulation of the dopaminergic neurotransmission. In this study, we sought to determine the possible association of the DAT1 gene core promoter polymorphism −67A/T with schizophrenia in a case/control study. The allele and genotype frequencies of the polymorphism were studied in 100 patients and 100 controls, which were matched on the basis of sex, age, and ethnicity. The genotype frequencies in the patients group were as follows: AA 29%; AT 59%; TT 12% versus the genotype frequencies in the control group: AA 57%; AT 38%; TT 5% [χ2 = 16.54, df = 2, OR = 2.25 (95% CI 1.46–3.45, P ≤ 0.0003]. For the first time, these findings provide tentative evidence for the contribution of the DAT1 gene core promoter polymorphism to the etiopathophysiology of schizophrenia at least in the Iranian male population that we studied. Replication studies of independent samples and family‐based association studies are necessary to further evaluate the significance of our findings. © 2004 Wiley‐Liss, Inc.
Mutation screening of X‐chromosomal neuroligin genes: No mutations in 196 autism probands
Authors: Vincent John B. , Kolozsvari Debbie , Roberts Wendy S. , Bolton Patrick F. , Gurling Hugh M.D. , Scherer Stephen W. 
Published: June 2004

AbstractAutism, a childhood neuropsychiatric disorder with a strong genetic component, is currently the focus of considerable attention within the field of human genetics as well many other medical‐related disciplines. A recent study has implicated two X‐chromosomal neuroligin genes, NLGN3 and NLGN4, as having an etiological role in autism, having identified a frameshift mutation in one gene and a substitution mutation in the other, segregating in multiplex autism spectrum families (Jamain et al. [2003: Nat Genet 34:27–29]). The function of neuroligin as a trigger for synapse formation would suggest that such mutations would likely result in some form of pathological manifestation. Our own study, screening a larger sample of 196 autism probands, failed to identify any mutations that would affect the coding regions of these genes. Our findings suggest that mutations in these two genes are infrequent in autism. © 2004 Wiley‐Liss, Inc.
Acetylation phenotype status in a Bangladeshi population and its comparison with that of other Asian population data
Authors: Zaid R.B. , Nargis M. , Neelotpol S. , Hannan J.M.A. , Islam S. , Akhter R. , Ali L. , Azad Khan A.K. 
Published: June 2004

AbstractThe objective of the present study was to determine the acetylator status of the Bangladeshi population and to compare the findings with the acetylator status of other Asian populations. The acetylator phenotype was determined in 517 unrelated healthy Bangladeshi subjects. The phenotyping procedure was done according to Price Evans' method using the NAT2 specific probe drug—sulphadimidine. The Bangladeshi population showed a bimodal distribution of fast and slow acetylators. Of a total of 517 healthy Bangladeshi, 79.5% (n=411) were fast acetylators and the rest 20.5% (n=106) were slow acetylators. The high frequency of the fast acetylators in the population of Bangladesh was comparable to other populations in East Asia. When this acetylator status was compared with other Asian data, the Asian population showed a positive correlation between the acetylator status and the geographical longitude (r=0.919; t=7.37; p>0.001; d.f.=10). The regression line of the scatter diagram showed that the frequency of acetylating capacity increasingly occurred in the populations towards eastern Asia (regression coefficient=0.54; constant=52.36). This line was termed as the Asian fast acetylator longitude (AFAL). Thus the AFAL was able to predict the acetylator status of the Asian population by the east–west geographical longitude. The AFAL could be a useful prognosticator in the disposition for the effective and safe use of numerous drugs and xenobiotic compounds in humans. Copyright © 2004 John Wiley & Sons, Ltd.
High rates of neural tube defects in Ukraine
Authors: Yuskiv Nataliya , Andelin Clark O. , Polischuk Svitlana , Shevchuk Oleksandr , Sosynyuk Zoryana , Vihovska Tetyana , Yevtushok Lyubov , Oakley Godfrey P. , Wertelecki Wladimir 
Published: June 2004

AbstractBACKGROUNDOral consumption of synthetic folic acid can prevent neural tube defects (NTDs), which are some of the most severe congenital anomalies. The prevalence of NTDs in Ukraine and other countries of the former U.S.S.R. has not been well studied. We determined the prevalence of NTD‐affected pregnancies in Northwestern Ukraine as background for policy decisions related to flour fortification in this country.METHODSThe Ukrainian‐American Birth Defects Program was established in 1999 and conducts population‐ based surveillance of birth defects in several oblasts (states) of Ukraine. We determined the prevalence of NTDs in the Volyn and Rivne oblasts of Northwestern Ukraine for three years, 2000–2002.RESULTSThere were 75,928 births in the two oblasts in 2000–2002. There were 159 cases of NTDs among live births, stillbirths, and induced abortions. The prevalence of NTDs in the two oblasts in Northwestern Ukraine is 2.1 per 1000 births.CONCLUSIONSThe prevalence of NTD‐affected pregnancies we found in Northwestern Ukraine is almost four times what it should be. This prevalence suggests that population folate deficiency is widespread in Ukraine. Universal folic acid fortification of flour milled in Ukraine is urgently needed to end this epidemic of birth defects. Such fortification would be expected to prevent folate deficiency anemia, heart attacks, and strokes. Birth Defects Research (Part A) 2004. © 2004 Wiley‐Liss, Inc.
Maternal autoimmune diseases and immunologically induced embryonic and fetoplacental damage
Authors: Ornoy Asher , Chen Limor , Silver Robert M. , Miller Richard K. 
Published: June 2004

AbstractBACKGROUNDAutoimmune diseases are a group of illnesses in which autoantibodies are produced against various organs, presenting with a variety of clinical symptoms. In this review, we discuss the different aspects of autoimmune diseases in pregnancy. We also describe experimental models that help to understand the etiology and pathogenesis of the effects of this maternal disease on the developing embryo, fetus and placenta.METHODSThe possible direct effects of sera or IgG obtained from women with systemic lupus erythematosus/antiphospholipid syndrome (SLE/APS) and recurrent pregnancy loss (RPL) were examined on cultured 10.5‐ and 11.5‐day‐old rat embryos and on cultured human placental explants, as compared to sera from healthy women or synthetic medium that were used as controls. In addition, we examined the effects of the sera obtained from these women after successful treatment that allowed the birth of normal infants.RESULTSWe observed increased embryonic death and anomalies in embryos cultured on sera and IgG from SLE/APS women. Similarly, when human placental explants were cultured on these sera, trophoblastic cell growth was reduced and apoptotic rate was increased. Successful treatment also reduced the damage caused by the sera from these women in the cultured embryos and placentas.CONCLUSIONSOur results, and the cited studies, point to the important role of the placental damage in the etiology of RPL associated with SLE/APS. Animal models, both in vivo and in vitro, as well as cultured early human placental explants can be used successfully to understand some of the pathogenic aspects of SLE/APS and RPL. Birth Defects Research (Part A), 2004. © 2004 Wiley‐Liss, Inc.
Effectiveness of a free folic acid supplement program in family planning clinics
Authors: Watkins Margaret L. , Brustrom Jennifer , Schulman Jane 
Published: June 2004

AbstractBACKGROUNDAdequate periconceptional folic acid consumption lowers the risk for neural tube defects. We report the results of an evaluation of a folic acid intervention in Georgia family planning clinics that provided free folic acid supplements or fortified breakfast cereal.METHODSSix family planning clinics participated in the evaluation. Three clinics provided folic acid pills and educational materials to clients, two provided super‐fortified cereal and educational materials, and one clinic provided educational materials only. Participants between the ages of 18 and 45 who visited the clinics in 2000 completed a brief survey and provided a blood sample. Of the 1093 women who participated, we evaluated the 165 women who had returned to the clinic at least once during the study period. We compared participants' survey and serum folate data from their first and subsequent visits.RESULTSParticipation in the intervention was associated with increased knowledge about folic acid, (odds ratio, 1.94; 95% confidence interval, 1.37–2.76), but was not directly associated with increased self‐reported folic acid consumption or increased serum folate levels. Reported use of folic acid supplements or cereal within two days of a visit was associated with higher serum folate levels. Knowledge about folic acid was one of the best predictors of self‐reported folic acid consumption.CONCLUSIONSParticipation in the intervention increased clients' knowledge about folic acid but did not directly increase reported folic acid consumption. Because knowledge predicted folic acid consumption, the intervention may be indirectly associated with increased consumption of folic acid. Birth Defects Research (Part A), 2004. Published 2004 Wiley‐Liss, Inc.
Dissociation of double‐headed cytoplasmic dynein into single‐headed species and its motile properties
Authors: Toba Shiori , Toyoshima Yoko Yano 
Published: June 2004

AbstractCytoplasmic dynein is a minus‐end directed microtubule motor and plays important roles in the transport of various intracellular cargoes. Cytoplasmic dynein comprises two identical heavy chains and forms a dimer (double‐headed dynein); the total molecular weight of the cytoplasmic dynein complex is about 1.5 million. The dynein motor domain is structurally very different from those of kinesin and myosin, and our understanding of the mechanisms of dynein energy transduction is limited mainly because of the difficulty in obtaining a sufficient quantity of purified and active cytoplasmic dynein. We purified cytoplasmic dynein, which was free from dynactin and other dynein‐associated proteins. The purified cytoplasmic dynein was active in an in vitro motility assay. The controlled dialysis of the purified dynein against 4 M urea resulted in its complete dissociation into monomeric species (single‐headed dynein). The separation of the dynein heads by the treatment was reversible. The MgATPase activities of the single‐headed and reconstituted double‐headed dynein were comparable to that of intact dynein. The double‐headed dynein bundled microtubules in the absence of ATP; the single‐headed dynein did not. The single‐headed dynein produced in vitro microtubule‐gliding motility at velocities very similar to those of double‐headed dynein at various ATP concentrations. These results indicate that a single cytoplasmic dynein heavy chain is sufficient to produce robust microtubule motility. Application of the double‐ and single‐headed dynein molecules in various assay systems will elucidate the mechanism of action of the cytoplasmic dynein. Cell Motil. Cytoskeleton 58:281–289, 2004. © 2004 Wiley‐Liss, Inc.
Reproductive factors and risk of breast carcinoma in a study of white and African‐American women
Authors: Ursin Giske , Bernstein Leslie , Wang Yaping , Lord Sarah J. , Deapen Dennis , Liff Jonathan M. , Norman Sandra A. , Weiss Linda K. , Daling Janet R. , Marchbanks Polly A. , Malone Kathleen E. , Folger Suzanne G. , McDonald Jill A. , Burkman Ronald T. , Simon Michael S. , Strom Brian L. , Spirtas Robert 
Published: June 2004

AbstractBACKGROUNDFew studies have investigated the association between reproductive factors and the risk of breast carcinoma among African‐American women. The authors assessed whether the number of full‐term pregnancies, age at first full‐term pregnancy, and total duration of breastfeeding were associated with similar relative risk estimates in white and African‐American women in a large multicenter, population‐based case–control study of breast carcinoma.METHODSCase patients were 4567 women (2950 white women and 1617 African‐American women) ages 35–64 years with newly diagnosed invasive breast carcinoma between 1994 and 1998. Control patients were 4668 women (3012 white women and 1656 African‐American women) who were identified by random‐digit dialing and were frequency matched to case patients according to study center, race, and age. Adjusted odds ratios and 95% confidence intervals were estimated using unconditional logistic regression.RESULTSFor white women, the reduction in risk of breast carcinoma per full‐term pregnancy was 13% among younger women (ages 35–49 years) and 10% among older women (ages 50–64 years). The corresponding risk reductions for African‐American women were 10% and 6%, respectively. Risk decreased significantly with increasing number of full‐term pregnancies for both races and both age categories. Duration of lactation was inversely associated with breast carcinoma risk among younger parous white (trend P = 0.0001) and African‐American (trend P = 0.01) women. African‐American women tended to have more children compared with white women, but parity rates were lower in younger women than in older women in both racial groups. However, breastfeeding was substantially more common in young white women than in young African‐American women.CONCLUSIONSOverall, parity and lactation had similar effects on breast carcinoma risk in white and African‐American women. If younger African‐American women now are giving birth to fewer children than in the past, without a substantial increase in breastfeeding, breast carcinoma rates may continue to increase at a more rapid rate among these women compared with white women. Cancer 2004. Published 2004 by the American Cancer Society.
Two‐ and Three‐Dimensional Hydrogen‐Bonded Networks Built from 1,3,5‐[(HO)2(O)P]3C6H3 and 4‐(Dimethylamino)pyridine
Authors: Mehring Michael 
Published: June 2004

AbstractCrystallisation of 3,5‐bis(phosphonophenyl)phosphonic acid, 1,3,5‐[(HO)2(O)P]3C6H3, from MeOH/H2O in the presence of 4‐(dimethylamino)pyridine, 4‐(Me2N)C5H4N, gave [1‐{(HO)2(O)P}‐3,5‐{(HO)(O)2P}2C6H3]2−[{4‐(Me2N)C5H4NH}+]2 (2) and [1,3‐{(HO)2(O)P}2‐5‐{(HO)(O)2P}C6H3]−[4‐(Me2N)C5H4NH]+ (3). Single‐crystal X‐ray diffraction analyses revealed a two‐ and a three‐dimensional hydrogen‐bonded network for compounds 2 and 3, respectively. Compound 2 is composed of layers which are formed by hydrogen‐bonded motifs of the type R2,2(8) and R4,4(16). These motifs are connected within the layer by additional hydrogen bonds and the benzene spacer. The cation [4‐(Me2N)C5H4NH]+ is located between the layers and determines the interlayer separation of approximately 6.5 Å. In compound 3 a layered network of the hydrogen‐bonded building units R2,3(10) was observed. These units are interconnected by four additional hydrogen bonds within the network. The benzene spacer links the adjacent layers to give a three‐dimensional structure. Within this network, channels with internal dimensions of ca. 8.5 × 11.3 Å2 which are occupied by the [4‐(Me2N)C5H4NH]+ cations were observed. (© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2004)
Zwitterionic Phosphorus Ylide Adducts of Boron‐Bridged ansa‐Zirconocene Complexes as Precatalysts for Olefin Polymerization
Authors: Shapiro Pamela J. , Jiang Feilong , Jin Xiaoping , Twamley Brendan , Patton Jasson T. , Rheingold Arnold L. 
Published: June 2004

AbstractMethylenetriphenylphosphorane was coordinated to the boron of phenylborylidene‐bridged bis(cyclopentadienyl)‐ and bis(2‐Me,4‐Ph‐indenyl)zirconium dichloride to form zwitterionic ansa‐zirconocene complexes. The cyclopentadienyl complex 2, when activated with MAO, exhibits remarkable polymerization activity that is more than an order of magnitude greater than that of a related amidoborylidene‐bridged complex as well as the commercially important precatalyst [Cp′−SiMe2−N−tBu]TiCl2 (Cp′ = C5Me4). The zwitterionic bis(2‐Me,4‐Ph‐indenyl)zirconium dichloride species is isolated as a mixture of rac and meso isomers 4−6. The propylene polymerization efficiency of the isomer mixture activated by MAO is greater than that of a related silylene bridged system at 70 and 85 °C; however, the activity of the zwitterionic system decreased with further increase in temperature. The high level of isotactic triads (63.6%) and pentads (52.4%) in the polypropylene formed by 4−6 indicates that the rac isomer is the most active precatalyst of the mixture. The molecular structures of 2 and the rac bis‐indenylzirconium isomer 4 and one of the meso isomers 5 are described. (© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2004)
RuII Complexes of Bis(1,10‐phenanthrolin‐2‐yl)diazines
Authors: Brown Darren , Zong Ruifa , Thummel Randolph P. 
Published: June 2004

AbstractA series of three bis‐tridentate bridging ligands has been prepared in which two 1,10‐phenanthroline units have been symmetrically appended to a central pyridazine, pyrimidine, or pyrazine ring. These ligands have been treated with [Ru(tpy‐d11)Cl3] to afford both mono‐ and dinuclear complexes whose photo‐ and electrochemical properties have been evaluated (tpy = 2,2′:6′,2′′‐terpyridine). A structural comparison is made between [(tpy)Ru(3)Ru(tpy)](PF6)4 and a previously reported complex involving 2,2′‐bipyridines in place of phenanthrolines on the bridging ligand and surprisingly little difference is found. (© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2004)