bluuebunny/crossref_metadata_2025_split huggingface dataset:
NLO‐active maleimide copolymers with ­high glass transition temperatures
Authors: Kato Masao , Shiraga Takao , Kimura Tatsumi , Fukuda Takashi , Matsuda Hiro , Nakanishi Hachiro 
Published: August 2002

AbstractWe synthesized some novel rigid NLO‐active maleimide copolymers bearing DR‐1 moieties (PMPD, PHSD and PHND). All copolymers exhibited high Tg's (190∼197 °C), good solubilities for common solvents and excellent film‐forming properties. Dependence of film thickness on the d33 value for the poled copolymer films induced by corona poling was investigated and it was demonstrated that in less than thickness of 0.3 µm decrease of the thickness gives rise to remarkable increase in the d33 value. The poled copolymer films exhibited large d33 values (270 × 10−9 esu (film thickness 0.13 µm) for PMPD, 290 × 10−9 esu (0.12 µm) for PHSD and 350 × 10−9 esu (0.08 µm) for PHND) as well as large r33 values (51.0 pmV−1 for PMPD and 60.4 pmV−1 for PHND) which are significantly large compared to the value of LiNbO3 (31 pmV−1) as a typical EO material. The d33 values of the poled copolymers were kept constant even after standing 1000h at 80 °C, although a small decrease was observed at an initial stage. Further, the d33 values did not change up to ca. 123 °C upon heating at the rate of 10 °C/min in all cases. Copyright © 2002 John Wiley & Sons, Ltd.
Oxidation assisted new reaction of glycerol
Authors: Kimura Hiroshi 
Published: August 2002

AbstractCatalytic oxidation of tartronic acid (TA) in water over a BiPt/C catalyst generates ketomalonic acid (KM) which polymerizes via ketone‐carbonyl to form the corresponding polyether, poly(ketomalonate) (PKM), preventing the competitive formation of KM‐hydrate available as reagent. Formation of the polyether (I) and of the hydrate (II) constitute the relaxation processes of generated active KM (keto‐form). Polymerization of KM proceeds cationically or anionically depending on pH, which shows that ketone‐carbonyl of KM is a dipole. TA, which can be prepared by catalytic oxidation of glycerol (GLY), functions as a precursor for KM as well as initiators such as proton or TA‐carbanion for cationic and anionic polymerization of KM, respectively. Perchloric acid and zinc chloride are effective promoters for polymerization of KM. The CeBiPt/C is an excellent multi‐functional catalyst which has three functions; (a) oxidation of the two primary hydroxy groups of GLY to form TA; (b) oxidation of the secondary hydroxy group of TA to generate KM; (c) polymerization of generated KM. PKM prepared by anionic polymerization of KM has no hydrogens bonded to the carbon atoms of the polyether chain. Decarboxylation of PKM can be easily performed by adding mineral acid. This shows that PKM is a polymer of carbon dioxide which is bonded to carbon of the polyether chain and is stabilized by sodium ion. Excess oxidation of PKM formed by pure oxygen accelerates complete decarboxylation to form poly(oxymethylene). These observations, assisted by catalytic oxidation, demonstrate new chemistry of GLY as a renewable resource. TA‐carbanion can also be used as an initiator for the anionic polymerization of glyoxylic acid (GOA) in a basic aqueous media to form poly(glyoxylate).Zinc chloride, a Lewis acid, can be an initiator for cationic polymerization of half‐neutralized GOA in water. GOA, which has been generally used as an ester for polyether synthesis, can be polymerized in water by controlling pH‐dependent hydration equilibrium of GOA to aldehyde‐form. Copolymer of KM and pyruvic acid prepared by anionic copolymerization initiated by TA‐carbanion shows excellent Ca‐sequestrancy as a detergent builder. Polymerization of a substituted ketone, generated by catalytic oxidation of a corresponding precursor, polymerizes via ketone‐carbonyl even in water to form the corresponding polyether. Oxidative polymerization in water of an aliphatic hydroxy compound is a new methodology for the advancement of fine chemistry and functional polymers. Copyright © 2001 John Wiley & Sons, Ltd.
Immunomodulation of experimental colitis: the role of NK1.1 liver lymphocytes and surrogate antigens – bystander effect
Authors: Shlomai Amir , Trop Shivti , Gotsman Israel , Jurim Oded , Diment Judith , Alper Ruslana , Rabbani Elazar , Engelhardt Dean , Ilan Yaron 
Published: August 2002

AbstractThe imbalance between Th1 pro‐inflammatory and Th2 anti‐inflammatory cytokine‐producing cells plays a major role in the pathogenesis of inflammatory bowel disease (IBD). Induction of oral tolerance to colitis‐extracted proteins was previously shown to down‐regulate the anti‐colon immune response, thereby alleviating experimental colitis. Immune bystander effect and liver‐associated lymphocytes expressing the NK1.1 marker (NK1.1+ LAL) have been suggested as being important in tolerance induction. The aims of the present study were to determine whether oral administration of inflammatory and non‐inflammatory colon‐extracted proteins of different species can induce peripheral immune tolerance and alleviate experimental colitis; and to examine the role of NK1.1+ LAL in oral tolerance induction. Colitis was induced in C57/B6 mice by intracolonic instillation of trinitrobenzene sulphonic acid (TNBS). Mice received six oral doses of colonic proteins extracted from TNBS‐colitis colonic wall, or normal colonic wall, from four different species. Standard clinical, macroscopic, and microscopic scores were used for colitis assessment. Serum interferon γ (IFNγ) and interleukin 10 (IL10) levels were measured by ELISA. To evaluate the role of NK1.1+ LAL in maintaining the balance between immunogenic and tolerogenic subsets of cells, their cytotoxicity functions were tested in tolerized and non‐tolerized‐mice. The administration of mouse‐derived colitis‐extracted proteins, or of surrogate proteins extracted from normal mouse colon, or from rat or human inflammatory colons, was found to alleviate experimental colitis. Tolerized mice had less diarrhoea; showed a marked reduction of colonic ulceration, intestinal and peritoneal adhesions, wall thickness, and oedema; and demonstrated a significant improvement of all microscopic parameters for colitis. Induction of tolerance led to an increase in IL10 and a decrease in IFNγ serum levels. NK1.1+ LAL cytotoxicity function increased markedly in tolerized mice. In contrast, mice fed with proteins extracted from normal rat, rabbit, and human colon, or from rabbit inflammatory colon, developed severe colitis, with a marked increase in IFNγ and a decrease in IL10 serum levels, and down‐regulation of NK1.1+ LAL function. This study has shown that oral tolerance can be induced in experimental colitis by means of the feeding of surrogate antigens; this alleviates experimental colitis. NK1.1+ LAL cytotoxicity function is associated with peripheral tolerance induction and may help to maintain the Th1/Th2 immune balance. Copyright © 2001 John Wiley & Sons, Ltd.
Localization of angiotensin‐converting enzyme in the human prostate: pathological expression in benign prostatic hyperplasia
Authors: Nassis Labrini , Frauman Albert G. , Ohishi Mitsuru , Zhuo Jialong , Casley David J. , Johnston Colin I. , Fabiani Maurice E. 
Published: August 2002

AbstractBenign prostatic hyperplasia (BPH) is the most common hyperplastic disease in man and it is characterized by increased cellular growth (stromal and epithelial hyperplasia) and enhanced local sympathetic tone, both of which are known to be augmented by activation of the renin–angiotensin system (RAS) in other tissues. Angiotensin‐converting enzyme (ACE) is an integral component of the RAS that is responsible for the production of the active peptide angiotensin II from the inactive precursor angiotensin I. The present study was undertaken to map the anatomical localization of ACE protein and messenger ribonucleic acid (mRNA) in the normal human prostate and to establish whether their expression is pathologically altered in BPH. Human prostate samples were obtained at post‐mortem and histologically defined as normal or hyperplastic. ACE protein binding/expression was determined by in vitro autoradiography and immunohistochemistry using the ACE‐specific radioligand [125I]‐MK351A and a mouse anti‐ACE polyclonal antibody, respectively, whereas the spatiotemporal distribution of ACE mRNA was determined by in situ hybridization using 35S‐labelled oligonucleotide probes. ACE protein was localized to the glandular epithelium in the human prostate. ACE binding and immunostaining were increased in BPH compared with normal (non‐hyperplastic) prostate specimens [X‐ray film autoradiography: normal 873±48 dpm/mm2 (n=8) vs. BPH 1631±274 dpm/mm2 (n=6), p<0.05; emulsion autoradiography: normal 3.1±0.5 grains/mm2 (n=6) vs. BPH 32.8±8.6 grains/mm2 (n=5), p<0.01]. ACE mRNA was also localized to glandular epithelial cells in the human prostate with a significant increase in ACE mRNA expression in BPH compared with the normal prostate [normal 11.04±2.03 grains/cell (n=220 cells total) vs. BPH 22.29±1.34 grains/cell (n=198 cells total), p<0.05]. The findings of the present study suggest that ACE is localized to the glandular epithelium of the human prostate and that its expression, at both protein and mRNA level, is aberrantly increased in BPH. These data support the concept that hyperactivity of the local RAS in the prostate may be involved in the pathogenesis of BPH. Copyright © 2001 John Wiley & Sons, Ltd.
Prenatal diagnosis of Pelizaeus‐Merzbacher disease: detection of proteolipid protein gene duplication by quantitative fluorescent multiplex PCR
Authors: Regis Stefano , Filocamo Mirella , Mazzotti Raffaella , Cusano Roberto , Corsolini Fabio , Bonuccelli Gloria , Stroppiano Marina , Gatti Rosanna 
Published: August 2002

AbstractA prenatal diagnosis of Pelizaeus‐Merzbacher disease (PMD) resulting from proteolipid protein gene (PLP) duplication was performed by a quantitative fluorescent multiplex PCR method. PLP gene copy number was determined in the proband, the pregnant mother, the male fetus and two aunts. Small amounts of genomic DNA extracted from peripheral blood and from chorionic villi were used. The fetus, in common with the proband, was identified as PMD‐affected being a carrier of the PLP gene duplication, inherited from the mother, while the two aunts were non‐carriers. The data obtained were confirmed by segregation analysis of a PLP‐associated dinucleotide‐repeat polymorphism amplified by the same multiplex PCR. Copyright © 2001 John Wiley & Sons, Ltd.
Maternal uniparental heterodisomy for chromosome 2: detection through ‘atypical’ maternal AFP/hCG levels, with an update on a previous case
Authors: Wolstenholme J. , White I. , Sturgiss S. , Carter J. , Plant N. , Goodship J. A. 
Published: August 2002

AbstractWe report a case of maternal uniparental disomy 2, detected through routine screening of placental karyotypes following the finding of ‘atypical’ AFP/hCG levels in the second trimester, with intrauterine growth retardation (IUGR) but otherwise normal outcome at term. Although the child remained small, subsequent early physical and mental development has also been normal. Additionally, we report long‐term follow‐up of an earlier case, again with relatively normal physical and mental development. The significance of atypical AFP/hCG results and the predictive value of prenatal testing for UPD2 in trisomy 2 confined placental mosaicism (CPM) cases are discussed. Copyright © 2001 John Wiley & Sons, Ltd.
Fetal and maternal progenitor cells in co‐culture respond equally to erythropoietin
Authors: Bohmer Ralph M. , Johnson Kirby L. , Bianchi Diana W. 
Published: August 2002

AbstractTo explore potentially selective growth conditions for fetal cells in cultures from the blood of pregnant women, we investigated if fetal and adult erythroid progenitors with different hemoglobin expression programs are differentially responsive to erythropoietin (EPO). Co‐cultures of clonogenic cells from 12‐week fetal and adult peripheral blood were established, and the development of erythropoietic cells was monitored using flow cytometric profiles of correlated cellular contents of fetal and adult hemoglobin (HbF and HbA, respectively). Adult nucleated red cells were classified as F+A−, F+A+ or F−A+. All fetal cells were F+A−. The population of F+A− cells was flow‐sorted and fetal cells were identified by fluorescence in situ hybridization (FISH) using chromosome‐specific probes. Delayed EPO addition revealed that all types of erythroid cells entered the EPO‐dependent phase with similar kinetics, beginning at about Day 4. The data suggest that fetal and adult erythroid stem/progenitor cells have the same initial maturation kinetics in culture independent of their hemoglobin chain expression program. Fetal and adult cells with different hemoglobin profiles also showed similar EPO dose–response curves, determined for different intervals during the first 2 weeks of culture. Thus, the kinetics of entry into the phase of EPO dependence, as well as the sensitivity to EPO at various stages of development, are essentially the same for erythropoietic progenitor cells derived from adult and early fetal blood, which rules out the possibility of using the timing or concentration of EPO for the selective growth of fetal cells from the blood of pregnant women. Copyright © 2001 John Wiley & Sons, Ltd.
Significantly higher number of fetal cells in the maternal circulation of women with pre‐eclampsia
Authors: Jansen Mieke W. J. C. , Korver‐Hakkennes Karin , van Leenen Dik , Visser Willy , in 't Veld Peter A. , de Groot Christianne J. M. , Wladimiroff Juriy W. 
Published: August 2002

AbstractAlthough the pathophysiology of pre‐eclampsia is unknown, several studies have indicated that abnormal placentation early in pregnancy might play a key role. It has recently been suggested that this abnormal placentation may result in transfusion of fetal cells (feto‐maternal transfusion) in women with pre‐eclampsia. In the present study, fetal nucleated red blood cells were isolated from 20 women with pre‐eclampsia and 20 controls using a very efficient magnetic activated cell sorting (MACS) protocol. The number of male cells was determined using two‐color fluorescence in situ hybridization (FISH) for X and Y chromosomes. Significantly more XY cells could be detected in women with pre‐eclampsia (0.61±1.2 XY cells/ml blood) compared to women with uncomplicated pregnancies (0.02±0.04 XY cells/ml blood) (Mann–Whitney U‐test, p<0.001). These results suggest that fetal cell trafficking is enhanced in women with pre‐eclampsia, and this finding may contribute to the understanding of the pathophysiology of the disease. Copyright © 2001 John Wiley & Sons, Ltd.
Prenatal interphase FISH diagnosis of PLP1 duplication associated with Pelizaeus–Merzbacher disease
Authors: Inoue Ken , Kanai Makoto , Tanabe Yuzo , Kubota Takeo , Kashork Catherine D. , Wakui Keiko , Fukushima Yoshimitsu , Lupski James R. , Shaffer Lisa G. 
Published: August 2002

AbstractA submicroscopic genomic duplication in Xq22.2 that contains the entire proteolipid protein 1 gene (PLP1) is responsible for the majority of Pelizaeus–Merzbacher disease (PMD) patients. We previously developed an interphase FISH assay to screen for PLP1 duplications in PMD patients using peripheral blood and lymphoblastoid cell lines. This assay has been utilized as a clinical diagnostic test in our cytogenetics laboratory. To expand usage of the interphase FISH assay to prenatal diagnosis of PLP1 duplications, we examined three PMD families with PLP1 duplications utilizing aminiotic fluid samples. In two families the FISH assay revealed fetuses with PLP1 duplications, whereas the other fetus showed a normal copy number of PLP1. Haplotype analyses, as well as an additional FISH analysis using postnatal blood samples, confirmed the results of the prenatal analyses. Our study demonstrates utility of the interphase FISH assay in the prenatal diagnosis of PLP1 duplications in PMD. Copyright © 2001 John Wiley & Sons, Ltd.
Identification of triploid trophoblast cells in peripheral blood of a woman with a partial hydatidiform molar pregnancy
Authors: van Wijk I. J. , de Hoon A. C. , Griffioen S. , Mulders M. A. M. , Tjoa M. L. , van Vugt J. M. G. , Oudejans C. B. M. 
Published: August 2002

AbstractIn a woman with a partial hydatidiform molar pregnancy with 69,XXY karyotype, the presence of male fetal cells of trophoblastic origin was demonstrated in maternal blood by X/Y‐chromosome specific PCR and by immunostaining combined with FISH on two cell populations isolated from maternal blood. Blood was obtained three weeks prior to the detection of fetal demise, at 13 weeks' gestation. Results were confirmed on formalin‐fixed paraffin‐embedded molar tissue, removed at 16 weeks' gestational age for therapeutic reasons. The results indicate that both plasma and cells from maternal peripheral blood might be useful for non‐invasive prenatal diagnosis of fetal aneuploidies, as described in the current case with a partial molar pregnancy. Copyright © 2001 John Wiley & Sons, Ltd.
Fetal renal anomalies and genetic syndromes
Authors: Wellesley Diana , Howe David T. 
Published: August 2002

AbstractRenal abnormalities are some of the commonest and most easily detectable anomalies on ultrasound. Many are an isolated finding but the prognosis may be altered considerably by the detection of other anomalies which could indicate a genetic disorder or syndrome. It is often easier to detect presupposed anomalies and the purpose of this article is to introduce and discuss those syndromes that may present with a renal abnormality on ultrasound. Common renal findings are presented with the range of additional anomalies that should be sought and suggested diagnostic tests. It should be remembered that although for many genetic conditions specific mutation analysis is now available, this usually requires pre‒pregnancy investigations. Furthermore, in some cases the definitive diagnosis may not be suspected until post mortem. By this time it may be too late to establish a cell line to confirm the suspicion using laboratory methods. It is therefore important to take tissue samples antenatally where possible, or at delivery, as postnatal samples may have a high culture failure rate. Copyright © 2001 John Wiley & Sons, Ltd.
New technique using galactose‐specific lectin for isolation of fetal cells from maternal blood
Authors: Kitagawa Michihiro , Sugiura Kentaro , Omi Hiroko , Akiyama Yoshiaki , Kanayama Kiyoko , Shinya Masaru , Tanaka Tadao , Yura Hirobumi , Sago Haruhiko 
Published: August 2002

AbstractTo isolate fetal cells from maternal blood, we developed a new method based on galactose‐bearing conjugation. Nucleated red blood cells (NRBCs), which highly express galactose on their surface, were selectively attached to a substrate coated with a galactose‐containing polymer via soybean agglutinin (SBA), a galactose‐specific lectin. Cord blood samples were used to evaluate enrichment efficacy of NRBCs by this method. Blood samples were obtained from 131 pregnant women between 6 and 27 gestational weeks. After preliminary condensation of fetal cells by Ficoll gradient centrifugation, NRBCs were enriched using galactose‐positive selection by adjusting SBA concentration. We isolated one to severalhundred NRBCs (mean±SD, 7.8±8.5) in 2.3 ml of peripheral blood samples from 96% of pregnantwomen. The isolated NRBCs were analyzed by a Y‐chromosome FISH probe in eight cases carrying male fetuses. Y‐signals were detected in all eight cases and more than half of the NRBCs wereoffetal origin. The study demonstrates that our new method using galactose‐specific lectin provides effective enrichment of fetal NRBCs allowing non‐invasive prenatal diagnosis. Copyright © 2002 John Wiley & Sons, Ltd.
Maternal serum levels of total activin‐A in first‐trimester trisomy 21 pregnancies
Authors: Spencer Kevin , Liao Adolfo W , Skentou Hariklea , Ong Charas YT , Nicolaides Kypros H 
Published: August 2002

AbstractMaternal serum total activin‐A concentration was measured in 45 pregnancies affected by trisomy 21 and 493 control unaffected pregnancies at 10–14 weeks of gestation. In the trisomy 21 pregnancies total activin‐A concentration was significantly higher (1.36 MoM of the unaffected pregnancies) and in 16% of cases the level was above the 95th centile of normal. The log10 SD for the control group and the trisomy 21 group were 0.17 and 0.22, respectively. The median pregnancy associated plasma protein‐A (PAPP‐A) in this trisomy 21 series was 0.49 and for free β‐hCG was 2.05. In the trisomy group there were significant positive associations between total activin‐A and PAPP‐A (0.6071) and free β‐hCG (0.4255). The low median difference and the high overlap in values between trisomic and unaffected pregnancies make total activin‐A of little practical use in first‐trimester screening for trisomy 21. Copyright © 2001 John Wiley & Sons, Ltd.
Prenatal diagnosis of congenital cytomegalovirus infection in 189 pregnancies with known outcome
Authors: Enders Gisela , Bäder Ursula , Lindemann Lisa , Schalasta Gunnar , Daiminger Anja 
Published: August 2002

AbstractAn Erratum has been published for this article in Prenatal Diagnosis 21(7) 2001, 605.Prenatal diagnosis (PD) of fetal cytomegalovirus (CMV) infection was performed in 242 pregnancies, with known outcome in 189 cases. In 141/189 pregnancies, PD was carried out on account of suspicious maternal CMV serology up to gestational week (WG) 23, and in 48 cases on account of abnormal ultrasonic findings detected between WG 18 and 39. Chorionic villus samples (n=6), amniotic fluid (AF, n=176) and/or fetal blood specimens (n=80) were investigated for detection of virus by cell culture, shell vial assay, PCR and/or CMV‐specific IgM antibodies. Of 189 fetuses correctly evaluated by CMV detection either in fetal tissue following therapeutic abortion/stillbirth (n=24) or in urine of neonates within the first 2 weeks of life (n=33), 57 were congenitally infected. In women with proven or suspected primary infection, the intrauterine transmission rates were 20.6% (7/34) and 24.4% (10/41), respectively. Of the congenitally infected live‐born infants, 57.6% (19/33) had symptoms of varying degree. The overall sensitivity of PD in the serologic and ultrasound risk groups was 89.5% (51/57). A sensitivity of 100% was achieved by combining detection of CMV‐DNA and CMV‐specific IgM in fetal blood or by combined testing of AF and fetal blood for CMV‐DNA or IgM antibodies. There was no instance of intrauterine death following the invasive procedure. The predictive value of PD for fetal infection was 95.7% (132/138) for negative results and 100% (51/51) for positive results. Correct results for congenital CMV infection by testing AF samples can be expected with samples obtained after WG 21 and after a time interval of at least 6 weeks between first diagnosis of maternal infection and PD. In case of negative findings in AF or fetal blood and the absence of ultrasound abnormalities at WG 22–23, fetal infection and neonatal disease could be excluded with high confidence. Positive findings for CMV infection in AF and/or fetal blood in combination with CMV suspicious ultrasound abnormalities predicted a high risk of cytomegalic inclusion disease (CID). Furthermore, detection of specific IgM antibodies in fetal blood was significantly correlated with severe outcome for the fetus or the newborn (p=0.0224). However, normal ultrasound of infected fetuses at WG 22–23 can neither completely exclude an abnormal ultrasound at a later WG and the birth of a severely damaged child nor the birth of neonates which are afflicted by single manifestations at birth or later and of the kind which are not detectable by currently available ultrasonographic techniques. Copyright © 2001 John Wiley & Sons, Ltd.