Library

X
feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Electronic Resource
    Electronic Resource
    Preliminary evidence for an association of Epstein-Barr virus with pre-ulcerative oral lesions in patients with recurrent aphthous ulcers or Behiçet's disease (1998)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of oral pathology & medicine 27 (1998), S. 0 
    Details
    ISSN: 1600-0714
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: In this study we used the polymerase chain reaction (PCR), slot blot and Southern blot hybridization, direct sequencing and in situ hybridization (ISH) to show the possible presence of EBV-DNA in pre-ulcerative oral aphthous lesions of patients with recurrent aphthous ulcers (RAU) or Behet's disease (BD). For this purpose, formalin-fixed biopsy specimens were obtained from 13 pre-ulcerative oral aphthous lesions of nine RAU and four BD patients. Five specimens of normal oral mucosa (NOM) from five normal control subjects and 10 specimens of oral erosive or ulcerative lesions from 10 patients with erosive lichen planus (ELP) were also included. EBV-DNA was detected by PCR in 5 of the 13 (38.5%) pre-ulcerative oral aphthous lesions, two from RAU patients and three from BD patients. However, no EBV-DNA was demonstrated in five NOM specimens from normal control subjects and in 10 specimens of oral lesions from ELP patients. EBV-DNA was also demonstrated in patients’peripheral blood lymphocytes and/ or plasma, suggesting that the lymphocytes may be the reservoir of latent EBV infection and there is EBV shedding in the plasma. EBV-DNA was detected by ISH in only one PCR-positive case; the reaction product was found to deposit on the nuclei of some of the epithelial cells and lymphocytes. By immunohistochemistry, expression of Epstein-Barr nuclear antigen and EBV/C3d receptors was also noted in some of the epithelial cells and lymphocytes in this ISH-positive case. Therefore, we suggest that the epithelial cells of pre-ulcerative oral aphthous lesions may be infected by EBV through EBV-infected lymphocytes; also, the cytotoxic T lymphocyte-induced lysis of the EBV-infected epithelial cells, but not the virus-induced cytolysis, may be the main mechanism causing oral ulcer formation. Our data provide preliminary evidence for an association of EBV with pre-ulcerative oral aphthous lesions in RAU and BD patients.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1600-0714.1998.tb01935.x
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    Human cytomegalovirus as a potential etiologic agent in recurrent aphthous ulcers and Behçet's disease (1996)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of oral pathology & medicine 25 (1996), S. 0 
    Details
    ISSN: 1600-0714
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: In a preliminary study on anti-human cytomegalovirus (HCMV) antibody (Ab) by ELISA. the serum anti-HCMV/IgG Ab concentrations in 22 patients with recurrent aphthous ulcers (RAU) in the remission stage were found to be significantly higher than in 22 control subjects (121±42 vs 100±27, P〈0.05) and in 39 patients with RAU in the active stage (121±42 vs 88±45, P〈0.01). Therefore, the potential of HCMV as an etiologic agent in RAU was proposed and studies using the polymerase chain reaction (PCR) and in situ hybridization (ISH) have been performed to investigate the possible presence of HCMV DNA in pre-ulcerative oral aphthous lesions in patients with RAU or Behçet's disease (BD) of the mucocutaneous type. For this purpose, formalin-fixed biopsy specimens were obtained from 13 pre-ulcerative oral aphthous lesions, 2 samples of normal oral mucosa and 1 ileal mucosal lesion from 9 RAU patients and 4 BD patients. Five specimens of normal oral mucosa from 5 normal control subjects and 12 specimens of oral erosive or ulcerative lesions from 12 patients with erosive lichen planus (ELP) were also included. By PCR, HCMV DNA was detected in 5 of the 13 (38.5%) pre-ulcerative oral aphthous lesions. 3 from RAU patients and 2 from BD patients. The ileal mucosa specimen was also HCMV DNA-positive, whereas HCMV DNA was not demonstrated in any of the 7 specimens of normal oral mucosa from RAU patients and normal control subjects; 12 specimens of oral lesions from ELP patients were similarly negative. ISH did not detect HCMV DNA in any of the biopsy specimens from RAU patients and control subjects. Our findings suggest that HCMV may be an etiologic agent in some cases of RAU and BD.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1600-0714.1996.tb01374.x
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Molecular analysis of survival motor neuron (SMN) and neuronal apoptosis inhibitory protein (NAIP) genes of spinal muscular atrophy patients and their parents (1997)
    Springer
    Human genetics 〈Berlin〉 100 (1997), S. 577-581 
    Details
    ISSN: 1432-1203
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract We have assayed deletions of two candidate genes for spinal muscular atrophy (SMA), the survival motor neuron (SMN) and neuronal apoptosis inhibitory protein (NAIP) genes, in 101 patients from 86 Chinese SMA families. Deletions of exons 7 and 8 of the telomeric SMN gene were detected in 100%, 78.6%, 96.6%, and 16.7%, in type I, II, III, and adult-onset SMA patients, respectively. Deletion of exon 7 only was found in eight type II and one type III patient. One type II patient did not have a deletion of either exon 7 or 8. The prevalence of deletions of exons 5 and 6 of the NAIP gene were 22.5% and 2.4% in type I and II SMA patients, respectively. We also examined four polymorphisms of SMN genes and found that there were only two, SMN-2 and CBCD541-2, in Chinese subjects. In our study, analysis of the ratio of the telomeric to centromeric portion (T/C ratio) of the SMN gene after enzyme digestion was performed to differentiate carriers, normals, and SMA patients. We found the T/C ratio of exon 7 of the SMN gene differed significantly among the three groups, and may be used for carrier analysis. An asymptomatic individual with homozygous deletion of exons 7 and 8 of the SMN gene showed no difference in microsatellite markers in the SMA-related 5q11.2–5q13.3. In conclusion, SMN deletion in clinically presumed child-onset SMA should be considered as confirmation of the diagnosis. However, adult-onset SMA, a heterogeneous disease with phenotypical similarities to child-onset SMA, may be caused by SMN or other gene(s).
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004390050555
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 4
    Electronic Resource
    Electronic Resource
    Lewis (FUT3) genotypes in Taiwanese, Thai, and Filipino populations (2000)
    Springer
    Annals of hematology 79 (2000), S. 599-603 
    Details
    ISSN: 1432-0584
    Keywords: Key words Lewis blood group ; α (1,3/1,4)-Fucosyltransferase (FUT3) ; Taiwanese ; Thai ; Filipino
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  The Lewis (Le) blood type comprises two major antigens, Lea and Leb, which are encoded by α (1,2)-fucosyltransferase (FUT2) and α (1,3/1,4)-fucosyltransferase (FUT3). In this study, we analyzed the mutations of FUT3 in Taiwanese, Thai, and Filipino populations and correlated these with serologic phenotypes. One hundred and thirty-seven Taiwanese, 71 Thai, and 125 Filipino were studied unselectively. The frequency of the normal and four other mutant alleles for Taiwanese, Thai, and Filipino, respectively, were as follows: 187/274 (68.2%), 87/142 (61.3%), and 160/250 (64.0%) were wild type (Le); 14/274 (5.1%), 1/142 (0.7%), and 1/250 (0.4%) were a T202C/C314T mutation (le202,314); 35/274 (12.8%), 15/142 (10.6%), and 22/250 (8.8%) had the G508A mutation (le508); and 38/274 (13.9%), 39/142 (27.4%), and 67/250 (26.8%) carried the T1067A mutation (le1067). The le445 and le1007 were not detected in this study. Our result provided the first genetic data of the FUT3 gene in these three populations, and the frequency distribution of mutant alleles among Taiwanese, Thai, and Filipinos demonstrates a significant difference (P〈0.001). In our study, the le202,314 mutation had considerable frequency in the Taiwanese, but the le1067 mutation had a higher frequency in Thai and Filipinos.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002770000212
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 5
    Electronic Resource
    Electronic Resource
    Rapid detection of −α 4.2 deletion of α-thalassemia-2 by polymerase chain reaction (1994)
    Springer
    Annals of hematology 69 (1994), S. 205-209 
    Details
    ISSN: 1432-0584
    Keywords: −α 4.2 Deletion ; α-Thalassemia-2 ; −α G-Taichung
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We sequenced part of the X boxes ofα-thalassemia-1 of Southeast Asia type (- -SEA) with−α 4.2,−α 3.7,−α G-Taichung, andα CSα. We found the X box of−α 3.7 belonged to the X box of α2 globin gene and the X box ofα csα contained X boxes of both al andα2 globin gene, whereas the X box of−α 4.2 and−α G-Taichung was a hybrid of X boxes of α2 and α1 globin gene. We also found there are two types of−α 4.2 deletion; type 1 is a common type of−α 4.2 deletion and type 2 is linkage to−α G-Taichung. We used a combination of two methods, the amplification refractory mutation system (ARMS) and the amplified created restriction sites (ACRS), to amplify the hybrids of X boxes specifically. The upstream primer for X box ofα2 globin gene was designed following the standard ARMS procedure to amplify the X segment of theα-globin gene. The downstream primer was designed according to the ACRS method to check the specificity of PCR products. Using this approach, we can diagnose the different types of−α 4.2 deletion. This kind of approach can also be used to amplify the specific region from the cluster of highly homologous genes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02215955
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 6
    Electronic Resource
    Electronic Resource
    Molecular characterization of secretor type α(1,2)-fucosyltransferase gene deficiency in the Philippine population (1999)
    Springer
    Annals of hematology 78 (1999), S. 463-467 
    Details
    ISSN: 1432-0584
    Keywords: Key words Filipino ; α(1,2)-fucosyltransferase ; Secretor phenotype ; Nonsecretor ; Mutation analysis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  We analyzed the seven mutations which are responsible for the deficiency of the secretor type α(1,2)-fucosyltransferase gene product, Se enzyme, in the Philippine population. One hundred and one unrelated Filipinos in Taiwan were studied. A new mutation, a 3-base pair deletion from nt 688 through 690, was found in two (0.1%) of 202 chromosomes. The frequencies of six other mutated alleles were as follows: 71/202 (35.2%) were cDNA 385 A→T missensed mutation (se2), 28/202 (13.9%) were C571T nonsense mutation (se3), 16/202 (7.9%) were G849A nonsense mutation (se4), 4/202 (1.9%) were G428A nonsense mutation (se1), and 81/202 (40.1%) were wild-type allele (Se). No C628T nonsense mutations (se5) or fusion genes of pseudogene and FUT2 gene (se 6) were found in this population. For the molecular basis of phenotype Le(a+ b–): eight cases had se2/se2, six cases had se2/se3, two cases had se3/se4, one case was homozygous of se4, one case was se3/se1, and two cases were se2/se7. For the Le(a+ b+) phenotype: four cases had se2/se2, two cases had se2/se3, one case was se3/se3, and one case was se2/se4. For the Le(a– b+) phenotype: 16 cases were Se/Se, 21 cases were Se/se2, six cases were Se/se3, five cases were Se/se4, and two cases had Se/se1. Our results suggest that the genotypes of the α(1,2)-fucosyltransferase gene in phenotypes Le(a+ b+) and Le(a+ b–) are the same. Other factors that play important roles may cause the differences between these two phenotypes. Several hotspot mutations in the α(1,2)-fucosyltransferase gene are responsible for the nonsecretor phenotype.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002770050599
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 7
    Electronic Resource
    Electronic Resource
    Rapid molecular characterization of Hb H disease in Chinese by polymerase chain reaction (1994)
    Springer
    Annals of hematology 68 (1994), S. 33-37 
    Details
    ISSN: 1432-0584
    Keywords: Hb H disease ; Polymerase chain reaction Chinese
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We have developed a rapid method to molecularly distinguish different types of Hb H disease. The study depended on (a) most of the Hb H disease in Taiwan having anα-thalassemia-1 of the Southeast Asia type (-SEA) in one allele and (b) the differences of X box ofα-globin gene cluster in the other allele. To detect the -SEA allele, we utilized the primers located on either side of the breakpoint to do PCR, then characterized the amplified products. For the other allele, we sequenced part of the X box, and found that bases −2803 to −2461 of the X box of −α 3.7 belonged to the X box ofα 2 globin gene. In −α 4.2, the bases belonged to the X box ofα 1 globin gene, whereas inα cs α it contained both X boxes ofα 1 andα 2 globin genes. There was anMboII site at this region of the X box ofα 2 globin gene. We utilized PCR to amplify this region and digested it with restriction enzymeMboII, then combined it with another PCR of different primer pairs to molecularly diagnose different types of Hb H disease. One hundred and one cases of Hb H disease from different families were studied: all of the cases had one allele of -SEA deletion, while the other allele showed that 52/101 were −α 3.7, 41/101 wereα cs α, 7/101 were −α 4.2, and 1/101 was −α G.Taichung. Of 52 cases of Hb H with −α 3.7, 47 were type-I deletion and five were type-II deletion.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01695917
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 8
    Electronic Resource
    Electronic Resource
    Rapid detection of hemoglobin variants by mutagenically separate polymerase chain reaction (MS-PCR) (1995)
    Springer
    Annals of hematology 71 (1995), S. 97-100 
    Details
    ISSN: 1432-0584
    Keywords: Hemoglobin variant ; MS-PCR ; Allele-specific primer
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The detection of molecular defects of hemoglobin variants using mutagenically separated polymerase chain reaction (MS-PCR) was applied in this study. Using different lengths of allele-specific mutagenic primers, normal and mutant alleles of hemoglobin genes were amplified in the same reaction tube. Subsequent gel electrophoresis showed at least one of the two allelic products at the same loci or at least two of the several allelic products at different loci. We employed MS-PCR to test the following hemoglobin variants: Hb Constant Spring (Hb CS), Hb E, Hb G-Taichung, Hb J-Meinung, and Hb Kaohsiung. The results were the same as those obtained by amplified created reaction sites (ACRS) or direct sequencing. We conclude that the MS-PCR provides a rapid and simple alternative to other techniques for mutation detection in hemoglobin variants. Moreover, the principle can be extended to other genetic diseases.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01699253
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 9
    Electronic Resource
    Electronic Resource
    Rapid detection of hemoglobin variants by mutagenically separated polymerase chain reaction (MS-PCR) (1995)
    Springer
    Annals of hematology 71 (1995), S. 97-100 
    Details
    ISSN: 1432-0584
    Keywords: Key words Hemoglobin variant ; MS-PCR ; Allele-specific primer
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  The detection of molecular defects of hemoglobin variants using mutagenically separated polymerase chain reaction (MS-PCR) was applied in this study. Using different lengths of allele-specific mutagenic primers, normal and mutant alleles of hemoglobin genes were amplified in the same reaction tube. Subsequent gel electrophoresis showed at least one of the two allelic products at the same loci or at least two of the several allelic products at different loci. We employed MS-PCR to test the following hemoglobin variants: Hb Constant Spring (Hb CS), Hb E, Hb G-Taichung, Hb J-Meinung, and Hb Kaohsiung. The results were the same as those obtained by amplified created reaction sites (ACRS) or direct sequencing. We conclude that the MS-PCR provides a rapid and simple alternative to other techniques for mutation detection in hemoglobin variants. Moreover, the principle can be extended to other genetic diseases.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01699253
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 10
    Electronic Resource
    Electronic Resource
    NUMERICAL MODELLING OF TWIN-ROLL CASTING BY THE COUPLED FLUID FLOW AND HEAT TRANSFER MODEL (1997)
    Chichester [u.a.] : Wiley-Blackwell
    International Journal for Numerical Methods in Engineering 40 (1997), S. 493-509 
    Details
    ISSN: 0029-5981
    Keywords: twin-roll casting process ; phase change ; Engineering ; Numerical Methods and Modeling
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Mathematics , Technology
    Notes: The twin-roll process is modelled by a coupled fluid flow and phase change model by means of a versatile finite element method. Here, a simple numerical scheme is proposed to solve the problem of determining the interface shape under the thermal equilibrium condition. The procedure is based on a finite element method using a transform technique. The simple numerical method provides an efficient and accurate way to find the interface position and shape with arbitrary boundary geometry. This method can easily be implemented on the existing finite element program, and provides a simple and efficient tool to simulate the solidification as well as the fluid flow problem of the twin-roll casting process. © 1997 by John Wiley & Sons, Ltd.
    Additional Material: 14 Ill.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...