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  1. AU="Ahammad, Rijwan U"
  2. AU="Wong, Man Yu"
  3. AU="Yilmaz, Adnan"
  4. AU="Turkyilmaz, Ayberk"
  5. AU="Ryan, Sophia C"
  6. AU="Stino, Heiko"
  7. AU=Fischbeck K H
  8. AU="Giadinis, Nektarios D"
  9. AU="Patten, Scott"
  10. AU="Verma, Deepika"
  11. AU="Foo, Anthony Tun Lin"
  12. AU="Georgia Panagiotakos"
  13. AU="Tennankore, Karthik K."
  14. AU=Kubota Kenji
  15. AU="Vieille, Peggy"
  16. AU="Kan, Yin-Shi"
  17. AU="Jasińska-Balwierz, Agata"
  18. AU="Hargitai, Rita"
  19. AU=Ueda Kazumitsu
  20. AU="Andrew N. Jordan"
  21. AU="Millemaggi, Alessia"
  22. AU=Paulsen Paige
  23. AU="Fan, Su-Su"
  24. AU="de Azeredo, Andressa Cardoso"
  25. AU="Miller, Russell"
  26. AU="A Mombet"

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  1. Artikel ; Online: Novel systemic delivery of a peptide-conjugated antisense oligonucleotide to reduce α-synuclein in a mouse model of Alzheimer's disease.

    Leitão, André D G / Ahammad, Rijwan U / Spencer, Brian / Wu, Chengbiao / Masliah, Eliezer / Rissman, Robert A

    Neurobiology of disease

    2023  Band 186, Seite(n) 106285

    Abstract: Neurodegenerative disorders of aging are characterized by the progressive accumulation of proteins such as α-synuclein (α-syn) and amyloid beta (Aβ). Misfolded and aggregated α-syn has been implicated in neurological disorders such as Parkinson's disease, ...

    Abstract Neurodegenerative disorders of aging are characterized by the progressive accumulation of proteins such as α-synuclein (α-syn) and amyloid beta (Aβ). Misfolded and aggregated α-syn has been implicated in neurological disorders such as Parkinson's disease, and Dementia with Lewy Bodies, but less so in Alzheimer's Disease (AD), despite the fact that accumulation of α-syn has been confirmed in over 50% of postmortem brains neuropathologically diagnosed with AD. To date, no therapeutic strategy has effectively or consistently downregulated α-syn in AD. Here we tested the hypothesis that by using a systemically-delivered peptide (ApoB
    Mesh-Begriff(e) Animals ; Mice ; Oligonucleotides, Antisense/pharmacology ; alpha-Synuclein/genetics ; Alzheimer Disease/drug therapy ; Amyloid beta-Peptides ; Apolipoproteins B ; Disease Models, Animal
    Chemische Substanzen Oligonucleotides, Antisense ; alpha-Synuclein ; Amyloid beta-Peptides ; Apolipoproteins B
    Sprache Englisch
    Erscheinungsdatum 2023-09-09
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 1211786-9
    ISSN 1095-953X ; 0969-9961
    ISSN (online) 1095-953X
    ISSN 0969-9961
    DOI 10.1016/j.nbd.2023.106285
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: Association of mannose-binding lectin 2 gene polymorphisms with Guillain-Barré syndrome.

    Jahan, Israt / Hayat, Shoma / Khalid, Mir M / Ahammad, Rijwan U / Asad, Asaduzzaman / Islam, Badrul / Mohammad, Quazi D / Jacobs, Bart C / Islam, Zhahirul

    Scientific reports

    2022  Band 12, Heft 1, Seite(n) 5791

    Abstract: Complement activation plays a critical role in the pathogenesis of Guillain-Barré syndrome (GBS), a debilitating immune-mediated neuropathy. Mannose-binding lectin (MBL) is a complement activation factor of lectin pathway which as genetic host factor may ...

    Abstract Complement activation plays a critical role in the pathogenesis of Guillain-Barré syndrome (GBS), a debilitating immune-mediated neuropathy. Mannose-binding lectin (MBL) is a complement activation factor of lectin pathway which as genetic host factor may influence the susceptibility or severity of GBS. We investigated the frequency of MBL2 promoter (- 550H/L and - 221X/Y) and functional region (exon 1 A/O) polymorphisms and their association with disease susceptibility, clinical features and serum MBL among GBS patients (n = 300) and healthy controls (n = 300) in Bangladesh. The median patient age was 30 years (IQR: 18-42; males, 68%). MBL2 polymorphisms were not significantly associated with GBS susceptibility compared to healthy controls. HL heterozygosity in GBS patients was significantly associated with mild functional disability at enrolment (P = 0.0145, OR, 95% CI 2.1, 1.17-3.82). The HY, YA, HA and HYA heterozygous haplotypes were more common among mildly affected (P = 0.0067, P = 0.0086, P = 0.0075, P = 0.0032, respectively) than severely affected patients with GBS. Reduced serum MBL was significantly associated with the LL, OO and no HYA variants and GBS disease severity. No significant association was observed between MBL2 polymorphisms and electrophysiological variants, recent Campylobacter jejuni infection or anti-ganglioside (GM1) antibody responses in GBS. In conclusion, MBL2 gene polymorphisms are related to reduced serum MBL and associated with the severity of GBS.
    Mesh-Begriff(e) Adolescent ; Adult ; Complement Activation ; Exons ; Genetic Predisposition to Disease ; Genotype ; Guillain-Barre Syndrome/genetics ; Haplotypes ; Humans ; Male ; Mannose-Binding Lectin/genetics ; Polymorphism, Genetic ; Young Adult
    Chemische Substanzen MBL2 protein, human ; Mannose-Binding Lectin
    Sprache Englisch
    Erscheinungsdatum 2022-04-06
    Erscheinungsland England
    Dokumenttyp Journal Article
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-022-09621-y
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel ; Online: FAS promoter polymorphisms and serum sFas level are associated with increased risk of nerve damage in Bangladeshi patients with Guillain-Barré syndrome.

    Islam, Zhahirul / Jahan, Israt / Ahammad, Rijwan U / Shahnaij, Mohammad / Nahar, Shamsun / Mohammad, Quazi D

    PloS one

    2018  Band 13, Heft 2, Seite(n) e0192703

    Abstract: Guillain-Barré syndrome (GBS) is an autoimmune disorder of the peripheral nervous system triggered by molecular mimicry between pathogen lipopolysaccharides and host nerve gangliosides. Polymorphisms in the Fas receptor (FAS) and Fas ligand (FASL) genes ... ...

    Abstract Guillain-Barré syndrome (GBS) is an autoimmune disorder of the peripheral nervous system triggered by molecular mimicry between pathogen lipopolysaccharides and host nerve gangliosides. Polymorphisms in the Fas receptor (FAS) and Fas ligand (FASL) genes may potentially alter the elimination of autoreactive immune cells and affect disease susceptibility or disease severity in GBS. We detected single nucleotide polymorphisms (SNPs) in FAS (-1377G/A and -670A/G) and FASL (-843C/T) in a prospective cohort of 300 patients with GBS and 300 healthy controls from the Bangladeshi population. Genotype distributions were not significantly different between patients with GBS and healthy controls. The FAS -670 AG heterozygous (P = 0.0005, OR = 2.5, 95% CI = 1.5-4.2) and GG homozygous (P = 0.0048, OR = 2.6, 95% CI = 1.3-5.0) genotypes were more common in patients with anti-GM1 antibodies than patients without anti-GM1 antibodies. The FAS -670 G allele was more prevalent in anti-GM1 antibody-positive than -negative patients (P = 0.0002, OR = 1.9, 95% CI = 1.4-2.7) and also in patients with the axonal subtype than demyelinating subtype (P < 0.0001, OR = 4.8, 95% CI = 2.3-10.1). The 1377G/-670G GG haplotype was significantly associated with the axonal subtype (P < 0.0001) and anti-ganglioside antibody-positivity (P = 0.0008) in GBS. Serum sFas (237.5 pg/mL vs. 159.5 pg/mL; P < 0.0001) and sFasL (225.1 pg/mL vs. 183.4 pg/mL; P = 0.0069) were elevated in patients with GBS compared to healthy controls, and among patients with high serum sFas was associated with severe GBS (P = 0.0406). In conclusion, this study indicates FAS-FASL promoter SNPs may promote the production of cross-reactive anti-ganglioside antibodies in GBS.
    Mesh-Begriff(e) Adolescent ; Adult ; Bangladesh ; Case-Control Studies ; Child ; Child, Preschool ; Fas Ligand Protein/genetics ; Female ; G(M1) Ganglioside/immunology ; Guillain-Barre Syndrome/blood ; Guillain-Barre Syndrome/pathology ; Humans ; Male ; Middle Aged ; Peripheral Nervous System/pathology ; Polymorphism, Single Nucleotide ; Promoter Regions, Genetic ; Prospective Studies ; Young Adult ; fas Receptor/blood ; fas Receptor/genetics
    Chemische Substanzen Fas Ligand Protein ; fas Receptor ; G(M1) Ganglioside (37758-47-7)
    Sprache Englisch
    Erscheinungsdatum 2018
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 1932-6203
    ISSN (online) 1932-6203
    DOI 10.1371/journal.pone.0192703
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel: Toll-like receptor-4 299Gly allele is associated with Guillain-Barré syndrome in Bangladesh.

    Jahan, Israt / Ahammad, Rijwan U / Khalid, Mir M / Rahman, Mohammad I / Hayat, Shoma / Islam, Badrul / Mohammad, Quazi D / Islam, Zhahirul

    Annals of clinical and translational neurology

    2019  Band 6, Heft 4, Seite(n) 708–715

    Abstract: Objective: TLR4 plays an important role in the pathogenesis of Guillain-Barré syndrome (GBS). The relationships between : Methods: A total of 290 subjects were included in this study: 141 patients with GBS and 149 unrelated healthy controls. The : ... ...

    Abstract Objective: TLR4 plays an important role in the pathogenesis of Guillain-Barré syndrome (GBS). The relationships between
    Methods: A total of 290 subjects were included in this study: 141 patients with GBS and 149 unrelated healthy controls. The
    Results: The minor 299Gly allele was significantly associated with GBS susceptibility (
    Interpretation: The
    Mesh-Begriff(e) Adolescent ; Adult ; Aged ; Alleles ; Bangladesh ; Female ; Gene Frequency/genetics ; Genotype ; Guillain-Barre Syndrome/etiology ; Guillain-Barre Syndrome/genetics ; Humans ; Male ; Middle Aged ; Polymorphism, Single Nucleotide/genetics ; Toll-Like Receptor 4/genetics ; Young Adult
    Chemische Substanzen TLR4 protein, human ; Toll-Like Receptor 4
    Sprache Englisch
    Erscheinungsdatum 2019-03-03
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 2740696-9
    ISSN 2328-9503
    ISSN 2328-9503
    DOI 10.1002/acn3.744
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  5. Artikel ; Online: CD1A and CD1E gene polymorphisms are not associated with susceptibility to Guillain-Barré syndrome in the Bangladeshi population.

    Rahman, Mohammad I / Jahan, Iffat / Khalid, Mir M / Jahan, Israt / Ahammad, Rijwan U / Nahar, Shamsun / Islam, Zhahirul

    Journal of neuroimmunology

    2017  Band 314, Seite(n) 8–12

    Abstract: The post-infectious autoimmune polyradiculoneuropathy Guillain-Barré syndrome (GBS) is triggered by molecular mimicry between microbial glycolipid antigens and human peripheral nerve gangliosides. Single nucleotide polymorphisms in exon 2 of CD1A (*01/* ... ...

    Abstract The post-infectious autoimmune polyradiculoneuropathy Guillain-Barré syndrome (GBS) is triggered by molecular mimicry between microbial glycolipid antigens and human peripheral nerve gangliosides. Single nucleotide polymorphisms in exon 2 of CD1A (*01/*02) and CD1E (*01/*02) were assessed using PCR-RFLP; no significant differences in genotype or allele frequency were observed between 200 patients with GBS and 200 healthy controls. CD1 gene polymorphisms cannot be recognized as a susceptibility or disease-causative factor for GBS in the Bangladeshi population. However, further studies are necessary to investigate the CD1A*01/CD1E*01 haplotype distribution and its potential causative role in the axonal form of GBS.
    Mesh-Begriff(e) Adult ; Antigens, CD1/genetics ; Antigens, CD1/immunology ; Bangladesh ; Female ; Genetic Predisposition to Disease/genetics ; Guillain-Barre Syndrome/genetics ; Guillain-Barre Syndrome/immunology ; Haplotypes ; Humans ; Male ; Middle Aged ; Molecular Mimicry ; Polymorphism, Single Nucleotide
    Chemische Substanzen Antigens, CD1 ; CD1a antigen ; CD1e antigen
    Sprache Englisch
    Erscheinungsdatum 2017-11-22
    Erscheinungsland Netherlands
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 8335-5
    ISSN 1872-8421 ; 0165-5728
    ISSN (online) 1872-8421
    ISSN 0165-5728
    DOI 10.1016/j.jneuroim.2017.11.013
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  6. Artikel ; Online: Tumor necrosis factor-alpha -863C/A polymorphism is associated with Guillain-Barré syndrome in Bangladesh.

    Jahan, Israt / Ahammad, Rijwan U / Farzana, Kaniz S / Khalid, Mir M / Islam, Mohammad B / Rahman, Mohammad I / Nahar, Shamsun / Kabir, Yearul / Mohmmad, Quazi D / Islam, Zhahirul

    Journal of neuroimmunology

    2017  Band 310, Seite(n) 46–50

    Abstract: Guillain-Barré syndrome (GBS) is a post-infectious autoimmune polyneuropathy regulated by pro- and anti-inflammatory cytokines; TNFA polymorphisms may exert immune pathogenic roles in GBS. We assessed TNFA promoter region polymorphisms (-238G/A, -308G/A, ...

    Abstract Guillain-Barré syndrome (GBS) is a post-infectious autoimmune polyneuropathy regulated by pro- and anti-inflammatory cytokines; TNFA polymorphisms may exert immune pathogenic roles in GBS. We assessed TNFA promoter region polymorphisms (-238G/A, -308G/A, -857C/T, -863C/A) in Bangladeshi patients with GBS (n=300) and healthy controls (n=300) by PCR-RFLP and ASO-PCR. TNFA -863CA was significantly associated with GBS disease susceptibility (P=0.0154) and disease severity (P=0.0492). TNFA -238A allele was more frequent among anti-ganglioside (GM1) antibody-positive patients (P=0.0092) and -863AA associated with AMAN subtype of GBS (P=0.0398). TNFA -863C/A may contribute to GBS severity and pathogenesis in Bangladeshi patients.
    Mesh-Begriff(e) Adolescent ; Adult ; Aged ; Antibodies/blood ; Bangladesh/epidemiology ; Child ; Child, Preschool ; Female ; Gangliosides/immunology ; Genetic Association Studies ; Genetic Predisposition to Disease/genetics ; Genotype ; Guillain-Barre Syndrome/genetics ; Humans ; Longitudinal Studies ; Male ; Middle Aged ; Polymorphism, Single Nucleotide/genetics ; Tumor Necrosis Factor-alpha/genetics ; Young Adult
    Chemische Substanzen Antibodies ; Gangliosides ; Tumor Necrosis Factor-alpha
    Sprache Englisch
    Erscheinungsdatum 2017-06-20
    Erscheinungsland Netherlands
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 8335-5
    ISSN 1872-8421 ; 0165-5728
    ISSN (online) 1872-8421
    ISSN 0165-5728
    DOI 10.1016/j.jneuroim.2017.06.005
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

    Volltext online

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