GLORIA

GEOMAR Library Ocean Research Information Access

X

Your email was sent successfully. Check your inbox.

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

Proceed reservation?

Export
Filter
  • English  (256)
Material
Publisher
Person/Organisation
Language
  • English  (256)
Years
FID
Subjects(RVK)
  • 1
    Online Resource
    Online Resource
    Identical and Nonidentical Twins: Risk and Factors Involved in Development of Islet Autoimmunity and Type 1 Diabetes
    American Diabetes Association ; 2019
    In:  Diabetes Care Vol. 42, No. 2 ( 2019-02-01), p. 192-199
    Details
    In: Diabetes Care, American Diabetes Association, Vol. 42, No. 2 ( 2019-02-01), p. 192-199
    Abstract: There are variable reports of risk of concordance for progression to islet autoantibodies and type 1 diabetes in identical twins after one twin is diagnosed. We examined development of positive autoantibodies and type 1 diabetes and the effects of genetic factors and common environment on autoantibody positivity in identical twins, nonidentical twins, and full siblings. RESEARCH DESIGN AND METHODS Subjects from the TrialNet Pathway to Prevention Study (N = 48,026) were screened from 2004 to 2015 for islet autoantibodies (GAD antibody [GADA], insulinoma-associated antigen 2 [IA-2A] , and autoantibodies against insulin [IAA]). Of these subjects, 17,226 (157 identical twins, 283 nonidentical twins, and 16,786 full siblings) were followed for autoantibody positivity or type 1 diabetes for a median of 2.1 years. RESULTS At screening, identical twins were more likely to have positive GADA, IA-2A, and IAA than nonidentical twins or full siblings (all P & lt; 0.0001). Younger age, male sex, and genetic factors were significant factors for expression of IA-2A, IAA, one or more positive autoantibodies, and two or more positive autoantibodies (all P ≤ 0.03). Initially autoantibody-positive identical twins had a 69% risk of diabetes by 3 years compared with 1.5% for initially autoantibody-negative identical twins. In nonidentical twins, type 1 diabetes risk by 3 years was 72% for initially multiple autoantibody–positive, 13% for single autoantibody–positive, and 0% for initially autoantibody-negative nonidentical twins. Full siblings had a 3-year type 1 diabetes risk of 47% for multiple autoantibody–positive, 12% for single autoantibody–positive, and 0.5% for initially autoantibody-negative subjects. CONCLUSIONS Risk of type 1 diabetes at 3 years is high for initially multiple and single autoantibody–positive identical twins and multiple autoantibody–positive nonidentical twins. Genetic predisposition, age, and male sex are significant risk factors for development of positive autoantibodies in twins.
    Type of Medium: Online Resource
    ISSN: 0149-5992 , 1935-5548
    URL: Article
    DOI: 10.2337/dc18-0288
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2019
    detail.hit.zdb_id: 1490520-6
    detail.hit.zdb_id: 441231-X
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 2
    Online Resource
    Online Resource
    A Type 1 Diabetes Genetic Risk Score Predicts Progression of Islet Autoimmunity and Development of Type 1 Diabetes in Individuals at Risk
    American Diabetes Association ; 2018
    In:  Diabetes Care Vol. 41, No. 9 ( 2018-09-01), p. 1887-1894
    Details
    In: Diabetes Care, American Diabetes Association, Vol. 41, No. 9 ( 2018-09-01), p. 1887-1894
    Abstract: We tested the ability of a type 1 diabetes (T1D) genetic risk score (GRS) to predict progression of islet autoimmunity and T1D in at-risk individuals. RESEARCH DESIGN AND METHODS We studied the 1,244 TrialNet Pathway to Prevention study participants (T1D patients’ relatives without diabetes and with one or more positive autoantibodies) who were genotyped with Illumina ImmunoChip (median [range] age at initial autoantibody determination 11.1 years [1.2–51.8] , 48% male, 80.5% non-Hispanic white, median follow-up 5.4 years). Of 291 participants with a single positive autoantibody at screening, 157 converted to multiple autoantibody positivity and 55 developed diabetes. Of 953 participants with multiple positive autoantibodies at screening, 419 developed diabetes. We calculated the T1D GRS from 30 T1D-associated single nucleotide polymorphisms. We used multivariable Cox regression models, time-dependent receiver operating characteristic curves, and area under the curve (AUC) measures to evaluate prognostic utility of T1D GRS, age, sex, Diabetes Prevention Trial–Type 1 (DPT-1) Risk Score, positive autoantibody number or type, HLA DR3/DR4-DQ8 status, and race/ethnicity. We used recursive partitioning analyses to identify cut points in continuous variables. RESULTS Higher T1D GRS significantly increased the rate of progression to T1D adjusting for DPT-1 Risk Score, age, number of positive autoantibodies, sex, and ethnicity (hazard ratio [HR] 1.29 for a 0.05 increase, 95% CI 1.06–1.6; P = 0.011). Progression to T1D was best predicted by a combined model with GRS, number of positive autoantibodies, DPT-1 Risk Score, and age (7-year time-integrated AUC = 0.79, 5-year AUC = 0.73). Higher GRS was significantly associated with increased progression rate from single to multiple positive autoantibodies after adjusting for age, autoantibody type, ethnicity, and sex (HR 2.27 for GRS & gt;0.295, 95% CI 1.47–3.51; P = 0.0002). CONCLUSIONS The T1D GRS independently predicts progression to T1D and improves prediction along T1D stages in autoantibody-positive relatives.
    Type of Medium: Online Resource
    ISSN: 0149-5992 , 1935-5548
    URL: Article
    DOI: 10.2337/dc18-0087
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2018
    detail.hit.zdb_id: 1490520-6
    detail.hit.zdb_id: 441231-X
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 3
    Online Resource
    Online Resource
    Regulation of thalamic neurite outgrowth by the Eph ligand ephrin-A5: Implications in the development of thalamocortical projections
    Proceedings of the National Academy of Sciences ; 1998
    In:  Proceedings of the National Academy of Sciences Vol. 95, No. 9 ( 1998-04-28), p. 5329-5334
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 95, No. 9 ( 1998-04-28), p. 5329-5334
    Abstract: The cerebral cortex is parcellated into different functional domains that receive distinct inputs from other cortical and subcortical regions. The molecular mechanisms underlying the specificity of connections of cortical afferents remain unclear. We report here that the Eph family tyrosine kinase receptor EphA5 and the ligand ephrin-A5 may play a key role in the exclusion of the limbic thalamic afferents from the sensorimotor cortex by mediating repulsive interactions. In situ hybridization shows that the EphA5 transcript is expressed at high levels in both cortical and subcortical limbic regions, including the frontal cortex, the subiculum, and the medial thalamic nuclei. In contrast, ephrin-A5 is transcribed abundantly in the sensorimotor cortex. Consistent with the complementary expression, the ligand inhibited dramatically the growth of neurites from neurons isolated from the medial thalamus but was permissive for the growth of neurites from lateral thalamic neurons, which is primarily nonlimbic. Similarly, the growth of neurites from Eph-A5-expressing neurons isolated from the subiculum was inhibited by ephrin-A5. Our studies suggest that the Eph family ligand ephrin-A5 serves as a general inhibitor of axonal growth from limbic neurons, which may serve to prevent innervation of inappropriate primary sensorimotor regions, thus contributing to the generation of specificity of thalamic cortical afferents.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.95.9.5329
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 1998
    detail.hit.zdb_id: 209104-5
    detail.hit.zdb_id: 1461794-8
    SSG: 11
    SSG: 12
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 4
    Online Resource
    Online Resource
    Immediate nephrectomy versus preoperative chemotherapy in the management of non-metastatic Wilms’ tumour: Results of a randomised trial (UKW3) by the UK Children’s Cancer Study Group
    Elsevier BV ; 2006
    In:  European Journal of Cancer Vol. 42, No. 15 ( 2006-10), p. 2554-2562
    Details
    In: European Journal of Cancer, Elsevier BV, Vol. 42, No. 15 ( 2006-10), p. 2554-2562
    Type of Medium: Online Resource
    ISSN: 0959-8049
    URL: Article
    DOI: 10.1016/j.ejca.2006.05.026
    RVK:
    XA 42017.A
    RVK:
    XA 42017
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2006
    detail.hit.zdb_id: 1120460-6
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 5
    Online Resource
    Online Resource
    Noradrenaline neuron innervation of the neocortex in the rat
    Elsevier BV ; 1978
    In:  Brain Research Vol. 139, No. 2 ( 1978-01), p. 219-231
    Details
    In: Brain Research, Elsevier BV, Vol. 139, No. 2 ( 1978-01), p. 219-231
    Type of Medium: Online Resource
    ISSN: 0006-8993
    URL: Article
    DOI: 10.1016/0006-8993(78)90925-3
    RVK:
    XA 10000
    Language: English
    Publisher: Elsevier BV
    Publication Date: 1978
    detail.hit.zdb_id: 1200-2
    SSG: 12
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 6
    Online Resource
    Online Resource
    Regionally restricted expression of the transcription factor c‐ myc intron 1 binding protein during brain development
    Wiley ; 2003
    In:  Journal of Comparative Neurology Vol. 467, No. 4 ( 2003-12-22), p. 581-592
    Details
    In: Journal of Comparative Neurology, Wiley, Vol. 467, No. 4 ( 2003-12-22), p. 581-592
    Abstract: Transcription factors regulate proliferation, differentiation, and regionalization of the central nervous system. In a screen of developing cerebral cortex, we identified the transcription factor c‐ myc intron 1 binding protein ( mibp1 ) due to its abundant expression. In this study, we analyzed the temporal and spatial expression patterns of mibp1 mRNA in developing mouse brain to address the putative role of this transcription factor in neural differentiation. Northern hybridization studies revealed that mibp1 is expressed first in the mouse dorsal telencephalon at embryonic day (E) 14.5, during peak neuronal production. In situ hybridization experiments revealed that mibp1 expression in the cerebral wall is most abundant in postmitotic cells of the cortical plate and absent from proliferative zones. Moreover, mibp1 is restricted to dorsal telencephalon during embryogenesis with expression only in the cerebral wall, olfactory bulb, and hippocampus. N‐ myc , a potential target of mibp1 regulation, exhibited complementary, nonoverlapping expression patterns in the telencephalon with greatest expression in proliferating cells of the ventricular zone from E12.5 to E14.5; N‐ myc was absent from the telencephalon by E15.5. The specificity and timing of mibp1 expression in the cerebral cortex suggests a role in maintaining a state of neuronal differentiation in the dorsal telencephalon. J. Comp. Neurol. 467:581–592, 2003. © 2003 Wiley‐Liss, Inc.
    Type of Medium: Online Resource
    ISSN: 0021-9967 , 1096-9861
    URL: Issue
    URL: Article
    DOI: 10.1002/cne.v467:4
    DOI: 10.1002/cne.10958
    Language: English
    Publisher: Wiley
    Publication Date: 2003
    detail.hit.zdb_id: 3086-7
    detail.hit.zdb_id: 1474879-4
    SSG: 12
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 7
    Online Resource
    Online Resource
    Subclass‐specific expression patterns of MET receptor tyrosine kinase during development in medial prefrontal and visual cortices
    Wiley ; 2023
    In:  Journal of Comparative Neurology Vol. 531, No. 1 ( 2023-01), p. 132-148
    Details
    In: Journal of Comparative Neurology, Wiley, Vol. 531, No. 1 ( 2023-01), p. 132-148
    Abstract: Met encodes a receptor tyrosine kinase (MET) that is expressed during development and regulates cortical synapse maturation. Conditional deletion of Met in the nervous system during embryonic development leads to deficits in adult contextual fear learning, a medial prefrontal cortex (mPFC)‐dependent cognitive task. MET also regulates the timing of critical period plasticity for ocular dominance in primary visual cortex (V1). However, the underlying circuitry responsible remains unknown. Therefore, this study determines the broad expression patterns of MET throughout postnatal development in mPFC and V1 projection neurons (PNs), providing insight into similarities and differences in the neuronal subtypes and temporal patterns of MET expression between cortical areas. Using a transgenic mouse line that expresses green fluorescent protein (GFP) in Met + neurons, immunofluorescence and confocal microscopy were performed to visualize MET‐GFP + cell bodies and PN subclass‐specific protein markers. Analyses reveal that the MET expression is highly enriched in infragranular layers of mPFC, but in supragranular layers of V1. Interestingly, temporal regulation of the percentage of MET + neurons across development not only differs between cortical regions but also is distinct between lamina within a cortical region. Further, MET is expressed predominantly in the subcerebral PN subclass in mPFC, but the intratelencephalic PN subclass in V1. The data suggest that MET signaling influences the development of distinct circuits in mPFC and V1 that underlie subcerebral and intracortical functional deficits following Met deletion, respectively.
    Type of Medium: Online Resource
    ISSN: 0021-9967 , 1096-9861
    URL: Issue
    URL: Article
    DOI: 10.1002/cne.v531.1
    DOI: 10.1002/cne.25418
    Language: English
    Publisher: Wiley
    Publication Date: 2023
    detail.hit.zdb_id: 3086-7
    detail.hit.zdb_id: 1474879-4
    SSG: 12
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 8
    Online Resource
    Online Resource
    Waved‐1 mutant mice are hypersensitive to the locomotor actions of cocaine
    Wiley ; 2007
    In:  Synapse Vol. 61, No. 4 ( 2007-04), p. 259-262
    Details
    In: Synapse, Wiley, Vol. 61, No. 4 ( 2007-04), p. 259-262
    Abstract: Transforming growth factor‐α (TGFα) is a well‐known regulator of many developmental processes, and is expressed heavily in basal forebrain and striatal regions. When TGFα is reduced in Waved‐1 (Wa‐1) mutant mice, brain anatomy, biogenic amines, stress response, and behavior are normal prior to, but altered following puberty. As an initial screen for possible alterations in nigrostriatal and mesolimbic dopamine (DA) systems, we tested adult Wa‐1 mutant mice in an open field, following acute injection with cocaine (15 mg/kg). Wa‐1 mice exhibited significantly greater ambulatory distance, number of ambulatory episodes, and cocaine‐induced motor stereotypies than do controls. These data indicate that adult Wa‐1 mice are hypersensitive to the locomotor effects of cocaine and provide a new potential link between neurodevelopmental processes and adult psychostimulant responsiveness. Synapse 61:259–262, 2007. © 2007 Wiley‐Liss, Inc.
    Type of Medium: Online Resource
    ISSN: 0887-4476 , 1098-2396
    URL: Issue
    URL: Article
    DOI: 10.1002/syn.v61:4
    DOI: 10.1002/syn.20364
    Language: English
    Publisher: Wiley
    Publication Date: 2007
    detail.hit.zdb_id: 1474927-0
    detail.hit.zdb_id: 639061-4
    SSG: 12
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 9
    Online Resource
    Online Resource
    Disruption of cerebral cortex MET signaling in autism spectrum disorder
    Wiley ; 2007
    In:  Annals of Neurology Vol. 62, No. 3 ( 2007-09), p. 243-250
    Details
    In: Annals of Neurology, Wiley, Vol. 62, No. 3 ( 2007-09), p. 243-250
    Abstract: Multiple genes contribute to autism spectrum disorder (ASD) susceptibility. One particularly promising candidate is the MET gene, which encodes a receptor tyrosine kinase that mediates hepatocyte growth factor (HGF) signaling in brain circuit formation, immune function, and gastrointestinal repair. The MET promoter variant rs1858830 allele “C” is strongly associated with ASD and results in reduced gene transcription. Here we examined expression levels of MET and members of the MET signaling pathway in postmortem cerebral cortex from ASD cases and healthy control subjects. Methods Protein, total RNA, and DNA were extracted from postmortem temporal cortex gray matter samples (BA 41/42, 52, or 22) belonging to eight pairs of ASD cases and matched control subjects. MET protein expression was determined by Western blotting; messenger RNA expression of MET and other related transcripts was assayed by microarray and quantitative reverse transcriptase polymerase chain reaction. Results MET protein levels were significantly decreased in ASD cases compared with control subjects. This was accompanied in ASD brains by increased messenger RNA expression for proteins involved in regulating MET signaling activity. Analyses of coexpression of MET and HGF demonstrated a positive correlation in control subjects that was disrupted in ASD cases. Interpretation Altered expression of MET and related molecules suggests dysregulation of signaling that may contribute to altered circuit formation and function in ASD. The complement of genes that encode proteins involved in MET activation appears to undergo long‐term compensatory changes in expression that may be a hallmark contribution to the pathophysiology of ASD. Ann Neurol 2007
    Type of Medium: Online Resource
    ISSN: 0364-5134 , 1531-8249
    URL: Issue
    URL: Article
    DOI: 10.1002/ana.v62:3
    DOI: 10.1002/ana.21180
    Language: English
    Publisher: Wiley
    Publication Date: 2007
    detail.hit.zdb_id: 80362-5
    detail.hit.zdb_id: 2037912-2
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 10
    Online Resource
    Online Resource
    Evidence of cell‐nonautonomous changes in dendrite and dendritic spine morphology in the met‐signaling–deficient mouse forebrain
    Wiley ; 2010
    In:  Journal of Comparative Neurology Vol. 518, No. 21 ( 2010-11), p. 4463-4478
    Details
    In: Journal of Comparative Neurology, Wiley, Vol. 518, No. 21 ( 2010-11), p. 4463-4478
    Abstract: Human genetic findings and murine neuroanatomical expression mapping have intersected to implicate Met receptor tyrosine kinase signaling in the development of forebrain circuits controlling social and emotional behaviors that are atypical in autism‐spectrum disorders (ASD). To clarify roles for Met signaling during forebrain circuit development in vivo, we generated mutant mice (Emx1 Cre /Met fx/fx ) with an Emx1‐Cre‐driven deletion of signaling‐competent Met in dorsal pallially derived forebrain neurons. Morphometric analyses of Lucifer yellow‐injected pyramidal neurons in postnatal day 40 anterior cingulate cortex (ACC) revealed no statistically significant changes in total dendritic length but a selective reduction in apical arbor length distal to the soma in Emx1 Cre /Met fx/fx neurons relative to wild type, consistent with a decrease in the total tissue volume sampled by individual arbors in the cortex. The effects on dendritic structure appear to be circuit‐selective, insofar as basal arbor length was increased in Emx1 Cre /Met fx/fx layer 2/3 neurons. Spine number was not altered on the Emx1 Cre /Met fx/fx pyramidal cell populations studied, but spine head volume was significantly increased (∼20%). Cell‐nonautonomous, circuit‐level influences of Met signaling on dendritic development were confirmed by studies of medium spiny neurons (MSN), which do not express Met but receive Met‐expressing corticostriatal afferents during development. Emx1 Cre /Met fx/fx MSN exhibited robust increases in total arbor length (∼20%). As in the neocortex, average spine head volume was also increased (∼12%). These data demonstrate that a developmental loss of presynaptic Met receptor signaling can affect postsynaptic morphogenesis and suggest a mechanism whereby attenuated Met signaling could disrupt both local and long‐range connectivity within circuits relevant to ASD. J. Comp. Neurol. 518:4463–4478, 2010. © 2010 Wiley‐Liss, Inc.
    Type of Medium: Online Resource
    ISSN: 0021-9967 , 1096-9861
    URL: Issue
    URL: Article
    DOI: 10.1002/cne.v518:21
    DOI: 10.1002/cne.22467
    Language: English
    Publisher: Wiley
    Publication Date: 2010
    detail.hit.zdb_id: 3086-7
    detail.hit.zdb_id: 1474879-4
    SSG: 12
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...