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  • Wiley  (8)
  • English  (8)
  • Natural Sciences  (8)
  • 1
    Online Resource
    Online Resource
    Tumor‐induced osteomalacia combined with acromegaly: A case report
    Wiley ; 2022
    In:  Annals of the New York Academy of Sciences Vol. 1517, No. 1 ( 2022-11), p. 88-92
    Details
    In: Annals of the New York Academy of Sciences, Wiley, Vol. 1517, No. 1 ( 2022-11), p. 88-92
    Abstract: Both acromegaly and tumor‐induced osteomalacia (TIO) are rare diseases caused by an excess hormone secreted by neuroendocrine neoplasms, which are growth hormone (GH) and fibroblast growth factor 23 (FGF23), respectively. GH elevates phosphate reabsorption via the effect of insulin‐like factor 1 (IGF‐1), while FGF23 inhibits phosphate reabsorption and reduces serum phosphate level markedly. A patient who developed a typical acromegaly appearance but was accompanied with height loss and hypophosphatemia for 2 years visited our hospital. Laboratory investigations showed GH and IGF‐1 hypersecretion, as well as hypophosphatemia caused by renal phosphate wasting. Magnetic resonance image revealed a pituitary somatotroph adenoma. Octreoscan scintigraphy also found a causative tumor on the right foot for hypophosphatemia. Then, he underwent resection of the tumor on the right foot. His serum phosphate returned to normal immediately but elevated gradually. Then, we removed the pituitary adenoma of the patient, and the GH and phosphate levels returned to the normal range. Here, we report the first case with acromegaly combined with TIO, the changing process of his phosphate concentration suggests an interesting concurrent effect of excess GH and FGF23 in this rare condition.
    Type of Medium: Online Resource
    ISSN: 0077-8923 , 1749-6632
    URL: Issue
    URL: Article
    DOI: 10.1111/nyas.v1517.1
    DOI: 10.1111/nyas.14893
    RVK:
    TD 7650
    Language: English
    Publisher: Wiley
    Publication Date: 2022
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  • 2
    Online Resource
    Online Resource
    PAX9 mutations and genetic synergism in familial tooth agenesis
    Wiley ; 2023
    In:  Annals of the New York Academy of Sciences Vol. 1524, No. 1 ( 2023-06), p. 87-96
    Details
    In: Annals of the New York Academy of Sciences, Wiley, Vol. 1524, No. 1 ( 2023-06), p. 87-96
    Abstract: Familial tooth agenesis (FTA) is one of the most common craniofacial anomalies in humans. Loss‐of‐function mutations in PAX9 and WNT10A have been known to cause FTA with various expressivity. In this study, we identified five FTA kindreds with novel PAX9 disease‐causing mutations: p.(Glu7Lys), p.(Val83Leu), p.(Pro118Ser), p.(Ser197Argfs*23), and c.771+4A 〉 G. Concomitant PAX9 and WNT10A pathogenic variants found in two probands with severe phenotypes suggested an effect of mutational synergism. All overexpressed PAX9s showed proper nuclear localization, excepting the p.(Pro118Ser) mutant. Various missense mutations caused differential loss of PAX9 transcriptional ability. PAX9 overexpression in dental pulp cells upregulated LEF1 and AXIN2 expression, indicating a positive regulatory role for PAX9 in canonical Wnt signaling. Analyzing 176 cases with 63 different mutations, we observed a distinct pattern of tooth agenesis for PAX9 ‐associated FTA: Maxillary teeth are in general more frequently affected than mandibular ones. Along with all second molars, maxillary bicuspids and first molars are mostly involved, while maxillary lateral incisors and mandibular bicuspids are relatively less affected. Genotypically, missense mutations are associated with fewer missing teeth than frameshift and nonsense variants. This study significantly expands the phenotypic and genotypic spectrums of PAX9 ‐associated disorders and reveals a molecular mechanism of genetic synergism underlying FTA variable expressivity.
    Type of Medium: Online Resource
    ISSN: 0077-8923 , 1749-6632
    URL: Issue
    URL: Article
    DOI: 10.1111/nyas.v1524.1
    DOI: 10.1111/nyas.14988
    RVK:
    TD 7650
    Language: English
    Publisher: Wiley
    Publication Date: 2023
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  • 3
    Online Resource
    Online Resource
    Vitamin D deficiency worsens maternal diabetes induced neurodevelopmental disorder by potentiating hyperglycemia‐mediated epigenetic changes
    Wiley ; 2021
    In:  Annals of the New York Academy of Sciences Vol. 1491, No. 1 ( 2021-05), p. 74-88
    Details
    In: Annals of the New York Academy of Sciences, Wiley, Vol. 1491, No. 1 ( 2021-05), p. 74-88
    Abstract: Many studies have shown that vitamin D (VD) deficiency may be a risk factor for neurodevelopmental disorders, such as autism spectrum disorders (ASDs) and schizophrenia, although causative mechanisms remain unknown. In this study, we investigated the potential role and effect of VD on maternal diabetes induced autism‐related phenotypes. The in vitro study found that enhancing genomic VD signaling by overexpressing the VD receptor (VDR) in human neural progenitor cells ACS‐5003 protects against hyperglycemia‐induced oxidative stress and inflammation by activating Nrf2 and its target genes, including SOD2 and HMOX1 , and accordingly, VDR gene knockdown worsens the problem. In the two in vivo models we explored, maternal diabetes was used to establish an animal model of relevance to ASD, and mice lacking 25‐hydroxyvitamin D 1‐alpha‐hydroxylase (the rate‐limiting enzyme in the synthesis of 1,25(OH)2D3) were used to develop a model of VD deficiency (VDD). We show that although prenatal VDD itself does not produce ASD‐relevant phenotypes, it significantly potentiates maternal diabetes induced epigenetic modifications and autism‐related phenotypes. Postnatal manipulation of VD has no effect on maternal diabetes induced autism‐related phenotypes. We conclude that VDD potentiates maternal diabetes induced autism‐related phenotypes in offspring by epigenetic mechanisms. This study adds to other preclinical studies linking prenatal VDD with a neurodevelopmental disorder.
    Type of Medium: Online Resource
    ISSN: 0077-8923 , 1749-6632
    URL: Issue
    URL: Article
    DOI: 10.1111/nyas.v1491.1
    DOI: 10.1111/nyas.14535
    RVK:
    TD 7650
    Language: English
    Publisher: Wiley
    Publication Date: 2021
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  • 4
    Online Resource
    Online Resource
    Increased Oxidative Damage with Altered Antioxidative Status in Type 2 Diabetic Patients Harboring the 16189 T to C Variant of Mitochondrial DNA
    Wiley ; 2005
    In:  Annals of the New York Academy of Sciences Vol. 1042, No. 1 ( 2005-05), p. 64-69
    Details
    In: Annals of the New York Academy of Sciences, Wiley, Vol. 1042, No. 1 ( 2005-05), p. 64-69
    Abstract: A bstract : A transition of T to C at nucleotide position 16189 in mitochondrial DNA (mtDNA) has attracted biomedical researchers for its probable correlation with the development of diabetes mellitus in adult life. In diabetes, persistent hyperglycemia may cause high production of free radicals. Reactive oxygen species are thought to play a role in a variety of physiologic and pathophysiologic processes in which increased oxidative stress may play an important role in disease mechanisms. The aim of the present study was to clarify the degree of oxidative damage and plasma antioxidant status in diabetic patients and to see the potential influence of the 16189 variant of mtDNA on the oxidative status in these patients. An indicative parameter of lipid peroxidation, malondialdehyde (MDA), and total free thiols were measured from plasma samples of 165 type 2 diabetic patients with or without this variant and 168 normal subjects. Here we report an increase in the plasma levels of MDA and total thiols in type 2 diabetic patients compared with control subjects. The levels of plasma thiols in diabetic patients with the 16189 variant of mtDNA were not different from those in controls. These results suggest an increase in the oxidative damage and a compensatory higher antioxidative status in patients with type 2 diabetes. Harboring the 16189 mtDNA variant may impair the ability of a cell to respond properly to oxidative stress and oxidative damage.
    Type of Medium: Online Resource
    ISSN: 0077-8923 , 1749-6632
    URL: Article
    DOI: 10.1196/annals.1338.007
    RVK:
    TD 7650
    Language: English
    Publisher: Wiley
    Publication Date: 2005
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  • 5
    Online Resource
    Online Resource
    Future Anti‐Catabolic Therapeutic Targets in Bone Disease
    Wiley ; 2006
    In:  Annals of the New York Academy of Sciences Vol. 1068, No. 1 ( 2006-04), p. 447-457
    Details
    In: Annals of the New York Academy of Sciences, Wiley, Vol. 1068, No. 1 ( 2006-04), p. 447-457
    Abstract: Abstract:  Understanding of the regulation of bone catabolism has advanced significantly over the past two decades with the identification of key enzymes that regulate osteoclast formation, activation, and survival following their knockout in mice or recognition of mutations in humans. This led to the discovery of specific inhibitors of some of these key enzymes as proof‐of‐concept lead compounds or potential clinical candidates for the prevention of osteoporosis and other diseases associated with increased bone resorption. Bisphosphonates have been the major therapeutic agents prescribed for the prevention of bone loss in a variety of pathologic conditions for over 30 years. More potent amino bisphosphonates have increased efficacy than earlier drugs, but side effects such as upper gastrointestinal symptoms and the requirement to take them at least 2 h before food have limited patient compliance. This, coupled with the growing knowledge of the pathways regulating osteoclast function, has driven efforts to identify small molecular lead compounds that could be developed into new therapeutic agents with efficacy that matches or supersedes that of bisphosphonates for the prevention of bone loss. In this article, we review briefly the effects of specific inhibitors of bone resorption that have been developed to date and highlight in a variety of models of increased bone resorption the effects of Src kinase inhibitors that have been targeted to bone to limit potential unwanted side effects on other cells.
    Type of Medium: Online Resource
    ISSN: 0077-8923 , 1749-6632
    URL: Article
    DOI: 10.1196/annals.1346.042
    RVK:
    TD 7650
    Language: English
    Publisher: Wiley
    Publication Date: 2006
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    detail.hit.zdb_id: 211003-9
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    SSG: 11
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  • 6
    Online Resource
    Online Resource
    The Host Responses in Sheep Artificially Infected with Theileria sp. (China)
    Wiley ; 2006
    In:  Annals of the New York Academy of Sciences Vol. 1081, No. 1 ( 2006-10), p. 465-467
    Details
    In: Annals of the New York Academy of Sciences, Wiley, Vol. 1081, No. 1 ( 2006-10), p. 465-467
    Abstract: Abstract:  Studies on host responses in sheep artificially infected with Theileria sp. (China) were discussed and summarized mainly on typical high fever periods, merozoits and schizoon observation, antibody response.
    Type of Medium: Online Resource
    ISSN: 0077-8923 , 1749-6632
    URL: Article
    DOI: 10.1196/annals.1373.066
    RVK:
    TD 7650
    Language: English
    Publisher: Wiley
    Publication Date: 2006
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    detail.hit.zdb_id: 2071584-5
    SSG: 11
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  • 7
    Online Resource
    Online Resource
    Ascorbic Acid Bioavailability in Humans : Ascorbic Acid in Plasma, Serum, and Urine
    Wiley ; 1992
    In:  Annals of the New York Academy of Sciences Vol. 669, No. 1 ( 1992-09), p. 383-386
    Details
    In: Annals of the New York Academy of Sciences, Wiley, Vol. 669, No. 1 ( 1992-09), p. 383-386
    Type of Medium: Online Resource
    ISSN: 0077-8923 , 1749-6632
    URL: Issue
    URL: Article
    DOI: 10.1111/nyas.1992.669.issue-1
    DOI: 10.1111/j.1749-6632.1992.tb17130.x
    RVK:
    TD 7650
    Language: English
    Publisher: Wiley
    Publication Date: 1992
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    SSG: 11
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  • 8
    Online Resource
    Online Resource
    Hematopoietic stem cell transplantation ameliorates maternal diabetes–mediated gastrointestinal symptoms and autism‐like behavior in mouse offspring
    Wiley ; 2022
    In:  Annals of the New York Academy of Sciences Vol. 1512, No. 1 ( 2022-06), p. 98-113
    Details
    In: Annals of the New York Academy of Sciences, Wiley, Vol. 1512, No. 1 ( 2022-06), p. 98-113
    Abstract: Epidemiological studies have shown that maternal diabetes is associated with autism spectrum disorder development, although the detailed mechanism remains unclear. We have previously found that maternal diabetes induces persistent epigenetic changes and gene suppression in neurons, subsequently triggering autism‐like behavior (ALB). In this study, we investigated the potential role and effect of hematopoietic stem cells (HSCs) on maternal diabetes–mediated gastrointestinal (GI) dysfunction and ALB in a mouse model. We show in vitro that transient hyperglycemia induced persistent epigenetic changes and gene suppression of tight junction proteins. In vivo , maternal diabetes–mediated oxidative stress induced gene suppression and inflammation in both peripheral blood mononuclear cells and intestine epithelial cells, subsequently triggering GI dysfunction with increased intestinal permeability and altered microbiota compositions, as well as suppressed gene expression in neurons and subsequent ALB in offspring; HSC transplantation (HSCT) ameliorates this effect by systematically reversing maternal diabetes–mediated oxidative stress. We conclude that HSCT can ameliorate maternal diabetes–mediated GI symptoms and autism‐like behavior in mouse offspring.
    Type of Medium: Online Resource
    ISSN: 0077-8923 , 1749-6632
    URL: Issue
    URL: Article
    DOI: 10.1111/nyas.v1512.1
    DOI: 10.1111/nyas.14766
    RVK:
    TD 7650
    Language: English
    Publisher: Wiley
    Publication Date: 2022
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    detail.hit.zdb_id: 2071584-5
    SSG: 11
    Location Call Number Limitation Availability
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