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  1. Article ; Online: Thyrotoxicosis: an under-recognised aetiology.

    Dave, Anjalee / Ludlow, Jason / Malaty, John

    BMJ case reports

    2015  Volume 2015

    Abstract: A 53-year-old woman presented for evaluation of dizziness, shortness of breath and chest pain. She was found to be in atrial fibrillation with rapid ventricular response that was determined to be caused by iodine-induced thyrotoxicosis (from a CT scan ... ...

    Abstract A 53-year-old woman presented for evaluation of dizziness, shortness of breath and chest pain. She was found to be in atrial fibrillation with rapid ventricular response that was determined to be caused by iodine-induced thyrotoxicosis (from a CT scan with intravenous contrast 2 months prior to presentation). Jod-Basedow syndrome (iodine-induced hyperthyroidism) is infrequently considered as a cause of thyrotoxicosis, even when typical risk factors are present. However, this patient did not have typical risk factors: she did not reside in an iodine deficient area, did not have a prior diagnosis of thyroid disorder or goitre, had never been treated with thyroid medications or medications known to cause thyroid dysfunction and she presented later than is typical with this syndrome (2 months after receiving iodinated contrast). She had complete resolution of hyperthyroidism and atrial fibrillation 2 weeks later with no recurrence over the following 7 months.
    MeSH term(s) Atrial Fibrillation/etiology ; Contrast Media/adverse effects ; Diagnostic Imaging/adverse effects ; Female ; Humans ; Hyperthyroidism/chemically induced ; Iodine/adverse effects ; Middle Aged ; Risk Factors ; Thyroid Gland/pathology ; Thyrotoxicosis/chemically induced ; Thyrotoxicosis/complications
    Chemical Substances Contrast Media ; Iodine (9679TC07X4)
    Language English
    Publishing date 2015-05-20
    Publishing country England
    Document type Case Reports ; Journal Article
    ISSN 1757-790X
    ISSN (online) 1757-790X
    DOI 10.1136/bcr-2014-208119
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Prompt initiation of ART With therapeutic food is associated with improved outcomes in HIV-infected Malawian children with malnutrition.

    Kim, Maria H / Cox, Carrie / Dave, Anjalee / Draper, Heather R / Kabue, Mark / Schutze, Gordon E / Ahmed, Saeed / Kazembe, Peter N / Kline, Mark W / Manary, Mark

    Journal of acquired immune deficiency syndromes (1999)

    2011  Volume 59, Issue 2, Page(s) 173–176

    Abstract: This retrospective observational study of 140 HIV-infected children with uncomplicated malnutrition in urban Malawi tested the hypothesis that initiation of antiretroviral therapy (ART) within 21 days of outpatient therapeutic feeding (prompt ART) ... ...

    Abstract This retrospective observational study of 140 HIV-infected children with uncomplicated malnutrition in urban Malawi tested the hypothesis that initiation of antiretroviral therapy (ART) within 21 days of outpatient therapeutic feeding (prompt ART) improved clinical outcomes. Children receiving prompt ART were more likely to recover nutritionally (86% vs. 60%, P < 0.01) and had higher rates of weight gain (3.6 vs. 1.6 g/k/day; P = 0.02). Logistic regression modeling found prompt ART was associated with increased likelihood of nutritional recovery (odds ratio: 5.4, 95% confidence interval: 2.0 to 14.5). This suggests that prompt ART is associated with improved outcomes in HIV-infected Malawian children with uncomplicated malnutrition.
    MeSH term(s) Anti-HIV Agents/therapeutic use ; Child, Preschool ; Combined Modality Therapy/methods ; Female ; Food, Formulated ; HIV Infections/complications ; HIV Infections/drug therapy ; Humans ; Infant ; Logistic Models ; Malawi ; Male ; Malnutrition/complications ; Malnutrition/diet therapy ; Retrospective Studies
    Chemical Substances Anti-HIV Agents
    Language English
    Publishing date 2011-11-22
    Publishing country United States
    Document type Journal Article
    ZDB-ID 645053-2
    ISSN 1944-7884 ; 1077-9450 ; 0897-5965 ; 0894-9255 ; 1525-4135
    ISSN (online) 1944-7884 ; 1077-9450
    ISSN 0897-5965 ; 0894-9255 ; 1525-4135
    DOI 10.1097/QAI.0b013e3182405f8f
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 2442: Show issues Location:
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  3. Article ; Online: Morphology and physiology of the epiphyseal growth plate.

    Burdan, Franciszek / Szumiło, Justyna / Korobowicz, Agnieszka / Farooquee, Rabia / Patel, Sagar / Patel, Ankit / Dave, Anjalee / Szumiło, Michał / Solecki, Michał / Klepacz, Robert / Dudka, Jarosław

    Folia histochemica et cytobiologica

    2009  Volume 47, Issue 1, Page(s) 5–16

    Abstract: The epiphyseal growth plate develops from the cartilaginous-orientated mesenchymal cells that express SOX family genes. This multilayer structure is formed by the proliferation and hypertrophy of cells that synthesize the extracellular matrix composed of ...

    Abstract The epiphyseal growth plate develops from the cartilaginous-orientated mesenchymal cells that express SOX family genes. This multilayer structure is formed by the proliferation and hypertrophy of cells that synthesize the extracellular matrix composed of collagen (mainly type II, IX, X, XI) and proteoglycans (aggrecan, decorin, annexin II, V and VI). The resting zone is responsible for protein synthesis and maintaining a germinal structure. In the proliferative zone, cells rapidly duplicate. The subsequent morphological changes take place in the transformation zone, divided into the upper and lower hypertrophic layers. In the degenerative zone, the mineralization process becomes intensive due to increased release of alkaline phosphate, calcium and matrix vesicles by terminally differentiated chondrocytes and some other factors e.g., metaphyseal ingrowth vessels. At this level, as well as in the primary and secondary spongiosa zones, chondrocytes undergo apoptosis and are physiologically eliminated. Unlike adult cartilage, in fetal and early formed growth plates, unusual forms such as authophagal bodies, paralysis and dark chondrocytes were also observed. Their ultrastructure differs greatly from apoptotic and normal cartilage cells. Chondrocyte proliferation and differentiation are regulated by various endocrine, paracrine, and autocrine agents such as growth, thyroid and sex hormones, beta-catenin, bone morphogenetic proteins, insulin-like growth factor, iodothyronine deiodinase, leptin, nitric oxide, transforming growth factor beta and vitamin D metabolites. However, the most significant factor is parathyroid hormone-related protein (PTHrP) which is synthesized in the perichondrium by terminally differentiated chondrocytes. Secondary to activation of PTH/PTHrP receptors, PTHrP stimulates cell proliferation by G protein activation and delays their transformation into prehypertrophic and hypertrophic chondrocytes. When proliferation is completed, chondrocytes release Indian hedgehog (Ihh), which stimulates PTHrP synthesis via a feedback loop. Any disturbances of the epiphyseal development and its physiology result in various skeletal abnormalities known as dysplasia.
    MeSH term(s) Animals ; Chondrocytes/cytology ; Chondrocytes/ultrastructure ; Chondrogenesis ; Growth Plate/anatomy & histology ; Growth Plate/physiology ; Humans
    Language English
    Publishing date 2009
    Publishing country Poland
    Document type Journal Article ; Review
    ZDB-ID 605761-5
    ISSN 1897-5631 ; 0015-5586 ; 0239-8508
    ISSN (online) 1897-5631
    ISSN 0015-5586 ; 0239-8508
    DOI 10.2478/v10042-009-0007-1
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.B 6: Show issues Location:
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    Zs.MO 545: Show issues

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  4. Article ; Online: Morphology and physiology of the epiphyseal growth plate.

    Robert Klepacz / Michał Solecki / Michał Szumiło / Anjalee Dave / Ankit Patel / Sagar Patel / Rabia Farooquee / Agnieszka Korobowicz / Justyna Szumiło / Franciszek Burdan / Jarosław Dudka

    Folia Histochemica et Cytobiologica, Vol 47, Iss 1, Pp 5-

    2009  Volume 16

    Abstract: The epiphyseal growth plate develops from the cartilaginous-orientated mesenchymal cells that express SOX family genes. This multilayer structure is formed by the proliferation and hypertrophy of cells that synthesize the extracellular matrix composed of ...

    Abstract The epiphyseal growth plate develops from the cartilaginous-orientated mesenchymal cells that express SOX family genes. This multilayer structure is formed by the proliferation and hypertrophy of cells that synthesize the extracellular matrix composed of collagen (mainly type II, IX, X, XI) and proteoglycans (aggrecan, decorin, annexin II, V and VI). The resting zone is responsible for protein synthesis and maintaining a germinal structure. In the proliferative zone, cells rapidly duplicate. The subsequent morphological changes take place in the transformation zone, divided into the upper and lower hypertrophic layers. In the degenerative zone, the mineralization process becomes intensive due to increased release of alkaline phosphate, calcium and matrix vesicles by terminally differentiated chondrocytes and some other factors e.g., metaphyseal ingrowth vessels. At this level, as well as in the primary and secondary spongiosa zones, chondrocytes undergo apoptosis and are physiologically eliminated. Unlike adult cartilage, in fetal and early formed growth plates, unusual forms such as authophagal bodies, paralysis and dark chondrocytes were also observed. Their ultrastructure differs greatly from apoptotic and normal cartilage cells. Chondrocyte proliferation and differentiation are regulated by various endocrine, paracrine, and autocrine agents such as growth, thyroid and sex hormones, beta-catenin, bone morphogenetic proteins, insulin-like growth factor, iodothyronine deiodinase, leptin, nitric oxide, transforming growth factor beta and vitamin D metabolites. However, the most significant factor is parathyroid hormone-related protein (PTHrP) which is synthesized in the perichondrium by terminally differentiated chondrocytes. Secondary to activation of PTH/PTHrP receptors, PTHrP stimulates cell proliferation by G protein activation and delays their transformation into prehypertrophic and hypertrophic chondrocytes. When proliferation is completed, chondrocytes release Indian hedgehog (Ihh), which stimulates PTHrP synthesis via a feedback loop. Any disturbances of the epiphyseal development and its physiology result in various skeletal abnormalities known as dysplasia.
    Keywords Biology (General) ; QH301-705.5 ; Science ; Q ; DOAJ:Biology ; DOAJ:Biology and Life Sciences
    Subject code 610
    Language English
    Publishing date 2009-05-01T00:00:00Z
    Publisher Polish Histochemical and Cytochemical Society
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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