-
Nature Reviews. Endocrinology Mar 2014Iodine is a micronutrient that is essential for the production of thyroid hormones. The primary source of iodine is the diet via consumption of foods that have been... (Review)
Review
Iodine is a micronutrient that is essential for the production of thyroid hormones. The primary source of iodine is the diet via consumption of foods that have been fortified with iodine, including salt, dairy products and bread, or that are naturally abundant in the micronutrient, such as seafood. Recommended daily iodine intake is 150 µg in adults who are not pregnant or lactating. Ingestion of iodine or exposure above this threshold is generally well-tolerated. However, in certain susceptible individuals, including those with pre-existing thyroid disease, the elderly, fetuses and neonates, or patients with other risk factors, the risk of developing iodine-induced thyroid dysfunction might be increased. Hypothyroidism or hyperthyroidism as a result of supraphysiologic iodine exposure might be either subclinical or overt, and the source of the excess iodine might not be readily apparent.
Topics: Humans; Hyperthyroidism; Hypothyroidism; Iodine; Thyroid Gland
PubMed: 24342882
DOI: 10.1038/nrendo.2013.251 -
American Family Physician Jun 2014Salivary gland disorders include inflammatory, bacterial, viral, and neoplastic etiologies. The presentation can be acute, recurrent, or chronic. Acute suppurative... (Review)
Review
Salivary gland disorders include inflammatory, bacterial, viral, and neoplastic etiologies. The presentation can be acute, recurrent, or chronic. Acute suppurative sialadenitis presents as rapid-onset pain and swelling and is treated with antibiotics, salivary massage, hydration, and sialagogues such as lemon drops or vitamin C lozenges. Viral etiologies include mumps and human immunodeficiency virus, and treatment is directed at the underlying disease. Recurrent or chronic sialadenitis is more likely to be inflammatory than infectious; examples include recurrent parotitis of childhood and sialolithiasis. Inflammation is commonly caused by an obstruction such as a stone or duct stricture. Management is directed at relieving the obstruction. Benign and malignant tumors can occur in the salivary glands and usually present as a painless solitary neck mass. Diagnosis is made by imaging (e.g., ultrasonography, computed tomography, magnetic resonance imaging) and biopsy (initially with fine-needle aspiration). Overall, most salivary gland tumors are benign and can be treated with surgical excision.
Topics: Humans; Mumps; Parotitis; Salivary Gland Calculi; Salivary Gland Diseases; Salivary Gland Neoplasms; Sialadenitis
PubMed: 25077394
DOI: No ID Found -
Journal of Veterinary Diagnostic... Jul 2018Ong CB, Herdt TH, Fitzgerald SD. Hyperplastic goiter in two adult dairy cows. J Vet Diagn Invest 2014;26:810-814. (Original doi: 10.1177/1040638714554441). The use of...
Ong CB, Herdt TH, Fitzgerald SD. Hyperplastic goiter in two adult dairy cows. J Vet Diagn Invest 2014;26:810-814. (Original doi: 10.1177/1040638714554441). The use of mineral supplements as a top dressing and trace mineralized salt noted by the authors was based on non-documented verbal comments and not based on direct observation. Therefore, the definitive source of the excess iodine measured in the thyroid gland of the 2 cows examined was not identified. The acknowledgments for this case report have been revised to reflect appropriate contributors to the case. We thank Tom Wood and the Histology Section of the Diagnostic Center for Population and Animal Health (DCPAH) for technical assistance processing the slides of the cases in this report. We also thank Drs. Tim Lyons, Daron Jones, and James Averill for their contributions to this case.
PubMed: 29952743
DOI: 10.1177/1040638718784917 -
Frontiers in Plant Science 2022is a dicotyledonous recretohalophyte with several multicellular salt glands on the leaves. The plant can directly secrete excess salt onto the leaf surface through the...
is a dicotyledonous recretohalophyte with several multicellular salt glands on the leaves. The plant can directly secrete excess salt onto the leaf surface through the salt glands to maintain ion homeostasis under salt stress. Therefore, it is of great significance to study the functions of genes related to salt gland development and salt tolerance. In this study, an R1-type MYB transcription factor gene was screened from , named , and its expression was strongly induced by salt stress. Subcellular localization analysis showed that was localized in the nucleus. LbMYB48 protein has transcriptional activation activity shown by transcriptional activation experiments. The density of salt glands in the leaves and the salt secretion capacity of -silenced lines were decremented, as demonstrated by the leaf disc method to detect sodium ion secretion. Furthermore, salt stress index experiments revealed that the ability of -silenced lines to resist salt stress was significantly reduced. regulates salt gland development and salt tolerance in mainly by regulating the expression of epidermal cell development related genes such as and and salt stress-related genes (, , and ) as demonstrated by RNA-seq analysis of LbMYB48-silenced lines. The heterologous over-expression of in improves salt tolerance of plants by stabilizing ion and osmotic balance and is likely to be involved in the abscisic acid signaling pathway. Therefore, , a transcriptional activator regulates the salt gland development of and salt tolerance of and
PubMed: 36388592
DOI: 10.3389/fpls.2022.1039984 -
Journal of Ophthalmology 2016The human tear film is a 3-layered coating of the surface of the eye and a loss, or reduction, in any layer of this film may result in a syndrome of blurry vision and... (Review)
Review
The human tear film is a 3-layered coating of the surface of the eye and a loss, or reduction, in any layer of this film may result in a syndrome of blurry vision and burning pain of the eyes known as dry eye. The lacrimal gland and accessory glands provide multiple components to the tear film, most notably the aqueous. Dysfunction of these glands results in the loss of aqueous and other products required in ocular surface maintenance and health resulting in dry eye and the potential for significant surface pathology. In this paper, we have reviewed products of the lacrimal gland, diseases known to affect the gland, and historical and emerging dry eye therapies targeting lacrimal gland dysfunction.
PubMed: 27042343
DOI: 10.1155/2016/7542929 -
Pflugers Archiv : European Journal of... Aug 2022Hypertension is one of the leading causes of premature death in humans and exhibits a complex aetiology including environmental and genetic factors. Mutations within the... (Review)
Review
Hypertension is one of the leading causes of premature death in humans and exhibits a complex aetiology including environmental and genetic factors. Mutations within the glucocorticoid receptor (GR) can cause glucocorticoid resistance, which is characterized by several clinical features like hypercortisolism, hypokalaemia, adrenal hyperplasia and hypertension. Altered glucocorticoid receptor signalling further affects sodium and potassium homeostasis as well as blood pressure regulation and cell proliferation and differentiation that influence organ development and function. In salt-sensitive hypertension, excessive renal salt transport and sympathetic nervous system stimulation may occur simultaneously, and, thus, both the mineralocorticoid receptor (MR) and the GR-signalling may be implicated or even act interdependently. This review focuses on identified GR mutations in human primary generalized glucocorticoid resistance (PGGR) patients and their related clinical phenotype with specific emphasis on adrenal gland hyperplasia and hypertension. We compare these findings to mouse and rat mutants harbouring genetically engineered mutations to further dissect the cause and/or the consequence of clinical features which are common or different.
Topics: Adrenal Glands; Animals; Glucocorticoids; Humans; Hyperplasia; Hypertension; Metabolism, Inborn Errors; Mice; Mutation; Rats; Receptors, Glucocorticoid; Receptors, Mineralocorticoid
PubMed: 35732960
DOI: 10.1007/s00424-022-02715-6 -
Immunologic Research Apr 2021Adequate iodine intake is necessary for normal thyroid function. Iodine deficiency is associated with serious complications, but also iodine excess can lead to thyroid... (Review)
Review
Adequate iodine intake is necessary for normal thyroid function. Iodine deficiency is associated with serious complications, but also iodine excess can lead to thyroid dysfunction, and iodine supplementation aimed to prevent iodine deficiency disorders has been associated with development of thyroid autoimmunity. The epidemiology of thyroid diseases has undergone profound changes since the implementation of iodoprophylaxis, notably by means of iodine-enriched salt, specifically resulting in decreased prevalence of goiter and neonatal hypothyroidism, improved cognitive function development in infancy, and reduced incidence of more aggressive forms of thyroid cancer. The main question we address with this review is the clinical relevance of the possible effect on autoimmunity exerted by the use of iodine-enriched salt to correct iodine deficiency. In animal models, exogenous iodine is able to trigger or exacerbate thyroid autoimmunity, but it is still not clear whether the observed immunological changes are due to a direct effect of iodine on immune response, or whether they represent a secondary response to a toxic effect of iodine on thyroid tissue. Previous iodine status of a population seems to influence the functional thyroid response to increased iodine intake and possibly the development of thyroid autoimmunity. Moreover, the prevalence of thyroid antibodies, regarded as hallmark of autoimmune thyroid disease, varies between populations under the influence of genetic and environmental factors, and the presence of thyroid antibodies does not always coincide with the presence of thyroid disease or its future development. In addition, the incidence of autoimmune diseases shows a general increasing trend in the last decades. For all these reasons, available data are quite heterogeneous and difficult to analyze and compare. In conclusion, available data from long-term population surveys show that a higher than adequate population iodine intake due to a poorly controlled program of iodine prophylaxis could induce thyroid dysfunction, including thyroid autoimmunity mostly represented by euthyroid or subclinical hypothyroid autoimmune thyroiditis. Close monitoring iodine prophylaxis is therefore advised to ensure that effects of both iodine deficiency and iodine excess are avoided.
Topics: Animals; Autoimmune Diseases; Autoimmunity; Humans; Iodine; Sodium Chloride, Dietary; Thyroid Diseases; Thyroid Gland
PubMed: 33914231
DOI: 10.1007/s12026-021-09192-6