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        <title>Thyroid Research - Most accessed articles</title>
        <link>http://www.thyroidresearchjournal.com</link>
        <description>The most accessed research articles published by Thyroid Research</description>
        <dc:date>2012-05-01T00:00:00Z</dc:date>
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        <item rdf:about="http://www.thyroidresearchjournal.com/content/2/1/4">
        <title>The mechanisms of atrial fibrillation in hyperthyroidism.</title>
        <description>Atrial fibrillation (AF) is a complex condition with several possible contributing factors. The rapid and irregular heartbeat produced by AF increases the risk of blood clot formation inside the heart. These clots may eventually become dislodged, causing embolism, stroke and other disorders. AF occurs in up to 15% of patients with hyperthyroidism compared to 4% of people in the general population and is more common in men and in patients with triiodothyronine (T3) toxicosis. The incidence of AF increases with advancing age. Also, subclinical hyperthyroidism is a risk factor associated with a 3-fold increase in development of AF. Thyrotoxicosis exerts marked influences on electrical impulse generation (chronotropic effect) and conduction (dromotropic effect). Several potential mechanisms could be invoked for the effect of thyroid hormones on AF risk, including elevation of left atrial pressure secondary to increased left ventricular mass and impaired ventricular relaxation, ischemia resulting from increased resting heart rate, and increased atrial eopic activity. Reentry has been postulated as one of the main mechanisms leading to AF. AF is more likely if effective refractory periods are short and conduction is slow. Hyperthyroidism is associated with shortening of action potential duration which may also contribute to AF.</description>
        <link>http://www.thyroidresearchjournal.com/content/2/1/4</link>
                <dc:creator>Agata Bielecka-Dabrowa</dc:creator>
                <dc:creator>Dimitri Mikhailidis</dc:creator>
                <dc:creator>Jacek Rysz</dc:creator>
                <dc:creator>Maciej Banach</dc:creator>
                <dc:source>Thyroid Research 2009, null:4</dc:source>
        <dc:date>2009-04-02T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1756-6614-2-4</dc:identifier>
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        <prism:startingPage>4</prism:startingPage>
        <prism:publicationDate>2009-04-02T00:00:00Z</prism:publicationDate>
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        <item rdf:about="http://www.thyroidresearchjournal.com/content/4/1/14">
        <title>Assessment of Japanese iodine intake based on seaweed consumption in Japan: A literature-based analysis
</title>
        <description>Japanese iodine intake from edible seaweeds is amongst the highest in the world. Predicting the type and amount of seaweed the Japanese consume is difficult due to day-to-day meal variation and dietary differences between generations and regions. In addition, iodine content varies considerably between seaweed species, with cooking and/or processing having an influence on iodine content. Due to all these factors, researchers frequently overestimate, or underestimate, Japanese iodine intake from seaweeds, which results in misleading and potentially dangerous diet and supplementation recommendations for people aiming to achieve the same health benefits seen by the Japanese. By combining information from dietary records, food surveys, urine iodine analysis (both spot and 24-hour samples) and seaweed iodine content, we estimate that the Japanese iodine intake--largely from seaweeds--averages 1,000-3,000 &#956;g/day (1-3 mg/day).</description>
        <link>http://www.thyroidresearchjournal.com/content/4/1/14</link>
                <dc:creator>Theodore Zava</dc:creator>
                <dc:creator>David Zava</dc:creator>
                <dc:source>Thyroid Research 2011, null:14</dc:source>
        <dc:date>2011-10-05T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1756-6614-4-14</dc:identifier>
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                <prism:publicationName>Thyroid Research</prism:publicationName>
        <prism:issn>1756-6614</prism:issn>
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        <prism:startingPage>14</prism:startingPage>
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        <item rdf:about="http://www.thyroidresearchjournal.com/content/5/1/3">
        <title>Phylogenetic analysis of the human thyroglobulin regions</title>
        <description>Thyroglobulin is a large protein present in all vertebrates. It is synthesized in the thyrocytes and exported to lumen of the thyroid follicle, where its tyrosine residues are iodinated . The iodinated thyroglobulin is reintegrated into the cell and processed (cleaved to free its two extremities) for thyroid hormone synthesis. Thyroglobulin sequence analysis has identified four regions of the molecule: Tg1, Tg2, Tg3 and ChEL. Structural abnormalities and mutations result in different pathological consequences, depending on the thyroglobulin region affected. We carried out a bioinformatic analysis of thyroglobulin, determining the origin and the function of each region. Our results suggest that the Tg1 region acts as a binding protein on the apical membrane, the Tg2 region is involved in protein adhesion and the Tg3 region is involved in determining the three-dimensional structure of the protein. The ChEL domain is involved in thyroglobulin transport, dimerization and adhesion. The presence of repetitive domains in the Tg1, Tg2 and Tg3 regions suggests that these domains may have arisen through duplication.</description>
        <link>http://www.thyroidresearchjournal.com/content/5/1/3</link>
                <dc:creator>Abdelaziz Belkadi</dc:creator>
                <dc:creator>Caroline Jacques</dc:creator>
                <dc:creator>Frédérique Savagner</dc:creator>
                <dc:creator>Yves Malthièry</dc:creator>
                <dc:source>Thyroid Research 2012, null:3</dc:source>
        <dc:date>2012-05-01T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1756-6614-5-3</dc:identifier>
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                <prism:publicationName>Thyroid Research</prism:publicationName>
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        <prism:publicationDate>2012-05-01T00:00:00Z</prism:publicationDate>
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        <item rdf:about="http://www.thyroidresearchjournal.com/content/3/1/11">
        <title>Hashimoto thyroiditis is more frequent than expected when diagnosed by cytology which uncovers a pre-clinical state</title>
        <description>Background:
Our Thyroid-Multidisciplinary Clinic is a large referral site for thyroid diseases. Thyroid biopsies are mainly performed for thyroid cancer screening. Yet, Hashimoto thyroiditis (HT) is being too frequently diagnosed. The prevalence of HT is reported as 0.3-1.2% or twice the prevalence of type 1 diabetes. However, the prevalence of HT confirmed by cytology is still uncertain. To evaluate different aspects of thyroid physiopathology including prevalence of Hashimoto&apos;s, a database of clinical features, ultrasound images and cytology results of patients referred for FNA of thyroid nodules was prospectively developed.
Methods:
We retrospectively studied 811 consecutive patients for whom ultrasound guided thyroid FNA biopsies were performed at our clinic over 2.5 year period (Mar/2006-Sep/2008).
Results:
The analysis of our database revealed that from 761 patients, 102 (13.4%) had HT, from whom 56 (7.4%) were euthyroid or had sub-clinical (non-hypothyroid) disease, and 46 (6%) were clinically hypothyroid.
Conclusions:
This is the first study to show such a high prevalence of HT diagnosed by ultrasound-guided FNA. More strikingly, the prevalence of euthyroid HT, appears to be &gt;5% similar to that of type 2 diabetes. Based on our results, there might be a need to follow up on cytological Hashimoto&apos;s to monitor for thyroid failure, especially in high risk states, like pregnancy. The potential risk for thyroid cancer in patients with biopsy-proven inflammation of thyroid epithelium remains to be established prospectively. However, it may explain the increased risk for thyroid cancer observed in patients with elevated but within normal TSH.</description>
        <link>http://www.thyroidresearchjournal.com/content/3/1/11</link>
                <dc:creator>Anca Staii</dc:creator>
                <dc:creator>Sarah Mirocha</dc:creator>
                <dc:creator>Kristina Todorova-Koteva</dc:creator>
                <dc:creator>Simone Glinberg</dc:creator>
                <dc:creator>Juan Jaume</dc:creator>
                <dc:source>Thyroid Research 2010, null:11</dc:source>
        <dc:date>2010-12-20T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1756-6614-3-11</dc:identifier>
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                <prism:publicationName>Thyroid Research</prism:publicationName>
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        <prism:startingPage>11</prism:startingPage>
        <prism:publicationDate>2010-12-20T00:00:00Z</prism:publicationDate>
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        <item rdf:about="http://www.thyroidresearchjournal.com/content/4/1/5">
        <title>Assessment of RET/PTC1 and RET/PTC3 rearrangements in fine-needle aspiration biopsy specimens collected from patients with Hashimoto&apos;s thyroiditis</title>
        <description>Background:
RET/PTC rearrangements are the most frequent molecular changes in papillary thyroid carcinoma (PTC). So far, 15 main RET/PTC rearrangements have been described, among which RET/PTC1 and RET/PTC3 are the most common in PTC - especially in radiation-induced tumours. RET/PTC1 and RET/PTC3 are the result of intrachromosomal paracentric inversions in chromosome 10, where RET and the activating genes (H4 and ELE1, respectively) are located. Recently, RET/PTC rearrangements have been shown not only in PTC but also in benign thyroid lesions, including Hashimoto&apos;s thyroiditis (HT). The aim of study was an assessment of RET/PTC1 and RET/PTC3 rearrangements in patients with Hashimoto&apos;s thyroiditis.Materials and methodsThyroid aspirates, eligible for the study, were obtained from 26 patients with Hashimoto&apos;s thyroiditis by fine-needle aspiration biopsy (FNAB). Each aspirate was smeared for conventional cytology, while its remaining part was immediately washed out of the needle. The cells, obtained from the needle, were used in further investigation. Total RNA from FNAB was extracted by use of an RNeasy Micro Kit, based on modified Chomczynski and Sacchi&apos;s method and reverse transcription (RT-PCR) was done. Quantitative evaluation of RET/PTC1 and RET/PTC3 rearrangements by real-time PCR was performed by an ABI PRISM&#174; 7500 Sequence Detection System. In the study, PTC tissues with known RET/PTC1 and RET/PTC3 rearrangements served as a reference standard (calibrator), while &#946;-actin gene was used as endogenous control.
Results:
Amplification reactions were done in triplicate for each examined sample. No RET/PTC1 and RET/PTC3 rearrangements were found in the examined samples.
Conclusions:
Our results indicate that RET/PTC1 and RET/PTC3 rearrangements in Hashimoto&apos;s thyroiditis, if any, are rather rare events and further investigations should be conducted in order to determine molecular changes, connecting Hashimoto&apos;s thyroiditis with PTC.</description>
        <link>http://www.thyroidresearchjournal.com/content/4/1/5</link>
                <dc:creator>Anna Cyniak-Magierska</dc:creator>
                <dc:creator>Katarzyna Wojciechowska-Durczynska</dc:creator>
                <dc:creator>Kinga Krawczyk-Rusiecka</dc:creator>
                <dc:creator>Arkadiusz Zygmunt</dc:creator>
                <dc:creator>Andrzej Lewinski</dc:creator>
                <dc:source>Thyroid Research 2011, null:5</dc:source>
        <dc:date>2011-01-10T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1756-6614-4-5</dc:identifier>
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                <prism:publicationName>Thyroid Research</prism:publicationName>
        <prism:issn>1756-6614</prism:issn>
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        <prism:startingPage>5</prism:startingPage>
        <prism:publicationDate>2011-01-10T00:00:00Z</prism:publicationDate>
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        <item rdf:about="http://www.thyroidresearchjournal.com/content/2/1/2">
        <title>Association between primary hypothyroidism and metabolic syndrome and the role of C reactive protein: a cross - sectional study from South India</title>
        <description>Background:
Hypothyroidism (sub-clinical and overt) and metabolic syndrome are recognized risk factors for atherosclerotic cardiovascular disease. This study is an effort to identify the proposed association between these two disease entities and the risk factors involved in this association.
Methods:
A cross &#8211; sectional study from a tertiary care teaching hospital in Chennai city, South India. 420 patients with metabolic syndrome (NCEP &#8211; ATP III criteria) were included in the study group. 406 appropriately age and sex matched controls having no features of metabolic syndrome (0 out of the 5 criteria) were compared with the study group. The study extended over a 5 year period. TSH, FT4 were measured for both the groups using electrochemiluminescence immuno assay. HsCRP was measured for all the patients in the study group. The baseline characteristics between the groups were compared with Student&apos;s&apos;t&apos; test. Chi-square test was used to analyze the association between metabolic syndrome and hypothyroidism (overt and sub-clinical). Logistic regression analysis was applied to identify the association between hypothyroidism and the patient characteristics in the study group.
Results:
Of the 420 patients in the study group, 240 were females (57.1%), 180 were males (42.9%) with mean age 51 &#177; 9.4 years. Of the 406 patients in the control group, 216 were females (53.2%), 190 males (46.8%) with mean age 49 &#177; 11.2 years. In the study group, 92 had sub-clinical hypothyroidism (SCH) (21.9%), 31 were overtly hypothyroid (7.4%) and 297 were euthyroid (70.7%). In the control group 27 patients had sub-clinical hypothyroidism (6.6%), 9 patients had overt hypothyroidism (2.2%) and 370 patients were euthyroid (91.2%). On comparison SCH (P &lt; 0.001) and overt hypothyroidism (P &lt; 0.001) were significantly associated with the study group as compared to the control group. Logistic regression analysis recognized the association between female gender (P = 0.021) and HsCRP (P = 0.014) with sub-clinical hypothyroidism and female gender (P = 0.01) with overt hypothyroidism in the study group.
Conclusion:
Hypothyroidism is associated with metabolic syndrome and females are more at risk. Metabolic syndrome patients with a raised HsCRP are at significant risk of having sub-clinical hypothyroidism.</description>
        <link>http://www.thyroidresearchjournal.com/content/2/1/2</link>
                <dc:creator>Ghanshyam Palamaner Subash Shantha</dc:creator>
                <dc:creator>Anita Kumar</dc:creator>
                <dc:creator>Vijay Jeyachandran</dc:creator>
                <dc:creator>Deepan Rajamanickam</dc:creator>
                <dc:creator>Rajkumar K</dc:creator>
                <dc:creator>Shihas Salim</dc:creator>
                <dc:creator>Kuyilan Karai Subramanian</dc:creator>
                <dc:creator>Senthilkumar Natesan</dc:creator>
                <dc:source>Thyroid Research 2009, null:2</dc:source>
        <dc:date>2009-03-09T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1756-6614-2-2</dc:identifier>
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                <prism:publicationName>Thyroid Research</prism:publicationName>
        <prism:issn>1756-6614</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>2</prism:startingPage>
        <prism:publicationDate>2009-03-09T00:00:00Z</prism:publicationDate>
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                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
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        <item rdf:about="http://www.thyroidresearchjournal.com/content/4/1/8">
        <title>Thyroid storm associated with Graves&apos; disease covered by diabetic ketoacidosis, A case report</title>
        <description>Background:
Thyroid storm is a condition in which multiple organ dysfunction results from failure of the compensatory mechanisms of the body owing to excessive thyroid hormone activity induced by some factors in patients with thyrotoxicosis. While diabetic ketoacidosis (DKA) is an important trigger for thyroid storm, simultaneous development of DKA and thyroid storm is rare.Case presentationA 59-year-old woman with no history of either diabetes mellitus or thyroid disease presented to our hospital because of developing nausea, vomiting and diarrhea for 2 days. Physical examination showed mild disturbance of consciousness, fever, and tachycardia. There were no other signs of thyrotoxicosis. Laboratory studies revealed elevation of random blood glucose and glycosylated hemoglobin, strongly positive of urine acetone, and metabolic acidosis. Since DKA was diagnosed, we initiated the patient on treatment with administration of insulin and adequate fluid replacement. Although the hyperglycemia and acidosis were immediately relieved, the disturbance of consciousness and tachycardia remained persistent. Levels of FT3 and FT4 were extremely high and TSH was below the detectable limit. TRAb was positive. The thyroid storm score of Burch &amp; Wartofsky was 75/140, and the thyroid storm diagnostic criteria of the Japan Thyroid Association were satisfied. Oral administration of thiamazole, potassium iodide and propranolol resulted in immediate relief of the tachycardia.DiscussionWe encountered a case of thyroid storm associated with Graves&apos; disease covered by DKA. Thyroid storm and DKA are both potentially fatal, and the prognosis varies depending on whether or not these conditions are detected and treated sufficiently early. The thyroid storm diagnostic criteria prepared in 2008 by the Japan Thyroid Association are very simple as compared to the Burch &amp; Wartofsky scoring system for thyroid storm. The Japanese criteria may be useful in the diagnosis of this condition since they enable clinicians to identify a broad range of cases with thyroid storm. When dealing with cases of DKA or thyroid storm, it seems essential to bear in mind the possibility of the coexistence of these two diseases.</description>
        <link>http://www.thyroidresearchjournal.com/content/4/1/8</link>
                <dc:creator>Erika Osada</dc:creator>
                <dc:creator>Naoki Hiroi</dc:creator>
                <dc:creator>Mariko Sue</dc:creator>
                <dc:creator>Natsumi Masai</dc:creator>
                <dc:creator>Ryo Iga</dc:creator>
                <dc:creator>Rika Shigemitsu</dc:creator>
                <dc:creator>Reiko Oka</dc:creator>
                <dc:creator>Masahiko Miyagi</dc:creator>
                <dc:creator>Kaoru Iso</dc:creator>
                <dc:creator>Koji Kuboki</dc:creator>
                <dc:creator>Gen Yoshino</dc:creator>
                <dc:source>Thyroid Research 2011, null:8</dc:source>
        <dc:date>2011-04-14T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1756-6614-4-8</dc:identifier>
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                <prism:publicationName>Thyroid Research</prism:publicationName>
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        <prism:startingPage>8</prism:startingPage>
        <prism:publicationDate>2011-04-14T00:00:00Z</prism:publicationDate>
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                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
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        <item rdf:about="http://www.thyroidresearchjournal.com/content/4/1/1">
        <title>Advantages and disadvantages of 3D ultrasound of thyroid nodules including thin slice volume rendering</title>
        <description>Background:
The purpose of this study was to assess the advantages and disadvantages of 3D gray-scale and power Doppler ultrasound, including thin slice volume rendering (TSVR), applied for evaluation of thyroid nodules.
Methods:
The retrospective evaluation by two observers of volumes of 71 thyroid nodules (55 benign, 16 cancers) was performed using a new TSVR technique. Dedicated 4D ultrasound scanner with an automatic 6-12 MHz 4D probe was used. Statistical analysis was performed with Stata v. 8.2.
Results:
Multiple logistic regression analysis demonstrated that independent risk factors of thyroid cancers identified by 3D ultrasound include: (a) ill-defined borders of the nodule on MPR presentation, (b) a lobulated shape of the nodule in the c-plane and (c) a density of central vessels in the nodule within the minimal or maximal ranges. Combination of features provided sensitivity 100% and specificity 60-69% for thyroid cancer.Calcification/microcalcification-like echogenic foci on 3D ultrasound proved not to be a risk factor of thyroid cancer.Storage of the 3D data of the whole nodules enabled subsequent evaluation of new parameters and with new rendering algorithms.
Conclusions:
Our results indicate that 3D ultrasound is a practical and reproducible method for the evaluation of thyroid nodules. 3D ultrasound stores volumes comprising the whole lesion or organ. Future detailed evaluations of the data are possible, looking for features that were not fully appreciated at the time of collection or applying new algorithms for volume rendering in order to gain important information. Three-dimensional ultrasound data could be included in thyroid cancer databases. Further multicenter large scale studies are warranted.</description>
        <link>http://www.thyroidresearchjournal.com/content/4/1/1</link>
                <dc:creator>Rafal Slapa</dc:creator>
                <dc:creator>Wieslaw Jakubowski</dc:creator>
                <dc:creator>Jadwiga Slowinska-Srzednicka</dc:creator>
                <dc:creator>Kazimierz Szopinski</dc:creator>
                <dc:source>Thyroid Research 2011, null:1</dc:source>
        <dc:date>2011-01-07T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1756-6614-4-1</dc:identifier>
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        <prism:startingPage>1</prism:startingPage>
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        <item rdf:about="http://www.thyroidresearchjournal.com/content/5/1/2">
        <title>Riedel&apos;s thyroiditis - a case report with genes&apos; expression studies</title>
        <description>Background:
Genetic background of Riedel&apos;s thyroiditis remains unknown. Herein, we describe our results of studies on genes expression levels in Riedel&apos;s thyroiditis.Case report and genetic findingsWe report the case of 48-year old woman with Riedel&apos;s thyroiditis who has presented unusual course of disease with non-specific cervical discomfort, though as with no pain and/or no compression symptoms. After surgery, thyroid specimens were quantitatively evaluated, regarding PIK3CA, PIK3CD, PIK3CG, Tg, TGFB1, THRB, COL1, CDKN1C, CDH3 and CACNA2D2 genes expression levels, by real-time PCR in the ABI PRISM&#174; 7500 Sequence Detection System. Out of 10 above genes, in 2 cases the expression was higher than in respective Controls of unchanged thyroid tissue. In the remaining 8 cases, expression in question became comparable or lower as in Controls.DiscussionThe association between increased expression levels of PIK3CA and CDH3 genes and Riedel&apos;s thyroiditis is not well-defined. However, the increased expression of PIK3CA and CDH3 genes in our case report and in previous studies of other authors on various malignancies may suggest possible molecular relation between Riedel&apos;s thyroiditis and certain neoplastic processes, the relation of which requires further genetic evaluation. It is to be stressed that gene expression studies in Riedel&apos;s thyroiditis are difficult to perform, mainly due to fibrosis, resulting in scarce thyroid specimens and - in consequence - small amount of genetic material.</description>
        <link>http://www.thyroidresearchjournal.com/content/5/1/2</link>
                <dc:creator>Katarzyna Wojciechowska-Durczynska</dc:creator>
                <dc:creator>Adam Durczynski</dc:creator>
                <dc:creator>Stanislaw Sporny</dc:creator>
                <dc:creator>Janusz Strzelczyk</dc:creator>
                <dc:creator>Andrzej Lewinski</dc:creator>
                <dc:source>Thyroid Research 2012, null:2</dc:source>
        <dc:date>2012-03-07T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1756-6614-5-2</dc:identifier>
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        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>2</prism:startingPage>
        <prism:publicationDate>2012-03-07T00:00:00Z</prism:publicationDate>
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                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
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        <item rdf:about="http://www.thyroidresearchjournal.com/content/5/1/1">
        <title>Gender-specific regulation of response to thyroid hormone in aging.</title>
        <description>Background:
Similar to other systems, the endocrine system is affected by aging. Thyroid hormone, the action of which is affected by many factors, has been shown to be associated with longevity. The most useful marker for the assessment of thyroid hormone action is TSH level. Although age and gender are believed to modify the pituitary set point or response to free thyroid hormone concentration, the precise age- and gender-dependent responses to thyroid hormone have yet to be reported.
Methods:
We analyzed the results of 3564 thyroid function tests obtained from patients who received medication at both out- and inpatient clinics of Shinshu University Hospital. Subjects were from among those with thyroid function test results in the normal or mildly abnormal range. Based on a log-linear relationship between the concentrations of FHs and TSH, we established the putative resistance index to assess the relation between serum FH and TSH levels.
Results:
Free thyroid hormone and TSH concentration showed an inverse log-linear relation. In males, there was a negative relationship between the free T3 resistance index and age. In females, although there were no relationships between age and FHs, the indices were positively related to age.
Conclusions:
These findings indicated that there is a gender-specific response to thyroid hormone with aging. Although the TSH level is a useful marker for the assessment of peripheral thyroid hormone action, the values should be interpreted carefully, especially with regard to age- and gender-related differences.</description>
        <link>http://www.thyroidresearchjournal.com/content/5/1/1</link>
                <dc:creator>Satoru Suzuki</dc:creator>
                <dc:creator>Shin-ichi Nishio</dc:creator>
                <dc:creator>Teiji Takeda</dc:creator>
                <dc:creator>Mitsuhisa Komatsu</dc:creator>
                <dc:source>Thyroid Research 2012, null:1</dc:source>
        <dc:date>2012-01-26T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1756-6614-5-1</dc:identifier>
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                <prism:publicationName>Thyroid Research</prism:publicationName>
        <prism:issn>1756-6614</prism:issn>
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        <prism:startingPage>1</prism:startingPage>
        <prism:publicationDate>2012-01-26T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
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