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M

M. De Jong

Researcher at Erasmus University Rotterdam

Publications -  34
Citations -  3057

M. De Jong is an academic researcher from Erasmus University Rotterdam. The author has contributed to research in topics: Triiodothyronine & Somatostatin receptor. The author has an hindex of 20, co-authored 34 publications receiving 2959 citations.

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Somatostatin receptor scintigraphy with [111In-DTPA-d-Phe1]- and [123I-Tyr3]-octreotide: the Rotterdam experience with more than 1000 patients

TL;DR: The successful application of radiolabelled octreotide in scintigraphy indicates the possible usefulness of other radiolABelled peptides, either native peptides or derivatives of these, in, for example, nuclear oncology.
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The sick euthyroid syndrome: changes in thyroid hormone serum parameters and hormone metabolism

TL;DR: In practice, the clinician must differentiate the changes in the serum thyroid hormone lcvels induced by illness from those caused by treatable disorders of thyroid function.
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Thyroxine and 3,3',5-triiodothyronine are glucuronidated in rat liver by different uridine diphosphate-glucuronyltransferases.

TL;DR: Measurement of the microsomal UDP-glucuronyltransferase (UDPGT) activities confirmed that T4 UDPGT was induced by TCB, whereas T3 glucuronidation was unaffected and T3 UDPGT activity showed a discontinuous variation, which completely matched the genetic heterogeneity in androsterone glucuronide in Wistar rats.
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Inhibition of thyroxine transport into cultured rat hepatocytes by serum of nonuremic critically ill patients: effects of bilirubin and nonesterified fatty acids.

TL;DR: Elevated bilirubin and NEFA and the low albumin level in non-uremic critical illness may be at least partly responsible for the T4 transport inhibition in T3-producing tissues (e.g. the liver) and, thus, the low plasma T3 levels in these critically ill patients.
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A furan fatty acid and indoxyl sulfate are the putative inhibitors of thyroxine hepatocyte transport in uremia

TL;DR: CMPF and indoxyl sulfate in concentrations normally present in the serum of uremic patients inhibit cellular transport and subsequent deiodination of T4, which may account for the low total T3 level in u Remic patients.