38 research outputs found

    Levothyroxine Treatment in Pregnancy: Indications, Efficacy, and Therapeutic Regimen

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    The prevalence of overt and subclinical hypothyroidism during pregnancy is estimated to be 0.3–0.5% and 2–3%, respectively. Thyroid autoantibodies are found in 5–18% of women in the childbearing age. The aim of this review is to underscore the clinical significance of these findings on the health of both the mother and her offspring. Methods of evaluation of thyroid function tests (TFTs) during pregnancy are described as are the threshold values for the diagnosis of overt and subclinical hypothyroidism or hypothyroxinemia. Anticipated differences in TFTs in iodine-sufficient and iodine-deficient areas are discussed and data are provided on potential complications of hypothyroidism/hypothyroxinemia and autoimmune thyroid disease during pregnancy and adverse effects for the offspring. The beneficial effects of levothyroxine therapy on pregnancy outcomes and offspring development are discussed with a proposed treatment regimen and follow up strategy

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    The prevalence of overt and subclinical hypothyroidism during pregnancy is estimated to be 0.3-0.5% and 2-3%, respectively. Thyroid autoantibodies are found in 5-18% of women in the childbearing age. The aim of this review is to underscore the clinical significance of these findings on the health of both the mother and her offspring. Methods of evaluation of thyroid function tests (TFTs) during pregnancy are described as are the threshold values for the diagnosis of overt and subclinical hypothyroidism or hypothyroxinemia. Anticipated differences in TFTs in iodine-sufficient and iodine-deficient areas are discussed and data are provided on potential complications of hypothyroidism/hypothyroxinemia and autoimmune thyroid disease during pregnancy and adverse effects for the offspring. The beneficial effects of levothyroxine therapy on pregnancy outcomes and offspring development are discussed with a proposed treatment regimen and follow up strategy

    Diffuse white matter loss in a transgenic rat model of cerebral amyloid angiopathy

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    Diffuse white matter (WM) disease is highly prevalent in elderly with cerebral small vessel disease (cSVD). In humans, cSVD such as cerebral amyloid angiopathy (CAA) often coexists with Alzheimer’s disease imposing a significant impediment for characterizing their distinct effects on WM. Here we studied the burden of age-related CAA pathology on WM disease in a novel transgenic rat model of CAA type 1 (rTg-DI). A cohort of rTg-DI and wild-type rats was scanned longitudinally using MRI for characterization of morphometry, cerebral microbleeds (CMB) and WM integrity. In rTg-DI rats, a distinct pattern of WM loss was observed at 9 M and 11 M. MRI also revealed manifestation of small CMB in thalamus at 6 M, which preceded WM loss and progressively enlarged until the moribund disease stage. Histology revealed myelin loss in the corpus callosum and thalamic CMB in all rTg-DI rats, the latter of which manifested in close proximity to occluded and calcified microvessels. The quantitation of CAA load in rTg-DI rats revealed that the most extensive microvascular Aβ deposition occurred in the thalamus. For the first time using in vivo MRI, we show that CAA type 1 pathology alone is associated with a distinct pattern of WM loss

    Fatty Acid Metabolites Combine with Reduced β Oxidation to Activate Th17 Inflammation in Human Type 2 Diabetes

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    Mechanisms that regulate metabolites and downstream energy generation are key determinants of T cell cytokine production, but the processes underlying the Th17 profile that predicts the metabolic status of people with obesity are untested. Th17 function requires fatty acid uptake, and our new data show that blockade of CPT1A inhibits Th17-associated cytokine production by cells from people with type 2 diabetes (T2D). A low CACT:CPT1A ratio in immune cells from T2D subjects indicates altered mitochondrial function and coincides with the preference of these cells to generate ATP through glycolysis rather than fatty acid oxidation. However, glycolysis was not critical for Th17 cytokines. Instead, β oxidation blockade or CACT knockdown in T cells from lean subjects to mimic characteristics of T2D causes cells to utilize 16C-fatty acylcarnitine to support Th17 cytokines. These data show long-chain acylcarnitine combines with compromised β oxidation to promote disease-predictive inflammation in human T2D. Although glycolysis generally fuels inflammation, Nicholas, Proctor, and Agrawal et al. report that PBMCs from subjects with type 2 diabetes use a different mechanism to support chronic inflammation largely independent of fuel utilization. Loss- and gain-of-function experiments in cells from healthy subjects show mitochondrial alterations combine with increases in fatty acid metabolites to drive chronic T2D-like inflammation

    Lawson criterion for ignition exceeded in an inertial fusion experiment

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    For more than half a century, researchers around the world have been engaged in attempts to achieve fusion ignition as a proof of principle of various fusion concepts. Following the Lawson criterion, an ignited plasma is one where the fusion heating power is high enough to overcome all the physical processes that cool the fusion plasma, creating a positive thermodynamic feedback loop with rapidly increasing temperature. In inertially confined fusion, ignition is a state where the fusion plasma can begin "burn propagation" into surrounding cold fuel, enabling the possibility of high energy gain. While "scientific breakeven" (i.e., unity target gain) has not yet been achieved (here target gain is 0.72, 1.37 MJ of fusion for 1.92 MJ of laser energy), this Letter reports the first controlled fusion experiment, using laser indirect drive, on the National Ignition Facility to produce capsule gain (here 5.8) and reach ignition by nine different formulations of the Lawson criterion

    Lawson Criterion for Ignition Exceeded in an Inertial Fusion Experiment

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    \u3csup\u3e124\u3c/sup\u3eI Positron Emission Tomography/Computed Tomography Versus Conventional Radioiodine Imaging in Differentiated Thyroid Cancer: A Review

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    © Copyright 2019, Mary Ann Liebert, Inc., publishers 2019. Background: Studies report a wide spectrum of 124I positron emission tomography (PET)/computed tomography (CT) sensitivity and specificity in the detection of differentiated thyroid cancer (DTC) lesions. This study reviews the lesion detection rate of pretherapy 124I PET/CT in different patient populations and further analyzes the factors necessary for a better detection on 124I PET/CT. Methods: A literature search was performed using multiple different databases (MEDLINE, EMBASE, Northern Lights, and handsearching) covering 1996 to April 2018. Two reviewers reviewed and extracted study data for 124I, 123I, and 131I scans in DTC. Results: This review includes 4 retrospective and 10 prospective studies in which 495 DTC patients underwent 124I and 131I imaging; no studies made comparisons with 123I. In the reports that compared 124I PET/CT with diagnostic 131I scans, there were a total of 72 patients in whom 120 lesions were detected on 124I imaging, whereas only 52 were detected on diagnostic 131I scans. In publications that compared 124I with post-therapy 131I scans in 266 patients, 410 lesions were detected with 124I PET, whereas 390 were detected on post-therapy 131I scans. Based on 124I PET/CT in six studies, TNM staging was revised in 15-21% of patients, and disease management was altered in 5-29% of patients. Conclusions: 124I PET/CT is able to identify a greater number of foci compared with diagnostic 131I scans. 124I PET may have better detection compared with post-therapy 131I scans in patients who are 131I therapy naive, have less aggressive pathology, or do not have disseminated lung metastases. Additional metastatic lesion detection by 124I PET may have a significant clinical impact in the management of patients before 131I therapy in some patients
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