Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0009443 (cold)
 92,137 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Low TSH levels are frequently encountered in patients presenting with goiter. We assayed TSH in 599 goitrous patients who were referred to us for scintigraphy and ultrasonography. When TSH levels were low or when a hot nodule was discovered at scintigraphy, free T3, free T4 and sex hormone-binding globulin (SHBG) were also assayed. TSH levels were always low in overt hyperthyroidism with elevated free T3. TSH levels were also low in patients with normal free T3 and free T4 in circumstances leading to mild hyperthyroidism such as hot nodules that suppressed extranodular thyroid tissue uptake, toxic multinodular goiter, De Quervain thyroiditis and some patients on amiodarone treatment. Low TSH levels were also encountered in 29% of the clinically euthyroid patients presenting with a multinodular goiter with normal iodine uptake, no hot area and normal free T3 levels. In diffuse goiter, low TSH and normal free T3 levels were more frequently associated when iodine uptake was low, mainly due to subacute thyroiditis which can be clinically silent. Low TSH levels were rarely observed in patients with "simple" goiter or uninodular goiter without hot areas. SHBG, which was elevated in 94% of the Graves' disease patients tested, was normal in all but two patients with low TSH and normal free T3 levels. This assay appeared to be of little relevance in goiter. In addition to imaging techniques which are usually performed first, TSH should be systematically assayed in goiter, except in cases of solitary cold nodules. When low, the patient is at risk of developing overt hyperthyroidism. Conversely, when an isolated low TSH level is observed, scintigraphy should be performed.
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PMID:Low thyrotropin (TSH) levels in goiter. Relationship with scintigraphic findings and other biological parameters. 248 6

The prevalence and characteristics of TSH receptor blocking activity were examined in patients with different thyroid disorders. Studies were also performed on the in-vitro synthesis and immunoregulation of the blocking antibody. Blocking activity was tested by measuring the inhibition of TSH-stimulated cAMP production of cultured human thyroid cells by patient immunoglobulin (Ig) preparations. The following patients were investigated (number of cases in parentheses): Hashimoto's thyroiditis (33); primary myxoedema (17); euthyroid ophthalmopathy (8); active Graves' disease (19); cold nodule (5); non-toxic goitre (14); toxic adenoma (8); toxic multinodular goitre (9) and 22 normal controls. TSH receptor blocking activity was only detected in primary hypothyroidism with the following characteristics: (i) Such activity was present in only 16% of the patients (both goitrous, i.e. Hashimoto's thyroiditis, and non-goitrous, i.e. primary myxoedema), and in three patients with previously active Graves' hyperthyroidism who had become hypothyroid. (ii) Blocking activity seems to be associated with the Ig fraction of serum as indicated by protein A adsorption. (iii) The block-positive samples did not bind 125I-TSH, which seems to rule out an antibody directed against TSH. (iv) The specificity of the blocking activity seems to be directed towards the TSH-(thyroid stimulating immunoglobulin, TSI) receptor-mediated cAMP response since no inhibition of prostaglandin E1-stimulated cAMP production was found. Moreover, all cases in which an inhibitory effect was demonstrated towards TSH also exhibited blocking of TSI-stimulated cAMP, with a high correlation between the degree of inhibition of the TSH to that of the TSI response (r = 0.89, P less than 0.001, n = 11). The blocking activity may contribute to the pathogenesis of some cases of primary hypothyroid autoimmune thyroiditis, both goitrous and non-goitrous, as well as in the evolution of hyper- to hypothyroidism. By culturing peripheral blood lymphocytes, as well as B/T lymphocyte co-cultures isolated from three patients with blocking activity present in serum, the in-vitro synthesis of the blocking antibody was demonstrated for the first time. Moreover, in-vitro secretion of the antibody by patients B lymphocytes, as well as T cell regulation of autoantibody production, were also shown.
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PMID:Thyrotrophin receptor blocking antibodies: incidence, characterization and in-vitro synthesis. 283 61

The aim of this study was to examine whether at least a subgroup of patients with toxic multinodular goiter may have autoimmune thyroid disease. Thyroid-stimulating immunoglobulin (TSI) activity, measured by a sensitive bioassay employing cultured human thyroid cells, was determined in patients with toxic multinodular goiter and other thyroid disorders. All patients with active Graves' disease (n = 47) had detectable serum TSI activity, whereas TSI was undetectable in patients with thyroid disease not believed to be of autoimmune origin: toxic adenoma (n = 13), cold nodule (n = 5), and nontoxic goiter (n = 19), with a single exception in the latter group. Toxic multinodular goiter (n = 26) was diagnosed based on clinical and laboratory evidence of hyperthyroidism associated with a multinodular goiter on palpation and scintiscan. The toxic multinodular goiter group was then subclassified according to scintiscan pattern (type A, diffuse but uneven distribution of technetium uptake; type B, multiple discrete nodules of varying size and function). All but 1 of the 11 TSI-positive toxic multinodular goiter patients had a type A scintiscan pattern. The patients with the type A scintiscan pattern were younger and more often had elevated antithyroid antibody titers, ophthalmopathy, and concurrent development of goiter and hyperthyroidism (rather than long-standing goiter preceding hyperthyroidism) compared to the type B patients. Thus, a subgroup of patients with clinically defined toxic multinodular goiter (type A) probably have autoimmune hyperthyroidism (a variant of Graves' disease), while in another subgroup (type B) hyperthyroidism is not related to an autoimmune etiology (a variant of toxic adenoma).
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PMID:Toxic multinodular goiter: a variant of autoimmune hyperthyroidism. 288 84

Water relations of Engelmann spruce (Picea engelmannii Parry) and subalpine fir (Abies lasiocarpa (Hook.) Nutt.) trees growing at an elevation of 3230 m on Mt. Evans, Colorado, USA, were studied during the winters of 1995-1996 and 1996-1997. During both winters, current-year and 1-year-old shoots were collected weekly and their relative water contents (RWC) determined. Measured meteorological parameters were used in a conifer winter water relations model, WINWAT, to simulate changes in shoot RWC of P. engelmannii and A. lasiocarpa during the winter. The model failed to predict shoot RWCs in 1996-1997 when calibrated with 1995-1996 data. The cold early summer of 1995 inhibited xylem formation, which appears to have caused lower rates of water recharge to the needles during the 1995-1996 winter than during the 1996-1997 winter. We conclude that summer climate strongly affects winter water relations in these subalpine species, and that changes in both summer and winter climate must be considered when predicting future ranges of these species.
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PMID:Dependence of winter water relations of mature high-elevation Picea engelmannii and Abies lasiocarpa on summer climate. 1126 59

Follicular thyroid carcinoma typically manifests under euthyroid conditions, and diagnostic scintigraphy usually identifies a cold nodule. Sometimes, such tumors can appear in the context of hyperthyroidism, which can be caused by a toxic multinodular goitre, a toxic adenoma, or even carcinoma. We report a case of follicular thyroid carcinoma discovered after surgical treatment of a toxic multinodular goiter, in which solitary adrenal gland metastasis was detected five years later. A (131)I whole body scan is the diagnostic method of choice for functioning thyroid metastasis.
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PMID:Solitary adrenal gland metastasis of a follicular thyroid carcinoma presenting with hyperthyroidism. 1145 74

Toxic nodular goiter (TNG) is the most frequent cause of thyrotoxicosis in the elderly, specially in iodine deficient areas. Epidemiological studies have shown that in iodine deficient areas (Jutland) the incidence of hyperthyroidism is significantly higher with respect to areas with normal iodine intake (Iceland) and it is due to TNG. A careful epidemiological study recently carried out in Pescopagano, in southern Italy, an area characterized by a mild to moderate iodine deficiency, indicates that, in its natural history, nodular goiter contributes to the development of functional autonomy and eventually hyperthyroidism. Somatic activating mutations of the TSH receptor are involved in the pathogenesis of TNG. It is supposed that the prolonged iodine deficiency associated with chronic TSH stimulation increases the replication of follicular thyroid cells, and favor the appearance and expression of mutations of the TSH receptor gene. The clinical signs are usually more subtle than those observed in Graves' disease: a long phase of subclinical hyperthyroidism (normal circulating thyroid hormones and undetectable TSH levels) can precede the appearance of the symptoms. Cardiac symptoms are most frequent, (arrhythmia and atrial fibrillation). Thyroid scintigraphy in toxic multinodular goiter shows an uneven distribution of the radionuclide with multiple hyperfunctioning nodules and cold nodules. Thyroid US shows goiter with inhomogeneous solid nodules often with ill-defined borders. The treatment with antithyroid drug does not allow a permanent remission of hyperthyroidism, but its use is indicated to achieve euthyroidism before the definitive treatment. The definitive treatment is radioiodine or thyroidectomy.
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PMID:Toxic multinodular goiter in the elderly. 1250 7

Greenhouse-cultured, container-grown ponderosa pine (Pinus ponderosa var. scopulorum Engelm.), interior Douglas-fir (Pseudotsuga menziesii var. glauca (Beissn.) Franco), and Engelmann spruce (Picea engelmannii (Parry) Engelm.) were cold acclimated and deacclimated in growth chambers over 19 weeks. Cold hardiness was measured weekly by a whole-plant freeze test and by two quick tissue tests: freeze-induced electrolyte leakage of needles, and differential thermal analysis of buds. The whole-plant freeze test provided results in 7 days, and indicated differences in cold hardiness among stems, buds, and needles. Although the whole-plant freeze test could accurately measure cold hardiness, it was not precise, and it required destructive sampling. Results from freeze-induced electrolyte leakage and differential thermal analysis were available in 2 days and 1 hour, respectively. The freeze-induced electrolyte leakage test was a precise, sensitive and objective predictor of changes or differences in tissue cold hardiness. To determine actual cold hardiness, results could be calibrated to the response of the same tissue in the whole-plant freeze test. The speed and objectivity of differential thermal analysis made this test useful for rapid, general assessment of cold hardiness status, but calibration was difficult, and precision varied.
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PMID:Comparison of three cold hardiness tests for conifer seedlings. 1497 28

Greenhouse-cultured, container-grown ponderosa pine (Pinus ponderosa var. scopulorum Engelm.), interior Douglas-fir (Pseudotsuga menziesii var. glauca (Beissn.) Franco) and Engelmann spruce (Picea engelmannii (Parry) Engelm.) were cold acclimated and deacclimated in growth chambers over 19 weeks. Stem cold hardiness, total new root length at 14 days and days to bud break were measured weekly. Relationships among cold hardiness, root growth potential (RGP) and bud dormancy suggest that cold hardiness, which can be measured quickly, could provide a useful basis for estimating the two other parameters. During cold acclimation, there was a lag period in which stem cold hardiness remained at -15 degrees C and RGP was at a minimum, in all three species. Douglas-fir and Engelmann spruce buds remained fully dormant during this lag period. Ponderosa pine buds had no chilling requirement for the loss of dormancy, and reached quiescence during the lag period. Immediately following the lag period, as stem cold hardiness progressed to -22 degrees C, RGP increased to a high plateau in all three species, and Douglas-fir and Engelmann spruce buds approached quiescence. Cold deacclimation and bud development began immediately on exposure to warm, long days, but RGP remained high until stem cold hardiness returned to approximately -15 degrees C. At bud break, cold hardiness and RGP were at the minimum.
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PMID:Relationships among cold hardiness, root growth potential and bud dormancy in three conifers. 1497 75

A model was developed earlier describing conductance for three conifers (Picea engelmannii Parry ex Engelm., Abies lasiocarpa [Hook.] Nutt., and Pinus contorta var. latifolia Engelm.) and one hardwood (Populus tremuloides Michx.) using only two terms, photosynthetic photon flux density (PPFD) and absolute humidity difference from leaf to air (DAH). Using residual analysis techniques (actual minus estimated conductance), it was determined that no seasonal or temperature effects existed that were not taken into account with PPFD and DAH. However, conductance was reduced on days following cold nights (below 4 degrees C) or, in aspen, when xylem pressure potential was below -20 bars (1 bar = 10(5) Pa). The following model takes these terms into account: Conductance = b(1) ( radicalPPFD/ radicalDAH) + b(2) ( radicalPPFD/DAH) + b(3) ( radicalPPFD/DAH(2)) + b(4)f(T(min)) + b(5)f(psi(threshold)), where the first three terms describe normal conductance, and the last two terms account for reductions in conductance caused by cold night temperatures or water stress.
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PMID:Evaluation of season, temperature, and water stress effects on stomata using a leaf conductance model. 1666 37

The regulation of striated muscle contraction involves changes in the interactions of troponin and tropomyosin with actin thin filaments. In resting muscle, myosin-binding sites on actin are thought to be blocked by the coiled-coil protein tropomyosin. During muscle activation, Ca2+ binding to troponin alters the tropomyosin position on actin, resulting in cyclic actin-myosin interactions that accompany muscle contraction. Evidence for this steric regulation by troponin-tropomyosin comes from X-ray data [Haselgrove, J.C., 1972. X-ray evidence for a conformational change in the actin-containing filaments of verterbrate striated muscle. Cold Spring Habor Symp. Quant. Biol. 37, 341-352; Huxley, H.E., 1972. Structural changes in actin and myosin-containing filaments during contraction. Cold Spring Habor Symp. Quant. Biol. 37, 361-376; Parry, D.A., Squire, J.M., 1973. Structural role of tropomyosin in muscle regulation: analysis of the X-ray diffraction patterns from relaxed and contracting muscles. J. Mol. Biol. 75, 33-55] and electron microscope (EM) data [Spudich, J.A., Huxley, H.E., Finch, J., 1972. Regulation of skeletal muscle contraction. II. Structural studies of the interaction of the tropomyosin-troponin complex with actin. J. Mol. Biol. 72, 619-632; O'Brien, E.J., Gillis, J.M., Couch, J., 1975. Symmetry and molecular arrangement in paracrystals of reconstituted muscle thin filaments. J. Mol. Biol. 99, 461-475; Lehman, W., Craig, R., Vibert, P., 1994. Ca2+-induced tropomyosin movement in Limulus thin filaments revealed by three-dimensional reconstruction. Nature 368, 65-67] each with its own particular strengths and limitations. Here we bring together some of the latest information from EM analysis of single thin filaments from Pirani et al. [Pirani, A., Xu, C., Hatch, V., Craig, R., Tobacman, L.S., Lehman, W. (2005). Single particle analysis of relaxed and activated muscle thin filaments. J. Mol. Biol. 346, 761-772], with synchrotron X-ray data from non-overlapped muscle fibres to refine the models of the striated muscle thin filament. This was done by incorporating current atomic-resolution structures of actin, tropomyosin, troponin and myosin subfragment-1. Fitting these atomic coordinates to EM reconstructions, we present atomic models of the thin filament that are entirely consistent with a steric regulatory mechanism. Furthermore, fitting the atomic models against diffraction data from skinned muscle fibres, stretched to non-overlap to preclude crossbridge binding, produced very similar results, including a large Ca2+-induced shift in tropomyosin azimuthal location but little change in the actin structure or apparent alteration in troponin position.
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PMID:A comparison of muscle thin filament models obtained from electron microscopy reconstructions and low-angle X-ray fibre diagrams from non-overlap muscle. 1679 85


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