967 research outputs found
Postpartum thyroiditis and autoimmune thyroiditis in women of childbearing age: recent insights and consequences for antenatal and postnatal care
Postpartum thyroiditis is a syndrome of transient or permanent thyroid
dysfunction occurring in the first year after delivery and based on an
autoimmune inflammation of the thyroid. The prevalence ranges from 5-7%.
We discuss the role of antibodies (especially thyroid peroxidase
antibodies), complement, activated T cells, and apoptosis in the outbreak
of postpartum thyroiditis. Postpartum thyroiditis is conceptualized as an
acute phase of autoimmune thyroid destruction in the context of an
existing and ongoing process of thyroid autosensitization. From pregnancy
an enhanced state of immune tolerance ensues. A rebound reaction to this
pregnancy-associated immune suppression after delivery explains the
aggravation of autoimmune syndromes in the puerperal period, e.g., the
occurrence of clinically overt postpartum thyroiditis. Low thyroid reserve
due to autoimmune thyroiditis is increasingly recognized as a serious
health problem. 1) Thyroid autoimmunity increases the probability of
spontaneous fetal loss. 2) Thyroid failure due to autoimmune
thyroiditis-often mild and subclinical-can lead to permanent and
significant impairment in neuropsychological performance of the offspring.
3) Evidence is emerging that as women age subclinical hypothyroidism-as a
sequel of postpartum thyroiditis-predisposes them to cardiovascular
disease. Hence, postpartum thyroiditis is no longer considered a mild and
transient disorder. Screening is considered
Decrease of free thyroxine levels after controlled ovarian hyperstimulation
Controlled ovarian hyperstimulation could lead to opposing effects on
thyroid function. Therefore, in a prospective study of 65 women undergoing
controlled ovarian hyperstimulation, thyroid hormones, T4-binding
globulin, TPO antibodies, gonadotropins, estradiol, and PRL were measured
before and after controlled ovarian hyperstimulation. After ovarian
stimulation (mean +/- SE of mean): free T4 decreased, 14.4 +/- 0.2 vs.
12.9 +/- 0.2 pmol/L (P < 0.0001); thyroid-stimulating hormone increased,
2.3 +/- 0.3 vs. 3.0 +/- 0.4 mU/L (P < 0.0001); T4-binding globulin
increased, 25.2 +/- 0.7 vs. 33.9 +/- 0.9 mg/L (P < 0.0001); total T4
increased, 98.1 +/- 2.3 vs. 114.6 +/- 2.5 nmol/L (P < 0.0001); total T3
increased, 2.0 +/- 0.04 vs. 2.3 +/- 0.07 nmol/L (P < 0.0001); TPO
antibodies decreased, 370 +/- 233 U/mL vs. 355 +/- 224 U/mL (P < 0.0001);
LH decreased, 8.1 +/- 1.1 vs. 0.4 +/-0.1 U/L (P < 0.0001); FSH did not
change, 6.5 +/- 0.6 vs. 7.9 +/- 0.9 U/L (P = 0.08); human CG increased, <2
+/- 0.0 vs. 195 +/- 16 U/L (P < 0.0001); estradiol increased, 359.3 +/-
25.9 pmol/L vs. 3491.8 +/-298.3 pmol/L (P < 0.0001); and PRL increased,
0.23 +/- 0.02 vs. 0.95 +/- 0.06 U/L (P < 0.0001). Because low maternal
free T4 and elevated maternal thyroid-stimulating hormone levels during
early gestation have been reported to be associated with impaired
psychomotor development in the offspring, our findings indicate the need
for additional studies in the children of women who where exposed to high
levels of estrogens around the time of conception
Reversible magnetization below Tc in high-quality superconducting ceramics
International audienceWe have investigated the reversible magnetization below Tc in high-quality YBa2Cu307_d (Y-123), YBa2Cu4Os (Y-124), Y2Ba4Cu7O15+x (Y-247) and Bi2Sr2CaCu2O8+x (Bi-2212), Tl2Ba2Cu106+d (Tl-2201) and Tl2Ba2CalCu2O8+d (T1-2212) ceramics. Except for the stoichiometric Y-124 phase, the oxygen concentration was optimized in order to obtain the highest value of the critical temperature for which the normal-state susceptibility becomes temperature independent. Using the simple London model, we are able to fit the reversible magnetization M(T, H) outside the region near Tc with good accuracy for the nearly three-dimensional YBaCuO phases. For the very anisotropic BiSrCaCuO and TlBaCaCuO phases, we have to include an additional term to take into account the fluctuations of vortices. An important result is that Y-123 exhibits a critical field clearly higher than those of the BiSrCaCuO or TlBaCaCuO phases. We obtain for the Y-123 phase a slope at Tc μodHC2,C/dT = -4.3 T/K and an extrapolated μoHC2,C (0) = 280 T
Acute effect of pegvisomant on cardiovascular risk markers in healthy men: implications for the pathogenesis of atherosclerosis in GH deficiency
Cardiovascular risk is increased in GH deficiency (GHD). GHD adults are
frequently abdominally obese and display features of the metabolic
syndrome. Otherwise healthy abdominally obese subjects have low GH levels
and show features of the metabolic syndrome as well. We investigated in
healthy nonobese males the effect of the GH receptor antagonist
pegvisomant in different metabolic conditions. This is a model for acute
GHD without the alterations in body composition associated with GHD. We
compared the effect of pegvisomant with that of placebo before and after 3
d of fasting. In addition, we investigated the effect of pegvisomant under
normal, i.e. fed, conditions. Three days of fasting as well as pegvisomant
alone decreased serum free IGF-I levels (1.0 +/- 0.15 vs. 0.31 +/- 0.05
ng/ml and 0.86 +/- 0.23 vs. 0.46 +/- 0.23 ng/ml, respectively). Fasting in
combination with pegvisomant also decreased serum free IGF-I levels (1.0
+/- 0.15 vs. 0.31 +/- 0.07 ng/ml). Treatment with pegvisomant had no
additional influence on the decline of free IGF-I induced by fasting.
Pegvisomant alone had no influence on insulin sensitivity. The increase in
insulin sensitivity induced by fasting was comparable to the increase in
insulin sensitivity induced by fasting combined with pegvisomant. Among
serum lipid concentrations, only serum triglycerides increased
significantly as a result of pegvisomant alone (1.0 +/- 0.2 vs. 1.6 +/-
0.4 mmol/liter). The changes in lipid concentrations induced by fasting
alone or pegvisomant were not different from those induced by pegvisomant
alone. von Willebrand factor antigen levels declined significantly under
the influence of pegvisomant alone (1.1 +/- 0.07 vs. 0.8 +/- 0.06 U/ml).
In conclusion, in different metabolic conditions the GH receptor
antagonist pegvisomant induces no significant acute changes in the major
risk markers for cardiovascular disease. These data suggest that the
secondary metabolic changes, e.g. abdominal obesity or inflammatory
factors, that develop as a result of long-standing GHD are of primary
importance in the pathogenesis of atherosclerosis in patients with GHD
Cytoplasmic continuity revisited: closure of septa of the filamentous fungus Schizophyllum commune in response to environmental conditions
Background: Mycelia of higher fungi consist of interconnected hyphae that are compartmentalized by septa. These septa contain large pores that allow streaming of cytoplasm and even organelles. The cytoplasm of such mycelia is therefore considered to be continuous.Methodology/Principal Findings: Here, we show by laser dissection that septa of Schizophyllum commune can be closed depending on the environmental conditions. The most apical septum of growing hyphae was open when this basidiomycete was grown in minimal medium with glucose as a carbon source. In contrast, the second and the third septum were closed in more than 50% and 90% of the cases, respectively. Interestingly, only 24 and 37% of these septa were closed when hyphae were growing in the absence of glucose. Whether a septum was open or closed also depended on physical conditions of the environment or the presence of toxic agents. The first septum closed when hyphae were exposed to high temperature, to hypertonic conditions, or to the antibiotic nourseothricin. In the case of high temperature, septa opened again when the mycelium was placed back to the normal growth temperature.Conclusions/Significance: Taken together, it is concluded that the septal pores of S. commune are dynamic structures that open or close depending on the environmental conditions. Our findings imply that the cytoplasm in the mycelium of a higher fungus is not continuous perse
Control of tumor size and disease activity during cotreatment with octreotide and the growth hormone receptor antagonist pegvisomant in an acromegalic patient
We describe the case of an acromegalic subject, who was the first patient
ever treated with the GH receptor antagonist pegvisomant. Furthermore, in
this particular patient, progression in tumor size was encountered during
treatment with pegvisomant. The patient described did benefit from
cotreatment with pegvisomant and octreotide, including decreased GH
levels, normalization of serum insulin-like growth factor I
concentrations, and improvement of visual field defects
Blockade of the growth hormone (GH) receptor unmasks rapid GH-releasing peptide-6-mediated tissue-specific insulin resistance
The roles of GH and its receptor (GHR) in metabolic control are not yet
fully understood. We studied the roles of GH and the GHR using the GHR
antagonist pegvisomant for metabolic control of healthy nonobese men in
fasting and nonfasting conditions. Ten healthy subjects were enrolled in a
double blind, placebo-controlled study on the effects of pegvisomant on
GHRH and GH-releasing peptide-6 (GHRP-6)-induced GH secretion before and
after 3 days of fasting and under nonfasting conditions (n = 5). Under the
condition of GHR blockade by pegvisomant in the nonfasting state, GHRP-6
(1 microg/kg) caused a increase in serum insulin (10.3 +/- 2.1 vs. 81.3
+/- 25.4 mU/L; P < 0.001) and glucose (4.2 +/- 0.3 vs. 6.0 +/- 0.6 mmol/L;
P < 0.05) concentrations. In this group, a rapid decrease in serum free
fatty acids levels was also observed. These changes were not observed
under GHR blockade during fasting or in the absence of pegvisomant. We
conclude that although these results were obtained from an acute study,
and long-term administration of pegvisomant could render different
results, blockade of the GHR in the nonfasting state induces
tissue-specific changes in insulin sensitivity, resulting in an increase
in glucose and insulin levels (indicating insulin resistance of
liver/muscle), but probably also in an increase in lipogenesis (indicating
normal insulin sensitivity of adipose tissue). These GHRP-6-mediated
changes indicate that low GH bioactivity on the tissue level can induce
changes in metabolic control, which are characterized by an increase in
fat mass and a decrease in lean body mass. As a mechanism of these
GHRP-6-mediated metabolic changes in the nonfasting state, direct
nonpituitary-mediated GHRP-6 effects on the gastroentero-hepatic axis seem
probable
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