Higher thyroid level during pregnancy,2 days after conception pregnancy test,pregnancy 50 thinned cervix - You Shoud Know

Hypothyroidism leads to a suppression of humoral and cell-mediated immune responses, effects that are often reversed by restoration of the euthyroid state. By this method, we analysed the correlation between pregnancy outcome, neonatal thyroid stimulating hormone (TSH) level and maternal thyroid diseases. In accordance, chronic stress induces a decrease in thyroid hormone levels that in turn, lead to impaired humoral and T-cell mediated responses. Despite the existence of contradictory results, in general, hyperthyroidism has been shown to up-regulate immunity.
Circulating thyroid hormone levels seem to be related to the immune function in subjects with altered thyroid status. The levels of TSH, free thyroxine (FT4) and thyroid peroxidase antibodies (TPO-Ab) of mothers were quantified by electrochemistry immunoassay (ECL). Here, we discuss the participation of these interactions in immune homeostasis, as well as in the development and course of autoimmune thyroid diseases.IntroductionFor many years the immune system has been considered to be autoregulated to avoid the perpetuation of protective responses once the pathogen has been eliminated and to prevent harmful autoimmune responses. The levels of neonatal blood TSH were detected by time-resolved fluorescence immunoassay (TRFIA).
Thus, the control of self-reactive T cells takes place in the thymus during ontogeny and in the periphery after birth, while regulatory mechanisms against effector cell responses to foreign antigens act in the peripheral lymphoid organs throughout  life.Many immune cells participate in immune responses, but control mechanisms are mainly exerted through T helper (Th) lymphocytes. Th cells are able to recruit and activate other immune cells including B lymphocytes, cytotoxic T cells, macrophages, mast cells, neutrophils, eosinophils and basophils. Naive CD4 T cells are categorized according to their functions, their pattern of cytokine secretion and their expression of specific transcription factors. Although other Th lineages may exist, there are four major lineages, Th1, Th2, Th17 and T regulatory (Treg) cells. The differentiation of Th cells usually depends on a unique combination of stimulants and on the subsequent activation of diverse transcription factors [1].
Being positive for thyroid peroxidase antibodies was a significant risk factor of subclinical hypothyroidism during pregnancy. Th1 cells direct cell-mediated immune responses that control intracellular infections, whereas Th2 cells essentially eliminate extracellular antigens, supporting humoral immunity and being involved in allergic reactions.
The cross-regulation between both cell types is managed by the secretion of different cytokines released by each T cell subtype that can inhibit the function of the other subset [2, 3].
Recently, other Th cells have come onto the scene, with Th17 cells facilitating various aspects of immune activation including inflammation, and being recognized as the central effectors in organ-related autoimmune diseases [3]. Treg cells, on the other hand, are in charge of suppressing potentially deleterious activities of the other Th cells. Interestingly, it has been indicated that a dichotomy exists in the generation of Th17 and Treg cells, depending on whether they are activated in the presence of TGF-beta or TGF-beta plus inflammatory cytokines such as IL-6 [4], which takes part in the control of inflammatory and autoimmune diseases.Besides the autoregulatory mechanisms mentioned above, the immune system is also controlled by the neuroendocrine system. A bidirectional network exists between both systems in which hormones and neurotransmitters are able to affect immune function and, thereby also affecting immune mediators that are then capable of inducing neuroendocrine changes. This two-way communication is possible as both systems share receptors for common ligands and their coupled signaling pathways.
The back and forth information, which flows between the neuroendocrine and the immune systems, functions to maintain and protect the internal homeostasis of the organism [5, 6].In this network, hormones and neuropeptides provide the link between the neuroendocrine and the immune systems constituting specific axes. Amongst these are two well studied axes, the hypothalamic-pituitary-adrenal (HPA) axis and the hypothalamic-pituitary-thyroid (HPT) axis.
Furthermore, the autonomic nervous system, through the innervation of lymphoid organs, also communicates with the lymphoid compartment by releasing neurotransmitters able to regulate immune cell physiology [7].
Thus, it appears that multidirectional communication networks exist within the body that permit the signal transmission between these various systems to keep homeostasis during times of stress, injury, disease or other pathological conditions. Los niveles de TSH en la sangre de los neonatos, fueron determinados mediante inmunoensayo por fluorescencia resuelto en el tiempo (TRFIA). Of note, the participation of HPT axis hormones in immune system regulation has received comparatively less attention than the effects exerted by hormones of the HPA axis.
This is perhaps related to the dominating role of autoimmunity in the pathogenesis of thyroid disorders that makes it difficult to explore the role of the HPT axis hormones in the physiologic control of immunity. In this overview we discuss the immunomodulatory effects of thyroid hormones, as well as their participation in immune dysfunction during stress conditions. Ser positivo a los anticuerpos de la peroxidasa tiroidea fue un factor de riesgo significativo del hipotiroidismo subclínico durante el embarazo. The role of thyroid hormones under physiological conditions and their potential contribution to the progress of autoimmune thyroid diseases are briefly outlined as well.How Do Thyroid Hormones Regulate Immunity?Thyroid hormones play critical roles in differentiation, growth and metabolism [8].
Their release from the thyroid gland involves a fine tuned regulated mechanism that includes structures of the central nervous system. Low circulating levels of thyroid hormones are sensed in the hypothalamus, which responds by releasing thyrotropin releasing hormone (TRH).
The TRH stimulates the pituitary to produce thyrotropin or thyroid stimulating hormone (TSH), which, in turn, stimulates the thyroid gland to produce thyroid hormone until levels in the blood return to normal.
These hormones are then transported by the blood to many different target tissues where they regulate the transcription of genes controlling cell metabolism. El tamizaje de rutina de la función tiroidea materna es importante y debe recomendarse. The authors hypothesized that thyroid hormones are involved in immune system homeostasis maintenance in response to environmental changes or stress-mediated immunosuppression [11, 12].
Although knockout mice studies have demonstrated that hormone deficiency is not incompatible with life, many of the effects on peripheral tissues were milder in these animals than those seen in congenital hypothyroidism [8].On the other hand, the presence of functional receptors for HPT hormones on lymphocytes as well as the frequent immune alterations observed during physiological or pathological fluctuations of thyroid hormones strengthens the interactions between the HPT axis hormones and the immune system [9]. The presence of triiodothyronine (T3) in lymphocytes, mast cells, monocytes, macrophage and granulocytes from rat peritoneal fluid and blood, and in thymic lymphocytes was demonstrated as well [13]. The increased prevalence of gestation-related thyroid disorders and the importance for both mother and child were reported in multiple studies throughout the world. This extrathyroidal source of T3 is regulated by TSH and is needed for maintaining cell proliferation and the normal status in the immune system [13, 14]. Maternal hypothyroidism, even very mild, can have adverse effects on both pregnancy outcome and children's development (2). In these patients, a significant correlation was observed between serum IgA and IgM concentrations, and free thyroxine (T4) levels, and with the severity of congenital hypothyroidism, as well [22].Many of the immune consequences of hypothyroidism can be reversed by treatment with thyroid hormones [14, 15]. Thus, restoration of thyroid function, after thiourea-induced blockade, recomposed the humoral response to sheep red blood cells (SRBCs) in birds [23] and similar results were obtained after T3 administration in propylthiouracil-induced hypothyroid mice for both humoral and cell-mediated immune responses [24, 25]. The fact that T3 is able to revert the effects of the thyrostatic drug on the immune response implies that the immunomodulatory actions are not related to a direct effect of the anti-thyroid agent, but to the levels of the thyroid hormone itself.
In addition, the suppression of cell-mediated immunity in severe human hypothyroidism was accompanied by an improvement of lymphocyte function with the gradual return to a euthyroid condition [26].On the other hand, contradictory results exist in the literature on the effects of experimental hyperthyroidism on immunity. Because of complicated physiological changes during pregnancy, it is vital to establish the normal gestational-specific reference values for thyroid function. In fact, it was shown that hyperthyroid condition can lead to either suppressing [27] or enhancing [24, 28, 29] effects on primary antibody responses or on T and B lymphocyte proliferation [16, 24, 25]. These controversial results might have been  due to the different species used or to the diverse hormonal treatment established (dose, duration, type of hormone).
In our last study, we established a new self- sequential longitudinal reference interval which was based on the same pregnant women group (10). On the contrary, treatment with higher doses of T4 for few (3 to 7) days induced both a decreased expression of T-cell type cytokines, both at the mRNA and the protein levels, and an impaired lymphocyte response to mitogen stimulation [30]. Our method could reflect the changes of thyroid function in pregnant women more realistically, and could decrease the percentage of potential misclassification of thyroid dysfunction during pregnancy.
In addition, most studies in experimental models have not evaluated the status of the HPT axis because thyrotropic hormone activity is difficult to evaluate in rodents. An integrative study of the HTP axis function and the immune status was recently performed in mice, showing that T and B-cell mitogen-induced proliferation of lymphocytes from hyperthyroid mice was higher than that of euthyroid animal cells [25]. This effect was related to an increase in the activation of intracellular signals and in the release of cytokines involved in T lymphocyte activation, such as IL-2 and IFN-? and of the pro-inflammatory cytokines IL-6 and TNF-?, after an inflammatory stimulus [25]. Most researchers focussed on how maternal thyroid dysfunction affected children's development, such as cognitive functioning (18), neuropsychological development (19) and so on.
Moreover, these effects seem not to be due to altered TSH or TRH hormone levels, as the low levels of TSH or TRH that accompany the hyperthyroid condition would lead to a decrease in immune function, as was previously shown for these hormones [31]. It is well known that thyroid hormones are important factors for neonatal normal growth, bone development and neural development, particularly within six months after birth. In support of this, direct actions of thyroid hormones were demonstrated on immune cells when the addition to T lymphocytes led to stimulation of cell proliferation [32] or of dendritic cell maturation and function [33]. Congenital hypothyroidism (CH) is the most prevalent endocrine disorder in the newborn and affects 1 in 3000–4000 newborn babies (20). The preponderance of evidence indicates an enhancing role of thyroid hormones on immune function.In conclusion, one could generalize that low levels of thyroid hormones in vivo lead to a decrease of the immune function, while the opposite occurs when circulating levels of these hormones are high.
Despite the proven direct action of thyroid hormones on immune cells, the possible involvement of other endocrine factors regulated by thyroid status cannot be ruled out.  An important example of the regulation of immunity exerted by low serum levels of thyroid hormones is found during the course of chronic stress conditions.
This issue is briefly discussed below.Thyroid Hormones in Stress-Mediated Alteration of ImmunityStress is defined as any situation capable of perturbing the physiological or psychological homeostasis.


We therefore emphasized the importance of neonatal screening in this study and questioned whether maternal thyroid diseases can also affect neonatal thyroid hormones. While response to stress is a necessary survival mechanism, prolonged stress can have several repercussions affecting behavioral, endocrine and immunological parameters [34]. Recently, Papendieck et al (22) reported that maternal hyperthyroidism implies the risk of thyroid abnormalities in the newborn.
The recognition of these effects has led McEwen [34] to develop a new terminology to link the protective and damaging biologic response to stressors, namely, allostasis and allostatic overload.  Allostasis refers to the adaptive processes that maintain homeostasis through the production of neuroendocrine mediators and cytokines. Neonates born from women with thyroid dysfunction were prone to get neonatal thyroid disorders.
Rovelli et al (23) also found that higher serum thyroid stimulating hormone (TSH) level was frequently observed in infants born to mothers affected by autoimmune thyroiditis. One of these mechanisms includes alterations of the endocrine system that in turn modulate the immune function [40]. The investigations have traditionally focused on the activation of the HPA axis and the sympathetic adrenal medullary system [41].
In this respect less attention has been given to the role of the HPT axis, although there is strong evidence of an important relationship between stress and thyroid function [42].  Differences in adaptative responses to stress would be related to either activation or suppression of the thyroid system.
Thus, traumatic stress is accompanied by activation of thyroid function, and patients with hyperthyroidism report more stressful life events than members of a control population [43, 44]. Using the self-sequential longitudinal reference intervals (SLRI) of thyroid function during pregnancy which we established, we analysed the correlation between pregnancy complication and maternal thyroid diseases. Conversely, in chronic posttraumatic stress disorder patients, significantly lower plasma cortisol and TSH levels are reported with respect to control subjects [45]. After follow-up of their newborn babies,we detected the neonatal blood TSH level and analysed the relationship between maternal thyroid function and fetal TSH screening. In addition, chronic stress has been generally associated with suppression of thyroid axis function [46].A reduction in serum levels of thyroid hormones, mainly of the biologically active T3, was found in stressed animals that correlated with lower titers of specific antibodies after alloimmunization [47] and reduced lymphocyte reactivity in response to mitogens [38]. Thyroidal inhibition after exposure to diverse stressors was also described in other species [48].  A very important finding was that restoration of physiologic thyroid hormone levels by T4 treatment in stressed animals not only restored thyroid hormone serum levels, but also reverted stress-mediated effects on immunity, thus suggesting that chronic stress induces an alteration of thyroid axis function that in turn alters the immune response [47].
During stress, suppressed secretion of TSH and decreased conversion of T4 to the potent biologically active T3 in peripheral tissues have been described [49], so a major decrease in T3 levels could be responsible for the alterations in the immune response. The cases of this study comprised the pregnant women who regularly checked in to our hospital for early prenatal care from June 2008 to June 2009. The study design and protocol were reviewed and approved by the ethics committee of Changzhou Women and Children Health Hospital affiliated to Nanjing Medical University. Despite that in humans the role of stress as a risk factor for cancer development has not been conclusively established, several epidemiological and clinical studies have linked psychological factors such as stress, chronic depression, and lack of social support to the incidence and progression of cancer [53].The increment of tumor development and progression mediated by stress was demonstrated in several types of cancer animal models. Although the mechanisms underlying this relation are not completely understood, recent studies have begun to unravel some of the immune components, modulated by neuroendocrine effects that may affect tumor growth and metastasis [53].
Several findings indicate that different types of stressful conditions result in the promotion of distinct murine tumors, namely ovarian carcinoma [54], B16F10 melanoma [55] and Ehrlich tumor [56] among others. One thousand seven hundred and forty-seven babies were born from those pregnant women (three bore twins). Regarding the T-lymphocyte subset distribution, these authors [58] demonstrated that chronic stress resulted in a reduction of CD4+, but not CD8+ or T-lymphocytes in the lymph nodes, indicating that stress mainly affects T-helper immunity, as previously suggested [59]. Although the participation of NK cells in these processes cannot be ruled out, NK activity has classically been related to the inhibition of metastasis [60] rather than to the control of tumor cell proliferation which is mainly mediated by T cells [61].Additionally, Frick et al.
In contrast, thyroid hormones were down regulated only after chronic restraint stress [62], as it was shown in other animal models of stress [47, 63, 64].
This decrease in thyroid hormone levels that is accompanied by impairment in T-cell reactivity was also observed in chronically stressed mice bearing solid tumors [62]. At the molecular level, it was also reported that chronic stress reduces the activation of specific protein kinase C (PKC), isoforms known to be involved in T-cell activation, namely PKC ? and ? isoenzymes [62]. Moreover, T4 replacement in these animals, which restored the euthyroid status, not only reversed the effect on T lymphocyte function and signaling events, but also prevented the exacerbation of tumor growth and the inhibition of the specific cytotoxic response against lymphoma cells [62].
These studies demonstrate that altered thyroid hormone concentration is associated with altered immunity, but whether these observations are directly due to the actions of thyroid hormones or underlying autoimmunity can not be well established. In this sense, the autoimmune condition in hyperthyroid patients is mainly related to antibodies against the TSH receptor that mimic the function of TSH, and has already been shown to alter the immune function of the TSH hormone as well [67].Results from animal models of hypo- and hyperthyroidism without autoimmune condition, not only show the importance of thyroid hormone circulating levels in immune modulation, but also suggest their participation in autoimmune thyroid diseases (AITD). In fact, these altered levels of thyroid hormones would have an effect in the pathological immune process of AITD. The question that arises is how and to what extent do thyroid hormone levels affect the immune response function in autoimmune thyroid conditions? Mann-Whitney (U test) was used to compare the difference between the two different groups.
The possible consequences of altered levels of thyroid hormones in the course of AITD are outlined below.Autoimmune thyroid diseases (AITD), one of the most common organ specific autoimmune disorders, affect approximately 5% of the overall population, mainly women. These disorders result in dysfunction (hyperfunction, hypofunction or both) of the thyroid gland, and the two most common entities have opposing effects i.e. Several pieces of evidence suggest that the phenotypic expression of thyroid autoimmunity toward one or the other clinical entity is largely dependent on the pattern of immune response that predominates at a given time [69].  The main thyroid autoantigens in HT and GD are thyroglobulin (Tg), thyroid peroxidase (TPO), the primary enzyme involved in the production of thyroid hormones, and the TSH receptor (TSH-R). The potential for misclassification of TSH results was greatest in the 1st trimester (31.0%).
Unlike antibodies against Tg, TPO antibodies are capable of inducing antibody-dependent cell-mediated cytotoxicity.
The intrathyroidal immune cells are B and T lymphocytes, the latter predominating mainly as the CD4+ Th1-subtype.In GD, the infiltration is mild and induces the production of antibodies that bind to the TSH-R stimulating the growth and the function of thyroid follicular cells and consequently leading to hyperthyroidism. Thus, it was demonstrated that intrathyroidal Treg cells are decreased in response to apoptosis in patients with AITD, suggesting that this decrease may contribute to the incomplete regulation of autoreactive T cells in AITD [71], and that naturally existing Treg cells are required for tolerance to experimental autoimmune thyroiditis [72]. A role for Treg in the natural progression of hyperthyroid GD to HT and hypothyroidism in humans has also been suggested [73].  With respect to Th17, an increased differentiation of these lymphocytes and an enhanced synthesis of Th17 cytokines in AITD, mainly in HT, has been described and the possibility that these phenomena have an important role in the pathogenesis of thyroid autoimmunity has been also suggested [74].
With respect to the genetic background, a Human-Leukocyte-Antigen gene locus was the first AITD susceptibility gene identified, followed by other loci of both class II and class I genes and by other non-HLA genes, including immune-modulating (CTLA-4, CD40 and PTPN22) and thyroid-specific (Tg and TSH-R) genes [77].
Thus, low thyroid hormone levels accompanying HT could ameliorate the autoimmune reaction through the inhibition of the cell-mediated mechanisms or the diminished autoantibody secretion. Alternatively, it would exert a negative control on regulatory lymphocytes, thus worsening clinical status.
Conversely, in GD, the increment in the humoral immune response during the hyperthyroid state would increase the levels of anti-TSH-R antibodies affecting the course of the autoimmune disease (see Figure 1).Figure 1. Role of neuroendocrine factors in the establishment and course of autoimmune thyroid diseases (AITD).
The direction of the response depends mainly on the antigen presenting cells (APC), which are influenced by  thyroid autoantigens and the environment of cytokines or neuroendocrine factors being encountered. The course of the thyroid autoimmune disorder is also regulated by thyroid hormone circulating levels, which in turn could aggravate or ameliorate the autoimmune pathology. For example, low levels of thyroid hormones in HT may down regulate the autoimmune reaction but could contribute to a decrease in T reg subsets thereby worsening the clinical status of the patient. In GD, high levels of thyroid hormones may up regulate the humoral responses, which would lead to higher levels of anti-TSH-R antibodies or alternatively may improve Treg function to counteract their action.ConclusionsA bidirectional circuit exists between the neuroendocrine and immune systems that functions to maintain and protect the internal homeostasis of the organism. In this context, interactions between thyroid hormones and the immune system are important to elicit appropriate immune responses, especially when the immune system is challenged as in stressful conditions. The possibility also exists that altered levels of thyroid hormones during the course of the AITD may alter immune function that in turn could influence the evolution of the disease.Both immune alterations leading to AITD, as well as AITD consequences on immunity, complete the picture for finding therapeutic solutions for the management of these endocrine disorders. Further studies on animal models with non autoimmune hypo- and hyperthyroidism would be useful tools to analyze the role that circulating hormone levels exert on immune function. A study in healthy elderly subjects devoid of thyroid illness showed the intricate network of hormones and factors involved in immune response regulation during a healthy euthyroid state [81].
This study demonstrated that thyroid hormone concentrations are positively associated with markers of inflammation, NK-like T cells, expression of IL-6 by activated monocytes, percentage of memory T-lymphocytes, and higher IL-2 receptor density in T-cells [81]. Neurohormonal-cytokine interactions: implications for inflammation, common human diseases and well-being. When we clinically evaluate the maternal thyroid function, it is advised to use a gestational-specific reference range. In a previous study (10), we have established a new SLRI which was based on the same group of pregnant women. Humoral and cell-mediated immunity in mice with genetic deficiencies of prolactin, growth hormone, insulin-like growth factor-I, and thyroid hormones. Self-sequential longitudinal reference interval could reduce the variation caused by sampling error from different groups and reflect the changes of thyroid function in pregnant women more realistically, resulting in a more important value for clinical diagnosis and therapy. The roles of prolactin, growth hormone, insulin-like growth factor-I, and thyroid hormones in lymphocyte development and function: insights from genetic models of hormone and hormone receptor deficiency. Immunologically demonstrable hormones and hormone-like molecules in rat white blood cells and mast cells. Thyroid hormone deficiency was the most common maternal thyroid disorder and accounted for about 71.2% of all thyroid disorders during pregnancy.


Thyrotropic hormone (TSH) regulation of triiodothyronine (T3) concentration in immune cells. Immunology, signal transduction, and behavior in hypothalamic-pituitary-adrenal axis-related genetic mouse models.
Immunomodulatory role of thyroid hormones: in vivo effect of thyroid hormones on the blastogenic response to lymphoid tissue.
Because of physiological changes in the mother, serum TSH level decreased during the 1st trimester, and then increased gradually which resulted in the difficulties of clinical diagnosis.
Effects of thyroid hormones on lymphocyte phenotypes in rats: changes in lymphocyte subsets related to thyroid function.
Therefore, it is reasonable and necessary to diagnose thyroid hormone deficiency in pregnant women with gestational-specific reference.
Here, we recommend the SLRI which we established, to clinically evaluate maternal thyroid function and our results demonstrated that it can give more accurate value for diagnosis and therapy. A new assay system for evaluation of developmental immunotoxicity of chemical compounds using respiratory syncytial virus infection to offspring mice. Assessment of the factors involving in the development of hypothyroidism in HIV-infected patients: a case-control study.
Recently, some researchers showed that maternal subclinical hypothyroidism is also associated with pregnancy outcome, and it could result in adverse effects on baby's growth, but there were different opinions (1, 2, 18, 19, 27). At the same time, it is a bone of contention whether all pregnant women should be routinely screened and treated for subclinical hypothyroidism (25, 28). Our study showed that mothers with subclinical hypothyroidism were prone to have pregnancy complications, including anaemia, HDCP, GDM, fetal distress, ICP, pre-eclampsia etc. Undetectable serum IgA and low IgM concentration in children with congenital hypothyroidism.
It is well known that thyroid hormones are important factors for neonatal normal growth, bone and neural development, particularly within six months after birth.
Fu et al found that mothers with hypothyroidism had greater effect on neonatal thyroid function (29). Experimental evidence pointing to the bidirectional interaction between the immune system and the thyroid axis. Recently, the relationship between maternal and fetal thyroid function were reported in a few studies throughout the world (22, 23).
Integrative study of hypothalamus- pituitary-thyroid-immune system interaction: thyroid hormone mediated modulation of lymphocyte activity through the protein kinase C signaling pathway. All 20 newborn babies whose TSH was higher than the cut-off value had transient hypothyroidism.
All suspected infants should be treated as having CH for the first three years of life, due to the risks of mental retardation (30). Potentiation of humoral immune response and activation of NF-kappaB pathway in lymphocytes in experimentally induced hyperthyroid rats.
But based on our results, we emphasize the importance of routine antenatal subclinical hypothyroidism screening.
Immunomodulation of peripheral lymphocytes by hormones of the hypothalamus-pituitary-thyroid axis.
Thyroid hormones increase inducible nitric oxide synthase gene expression down-stream PKC ? in tumor murine T lymphocytes. Some reports showed that mothers who are TPO-Ab positive are also at risk for pregnancy complication and poor fetal outcome (34, 35). Compared with the control group, women who were TPO-Ab positive were prone to have any kind of pregnancy complication. Central effects of stress hormones in health and disease: understanding the protective and damaging effects of stress and stress mediators. Overall, we think screening for TPO-Ab in pregnant women is also recommended and important, especially to mothers.
Based on our results, we found that thyroid disorders, especially subclinical hypothyroidism, are common in pregnant women. It is a risk factor for pregnancy complications and can affect the level of neonatal blood TSH. Acute and chronic stress exert opposing effects on antibody responses associated with changes in stress hormone regulation of T-lymphocyte reactivity. We therefore recommend routine maternal thyroid function screening for both mothers and newborns.
Cytokine production by spleen cells after social defeat in mice: Activation of T cells and reduced inhibition by glucocorticoids. This study was supported by grants from Changzhou Health Bureau and Key Laboratory of Changzhou City. Effects of chronic mid stress (CMS) and imipramine administration on spleen mononuclear cell proliferative response, serum corticosterone level and brain norepinephrine content in male mice.
Persistent neuroendocrine changes in multiple hormonal axes after single or repeated stressor exposures.
Elevations of serum T3 levels and their association with symptoms in World War II veterans with combat-related posttraumatic stress disorder: replication of findings in Vietnam combat veterans. Thyroidal inhibition following diverse stress in soft-shelled turtle, Lissemys punctata punctata bonnoterre.
Acute effects of thyroid hormones on the production of adrenal cAMP and corticosterone in male rats. Experimentally-induced hyperthyroidism is associated with activation of the rat hypothalamic-pituitary-adrenal axis.
Immunomodulatory activities of glucocorticoids: insights from transgenesis and gene targeting. Maternal hypothyroidism in early and late gestation: effects on neonatal and obstetric outcome. Variations in behavior, innate immunity and host resistance to B16F10 melanoma growth in mice that present social stable hierarchical ranks. Stress system activity, innate and T helper cytokines, and susceptibility to immune-related diseases. Human neuroblastoma cell growth in xenogeneic hosts: Comparison of T cell-deficient and NK-deficient hosts, and subcutaneous or intravenous injection routes. Involvement of thyroid hormones in the alterations of T-cell immunity and tumor progression induced by chronic stress. Relation between the hypothalamic-pituitary-thyroid (HPT) axis and the hypothalamic-pituitary-adrenal (HPA) axis during repeated stress. Exercise as a stress model and the interplay between the hypothalamus-pituitary-adrenal and the hypothalamus-pituitary-thyroid axes. A study for maternal thyroid hormone deficiency during the first half of pregnancy in China. Apoptosis-induced decrease of intrathyroidal CD4(+)CD25(+) regulatory T cells in autoimmune thyroid diseases. Naturally-existing CD4(+)CD25(+)Foxp3(+) regulatory T cells are required for tolerance to experimental autoimmune thyroiditis induced by either exogenous or endogenous autoantigen. Determination of trimester specific reference intervals for thyroid hormones during pregnancy in Malaysian women. Establishment of a self-sequential longitudinal reference intervals of maternal thyroid function during pregnancy. Preliminary evidence of immune function modulation by thyroid hormones in healthy men and women aged 55–70 years.
Gestational month-specific reference ranges for TSH and thyroxine in Han nationality women in iodine sufficient area of China. A study to establish gestation-specific reference intervals for thyroid function tests in normal singleton pregnancy. Reference intervals in evaluation of maternal thyroid function during the first trimester of pregnancy.
Henrichs J, Bongers-Schokking JJ, Schenk JJ, Ghassabian A, Schmidt HG, Visser TJ et al. Maternal thyroid function during early pregnancy and cognitive functioning in early childhood: the generation R study. Serum thyroid autoantibodies in patients with idiopathic either acute or chronic urticaria.



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