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Lead exposure is known to affect the pituitary-thyroid axis. Likewise, ascorbic acid (AA) has a protective action against lead poisoning. We examine the protective role of AA in lead-induced damage to the thyroid gland. The Wistar rats were divided into three groups: control that received 0.2% AA in drinking water throughout the experiment (15 days), intoxicated with lead acetate (20 mg/kg) intraperitoneally every 48 h for 15 days, and the experimental group treated with lead acetate and 0.2% AA in drinking water throughout the experiment. Plasma thyroid-stimulating hormone, triiodothyronine, thyroxine, and lead were determined. The thyroid gland was weighed, then epithelial cell height and nuclear volume were measured on histological slides. The results show that AA reduced the thyroid atrophy caused by lead acetate, as well as the loss of weight of the gland. In addition, it prevented the decrease of the hormone triiodothyronine, although the thyroxine hormone remained lower than the control values ​​and the thyroid-stimulating hormone remains high. Our results indicated that AA could play a protective role in lead poisoning in the thyroid gland.

Most infectious diseases are unequally distributed between male and female subjects. This sex dimorphism is confirmed by epidemiologic studies which suggest an increased number of male septic patients, while, due to the class age of septic patients, an overrepresentation of female patients would be expected. Lifestyle, recreational activities, professional exposition and access to care are plausible reasons for this dimorphism. However, biological differences should be carefully considered, particularly the weight of X-linked variability and the role of sex hormones. Animal models clearly show that clinical response to infection is more exuberant in males than in females. This is partly explained by an attenuation of the inflammatory response by female sex hormones. However, the translation from experimental studies to the bedside remains challenging as a result of confounding factors like age, hormone changes and response to treatment. Keywords: Bacteria, estradiol, gender, infection, sex

Alternatives to bisphenol A (BPA) are more and more used in thermal paper receipts. To get an overview of the situation in Switzerland, 124 thermal paper receipts were collected and analyzed. Whereas BPA was detected in most samples (n=100), some alternatives, namely bisphenol S (BPS), Pergafast® 201 and D-8 have been found in 4, 11 and 9 samples respectively. As no or few data on their endocrine activity are available, these chemicals and bisphenol F (BPF) were tested in vitro using the H295R steroidogenesis assay. 17β-Estradiol production was induced by BPA and BPF, whereas free testosterone production was inhibited by BPA and BPS. Both non-bisphenol substances did not show significant effects. The binding affinity to 16 proteins and the toxicological potential (TP) were further calculated in silico using VirtualToxLab™. TP values lay between 0.269 and 0.476 and the main target was the estrogen receptor β (84.4 nM to 1.33 μM). A substitution of BPA by BPF and BPS should be thus considered with caution, since they exhibit almost a similar endocrine activity as BPA. D-8 and Pergafast® 201 could be alternatives to replace BPA, however further analyses are needed to better characterize their effects on the hormonal system.

Screening for congenital hypothyroidism for all newborns of the former western parts of the city of Berlin was instituted in 1978 by determination of the TSH levels in dried filter paper blood spots of the 3rd to 5th day of life. Since 1991 the newborns of the former eastern parts have been also included in the same screening program. From 1978 to 1995 a total number of 104 newborns with permanent congenital hypothyroidism have been detected resulting in a prevalence of congenital hypothyroidism of 1:3800. The etiological diagnosis of hypothyroidism was made by imaging studies (ultrasonography or 99mTc scintigraphy) and assessment of serum thyroglobulin and thyroid hormone levels. Using this approach in 37 children (30 female, 7 male) the diagnosis of athyrosis, in 20 children (15 female, 5 male) the diagnosis of ectopy and in 21 children (18 female, 3 male) the diagnosis of thyroid hypoplasia was made, 16 children (8 female, 8 male) had a normally sized gland and 4 (1 female, 3 male) had congenital goiter. In 86% of all patients the age at onset of thyroxine (L-T4) replacement therapy was 8 or 9 days of life (3-42 days) and the median initial L-T4 dose was 14 micrograms/kg/day (10-16 micrograms/kg/day). The intellectual outcome of 77 children (2-16 years) was studied and normal scores for the intelligence (IQ) and developmental (DQ) quotients were found in 71 (92%). Outcome was not correlated to the age at onset of treatment, the initial dose and the severity of hypothyroidism, but there was a positive correlation of the socioeconomic status of the family and the IQ of the patients. The results of the screening program in Berlin document that an early and efficient thyroxine replacement can normalize the intellectual outcome of patients with congenital hypothyroidism independent of the severity of the disease as assessed by the residual thyroid function detectable at diagnosis.

Stress is known to suppress immune function and increase susceptibility to infections and cancer. Paradoxically, stress is also known to exacerbate asthma, and allergic, autoimmune and inflammatory diseases, although such diseases should be ameliorated by immunosuppression. Moreover, the short-term fight-or-flight stress response is one of nature’s fundamental defense mechanisms that enables the cardiovascular and musculoskeletal systems to promote survival, and it is unlikely that this response would suppress immune function at a time when it is most required for survival (e.g. in response to wounding and infection by a predator or aggressor). These observations suggest that stress may suppress immune function under some conditions while enhancing it under others. The effects of stress are likely to be beneficial or harmful depending on the type (immunoprotective, immunoregulatory/inhibitory, or immunopathological) of immune response that is affected. Studies have shown that several critical factors influence the direction (enhancing vs. suppressive) of the effects of stress or stress hormones on immune function: (1) Duration (acute vs. chronic) of stress: Acute or short-term stress experienced at the time of immune activation can enhance innate and adaptive immune responses. Chronic or long-term stress can suppress immunity by decreasing immune cell numbers and function and/or increasing active immunosuppressive mechanisms (e.g. regulatory T cells). Chronic stress can also dysregulate immune function by promoting proinflammatory and type-2 cytokine-driven responses. (2) Effects of stress on leukocyte distribution: Compartments that are enriched with immune cells during acute stress show immunoenhancement, while those that are depleted of leukocytes, show immunosuppression. (3) The differential effects of physiologic versus pharmacologic concentrations of glucocorticoids, and the differential effects of endogenous versus synthetic glucocorticoids: Endogenous hormones in physiological concentrations can have immunoenhancing effects. Endogenous hormones at pharmacologic concentrations, and synthetic hormones, are immunosuppressive. (4) The timing of stressor or stress hormone exposure relative to the time of activation and time course of the immune response: Immunoenhancement is observed when acute stress is experienced at early stages of immune activation, while immunosuppression may be observed at late stages of the immune response. We propose that it is important to study and, if possible, to clinically harness the immunoenhancing effects of the acute stress response, that evolution has finely sculpted as a survival mechanism, just as we study its maladaptive ramifications (chronic stress) that evolution has yet to resolve. In view of the ubiquitous nature of stress and its significant effects on immunoprotection as well as immunopathology, it is important to further elucidate the mechanisms mediating stress-immune interactions and to meaningfully translate findings from bench to bedside.

Aims: 3,4-Methylenedioxymethamphetamine (MDMA) can affect both neurotransmitter and neurohormonal activity. This review will debate the role of the metabolic activation hormone cortisol for the psychobiological effects of ecstasy/MDMA. Methods: The empirical literature on cortisol release following acute MDMA administration and cortisol functioning in drug-free recreational ecstasy/MDMA users will be reviewed. This will be followed by an overview of cortisol as a bioenergetic stress neurohormone, and a debate on how it could be modulating the acute and chronic psychobiological effects of MDMA. Results: Cortisol release is increased by stimulatory factors, including physical activity, thermal stress and stimulant drugs. In laboratory studies MDMA leads to an acute cortisol increase of around 150% in sedentary humans. In MDMA-using dance clubbers, the cortisol levels are increased by around 800%, possibly due to the combined factors of stimulant drug, physical exertion and psychosocial stimulation. Regular ecstasy/MDMA users also demonstrate changes in baseline cortisol levels and cortisol reactivity, with compromised hypothalamic-pituitary-adrenal activity. Nonpharmacological research has shown how cortisol is important for psychological aspects such as memory, cognition, sleep, impulsivity, depression and neuronal damage. These same functions are often impaired in recreational ecstasy/MDMA users, and cortisol may be an important modulatory co-factor. Conclusions: The energizing hormone cortisol is involved in the psychobiology of MDMA, probably via its effects on energy metabolism. Acute cortisol release may potentiate the stimulating effects of MDMA in dance clubbers. Chronically, cortisol may contribute to the variance in functional and structural consequences of repeated ecstasy usage.

Objectives Clinical laboratories store filter paper samples used in neonatal screening for various periods of time after performing hormonal measurements. However, due to lack of data concerning specimen stability, it is unclear for how long these samples should be stored. The objective of this study is to determine the stability and reproducibility of thyroid-stimulating hormone (TSH), thyroxine (T4) and 17-hydroxyprogesterone (17-OHP) measurements in filter paper blood samples stored for up to 60 months. Methods Two hundred and twenty-eight blood samples, drawn between the second and the fourth day of life, were divided into seven distinct groups and kept at 4–8°C for one day or 2, 12, 24, 36, 48 or 60 months after basal hormonal measurements. In each group, TSH, T4 and 17-OHP levels were initially assayed 24–48 hours after collection (basal) and repeated once at the end of storage timing. All the measurements were performed by time-resolved fluorometry (1235 AutoDELFIA, Wallac Oy, Turku, Finland). Repeated and basal levels of each hormone were compared within the same group by Student's paired t-test. Differences were considered significant at P < 0.05. Results Compared with basal measurements, TSH and T4 levels declined significantly only when these hormones were re-assayed at 48 or 60 months of sample storage. In contrast, 17-OHP concentrations decreased earlier, starting at 24 months and continuing throughout the remaining period. Conclusion Our data suggest that neonatal screening of filter paper samples kept at 4–8°C are reliable for repeating the hormonal measurements when specimens are stored for up to one year, in the case of 17-OHP, or three years, in the case of T4 and TSH.

Thyroid-antibody screening is recommended for several adult populations, including the elderly and pregnant and postpartum women, and analysis of filter paper-dried blood spots (DBSs) has been a cost-effective means of screening newborns for hypothyroidism for more than 30 years. The aim of this study was to show that DBS specimens can be used to test adults for thyroid-stimulating hormone (TSH) antibodies and thyroid antibodies during screening for thyroid disease in a community setting. Thyroid peroxidase antibody and thyroglobilin antibody enzyme-linked immunosorbent assay kits for serum have been adapted for use with DBSs. A TSH assay for newborn DBSs was adapted for the screening of adults. Parallel specimens, serum and DBSs, were collected during routine care of patients attending a thyroid clinic. In addition, 962 DBS specimens were collected from volunteers at community centers and nursing homes. Twelve months later, a second specimen was collected from each of 411 original volunteers. Antibody results are reported as normal and positive. Ninety-seven percent of the serum/DBS results correlated exactly. Of 962 volunteers from nursing homes and community centers, testing for antibodies was positive or indeterminate (borderline) in 266 (27%). Eighty percent of the patients with an initially normal TSH reading who were positive on the 12-month collection were positive for at least one antibody in the first collection. The use of DBSs is a convenient and efficient way to screen for thyroid antibody as a means of detecting occult thyroid disease in adults.

Epilepsy is commonly associated with reproductive endocrine disorders. These include polycystic ovary syndrome (PCOS), isolated components of this syndrome such as polycystic ovaries, hyperandrogenaemia, hypothalamic amenorrhoea, and functional hyperprolactinaemia.To summarise the currently known relations between epilepsy and reproductive endocrine disorders.A review of clinical experience and published reports.The most likely explanations for endocrine disorders related to epilepsy or antiepileptic drugs are: (1) a direct influence of the epileptogenic lesion, epilepsy, or antiepileptic drugs on the endocrine control centres in the brain; (2) the effects of antiepileptic drugs on peripheral endocrine glands; (3) the effects of antiepileptic drugs on the metabolism of hormones and binding proteins; and (4) secondary endocrine complications of antiepileptic drug related weight changes or changes of insulin sensitivity. Regular monitoring of reproductive function at visits is recommended, including questioning about menstrual disorders, fertility, weight, hirsutism, and galactorrhoea. Particular attention should be paid to patients on valproate and obese patients or those experiencing significant weight gain. Single abnormal laboratory or imaging findings without symptoms may not constitute a clinically relevant endocrine disorder. However, patients with these kinds of abnormalities should be monitored to detect the possible development of a symptomatic disorder associated with, for example, menstrual disorders or fertility problems.If a reproductive endocrine disorder is found, antiepileptic drug treatment should be reviewed to ensure that it is correct for the particular seizure type and that it is not contributing to the endocrine problem. The possible benefits of a change in treatment must be balanced against seizure control and the cumulative side effect of alternative agents.

Aims —To determine mechanisms regulating the production of connective tissue growth factor (CCN2; CTGF) and transforming growth factor β1 (TGF-β1) in the mouse uterus. Methods —In situ hybridisation and immunohistochemistry were used to localise CCN2 (CTGF) and TGF-β1 in uteri from sexually mature female mice that had either been (1) mated with sterile males to induce pseudopregnancy or (2) ovariectomised (OVX) and administered estradiol-17β (E 2 ) or progesterone (P 4 ), either alone or in combination. Uteri collected on days 0.5, 1.5, 2.5, 3.5, 4.5, or 5.5 of pseudopregnancy or at one, three, six, 12, or 24 hours after steroid administration were fixed, sectioned, and incubated with specific riboprobes or antibodies to permit detection and localisation of mRNA or protein for CTGF and TGF-β1. Results —On days 0.5–2.5 of pseudopregnancy, CCN2 (CTGF) and TGF-β1 were principally colocalised to uterine epithelial cells, with much smaller amounts in the stroma. On days 3.5–4.5, there was a reduction of CCN2 (CTGF) and TGF-β1 in the epithelium but an increase in stromal and endothelial cells, corresponding to a period of extracellular matrix remodelling and neovascularisation within the endometrium. In OVX mice, epithelial cells were weakly positive for both CCN2 (CTGF) and TGF-β1 in the absence of steroid hormones. Epithelial CTGF mRNA production were strongly but transiently stimulated in OVX mice cells by E 2 . These effects were antagonised by P 4 , which itself transiently stimulated epithelial CCN2 (CTGF) production, although less robustly than E 2 . CTGF and TGF-β1 protein amounts were high in epithelial cells throughout steroid treatment and were increased in the stroma, where they were relatively long lived. Stromal CCN2 (CTGF) and TGF-β1 were lower after co-administration of E 2 and P 4 than in response to each hormone individually. Although ccn2 (ctgf) is a TGF-β1 inducible gene in other systems, and both growth factors were often co-localised in uterine tissues in these studies, several treatment regimens resulted in high amounts of TGF-β1 protein in stromal cells without the concomitant production of ccn2 (ctgf) mRNA. Conclusions— Maternal factors are principal cues for CCN2 (CTGF) and TGF-β1 production in the uterus because (1) their expression during pseudopregnancy is comparable to that seen in pregnancy and (2) they are regulated by ovarian steroids. TGF-β dependent and independent mechanisms of ccn2 (ctgf) gene transcription exist in the uterus that are variably regulated by steroid hormones. Collectively, the data support a role for CCN2 (CTGF) in mediating the effects of steroid hormones and TGF-β on endometrial function.

Molecular genetic techniques were used to establish new characteristics in the animals and plants. Fishes are good animal protein resources and are suitable for genetic researches because of their short maturation time, high number of egg production in each spawning, and easy rearing. New characteristic can be establishes by it's related gene transfer. Transgenic researches in the fishes started about ten years ago. Different gene constructs were used in these researches. More than 60% of works were pure research to find the principal of gene transfers in the fishes. About 37.5% of research used growth hormone gene to improve fish growth; the rest of researches used anti-freeze protein gene. Adjustment of DNA forms, buffer contents transferring method for gene transfer are the main factors in the success of fish transgenic. There are different published researches to meet these problems in the last decade. In this paper these research is going to be reviewed and discussed......

We have recently developed an immunoassay that can measure thyroxine rapidly and accurately in the eluate of 40 mul of dried blood spotted on filter paper at the fifth day of life. The method is completely automated and by using the samples received by the Central Laboratory of the Quebec Network for Genetic Medicine and their follow-up facilities, we are now screening every newborn in the province of Quebec for neonatal hypothyroidism. To date, from 47,000 measurements, three newborn infants with abnormally low TBG and seven hypothyroid infants have been detected. From these data we conclude that the frequency of congenital hypothyroidism is about one in 7,000 births and that our method is effective in detecting thyroid hormone abnormalities with an acceptable percentage of false positive measurements; no false negative results have occurred to our knowledge.

Based on our method for the qualitative test for steriod hormones by paper chromatography Fujisaki, et al.(1953) the quantitative determinations of several steroids were investigated. It was found that within a certain range of the amount the logarithms of each spot area of estrone, α-estradiol, dehydroepiandrosterone, Δ5-androstendiol, methyltestosterone, mcthylandrostendiol and androstane-17β-ol-3-one were directly proportional to the logarithms of the amount of the hormone, thus rendering the quantitative assay possible.

Reversed-phase high-performance liquid chromatography with UV detection is studied for the determination of both progestogenic and oestrogenic components of oral contraceptive formulations. The applicability of the assay is demonstrated for a number of different progestogen—oestrogen combinations in both conventional tablet and novel “paper” formulations. The results show that the method developed is a versatile technique for the routine assay of these pharmaceutical formulations.

1. RNA-iodo-proteinaceous complexes occur in the tRNA fractions isolated from bovine, ovine, and porcine thyroids. The calf thyroid complex has been partially characterized and contains diiodotyrosine and probably the hormone thyroxine in addition to several other amino acids. 2. Different preparative procedures and techniques capable of disrupting a variety of non-covalent bonds and aminoacyl and peptidyl ester bonds had no obvious effect on the calf thyroid RNA-iodo-proteinaceous complex which remained associated with tRNA. 3. Nucleolytic enzymes can degrade the complex to lower molecular weight products that contain iodine, proteinaceous, and RNA components. However, most of the iodine and proteinaceous material is associated with a relatively high molecular weight, ribonuclease-resistant, RNA-containing core. 4. It is concluded that the tRNA fractions of bovine and probably other mammalian thyroid glands contain a low molecular weight RNA linked to proteinaceous material that contains iodinated amino acids.

VERTEBRATE neurohypophysial hormones have a common structural pattern characterized by a chain of nine amino-acid residues with a disulphide bridge connecting the amino-acids in positions 1 and 6. There are usually two hormones in each species, the active principles rarely varying from one species to another within a given class. Thus oxytocin and arginine vasopressin have been chemically identified in five species of mammals belonging to the orders Primates, Artiodactyla, Perissodactyla and Cetacea. Isotocin (Ser4-Ile8-oxytocin) and vasotocin (Arg8-oxytocin) have up to now been isolated from six species of bony fish belonging to the families Gadidae, Scombridae and Cyprinidae. The structural variations which occur between one vertebrate class and another are confined to one or two amino-acid substitutions in positions 3, 4 or 8 (for a review of this subject see ref. 1).