Electronic Library of Scientific Literature - © Academic Electronic Press
Volume 37 / No. 1 / 2003
Kovacikova L, Kunovsky P, Lakomy M, Skrak P, Misikova Z, Siman J, Kostalova L, Tomeckova E (Bratislava, Slovakia)
Thyroid hormone status after cardiac surgery in infants with delayed sternal closure and continued use of cutaneous povidone-iodine
Augustowska A, Gregoraszczuk EL, Milewicz T, Krzysiek J, Grochowalski A, Chrzaszcz R (Krakow, Poland)
Effects of dioxin (2,3,7,8-TCDD) and PCDDs/PCDFs congeners mixture on steroidogenesis in human placenta tissue culture
Or³owska-Majdak M, Kolodziejski P, Traczyk WZ (Lodz, Poland)
Centrally applied oxytocin has no effect on eylid conditioning in rabbits
Zajickova K, Zofkova I (Prague, Czech Republic)
Osteoporosis: Genetic analysis of multifactorial disease
Letter to the Editor
Masi AT (Peoria, Illinois)
Comments to: Imrich R: The role of neuroendocrine system in the pathogenesis
Thyroid Hormone Receptors: Methods and protocols
Endocrine Regulations (since 1967 to 1990 Endocrinologia Experimentalis) is an international journal on experimental and clinical endocrinology edited quarterly in English by care of the Institute of Experimental Endocrinology, Slovak Academy of Sciences (Bratislava, Slovakia) and published by the Slovak Academic Press (Bratislava, Slovakia).
This journal aims to publish original manuscripts or minireviews on experimental and clinical endocrinology and diabetes.
The submission of a manuscript to Endocrine Regulations implies that it has not been previously published or is not being submitted for publication elsewhere and that the manuscript has been approved by all authors who are ready to take public responsibility for the content.
All materials relating to human investigation will be published upon the understanding that design of the work has been approved by the local Ethical Committee or that it conforms to ethical guidelines of the Declaration of Helsinki. The animal experiments should state the conformance to guidelines on animal care.
Manuscripts in triplicate with three sets of illustrations (of which one is an original) should be sent to:
Richard Kvetnansky, Ph.D., Dr.Sc., Chief Editor,
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All text must be printed on one side of the sheet only with appropriate margins and double spacing to give adequate space for editorial notes. The corresponding author should indicate his/her full mailing address including phone and fax numbers and the e-mail address.
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Types of manuscripts. Standard original papers should contain following sections: * Title, * Abstract (divided into sections Objective, Methods, Results, Conclusions), * Key Words, * Introduction, * Materials and Methods (in clinical papers this section should read * Subjects and Methods), * Results, * Discussion, (* Acknowledgements), * References. There is no length limit for these papers.
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Itoh M, Okugawa T, Shiratori N, Ohashi H: Treatment with triiodothyronine (T3) against multinodular goiter fails to prevent the onset of Graves disease. Endocrine Regul 29, 151-156, 1995
B. Book Chapters:
Mornex R, Orgiazzi JJ: Hyperthyroidism. In: The Thyroid Gland (Ed. M de Visscher), pp. 279-362, Raven Press, New York 1980
Podoba J: Endemic goiter in Slovakia. VEDA, Bratislava, 1962
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Lubica Kovacikova, Pavol Kunovsky, Miroslav Lakomy, Peter Skrak, 1Zelmira Misikova, Jaroslav Siman, 1Ludmila Kostalova, 2Eva Tomeckova
Cardiac Intensive Care Unit, Department of Cardiosurgery, 1Department of Pediatrics and 2Department of Biochemistry, Children´s University Hospital, 833 40 Bratislava, Slovakia
Objective. The aim of this prospective study was to examine whether povidone-iodine used for sternal wound protection in infants with delayed sternal closure (DSC) influences the thyroid function.
Patients and methods. Thyroid hormones (see bellow) and thyroxine binding globulin (TBG) were estimated by radioimmunoassay and ioduria by mass spectrometry in 20 infants in whom cutaneous povidone-iodine was continuously applied on the skin for 1-7 days before DSC after open heart surgery.
Results. In the early postoperative period the median levels of total triiodothyronine (TT3), total thyroxine (TT4) and thyroxine-binding globulin (TBG) were below the lower limit of normal, while these of reverse triiodothyronine (rT3) were above normal. The median levels of free triiodothyronine (FT3), free thyroxine (FT4), and thyroid stimulating hormone (TSH) were normal. Two weeks after the sternal closure, the levels of TT3, TT4 and TBG increased significantly (P<0.001), while these of rT3 decreased, but not significantly. The levels of TSH increased (P<0.001), being above normal in 7 patients. Four weeks after the sternal closure, TSH levels remained markedly increased in 4 infants. These patients were considered to be hypothyroid and were started on thyroxine replacement therapy. Such replacement treatment was withdrawn at a median age of 6.5 months (range 5-8 months). Urinary iodine concentration on the last day of povidone-iodine exposure was several times higher (P< 0.001) than that in the control group of healthy infants.
Conclusions. Transient hypothyroidism was found in four of 20 infants with DSC who were exposed to povidone-iodine. It is suggested to monitor TSH level in these patients, optimally at 4 weeks after closure of the sternum, when findings may show true hypothyroidism.
Keywords: Thyroid hormones – Cardiac surgery – Infants – Delayed sternal closure – Povidone-iodine
ENDOCRINE REGULATIONS, Vol. 37, pages 3-9, 2003
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EFFECTS OF DIOXIN (2,3,7,8-TCDD) AND PCDDs/PCDFs CONGENERS MIXTURE ON STEROIDOGENESIS IN HUMAN PLACENTA TISSUE CULTURE
Katarzyna Augustowska, Ewa L Gregoraszczuk,Tomasz Milewicz1, Jozef Krzysiek1, Adam Grochowalski2, Ryszard Chrzaszcz2Laboratory of Physiology and Toxicology of Reproduction, Department of Animal Physiology, Institute of Zoology, Jagiellonian University, Krakow, Poland; 2 Department of Endocrinology and Fertility, Collegium Medicum, Jagiellonian University, Krakow, Poland; 3 Department of Chemistry, Krakow, University of Technology, Krakow, Poland
Objective. The aim was to compare the direct effect of most toxic 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) as well as of naturally occurring congener mixture of polychlorinated dibenzodioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs) extracted from fly ash on the placental steroidogenesis. The concentration of all 17 toxic congeners was reported and the toxic equivalent (TEQ) was calculated as a 27.7 mg-TEQ/kg of fly ash.
Methods. Placental cotyledons were harvested immediately after expulsion of placenta. The cells were prepared according to Kliman et al. (1986). To examine TCDD and PCDDs/PCDFs mixture action on cytochrome P450 side change cleavage enzyme (P450 scc) and 3b-hydroxysteroid dehydrogenase (3b-HSD) activity the placental cells were cultured either in basal conditions or with the addition of 25-hydroxycholesterol (25-OH) or pregnenolone (P5).
Results. TCDD in all doses used decreased basal P4 secretion, while did not show any effect on 25-hydroxycholesterol (25-OH) and pregnenolone (P5) supplemented cultures. In all variants of culture PCDDs/PCDFs mixture was without effect on basal and substrate supplemented progesterone (P4) secretion suggesting a reduction in the activity of cytochrome P450scc or 3b-HSD. To examine TCDD and PCDDs/PCDFs mixture action on aromatase cytochrom P450 (P450 arom) activity the placental cells were cultured in basal condition or with the addition of dehydroepiandrosterone (DHEA) or testosterone (T). Significant increase of estradiol secretion under the influence of TCDD in DHEA and T supplemented cultures suggests its action on the activity of P450 arom.
Conclusion. The discrepancy found between the action of pure TCDD and dioxin mixture on placental steroids secretion is possibly due to an additional effect of pentachlorodibenzo-p-dioxin (PeCDD) and pentachlorodibenzo-furan (PeCDF) which covered >50 % of the total toxic equivalents (TEQ) present in this mixture.
Key words: TCDD – PCDDs/PCDFs mixture – Human placenta – Hormonal status
ENDOCRINE REGULATIONS, Vol. 37, pages 11-20, 2003
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Monika Or³owska-Majdak, Pawe³ Kolodziejski, W³adyslaw Z. Traczyk
Department of Experimental and Clinical Physiology, Institute of Physiology and Biochemistry,
Medical University of Lodz, 92-215 Lodz, Poland
Objective. The classically conditioned rabbit eyelid reflex has proven to be useful for studying memory processes. The role of oxytocin (OXT) dialyzed into the hippocampus or caudate nucleus in the acquisition and extinction of this reflex was investigated.
Methods. Microdialysis probes were unilaterally, chronically, alternatively implanted into the mentioned brain structures. OXT was repeatedly dialyzed into each brain structure during the extinction of the conditioned eyelid reflex. An air puff was applied as an unconditioned and the tone as a conditioned stimulus to create conditioned eyelid reflex. Eyelid responses were detected by opto-electronic sensor and recorded. Thus obtained conditioned responses were calculated as a percentage of all 120, daily applied, trials of stimuli. ANOVA was used for statistical evaluation.
Results. Neither OXT dialyzed into the hippocampus nor into the caudate nucleus significantly changed the course of acquisition and extinction of the conditioned eyelid reflex. However, some tendency to the impairment of forgetting when dialyzed into the hippocampus and to its facilitation during caudate nucleus dialysis was observed.
Conclusion. Conditioning of the eyelid reflex applied as the experimental model for the study of the memory processes did not show OXT participation in these processes neither in the hippocampus nor in the caudate nucleus, but this problem needs to be further studied.
Key words: Conditioned eyelid reflex – Oxytocin – Hippocampus – Caudate nucleus – Microdialysis – Rabbit
ENDOCRINE REGULATIONS, Vol. 37, pages 21-30, 2003
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Katerina Zajickova, Ivana.Žofkova
Institute of Endocrinology, 116 94 Prague, Czech Republic
Osteoporosis is a common disorder with a complex pathophysiology involving both endogenous and environmental factors. Family and twin studies have shown that genetic factors play an essential role in bone mass regulation and that apart from rare instances the heritability of bone mineral density (BMD) and osteoporosis is polygenic. Linkage analysis and association studies with numerous DNA markers (single nucleotide polymorphisms or microsatellites) have analysed several bone-related candidate genes encoding vitamin D, calcium-sensing, calcitonin and estrogen alpha receptors, insulin growth factor I, collagen type I alpha 1 chain and others. Despite this, the definite polymorphic marker has not been found in different populations which reflects the divergent results of association studies with their frequent limitations, and probably the fact that the relevant polymorphism is still awaiting identification. Once the genetic determinants can be defined, the clinical implications would be extensive both in diagnostics and in pharmacogenetics.
Key words: Osteoporosis – Bone mineral density – Candidate genes – DNA polymorphisms – Association studies
ENDOCRINE REGULATIONS, Vol. 37, pages 31-44, 2003
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Masi AT (Peoria, Illinois)
College of Medicine at Peoria
To the editor:
The concept promoted by collaborators and myself that rheumatoid arthritis (RA) seems to result from the accumulative effects of multiple determinants [e.g., genetic, neuroendocrine, behavioral (smoking), other somatic and environmental factors] during a long preclinical period has been recently reviewed in your Journal (Imrich 2002). The concept is also important that risk factor profiles for RA may differ among subsets of susceptibles, i.e., premenopausal- vs postmenopausal-onset women and men. As was mentioned in the paper, and by the Masi collaborators, such knowledge may lead to possible approaches to primary prevention or modulation of RA risks.
One reason for this letter is to update on several additional studies by collaborators and myself, which reinforce the preceding concepts. Our paper (Masi et al. 2002), which was recently published, indicated independent laboratory confirmation of low serum dehydroepiandrosterone sulfate (DHEAS) levels many years prior to the onset of premenopausal RA.
Evidence for relative adrenal androgen deficiency (i.e., low serum DHEAS levels) prior to onset of RA in adolescent and younger women is now quite strong (see my discussion of the contrary Heikkillä et al 1998). Nevertheless, this hormone per se is not likely to be a pathogenetic factor for RA. Rather, it seems to be a marker for relative adrenal cortical and glucocorticoid (GC) insufficiency. This interpretation was summarized in Table 5 of my review article (Masi 2000).
Data supporting subtle GC dysfunction in younger female RA patients, and even many years before clinical onset, were summarized in the German literature (Masi et al 2000). As you know, the negative GC feedback control of the hypothalamic - pituitary - adrenal (HPA) axis tends to obscure detection of subtle degrees of insufficiency of this hormone, unlike the more reliable indicator of low serum levels of DHEAS, which has a much longer half-life than cortisol in the circulation.
If one proposes a concept that relative adrenal cortical glucocorticoid hypofunction may be a predisposing factor to RA in a minority of younger-onset women (estimated at about one-third), then the next question is how does one explain such a state? This area of human physiology is essentially unexplored. In fact, it is rarely mentioned in the literature.
In a detailed earlier review (Masi et al. 1996), collaborators and myself proposed an hypothesis regarding possible mechanisms operating in this challenging question. The occurrence of relative adrenal cortical and gonadal trophic (i.e., functioning cell capacities/mass) hypocompetence was hypothesized as a constitutional polymorphic variant. For women, subtle adrenal/gonadal mass hypocompetence would be clinically unnoticed. Such status could be the polar opposite of the polymorphic polycystic ovarian syndrome (PCOS), which, of course, is usually clinically evident. As you know, increased ovary (especially) and adrenal mass has been documented in PCOS as well as robust androgenic and glucocorticoid functions. Endocrinologists need to explore more critically the occurrence or non-occurrence of intrinsic adrenal/gonadal hypocompetence in younger women, as a possible polymorphic polar opposite to PCOS. Whether or not such polymorphisms might be part of a population continuum, from hypo to normal to hyper competencies (cell capacities/mass) also remains to be investigated.
When our hypothesis of intrinsic adrenal and gonadal androgenic hypocompetence was proposed in 1996, it was believed to apply only to a minority subset of premenopausal-onset RA women. However, as shown in Table 1 of our article (Masi et al. 2002), low serum cortisol (<140 nmol/L) and relatively low serum total testosterone (<15 nmol/L) were significantly correlated in 18 pre-RA males, but not in 72 controls. In Table 7 of my review (Masi 2000), it has been noted that low serum cortisol and definitely low serum testosterone (<10 nmol/L) is a significant, independent long-term predictor of RA in men. However, this risk factor occurs in only a small minority (circa 10 %) of susceptible men.
Interestingly, in postmenopausal women, combined low serum cortisol (<140 nmol/L) and low total testosterone (<3.5 nmol/L) levels were also a significant predictor of RA. Among subjects having such assays, the combination occurred in 6 (33.3 percent) of 18 pre-RA women, 4 to 17 (mean 11) years prior to clinical onset at age 50 years or older. Among 61 control women matched for age at entry into this cohort study, the combination of low serum cortisol and testosterone was found in 6 (9.8 percent), odds ratio 4.58, 95 % confidence intervals 1.25, 16.69.
Varied profiles of presumably constitutional hypocompetences of adrenal glucocorticoids and/or gonadal androgens (i.e., low serum testosterone) have now been observed in our controlled prospective studies of females with premenopausal-and postmenopausal-onsets of RA and of males, albeit in minority subsets of each.
The physiopathogenesis of RA is profoundly complex. The hypothesized neuroendocrine dysfunctions are believed to contribute to chronic preclinical upregulation of inflammatory pathways and endothelial microvascular activation, and perhaps even to somatic remodeling of the immune system (reviewed in Masi 2000). The author indicated such interactions in the mini-review and illustrated them in Fig 1 (Imrich 2002). However, in the Table 1, the effects of glucocorticoids were indicated as “increased overall cytokine synthesis”. Most investigators would summarize physiological and pharmacological effects of glucocorticoids as “decreased overall cytokine synthesis”. Could the author please provide evidence available for the Table 1 entry on glucocorticoids and submit a corrected Table, if appropriate.
Alfonse T. Masi, MD., DR.P.H.
Professor of Medicine
University of Illinois
College of Medicine at Peoria
Richard Imrich, MD
Slovak Academy of Sciences
To the editor:
I thank Professor Masi for his supportive comments regarding my minireview entitled “The role of neuroendocrine system in the pathogenesis of rheumatic diseases” (Imrich 2002).
The concepts, which Masi and colleagues (2000), raise many new questions to endocrinologists and rheumatologists as well as to investigators in the field of human physiology itself.
As mentioned, relative adrenal cortical glucocorticoid hypofunction indicated by low serum levels of dehydroepiandrosterone sulfate (DHEAS), may be a predisposing factor to rheumatoid arthritis in a subset of younger onset women. The hypotheses proposed by Masi and collaborators assume the presence of subclinical adrenal/gonadal mass hypocompetence as a constitutional polymorphic variant opposite to polycystic ovarian syndrome (PCOS). One of the possible alternative mechanisms, which may contribute to androgen insufficiency, may result from the interindividual variability of feedback sensitivity of the HPA or HPG axes. Different set points of HPA or HPG axes would thus result in different baseline levels of peripheral hormones (e.g. glucocorticoids or androgens). Such dysfunctions of feedback mechanism could further contribute to chronic preclinical upregulation of inflammatory pathways and endothelial microvascular activation, as reviewed by Masi (2000). These alternative mechanisms have been previously mentioned by Masi et al. (1996) and the Fig. 10 of this review attempts to differentiate trophic from tropic dysfunctions. The dilemma of trophic vs. tropic dysfunctions needs further critical investigation. However, to reveal such subtle changes of HPA or HPG axes activity, it seems necessary to develop new methodological approaches.
Recently debated questions of female androgen insufficiency supports the perspectives outlined in Masi’s letter. It was concluded that the role of androgens in women’s health has been generally neglected and is not well recognized or understood (Bachmann et al 2002). The presented definition and guidelines together with identified research needs and priorities are giving hope that androgen insufficiency will be better evaluated and treated in the future as well as in the subgroup of patients affected with chronic inflammatory diseases such as RA.
Regarding the question of “the glucocorticoids cause increased overall cytokine synthesis” indicated in Table 1 of my minireview (Imrich 2002), I would like to apologize for incorrect direction of arrows caused by technical problems during the processing of the manuscript. Table 1 as was originally intended is shown below.
Richard Imrich, MD.
Institute of Experimental Endocrinology
Slovak Academy of Sciences
ENDOCRINE REGULATIONS, Vol. 37, pages 45-48, 2003
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Editor: Aria Baniahmad
Published by: Humana Press, Totowa, New Jersey, USA.
Price: US $ 99.50
The book has been written by hands-on experts in the field who, to my consideration, addressed important questions concerning the role of the nuclear thyroid hormone receptor signalling pathway in vertebrates. Thyroid hormone receptors – thyroid hormone inducible transcription factors are regulators of a variety of biological processes in animal and human physiology of crucial importance. The above book consists of eleven chapters, 223 pages, the content of them sounds clear, well written, and of a very high impact. The topics include the analysis of heart rate, amphibian morphogenesis, target gene analysis in brain and heart or liver, and transcriptional analysis by thyroid hormone receptors in cell-free systems as well as in living cells.
Methodology comprises a wide variety of modern and sophisticated methods of up-to-date research (cloning techniques, a model of null mutant mice for thyroid hormone receptor, molecular analysis of human resistance to thyroid hormone syndrome, in situ hybridisation methodology, RT-PCR and microarray chip techniques, electrophoretic mobility and “super” shift assays, etc.). Each methodology protocol contains full explanatory notes as well as troubleshooting tips, and helpful comments on avoiding pitfalls. Thus, those sophisticated methods enable a variety of basic and applied researchers (endocrinologists, geneticists, biochemists, and physicians) to learn those modern technique in order to achieve in their laboratories novel and original data on specific gene expression mediated by thyroid hormone via nuclear receptors. Thus, the use of know-how described in details in each single chapter may generate new knowledge in the field of thyroid hormone signalling pathway.
From my point of view, use of up-to-date information together with methodology described in the above book may represent a marked “push forward“ in signalling pathways via nuclear thyroid hormone receptors.
ENDOCRINE REGULATIONS, Vol. 37, page 10, 2003
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