bluuebunny/crossref_metadata_2025_split huggingface dataset:
Immunoreactive thyrotrophin-releasing hormone like material (IR-TRH LM) in human cord blood: high circulating serum levels but possible non-identity with hypothalamic TRH
Authors: Kaufman J. M. , Elewaut A. , Vermeulen A. 
Published: December 2008

Abstract. Levels of immunoreactive thyrotrophin-releasing hormone like material (IR-TRH LM) were measured in paired maternal and umbilical cord serum samples (n = 45) and in serum of non-pregnant women (n = 63), using a sensitive and specific radioimmunoassay.
In all pairs IR-TRH LM in venous cord serum (mean 91.3 pg/ml, range 20–270) was markedly elevated as compared to maternal serum (mean 13.5 pg/ml, range 0–37, P < 0.001, the maternal levels being similar to those in non-pregnant women (mean 12.0 pg/ml, range 0–39, P > 0.1). In 23 cases IR-TRH LM was also measured in arterial cord serum: arterial and venous cord levels were highly significantly correlated (r = 0.904) with higher arterial levels in 22 out of 23 cases (mean 117.8 pg/ml, range 32–280 and 90.6 pg/ml, range 20–270, P < 0.001), suggesting that cord IR-TRH LM is not of placental origin. There was no correlation between individual levels of IR-TRH LM and either TSH, T4, T3 or FT4 levels in either maternal or cord serum.
Agar gel electrophoresis and equilibrium dialysis of adult and cord serum pre-incubated with [125I]TRH or [3H]TRH revealed no protein binding. Cord IR-TRH LM was immunologically, as well as in paper electrophoresis and in gelfiltration, indistinguishable from synthetic and hypothalamic TRH.
In vitro degradation of synthetic TRH was much slower in cord serum as compared to maternal and control serum (P < 0.001). In vitro degradation of cord IRTRH LM could not be demonstrated, neither by cord serum itself nor by adult serum, this in contrast to hypothalamus extracted TRH which was readily degraded by adult serum. Neither the presence of an inhibiting substance, nor methodological factors seem to account for the apparently different behaviour of cord IR-TRH. It is suggested that circulating IR-TRH could be closely related, but still different from tissue extracted and synthetic TRH.
β-Neoendorphin inhibits thyrotrophin secretion in rats
Authors: Mitsuma Terunori , Nogimori Tsuyoshi 
Published: December 2008

Abstract. The effects of β-neoendorphin on thyrotrophin-releasing hormone (TRH) and thyrotrophin (TSH) secretion in rats were studied. β-neoendorphin (500 μg/kg) was injected iv, and the rats were decapitated serially. TRH, TSH, thyroxine (T4) and 3,3',5-triiodothyronine (T3) were measured by means of a specific radioimmunoassay for each.
Hypothalamic immunoreactive TRH (ir-TRH) content increased significantly after β-neoendorphin injection, and plasma concentrations tended to decrease, but not significantly so. Plasma TSH levels decreased significantly in a dose-related manner with a nadir at 40 min. Plasma T4 and T3 levels did not change after the injection. Plasma ir-TRH and TSH responses to cold were significantly inhibited by β-neoendorphin, but the plasma TSH response to TRH was not. Naloxone partially prevented the inhibitory effect of β-neoendorphin on TSH release. In the haloperidol- or 5-hydroxytryptophan-pretreated group, the inhibitory effect of β-neoendorphin on TSH release was prevented, but not in the l-dopa- or para-chlorophenylalanine-pretreated group. These drugs alone did not affect plasma TSH levels at the dose used.
These findings suggest that β-neoendorphin acts on the hypothalamus by inhibiting TRH release, which may be modified by amines of the central nervous system.
Increased frequency of HLA-Cw4 in type 2 diabetes
Authors: Groop L. , Koskimies S. , Pelkonen R. , Tolppanen E.-M. 
Published: December 2008

Abstract. In order to investigate whether there is an association between the HLA system and type 2 diabetes, we have determined HLA-A, B- and C-antigens in 227 patients with onset of diabetes between the ages of 35 and 70 years and compared them with the HLA-antigen frequencies in Finnish blood donors.
One hundred and sixty-eight patients (74%) were treated with diet or oral antidiabetic drugs (non-insulin dependent), whereas 59 patients (26%) were treated with insulin (insulin-dependent).
The HLA-antigen Cw4 was found in 38.7% of the non-insulin dependent patients (relative risk 2.67, P = 0.00005) and in 15.6% of the insulin dependent diabetics (relative risk 0.785 NS) compared with 19.1% in blood donors. In addition, there was an increase in the frequency of HLA-Bw35 antigen among the non-insulin dependent patients (relative risk 1.6, P = 0.007), which could be explained by the known positive linkage disequilibrium between HLA-Bw35 and HLA-Cw4.
In insulin-dependent patients there was a decrease in the frequency of HLA-B7 (relative risk 0.226, P = 0.001) and an increase in the frequencies of HLA-B8 (relative risk 1.91, P = 0.031), B12 (relative risk 2.22, P = 0.01) and B15 (relative risk 2.04, P = 0.019) compared with blood donors.
Conclusion: these data provide evidence that genes in the HLA region may have some influence in genetic susceptibility to type 2 diabetes. They further suggest that maturity onset (type 2) diabetes is a heterogeneous disease in terms of HLA antigens. Consequently, there is a need for re-evaluation of the definition of type 2 diabetes.
Aggression-provoked huge release of submaxillary mouse renin to saliva
Authors: Pedersen Erik Bækkelund , Poulsen Knud 
Published: December 2008

Abstract. In a normal male mouse, which had been kept isolated for some time, confrontation with another male mouse, resulted in aggressive behaviour, including fighting. The aggressive behaviour resulted in secretion of a few microlitre of saliva with vast renin concentration. The renin concentration in saliva reached values of 6000 Goldblatt units × ml−1, corresponding to 15 mg/ml of renin. This concentration is 6 orders of magnitude higher than normal plasma renin concentrations. The secretory pattern could be mimicked by ip injection of pharmacological doses (2–18 mg/kg) of the α-adrenergic agonist phenylephrine.
This is probably the first demonstration of a physiological secretion of renin to saliva which may be of importance since renin most likely is injected into the opponent or prey through bites.
Prolactin secretion from human prolactinomas perifused in vitro: effect of TRH, prostaglandin E1, theophylline, dopamine and dopamine receptor blockers
Authors: Chihara Kazuo , Iwasaki Junji , Minamitani Naoto , Kaji Hidesuke , Kodama Hitoshi , Fujita Takuo , Shirataki Kunio , Tamaki Norihiko , Matsumoto Satoshi 
Published: December 2008

Abstract. To clarify the functional characteristics of prolactin (Prl)-producing adenoma cells, the effect of TRH, prostaglandin E1 (PGE1), theophylline, dopamine and dopaminergic antagonists on Prl secretion was examined in vitro in perifused pituitary adenoma tissues obtained at surgery from 8 patients with prolactinoma. Perifusion with TRH at a concentration of 10−6 to 10−5 m resulted in a significant increase in effluent Prl levels in 3 of the 8 adenoma tissues. In the remaining 5 adenomas, TRH produced no effect on Prl release in vitro. On the other hand, PGE1 (10−5 m) stimulated Prl secretion in 2 of the 4 adenomas examined. Addition of theophylline (5.5 mm) caused a marked increase of effluent Prl levels in all 8 prolactinomas regardless of the reactivity to TRH or PGE1.
Dopamine (5 × 10−7 m) suppressed Prl secretion from adenoma tissue in 5 of 7 patients tested but had no effect in the remaining two adenomas. When perifused simultaneously with dopamine, sulpiride (D2-selective dopamine receptor blocker, 5 × 10−7 m) blocked the inhibitory effect of dopamine on Prl release in 3 of the 4 dopamine-sensitive prolactinomas. In one adenoma responsive to dopamine but resistant to sulpiride, YM-09151-2 (relatively specific D1-dopamine receptor blocker, 5 × 10−7 m) antagonized the dopaminergic inhibition of Prl release. When perifused alone, neither sulpiride nor YM-09151-2 affected Prl release from any of the adenoma tissues tested.
These findings suggest that a direct action of TRH on the adenoma cells in stimulating Prl release may be lacking in some prolactinoma cells, and that quantitative and qualitative changes in the dopaminergic inhibition of Prl release may occur in some adenomatous lactotrophs.
Vascularization and iodide transport down regulation in rat goitre
Authors: Rognoni J. B. , Penel C. , Ducret F. 
Published: December 2008

Abstract. This study was designed to investigate, in the rat, the regulation of the amount of thyroid iodide and of its organification during the involution of an experimentally induced goitre. The goitre was obtained by drastic iodine deficiency; male Wistar rats received an iodide deficient diet for 6 months, supplemented with PTU during the last 2 months. The study was followed for 16 days after the beginning of iodide refeeding (daily iodine intake = 50 μg).
The thyroid iodide, total thyroid organic iodine and plasma iodide, PBI and TSH concentrations were determined from day 0 to 16 and compared to their control values (rats on a normal iodide diet for 6 months). In addition, a stereological study was carried out to determine if the extent of the gland vasculature might be implicated in the regulation of the thyroid iodide content.
The plasma TSH concentration was very high and constant for 8 days (2.40 ± 0.37 and 2.45 ± 0.43 on day 0 and 8 respectively vs 0.25 ± 0.12 μg/ml in control rats), whereas iodination and secretion were blocked for 4 days (0.34 ± 0.19 and 0.5 ± 0.1 on day 0 and 4 respectively vs 14.4 ± 2.0 μg 127I/gland in control rats) (Wolff-Chaikoff effect). Thyroid iodide amount increased enormously for 2 days (2.5 ± 0.6 and 2.45 ± 0.55 respectively on day 1 and 2 vs 0.09 ± 0.01 μg 127I/gland on day 0), then strongly decreased between 2 and 4 days (1.15 ± 0.27 127I/gland). The thyroid/serum (T/S) ratio (iodide pump), which was very important between 0 and 2 days (115), decreased strikingly on day 4 (55). Moreover, the thyroid homogenates were shown to contain a new (nonproteic) iodocompound which escaped classical iodination. Its mobility during polyacrylamide gel electrophoresis was intermediary between those of iodoaminoacids and iodide. Its turnover rate was practically similar to that of thyroid iodide. This compound (termed 'X') accumulated until day 2 (0.39 ± 0.03 μg 127I/gland), then decreased sharply as did thyroid iodide, whereas neoiodination resumed (Wolff-Chaikoff escape). The stereological results showed that as soon as the iodide refeeding started, the volume density as well as the surface density of vessels sharply decreased (0.23 ± 0.03 μm3/μm3 and 0.06 ± 0.03 μm2/μm3 on day 0 and 8, respectively), whereas the same parameters for thyroid epithelial cells remained constant (0.35 ± 0.02 μm3/μm3 and 0.32 ± 0.03 μm2/μm3 on day 0 and 8, respectively.
From these data we can conclude that a great iodide influx in hyperstimulated thyroid epithelial cells induces a cellular control, antagonist to the TSH action on the amount of thyroid iodide. This control acts sequentially: an early regression of the thyroid vasculature is observed, which is followed by a regulation of iodide active transport. The 'X' iodocompound might be one of the factors implicated in this control.
Changes in the multiple components of rat pituitary TSH and TSHβ subunit following thyroidectomy
Authors: Mori Masatomo , Ohshima Kihachi , Fukuda Hitoshi , Kobayashi Isao , Wakabayashi Katsumi 
Published: December 2008

Abstract. Heterogeneity of pituitary TSH was investigated in rats following thyroidectomy. Adult male rats were sacrificed at varying periods (2–28 days) after thyroidectomy. In another experiment, thyroidectomized rats were injected daily with various doses of l-T4 (0.3–7.5 μg/100 g body weight, ip) and sacrificed 2 weeks later. The homogenate of the pituitaries was applied on an isoelectric focusing column or a Sephacryl S-200 column.
The normal rat pituitary contained 5 major components of immunoreactive (IR) TSH in isoelectric focusing, in which the isoelectric point (pi) ranged from 6.6 to 8.8. The multiple components of IR-TSGβ were observed almost in the same areas as those of IR-TSH. Following thyroidectomy IR-TSH components with more acidic pI, associated with IR-TSHβ, were evident. A large amount of IR-TSHβ in the pituitaries of thyroidectomized rats appeared near the void volume in gel filtration, suggesting the presence of big TSHβ Supplement of l-T4 minimized these thyroidectomy-induced changes in isoelectric focusing and gel filtration. Furthermore, big IR-TSHβ was little affected by ultracentrifugation and was relatively stable after treatment with 6 m guanidine hydrochloride.
We demonstrated that the rat pituitary gland contained multiple components of IR-TSH and IR-TSHβ, both of which became variegated after thyroidectomy. It is suggested that a discernible degree of heterogeneity of TSH, particularly of TSHβ, is dependent upon the increased rate of TSH biosynthesis at the pituitary level.
In vitro lymphocyte recognition of islet cells following in vivo priming with allogeneic murine pancreatic islets
Authors: Scott Joanne , MacKay Peter G. , Lernmark Åke 
Published: December 2008

Abstract. Lymphocytes from patients with insulin-dependent diabetes have been shown to be sensitized to pancreatic tissue antigens. Mice immunized with homologous pancreatic islets have been found to develop glucose intolerance and insulitis. Since lymphocytes may be involved in diabetogenesis, we wished to determine if lymph node cells from islet-immunized mice can recognize and respond to islet cells in vitro.
A.TL female mice were immunized with an emulsion of BALB/c islet homogenate and complete Freund's adjuvant (CFA); sham-treated A.TL mice were injected with adjuvant and water. Mice were sacrificed 7–8 days later and the draining lymph nodes were removed. The lymph node cells were co-cultured with freshly prepared irradiated BALB/c islet cell, which served as stimulator cells. The co-cultures were incubated for 24–26 h at 37°C, followed by a 16 h [3H]thymidine (TdR) pulse.
A significant proliferation of lymph node cells from islet-primed mice was induced during the in vitro stimulation with irradiated islet cells when compared with lymph node cells from sham-treated mice (P < 0.001). The response may be islet-cell-specific, since irradiated lymph node cells from BALB/c mice failed to proliferative response under the same culture conditions (P > 0.80).
Prolactin secretion in polycystic ovary syndrome (PCO): correlation with the steroid pattern
Authors: Carmina Enrico , Rosato Francesca , Maggiore Michele , Gagliano Anna Maria , Indovina Daniela , Jannì Alberto 
Published: December 2008

Abstract. To evaluate the prevalence of hyperprolactinaemia in PCO patients and its possible correlation with a steroid pattern, we studied prolactin secretion (basal and after TRH stimulation) in 40 women affected by typical PCO. LH, FSH, testosterone, oestradiol, oestrone, DHEA-s and 17-OHP serum levels were also evaluated. Twenty-one patients had prolactin (Prl) values in the normal range both in baseline conditions and after TRH stimulation; 10 patients had normal basal values of Prl but an exaggerated response to TRH stimulation; 9 patients had high Prl basal values and an exaggerated response to TRH. The presence of hyperprolactinaemia was associated with increased serum levels of oestrone (P < 0.01), DHEA-s (P < 0.01) and 17-OHP (P < 0.05).
In conclusion, hyperprolactinaemia is as relatively frequent condition which affects almost half the patients suffering from PCO and is probably related to an increase of serum oestrogens, mostly oestrone. Moreover, in patients with PCO and hyperprolactinaemia, the production of some other steroids is also affected.
The effect of d,l-4-hydroxypropranolol on the thyroxine to 3,5,3'-triiodothyronine conversion in rat renal and liver microsomes
Authors: Jørgensen Preben Holme , Lumholtz lb Bo , Faber Jens , Kirkegaard Carsten , Siersbæk-Nielsen Kaj , Friis Thorkild 
Published: December 2008

Abstract. The in vitro effect of d,l-4-hydroxypropranolol, a major pharmacological active metabolite of the beta adrenoceptor blocking drug d,l-propranolol, on the thyroxine (T4) to 3,5,3'-triiodothyronine (T3) conversion has been studied using rat renal and liver microsomal fractions. The results showed, that primarily the metabolite, but also the parent drug inhibits the T3-production in a dose dependent manner. The potency, expressed as the 50% inhibition of the T3-production, was reached using 65 ± 12 (sd) μm d,l-4-OH-propranolol and 1000 ± 22 (sd) μm d,l-propranolol, respectively in both tissues. The efficacy of 4-OH-propranolol corresponded to a maximal inhibition of 86 ± 7% while it for d,l-propranolol corresponded to 58 ± 6% (P < 0.001). The beta adrenoceptor agonist isoprenaline itself did not effect the T4 to T3 conversion but considerably opposed the inhibitory effect of d,l-4-OH-propranolol but not of d,l-propranolol. The D-isomer form of propranolol, which is without beta receptor blocking activity inhibited the T3-production in the same degree as d,l-propranolol. Evaluation of the enzyme kinetic data suggested that 4-OH-propranolol caused a competitive inhibition of both T4 and DTT.
It is concluded, that the metabolite d,l-4-OH-propranolol is a much more potent and efficacious inhibitor of the T4-5'-deiodination than d,l-propranolol.
Absorption of soluble and isophane semi-synthetic human and porcine insulin in insulin-dependent diabetic subjects
Authors: Pramming Stig , Lauritzen Torsten , Thorsteinsson Birger , Johansen Klaus , Binder Christian 
Published: December 2008

Abstract. A double-blind cross-over study of the sc absorption of radiolabelled semi-synthetic human (SHI) and purified porcine (PPI) insulin was made. Absorption of both isophane (n = 10) and soluble insulin (n = 8) was studied. There was no significant difference between the disappearance from the injection site, the plasma free insulin concentrations, or blood glucose levels after sc injection of the isophane preparations.
A faster disappearance of the soluble SHI (as judged from T/50 and AUC) was found (both P-values < 0.01). However, no difference was observed between the plasma insulin concentrations at any time point (P < 0.05). Blood glucose levels showed no statistical differences between the two soluble preparations. The data indicate minor differences between the pharmaco-kinetics of SHI and PPI, but these seem of no clinical importance.
Ovarian production of progesterone and 20α-dihydroprogesterone in vitro following prostaglandin F2α induced luteolysis in the superluteinized rat
Authors: Torjesen P. A. , Aakvaag A. 
Published: December 2008

Abstract. Superluteinized rats were injected with the prostaglandin F2α (PGF2α) analogue cloprostenol to induce luteolysis. The treatment decreased progesterone production of ovarian homogenates from 8.9 ± 0.5 to 4.0 ± 0.7 nmol/ovary/10 min (mean ± sem) within 40 min. tochondrial fractions isolated from control and cloprostenol treated animals produced 4.7 ± 0.4 and 2.8 ± 0.3 nmol progesterone/ovary/10 min, respectively. Thus, the PGF2α analogue treatment significantly reduced mitochondrial progesterone production. Addition of the 15 000 × g supernatant fraction did not influence the progesterone production rates of the mitochondrial fraction. The basal progesterone secretion from quartered ovaries decreased from 1.50 ± 0.15 to 0.38 ± 0.05 nmol/ovary during the initial 15 min of incubation following cloprostenol administration. hCG and N6,O2'-dibutyryladenosine 3':5'-cyclic monophosphate (DBC) stimulated the progesterone secretion from quartered ovaries, but the response was delayed in ovaries obtained from cloprostenol treated animals. Although the response was delayed, the progesterone secretion following cloprostenol treatment was re-activated with cAMP either directly or via hCG. The increment in progesterone secretion above unstimulated controls in response to DBC was not influenced by the cloprostenol treatment while the increment caused by hCG was decreased.
Our data suggest that: 1) PGF2α deactivates mitochondrial progesterone production, 2) this deactivation may be overcome by cAMP, and 3) PGF2α decreases gonadotrophin responsive adenylyl cyclase.
Growth hormone and insulin-like growth factor I in German Shepherd dwarf dogs
Authors: Eigenmann J. E. , Zanesco S. , Arnold U. , Froesch E. R. 
Published: December 2008

Abstract. The roles of growth hormone (GH) and insulin-like growth factor I (IGF I) were studied in 9 German Shepherd dwarf dogs. GH deficiency was evidenced in all dogs by an absence of increase in GH levels in response to clonidine administration. While the mean IGF I concentration in normal adult German Shepherds was 280 ± 23 ng/ml and 345 ± 50 ng/ml in immature animals, the mean IGF I concentration in the dwarf dogs was 11 ± 2 ng/ml (mean ± sem, P < 0.001).
In the affected animals, plasma thyroxine (T4) levels were only slightly subnormal and there was an increase in these levels in response to thyroid stimulating hormone (TSH) administration. The findings indicate 1) that dwarfism in German Shepherds is caused by primary GH-deficiency resulting in low circulating levels of IGF I and 2) that IGF I levels in the dog as in man are subject to control by GH.
Uptake, metabolism and subcellular distribution of [125I]T4 in calf thyroid slices
Authors: Chazenbalk G. D. , de Pisarev D. L. Kleiman , Juvenal G. J. , Pisarev M. A. 
Published: December 2008

Abstract. Previous work from our laboratory has shown that iodothyronines have a direct inhibitory action on the thyroid. In the present studies the uptake, metabolism and subcellular distribution of labelled thyroxine were analyzed. The entry of this hormone reaches a plateau after 15–20 min incubation and is temperature-dependent. The T/M values for T4 were much lower than those of labelled T3 and the curve was different from that obtained with [125I]. The influence of a series of compounds on the T/M values for thyroxine was studied. KI, T3, IOP PTU and MMI were without effect. Absence of Ca++ in the buffer, or addition of KClO4 or ouabain caused a slight decrease, while TSH produced a stimulation in the T/M ratio. Calf thyroid slices dehalogenated thyroxine, producing both T3 and rT3. TSH increased the generation of these two compounds. Neither PTU nor IOP altered the production of T3 and rT3 significantly. The lack of effect of IOP on T3 and rT3 generation was confirmed in calf thyroid homogenates. However, and in agreement with previous reports, IOP significantly decreased production of both triiodothyronines in rat liver slices and in rat liver homogenates.
When the subcellular distribution of labelled thyroxine was examined most of the radioactivity appeared in the soluble fraction and less than 1 % was present in purified nuclei. The addition of unlabelled thyroxine to the slices only caused a significant displacement in the radioactivity of purified nuclei. The presence of labelled thyroxine in the nuclei was confirmed by paper chromatography.