bluuebunny/crossref_metadata_2025_split huggingface dataset:
Correlation of pinopod development on uterine luminal epithelial surface with hormonal events and endometrial sensitivity in rat
Authors: Singh MM , Chauhan SC , Trivedi RN , Maitra SC , Kamboj VP 
Published: December 2008

Singh MM, Chauhan SC, Trivedi RN, Maitra SC, Kamboj VP. Correlation of pinopod development on uterine luminal epithelial surface with hormonal events and endometrial sensitivity in rat. Eur J Endocrinol 1996;135:107–17. ISSN 0804–4643
Intrinsic role of preovulatory and nidatory estrogen and progesterone and presence of viable blastocysts in utero in pinopod development on the uterine luminal epithelial surface and correlation between time of their development and onset of endometrial sensitivity were investigated. In adult rats, pinopods were observed on the entire epithelium even before secretion of nidatory estrogen, i.e. at 14.00 h on day 4 post-coitum (p.c.). Apparently, their number increased, more so on the antimesometrial than the mesometrial side, at 10.00 h on day 5, but were fewer and mostly collapsed at 10.00 h on day 6. Pinopods on day 4 were located within epithelial depressions and foldings, but protruded from the surface on days 5 and 6. Normal pinopods were also present on day 8 p.c. in rats under delayed implantation, but an implantation-inducing dose of estradiol-17β administered about 18 h earlier caused their collapse like that on day 6 in intact rats. Development and appearance of pinopods in intact or delayed rats was unaffected when native preimplantation embryos were prevented from entering the uterus. Normal pinopods were seen in immature rats receiving progesterone for at least 3 days or cyproterone acetate for 4 days, but not after estradiol alone. In animals receiving progesterone or priming/sensitizing estradiol in addition to progesterone, the decidual response was suboptimal, irrespective of the presence of pinopods on the day of stimulation. In animals in which a condition mimicking preimplantation had been produced by suitable hormone supplementation, optimal endometrial sensitivity and decidual response were elicited, even though most pinopods appeared collapsed, resembling those on day 6 in intact rats and about 18 h after estradiol in implantation-delayed rats. Findings confirm that pinopod development on uterine luminal epithelium was dependent on progesterone alone and demonstrate that: (i) preovulatory (priming) or nidatory (endometrial sensitizing) estrogen or viable blastocysts in utero have no role in their development. Nidatory estrogen, instead, appears to limit pinopod development by causing their collapse; (ii) pinopod development/presence on the endometrial surface might indicate the uterus coming into a period of sensitivity rather than actually being in it and might thus serve as a useful marker of "transfer window" rather than "implantation window"; (iii) in the rat, pinopod development might serve as an alternate assay for evaluation of progestational activity of newer test agents.
MM Singh, Division of Endocrinology, Central Drug Research Institute, Lucknow 226 001, India
Three-step immunoscintigraphy with anti-chromogranin A monoclonal antibody in tumours of the pituitary region
Authors: Colombo Paolo , Siccardi Antonio G , Paganelli Giovanni , Magnani Patrizia , Songini Cristina , Buffa Roberto , Faglia Giovanni , Fazio Ferruccio 
Published: December 2008

Colombo P, Siccardi AG, Paganelli G, Magnani P, Songini C, Buffa R, Faglia G, Fazio F. Three-step immunoscintigraphy with anti-chromogranin A monoclonal antibody in tumours of the pituitary region. Eur J Endocrinol 1996;135:216–21. ISSN 0804–4643
In the present paper we evaluated the ability of pretargeted immunoscintigraphy (ISG) with antichromogranin A (CgA) monoclonal antibody (Mc-ab A11) in visualizing pituitary masses. The results obtained in 23 patients are described along with those of [111In]pentetreotide scintigraphy (Octreoscan®) in 18 cases. Positive ISG was obtained in 9/11 (82%) non-functioning, 1/4 growth hormone-, 1/2 prolactin-, 1/2 thyrotropin-, 1/1 follicle-stimulating hormone-, 0/1 adrenocorticotrophin-secreting pituitary adenomas. In one patient with a positive ISG scan of a non-functioning pituitary adenoma, an associated neurinoma of the acoustic nerve was not imaged. The same occurred in one patient with a pituitary deposit from a mammary carcinoma and in another one with a cyst of the Rathke's pouch. Chromogranin A immunohistochemistry, carried out in 10 tumours, was positive in eight pituitary adenomas and negative in two non-adenomatous lesions. A concordant ISG occurred in all cases except for two pituitary adenomas: one cystic and necrotized and one post-operative remnant very small in size. In 18 patients with pituitary adenoma both ISG and Octreoscan® were positive in 61% of cases but with a different distribution among tumours. At variance with ISG, Octreoscan® visualized only 5/10 (50%) non-functioning pituitary adenomas and all (4/4) somatotropinomas. In conclusion, ISG is able to image pituitary tumours and particularly non-functioning pituitary adenomas. In this respect, it may be helpful in discriminating non-neuroendocrine masses of the pituitary region from non-functioning pituitary adenomas.
G Faglia, Institute of Endocrine Sciences, University of Milan, Ospedale Maggiore IRCCS, via F. Sforza 35, 1-20122 Milan, Italy
Immunoglobulins from Graves' disease patients stimulate phospholipase A2 and C systems in FRTL-5 and human thyroid cells
Authors: Atwa Mohamed A , Smallridge Robert C , Burch Henry B , Gist Irene D , Lu Rui , Abo-Hashem Ekbal M , El-Kannishy Mohamed H , Burman Kenneth D 
Published: December 2008

Atwa MA, Smallridge RC, Burch HB, Gist ID, Lu R, Abo-Hashem EM, El-Kannishy MH, Burman KD. Immunoglobulins from Graves' disease patients stimulate phospholipase A2 and C systems in FRTL-5 and human thyroid cells. Eur J Endocrinol 1996;135:322–7. ISSN 0804–4643
We have studied the effects of immunoglobulin G from Graves' disease patients on phospholipase A2 (PLA2) and C (PLC) systems in FRTL-5 and human thyroid cells. Immunoglobulin G (IgG) from Graves' disease patients stimulated arachidonic acid (AA) release in a time- and dose-dependent manner. In FRTL-5 thyroid cells, removal of external calcium had no significant effect on the IgG (20 μg/ml)-induced AA release in FRTL-5 thyroid cells. U-73122 (3 μmol/l), a PLC inhibitor, and quinacrine (100 μmol/l) but not U-26384 (5 μmol/l), PLA2 inhibitors, blocked the IgG-induced (20 μg/ml) AA release in FRTL-5 thyroid cells. Immunoglobulin G (100 μg/ml) also stimulated accumulation of inositol-1,4,5-triphosphate (IP3) in a time- and dose-dependent (20–300 μg/ml) manner in FRTL-5 cells. Immunoglobulin G from Graves' disease patients induced a significant increase of IP3 production (p = 0.01) compared to IgG from normal subjects. Removal of external calcium had no significant effect on the IgG-induced IP3 production. The PLC inhibitor U-73122 completely blocked IgG-induced IP3 production from FRTL-5 thyroid cells. Also, in human thyroid cells, IgG from Graves' disease patients induced a significant increase of AA release (p = 0.001) and IP3 production (p = 0.004) compared to the IgG from normal subjects. These data indicate that IgG from Graves' disease patients induced PLA2 activity that was PLC dependent, a pattern referred to as sequential activation. Our studies suggest that IgG from Graves' disease patients activates PLA2 and PLC systems in FRTL-5 and human thyroid cells. These signal transduction pathways could be involved in the pathogenesis of Graves' disease and future studies are warranted to investigate this area.
Kenneth D Burman, Endocrine Section, Washington Hospital Center, 110 Irving St. NW, Washington, DC 20010, USA
Episodic secretion of activin A in pregnant women
Authors: Gallinelli A , Gallo R , Genazzani AD , Matteo ML , Caruso A , Woodruff TK , Petraglia F 
Published: December 2008

Gallinelli A, Gallo R, Genazzani AD, Matteo ML. Caruso A, Woodruff TK. Petraglia F. Episodic secretion of activin A in pregnant women. Eur J Endocrinol 1996,135:340–4. ISSN 0804–4643
The aim of the present study was to determine the characteristics of activin A secretion in women with normal and abnormal pregnancy. With this purpose, a prospective study was done to evaluate the putative pulsatile pattern of serum activin A in serial specimens of blood collected during a certain amount of time (every 15 min for 3 h). A group of pregnant women (N = 24) participated in a crosssectional study. They were subdivided into three groups: healthy pregnant women (N = 8), patients with preterm labor (N = 8) and patients with gestational diabetes (N = 8) before and after insulin therapy. Secretory pulses of serum activin A were determined in all patients with a specific frequency and amplitude by using two different computerized analyses, i.e. DETECT and CLUSTER. Mean ± sem values of serum activin A were significantly higher in patients with preterm labor and gestational diabetes than in controls (p < 0.01), showing a significant decrease following insulin therapy in diabetic patients (p < 0.01). Specific pulses of serum activin A levels were observed in all women. The mean pulse frequency did not change significantly between healthy controls and the different pathological groups. Patients with gestational diabetes after insulin therapy showed a pulse frequency that was significantly higher than in controls (p < 0.05). When the mean peak amplitude of activin A pulses was evaluated, patients with preterm labor or gestational diabetes showed values that were significantly higher than in healthy pregnant women (p < 0.01). A significant, inverse correlation between pulse frequency and amplitude was found both in healthy pregnant women (p < 0.05) and in patients with gestational diabetes (p < 0.001). The present study showed that circulating activin A levels in pregnant women change in a pulsatile pattern whose pulse amplitude is modified in the presence of gestational diseases, such as preterm labor or gestational diabetes.
Felice Petraglia, Department of Obstetrics and Gynecology, University of Pisa, via Roma 67, 56100 Pisa, Italy
Short-term administration of intranasal or oral Hexarelin, a synthetic hexapeptide, does not desensitize the growth hormone responsiveness in human aging
Authors: Ghigo E , Arvat E , Gianotti L , Grottoli S , Rizzi G , Ceda GP , Boghen MF , Deghenghi R , Camanni F 
Published: December 2008

Ghigo E, Arvat E, Gianotti L, Grottoli S. Rizzi G, Ceda GP, Boghen MF, Deghenghi R, Camanni F. Shortterm administration of intranasal or oral Hexarelin, a synthetic hexapeptide. does not desensitize the growth hormone responsiveness in human aging. Eur J Endocrinol 1996;135:417–12. ISSN 0804–4643
The function of the growth hormone–insulin-like growth factor I (GH–IGF-I) axis is reduced in aging, although the secretory capacity of somatotrope cells is preserved. Previous studies have suggested that continuous administration of GH-releasing peptides (GHRPs) results in homologous desensitization to the GH-releasing effect of the peptides. In the present study we have studied whether healthy elderly subjects would remain responsive to short-term, intermittent treatment with Hexarelin (HEX), a GHRP, and whether this treatment would result in an increase in serum IGF-I. In study I, the effect of an 8-day treatment with intranasal administration of 1.25 mg (about 18 μg/kg) t.i.d. HEX on the acute GH response to the hexapeptide and on serum IGF-I, IGF binding protein 3 (IGFBP-3), prolactin and cortisol levels was studied in seven elderly subjects (four males and three females, aged 67–80 years). In study II, the same parameters were studied before and after a 15-day treatment with oral administration of 20 mg (about 300 μg/kg) t.i.d. HEX in seven elderly women (aged 63–80 years). The GH response to the intranasal HEX administration was not significantly higher than that induced by 1 μg/kg iv GHRH (229.4± 35.9 vs 145.8 ± 26.9 μg·1−1·h−1) and was maintained with a trend towards increase after an 8-day treatment with the peptide (342.5 ± 199.3 μg·1−1·h−1). On the other hand, HEX treatment did not significantly modify IGF-I (138.7 ± 11.1 vs 122.4 ± 14.1 μg/l) but increased IGFBP-3 levels (2.4 ± 0.2 vs 1.6 ± 0.2 mg/l, p < 0.02). The GH response to the oral HEX administration was also not significantly higher than that to iv GHRH (257.6 ± 72.0 vs 179.0 ±42.8 μg·1−1·h−1) and did not change after a 15-day treatment with the peptide (237.8±42.8 μg·1−1·h−1). Both IGF-I and IGFBP-3 levels were slightly but significantly increased by oral HEX treatment (156.0 ± 10.7 vs 141.6 ± 13.6 μg/l. p< 0.03, 3.4 ±0.2 vs 3.1 ± 0.2 mg/l, p < 0.03, respectively). Neither intranasal nor oral HEX treatment modified PRL or cortisol levels and did not induce any side effect. In conclusion, these results indicate that chronic but intermittent treatment with HEX, administered either by intranasal or oral route, does not desensitize the GH response to the peptide. Moreover, after HEX treatment a trend towards increase was shown for IGF-I and IGFBP-3 levels. Thus, our findings strengthen the hypothesis that prolonged treatment with HEX may restore the reduced GH release in aging.
F Camanni, Divisione di Endocrinologia. Ospedale Molinette. C. so Dogliotti 14, 10126 Torino. Italy
Acute administration of recombinant human growth hormone inhibits the somatotrope responsiveness to growth hormone-releasing hormone in childhood
Authors: Bellone J , Aimaretti G , Valetto MR , Bellone S , Baffoni C , Arvat E , Seminara S , Camanni F , Ghigo E 
Published: December 2008

Bellone J. Aimaretti G, Valetto MR, Bellone S, Baffoni C, Arvat E, Seminara S, Camanni F, Ghigo E, Acute administration of recombinant human growth hormone inhibits the somatotrope responsiveness to growth hormone-releasing hormone in childhood. Eur J Endocrinol 1996:135: 421–4. ISSN 0804–4643
In adulthood the growth hormone (GH) response to growth hormone-releasing hormone (GHRH) is inhibited by previous acute administration of either GH or GHRH and it is restored by substances that inhibit hypothalamic somatostatin release. Because in children the GH response to GHRH is not affected by previous neurohormone administration, it has been suggested that in childhood a GH increase is not able to trigger the somatostatin-mediated negative GH autofeedback mechanism. To verify this hypothesis, in 25 children (8 girls and 17 boys; 15 prepubertal and 10 in pubertal stages II–IV) with familial short stature (normal height velocity and insulin-like growth factor I levels) we studied the effect of acute iv administration of different recombinant human GH doses (group 1, N = 5, 0.06U/kg; group 2, N = 6, 0.01 U/kg; group 3, N = 7, 0.005 U/kg at −150 min or saline on the GH response to GHRH (1 μg/kg iv at 0 min). In another group (N = 7), we studied the effect of 0.005 U/kg iv recombinant human GH or saline on the GH response to GHRH combined with arginine (0.5 g/kg iv over 30 min), which likely inhibits hypothalamic somatostatin release. Serum GH increases after recombinant human GH were dose-dependent (GH peak, mean±sem, 171.7 ± 24.4, 33.3 ± 3.9 and 21.8 ± 5.1 μg/l, respectively). The administration of recombinant human GH strongly inhibited the GHRH-induced GH rise in all groups (group 1, 7.1 ± 1.7 vs 23.1 ± 7.6 μg/l, p < 0.05; group 2, 9.5 ±2.8 vs 26.9±8.5 μg/l, p < 0.05; group 3, 9.1 ±2.7 vs 34.8 ± 7.2 μg/l, p< 0.02). The GH response to arginine + GHRH (56.9 ± 13.3 μg/l) was higher than that to GHRH alone recorded in group 1 (p < 0.005), group 2 (p < 0.01) and group 3 (p < 0.01), while exogenous recombinant human GH failed to inhibit it (45.0 ± 9.4 μg/l). Our results demonstrate that in childhood, as well as in adulthood, recombinant human GH administration inhibits the somatotrope responsiveness to GHRH. This inhibitory effect is likely to be mediated by hypothalamic somatostatin release.
Ezio Ghigo, Divisione di Endocrinologia, Ospedale Molinette, C.so Dogliotti 14, 10126 Torino, Italy
Altered parathyroid hormone-related protein secretion and mRNA expression in squamous carcinoma cells in vitro
Authors: Gröne Andrea , Weckmann Michelle T , Steinmeyer Carole L , Capen Charles C , Rosol Thomas J 
Published: December 2008

Gröne A, Weckmann MT, Steinmeyer CL, Capen CC, Rosol TJ. Altered parathyroid hormone-related protein secretion and mRNA expression in squamous carcinoma cells in vitro. Eur J Endocrinol 1996;135:498–505. ISSN 0804–4643
Parathyroid hormone-related protein (PTHrP), a major factor in the pathogenesis of humoral hypercalcemia of malignancy, is produced by many squamous carcinoma cells (SCCs). Two SCC lines were grown in multilayered culture systems and compared to cells grown as monolayers to evaluate the effects of cell proliferation, confluence and differentiation on PTHrP secretion and mRNA expression. Well-differentiated (SCC 2/88) and poorly differentiated (SCC-A253) SCCs were grown as monolayer and three-dimensional cultures on collagen-coated membranes to compare the regulation of PTHrP expression and secretion by the cell lines in vitro. Parathyroid hormone-related protein secretion was evaluated by radioimmunoassay and immunohistochemistry. Messenger RNA expression was analyzed by RNase protection assay and in situ hybridization. Secretion of PTHrP was greatest in preconfluent SCC 2/88 cells in monolayer culture and decreased after confluence, which was the result of decreased PTHrP mRNA expression. In contrast, PTHrP secretion in cultures of SCC-A2 5 3 cells reached maximal levels after confluence. In multilayered cultures, total PTHrP secretion and mRNA expression remained high in both SCC 2/88 and SCC-A253 cells, and secretion by the multi-layered cultures was principally in the basal direction. Parathyroid hormone-related protein was present in all cell layers in three-dimensional cultures as determined by immunohistochemistry. These results indicated that multilayered cultures of SCCs produced PTHrP continuously, whereas decreased proliferation in monolayer cultures was associated with decreased PTHrP production. Multilayered cultures represent a better system to investigate PTHrP secretion and mRNA expression in vitro and PTHrP secretion by SCCs in vivo may be greatest by proliferating cells.
Thomas J Rosol, 1925 Coffey Road, Columbus, OH 43210, USA
Effects of methimazole in the early and established phases of NG-nitro-l-arginine methyl ester hypertension
Authors: Vargas Félix , Fernandez-Rivas Antonio , Osuna Antonio 
Published: December 2008

Vargas F, Fernandez-Rivas A, Osuna A. Effects of methimazole in the early and established phases of NG-nitro 4643 c-nitro-l-arginine methyl ester hypertension. Eur J Endocrinol 1996;135:506–13. ISSN 0804–
In the present study we evaluated the effects of methimazole, an antithyroid drug, on blood pressure and other variables in the early and established phases of hypertension induced by the inhibition of nitric oxide synthesis with the oral administration of NG-nitro-l-arginine methyl ester (l-NAME), 75 mg/100 ml in the drinking water. Moreover, we also evaluated the acute pressor effect of l-NAME on systemic blood pressure in control and rats treated chronically with methimazole, administered via drinking water (30 mg/100 ml). Oral administration of methimazole maintained the blood pressure of l-NAME-treated rats at normal levels 25 days after induction of hypertension. However, after 25 days of methimazole treatment in rats made hypertensive with l-NAME (for 25 days), high blood pressure was similar in methimazole-treated and non-treated l-NAME rats, despite the fact that a hypothyroid state had been achieved in the methimazole-treated rats. Acute intravenous injection of l-NAME caused a similar increase in mean arterial pressure in control and methimazole-treated rats at the lowest dose; however, smaller pressor responses were observed with increasing doses in hypothyroid rats. These results clearly demonstrate that hypothyroidism induced by methimazole prevents, but does not reverse, l-NAME hypertension and reduces the acute pressor responsiveness to l-NAME administration.
F Vargas, Departamento de Fisiología, Facultad de Medicina, E-18012, Granada, Spain
Modulatory actions of progesterone on gonadotropin-releasing hormone-induced arachidonic acid liberation from perifused rat pituitary cells
Authors: Ortmann Olaf , Ansari-Pirsarai Bijan , Bloh Peter , Schulz Klaus-Dieter , Emons Günter 
Published: December 2008

Ortmann O, Ansari-Pirsarai B, Bloh P, Schulz K-D, Emons G. Modulatory actions of progesterone on gonadotropin-releasing hormone-induced arachidonic acid liberation from perifused rat pituitary cells. Eur J Endocrinol 1996;135:626–30. ISSN 0804–4643
The stimulatory action of gonadotropin-releasing hormone (GnRH) on gonadotropin secretion from cultured rat pituitary cells is modulated by estradiol and progesterone. Recent studies provided evidence that both steroids exert effects on different pathways of GnRH signal transduction, which might be responsible for their actions on luteinizing hormone (LH) release. Here we investigated whether the steroids are able to modulate GnRH-induced liberation of arachidonic acid, which is thought to be involved in GnRH signal transduction. Pituitary cells obtained from female rats were treated for 48 h with vehicle, 1 nmol/l estradiol or 1 nmol/l estradiol +100 nmol/l progesterone, 48 h with 1 nmol/l estradiol and 2 h with 100 nmol/l progesterone. In addition, these cells were prelabeled with [3H]arachidonic acid. Then the cells were transferred to a perifusion system and challenged with a 6-min pulse of 100 nmol/l GnRH. Estradiol treatment enhanced the LH secretory response while GnRH-induced [3H]arachidonic acid liberation remained unaffected. However, progesterone modulated both LH secretion and [3H]arachidonic acid release in response to the GnRH stimulus. The shortterm progesterone treatment paradigm enhanced the LH and arachidonic acid responses by up to 160 ±13 and 204 ±18%, respectively, while long-term treatment was inhibitory (59 ± 9 and 63 ± 4% vs control). Because arachidonic acid has been shown to be involved in GnRH signal transduction, it seems reasonable to speculate that the actions of progesterone described in the present study are related to its modulatory effect on GnRH-induced LH secretion.
O Ortmann, Department of Obstetrics and Gynecology, Medical University of Lübeck, Ratzeburger Allee 160, D-23538 Lübeck, Germany