bluuebunny/crossref_metadata_2025_split huggingface dataset:
A novel action of epidermal growth factor in rat granulosa cells: its potentiation of gonadotrophin action
Authors: Hattori M-A , Yoshino E , Shinohara Y , Horiuchi R , Kojima I 
Published: December 2008

ABSTRACT
It is well known that epidermal growth factor (EGF) induces down-regulation of LH receptors and desensitization to gonadotrophin stimulation in gonadal cells, including granulosa cells. In a previous study we showed that EGF receptor levels in rat granulosa cells were increased up to fourfold after 96 h of culture with human GH in the presence of FSH, and the present study has evaluated the action of EGF on these cells. The induced EGF receptors were identical in size to the pre-existing receptors as assessed by affinity labelling with 125I-EGF. After 48 h in culture, various amounts of EGF (0·5–10 ng) were added and the cells were cultured for a further 48 h. The addition of EGF caused down-regulation of LH receptors in cells expressing high levels of EGF receptors. However, this down-regulation was less than that in control cells. After the cells were washed, cAMP synthesis in response to human chorionic gonadotrophin (hCG) increased by two to three times the control value and this increase was closely correlated with an increase in EGF receptor content. However, stimulation with cholera toxin or forskolin showed no such augmentation, indicating that it may not be due to quantitative alterations in G proteins and their effector systems. Induction of EGF potentiation required long-term exposure to EGF, for at least more than 24 h. In addition, progesterone synthesis was sensitive to stimulation with lower doses of hCG. These findings indicate that the activation of hGH-induced EGF receptors may potentiate gonadotrophin action in granulosa cells.
Pancreastatin: further evidence for its consideration as a regulatory peptide
Authors: Sánchez-Margalet V , Lucas M , Goberna R 
Published: December 2008

ABSTRACT
Pancreastatin is a 49 amino acid peptide first isolated, purified and characterized from the porcine pancreas, and whose biological activity in different tissues can be assigned to the C-terminal part of the molecule. Pancreastatin has a prohormonal precursor, chromogranin A (CGA), which is a glycoprotein present in neuroendocrine cells, including the endocrine pancreas. Both intracellular and extracellular processing of CGA can yield pancreastatin. This processing is tissue-specific, with the pancreatic islet and antral gastric endocrine cells being the major source of fully processed pancreastatin. Most of the circulating CGA is secreted by chromaffin tissue. Therefore, peripheral processing of CGA is probably the major indirect source of pancreastatin. Pancreastatin seems to have a general modulatory control on endocrine (insulin, glucagon, parathormone) and exocrine (pancreatic, gastric) secretion from tissues close to the source of production. This has led to the assumption that pancreastatin may be a peptide with an autocrine and paracrine function. It has recently been revealed to be a peptide with a metabolic function counter-regulatory to insulin action. This effect, in conjunction with the inhibitory effect on insulin and pancreatic exocrine secretion, points to a role in the physiology of stress. The molecular mechanism of the glycogenolytic effect of pancreastatin is better known, although further work is still needed. In general, more studies should be carried out at the molecular level to investigate the mechanism of action of pancreastatin and thus to clarify its physiological role in the neuroendocrine system.
Developmental expression of the cyclo-oxygenase-1 and cyclo-oxygenase-2 genes in the peri-implantation mouse uterus and their differential regulation by the blastocyst and ovarian steroids
Authors: Chakraborty I , Das S K , Wang J , Dey S K 
Published: December 2008

ABSTRACT
Cyclo-oxygenase (COX) is a rate-limiting enzyme that converts arachidonic acid to prostaglandins (PGs) and exists in two isoforms, COX-1 and COX-2. In the rodent, increased uterine vascular permeability at sites of blastocyst apposition is one of the earliest prerequisite events in the implantation process. This event is preceded by generalized uterine edema and luminal closure, and coincides with the initial attachment reaction between the trophectoderm and luminal epithelium. Vasoactive PGs are implicated in these processes. Here we demonstrate that COX genes are differentially regulated in the peri-implantation mouse uterus. During the preimplantation period (days 1–4), the COX-1 gene was expressed in the uterine epithelium mainly on day 4 until the initiation of attachment reaction in the evening after which the expression was downregulated. This COX-1 expression coincides with the generalized uterine edema required for luminal closure. In contrast, the COX-2 gene was expressed in the luminal epithelium and subepithelial stromal cells at the anti-mesometrial pole exclusively surrounding the blastocyst at the time of attachment reaction on day 4 and persisted through the morning of day 5. This uterine gene was not expressed at the sites of blastocyst apposition during progesterone (P4) treated delayed implantation, but was readily induced in the uterus surrounding the activated blastocysts after termination of the delay by estradiol-17β (E2). The results suggest that PG synthesis catalyzed by COX-2 is important for localized increased uterine vascular permeability and attachment reaction. The COX-1 gene that was downregulated from the time of attachment reaction on day 4 was again expressed in the mesometrial and anti-mesometrial secondary decidual beds on days 7 and 8. These results suggest that PGs generated by COX-1 are involved in decidualization and/or continued localized endometrial vascular permeability observed during this period. In contrast, the COX-2 gene, expressed at the anti-mesometrial pole on days 4 and 5, switched its expression to the mesometrial pole from day 6 onward. These results suggest that PGs produced at this site by COX-2 are involved in angiogenesis for the establishment of placenta. In the ovariectomized mice, the COX-1 gene was induced in the epithelium by a combined treatment with P4 and E2. However, P4 and/or E2 treatments failed to influence the uterine COX-2 gene. Overall, the results suggest that the uterine COX-1 gene is influenced by ovarian steroids, while the COX-2 gene is regulated by the implanting blastocyst during early pregnancy.
Developmental and tissue-regulated expression of IGF-I and IGF-II mRNAs in Sparus aurata
Authors: Duguay S J , Lai-Zhang J , Steiner D F , Funkenstein B , Chan S J 
Published: December 2008

ABSTRACT
Recent studies have shown that homologues of the mammalian IGF-I and -II genes are also found in teleosts. We report here the cDNAs coding for IGF-I and IGF-II cloned from the gilthead seabream, Sparus aurata. Sequence comparisons revealed that both IGFs have been well conserved among teleosts, although Sparus IGF-I is shorter by three amino acid residues due to truncated B-and C-domains. Using the cloned cDNAs as probes, the relative expression of IGF-I and IGF-II mRNAs were assayed in different Sparus tissues. Sparus liver clearly contained the highest level of IGF-I mRNA while relatively high levels of IGF-II mRNA were found in liver, heart and gill using the ribonuclease protection assay. After GH administration the amount of IGF-I mRNA was increased by 220% in liver but no changes in IGF-II mRNA levels were detected in any tissue. We also assayed the expression of IGF-I and IGF-II in Sparus during early development. The IGF-II mRNA level was highest in larva 1 day after hatching and decreased thereafter. In contrast, IGF-I mRNA was detected in 1-day-old larva but there was an increase in expression in 12- and 16-day-old larva. These results demonstrated that the expression of IGF-I and IGF-II is highly regulated in teleosts and suggest that they play distinct roles during growth and development.
Monoclonal antibodies to the human TSH receptor: epitope mapping and binding to the native receptor on the basolateral plasma membrane of thyroid follicular cells
Authors: Nicholson L B , Vlase H , Graves P , Nilsson M , Molne J , Huang G C , Morgenthaler N G , Davies T F , McGregor A M , Banga J P 
Published: December 2008

ABSTRACT
We have characterized four murine monoclonal antibodies (mAbs) to the extracellular domain of the human TSH receptor (TSH-R.E), the target autoantigen of Graves' disease. Recombinant TSH-R.E used as immunogen, was produced in E. coli as a fusion protein with glutathione-S-transferase or in a baculovirus-insect cell system, as a non-fusion glycoprotein. To increase the epitope specificity of the mAbs, two different strains of mice (H-2b and H-2d) were immunized. The epitopes recognized by the mAbs were characterized by immunoblotting with various recombinant constructs of TSH-R.E and by binding to overlapping synthetic peptides of the receptor. The four IgG mAbs characterized recognized epitopes localized to different regions on the TSH-R.E; amino acids 22–35 (A10 and All, both IgG2b from H-2b animals), amino acids 402–415 (A7, IgG2b from H-2b animals) and amino acids 147–228 (A9, IgG1 from H-2d animals). Immunolocalization studies showed that mAb A9 recognized TSH-R.E on unfixed cryostat sections, where binding was localized to the basolateral plasma membrane of thyroid follicular cells, suggesting that this antibody reacts with the native receptor on thyroid cells. The binding of the mAbs A7, A10 and All was also restricted to the basal surface of thyroid cells, but only after acetone fixation of the sections, implying that the epitopes recognized on the amino and carboxyl terminus of the extracellular region of the receptor are not accessible on the native molecule. None of the mAbs stimulated cyclic AMP responses in COS-7 cells transiently transfected with full-length functioning TSH-R.E, whilst weak inhibition of binding of radiolabelled TSH to porcine membranes in a radioreceptor assay was apparent with mAb A10 and All, but only at high concentrations of IgG. The ability of mAb A9 to bind to the native receptor without stimulating activity or inhibition of TSH binding suggests that antibody can bind to the central region of the TSH-R.E without perturbing receptor function. The availability of mAbs that recognize epitopes on different regions of the extracellular domain of TSH-R will lead to a better understanding of the autoantigenic regions on TSH-R implicated in disease activity.
The human placenta expresses transcription enhancer factor-1 but there is no correlation with the expression of placental lactogen
Authors: Quinn G , Boam D S W , Davis J R E , Glazier J D , Mylona P , Sides K , Sibley C P 
Published: December 2008

ABSTRACT
A transcriptional enhancer which has a consensus binding sequence for transcription enhancer factor-1 (TEF-1) has been found 3′ of the hPL3 gene. We examined whether TEF-1 is expressed by the human placenta and whether such expression is co-ordinated with that of human placental lactogen (hPL). Probing Northern blots of total RNA from first trimester and term placenta, the choriocarcinoma-derived cell line JAr and primary cultured cytotrophoblast cells with a cDNA for TEF-1 revealed transcripts of 12–13 kb and 3–4 kb. The level of TEF-1 expression was the same in first trimester as compared with term placenta and in undifferentiated JAr as compared with differentiated cytotrophoblast cells. hPL expression was tenfold higher in term compared with first trimester placenta and, whilst detectable in cytotrophoblast cells, was undetectable in JAr cells. These data show that TEF-1 is expressed by the placenta but is not co-ordinated with hPL expression.
Anterior pituitary vasoactive intestinal peptide mRNA is colocalised with prolactin mRNA in hyperoestrogenised rats
Authors: Chew L-J , Seah V , Murphy D , Carter D 
Published: December 2008

ABSTRACT
It is well established that oestrogens can stimulate prolactin (PRL) secretion as well as the expression of the vasoactive intestinal peptide (VIP) gene whose product is also a potent PRL secretagogue. Previous evidence has supported both an autocrine and a paracrine role for pituitary VIP in PRL release in vitro; however, the cellular origin of VIP in pituitary tissue still remains poorly defined. In these studies, we have demonstrated by in situ hybridisation that VIP RNA is detected in the anterior pituitaries of chronically hyperoestrogenised rats, but not in those of untreated animals. Using a double-probe labelling procedure, VIP RNA has been shown to be present in a subpopulation of PRL-producing cells, while colocalisation of VIP and GH RNA was not observed. VIP gene expression in the rat anterior pituitary gland was characterised by the presence of two alternatively polyadenylated transcripts, 1·7 kb and 1·0 kb in size. We have generated a probe specific for the 1·7 kb transcript and double-labelling studies also showed definitive colocalisation with PRL mRNA. Our results demonstrating the presence of VIP RNA in PRL-producing cells thus suggest that VIP may play an autocrine role in PRL hypersecretion under conditions of oestrogen-induced hyperplasia.
The ARP-1 orphan receptor represses steroid-mediated stimulation of human placental lactogen gene expression
Authors: Stephanou A , Shah M , Richardson B , Handwerger S 
Published: December 2008

ABSTRACT
Studies were performed to determine whether ARP-1, which is an orphan receptor of the steroid receptor superfamily, inhibits basal activity of the human placental lactogen (hPL) promoter and the increase in hPL promoter activity in response to the receptors for thyroid hormone (TR) and retinoic acid (RAR). Co-transfection of an ARP-1 expression vector into BeWo choriocarcinoma cells, along with an expression vector containing 1·2 kb of the hPL promoter coupled to a CAT reporter gene, resulted in a dose-dependent inhibition of basal CAT activity. In addition, ARP-1 inhibited the stimulation of CAT activity by RARα and TRβ expression vectors. Mobility shift assays demonstrated that ARP-1 binds specifically to a composite steroid response element on the hPL promoter that confers retinoic acid and T3 responsiveness. The results implicate an inhibitory role for ARP-1 in the regulation of hPL gene expression and strongly suggest that hPL gene expression is regulated, at least in part, by the interaction of stimulatory and inhibitory members of the steroid receptor superfamily.
Mutational analysis of the estrogen receptor ligand-binding domain: influence of ligand structure and stereochemistry on transactivation
Authors: Kohno H , Bocchinfuso W P , Gandini O , Curtis S W , Korach K S 
Published: December 2008

ABSTRACT
The mouse estrogen receptor (mER) exhibits ligand stereochemical specificity for indenestrol A (IA), a stilbestrol estrogen. IA has a chiral C3 methyl group, and the mER preferentially binds the S-enantiomer (IA-S), resulting in elevated biological activity when compared with the IA-R enantiomer. To elucidate the mechanisms for this stereochemical recognition, we have constructed a series of mERs with individual amino acid substitutions at Met521, His528, Met532, and Val537. The abilities of yeast-expressed wild-type and mutant mERs to transactivate an estrogenresponsive reporter gene construct were measured in the presence of diethylstilbestrol (DES) and IA enantiomers. The concentration of IA-S required to induce half-maximal transactivation by wild-type mER was 10-fold lower than IA-R, which is attributed to the 15-fold greater binding affinity for IA-S. Wild-type mER displayed similar dose—response curves for IA-R and demethyl IA, which lacks a C3 methyl group, demonstrating that the presence and correct orientation of the C3 methyl group on the IA compound is required for high-affinity ligand binding and transcriptional activity. Each mutant exhibited a reduced preference for IA-S enantiomer with respect to transactivation, suggesting that this region of the mER functions in ligand stereochemical recognition and activation. A mutation at Met532 diminished DES-and IA-S-induced transactivation by 7·5-fold and 40-fold respectively, with minimal change on their binding affinity. These data suggest that Met532 is required for transactivation induced by the potent agonist, IA-S, and the M532G mutation effectively uncouples IA-S ligand binding from transactivation. Use of these stereochemically different ligands in combination with mutagenesis of the mER demonstrates that ligand structure could influence transactivation by specifically altering the conformation of the mER AF-2 region.
Farm-level economic analysis of the US National Johne's Disease Demonstration Herd Project
Authors: Groenendaal Huybert , Wolf Christopher A. 
Published: December 2008

Abstract
Objective—To evaluate farm-level economic costs and benefits related to control of paratuberculosis (Johne's disease) in dairy herds in the National Johne's Disease Demonstration Herd Project (NJDDHP).
Design—Economic analysis.
Sample Population—40 dairy herds enrolled in the NJDDHP.
Procedures—A farm-level economic analysis of the US NJDDHP was performed. Costs and benefits of management-related practices to control Johne's disease were estimated on the basis of results for 40 dairy operations enrolled in the project. From these costs and benefits, the net present value (NPV) for control of Johne's disease was estimated.
Results—Analysis revealed a mean NPV of $34/animal (equivalent to approx $3/animal/y) when there were no testing costs for producers and a mean NPV of −$14/animal when testing costs were borne by the producers.
Conclusions and Clinical Relevance—Management-related practices to control Johne's disease were typically found to be of marginal economic benefit when the costs of testing were not borne by producers. The continuation of the NJDDHP for another 2 to 4 years would allow more precise estimation of the economic benefits of a control program for Johne's disease.
Prevalence of anthelmintic resistance on sheep and goat farms in the southeastern United States
Authors: Howell Sue B. , Burke Joan M. , Miller James E. , Terrill Thomas H. , Valencia Elide , Williams Mimi J. , Williamson Lisa H. , Zajac Anne M. , Kaplan Ray M. 
Published: December 2008

Abstract
Objective—To determine prevalence of anthelmintic resistance on sheep and goat farms in the southeastern United States.
Design—Cross-sectional study.
Animals—Sheep and goats from 46 farms in 8 southern states, Puerto Rico, and St Croix in the US Virgin Islands.
Procedures—Parasite eggs were isolated from fecal samples, and susceptibility to benzimidazole, imidathiazole, and avermectin-milbemycin anthelmintics was evaluated with a commercial larval development assay.
Results—Haemonchus contortus was the most common parasite on 44 of 46 farms; Trichostrongylus colubriformis was the second most commonly identified parasite. Haemonchus contortus from 45 (98%), 25 (54%), 35 (76%), and 11 (24%) farms were resistant to benzimidazole, levamisole, ivermectin, and moxidectin, respectively. Resistance to all 3 classes of anthelmintics was detected on 22 (48%) farms, and resistance to all 3 classes plus moxidectin was detected on 8 farms (17%).
Conclusions and Clinical Relevance—Findings provided strong evidence that anthelmintic resistance is a serious problem on small ruminant farms throughout the southeastern United States. Owing to the frequent movement of animals among regions, the prevalence of resistance in other regions of the United States is likely to also be high. Consequently, testing of parasite eggs for anthelmintic resistance should be a routine part of parasite management on small ruminant farms.
Evaluation of progress made by dairy and beef herds enrolled in the Minnesota Johne's Disease Control Program
Authors: Wells Scott J. , Hartmann William L. , Anderson Paul L. 
Published: December 2008

Abstract
Objective—To evaluate progress made by cattle herds in the control of paratuberculosis (Johne's disease) through participation in the Minnesota Johne's Disease Control Program (MNJDCP).
Design—Retrospective records analysis.
Sample Population—Data for dairy and beef herds participating in the MNJDCP.
Procedures—Data for the MNJDCP were collected for analyses. Outcome measures included changes in numbers of participating cattle producers, risk assessment scores, and within-herd seroprevalence of Johne's disease by year of program participation.
Results—Results revealed steady increases in program participation by cattle producers in Minnesota over time, with > 30% of dairy producers and 2% of beef producers in the state participating by the end of 2006. Despite risk of introduction of Johne's disease to cattle herds through continued introduction of cattle from other herds, dairy and beef herds in the Management Program of the MNJDCP reduced their on-farm risk assessment scores during the program. Dairy herds in the Management Program reduced their mean within-herd seroprevalence 1.1% during the first year, 2.6% during the first 2 years, and 4.0% during the first 3 years of program participation. Significant within-herd seroprevalence reduction was also detected for beef herds that participated in the Management Program for at least 3 years.
Conclusions and Clinical Relevance—This study revealed a reduction in the risk of withinherd transmission of Johne's disease and seroprevalence over time in dairy and beef herds in the Management Program of the MNJDCP. This is consistent with a positive effect of the program for the control of Johne's disease in cattle.
Sourcing Through Auctions and Audits
Authors: Chen Ying‐Ju , Seshadri Sridhar , Zemel Eitan 
Published: December 2008

Buyers often find that obtaining complete information about suppliers is costly. In such scenarios, there is a trade‐off between the costs of obtaining information and the benefits that accrue to the owners of such information. There are also various ways in which the missing information can be obtained or inferred. In this paper, we compare the efficiency of obtaining information via the classical mechanism design approach, which relies on the information available before the contracts are designed, with that of an “audit‐based” approach, which relies on the information obtained after the fact. In our model, a single buyer (the Stackelberg leader) wishes to procure a package of products or services from various competing suppliers that possess private cost information. We allow for arbitrary cost and revenue functions and can incorporate multiple cost and revenue drivers. We show how the buyer can optimize her profit and at the same time coordinate the channel by using a contract scheme involving auctions, audits, and profit sharing. We also examine the behavior of this mechanism when the supplier can exert effort to reduce cost but the cost of effort cannot be verified. We propose several mechanisms for different precontract informational scenarios and compare their performance.