Search

This study demonstrates that a single subcutaneous injection of gonadotrophin-releasing hormone (GnRH) (60 ng) to GnRH-deficient (hpg) male mice causes a doubling of pituitary GnRH receptors (GnRH-R). No change in GnRH-R occurs during the time of LH release (15–60 min) or up until 4 h post-GnRH. Between 4 and 12 h there is a progressive increase in GnRH-R, which is still apparent 24 h later. No induction of GnRH-R occurs after the same treatment of intact adult normal mice. The same degree of GnRH-R induction occurs 12 h after a single GnRH injection (60 ng) to orchidectomised hpg male mice, indicating that this effect is mediated by a direct action of GnRH on the pituitary gonadotroph, rather than being secondary to stimulation of some gonadal product. Homologous ligand GnRH-R induction in hpg mouse pituitaries in vivo is prevented by prior treatment with cycloheximide, a non-specific protein synthesis inhibitor. Cycloheximide alone had no effect on GnRH-R in normal male mice but when combined with GnRH caused a 40% depletion of receptors, implying ligand-induced receptor loss without subsequent replenishment. The similarity between the extent, time-course, and dependence on protein synthesis of GnRH induction of its own receptors in vivo and in cultured pituitary cells in vitro indicates that the hpg mouse pituitary behaves like an in vivo pituitary cell culture system in this respect. Similarity of data derived from this in vivo model provides direct support for the view that in vitro studies on the cellular mechanism of GnRH action can be physiologically relevant to the intact animal.

Pre- and postcastration changes in LH beta and common alpha mRNAs were correlated with pituitary and serum LH levels in two different species after abolition of pituitary stimulation by GnRH. A GnRH antagonist (GnRH-ANT) was used to block gonadotroph GnRH receptors in male rats, and a GnRH antiserum (GnRH-AS) was used to inhibit GnRH stimulation of female and male mouse and male rat pituitaries. The postcastration increases in LH beta and common alpha mRNA levels (2- and 3.5-fold, respectively) were abolished in male rats after 7 days of continuous GnRH-ANT infusion. The postcastration increases in LH beta and common alpha mRNA in female (1.9- and 2.2-fold respectively) and male mice (1.4- and 3.6-fold, respectively) were also prevented after daily sc injection of GnRH-AS, as were the rises in LH beta (3-fold) and common alpha (4-fold) in castrated male rats. The pituitary LH content (postgonadectomy) was no different from intact control levels in all experimental animals regardless of treatment, while the increase in serum LH concentration in rats (7- and 8-fold) and in female (4.8-fold) and male mice (9.8-fold) was prevented by both GnRH-ANT and GnRH-AS administration. In intact rats treated with GnRH-ANT the LH beta mRNA level decreased (57%) while the common alpha mRNA level was unaffected after 7 days. Neither pituitary nor serum LH levels were altered in intact rats or mice after appropriate treatments. We conclude that endogenous GnRH is required for the postcastration rise of both LH beta and common alpha-subunit mRNA levels in rats and mice.

GnRH receptor values are 30-50% of normal in pituitaries of hpg male mice, and testicular LH receptors only 8% of normal (160.4 +/- 17.6 and 2013 +/- 208.1 fmol/testis respectively). In male hpg mice bearing fetal preoptic area (POA) hypothalamic implants for 10 days there was no change in pituitary GnRH receptors, pituitary gonadotrophin content, or seminal vesicle weight. However, testicular weights and LH receptors were doubled in 4/10 mice and 2 had increased serum FSH levels. Between 26 and 40 days after implantation pituitary GnRH receptors and pituitary LH increased to normal male levels, although at 40 days serum and pituitary FSH concentrations had reached only 50% of normal values. Testicular and seminal vesicle weights increased more than 10-fold by 40 days after implantation and LH receptors to 70% of normal. In hpg female mice bearing hypothalamic implants for 30-256 days pituitary gonadotrophin concentrations were normal, even though GnRH receptors reached only 60% of normal values (6.18 +/- 0.4 and 9.8 +/- 0.4 fmol/pituitary respectively). Serum FSH was substantially increased from values of less than 30 ng/ml in hpg mice to within the normal female range in hypothalamic implant recipients. Ovarian and uterine weights increased after hypothalamic grafting from only 4-5% to over 74% of normal values. LH receptors increased from 6.5 +/- 1.3 fmol/ovary for hpg mice to 566.9 +/- 39.2 fmol/ovary for implant recipients. Vaginal opening occurred about 23 days after implantation and these animals displayed prolonged periods of oestrus.(ABSTRACT TRUNCATED AT 250 WORDS)

In this study we investigated changes in steady state cytoplasmic mRNA levels for LH subunits in pituitaries of male rats desensitized by continuous infusion of GnRH in vivo. Seven days of GnRH infusion (340 micrograms/day) reduced (P less than 0.01) LH beta mRNA levels in intact adult male rats and prevented the LH beta mRNA rise observed after castration. In contrast, common alpha mRNA doubled (P less than 0.05) in intact rats, and the elevated alpha mRNA after 7 days castration was unchanged. Serum and pituitary LH levels were suppressed below values of intact controls. Fourteen days of GnRH infusion (290 micrograms/day) further reduced LH beta mRNA levels in both intact and castrated male rat pituitaries. alpha mRNA levels in intact rat pituitaries were unchanged by 14 days of GnRH infusion, while in castrated rats there was a 23% (P less than 0.05) decrease, though values were still twice those of intact controls. As at 7 days, serum and pituitary LH were suppressed. Infusion of a superagonist analog (Buserelin) at a dose of 14 micrograms/day for 28 days reduced LH beta mRNA to 15% of intact control values in both castrated and intact rats. Common alpha mRNA was significantly (P less than 0.05) increased in intact rats and reduced by 13% (P less than 0.05) in castrates by superagonist infusion. These results were similar to those produced by 20- to 30-fold higher doses of native GnRH. GnRH and agonist analog effects were specific since no changes were observed in other mRNA species (GH, PRL, actin). These results indicate that in GnRH-desensitized gonadotropes LH beta gene expression is inhibited, and this may largely explain the reduced LH biosynthesis. However, there is a differential effect of continuous GnRH or agonist analog treatment on LH subunit gene expression, with a time-dependent stimulation of common alpha gene expression in intact rats. This may be caused by a stimulatory interaction between GnRH and progestagens at the level of the gonadotrope. Thus, common alpha gene expression is less tightly coupled than that of LH beta to GnRH action.

The cellular mechanisms involved in GH biosynthesis have been investigated by the measurement of steady-state levels of cytosolic GH messenger RNA (mRNA) in primary cultures of rat pituitary cells using an RNA–complementary DNA (cDNA) hybridization assay. Growth hormone mRNA–cDNA hybridization increased in a linear manner with increasing cytosol concentration. Cellular GH mRNA levels rose by an average of 2·4-fold (range, 1·6–3·3; n = five experiments) after exposure to GH-ieleasing factor (GRF(1–40); 10 nmol/l) for 3 days. Treatment with GRF increased the release of GH into the culture medium, and depleted the cellular GH content by 40%. Total GH (in the medium plus cells) after GRF treatment increased by between 1·5- and 3·8-fold, a magnitude similar to the increase in GH mRNA levels. Treatment of cells with dibutyryl adenosine 3′:5′-cyclic monophosphate (1 mmol/l) or forskolin (5 μmol/l) increased the levels of cytosolic GH mRNA by between 1·6- and 4·7-fold. These agents increased GH release into the medium, depleted cellular GH content and increased total GH in the system to the same extent as GRF (10 nmol/l). These data demonstrate that cyclic adenosine nucleotides may mediate the GRF induction of GH gene transcription. In addition, we have shown that increases in the levels of cellular GH mRNA are reflected by increased GH biosynthesis, suggesting that the regulation of hormone gene transcription is one cellular site for the control of hormone biosynthesis and, ultimately, hormone available for release. J. Endocr. (1986) 110, 51–57

The purpose of this study was to examine the physiological functions of the gonadotropin releasing hormone (GnRH) receptors present in the rat testis. The receptors were blocked in situ by infusing one testis of adult rats for 7 days with 10-100 ng/h of a potent GnRH antagonist (N-Ac-Ala1, D-p-Cl-Phe2, D-Trp3,6-GnRH) using Alzet osmotic minipumps. The contents of the pump were delivered to the testis through a cannula perforating, and fixed, to the tunica albuginea. A plastic cannula alone was attached to the contralateral testis, to act as a control. Infusion of the antagonist resulted in a dose-dependent decrease of testicular GnRH receptors, up to 90%. Some of the antagonist also occupied GnRH receptors in the contralateral testis and pituitary, but these effects were always clearly less than in the infused testis. None of the doses used affected circulating levels of gonadotropins, prolactin (Prl) or testosterone. However, when the endocrine parameters of the two testes were compared, the 100 ng/h dose of the antagonist resulted in a significant (P less than 0.01-0.05) 16-32% decrease in the testicular content of testosterone, and LH, FSH and lactogen receptors. Similar effects (inhibition of the same parameters by 22-42%) were observed when immature (30-day-old) male rats were treated for 1 week with intratesticular infusions of the antagonist. It is inferred from these observations that, in physiological circumstances, testicular GnRH receptors may mediate stimulatory effects of Leydig cell LH and lactogen receptors, and testosterone synthesis.(ABSTRACT TRUNCATED AT 250 WORDS)

Grafts of normal mouse preoptic area (POA) tissue into the third ventricle of gonadotrophin-releasing hormone (GnRH)-deficient hypogonadal (hpg) mice resulted in an elevation of pituitary GnRH receptors, an increased synthesis of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) by the pituitary gland, an elevation of gonadal LH receptors and in the stimulation of steroidogenesis and spermatogenesis in the testis. In normal mice both castration or the subcutaneous implantation of testosterone capsules for 10 days reduced GnRH receptors, pituitary LH and FSH content, and the latter treatment also caused a 50% reduction in testicular LH receptors. In hpg mice bearing POA grafts testosterone implants failed to affect any of the above parameters, and castration failed to affect pituitary gonadotrophin hormone content, although there was a slight reduction in pituitary GnRH receptors after castration. These experiments suggest that neither the pituitary gonadotroph, nor the GnRH neurone represent major sites for the direct negative feedback of testosterone upon gonadotrophic hormone secretion in male mice.

A lower bound for the number of integer polynomials which simultaneously have “close” complex roots and “close” p-adic roots is obtained.

Isolated familial pseudohyperkalemia is a dominant red cell trait characterized by cold-induced ‘passive leak’ of red cell potassium ions into plasma. The causative gene of this condition is ABCB6, which encodes an erythrocyte membrane ABC transporter protein bearing the Langereis blood group antigen system. In this study analyzing three new families, we report the first functional characterization of ABCB6 mutants, including the homozygous mutation V454A, heterozygous mutation R276W, and compound heterozygous mutations R276W and R723Q (in trans). All these mutations are annotated in public databases, suggesting that familial pseudohyperkalemia could be common in the general population. Indeed, we identified variant R276W in one of 327 random blood donors (0.3%). Four weeks’ storage of heterozygous R276W blood cells resulted in massive loss of potassium compared to that from healthy control red blood cells. Moreover, measurement of cation flux demonstrated greater loss of potassium or rubidium ions from HEK-293 cells expressing ABCB6 mutants than from cells expressing wild-type ABCB6. The R276W/R723Q mutations elicited greater cellular potassium ion efflux than did the other mutants tested. In conclusion, ABCB6 missense mutations in red blood cells from subjects with familial pseudohyperkalemia show elevated potassium ion efflux. The prevalence of such individuals in the blood donor population is moderate. The fact that storage of blood from these subjects leads to significantly increased levels of potassium in the plasma could have serious clinical implications for neonates and infants receiving large-volume transfusions of whole blood. Genetic tests for familial pseudohyperkalemia could be added to blood donor pre-screening. Further study of ABCB6 function and trafficking could be informative for the study of other pathologies of red blood cell hydration.

The demonstration of GnRH receptor changes in a variety of physiological and abnormal states in animals has led to the general belief that these changes are functionally related to gonadotroph function. This idea was based largely on the apparently ‘tight’ qualitative positive correlation between GnRH receptor changes and changes in serum gonadotrophin levels in animals (reviewed in 1–3). That this may be an oversimplification was suggested by several lines of evidence derived either from in vitro studies in mice, or from in vitro studies designed to explore the cellular biochemical events involved in GnRH receptor regulation and action. This does not deny that GnRH receptors are a prerequisite for the hormone’s action in respective target tissues.

The relationship between pituitary GnRH receptors (GnRH-R) and LH responsiveness to GnRH stimulation is not straightforward. In some circumstances, e.g. post-gonadectomy of rats, in lactating rats, during the rat, hamster and monkey oestrous cycles there appears to be a good positive correlation between GnRH-R, basal serum LH values and LH responses to exogenous GnRH. However, in mice following gonadectomy GnRH-R fall by 50% while serum LH levels rise by 10-fold, and in cultured pituitary cells, GnRH exposure increases GnRH-R yet desensitizes cellular responsiveness to subsequent GnRH stimulation. Thus, our original hypothesis that GnRH-R regulation was closely coupled to gonadotroph secretory function does not always hold. Further, we and others, using the rat as an experimental model, hypothesised that the pituitary GnRH receptor content reflected the level of previous pituitary exposure to endogenous GnRH. This view is supported with studies in the GnRH deficient hypogonadotrophic hypogonadal (hpg) mouse in which exogenous GnRH rapidly normalises GnRH-R from very low levels, and is accompanied by rapid activation of pituitary FSH synthesis. However, the post-castration fall in GnRH-R in mice, which is opposite to that in rats, does not appear to be so closely related to endogenous GnRH secretion and cannot be reversed by exogenous GnRH. Using the ovariectomised mouse as an experimental model, evidence has been obtained that estradiol, in addition to GnRH, is essential for maintenance of pituitary GnRH-R in this species. Exogenous estradiol stimulates GnRH-R in OVX mice while it reduces the high values in OVX rats. In female mice estradiol and GnRH have additive stimulatory effects on GnRH-R. Thus, there is species variability in the predominant hormonal regulation of GnRH receptors. In rat pituitary cells in vitro up-regulation of GnRH-R can be effected by several agents which stimulate LH release (GnRH, KCl, DbCAMP) as well as some which do not (Ca ionophore at low concentrations). Receptor up-regulation requires Ca2+ mobilisation and protein synthesis. The data obtained from several in vivo and in vitro model systems supports the conclusion that GnRH receptor changes represent another, medium-term, consequence of GnRH action on the gonadotroph and are not always a locus for the modulation of gonadotrophin secretion and synthesis.

A single injection of gonadotrophin-releasing hormone (GnRH) (60 ng s.c., 42·9 nmol) induced biphasic GnRH receptor regulation in normal intact adult female mice. A transient 22% receptor decrease occurred 30–60 min after injection of GnRH when peak serum decapeptide concentrations were reached (137 ± 41 (s.e.m.) ng/l). This GnRH receptor decrease occurred shortly after the peak serum LH values at 15–30 min. The subsequent rapid (within 1 h) return of GnRH receptor levels to normal suggested transient receptor occupancy by GnRH rather than true receptor loss. At 8 h after injection of GnRH a significant 35% increase in GnRH receptors was consistently observed, when serum GnRH levels were undetectable and serum LH had returned to basal levels. This receptor increase was not due to increased receptor affinity, and was prevented by a non-specific protein synthesis inhibitor. Ovariectomy, which caused a 50% fall in GnRH receptors (59·4 ± 4·9 fmol/pituitary gland in intact controls; 26·9 ± 2·6 in ovariectomized mice) abolished the induction by GnRH of its own receptors, although the initial transient decrease occurred over the period of the acute serum LH and FSH rise. Despite a 50% reduction in GnRH receptors in ovariectomized mice, increased serum gonadotrophin levels and responsiveness to GnRH were maintained, indicating dissociation between receptor changes and gonadotrophin levels. No GnRH receptor up-regulation was observed 8 h after a single GnRH injection (60 ng s.c.) in either intact or orchidectomized normal male mice. However, the same treatment doubled GnRH receptors in GnRH-deficient (hpg) female mice. While GnRH appears to up-regulate its own receptors by a direct action on pituitary gonadotrophs in the GnRH-deficient mouse its action in the normal female mouse pituitary appears secondary to stimulation of a gonadal product, presumably oestrogens. J. Endocr. (1985) 107, 41–47

Evidence suggests that exogenous GnRH and agonist analogues have short-term stimulatory effects on rat Leydig cell function - when administered intratesticularly. Since rat Leydig cells possess GnRH receptors and their endogenous ligand has not yet been identified the physiological importance of the observations for testis function is unknown. To address this issue we have determined the consequences of blockade of testis GnRH receptors on Leydig cell function under both normogonadotrophic and hypogonadotrophic stimulation of the testis in vivo. A GnRH antagonist (ANT) was used to achieve receptor blockade but during continuous systemic infusion ANT occupied pituitary GnRH receptors and markedly reduced serum LH, FSH, testosterone, and intratesticular testosterone in adult and 30 d old immature male rats. These results were similar to those obtained by administration of a GnRH antiserum which did not bind to testis GnRH receptors. Thus, blockade of testis GnRH receptors during hypogonadotrophism did not produce additional inhibition of steroidogenesis by Leydig cells. However, direct continuous infusion of ANT into one testis produced greater than 90% occupancy of GnRH receptors while reducing GnRH receptors by only 50% in the contralateral testis. Unilateral intratesticular infusion did not reduce serum LH, FSH, Prolactin or testosterone levels despite 75% occupancy of pituitary GnRH receptors. Thus, both ANT infused and saline infused testes were exposed to the same gonadotrophic stimulants but in the former GnRH-R were essentially non-existent. Compared to the control testis, the ANT infused testis showed a 20-30% reduction in LH, FSH, lactogen receptors and 30-40% fall in testosterone content. Identical results were obtained in adult and 30 d-old male rats.(ABSTRACT TRUNCATED AT 250 WORDS)

The ontogeny of hypothalamic GnRH, of pituitary and gonadal receptors and of pituitary LH and FSH was studied in the fetal and neonatal rat. Hypothalamic, hypophyseal and gonadal primordia were dissected from animals ranging in age from postconceptual day 12 to birth. Immunoreactive GnRH was detectable in the hypothalamus from fetal day 12 onwards at a low level until day 17, whereafter hypothalamic GnRH content and concentration increased until birth. GnRH receptors were reliably detectable in the pituitary anlage from fetal day 16 onwards and increased progressively with advancing age whether expressed as content or concentration. Signs of pituitary LH synthesis were evident as early as fetal day 12 but intrapituitary LH levels remained low until fetal day 17 when levels increased progressively until the end of gestation. Pituitary FSH was undetectable until fetal day 19, thereafter rising dramatically until the end of gestation. GnRH binding to testicular and ovarian tissues was undetectable throughout the period of fetal development. The possible relations among the developmental changes in hypothalamic GnRH, pituitary GnRH receptors and gonadotrophins are discussed.

A collection of folklore and local history stories from Díseart, Droichead Átha (school) (Dysart, Co. Louth), collected as part of the Schools' Folklore Scheme, 1937-1938 under the supervision of teacher M. Ní Ailpín., Hidden Treasure / Brien, Maisie O' -- Hidden Treasure / Campbell, Detta -- Hidden Treasure / Devin, Patrick -- Hidden Treasure / Rodgers, Jack -- Hidden Treasure / Howell, Evelyn -- Hidden Treasure / Fay, Donal -- Funny Stories / Campbell, Delta -- Funny Stories / Brien, Maisie O' -- Funny Stories / Murphy, Mildred -- Funny Stories / Campbell, Mary -- Funny Stories / Fitzpatrick, May -- Funny Stories -- Funny Stories / Howell, Evelyn -- Funny Stories / Fitzpatrick, Paddy -- Riddles -- Weather-Lore / Brien, Maisie O' -- Weather-Lore / Fay, Francis / Fay, Donal -- Weather-Lore -- Weather-Lore / Campbell, Mary -- Weather-Lore / Campbell, Detta -- Weeather-Lore / Molloy, Brendan -- Weather-Lore / Butterly, Evelynn -- Weather-Lore / Kenna, Tom Mc -- Weather-Lore / Howell, Evelynn -- Weather-Lore / Rourke, Phyllis -- Weather-Lore -- Stories About Cromwell / Molloy, Brendan -- Stories About Cromwell / Fay, Francis -- Stories About Cromwell / Butterly, Evelyn -- Stories About Cromwell / Butterly, Evelyn -- Stories About Cromwell / Fitzpatrick, May -- Potato Crop / Byrne, Vincent -- Potato Crop / Butterly, Donal -- Potato Crop -- Great Racer -- Great Walkers -- Great Walkers -- Great Disaster -- Great Disaster -- Great Disaster -- Famine -- Big Wind -- School Games -- School Games - Four Corner Fool -- School Games - Hide and Go Seek -- School Games - How Many Miles to Barneybridge -- School Games - Ghost in the Garden -- School Games - Clock -- School Games - Colours -- School Games - Fox and Geese -- School Games - Ring a Rosy -- School Games - Frog in the Well -- School Games - Lueena -- School Games - Cat Cat the Rat -- School Games - I Wrote a Letter to my Mother -- School Games - Button -- School Games - Turn the Blankets Over -- School Games - Weigh the Butter -- School Games - Singing Games -- School Games - Green Gravel -- School Games - Sally, Sally, Waters -- School Games - Nuts in May -- School Games - The Farmer Wants a Wife -- School Games - The Big Ship Sails -- School Games - Indoor Games -- Old Crafts - Candle-Making -- Old Crafts - Basket-Making -- Old Crafts - Wheel-Making / Murphy, Mildred -- Old Crafts - Forge Work -- Old Crafts - Spinning -- Old Crafts - Weaving / Campbell, Detta -- Old Crafts - Candle-Making -- Old Crafts - Basket-Making -- Old Crafts - Forge Work / Brien, Maisie O' -- Old Crafts - Spinning / Brien, Maisie O' -- Old Crafts - Dyeing / Brien, Maisie O' -- Old Crafts - Thatching / Brien, Maisie O' -- Old Crafts -- Old Crafts -- Local Marriage Customs / Campbell, Mary -- Local Marriage Customs / Fay, Francis -- Local Marriage Customs / Butterly, Evelyn -- In Penal Times / Fay, Francis -- In Penal Times / Kenna, Tommy Joe Mc -- In Penal Times / Campbell, Detta -- In Penal Times / Molloy, Brendan -- In Penal Times / Byrne, Vincent -- In Penal Times / Brien, Maisie O' -- Local Patron Saint -- Place Names - Fields -- Townland of Hitchestown -- Townland of Skeaghmore -- Stray Sods -- Townland of Thornogs -- Townland of Kilally -- Townland of Clonmore -- Townland of Rath Drummion -- Townland of Mountainstown -- Townland of Dysart -- Bird-Lore -- Migratory Birds -- Nests -- Bird's Eggs -- Bird-Lore / Fitzpatrick, Paddy -- Bird-Lore / Kenna, Tommy Joe Mc -- Bird-Lore / Brien, Maisie O' -- Bird-Lore / Molloy, Brendan -- Bird-Lore / Campbell, Detta -- Bird-Lore / Campbell, Mary -- Bird-Lore / Fay, Donal -- Local Cures / Brien, Maisie O' -- Local Cures / Butterly, Donal -- Local Cures / Murphy, Mildred -- Local Cures / Molloy, Brendan -- Local Cures / Campbell, Marie -- Local Cures / Kenna, Tom Mc -- Local Cures / Campbell, Mary -- Local Cures / Fay, Donal -- Local Cures / Fay, Francis -- Local Cures / Butterly, Evlynn -- Local Cures / Reynolds, Pete -- Homemade Toys / Brien, Maisie O' -- Homemade Toys / Campbell, Marie -- Homemade Toys / Butterly, Evlyn -- Fairy Forts -- Kilally Moat -- Rath Moat -- Butterly's Moat -- O'Reilly's Moat -- Mountainstown Moat / Brien, Maisie O' -- Rathdrummion Moat -- Local Poets / Butterly, Evlyn -- Famine / Levins, Mona -- Famine / Butterly, Evlynn -- Famine / Butterly, Donal -- Local Roads / Brien, Maisie O' -- Local Roads / Byrne, Vincent -- Local Roads / Fitzpatrick, May -- Local Roads / Campbell, Detta -- Local Roads / Campbell, Mary -- Local Roads / Hay, Donal -- Local Roads / Molloy, Brendan -- Local Roads / Campbell, Marie -- Local Roads / Kenna, Tom Mc -- Holy Wells / Butterly, Evlynn -- Holy Wells / Brien, Maisie O' -- Travelling Folk -- Tramps / Butterly, Donal -- My Home District / Brien, Maisie O' -- My Home District / Butterly, Evelyn -- My Home District / Molloy, Brendan -- My Home District / Campbell, Ditta -- My Home District / Murphy, Mildred -- Herbs / Brien, Maisie O' -- Herbs / Fitzpatrick, May -- Herbs / Molloy, Brendan -- Herbs / Butterly, Evelyn -- Herbs / Kenna, Tom Mc -- Herbs / Fay, Francis -- Old Sayings / Brien, Maisie O' -- Old Sayings / Fitzpatrick, May -- Old Sayings / Campbell, Detta, Supported by funding from the Department of Arts, Heritage and the Gaeltacht (Ireland), University College Dublin, and the National Folklore Foundation (Fondúireacht Bhéaloideas Éireann), 2014-2016.

A collection of folklore and local history stories from Cill Cruain (C) (school) (Ballyglass South, Co. Galway), collected as part of the Schools' Folklore Scheme, 1937-1938 under the supervision of teacher Brighid Ní Náradaigh., agóid - touch me not, antaire - saucy -- Scéal -- Paidrín -- Seanrann -- Bia agus Nósanna -- Leasainmneacha -- Bia san Am Fadó / Caomhánaigh, Nóra Ní -- Nósanna Pósta / Eigcheartaigh, Máire Ní h -- Scoil Mhóta / Gríobhtha, Cáit Ní -- Scoil Mhóta / Ríain, Eibhlín Ní -- Scoileanna Mhóta / Ríain, Eibhlín Ní -- Seantithe / Gríobhtha, Cáit Ní -- Seantithe / Eighceartha, Máire Ní h -- Maistreadh / Ríain, Eibhlín Ní -- Maistreadh / Gríobhtha, Cáit Ní -- Maistreadh / Ríain, Eibhlín Ní -- Arán san Am Fadó / Mhuireagán, Máire Cáit Ní -- Cén Chaoi a Níodh siad Suidín Fadó -- Cén Chaoi a Níodh siad Scoith Fadó -- Stailc / Ceallaigh, Dettha Ní -- Daoine Siúil / Ríain, Eibhlín Ní -- Daoine Siúil / Eigceartha, Máire Ní h -- Cluichí - Sicín / Gríobhtha, Cáit Ní -- Cluichí / Nualláin, Máire Ní -- Oíche Shamhna / Muirgain, Máire Ní -- Cluichí / Eigcearta, Máire Ní h -- Cluichí / Ríain, Eibhlín Ní -- Cluichí - Hurley Burley / Ríain, Eibhlín Ní -- Aire na gCos - Pisreoga -- Paitíní -- Pisreoga / Nolan, Mary Joe -- Old Cures / Ryan, Eileen -- Fairy Forts / Nolan, Mary Joe -- Fairy Forts / Hegarty, Mary -- Old Story - Local History / Galvin, Mary Ellen -- Old Story - Local History / Ryan, Eileen -- Funny Story / Nolan, Mary Joe -- Funny Story / Nolan, Mary Joe -- Old Prayers / Keaveney, Nora / Nolan, Mary Joe -- Prayers / Hegarty, Mary -- Old Prayers / Dillon, Mary / Griffin, Kitty -- Local Heroes / Griffin, Kitty -- Local Heroes / Nolan, Mary Joe -- Local Heroes / Dillon, Mary -- Local Heroes -- Local Heroes -- Three Local Heroes / Nolan, Mary Joe -- Hidden Treasure / Ryan, Eileen -- Hidden Treasure / Griffin, Kitty -- Hidden Treasure / Galvin, Mary E. -- Hidden Treasures / Brien, Kathleen O' -- Famine Times / Dillon, Mary -- Famine Times / Griffin, Kitty -- Severe Weather / Griffin, Kitty -- Severe Weather / Morgan, Mary Kate -- Bird-Lore / Griffin, Kitty -- Old Crafts / Nolan, Mary Joe -- Old Crafts / Griffin, Kitty -- Lá an Dreoilín / Eighceartaigh, Máire Ní h -- Dá Lá Déag Nollag / Eigceartaigh, Máire Ní h -- Pisreoga agus Nósanna faoi Shochraid agus Tórramh / Nualláin, Máire Ní -- Pisreoga agus Nósanna faoi Shochraid / Ríain, Eibhlín Ní -- Pisreoga agus Nósanna faoi Shochraid agus Tórramh / Mhuirghain, Máire Cáit Ní -- Pisreoga agus Nósanna faoi Shochraid agus Tórramh / Gríobhtha, Cáit Ní -- Lá Fhéile Naomh Máirtín / Gríobhtha, Cait Ní -- Ainmhithe na Feilme / Gríobhtha, Cait Ní -- Seanfhocla -- Seanfhocla / Mhúiréagán, Máire Cháith Ní -- Fataí / Gríobhtha, Cait Ní -- Fataí / Cheallaigh, Detta Ní -- Fataí -- Seo é an Chaoi a Chuireann M'Athair Altrama na Prátaí / Nualláin, Máire Ní -- Na hAonaigh / Caomhánaigh, Máire Ní -- Old Crafts / Hegarty, Mary -- Old Crafts -- Local Landlords -- My Home District / Griffin, Kitty -- Our Holy Wells -- Holy Wells / Galvin, Mary E., Supported by funding from the Department of Arts, Heritage and the Gaeltacht (Ireland), University College Dublin, and the National Folklore Foundation (Fondúireacht Bhéaloideas Éireann), 2014-2016.

This thesis aims to discuss a deeper understanding of the body and being in relation to a\ud dance practice, culminating in the performance of a new solo created originally from a written\ud score devised by Deborah Hay. The research grows out of my curiosity in the potential of\ud awareness in motion, with the intention to invigorate a choreographic practice and enhance\ud what it is to perform.

The story of this research begins (and ends) with the body. We all own a personal container of bones, muscles, blood and fibres. I use mine in my work, teaching contemporary dance technique classes, choreographing, performing, and outside of that, as a transporter to get me from an A to a B, hopefully on time and prepared for one of the above. After 20 years of use in my career, I struggle to remember many moments where I have stopped and acknowledged just how remarkable the body is and how much of its capacity to sense, feel and learn passes most of us by unnoticed. This paper intends to unfold a journey of recognition, realisation, reassessment and reworking of a dancing body with the intention of fine tuning the art of noticing.\ud The spark that ignited the beginnings of this investigation came from a period of research and development with freelance dance artist Matthias Sperling, designed to unwrap, shake up, unsettle and explore what was then my working practice. Unsure where this would lead and what I might find along the way, I tentatively began a new chapter in my dance career. \ud In the summer of 2010 Sperling and I worked together for two weeks where he introduced me to his dance practice, influenced by the work of Deborah Hay. We explored notions of listening to feedback from the body and working with many questions to stimulate, challenge and trick the mind to allow the body to experience a sense of release and letting go of habitual movements. Sperling spoke of this work as offering ‘…the difference between wearing a mask and inviting being seen… an embodied research, a helpful lens to notice things that you may not have noticed before.’ (Aug, 2010).\ud In one of our practices, Sperling questioned whether, ‘I was seeing or appearing to see?’ This thought resonated and rebounded in my mind repeatedly as we practiced together in the studio and as part of my continued solo journey. As a consequence my seeing both internally and externally has been altered beyond recognition. I will attempt to record the phenomenal change I have experienced in my dance practice as a result of my dancing with new eyes, explaining how my refreshed vision has lead to my re-experiencing living and being within the dancing body.\ud I have chosen to explore, illuminate and share my investigation in a dance performance that will form 50% of this study. The chapters enclosed will act as a guide to navigate the reader through this varied and insightful journey. Each chapter, I hope will trigger a curiosity within you to notice, listen, receive and respond. By doing so you may sense colours, sounds, shifts of motion and new connections forming at a cellular/bodily level, and as part of your dialogue with the outside world.

Let $\cal C$ be a non--degenerate planar curve and for a real, positive decreasing function $\psi$ let $\cal C(\psi)$ denote the set of simultaneously $\psi$--approximable points lying on $\cal C$. We show that $\cal C$ is of Khintchine type for divergence; i.e. if a certain sum diverges then the one-dimensional Lebesgue measure on $\cal C$ of $\cal C(\psi)$ is full. We also obtain the Hausdorff measure analogue of the divergent Khintchine type result. In the case that $\cal C$ is a rational quadric the convergence counterparts of the divergent results are also obtained. Furthermore, for functions $\psi$ with lower order in a critical range we determine a general, exact formula for the Hausdorff dimension of $\cal C(\psi)$. These results constitute the first precise and general results in the theory of simultaneous Diophantine approximation on manifolds., Comment: With an Appendix by Bob Vaughan: Sums of two squares near perfect squares