Clonidine given i.v. at a dose of 0.1 mg and 0.2 mg was found to cause miosis in a placebo controlled double‐blind study in six healthy volunteers. In a further single‐blind placebo controlled study in three of these volunteers, the alpha 2‐adrenoreceptor antagonist RX 781094 at a dose of 0.1 mg/kg i.v. reversed the miosis induced by i.v. clonidine 0.2 mg. At a dose of 0.05 mg/kg the miosis was partially reversed.

Among the many responses to GH administration is suppression of voluntary feed intake (FI) in some species, attributed to improvement in the efficiency of nutrient utilization and, therefore, reduced need for ingested substrates. Commercial broiler chickens have been genetically selected for generations for rapid growth, realized largely via the major correlated response of increased voluntary feed consumption. Neuropeptide Y (NPY) and monoamines play very important roles in the central regulation of feeding. Preliminary studies from our laboratory suggest that the appetite-suppressive effect of GH may be independent of its actions as a repartitioning agent, and may involve alterations in NPY expression at the pre-translational level. The purpose of this investigation was to explore the dose-response nature of the appetite-suppressive effect of GH in juvenile broilers, and the possible involvement of NPY and monoamines in this process.A GH dose-response study was conducted using 8-week-old female broilers infused i.v. with GH in a pulsatile pattern for 7 days at 0, 10, 50, 100 or 200 µg/kg body weight per day. Hypothalamic NPY and epinephrine (EP) concentrations decreased in a dose-related manner with GH. At the highest dosage, voluntary FI decreased 19% (P<0·05) and hypothalamic NPY mRNA decreased approximately 50% in the infundibular nuclei and midline region (P<0·0001). In contrast, birds pairfed to the high-GH dosage group did not differ from controls, verifying that changes in NPY and monoamines were not secondary to reduced FI. We conclude that hypothalamic NPY and EP are likely candidates to explore further as mediators of the appetite-suppressive effect of GH.

The aim of this study was to localize expression of the prostaglandin D synthase gene in the reproductive tracts of Holstein bulls using northern blotting and in situ hybridization. For northern blotting, a digoxigenin-labelled prostaglandin D synthase cDNA probe was used to probe blots containing RNA isolated from the testes, epididymides, vas deferens, ampullae, seminal vesicles, prostate and bulbourethral glands of bulls. The digoxigenin-labelled cDNA for the bovine homologue of prostaglandin D synthase hybridized to a single band (approximately 0.9 kb) to RNA samples from the caput, corpus and cauda epididymides, as well as RNA samples from the vas deferens and the ampulla. The probe also detected a single band in testis samples, although the transcript size was slightly larger (approximately 1.0 kb) than the transcript found in the other tissues. The highest expression of prostaglandin D synthase was observed in the testes and caput epididymides. Prostaglandin D synthase transcripts were not found in the seminal vesicles or the prostate or bulbourethral glands using northern blotting. For in situ hybridization, antisense and sense riboprobes were synthesized and used to hybridize to cryosections obtained from the reproductive tissues of bulls. In situ hybridization of bull testes showed that prostaglandin D synthase transcripts were present within the germ cells in the adluminal compartment of the seminiferous tubules containing round and elongated spermatids, indicating that expression varied with stage of development of the seminiferous tubules. Prostaglandin D synthase expression was observed in the epithelial cells of the epididymides with greatest expression occurring in the caput epididymidis. Some expression was also observed in the epithelial cells of the vas deferens and a few cells of some lobules in the prostate and bulbourethral glands. Expression of the prostaglandin D synthase gene was not detected in ampullae or seminal vesicles by in situ hybridization.

In clinical practice, the assessment of nutritional status in children can be problematic. More than one indicator is often required: these may include anthropometric measurements, body compartment analysis and biochemical markers. The nutritional status of children at the time of admission to hospital can impact adversely on their hospital stay. Furthermore, children's medical conditions may also impact upon their nutrition during a hospital stay. In recent years a number of Nutrition Risk Screening (NRS) tools have been developed and validated, with the goals of providing rapid assessment of children's risk of nutritional change during a hospitalisation. This article reviews the current NRS tools, considers their benefits and shortcomings and evaluates the potential roles of these tools.

y b o t h a s an a n t i -e m e t i c and a l s o t o i n c r e a s e t h e r a t e o f g a s t r i c emptying ( P i n d e r g! o t h e r s , 1 9 7 6 ) . The a n t i -e m e t i c e f f e c t o f metoclopramide is p r o b a b l y r e l a t e d t o i t s a c t i o n i n b l o c k i n g dopamine r e c e p t o r s ( p e r i n g e r & o t h e r s , 1975; Day & Blower, 1 9 7 5 ) . However, t h e mechanism o f i t s a c t i o n on t h e g a s t r o i n t e s t i n a l t r a c t i s n o t c l e a r and a number of p o s s i b i l i t i e s have been s u g g e s t e d ( f o r review see P i n d e r & o t h e r s , 1 9 7 6 ) . I n t h e p r e s e n t i n v e s t i g a t i o n t h e a c t i o n o f metoclopramide h a s been examined on t h e smooth muscle o f t h e r a t g a s t r i c fundus p r e p a r a t i o n (Vane, 1957) i n which t h e i n t r i n s i c n e u r a l e l e m e n t s have been a c t i v a t e d by e l e c t r i c a l f i e l d s t i m u l a t i o n . F i e l d s t i m u l a t i o n s were a p p l i e d f o r t r a i n s o f 100 p u l s e s o f supramaximal s t r e n g t h (140 v o l t ) and 2 m.sec p u l s e w i d t h a t f r e q u e n c i e s o v e r t h e r a n g e 0 . 5 t o 20 H e r z . The r e s p o n s e s t o f i e l d s t i m u l a t i o n i n c o n t r o l p r e p a r a t i o n s were f r e q u e n c y -r e l a t e d c o n t r a c t i o n s which were p o t e n t i a t e d by n e o s t i g m i n e (10-100 ng/ml) o r e s e r i n e (10-100 ng/ml) and were a b o l i s h e d by e i t h e r t e t r o d o t o x i n (1 ug/ml) o r a t r o p i n e (20 t o 100 ng/ml). I t was c o n c l u d e d t h a t t h e c o n t r a c t i l e r e s p o n s e s were mediated v i a a c t i v a t i o n o f c h o l i n e r g i c n e r v e e l e m e n t s i n t h e muscle. Metoclopramide ( 1 t o 10 ug/ml) i n c r e a s e d t h e r e s p o n s e s to c h o l i n e r g i c n e r v e s t i m u l a t i o n a t a l l f r e q u e n c i e s of s t i m u l a t i o n a l t h o u g h t h e e f f e c t w a s most marked o v e r t h e f r e q u e n c y r a n g e 0 . 5 t o 2 Herz; r e s p o n s e s to added a c e t y l c h o l i n e (1 t o 5 0 ng/ml) were n o t s i g n i f i c a n t l y changed by metoclopramide. The p o s s i b i l i t y w a s i n v e s t i g a t e d t h a t metoclopramide was i n c r e a s i n g r e s p o n s e s t o c h o l i n e r g i c n e r v e s t i m u l a t i o n by b l o c k i n g e i t h e r i n h i b i t o r y n o r a d r e n e r g i c o r " p u r i n e r g i c " ( B u r n s t o c k , 1972) nervous e l e m e n t s a l s o a c t i v a t e d by f i e l d s t i m u l a t i o n . The s y m p a t h e t i c component of t h e f i e l d s t i m u l a t i o n r e s p o n s e s w e r e a b o l i s h e d by e i t h e r p h e n t o l a m i n e ( 1 t o 3 ug/ml) or b e t h a n i d i n e ( 1 t o 20 pg/ml) which r e s u l t e d i n a s m a l l i n c r e a s e i n t h e c o n t r a c t i l e r e s p o n s e s b u t d i d n o t p r e v e n t t h e u s u a l enhancement o f t h e r e s p o n s e s i n t h e p r e s e n c e o f...