Kainic acid is a linear competitive inhibitor (Kis 250 μm) of the ‘high affinity’ uptake of l‐glutamic acid into rat brain slices. Kainic acid inhibits the ‘high affinity’ uptake of l‐glutamic, d‐aspartic and l‐aspartic acids to a similar extent. Kainic acid is not actively taken up into rat brain slices and is thus not a substrate for the ‘high affinity’ acidic amino acid transport system or any other transport system in rat brain slices. Kainic acid (300 μm) does not influence the steady‐state release or potassium‐stimulated release of preloaded d‐aspartic acid from rat brain slices. Kainic acid binds to rat brain membranes in the absence of sodium ions in a manner indicating binding to a population of receptor sites for l‐glutamic acid. Only quisqualic and l‐glutamic acid inhibit kainic acid binding in a potent manner. The affinity of kainic acid for these receptor sites appears to be some 4 orders of magnitude higher than for the ‘high affinity’l‐glutamic acid transport carrier. Dihydrokainic acid is approximately twice as potent as kainic acid as an inhibitor of ‘high affinity’l‐glutamic acid uptake but is some 500 times less potent as an inhibitor of kainic acid binding and at least 1000 times less potent as a convulsant of immature rats on intraperitoneal injection. Dihydrokainic acid might be useful as a ‘control uptake inhibitor’ for the effects of kainic acid on ‘high affinity’l‐glutamic acid uptake since it appears to have little action on excitatory receptors. N‐Methyl‐d‐aspartic acid is a potent convulsant of immature rats, but does not inhibit kainic acid binding or ‘high affinity’l‐glutamic acid uptake. N‐Methyl‐d‐aspartic acid might be useful as a ‘control excitant’ that activates different excitatory receptors to kainic acid and does not influence ‘high affinity’l‐glutamic acid uptake.
The findings are presented of a conference on Outcomes of Hand Surgery organized by the audit committee of British Society for Surgery of the Hand in 1993. Measures of outcome in terms of movement, power, sensibility, pain, activities of daily living, complications and patient satisfaction are considered, and an example of a patient evaluation measure given as an appendix.
SummaryVariation in flowering time and response to overwintering has been exploited to breed brassica vegetables that can be harvested year‐round. Our knowledge of flowering time control now enables the investigation of the molecular basis of this important variation. Here, we show that a major determinant of heading date variation in Brassica oleracea is from variation in vernalization response through allelic variation at FLOWERING LOCUS C.C2 (BoFLC4). We characterize two alleles of BoFLC.C2 that are both functional and confer a requirement for vernalization, but they show distinct expression dynamics in response to cold. Complementation experiments in Arabidopsis thaliana revealed that the allelic variation results from cis polymorphism at BoFLC.C2, which quantitatively influences the degree of cold‐induced epigenetic silencing. This results in one allelic variant conferring consistently later heading under both glasshouse and field conditions through reduced environmental sensitivity. Our results suggest that breeding of brassica varieties for commercially valuable variation in heading date has been achieved through the selection of cis polymorphism at FLC, similar to that underpinning natural variation in A. thaliana. This understanding will allow for the selection of alleles with distinct sensitivities to cold and robust heading dates under variable climatic conditions, and will facilitate the breeding of varieties more resistant to climate change.
A specialist nurse-led, one-stop TWR clinic for suspected colorectal cancer is sustainable and can be run successfully with over 90% of referrals seen within the targeted time period. The proportion of non-conforming referrals was high and a large number of advanced and unstaged tumours was observed. Low numbers of proximal tumours were detected.
Abstract— The GABA analogue, muscimol, was taken up relatively inefficiently compared to GABA by slices of rat cerebral cortex at 37 C. Muscimol uptake followed saturation kinetics (Km ImM. Vm 0.1 μmol g mini and showed an absolute dependence on sodium ions. The relative susceptibilities of muscimol uptake and GABA high affinity uptake to a variety of inhibitors, including (‐)‐nipecotic acid. (+)‐2.4‐diaminobutyric acid and arecaidine, and the stimulation of muscimol efflux by 50μM‐GABA, suggest that muscimol and GABA share some common transport carriers. Since L‐histidine inhibited muscimol uptake hut not GABA high affinity uptake, at least part of the observed muscimol uptake may be mediated by the 'small basic’amino acid transport system. Muscimol appeared to he taken up into nerve terminals, since uptake was inhibited by the neuronal uptake inhibitor cis‐3‐aminocyclohexanecarboxylic acid but not by the glial uptake inhibitor β‐alanine. Muscimol efflux was stimulated in a calcium‐dependent manner by an increased potassium ion concentration. Sodium‐independent binding of muscimol was observed in slices of rat cerebral cortex at 4 C. Binding could be inhibited by a variety of substances. including GABA, isoguvacine and (+)‐bicuculline methochloride, which are known to inhibit the binding of muscimol to putative GABA receptors associated with synaptic membranes purified from rat brain.
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