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Bobby Jon goes down to one knee and Tom presses his advantage. Tom gets under Bobby Jon's pillow-cushion-bag-thing and lifts the boy off balance, tipping him over the side and into the water. Koror is up 5-2, and it's match point. Steph and Jenn meet again, but Jenn has learned a thing or two. Steph has the early advantage, but Jenn pushes back hard. Steph loses her footing and has to circle out of Jenn's reach. Steph tries to end the match quickly with a decisive shove, but Jenn hangs on by her toes. Jenn regains her balance and drives forward, pushing Steph back toward the edge; from somewhere deep inside, Steph finds a reserve of strength and gives Jenn a mighty push, knocking the smaller girl off her feet. Jenn crawls back up, and Steph knocks her down again. Jenn comes up a second time and goes after Steph for all she's worth, then Steph does the smartest thing I've seen her do in this whole game: She steps aside. She takes one step to her left and let's Jenn's momentum carry her toward the edge. Jenn drops to her hands and knees to try to keep from falling off, but the match is basically over at this point. Steph gives Jenn one last, definitive push, and Ulong begins to crawl back, 5-3. Gregg and Ibrehem meet again. Last time Gregg was able to take the initiative and batter Ibrehem off the platform. Not this time. As soon as Probst says "Go, " Ibrehem explodes into Gregg, translating every ounce of body weight into momentum, in one massive move shoving Gregg off the platform, into the air, and down into the water. Ulong is now only down by one point: 5-4. Starbuck and Caryn are back for their rematch. We know how this went down last time, and we expect nothing to change this time. Starbuck owns Caryn from the very first instant of the match, shoving the older woman off with no particular fuss. We're tied at match point: 5-5. The next bout will decide who wins the day. The literature on antitussive treatments is problematic because efficacy of these agents appears to depend on the cause of the cough. Acute or early cough due to colds or other viral upper respiratory tract infections does not appear to respond to dextromethorphan or codeine, whereas chronic cough 3 weeks' duration ; , cough associated with underlying lung disease, or experimentally induced cough appears to respond to these two agents. For patients with uncomplicated acute bronchitis for whom the average duration of cough is 2 to weeks ; , cough preparations containing dextromethorphan or codeine probably have a modest effect on cough severity and duration during the protracted phase of illness. Propofol has a high brain to blood concentration ratio5 with brain concentrations of 220 mol g1 recorded in the rat for plasma propofol concentrations of 29 mol litre1. We used a concentration of propofol 100 mol litre1 ; that, while below peak brain concentrations achieved, nonetheless represented a typical brain concentration after i.v. propofol anaesthesia in the rat. It is worth remembering that propofol is highly protein bound and thus the concentration at the active site s ; may be considerably lower. The experiments were predicated upon the hypothesis that propofol might block presynaptic D2 receptors, increasing dopamine release and thus explaining its apparent abuse potential. We have recently demonstrated that ketamine markedly increases dopamine release in the rat nucleus accumbens.4 Propofol decreased dopamine release, an effect suggesting an agonist action at D2 receptors. Certainly, propofol binds to D2 receptors, albeit weakly.3 However, metoclopramide did not block the propofol response at a concentration that rapidly increased dopamine release and has been shown in this laboratory to block autoreceptor stimulation. Thus propofol, at this concentration, has no detectable D2 agonist or antagonist activity on presynaptic D2 receptors in the rat nucleus accumbens. Furthermore, Appadu, Strange and Lambert3 showed that propofol, at typical serum concentrations, occupies no more than 15% of D2 dopamine receptors. Propofol is known to potentiate GABA-mediated synaptic inhibition and this might underlie its effect on dopamine release. However, failure of bicuculline, the specific GABAA receptor antagonist, to block propofol suggests that a GABAA agonist action does not mediate the observed effects. Propofol causes inhibition of NMDA receptors in vitro6 and this may mediate the hallucinations observed after propofol anaesthesia. However, although dextromethorphan itself decreased dopamine release, it was unable to block the action of propofol at a concentration known to block NMDA-mediated responses in vitro.7 The absence of involvement of D2, GABAA and NMDA receptors may suggest that the action of propofol is mediated via less specific mechanisms, such as calcium and sodium channels. Voltage-sensitive calcium channels can perhaps be excluded. Although propofol can block L- and T-type calcium channels, 8 9 we have shown that forebrain dopamine release is mainly under the control of N- and P Q-type calcium channels Phillips and Stamford, unpublished data ; . More likely is the involvement of sodium channels. Propofol has been shown to inhibit glutamate release evoked by 4-aminopyridine and veratridine but not by potassium.10 It is possible that the same phenomenon may apply to dopamine release. In summary, we found that propofol inhibited dopamine release in the rat nucleus accumbens in a manner dependent neither on D2, GABAA nor NMDA receptors. We suggest.

The information questions for the given examples are different. Wh-questions involve a proposition that is almost entirely presupposed except for one element Givn 1990: 714 ; . The response represents new information in the declarative correspondent sentence. i ; He runs as fast as I do. How fast does he run? quantification ; ii ; He runs exactly like me. How does he run? manner ; In text, adverbial arguments, such as manner, may attract the focus of new information. Givn 1984: 260 ; claims that when an optional adverbial is added to a clause it becomes the most salient communicatively cf. note 6 ; . 4 According to Stassen 1985: 105 ; , the linguistic codification of comparison is modelled on the concept of temporal chaining. From a cognitive point of view, the mental act of comparison must be seen as a conceptual extension of the mental operation by which two events are ordered with respect to their occurrence in time. Thus, comparison is a cognitive metaphor of temporal chaining, by which the mind establishes 'the relation between two events, A and B as overlapping, preceding or following each other' Traugott 1975: 208 ; . Stassen 1985: 59 ; points out that ".the result of this mapping into language is a temporal chain, i.e. a semantic configuration in which two tensed propositions are presented successively." Co-ordination is an example of syntactic temporal chaining, i.e. the formal linguistic correlate of the semantic chaining of propositions.

Staining in a radiating fashion Zackrisson et al., 1996 ; may represent infolding of theca-derived cells. This may correspond to the relatively dominating expression of eNOS to the theca lutein layer of the human CL, as found in the present study. In the human CL there is a higher quantity of precapillary NO-responsive vessels in this region. In luteinized tissue from hypophysectomized DES-treated rats, immunohistochemistry revealed that endothelial cells, and some of the parenchymal luteal cells, express NOS Olson and Jones-Burton, 1996 ; . This fits with our findings of immunoreactive eNOS in theca lutein cells. It also supports a recently published study Vega et al., 1998 ; , which shows the presence of eNOS in large luteal-like cells in human CL tissue. Taken together, the results of the present and other studies indicate that a subpopulation of the luteal cells in both the rat and the human CL express NO. These cells can by autocrine paracrine mechanisms influence most of the cells in the CL. The immunoblotting experiments suggested that the highest concentrations of eNOS are found during the late luteal phase, indicating a functional role for eNOS during this phase. A similar increase of eNOS protein concentrations during the later stages of the luteal phase was seen in the eCG HCG rat model, where maximal concentrations were seen during days 911 of the induced luteal phase Van Voorhis et al., 1995; Zackrisson et al., 1996; Jablonka-Shariff and Olson, 1997 ; . However, maximal eNOS mRNA expression, as assessed by quantitative reverse transcriptionpolymerase chain reaction RTPCR ; , was observed during the early and mid-luteal phases with an ~50% reduction during late luteal phase Vega et al., 1998 ; . The different time profiles of eNOS protein and mRNA expression can be explained by variations in posttranscriptional processing during the various stages of the luteal phase and also to the methodological difficulties involving quantitative RTPCR. Interestingly, eNOS was barely detectable in the regressing CL obtained during the next follicular phase, either by immunoblotting or by immunohistochemistry. This suggests that NOS activity, particularly that of eNOS, may be important only during the functional luteal phase. The vascularity of the CL changes throughout its life with maximal capillary networks Gaytan et al., 1999 ; during the mid-luteal phase. Since the number of endothelial cells and vasculature in the CL decrease during the late luteal phase Gaytan et al., 1999 ; when eNOS expression is elevated, it is possible that a considerable increase in eNOS expression takes place in the CL cells during this period of development. Inducible NOS appeared to be present in lower quantities in all CL studied by immunoblotting and immunohistochemistry techniques. The protein concentrations did not display any marked cycledependent changes. These findings are in line with earlier reports of expression of iNOS protein in the external layers of developing rat CL and also to a larger degree throughout the degenerating CL in the rat Jablonka-Shariff and Olson, 1997 ; . Inducible NOS has also been demonstrated in luteinized ovarian cells in vitro Olson and Jones-Burton, 1996 ; , confirming other studies in the rat Zackrisson et al., 1996 ; . The advantage of detection of immunoreactive protein is emphasized by earlier studies being unable to demonstrate iNOS mRNA in the rat CL Van Voorhis et al., 1995 ; . 401 and diamox.

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