68 research outputs found
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No full textTo show various forms of equivalence between programs Correctness of optimization � p opt ∼ p unopt: τ Secrecy as non-interference � p v ∼ p w: τ for v ≠ w Correspondence between CPS and direct style � p CPS ∼ p DS: τ This Talk Logical relations for wider range of programming constructs Perfect encryption [Sumii-Pierce 01] Cf. Type abstraction [Reynolds 83] Higher-order references [ongoing work] First-class channels [ongoing work] Everything is syntactic and operationa
Effect of histamine on rat gastric H(+)-K(+)-ATPase alpha-subunit expression
No full text The H(+)-K(+)-adenosinetriphosphatase (ATPase) is expressed in the parietal cell and is responsible for acid secretion by the stomach. Histamine binds to an H2 receptor and activates adenylate cyclase and intracellular calcium concentration ([Ca2+]i) elevation, stimulating acid secretion. It has been shown that omeprazole administered to rats increases serum gastrin and transiently increases the level of mRNA for the alpha-subunit of the pump, but this increase is blocked by the presence of the H2-receptor antagonist, famotidine [A. Tari, G. Yamamoto, K. Sumii, M. Sumii, Y. Takehara, K. Haruma, G. Kajiyama, V. Wu, G. Sachs, and J. H. Walsh. Am. J. Physiol. 265 (Gastrointest. Liver Physiol. 28): G752-G758, 1993]. These observations suggest that the release of histamine induced by gastrin is essential for the increase of the expression of mRNA induced by omeprazole. Infusion of histamine at 15 mumol.kg-1.h-1 i.v. for 1 h increased the alpha-subunit mRNA level by 144 +/- 2.4% and induced a stimulated morphological appearance of the parietal cell. These changes were inhibited completely by the competitive H2-receptor antagonist famotidine, which elevated gastric pH and serum gastrin. Famotidine also reduced the level of H(+)-K(+)-ATPase mRNA compared with control animals. No change in the expression of beta-actin mRNA was observed in any group of animals. These data provide direct evidence for histamine stimulation of H(+)-K(+)-ATPase alpha-subunit gene expression by activation of the H2 receptor. </jats:p
Abstract An Implementation of Transparent Migration on Standard Scheme
No full textI present a handy (though somewhat restrictive) way to implement mobile computation à la Telescript on top of standard Scheme. Background. Mobile computation is an efficient and effective approach to distributed programming where a program works by migrating from one host to another. The migration is called transparent if the execution state of the program is preserved before and after the migration. Transparent migration is preferable to non-transparent, because it is easier to use for application programmers. At the same time, however, it is harder to implement for language developers: all existing implementations (to my knowledge) of transparent migration need either a custom runtime system (e.g. [13]) or global source code transformation (e.g. [12]). Our Method. In this presentation, I describe a library to enable transparent migration in standard Scheme. Unlike existing implementations, it requires neither modification of the runtime system nor transformation of the source code. It works by (i) extracting a delimited continuation [5, 6] with control operators (shift and reset), (ii) reifying the delimited continuation—i.e., reconstructing its source code— with type-directed partial evaluation (TDPE) [2, 4], and (iii) evaluating the source code at the remote host (e.g. by invoking ssh). Assuming the function shift for delimitedcontinuation extraction and the operator ↓ for TDPE, the main part of the library looks like: (define (go rhost) (shift (lambda (k) ; extract the delimited continuation (let ([e ( ↓ ()→() k)]) ; reconstruct its source code (reval e rhost))))) ; remotely evaluate the source code Note that the delimited continuation k has the type () → (), because the transparent migration operator go works as a side effect. Since TDPE itself uses control operators, the library actually uses layered control operators [8]. For details of (layered) delimited continuations and TDPE, see Appendix A and B, respectively. Example 1. Consider the following program. (In the examples, we use the non-standard procedure system for the sake of convenience.
Role of histamine2 receptor in increased expression of rat gastric H(+)-K(+)-ATPase alpha-subunit induced by omeprazole
No full text Omeprazole is a specific inhibitor in vivo of the functioning gastric acid pump, the H(+)-K(+)-adenosinetriphosphatase (ATPase), in the secretory canaliculus of the parietal cell. It has been shown previously that omeprazole in rats led to an increase in the mRNA for the alpha-subunit of the H(+)-K(+)-ATPase. Omeprazole causes a marked increase in circulating gastrin in this species, which in turn stimulates release of histamine from the enterochromaffin-like cell. The possible role of this pathway was investigated by the in vivo administration of famotidine, a potent H2 receptor antagonist. A single intraperitoneal dose of famotidine, 200 mg/kg, produced a transient hypergastrinemia peaking at 3 h and normalizing at 12 h, inhibition of secretion that lasted for 12 h, but no change in the level of the alpha-subunit mRNA or of beta-actin mRNA. In contrast, a single dose of omeprazole,xs 100 mg/kg, inhibited acid secretion and produced hypergastrinemia, peaking at 12 h, both effects lasting for the 24-h observation period. Omeprazole elevated the alpha-subunit mRNA transiently by more than threefold at 3 h, with normal levels being restored at 24 h. The administration of famotidine 1 h after omeprazole did not change the effects of omeprazole on acid secretion but elevated the gastrin levels further. There was now no elevation of the alpha-subunit mRNA for the first 6 h, but a small increase at 12 h and a further increase to approximately 2.5-fold at 24 h.(ABSTRACT TRUNCATED AT 250 WORDS) </jats:p
Semantics for Prolog with Cut – Revisited
No full textThis paper revisits the semantics for Prolog with cut from the perspective of formulating a semantic base that is amenable to abstract interpretation. It argues that such a semantics should separate the question of divergence from questions pertaining to the number of answers and determinacy. It also shows how to replace prefix ordering, that is classically used in these semantics, with a domain that is setup for abstraction, whilst simultaneously retaining a fixpoint construction, albeit one in a stratified form
Evidence that endogenous GRP in rat stomach mediates omeprazole-induced hypergastrinemia
No full text To investigate the physiological role of endogenous gastrin-releasing peptide (GRP) in regulating the release of gastrin, we evaluated the response of intragastric pH, gastrin, and GRP after omeprazole treatment in rats. A significant elevation of the plasma level of GRP (P< 0.01) and a significant reduction of the antral content of GRP (P <0.05) were observed after the administration of 100 mg/kg omeprazole. The antral content of GRP was significantly decreased 12 h after omeprazole administration and thereafter gradually returned to control levels. Peak values for intragastric pH and plasma GRP were observed 3 h after omeprazole administration and before the peak of serum gastrin. The bombesin antagonist [D-Phe6]-bombesin-(6,13)-methyl ester significantly inhibited gastrin release after omeprazole treatment (P < 0.05). These observations indicate that omeprazole-induced inhibition of acid secretion stimulates the release of GRP and suggest that the secretion of GRP induced by omeprazole may stimulate the secretion of gastrin, at least in the early phase. </jats:p
Intracellular signal transduction systems do not regulate Na channel in frog ventricular cells
No full text The regulation of sodium channel activity through intracellular signal transduction systems was studied on isolated frog ventricular cells using a whole cell patch-clamp technique. Special care was exercised in evaluating the stability of the voltage-clamp condition by observing shifts in the steady-state inactivation curve (h infinity curve) and changes in series resistance. We applied the following reagents: isoproterenol (Iso; 0.1–10 microM) and forskolin (Fsk; 0.1–10 microM) to activate protein kinase A. 1-Oleoyl-2-acetyl-sn-glycerol (40 microM) and 12-O-tetradecanoylphorbol-13-acetate (80-800 nM) were used to activate protein kinase C, and phenylephrine (0.1–10 microM), dopamine (0.1-10 microM), and histamine (10 microM) were used to stimulate alpha-adrenergic, dopaminergic, and histaminergic receptors, respectively. The current-voltage relationship and the h infinity curve for the sodium channel remained unchanged regardless of the application of these reagents. Iso and Fsk did not affect the sodium current but substantially increased the calcium current, suggesting that the intracellular signal transduction systems remained intact. Therefore, it is concluded that sodium channel in frog ventricular cells is not regulated by intracellular signal transduction systems. </jats:p
Clinicoprognostical features of endometrial cancer patients with somatic mtDNA mutations
No full textSomatic mitochondrial DNA (mtDNA) mutations
have been found in a subset of endometrial cancers (EC) from
different populations. We have investigated the relationship
between mtDNA changes and clinical and pathological
variables of women affected by EC. mtDNA mutations were
detected both in early (3/32; 9%) and in advanced (1/8;
12%) stages of uterine tumors. However, patients carrying
the mtDNA mutations or the normal mtDNA sequence had
indistinguishable clinicopathological data, including age,
clinical stage, histological grade and type or depth of myometrial
invasion. It is noteworthy that mtDNA mutations
were not detected in hyperplastic endometrial tissues or in
ECs coexisting with hyperplasia, nor in a single case of
endometrial stromal sarcoma. LOH at the tumor suppressor
genes RB1 and TP53 as well as p16INK4A alterations (LOH,
gene deletion) were found in tumors carrying mtDNA
mutations. These results suggest that somatic mtDNA
mutations are detected in a subset of ECs, although they are
unrelated to clinicopathological variables of cancer
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