Characterization of Autographa californica multiple nucleopolyhedrovirus ORF17.

The expression of Autographa californica multiple nucleopolyhedrovirus (AcMNPV) ORF17 was examined. The respective transcript of 492 nts could be detected by RT-PCR at 3-72 hrs p.i., while the corresponding protein could be assessed by Western blot analysis at 6-72 hrs p.i. Its size was determined at about 19 K in agreement with the predicted value of 18.5 K, suggesting that no major posttranslational modification of primary gene product. The ORF17 protein was primarily located in the cytoplasm. All these results together with earlier data on early AcMNPV promoter motifs suggest that ORF17 as an early gene encoding a protein located in the cytoplasm of infected cells.

Visualization method for fingerprints on skin by impression on a polyethylene terephthalate (PET) semirigid sheet.

Based on the phenomenon that static electricity attracts dust, a polyethylene terephthalate (PET) semirigid sheet coated with printing ink was used to visualize impressions of fingerprints on the skin of living and dead bodies. Compared with visualization methods for perspiration fingerprints, this method recovers better images for a longer time after the fingerprint has been deposited on skin. Fingerprints transferred to the PET sheet are photographed with sidelighting using an ordinary light source. For fingerprints that yield inadequate contrast, an argon-ion laser can be used to improve the contrast.

Mesolimbic dopamine mediates gastric mucosal protection by central neurotensin.

Bilateral microinjection (1.0 microliter/side) of neurotensin (NT; 0.3, 1.5, and 3.0 micrograms/side) into the nucleus accumbens (NACB) and ventral tegmental area (VTA) but not in substantia nigra and striatum reduced gastric mucosal injury produced by 2 h of cold-water restraint (CWR). The minimal effective dose for NT-induced protection was 10-100 times lower when administered directly into NACB than into the lateral ventricle. These effects were blocked by pretreatment with the dopamine (DA) receptor antagonist, haloperidol (Hal; 0.5 microgram/side) given directly into NACB. Injection of 6-hydroxydopamine into VTA depleted endogenous DA and inhibited gastric mucosal protection against CWR-induced injury afforded by NT pretreatment. NT, given into either VTA and NACB, inhibited pentagastrin-stimulated gastric acid secretion. These results suggest that VTA and NACB, which represent the mesolimbic DA system, are important locations for interaction between NT and DA receptors to produce gastric mucosal protection against CWR-induced injury.

Effect of neurotensin on regional cerebral glucose utilization in cold water-restrained rats.

Neurotensin (NT), given intracerebroventricularly (icv), attenuates cold water restraint (CWR)-induced gastric mucosal injury; however, it is not clear which brain nuclear group or groups are involved. These studies tested the hypothesis that neuronal function, as measured by regional cerebral metabolic rate for glucose (rCMRGlc), is altered by icv NT with or without CWR. CWR resulted in a reduced global glucose utilization of 72 and 65% in control and NT-treated rats, respectively. NT, given icv, protected against ulcer formation induced by CWR. In those rats given NT icv, rCMRGlc was elevated significantly in amygdala, nucleus accumbens, substantia nigra, tuberculum olfactrium, hypothalamus, and cerebellum compared with CWR rats without NT pretreatment. This rCMRGlc increase was observed in both unstressed and stressed rats given NT icv in the nucleus accumbens and amygdala. These observations suggest that the nucleus accumbens and amygdala, both components of the mesolimbic dopamine system, are involved in the central action of NT on the gastric mucosa.

Monoamine oxidase B inhibition reduces gastric mucosal blood flow, basal acid secretion, and cold water restraint-induced gastric mucosal injury in rats.

Inhibition of monoamine oxidase B (MAO B) by selective inhibitors pargyline and L-deprenyl increases dopamine (DA) and norepinephrine (NE) concentrations in nucleus accumbens (NACB) and is associated with reduction in cold water restraint-induced gastric mucosal injury, inhibition of basal gastric acid output, and regional gastric mucosal blood flow. Similar effects were not observed with administration of MAO A inhibitors. These observations suggest that activation of central dopamine and norepinephrine receptors, particularly in NACB, are involved in the control of gastric mucosal function.

Central neurotensin inhibits gastric acid secretion: an adrenergic mechanism in rats.

Although parenteral neurotensin (NT) inhibits stimulated gastric acid secretion, published reports on the effect of centrally administered NT on gastric acid secretion are conflicting. This study provides evidence suggesting that, in chronic gastric fistula rats, intracerebroventricularly administered NT (15-60 micrograms) significantly reduces both basal and pentagastrin-, 2-deoxy-D-glucose-, and carbachol-but not histamine-stimulated gastric acid secretion. Using radioimmunoassay, the concentration of plasma immunoreactive NT increased from 30 to 200 pg/ml at 30 and 60 min, respectively after a single intracerebroventricular (i.c.v.) administration of NT at a dose of 60 micrograms. These serum NT concentrations can be reproduced by a constant NT i.v. infusion at 2 micrograms/kg.h. This parenteral infusion dose does not inhibit acid secretion as does i.c.v. NT. Pretreatment with the i.c.v. dopamine-2 receptor antagonists haloperidol or domperidone totally abolishes the inhibitory effect of i.c.v. NT on pentagastrin-stimulated gastric acid secretion. In contrast, pretreatment with the specific dopamine-1 receptor antagonist SCH 23900 or the specific dopamine-2 receptor antagonist sulpiride does not affect i.c.v. NT-induced inhibition of pentagastrin-stimulated gastric acid secretion. Pretreatment (intracerebroventricularly) with the alpha-adrenergic antagonist phentolamine blocks the antisecretory effect of i.c.v. NT. Administration of 3.0 micrograms NT per side directly into nucleus accumbens (NACB), using a stereotaxic technique, significantly reduces basal gastric acid secretion. This effect of central NT is blocked by pretreatment with intra-NACB haloperidol (0.5 microgram per side). These findings suggest that NT acts centrally to inhibit gastric acid secretion, an effect that may occur within NACB and be mediated by central nervous system alpha-adrenergic receptor activation.

Effect of furazolidone on gut catecholamine in cysteamine-induced duodenal ulcer in the rat.

The effect of furazolidone, a monoamine oxidase (MAO) inhibitor, on cysteamine-induced duodenal ulcer and gut catecholamines was studied in rats, since previous reports have suggested protective effects of MAO inhibitors against other forms of experimental mucosal injury. Furazolidone (100 mg kg-1, orally) pretreatment significantly reduced the frequency and severity of cysteamine-induced duodenal ulcer. By means of a spectrofluorometric technique, gastric and duodenal norepinephrine concentrations and duodenal dopamine concentrations were measured and found to be increased in animals treated with the MAO inhibitor. It is concluded that the protective effect of furazolidone against cysteamine-induced duodenal ulcer may in part be related to modulation of gut norepinephrine and dopamine concentrations.