Effects of chemically amended litter on broiler performances, atmospheric ammonia concentration, and phosphorus solubility in litter.

The effects of 6 different litter amendments on broiler performance, level of atmospheric ammonia (NH3) concentration, and soluble reactive phosphorus (SRP) in litter was determined. Through 3 experiments conducted on 2 different commercial farms, one chemical amendment was added to the litter and then was compared with a control. Broiler performance was not affected by any of the amendments except the ferrous sulfate amendment for which mortality was 25.5%. Application of aluminum chloride (AlCl3 x 6H2O) to the litter lowered atmospheric ammonia concentrations at 42 d by 97.2%, whereas ferrous sulfate (FeSO4 x 7H2O) lowered it by 90.77%. Ammonia concentrations were reduced by 86.18, 78.66, 75.52, and 69.00% by aluminum sulfate [alum or Al2(SO4)3 x 14H2O)], alum + CaCO3, aluminum chloride + CaCO3, and potassium permanganate (KMnO4), respectively, when compared with each control at 42 d. Each amendment except KMnO4 significantly reduced SRP contents. Alum and aluminum chloride were the effective compounds evaluated on the commercial farms with respect to reducing ammonia contents, phosphorus solubility, and mortality.

Quinoline alkaloids from the fruits of Evodia officinalis.

A new quinoline derivative, 2-hydroxy-4-methoxy-3-(3'-methyl-2'-butenyl)-quinoline and five known quinoline alkaloids were isolated from the fruits of Evodia officinalis. The structure of 1 was determined by spectroscopic methods.

Antinociceptive mechanisms of dipsacus saponin C administered intracerebroventricularly in the mouse.

1. Dipsacus saponin C (DSC) administered intracerebroventricularly (i.c.v.) showed an antinociceptive effect in a dose-dependent (from 3.75 to 30 micrograms) manner as measured by the tailflick assay. The antinociception induced by DSC at the dose of 30 micrograms was maintained at least 1 h. 2. Sulfated cholecystokinin (CCK, from 0.1 to 0.5 ng); muscimol (a GABAA receptor agonist, from 50 to 200 ng); MK-801 [(+/-)-5-methyl-10, 11-dihydro-5H-dibenzo (a,d) cyclohepten-5, 10-imine maleate, from 0.1 to 1 microgram], a noncompetitive N-methyl-D-aspartic acid (NMDA) receptor antagonist; or CNQX (6-cyano-7-nitroquinoxaline-2,3-dione, from 0.1 to 0.5 microgram), a non-NMDA receptor antagonist, injected i.c.v. significantly reduced the inhibition of the tail-flick response induced by DSC (30 micrograms) administered i.c.v. However, naloxone (an opioid receptor antagonist, 2 micrograms) or baclofen (a GABAB receptor antagonist, 10 ng) did not affect the inhibition of the tail-flick response induced by DSC. 3. The intrathecal (i.t.) injection of yohimbine (an alpha 2-adrenergic receptor antagonist, from 5 to 20 micrograms) and methysergide (a serotonin receptor antagonist, from 5 to 20 micrograms) but not naloxone (from 2 to 8 micrograms), significantly attenuated inhibition of the tail-flick response induced by DSC (30 micrograms) administered i.c.v. 4. Our results suggest that DSC has an antinociceptive effect when it is administered supraspinally and GABAA, NMDA and non-NMDA receptors, but not opioid and GABAB receptors located at the supraspinal level, may be involved in DSC-induced antinociception. Furthermore, DSC administered supraspinally may produce antinociception by stimulating descending alpha 2-adrenergic and serotonin pathways but not the opioidergic pathway.

Antinociceptive effect of smilaxin B administered intracerebroventricularly in the mouse.

We examined the antinociceptive effect of smilaxin B administered intracerebroventricularly (i.c.v.) in ICR mice. The tail-flick test was used as an analgesic assay. Smilaxin B showed a strong antinociceptive effect in a dose-dependent manner. Sulfated cholecystokinin (CCK-8s, 0.5 ng), muscimol (50ng), or MK-801 [(+/-)-5-methyl-10, 11-dihydro-5H-dibenzo [a,d]cyclohepten-5, 10-imine maleate, 1 microgram] injected i.c.v. significantly reduced inhibition of the tail-flick response induced by smilaxin B administered i.c.v. However, naloxone (2 microgram), baclofen (10 ng), or CNQX (6-cyano-7- nitroquinoxaline-2,3-dione, 0.5 microgram) injected i.c.v. did not affect inhibition of the tail-flick response induced by similaxin B administered i.c.v. The intrathecal (i.t.) injection of yohimbine (20 micrograms), but not methysergide (20 micrograms) and naloxone (2 microgram), significantly attenuated inhibition of the tail-flick response. induced by smilaxin B administered i.c.v. Our results suggest that GABAA or NMDA receptors but not opioid, GABAB, and non-NMDA receptors located at the supraspinal level may play important roles in the production of antinociception induced by smilaxin B administered supraspinally. Furthermore, smilaxin B administered supraspinally. may produce its antinociception by activating descending noradrenergic- but not opioidergic- and serotonergic-neurons.

Triterpene glycosides from the roots of Dipsacus asper.

The roots of Dipsacus asper have yielded two new triterpenoid saponins, dipsacus saponins B [1] and C [2], which have been characterized by chemical and spectral means and spectral means as hederagenin-3-O-beta-D-glucopyranosyl-(1-->4)-[alpha-L-rhamnopy ran osyl- (1-->6)]-beta-D-glucopyranosyl-(1-->3)-alpha-L-rhamnopyranosyl-(1-->2)-a lpha- L-arabinopyranoside [1] and hederagenin-3-O-beta-D-xylopyranosyl-(1-->4)- beta-D-glucopyranosyl-(1-->4)-beta-D-glucopyranosyl-(1-->3)-[alpha-L- rhamnopyranosyl-(1-->4)]-alpha-L-rhamnopyranosyl-(1-->2)-alpha-L- arabinopyranoside [2].

Steroidal saponins from the rhizomes of Polygonatum sibiricum.

Investigation of the rhizomes of Polygonatum sibiricum led to the isolation of the previously reported neoprazerigenin A 3-O-beta-lycotetraoside [3], its methyl proto-type congener 2, and two new steroidal saponins, sibiricosides A [1] and B [4]. The structures have been determined by spectral means and by comparison with literature data and authentic samples.