Effect of lesion age, humidity, and fungicide application on sporulation of Alternaria alternata, the cause of brown spot of tangerine

Alternaria brown spot, caused by Alternaria alternata, causes yield losses and fruit blemishes on many tangerines and their hybrids in most citrus areas of the world where susceptible cultivars are grown. Although the conditions affecting infection and disease severity are known, little information is available on inoculum production on infected tissue. We found that sporulation on leaves began about 10 days after symptoms developed, was abundant from 20 to 40 days, and declined thereafter. Conidial production was far greater on leaf than on fruit or twig lesions. Spore production per unit area of leaf lesion was greater on the more susceptible hybrids, Minneola and Orlando tangelos, than on the less susceptible Murcott tangor. At 74% relative humidity, conidial production on leaf lesions was low, but it was abundant at 85, 92.5, 96, and 100%. Application of Q(o)I or copper fungicides, but not ferbam, suppressed sporulation on leaf lesions for about 14 to 21 days after application. Additional applications did not appear to be more effective than a single spray in reducing inoculum production.

HIGH DIETARY CARBOHYDRATE AND PANCREATIC LESION

The ability of high dietary carbohydrate to induce acute pancreatitis was investigated in groups of 16,2 1-day and 15-month old rats fed different carbohydrate diets for 30 days. Significantly increased levels of serum amylase (2-fold), phospholipids (50%),phosphorus (2-fold), and lipoperoxides (8-fold) were observed in 15-month old rats fed a high-carbohydrate diet, compared to rats fed a diet with normal carbohydrate levels, indicating peroxidation of membrane lipids which caused final cell death and pancreatic lesion. Serum Cu-Zn superoxide dismutase activity was not altered. Daily administration of bovine Cu-Zn superoxide dismutase conjugated with polyediylene glycol prevented the serum level alterations and pancreatic lesions, indicating that the superoxide radical has a role in dietary carbohydrate-induced acute pancreatitis. No biochemical changes were observed in rats in which treatment was initiated on the 21st day of life indicating that this is an age-related lesion.

EFFECT OF ELECTROLYTIC AND CHEMICAL LESION BY IBOTENIC ACID OF THE AMYGDALA ON SALT INTAKE

Sodium chloride intake was studied in male Holtzman rats weighing 250-300 g submitted to electrolytic and chemical lesion of the cell bodies, not fibers of the amygdaloid complex. Sodium chloride (1.5%) intake increased in animals with electrolytic lesion of the corticomedial nucleus of the amygdala. Sodium chloride (1.5%) intake increased after ibotenic acid injection into the corticomedial nucleus of the amygdala to a larger extent (26.6 +/- 9.2 to 147.6 +/- 34.6 ml/5 days). The results indicate that sodium intake response can be induced by lesions, which involved only cell bodies. The fibers of passage of the corticomedial nucleus of the amygdala produce a water intake less consistent than that induced by ibotenic acid, which is more acute. The results show that cell bodies of this region of the amygdala are involved in the control of sodium chloride intake.

EFFECT OF TESTOSTERONE ON THE PRESSOR-RESPONSE TO COMMON CAROTID OCCLUSION IN GONADECTOMIZED CONSCIOUS MALE-RATS WITH LESION OF THE MEDIAN-EMINENCE

The influence of testosterone on the development of the pressor response to common carotid occlusion was investigated in control and median eminence-lesioned male rats. In control rats (N = 9), gonadectomy performed 21 days before the experiments reduced by 22% (from 51 +/- 2 to 40 +/- 2 mmHg) and treatment with testosterone (300-mu-g for 4 days before the measurements) increased the initial peak pressor response (from 51 +/- 2 to 57 +/- 2 mmHg) which depends on carotid innervation. The maintained response which is of central origin (probably ischemic) was less affected. In nongonadectomized rats (N = 6), lesions of the median eminence (6 days) decreased the initial peak by 19% (from 52 +/- 2 to 42 +/- 3 mmHg) and the maintained response by 56% (from 32 +/- 2 to 14 +/- 1 mmHg). Sham-operated rats served as controls. In gonadectomized animals (N = 6) the lesion reduced only the maintained response (from 23 +/- 2 to 11 +/- 1 mmHg). Testosterone supplementation restored the maintained response but did not alter the initial peak. These results indicate that the pressor response to common carotid occlusion in male rats is modulated by testosterone and that the depression in the maintained response caused by median eminence lesion can be reversed by steroid supplementation.

AV3V LESION REDUCES THE PRESSOR, DIPSOGENIC, AND NATRIURETIC RESPONSES TO VENTROMEDIAL HYPOTHALAMUS ACTIVATION

In the present study, we investigated the effect of anteroventral third ventricle (AV3V) lesion on pressor, tachycardic, dipsogenic, natriuretic, and kaliuretic responses induced by the injection of the cholinergic agonist carbachol into the ventromedial hypothalamic nucleus (VMH) of rats. Male rats with sham or AV3V lesion and a stainless steel cannula implanted into the VMH were used. Carbachol (2 nmol) injected into the VMH of sham rats produced pressor (32 +/- 4 mmHg). tachycardic (83 +/- 14 bpm), dipsogenic (8.2 +/- 1.1 ml/h). natriuretic (320 +/- 46-mu-Eq/120 min), and kaliuretic (155 +/- 20-mu-Eq/120 min) responses. In AV3V-lesioned rats (2 and 15 days), the pressor (4 +/- 2 and 15 +/- 2 mmHg. respectively), dipsogenic (0.3 +/-0.2 and 1.4 +/- 0.7 ml/h), natriuretic (17 +/- 7 and 99 +/- 21-mu-Eq/120 min), and kaliuretic (76 +/- 14 and 79 +/- 7-mu-Eq/120 min) responses induced by carbachol injection into the VMH were reduced. The tachycardia was also abolished (27 +/- 15 and -23 +/-29 bpm, respectively). These results show that the AV3V region is essential for the pressor, tachycardic, dipsogenic, natriuretic. and kaliuretic responses induced hy cholinergic activation of the VMH in rats.

Anxiolytic-like effects produced by bilateral lesion of the periaqueductal gray in mice: Influence of concurrent nociceptive stimulation

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Ventrolateral periaqueductal gray lesion attenuates nociception but does not change anxiety-like indices or fear-induced antinociception in mice

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)