Ecdysteroid titers in pupae of highly social bees relate to distinct modes of caste development.

Modifications in endocrine programs are common mechanisms that generate alternative phenotypes. In order to understand how such changes may have evolved, we analyzed the pupal ecdysteroid titers in two closely related, highly social bees: the honey bee, Apis mellifera, and a stingless bee, Melipona quadrifasciata. In both species, the ecdysteroid titers in queens reached their peak levels earlier than in workers. Titer levels at peak maxima did not differ for the honey bee castes, but in Melipona they were twofold higher in queens than in workers. During the second half of pupal development, when the ecdysteroid titers decrease and the cuticle progressively melanizes, the titer in honey bee queens remained higher than in workers, while the reverse situation was observed in Melipona. Application of the juvenile hormone analog Pyriproxyfen((R)) to spinning-stage larvae of Melipona induced queen development. Endocrinologically this was manifest in a queen-like profile of the pupal ecdysteroid titer. Comparing these data with previous results on preimaginal hormone titers in another stingless bee, we conclude that the timing and height of the pupal ecdysteroid peak may depend on the nature of the specific stimuli that initially trigger diverging queen/worker development. In contrast, the interspecific differences in the late pupal ecdysteroid titer profiles mainly seem to be related to caste-specific programs in tissue differentiation, including cuticle pigmentation.

Inhibition of vitellogenin synthesis in Apis mellifera workers by a juvenile hormone analogue, pyriproxyfen.

Insect juvenile hormone (JH) has been related to modulation of vitellogenin (Vg) synthesis, a protein produced by fat body cells, secreted in haemolymph and sequestered by developing oocytes. A stimulatory JH action has been described for the majority of species studied thus far. In some insects, however, Vg synthesis has been inhibited or unaffected by JH. The aim of this study was to re-examine the action of JH on Vg synthesis in Apis mellifera workers, since contrasting effects of this hormone were described. Newly emerged worker bees were treated with different doses of pyriproxyfen (PPN), a potent JH analogue. Vg and total protein were quantified in haemolymph samples of newly emerged up to 6-day-old worker bees. Protein synthesis activity of fat body cultured in vitro and ultrastructure of fat body cells were also examined. High doses (1.25, 2.5, 5 and 10 &mgr;g) of PPN inhibited the onset and accumulation of Vg in the haemolymph of young worker bees in a dose-dependent fashion. This inhibition was not a result of fat body cell degeneration or death, as illustrated by fat body cells ultrastructure analysis, but by impairing Vg synthesis, as demonstrated by in vitro culture of fat body cells. Low doses (0.001, 0.01 and 0.1 &mgr;g) neither affected the normal synthesis and secretion of Vg into the haemolymph nor caused an early onset of Vg in treated bees (which could be interpreted as a JH-activating effect), as shown by Vg quantification at 24-h intervals. The results suggest that a low JH titre in honey bee workers permits the onset and accumulation of Vg in haemolymph, whereas high JH levels turn off Vg synthesis.

The relationship between megacolon and carcinoma of the colon: an experimental approach.

'Carcinoma of the colon does not occur in cases of megacolon' is an axiom held by Brazilian physicians working in endemic areas for Chagas' disease. The objective of the present study was to test this axiom experimentally by submitting rats with experimental megacolon to a carcinogen which causes carcinoma of the colon. Eighty young male Wistar rats received serosal application of either saline (0.9% NaCl) or 2 mM benzalkonium chloride (BAC) to the distal colon. Ten months later randomly chosen saline and BAC rats were injected weekly with dimethylhydrazine (DMH) for 20 weeks. Non-DMH-treated rats from both original groups were maintained, for a total of four experimental groups. Three months after the injections all surviving rats were killed. At autopsy the presence of absence of carcinomas along the colon was recorded. The induction of megacolon was evaluated by morphometry of the wall from the distal colon and myenteric denervation was assessed by neuron counts. An increase of at least 2-fold in distal colon wall thickness confirmed the induction of megacolon in BAC-treated rats. Neuronal counts from BAC and control rats not treated with DMH showed an average denervation of 63%. The number of distal colon carcinomas in BAC+DMH-treated rats was significantly lower than that in DMH-treated rats. These findings appear to contradict the traditional concept of carcinogenesis of the colon. The clinical axiom was reproduced experimentally.

Experimental megaileum.

Typical megaileum occurred in young male Wistar rats three months after ileum myenteric plexus denervation. An average of 58.4% denervation of the Auerbach plexus was obtained by serosal application of benzalkonium chloride (0.2% v/v). Denervation was assessed by ganglion cell counts in an 8 nm ring-shaped histological sectfrom the midportion of the treated segment. A morphometric study showed that the increased thickness of the megaileum wall was due to muscle hypertrophy and mucosal hyperplasia. The potential usefulness of this model of megaileum is emphasized.

Peripheral and coronary sinus catecholamine levels in patients with severe congestive heart failure due to Chagas' disease.

The aim of this study was to assess the peripheral and cardiac autonomic system by catecholamine measurements in patients with severe chagasic and nonchagasic heart failure. Fifteen chagasic and 16 nonchagasic patients were enrolled in the study. Plasma venous norepinephrine levels (pg/ml) were 397.26 +/- 250.11 for chagasic and 660.05 +/- 455.57 for nonchagasic patients (p > 0.05), plasma venous epinephrine levels 215.84 +/- 254.04 for chagasic and 106.17 +/- 65.90 for nonchagasic patients (p > 0.05), aortic root norepinephrine levels 435.46 +/- 306.60 for chagasic and 668.16 +/- 512.82 for nonchagasic patients (p > 0.05), aortic root epinephrine levels 300.33 +/- 302.69 for chagasic and 199.98 +/- 162.88 for nonchagasic patients (p > 0.05), coronary sinus norepinephrine levels 636.10 +/- 495.22 for chagasic and 552.17 +/- 535.54 for nonchagasic patients (p > 0.05) and coronary sinus epinephrine levels 226.66 +/- 277.47 for chagasic and 69.21 +/- 35.62 for nonchagasic patients (p = 0.02). Myocardial and peripheral norepinephrine and epinephrine extractions were similar for both groups. Taken together, these findings may suggest that chagasic patients with congestive heart failure have biochemical evidence of cardiac autonomic dysfunction with preservation of the peripheral sympathetic activity.

Beneficial effects of gangliosides on the natural history of acute chagasic myocarditis in rats.

This study was designed to investigate the effects of ganglioside treatment on acutely Trypanosoma cruzi-infected rats with emphasis on the heart. Newly weaned Wistar rats were infected with T. cruzi (Colombian strain, 50,000 parasites/kg body weight injected intraperitoneally). Two groups of 25 infected rats received daily injections of saline or ganglioside (10 mg/kg body weight) intraperitoneally between the 14th and 30th days after infection. Two groups of 10 noninfected rats were similarly treated. On day 31, all surviving rats were killed. Hearts were collected for histopathology and norepinephrine assay. An arbitrary score for myocardial microscopic lesions was used to characterize each heart wall. Mortality was recorded throughout the experimental period. Seven of 25 (28%) ganglioside-treated and 14 of 25 (56%) saline-treated rats died spontaneously (p = 0.02). The histological score was 5.4 ± 3.2 for ganglioside-treated and 7.9 ± 3.0 for saline-treated rats (p < 0.05). No difference was detected in myocardial norepinephrine content. Thus, ganglioside treatment decreases mortality and myocardial inflammation in acute chagasic myocarditis in rats.

Changes in electrocardiographic patterns at different stages of Chagas' heart disease in rats.

1. The resting electrocardiogram was obtained from 25 Trypanosoma cruzi-infected rats 30 days after infection (phase I). The resting electrocardiogram was abnormal in 12 (group I) and normal in 13 (group II) animals. Nineteen similar but non-infected animals served as controls. Both the resting electrocardiogram and the ajmaline test were performed 120 and 350 days after infection (phases II and III, respectively). 2. With regard to the resting electrocardiogram of group I animals, left axis deviation was found in 10 of 12 (83%) in phase I, one of 12 (8%) in phase II (P less than 0.05) and in none of phase III (P less than 0.05). An intraventricular conduction delay was found in four of 12 (33%) rats in phase I, two of 12 rats (16%) in phase II (P greater than 0.05) and six of 12 rats (50%) in phase III (P greater than 0.05). The ajmaline test was abnormal in nine of 10 (90%) rats of group I with normal resting electrocardiogram in phase II, and in three of six (50%) animals in phase III (P greater than 0.05). 3. An intraventricular conduction delay was found in the resting electrocardiogram of one of 13 (7%) rats of group II in phase III. The ajmaline test was abnormal in one of 13 (7%) rats in phase II and in one of 12 (8%) rats in phase III. 4. No control rat showed pathological changes.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of long term metoprolol administration on the electrocardiogram of rats infected with T cruzi.

STUDY OBJECTIVE: The aim of the study was to evaluate the role of beta receptor antagonists in the evolution of experimental Chagas' disease. DESIGN: Rats were infected with T cruzi, 2000 parasites.g-1 body weight, soon after weaning. One group was then given metoprolol, 100 mg.kg-1.d-1, in drinking water. A comparison group received no metoprolol. Two control groups of non-infected rats were also studied, one with and one without metoprolol in the same dose. SUBJECTS: Adult male albino rats were used: 144 were infected with T cruzi and received metoprolol (group IM), 137 were infected and received no metoprolol (group IW), 46 non-infected rats received metoprolol (group CM), and 43 non-infected rats did not receive metoprolol (group CW). MEASUREMENTS and main results--30 d after infection, resting ECG was performed in all surviving rats. (There were 63 deaths in the infected groups and none in the non-infected groups.) Abnormal ECG was found in 20/81 infected rats in group IM and in 30/74 in group IW (p less than 0.05). No ECG changes were found in the non-infected rats. Of rats in group IM with normal resting ECG, 31 continued to take metoprolol (group IMNM), while 30 similar rats did not (group IMNW); in group IM with abnormal ECG, 10 rats continued to take metoprolol (group IMAM), while 10 similar rats did not (group IMAW). Of rats in group IW with normal ECG, 22 were started on metoprolol (group IWNM), while 22 similar rats were not (group IWNW); in group IW with abnormal ECG, 15 rats were started on metoprolol (group IWAM), while 15 similar rats did not (group IWAW). After 120 d and 300 d infection there were no differences in mortality rate and Ajmaline test in any of the matched groups (IMNM X IMNW; IMAM X IMAW; IWNM X IWNW; IWAM X IWAW). After 120 d there was no difference in ECG between the groups, but after 300 d there was a decrease in abnormal ECG in group IWAM (IWAM v IWAW, 0/12 v 5/12, p less than 0.05). No histological differences were found. CONCLUSIONS: Metoprolol decreases the proportion of rats with abnormal resting ECG in both the acute and the chronic stage of T cruzi infection.

Impending myocardial infarction in a patient with marked left ventricular hypertrophy and normal coronary arteriogram--a case report.

A middle-aged woman with long-term uncontrolled arterial hypertension developed a clinical picture of impending myocardial infarction. A normal coronary arteriogram was obtained. However, left heart catheterization showed a marked increase in left ventricular end-diastolic pressure, while left angiocardiography revealed marked left ventricular hypertrophy. She was successfully treated with a beta-blocking and calcium-antagonist agent. The present case shows that an impending myocardial infarction may occur in patients having normal coronary arteriogram but with left ventricular hypertrophy secondary to arterial hypertension.