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Auditory stimulation applied during rapid eye movement (REM) sleep enhances the duration of REM sleep in cats and humans. The present experiment investigated whether auditory stimulation would enhance REM sleep in young (3-6 months) rats, and also in old (22-24 months) rats which have impaired REM sleep. Baseline sleep records were obtained on two days. Sleep patterns were then assessed during auditory stimulation test sessions. In young rats, auditory stimulation was administered during each REM sleep bout. In old rats, auditory stimulation was administered on a fixed schedule (10 min of stimulation alternating with 15 min quiet). The day after the stimulation session, an additional sleep record (Day 2) was obtained for each rat. In young rats, auditory stimulation enhanced both REM sleep duration and total REM sleep time. In the old rats, which showed impaired sleep measures as compared to young animals, auditory stimulation enhanced both total REM sleep time and the number of REM sleep periods. Residual proactive effects of auditory stimulation (Day 2) were observed in both young and old rats. Thus, auditory stimulation is an effective manipulation with which to augment REM sleep in both young and old rats, and partially attenuates REM sleep impairments in old rats.

The results of treatments applied to 142 patients with breast carcinoma stage III, in the Oncology Service from 1965 to 1974 are as follows: successive cycles of treatments were applied: irradiation with X-rays of 280 Kv-20 mA for ulcerated tumors or Cobalt 60 for non-ulcerated tumors, using a dose of 5,500 rad in eight weeks. Subsequently, in cases of residual neoplasia, mastectomy was used or an extra dose of 1,500 to 3,000 rad. Later, at the first sign of the spread of carcinoma, hormonal therapy was given and then chemotherapy. Survival rate after five years was as follows: 41.54% of patients survived and 58.45% died from the cancer.

The anticonvulsant activity of a homologous series of phenyl alcohol amides is described. (+-)-2-Hydroxy-2-phenylbutyramide (1), (+-)-3-hydroxy-3-phenylpentanamide (2) and (+-)-4-hydroxy-4-phenylhexanamide (3) were prepared and tested for their anticonvulsant profile and neurotoxicity. 1, 2 and 3 exhibited a broad profile of anticonvulsant activity and a similar significant activity in the seizures provoked by maximal electroshock, pentetrazol, 4-aminopyridine, bicuculline and thiosemicarbazide, but in the strychnine and picrotoxin tests, the protection was variable. The rotarod ataxia test was used to evaluate their neurotoxicity. In this test 2 possesses the lowest neurotoxicity.

Hypertension and renal mass reduction induce glomerular hypertension (GH), hyperfiltration (HF) and renal injury. GH may contribute to allograft loss in post-transplant hypertensive patients (PT x HT). HF and GH may be evaluated by renal response to acute protein intake (API). Since ACE inhibition may prevent GH, the effects of fosinopril (Fos) were evaluated in 10 PT X HT on azathioprine and prednisone. Patients received 5 to 40 mg/day of Fos during 12 months. Baseline MAP (111.1 +/- 2.9 mm Hg) was significantly reduced by 10 to 12 mm Hg, rising to 114.7 +/- 2.7 mm Hg after Fos was administered. GFR (63.7 +/- 5.9 ml/min) decreased after 4 (48.1 +/- 4.6, P less than 0.05) and 12 months (50.7 +/- 4.6, P less than 0.05), rising to 59.4 +/- 5.6 after Fos was given. There was no GFR response to API before and after one month of Fos, however, a clear response became apparent at 4 (+ 27% P less than 0.05), and 12 months (+ 18%, P less than 0.05), disappearing after Fos discontinuation. Proteinuria (918.8 +/- 710.6 mg/d) decreased after 4 (72.3 +/- 21.6 mg/d, P less than 0.05) and 12 months, rising to 297.8 +/- 172.3 mg/day after therapy. GFR response to API in 22 controls and 17 uninephrectomized donors was 13 and 11%, respectively. Lack of response to API in PT x HT suggests HF and GH. Reduction of GFR, restoration of response to API and reduction of proteinuria, indicate that ACE inhibition with fosinopril ameliorates HF and GH. This effect may be beneficial in preventing hemodynamic-mediated allograft injury.

A morphometric study of intra-uterine and extra-uterine Leydig cell differentiation was carried out by the Weibel's technique which was adapted for morphometry on electronmicrography. The results obtained in rats, the animals studied in this investigation, were: a) Testis of intra-uterine life as well as those of extra-uterine life displayed Leydig cells with lipid droplets. b) The percentage of Leydig cells varied from one testis to another. c) This percentage increased at 20th day of intra-uterine life and between 60th and 90th day of extra-uterine life. d) The percentage of lipid droplets within cytoplasm of Leydig cell increased at 20th day of intra-uterine life, at 15th day of extra-uterine life and at the proximity of puberty. e) The percentages of mitochondria are at inverse ratio of percentage of lipid droplets until the 40th day of life.

It has been shown that REM sleep duration and ponto-geniculo-occipital (PGO) spike density can be enhanced by auditory stimulation. The purpose of this study was to determine whether this effect is restricted to the auditory sensory modality or whether somatic stimulation can produce similar effects. Cats implanted with electrodes for recording the sleep-wake cycle were additionally prepared with clip electrodes placed in the neck for somatic stimulation. Such stimulus was applied at the beginning and throughout each REM sleep period. The effect of this procedure was compared to a similar period when no stimulus was applied. The results showed that somatic stimulation induced a significant increase in REM duration (60.2%) and PGO spike density. Since the effects of somatic stimuli are identical to auditory ones, it is suggested that all sensory modalities may share the property of influencing the mechanisms which regulate the maintenance of REM sleep. Such mechanisms are discussed in terms of an increase in the excitability levels of polymodal medial reticular neurons.

It was previously shown that an auditory stimulus given prior to and throughout a rapid eye movement (REM) sleep period was capable of inducing a significant increase in REM sleep duration and pontogeniculo-occipital (PGO) spike density. The purpose of this study was to determine whether the increase in REM duration is dependent on PGO spike density. We administered atropine to cats at doses of 0.1-0.6 mg/kg and the effects on REM duration and PGO spikes was determined. The doses of 0.2 and 0.3 mg/kg of atropine were then utilized to compare REM sleep periods with and without auditory stimulation. The results showed that both REM duration and PGO spikes were decreased by atropine, but could be dissociated from each other depending on the doses. In addition, it was shown that the auditory stimulus protected the animals from the effects of atropine but only in relation to REM sleep duration. The results indicate that both REM sleep duration and PGO spikes have a cholinergic component and that the auditory stimulus exerts its REM enhancing properties in a manner which seems to be independent of the PGO spike density. The results are discussed in terms of receptor availability and/or excitability levels of medial reticular neurons.

Thirty one infants with moderate and severe protein-calorie malnutrition whose blood hemoglobin concentrations were higher than 10 g/dl were managed with diet supplements containing iron fortified cereals for three months. In addition, 17 of them were given an extra daily dose of elementary iron (3 mg/kg/day). Mean weight gain was similar in both subgroups but mean hemoglobin concentration raised by 1,2 g/dl among extra iron infants in contrast with no increase or even decreased hemoglobin levels at the end of follow up in controls, thus demonstrating the importance of adding supplementary iron to these children during the recovery period of under nutrition, even it the diet provides the usually recommended 8 to 10 mg/day of iron.

Rats which sustained lesions of the suprachiasmatic nucleus (SCN) were transplanted with fetal hypothalamic tissue which included the SCN. After the graft, animals were kept under a 12:12 light-dark (LD) cycle during 6 weeks at which time half the animals were placed in constant light (LL) and half in constant darkness (DD). The results showed that all grafted rats recovered the photoperiod under LD, but under constant conditions rats began to free-run only in DD. The results suggest that the grafted tissue functions as a self-sustained oscillator only in darkness.

It has been shown that auditory or somatic stimulation during rapid eye movement (REM) sleep is capable of producing a significant increase in ponto-geniculo-occipital (PGO) spike density as well as in REM sleep duration. The purpose of this study was to determine the role of the medial pontine reticular formation (PRF) in mediating such increase of REM sleep duration. After a baseline recording whereby on the same recording day the control and the stimulus (auditory or somatic) alternated with each REM, a group of cats was lesioned with kainic acid in the PRF. The sleep-wake cycle was recorded again on days 15, 30 and 45 post-lesion, following the same procedure. The results showed no changes in REM sleep duration and PGO spike density in the lesioned animals. However, when sensory stimulation was applied it was ineffective in producing REM sleep enhancement, although it was able to increase PGO spike density. These findings suggest that the effects of sensory stimulation on REM sleep duration are accomplished through the PRF, probably by inducing an increase in the excitability levels of such neurons, and further suggests that PGO spike density and REM duration are independent of each other.

In the past few years a steadily increasing number of substances have been suggested to qualify as sleep-inducing factors. Most 'sleep factors' appear to exert their effects on slow-wave sleep. Recently, however, it has been shown that the cerebrospinal fluid (CSF) of sleep-deprived cats may contain a rapid eye movement (REM) sleep factor, and that vasoactive intestinal peptide (VIP) may be a specific REM sleep inducer. The purpose of this study is to determine whether the CSF of sleep-deprived cats and VIP can reverse insomnia produced by parachlorophenylalanine (PCPA). Donor cats were sleep-deprived for 24 h and their CSF extracted. Some donor cats were additionally pre-treated with chloramphenicol, and some extracted CSF was heated. Recipient cats were injected with 400 mg/kg i.p. of PCPA on two consecutive days. Twenty-four h after the second injection, the recipient cats were intraventricularly injected with a 100-microliters of the various CSF types or 200 ng of VIP. The results showed that only CSF from sleep-deprived cats and VIP were capable of restoring REM sleep in the otherwise PCPA insomniac cats. Since the return of REM sleep was through an increase in its frequency, it is suggested that the CSF of sleep-deprived cats contains a VIP-like sleep factor possibly involved in triggering REM sleep.