Some effects of zinc on maternal and fetal intergrety in pregnancy

Summary: This study was undertaken to determine the effects of zinc sulphate on the weights of pregnant rats, on the food and water consumption during gestation, litters weight at birth, the number of litters at birth and the accumulation of zinc in selected organs of the litters. Zinc sulphate in the dose of 1 mg/liter and 20mg/liter drinking water was administered to both pregnant and non-pregnant for the period of gestation. The results indicated a significant (

Sleep-waking states and the endogenous opioid system

In the general introductory part of this thesis (Chapters and 2) a review of some pertinent literature related to sleep-waking states and opioid peptides is offered. A global view of the neurochemical mechanisms and theories of functions of sleep, as well as the physiological and possible clinical consequences of total or selective REM sleep deprivation is given in Chapter 1. In Chapter 2, which is concerned with the role of endogenous opioid peptides, particular attention is paid to the possible modulatory role of endogenously released opioid peptides in the regulation of some behavioural states in physiological and pathological conditions. It is generally known that exogenously administered opiates and opioid peptides can alter sleep pattern and decrease REM sleep. A possible interaction between sleep-waking states and endogenous opioid system is suggested by the report that the episodic release of plasma humoral endorphins during sleep is associated with the REM sleep phase (Chapter 1, section 1.1 .7). In addition, the concentrations of opioid peptides in some brain nuclei of the rat which are known to be important in sleep-waking regulation, are highest in the dark (active) phase, during which wakefulness is high and lowest in the light (rest) phase, when the propensity to sleep is at its highest (Chapter section 1 .3.2). Thus in order to clarify the effect of endogenously released opioid peptides in the regulation of sleep-waking pattern, we studied the effects of phosphoramidon, an inhibitor of enkephalinase A on sleep-waking states (Chapter 3). Several clinical studies suggest that the sleep-waking cycle may modulate the occurence of some types of epileptic phenomena in human subjects (Chapter 1, section 1 .5.2, iii). In addition, some studies indicate a similarity between enkephalin induced epileptic Therefore, phenomena and we studied petit the mal epilepsy effects of (Chapter 4 discussion). different sleep stages on enkephalin-induced epileptic phenomena using electrophysiological parameters (Chapter 4). These initial studies (Chapters 3 and 4) suggested an interaction between sleep-waking states and endogenous opioid system. The observation that REM sleep deprivation (REMSD) reduced the pain threshold to noxious electrical stimulation (Chapter 1 section 1 .5.2d i) was an indication of the importance of REM sleep in the regulation of nociception. Therefore in Chapters 5 and 6, the experiments were designed to explore a direct effect of REMSD on the analgesic effects of morphine, an enkephalinase inhibitor phosphoramdion and cold-water-swim. The profound antagonistic effect of REMSD on opiate/opioid peptide induced analgesia stimulated further interest to investigate the relationship between REMSD and other opiate/opioid peptide modulated behavioural phenomena. Therefore the following opioid modulated behaviours were investigated: akinetic-cataleptic syndrome, spontaneous vertical motor activity, convulsions, (Chapters 7-9). (Chapter 10) grooming, wet-dog-shakes and morphine withdrawal symptoms Additional experiments with nitrous oxide were performed since it is known that this anaesthetic agent can stimulate the release of endogenous enkephalins and induce opiate-like withdrawal symptoms (Chapter 2, section 2.5.2, iv). Finally, the possible clinical consequences of our findings are described in the relevant chapters

In vivo anti-malarial activity of propranolol against experimental Plasmodium berghei ANKA infection in mice

Background: Malaria is a mosquito-borne infectious disease caused by Plasmodium spp, which is widespread in tropical and subtropical regions of the world. The objective of this study is to evaluate in vivo antimalarial activity of propranolol against experimental Plasmodium berghei ANKA (PbA) infection in a mouse model.Methods: A total of 36 mice weighing between 15 to 18g were randomly divided into six groups of six mice each. Mice in the first group (SAL) were non-infected with P. berghei but received normal saline (control), second group (PbA) were mice infected without treatment (control), third group (PRL) were non-infected mice treated with propranolol at the dose of 7.5 mg/kg/bid, fourth group (PbA+PRL) were mice infected and treated with same dose of propranolol, fifth group (QUN) were non-infected mice treated with quinine at a dose of 20 mg/kg stat, then 10 mg/kg bid, and sixth group (PbA+QUN) were infected mice treated with quinine. Parasitaemia, physiological conditions (cognitive function, temperature) and lethality of infected mice were monitored over 7-day period to assess the antimalarial activity of propranolol and quinine. The Y-maze paradigm was used to assess cognitive impairment induced by PbA infection. The effects of propranolol on malaria indices and cognitive impairment were compared with that of quinine and the control using T-test statistical method.Results: Mortality of mice at day 7 in the infected group without treatment (PbA) was 100% (6/6) while mortality was 50% (3/6) in infected group treated with propranolol (PbA+PRL) and 33.3% (2/6) in infected group treated with quinine (PbA+QUN) (OR=2.000, p=1.000). No mortality was recorded in any of the three groups of uninfected mice. Propranolol reduced parasitaemia to a trough level of 1.40±0.07 three days after treatment, comparable to trough level of 1.39±0.0633 by quinine but did not reverse PbA-induced hypothermia, which quinine did.Conclusion: Propranolol demonstrated in vivo antimalarial activity against experimental PbA infection in mice comparable to that of quinine. Keywords: malaria, propranolol, quinine, Plasmodium, cerebral malaria French Title: Activité antipaludique in vivo du propranolol contre l'infection expérimentale par Plasmodium berghei ANKA chez la souris   Contexte: Le paludisme est une maladie infectieuse transmise par les moustiques causée par Plasmodium spp, qui est répandue dans les régions tropicales et subtropicales du monde. L'objectif de cette étude est d'évaluer l'activité antipaludique in vivo du propranolol contre une infection expérimentale à Plasmodium berghei ANKA (PbA) dans un modèle murin. Méthodes: Un total de 36 souris pesant entre 15 et 18 g ont été réparties au hasard en six groupes de six souris chacun. Les souris du premier groupe (SAL) n'étaient pas infectées par P. berghei mais ont reçu une solution saline normale (contrôle), le deuxième groupe (PbA) était des souris infectées sans traitement (contrôle), le troisième groupe (PRL) était des souris non infectées traitées par propranolol à la dose de 7,5mg/kg/bid, le quatrième groupe (PbA+PRL) étaient des souris infectées et traitées avec la même dose de propranolol, le cinquième groupe (QUN) étaient des souris non infectées traitées avec de la quinine à une dose de 20mg/kg stat, puis 10mg/kg bid et le sixième groupe (PbA+QUN) étaient des souris infectées traitées avec de la quinine. La parasitémie, les conditions physiologiques (fonction cognitive, température) et la létalité des souris infectées ont été surveillées sur une période de 7 jours pour évaluer l'activité antipaludique du propranolol et de la quinine. Le paradigme du labyrinthe en Y a été utilisé pour évaluer les troubles cognitifs induits par l'infection au PbA. Les effets du propranolol sur les indices du paludisme et les troubles cognitifs ont été comparés à ceux de la quinine et du témoin à l'aide de la méthode statistique du test T. Résultats: La mortalité des souris au jour 7 dans le groupe infecté sans traitement (PbA) était de 100% (6/6) tandis que la mortalité était de 50% (3/6) dans le groupe infecté traité avec du propranolol (PbA+PRL) et 33,3% ( 2/6) dans le groupe infecté traité par la quinine (PbA+QUN) (OR=2.000, p=1.000). Aucune mortalité n'a été enregistrée dans aucun des trois groupes de souris non infectées. Le propranolol a réduit la parasitémie à un niveau minimum de 1,40±0,07 trois jours après le traitement, comparable au niveau minimum de 1,39±0,0633 de la quinine, mais n'a pas inversé l'hypothermie induite par le PbA, ce que la quinine a fait. Conclusion: le propranolol a démontré une activité antipaludique in vivo contre l'infection expérimentale au PbA chez la souris comparable à celle de la quinine. Mots-clés: paludisme, propranolol, quinine, Plasmodium, paludisme cérébra

Anaphe venata larva extract-induced purposeless chewing in rats: the role of cholinergic, GABAergic and opioid systems

Seasonal ataxia was reported in humans following the consumption of Anaphe venata larva as protein supplement in diet and altered motor function in rodents when the extract was administered intraperitoneally. In this study we investigated the effect of the crude aqueous and Phosphate Buffer Saline (PBS) extracts of this larva on altered spontaneous rat behavior in a novel environment particularly chewing behaviour, with a view to determine the mechanism(s) involved in these behavioural alteration. Animals were randomly assigned into four groups (n = 6-12 per group) and graded doses of aqueous and PBS extracts (100-400 mg/kg) were administered dissolved in saline intraperitoneally (i.p.) to each animal in the experimental groups. The control group received an equivalent volume of saline. Behavioral scores were recorded for a period of 30 minutes after the administration of saline or extract. The role of various receptors in the extract induced chewing was evaluated using known receptor agonist/antagonists. Results revealed a significant increase in purposeless chewing (F (7, 95) = 7.85; p<0.05) by the aqueous extract compared to saline control at all dose levels, which was significantly attenuated by scopolamine (3 mg/kg, i.p) and thiamine (1 mg/kg, i.p) respectively (p<0.05); while flumazenil (2 mg/kg, i.p) and naloxone (2.5 mg/kg, i.p) did not alter the induced purposeless chewing behaviour. Also, administration of PBS induced a significant (F (7, 95) = 6.11; p<0.05) increase in chewing behaviour but only at 400 mg/kg dose level which was attenuated by scopolamine (3 mg/kg, i.p); while flumazenil (2 mg/kg, i.p), naloxone (2.5 mg/kg, i.p), and thiamine (1 mg/kg, i.p) potentiated purposeless chewing behaviour respectively. It may therefore be concluded from this study that Anaphe extract-induced purposeless chewing behaviour in rat is mediated via the activation of cholinergic neurotransmission which is modulated by GABAergic and opioid receptor systems

Medicinal and Economic Value of Spondias mombin

This article reviewed the folk medical value of Spondias mombin with the correlated research findings on the uses of Spondias mombin. Most of the folk uses had been scientifically proven in most of the regions where those beliefs are based. The plant was described with habitat, the local uses including the uses of its parts mentioned. We reviewed the ethnomedicinal uses, the biological activities and the phytochemistry of Spondias mombin

The Modulation of Pain by Circadian and Sleep-Dependent Processes: A Review of the Experimental Evidence

AbstractThis proceedings paper is the first in a series of three papers developing mathematical models for the complex relationship between pain and the sleep-wake cycle. Here, we briefly review what is known about the relationship between pain and the sleep-wake cycle in humans and laboratory rodents in an effort to identify constraints for the models. While it is well accepted that sleep behavior is regulated by a daily (circadian) timekeeping system and homeostatic sleep drive, the joint modulation of these two primary biological processes on pain sensitivity has not been considered. Under experimental conditions, pain sensitivity varies across the 24 h day, with highest sensitivity occurring during the evening in humans. Pain sensitivity is also modulated by sleep behavior, with pain sensitivity increasing in response to the build up of homeostatic sleep pressure following sleep deprivation or sleep disruption. To explore the interaction between these two biological processes using modeling, we first compare the magnitude of their effects across a variety of experimental pain studies in humans. To do this comparison, we normalize the results from experimental pain studies relative to the range of physiologicallymeaningful stimulation levels. Following this normalization, we find that the estimated impact of the daily rhythm and of sleep deprivation on experimental pain measurements is surprisingly consistent across different pain modalities. We also review evidence documenting the impact of circadian rhythms and sleep deprivation on the neural circuitry in the spinal cord underlying pain sensation. The characterization of sleep-dependent and circadian influences on pain sensitivity in this review paper is used to develop and constrain the mathematical models introduced in the two companion articles.</jats:p