Background: Staphylococcus epidermidis is the most frequently isolated species of the coagulase negative staphylococci from human stool. However, it is not clear how its presence in the gut affects the cellular structures and functions of this organ. In this study therefore, the pathogenicity of strains of S. epidermidis which were isolated from the stool samples of apparently healthy children was investigated in mice and rats.

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Background: Lopinavir/Ritonavir (LR) is a protease inhibitor used human immunodeficiency virus infection management. There have been issues regarding the effects of fat on LR efficacy and the possibility of neurological deficits following prolonged use, there is however a dearth of research examining this. Aims: The effects of LR administered with normal or High-Fat Diet (HFD) on neurobehaviour, neurochemistry and oxidative stress in healthy mice were examined. Methods: Mice were randomly-assigned into eight groups of ten (n=10) animals each. The groups were normal control [Standard Diet, (SD)], HFD control, 3 groups of LR incorporated into SD (100/25, 200/50 and 400/100 mg/kg of feed), and 3 groups of LR with HFD (100/25, 200/50 and 400/100 mg/kg of feed). Mice were fed daily for six weeks, following which open field, elevated-plus maze (EPM), radial-arm maze and Y-maze behaviours were scored. Twenty-four hours after tests, mice were euthanised and brains were homogenised for estimation of oxidative stress, L-glutamate level and acetylcholinesterase activity. Results: LR was associated with a reduction in HFD-induced weight gain, suppression of open-field behaviours with SD, and counteraction of HFD-induced changes in working-memory, open-field and anxiety-related behaviours. Also, LR causes increased lipid peroxidation and superoxide dismutase activity; and a decrease in brain glutamate, irrespective of dietary composition. Increased fat catabolism leading to increased oxidative stress could possibly account for the weight changes, while a decrease in brain glutamate could account for the changes in open-field behaviours in mice fed SD. Conclusion: LR alters neurobehaviour, oxidative stress and brain glutamate in mice; however, only its effects on neurobehaviour are affected by diet.

The worldwide burden of cancers is increasing at a very high rate, including the aggressive and resistant forms of cancers. Certain levels of breakthrough have been achieved with the conventional treatment methods being used to treat different forms of cancers, but with some limitations. These limitations include hazardous side effects, destruction of non-tumor healthy cells that are rapidly dividing and developing, tumor resistance to anti-cancer drugs, damage to tissues and organs, and so on. However, oncolytic viruses have emerged as a worthwhile immunotherapeutic option for the treatment of different types of cancers. In this treatment approach, oncolytic viruses are being modeled to target cancer cells with optimum cytotoxicity and spare normal cells with optimal safety, without the oncolytic viruses themselves being killed by the host immune defense system. Oncolytic viral infection of the cancer cells are also being genetically manipulated (either by removal or addition of certain genes into the oncolytic virus genome) to make the tumor more visible and available for attack by the host immune cells. Hence, different variants of these viruses are being developed to optimize their antitumor effects. In this review, we examined how grave the burden of cancer is on a global level, particularly in sub-Saharan Africa, major conventional therapeutic approaches to the treatment of cancer and their individual drawbacks. We discussed the mechanisms of action employed by these oncolytic viruses and different viruses that have found their relevance in the fight against various forms of cancers. Some pre-clinical and clinical trials that involve oncolytic viruses in cancer management were reported. This review also examined the toxicity and safety concerns surrounding the adoption of oncolytic viro-immunotherapy for the treatment of cancers and the likely future directions for researchers and general audience who wants updated information.

Aim of the Study: Conventional antimalarial drugs are used concurrently with herbal remedies in malarial endemic developing countries. Vernonia amygdalina is one of such popular herbs used in the treatment of malaria. This study aimed at investigating the antimalarial chemotherapeutic interaction of Vernonia amygdalina (VA) when combined with Amodiaquine (AQ) and/or Artesunate (AS) in a murine Plasmodium berghei malaria model. Methodology: Various doses of aqueous VA leaf extract (100-500 mg/kg/day), AQ (2-10 mg/kg/day) and AS (0.8-4 mg/kg/day) were administered orally to P berghei.-infected Swiss albino mice to determine their sub-therapeutic doses. These doses were subsequently used to investigate the chemotherapeutic interactions of VA with AQ and/or AS in both early and established malaria infection test models. The survival of animals with established infections that received different drug/herb treatments were determined using their mean survival time (days) and Kaplan-Meier survival curves (percentage). Using GraphPad Instat (version 3.10) and PrismR (version 5.01) the data obtained were subjected to One-way ANOVA, followed by Student-Newman-Keuls test. P < .05 was considered statistically significant. Results: The sub-therapeutic doses of VA, AQ and AS were found to be 100 mg/kg, 2 mg/kg and 2.4 mg/kg, respectively. The chemosuppressive effect of AQ or AS was significantly increased (p< 0.05) when administered in combination with the VA extract. Similarly, combination of VA extract with AQ or AS resulted in significant (P < .05) parasite clearance when compared to the effects of the herb or the conventional drugs administered separately. The mean survival period of animals with established infection was also significantly enhanced by the VA alone or with AQ (or AS) compared to placebo.

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 cérébral

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Insulin, an important regulator of peripheral metabolism, has been reported to interact with many neurotransmitter systems including those associated with convulsion. The effect of insulin against pentylenetetrazole and strychnine-induced convulsions in mice, as well as possible sex differences, were evaluated in this study. Mice of both sexes weighing between 20 and 25 g were administered insulin intraperitoneally at doses of 1, 2, 4 and 8 IU/kg. Each mouse received a convulsive dose of pentylenetetrazole (100 mg/kg, i.p.) or strychnine (2 mg/kg, i.p.) and was observed for the onset of convulsions and occurrence of death. Against pentylenetetrazole-induced convulsions, all the doses of insulin used significantly (p < 0.05) prolonged the onset of convulsions and significantly delayed the time of death in male mice when compared with control. However, in female mice, only insulin 8 IU/kg significantly prolonged the onset of convulsions, while insulin 4 IU/kg significantly delayed the time of death. Against strychnine-induced convulsions, insulin at the doses of 2 and 4 IU/kg significantly (p < 0.05) prolonged the onset of convulsions in male mice relative to control, while 8 IU/kg insulin significantly prolonged the time of death in male mice compared to control. However, none of the doses of insulin administered to female mice were effective against strychnine-induced convulsions. These results show that insulin produced sex-related protective effects against chemically-induced convulsions in mice.