The consumption of khat (Catha Edulis, Forsk) is on the rise despite the much publicized associated deleterious health effects. How chemicals present in khat, affect various physiological and biochemical processes requires further scrutiny. A clear understanding of these processes will provide an avenue for countering khat-driven negative effects using appropriate pharmacological and/or nutritional interventions. The current study investigated the effect of khat on vital physiological and biochemical processes such as oxidative stress, inflammation and immune responses and the role of Coenzyme-Q10 (CoQ10), a potent antioxidant and anti-inflammatory, in modulating any negative effects due to khat exposure. Three (3) weeks old forty (40) Swiss albino mice were randomly assigned into four treatment groups (n = 10). The first group was the control that was not administered with khat or CoQ10. The second group received 200 mg/kg body weight (b/w) of CoQ10, while the third group received 1500 mg/kg b/w of khat extract and finally the forth group was co-treated with 200 mg/kg b/w of CoQ10 and 1500 mg/kg b/w of khat extract. The experiment was conducted for 90 days after which samples were collected for physiological and biochemical analyses. The effects of khat and CoQ10 on the weights of brain, liver, kidney and spleen was determined. Administration of khat decreased the levels of RBCs and its subtypes (MCV, MCH, RDW-SD and RDW-CV), a clear indicator of khat-induced normochromic microcytic anemia. White blood cells (lymphocytes, monocytes, neutrophils and eosinophil) which are vital in responding to infections were markedly elevated by khat. Moreover, these results provide evidence for khat-induced liver and kidney injury as shown by increased biomarkers; AST, ALT, GGT and creatinine respectively. Standard histopathological analysis confirmed this finding for khat-driven liver and kidney injury. Further studies showed evidence for khat-induced inflammation and oxidative stress as depicted by increased levels of the pro-inflammatory cytokine TNF-alpha and elevation of GSH in the brain, liver and spleen. Remarkably, this is the first study to demonstrate the potential of CoQ10 in ameliorating khat-induced negative effects as outlined. CoQ10 supplementation restored the khat-induced reduction in RBC subtypes, and was protective against liver and kidney injury as shown by the appropriate biomarkers and standard histopathology analysis. The other significant finding was the CoQ10-driven normalization of GSH and TNF-α levels, indicating a protective effect from khat-driven oxidative stress and inflammation respectively. From this study, we conclude that CoQ10 may be useful in nullifying khat-driven deleterious events among chronic khat users.

Electrical stimulation with high-frequency (2–10 kHz) sinusoidal currents has previously been shown to produce a transient and complete nerve block in the peripheral nervous system. Modeling and in vitro studies suggest that this is due to a prolonged local depolarization across a broad section of membrane underlying the blocking electrode. Previous work has used cuff electrodes wrapped around the peripheral nerve to deliver the blocking stimulus. We extended this technique to central motor pathways, using a single metal microelectrode to deliver focal sinusoidal currents to the corticospinal tract at the cervical spinal cord in anesthetized adult baboons. The extent of conduction block was assessed by stimulating a second electrode caudal to the blocking site and recording the antidromic field potential over contralateral primary motor cortex. The maximal block achieved was 99.6%, similar to findings of previous work in peripheral fibers, and the optimal frequency for blocking was 2 kHz. Block had a rapid onset, being complete as soon as the transient activation associated with the start of the sinusoidal current was over. High-frequency block was also successfully applied to the pyramidal tract at the medulla, ascending sensory pathways in the dorsal columns, and the descending systems of the medial longitudinal fasciculus. High-frequency sinusoidal stimulation produces transient, reversible lesions in specific target locations and therefore could be a useful alternative to permanent tissue transection in some experimental paradigms. It also could help to control or prevent some of the hyperactivity associated with chronic neurological disorders.

Injuries, which affect survival and biological functioning, are common in the animal kingdom. This study systematically investigated whether the slow wound healing observed in humans is a unique characteristic within the primate order. First, we found no significant difference in wound-healing rates between baboons under experimental conditions and those in their natural environment (0.613 mm d ⁻¹ ). Second, comparisons among four non-human primates (velvet monkeys, Sykes’ monkeys, baboons and chimpanzees) revealed no significant differences in wound-healing rates. Furthermore, these rates showed no significant differences compared to those observed in rodents, suggesting a potential commonality in wound-healing rates across diverse animal species. In contrast, human wound-healing rates were found to be markedly slower (0.25 mm d ⁻¹ ), approximately three times slower than those observed in non-human primates. This finding indicates that the slow wound healing observed in humans is not a common characteristic among primate order and highlights the possibility of evolutionary adaptations in humans. Understanding these inter-species differences in wound-healing rates may provide valuable insights into the evolutionary implications of wound healing. This study also underscores the need for further research into the biological processes underlying wound healing in various species.

Background: Cryptosporidiosis causes high morbidity and mortality in children under 2 years of age globally. The lack of an appropriate animal model that mimics the pathogenesis of disease in humans has hampered the development and testing of potential therapeutic options. This study aimed to develop and validate an infant baboon infection model of cryptosporidiosis. Methods: Eighteen immunocompetent weaned infant baboons aged 12 to 16 months were used. The animals were n = 3 controls and three experimental groups of n = 5 animals each inoculated with Cryptosporidium parvum oocysts as follows: group 1: 2 × 10⁴, group 2: 2 × 10⁵, group 3: 2 × 10⁶ followed by daily fecal sampling for oocyst evaluation. Blood sampling for immunological assay was done on the day of infection and weekly thereafter until the end of the experiment, followed by necropsy and histopathology. Statistical analysis was performed using R, SPSS, and GraphPad Prism software. Analysis of variance (ANOVA) and Bonferroni post hoc tests were used for comparison of the means, with p < 0.05 considered as a significant difference. Correlation coefficient and probit analysis were also performed. Results: In all experimental animals but not controls, the onset of oocyst shedding occurred between days 2 and 4, with the highest oocyst shedding occurring between days 6 and 28. Histological analysis revealed parasite establishment only in infected animals. Levels of cytokines (TNF-α, IFN-γ, and IL-10) increased significantly in experimental groups compared to controls. Conclusion: For developing a reproducible infant baboon model, 2 × 10⁴ oocysts were an effective minimum quantifiable experimental infection dose. Graphic

The Pan-African Network for Laboratory Animal Science and Ethics (PAN-LASE) pro-vides professional education opportunities for all those involved in the care and use of animals in research across Africa, and supports the development of structures, policies and procedures to facilitate high-quality, humane research involving animals across the continent. To ensure the continued, sustainable growth and development of its activi-ties, PAN-LASE founding members and other key stakeholders convened in Kenya to co-create a forward-thinking Road Map for the organisation. The Road Map includes the following recommendations: creating Africa-centric learn-ing opportunities and resources; changing mind-sets on animal welfare; supporting the development of research animal sciences associations; creating structures, processes and organisations that reflect Africa; engaging with key national and pan-African reg-ulatory organisations and stakeholders; identifying unique selling points for African research involving animals; creating a PAN-LASE Steering Committee. These recommendations will enable the sustainable growth and development of PAN-LASE across Africa by providing solutions that will work for Africa. Our Road Map is also applicable to other animal welfare sectors, other pillars of the One Health Triad, and to other resource constrained countries or regions. A template for interested parties to develop similar activities in their own discipline, country or region.

In tropical and subtropical countries, malaria and leishmaniasis are significant vector-borne parasitic infections that can often be present at the same time, posing a risk of concurrent infections. However, their roles in disease progression and host responses are not well understood. In the present study, we investigated the effects of consecutive infection with L. major and P. berghei in BALB/c mice. BALB/c mice were randomly allocated to naïve, L. major mono-infected, P. berghei mono-infected and co-infected groups. We observed body weight, Leishmania parasite burden in the footpad, and hematological parameters over a 13-day follow-up after malaria infection. Co-infected mice developed more severe disease than either mono-infected group, exhibiting greater body weight reduction, with mean body weight declining to 24.8 ± 2.4 g by Day 13, compared with 28.1 ± 1.5 g in L. major-infected mice and 26.9 ± 1.9 g in P. berghei-infected mice. The co-infected mice also had higher parasitemia than P. berghei mono-infected mice (23.73 ± 3.02% vs. 19.63 ± 3.39%; p = 0.008), and higher Leishmania parasite burden than L. major mono-infected mice (34.00 ± 1.38 vs. 28.92 ± 6.16; p = 0.041). Co-infection induced anemia, thrombocytopenia, leukocytosis, neutrophilia, lymphopenia and monocytosis. These findings show that co-infection with L. major–P. berghei exacerbates disease severity, boosts the burden of malaria, and worsens hematological dysfunctions; thus, highlighting the need for an integrated approach to malaria–leishmaniasis co-infections in endemic areas.