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Background: Neuroimaging is important for determining etiology and guiding care in early childhood epilepsy. However, access to appropriate imaging in sub-Saharan Africa is modest, and as a consequence, etiological descriptions of childhood epilepsy in the region have been limited. We sought to describe MRI findings in children with epilepsy presenting to a tertiary hospital in Nairobi, Kenya, over a 6-year period of routine care. Materials and Methods: We undertook a retrospective review of MRI findings of children aged between 0 and 18 years with a diagnosis of epilepsy presenting to the pediatric neurology department of Aga Khan University Hospital in Nairobi, Kenya, between January 2014 and July 2020. Over this period, the hospital had 1.5T MRI machines (GE1.5T Signa Excite and GE 1.5T Signa Explorer) and a 3T MRI machine (Philips 3T Ingenia). MRI images were independently reviewed by two study radiologists, and the findings were summarized and categorized into a study database. Related clinical and electroencephalographic (EEG) details were extracted from patient records. Categorical data analysis methods were applied to investigate for relationships between clinically relevant neuroimaging findings and key clinical and EEG observations. Results: Over the study period, 288 children with a confirmed diagnosis of epilepsy had an MRI. They were of median age of 6 [interquartile range (IQR) 2-11] years. Ninety-five (33%) children had abnormal findings on imaging. The most common findings were encephalomalacia related to chronic infarcts (n = 18: 6.3%), cerebral atrophy (n = 11: 3.8%), disorders of neuronal migration (n = 11: 3.8%), periventricular leukomalacia (n = 9: 3.1%), and hippocampal sclerosis (n = 8: 2.8%). Findings related to infectious etiology were only observed in four children. Clinical comorbidity and inter-ictal epileptiform activity on EEG were independently associated with abnormal findings on imaging. Conclusion: Up to a third of the children who underwent an MRI had a positive yield for abnormal findings. Imaging findings related to infectious etiologies were little observed in our cohort, in contradistinction to etiology studies in similar settings. At the time of the study, comorbidity and inter-ictal epileptiform activity on EEG were associated with abnormal findings on imaging and should be considered in informing prioritization for imaging in childhood epilepsy in this setting.

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BACKGROUND: Tsetse fly-borne trypanosomiasis remains a significant problem in Africa despite years of interventions and research. The need for new strategies to control and possibly eliminate trypanosomiasis cannot be over-emphasized. Entomopathogenic fungi (EPF) infect their hosts through the cuticle and proliferate within the body of the host causing death in about 3-14 days depending on the concentration. During the infection process, EPF can reduce blood feeding abilities in hematophagous arthropods such as mosquitoes, tsetse flies and ticks, which may subsequently impact the development and transmission of parasites. Here, we report on the effects of infection of tsetse fly (Glossina fuscipes fuscipes) by the EPF, Metarhizium anisopliae ICIPE 30 wild-type strain (WT) and green fluorescent protein-transformed strain (GZP-1) on the ability of the flies to harbor and transmit the parasite, Trypanosoma congolense. RESULTS: Teneral flies were fed T. congolense-infected blood for 2 h and then infected using velvet carpet fabric impregnated with conidia covered inside a cylindrical plastic tube for 12 h. Control flies were fed with T. congolense-infected blood but not exposed to the fungal treatment via the carpet fabric inside a cylindrical plastic tube. Insects were dissected at 2, 3, 5 and 7 days post-fungal exposure and the density of parasites quantified. Parasite load decreased from 8.7 × 107 at day 2 to between 8.3 × 104 and 1.3 × 105 T. congolense ml- 1 at day 3 post-fungal exposure in fungus-treated (WT and GZP-1) fly groups. When T. congolense-infected flies were exposed to either fungal strain, they did not transmit the parasite to mice whereas control treatment flies remained capable of parasite transmission. Furthermore, M. anisopliae-inoculated flies which fed on T. congolense-infected mice were not able to acquire the parasites at 4 days post-fungal exposure while parasite acquisition was observed in the control treatment during the same period. CONCLUSIONS: Infection of the vector G. f. fuscipes by the entomopathogenic fungus M. anisopliae negatively affected the multiplication of the parasite T. congolense in the fly and reduced the vectorial capacity to acquire or transmit the parasite.

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Docetaxel (DCT) is an anticancer drug which acts by disrupting microtubule dynamics in the highly mitotic cancer cells. Thus, this drug has a potential to affect function and organization of tissues exhibiting high cellular turnover. We investigated, in the rabbit, the effects of a single human equivalent dose (6.26 mg/kg, i.v.) of DCT on the olfactory mucosa (OM) through light and electron microscopy, morphometry, Ki-67 immunostaining, TUNEL assay and the buried food test for olfactory sensitivity. On post-exposure days (PED) 5 and 10, there was disarrangement of the normal cell layering in the olfactory epithelium (OE), apoptotic death of cells of the OE, Bowman's glands and axon bundles, and the presence (including on PED 3) of blood vessels in the bundle cores. A decrease in bundle diameters, olfactory cell densities and cilia numbers, which was most significant on PED 10 (49.3%, 63.4% and 50%, respectively), was also evident. Surprisingly by PED 15, the OM regained normal morphology. Furthermore, olfactory sensitivity decreased progressively until PED 10 when olfaction was markedly impaired, and with recovery from the impairment by PED 15. These observations show that DCT transiently alters the structure and function of the OM suggesting a high regenerative potential for this tissue.

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