Daystar University Repository

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Conference/ Workshop/ Seminar/ Proceedings/ Lecture Series
A collection of conference, workshop, seminar, proceedings, and lecture series showcasing diverse topics and cutting-edge research from faculty and staff of Daystar University.
Daystar Archives
An archival collection chronicling the institutional history, academic achievements, and diverse heritage of Daystar University.
Daystar University Publications
A collection of Publications by faculty and staff showcasing research, academic achievements, and institutional insights of Daystar University.
Lectures and Speeches
A collection of Lectures and Speeches from distinguished speakers across various disciplines of Daystar University.
Policies
A collection Policies and Operational Manuals from different departments of Daystar University.

Recent Submissions

Co-administration of chloroquine and coenzyme Q10 improved treatment outcome during experimental cerebral malaria
(Indian Society for Parasitology, 2022) Nyambuga, Nyariki James; Amwayi, Peris W.; Ochola, Lucy A.; Wairagu, Peninah M.; Orina, Isaac Alfred
Development of cerebral malaria (CM) is drivenby parasitemia levels, harmful inflammatory response,oxidative stress and consequent breach of the blood brainbarrier. Use of adjunct therapy that utilizes an antioxidant and anti-inflammatory agent alongside chloroquine (CQ), may improve treatment outcome and shorten recovery from post-infection sequelae. Though withdrawn in some countries, CQ is still in use for prophylaxis and treatment of malaria in many countries. Current study investigated whether oral co-administration of 50 mg/kg CQ and 200 mg/kg of coenzyme Q10 (CoQ10) would improve treatment outcome against experimental cerebral malaria (ECM) and assuage the deleterious effects of oxidative stress and inflammation upon infection by Plasmodium berghei ANKA (PbA) in a C57BL/6 J mouse model. Treatment with CQ ? CoQ10 resulted in an improved parasite elimination; clearing the parasite one day early, when compared to mice on CQ alone. Remarkably, treatment with CQ and CoQ10 separately or in combination, assuaged PbA induced elevation of serum levels of TNF-a and IFN-c an indication of protection from ECM progression. Furthermore, CQ and CoQ10-administration, blocked parasite-driven elevation of aspartate transaminase (AST), alanine transaminase (ALT) and bilirubin. In the presence of CQ and CoQ10, severe PbA-induced systemic induction of oxidative stress and resultant GSH depletion was reduced in the brain, liver, spleen, and kidney. Overall, these findings demonstrate that administration of CQ and CoQ10 ameliorates harmful parasite-driven oxidative stress and inflammation, while slowing the progression to full blown ECM and may improve treatment outcome in CM
Empowering Older Adults to Utilise Neighbourhoods: A Healthy Ageing Perspective
(Springer Nature, 2024) Agyemang, Simon Mawulorm; Muhonja, Faith Hope; Sghaier, Sarra; Sorkpor, Richmond Stephen; Akude, Seyram Kafui
Chronic S. Mansoni Infection Critically Regulates PbA Infection-associated Severity and Pathological Events in a Mouse Model
(Elsevier, 2025) Nyambuga, Nyariki James; Owiti, Okonjo Edward; Kasiti, Muganda Andrew; Syokui, Yole Dorcas
The parasite Plasmodium is responsible for the severe infection known as malaria. The infection causes high mortality and morbidity, especially in endemic areas worldwide. Schistosomes which are blood flukes are the primary cause of schistosomiasis, which is the second most common parasitic illness in terms of morbidity and death after malaria. In many areas, both of these illnesses are co-endemic. Biochemically, each parasite utilizes the host protein differently and has defined immunological and physiological responses. This study sought to assess how persistent S. mansoni infection affected the severity of the P. berghei ANKA-associated illness and other pathological events in a mouse model during co-infection. Mice were infected with 200 Schistosoma mansoni cercaria. After chronic S. mansoni infection had been established, mice in the coinfection group were inoculated with 10,000 PbA-infected red blood cells. Physiological parameters were monitored at a two-day interval, to track the infection levels. Furthermore, liver andkidney function tests and oxidative stress markers were quantified at the end of the study and analyzed at a p < 0.05. Co-infection of S. mansoni and PbA enhanced the survival of mice whichwas independent of parasitemia preventing lethal experimental malaria in the majority of mice and prevented hepatosplenomegaly. Chronic S. mansoni infection resulted in hepatosplenomegaly which contributed to an increase in body weight while the introduction of malaria in the host reduced body weight. Liver functionality was disrupted by the measurement of the ALP enzyme, a marker of liver damage. Schistosomiasis reduced host metabolites such as protein, and lipids as schistosomes cannot synthesize their own de novo. Co-infection restored the disruptive effect of S. mansoni in the host. There was evident oxidative stress in the host, liver, and brain of mice infected with S. mansoni or PbA alone. However, coinfection of S. mansoni and PbA ameliorated oxidative stress with concomitant attenuation of organ injury hence reinforcing protection observed in experimental malaria. Overall, this study demonstrates that chronic S. mansoni infection is critical in the regulation of PbA infection-associated severity & pathological events in a mouse model.
Street Food Vendors
(Lap Lambert Academic Publishing, 2013) Muhonja, Faith Hope
Disaster Management: The Kenyan Perspective
(LAP LAMBERT Academic Publishing, 2012) Muhonja, Faith Hope