Plasmodium falciparum infection can cause microvascular dysfunction, cerebral encephalopathy and death if untreated. We have previously shown that high concentrations of free heme, and C-X-C motif chemokine 10 (CXCL10) in sera of malaria patients induce apoptosis in microvascular endothelial and neuronal cells contributing to vascular dysfunction, blood-brain barrier (BBB) damage and mortality. Endothelial progenitor cells (EPC) are microvascular endothelial cell precursors partly responsible for repair and regeneration of damaged BBB endothelium. Studies have shown that EPC’s are depleted in severe malaria patients, but the mechanisms mediating this phenomenon are unknown. Toll-like receptors recognize a wide variety of pathogen-associated molecular patterns generated by pathogens such as bacteria and parasites. We tested the hypothesis that EPC depletion during malaria pathogenesis is a function of heme-induced apoptosis mediated by CXCL10 induction and toll-like receptor (TLR) activation. Heme and CXCL10 concentrations in plasma obtained from malaria patients were elevated compared with non-malaria subjects. EPC numbers were significantly decreased in malaria patients (P < 0.02) and TLR4 expression was significantly elevated in vivo. These findings were confirmed in EPC precursors in vitro; where it was determined that heme-induced apoptosis and CXCL10 expression was TLR4-mediated. We conclude that increased serum heme mediates depletion of EPC during malaria pathogenesis.

Background:Adherence is the active, voluntary, and collaborative involvement of the patient in a mutually acceptable course of behaviour to produce a therapeutic result. The study is aimed at assessing adherence to medication and its relation to therapeutic outcomes among people living with diabetes in the Ho Municipality.Methodology:A cross-sectional study was conducted involving 150 diabetic patients attending the diabetic clinic at the Ho Municipal Hospital. Urine glucose and urine protein were measured using a two-parameter dipstick. The current fasting blood glucose and blood pressure, as well as the measurements of two previous visits, were documented. A semi-structured questionnaire including the Diabetes Complication Checklist and the Morisky, Green and Levine Adherence Scale were used to capture biodata, clinical information and medication adherence.Results:Optimal medication adherence was 60.67%. Glycaemic control and controlled blood pressure were 33.33% and 58.67%, respectively. The prevalence of glycosuria and proteinuria was 10.67% and 3.3%, respectively. Percentage glycaemic control and controlled blood pressure were found to be higher among the medication adherent group, while glycosuria and proteinuria were the highest among participants presenting with low medication adherence.Conclusion:In this group of patients living with diabetes in the Ho Municipality, high level of uncontrolled glycaemia and blood pressure exist.However, these two treatment outcomes may be modulated by optimal medication adherence.

Background Preserved blood cells undergo progressive structural and functional changes that may affect their function, integrity, and viability after transfusion. The impact of transfusion of stored blood on potassium, sodium, or acid-base balance in the recipient may be complex, but information on it is inconsistent. This study therefore sought to determine the changes in the potassium and sodium levels in whole blood stored at 4°C for 28 days and clinical outcomes when such blood are transfused. Methods Whole blood were taken into double CPDA-1 bags and 50 ml transferred into the satellite bags for the study. Electrolyte concentration determinations were made on each of the blood sample on days 0, 7, 14, 21, and 28 using the Vitalab Selectra Junior chemistry analyser. The remaining blood in the main bags was transfused after the 28-day period, and biochemical analysis carried out on the patients before and after the transfusion. One-way ANOVA was used for the analysis of variance between the weekly ion concentrations and independent sample Mann–Whitney U test for the data obtained from the patients. Results The mean potassium level of all the samples started with a normal value of 3.45 mmol/L on the first day followed by a sharp rise to 9.40 mmol/L on day 7, 13.40 mmol/L on day 14, 14.60 mmol/L on day 21, and 15.40 mmol/L on day 28. Sodium on the other hand started with a high value of 148.4 mmol/L on day 0 and then reduced to 146.4 mmol/L on day 7, 140.8 mmol/L on day 14, 135.6 mmol/L on day 21, and a low value of 130.8 mmol/L on day 28. No adverse clinical outcomes were seen in patients after they were transfused with the blood. Conclusion It can be deduced that potassium concentration in refrigerated blood increases, whilst sodium concentration reduces with time and when such blood is transfused, it may not result in any adverse clinical outcome.

In 2018, 228 million cases and 405,000 malaria-associated deaths were reported worldwide with a majority being in Africa. A wide range of factors, including parasitemia, host immunity, inflammatory responses to infection, and host hemoglobin genotype, mediate the severity of malaria. Among the hemoglobinopathies, hemoglobin S (HbS) is caused by a single amino acid substitution of Glutamic Acid replaced by Valine at the sixth position of the beta-globin chain (E6V). Hemoglobin C (HbC) on the other hand, involves a single amino acid substitution of Glutamic Acid by a Lysine (E6K), which has received the most attention. These substitutions alter the stability of Hb leading to wide-ranging hematological disorders. The homozygous state of hemoglobin S (HbSS) results in sickle cell anemia (SCA) whereas the heterozygous state (HbAS) results in sickle cell trait (SCT). Both mutations are reported to mediate the reduction in the severity and fatality of Plasmodium falciparum malaria. The mechanism underlying this protection is poorly understood. Since both malaria and sickle cell disease (SCD) are associated with the destruction of erythrocytes and widespread systemic inflammation, identifying which inflammatory factor(s) mediate susceptibility of individuals with different hemoglobin genotypes to Plasmodium infection could result in the discovery of new predictive markers and interventions against malaria or SCD severity. We hypothesized that hemoglobin genotypes modulate the inflammatory response to Plasmodium infection. We conducted a cross-sectional study in Ghana, West Africa, between 2014 and 2019 to ascertain the relationships between blood inflammatory cytokines, Plasmodium infection, and hemoglobin genotype. A total of 923 volunteers were enrolled in the study. A total of 74, age and sex-matched subjects were identified with various genotypes including HbAS, HbAC, HbSS, HbSC, HbCC, or HbAA. Complete blood counts and serum inflammatory cytokine expression levels were assessed. The results indicate that differential expression of CXCL10, TNF-α, CCL2, IL-8, and IL-6 were tightly linked to hemoglobin genotype and severity of Plasmodium infection and that these cytokine levels may be predictive for susceptibility to severe malaria or SCD severity.