Uptake of purines in <i>Plasmodium falciparum</i>-infected human erythrocytes is mostly mediated by the human Equilibrative Nucleoside Transporter and the human Facilitative Nucleobase Transporter

&lt;b&gt;Background&lt;/b&gt;: Plasmodium parasites are unable to synthesize purines de novo and have to salvage them from the host. Due to this limitation in the parasite, purine transporters have been an area of focus in the search for anti-malarial drugs. Although the uptake of purines through the human equilibrative nucleoside transporter (hENT1), the human facilitative nucleobase transporter (hFNT1) and the parasite-induced new permeation pathway (NPP) has been studied, no information appears to exist on the relative contribution of these three transporters to the uptake of adenosine and hypoxanthine. Using the appropriate transporter inhibitors, the role of each of these salvage pathways to the overall purine transport in intraerythrocytic Plasmodium falciparum was systematically investigated. &lt;b&gt;Methods&lt;/b&gt;: The transport of adenosine, hypoxanthine and adenine into uninfected and P. falciparum-infected human erythrocytes was investigated in the presence or absence of classical inhibitors of the hFNT1, hENT1 and NPP. The effective inhibition of the various transporters by the classical inhibitors was verified using appropriate known substrates. The ability of high concentration of unlabelled substrates to saturate these transporters was also studied. &lt;b&gt;Results&lt;/b&gt;: Transport of exogenous purine into infected or uninfected erythrocytes occurred primarily through saturable transporters rather than through the NPP. Hypoxanthine and adenine appeared to enter erythrocytes mainly through the hFNT1 nucleobase transporter whereas adenosine entered predominantly through the hENT1 nucleoside transporter. The rate of purine uptake was approximately doubled in infected cells compared to uninfected erythrocytes. In addition, it was found that the rate of adenosine uptake was considerably higher than the rate of hypoxanthine uptake in infected human red blood cells (RBC). It was also demonstrated that furosemide inhibited the transport of purine bases through hFNT1. &lt;b&gt;Conclusion&lt;/b&gt;: Collectively, the data obtained in this study clearly show that the endogenous host erythrocyte transporters hENT1 and hFNT1, rather than the NPP, are the major route of entry of purine into parasitized RBC. Inhibitors of hENT1 and hFNT1, as well as the NPP, should be considered in the development of anti-malarials targeted to purine transport

An unusual recurrence of pruritic creeping eruption after treatment of cutaneous larva migrans in an adult Ghanaian male: a case report with a brief review of literature

The hookworm related Cutaneous Larva Migrans is a common disease present in the tropic and subtropical areas of the world. The disease is self limiting and would naturally resolve within weeks. However, an unusual recurrence of the disease in a Ghanaian male after standard treatment was observed and is herein reported. A 52 year old Ghanaian male of Akan dissent was diagnosed with Cutaneous Larva Migrans in a clinic in Accra, Ghana. Symptoms of the disease persisted for three days after treatment with a 400mg single dose Albendazole and was only resolved after redosing with 400 mg daily of the same drug for three days. Two months post-treatment, the usual pruritic creeping eruption typical with the disease re-appeared even though the victim has not been re-exposed to any possible larva contaminated source. This could possibly be a case of hookworm- related larva resistance to a standard anti-helminthic therapy and host immunity

Regional tourism facts North West

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The evolving SARS-CoV-2 epidemic in Africa: Insights from rapidly expanding genomic surveillance

The past 2 years, during which waves of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) variants swept the globe, have starkly highlighted health disparities across nations. Tegally et al. show how the coordinated efforts of talented African scientists have in a short time made great contributions to pandemic surveillance and data gathering. Their efforts and initiatives have provided early warning that has likely benefited wealthier countries more than their own. Genomic surveillance identified the emergence of the highly transmissible Beta and Omicron variants and now the appearance of Omicron sublineages in Africa. However, it is imperative that technology transfer for diagnostics and vaccines, as well the logistic wherewithal to produce and deploy them, match the data-gathering effort