-associated Placentitis in the absence of maternal seroconversion.

Severe granulomatous chronic villitis with focal remnants of was confirmed by immunohistochemistry and DNA-based methods in the placenta from a child that died four days after birth. The immunocompetent mother was seronegative for at delivery and 10 months later. Placental infection may happen without maternal systemic infection.

Biomarkers for iron metabolism among patients hospitalized with community-acquired pneumonia caused by infection with SARS-CoV-2, bacteria, and influenza.

Ferritin, the central iron storage protein, has attracted attention as a biomarker of severe COVID-19. Few studies have investigated regulators of iron metabolism in the context of COVID-19. The aim was to evaluate biomarkers for iron metabolism in the acute phase response to community-acquired pneumonia (CAP) caused by SARS-CoV-2 compared with CAP caused by bacteria or influenza virus in hospitalized patients.

The disease burden of ocular toxoplasmosis in Denmark in 2019: Estimates based on laboratory testing of ocular samples and on publicly available register data.

Background: is an important zoonotic protozoan parasite with worldwide distribution. Information on the contribution of ocular toxoplasmosis to the disease burden caused by this parasite is limited or lacking from many countries.

Methods: We estimated the minimum occurrence of ocular toxoplasmosis in Denmark using results from direct detection of DNA with qPCR and determination of the Goldmann-Witmer coefficient on ocular samples submitted by ophthalmological clinics and departments to the national reference laboratory in 2003-2019.

Imaging of the Buccal Mucosa Shows Loss of the Endothelial Glycocalyx and Perivascular Hemorrhages in Pediatric Plasmodium falciparum Malaria.

Severe malaria is mostly caused by resulting in considerable, systemic inflammation and pronounced endothelial activation. The endothelium forms an interface between blood and tissue, and vasculopathy has previously been linked with malaria severity. We studied the extent to which the endothelial glycocalyx that normally maintains endothelial function is involved in falciparum malaria pathogenesis by using incident dark-field imaging in the buccal mucosa.

Infectious diseases detected by screening after arrival to Denmark in internationally adopted children.

Aim: To show the prevalence of selected infectious diseases among internationally adopted children (IAC) in Denmark.

Background: Each year approximately 200 IAC arrive in Denmark. These are at increased risk of infectious diseases rarely seen in Danish children.

Antibiotic use in surgical units of selected hospitals in Ghana: a multi-centre point prevalence survey.

Background: Improper use of antibiotics leads to the emergence of resistant microorganisms as well as drug toxicity, increased healthcare costs, morbidity and mortality. Globally, an estimated 25-68% of hospitalized patients receive suboptimal antibiotic regimes. Information on the extent of this problem in Ghana is currently limited, particularly in surgical units.

Antibiotic prescribing in paediatric inpatients in Ghana: a multi-centre point prevalence survey.

Background: Excessive and inappropriate use of antibiotics in hospitalised patients contributes to the development and spread of antibiotic resistance. Implementing a stewardship programme to curb the problem requires information on antibiotic use. This study describes a multicentre point prevalence of antibiotic use among paediatric inpatients in Ghana.

Experimental cerebral malaria is associated with profound loss of both glycan and protein components of the endothelial glycocalyx.

Vascular pathology is central to malaria pathogenesis and associated with severity of disease. We have previously documented shedding of the cerebral endothelial glycocalyx in experimental malaria and hypothesized that this action is implicated in the pathogenesis of cerebral malaria (CM). Quantification and characterization of the intraluminal vascular glycocalyx are technically challenging.

Binding of Plasmodium falciparum to CD36 can be shielded by the glycocalyx.

Background: Plasmodium falciparum-infected erythrocytes sequester in the microcirculation due to interaction between surface-expressed parasite proteins and endothelial receptors. Endothelial cells are covered in a carbohydrate-rich glycocalyx that shields against undesired leukocyte adhesion. It was investigated if the cellular glycocalyx affects the binding of P.

Erratum to: Glucagon-like peptide-1 analogue, liraglutide, in experimental cerebral malaria: implications for the role of oxidative stress in cerebral malaria.

[This corrects the article DOI: 10.1186/s12936-016-1486-0.].

Glucagon-like peptide-1 analogue, liraglutide, in experimental cerebral malaria: implications for the role of oxidative stress in cerebral malaria.

Background: Cerebral malaria from Plasmodium falciparum infection is major cause of death in the tropics. The pathogenesis of the disease is complex and the contribution of reactive oxygen and nitrogen species (ROS/RNS) in the brain is incompletely understood. Insulinotropic glucagon-like peptide-1 (GLP-1) mimetics have potent neuroprotective effects in animal models of neuropathology associated with ROS/RNS dysfunction.

GLP-1 improves neuropathology after murine cold lesion brain trauma.

Objectives: In this study, we address a gap in knowledge regarding the therapeutic potential of acute treatment with a glucagon-like peptide-1 (GLP-1) receptor agonist after severe brain trauma. Moreover, it remains still unknown whether GLP-1 treatment activates the protective, anti-neurodegenerative cAMP response element binding protein (CREB) pathway in the brain in vivo, and whether activation leads to observable increases in protective, anti-neurodegenerative proteins. Finally, we report the first use of a highly sensitive in vivo imaging agent to assess reactive species generation after brain trauma.

Systemic and Cerebral Vascular Endothelial Growth Factor Levels Increase in Murine Cerebral Malaria along with Increased Calpain and Caspase Activity and Can be Reduced by Erythropoietin Treatment.

The pathogenesis of cerebral malaria (CM) includes compromised microvascular perfusion, increased inflammation, cytoadhesion, and endothelial activation. These events cause blood-brain barrier disruption and neuropathology and associations with the vascular endothelial growth factor (VEGF) signaling pathway have been shown. We studied this pathway in mice infected with Plasmodium berghei ANKA causing murine CM with or without the use of erythropoietin (EPO) as adjunct therapy.

Investigation of hydrogen sulfide gas as a treatment against P. falciparum, murine cerebral malaria, and the importance of thiolation state in the development of cerebral malaria.

Introduction: Cerebral malaria (CM) is a potentially fatal cerebrovascular disease of complex pathogenesis caused by Plasmodium falciparum. Hydrogen sulfide (HS) is a physiological gas, similar to nitric oxide and carbon monoxide, involved in cellular metabolism, vascular tension, inflammation, and cell death. HS treatment has shown promising results as a therapy for cardio- and neuro- pathology.

CNS hypoxia is more pronounced in murine cerebral than noncerebral malaria and is reversed by erythropoietin.

Cerebral malaria (CM) is associated with high mortality and risk of sequelae, and development of adjunct therapies is hampered by limited knowledge of its pathogenesis. To assess the role of cerebral hypoxia, we used two experimental models of CM, Plasmodium berghei ANKA in CBA and C57BL/6 mice, and two models of malaria without neurologic signs, P. berghei K173 in CBA mice and P.