Delayed Diagnosis of a Diffuse Invasive Gastrointestinal Aspergillosis in an Immunocompetent Patient

Invasive aspergillosis represents a clinical picture frequently associated with host’s immunosuppression which usually involves a high morbidity and mortality. In general, the most frequent fungal entry is the lungs with secondary hematogenous dissemination, but there are other hypotheses like a gastrointestinal portal of entry. There are some rare publications of cases with invasive aspergillosis in immunocompetent patients. We present the case of an immunocompetent patient without any risk factors except for age, ICU stay, and surgical intervention, who developed a septic shock by invasive gastrointestinal aspergillosis as primary infection. Due to the unusualness of the case, despite all the measures taken, the results were obtained postmortem. We want to emphasize the need not to underestimate the possibility for an invasive aspergillosis in an immunocompetent patient. Not only pulmonary but also gastrointestinal aspergillosis should be taken into account in the differential diagnosis to avoid a delay of treatment

Spectrofluorimetric study of dissolved organic matter in River Salaca (Latvia) basin waters

Dissolved organic matter (DOM) in surface waters influences mineral weathering, nutrient cycling, aggregation of particulate matter and photochemical reactions in waters and aquatic communities. In this study, the effectiveness of UV and fluorescence measurements in distinguishing the origin of DOM and processes within the river basin were analyzed using the River Salaca basin as an example. The basin of River Salaca is characterized by low anthropogenic pressure, however, the water color during the last few decades has increased (an effect known as brownification). As tools to study the composition of dissolved organic substances in waters of the River Salaca and its tributaries the use of UV and fluorescence spectroscopy was evaluated. The use of the fluorescence index (a ratio of the emission intensity at a wavelength of 450 nm to that at 500 nm) allowed us to distinguish sources of aquatic DOM, characterize processes in the water body basin and to follow the changes in organic matter composition. Synchronous scan fluorescence spectrometry was more informative than excitation emission spectra and, provided information on the basic structural features of DOM

Chronic administration of dimebon does not ameliorate amyloid-β pathology in 5xFAD transgenic mice

Dimebon has been tested as a potential modifier of Alzheimer's disease (AD), resulting in mixed clinical trial outcomes. Originally utilized as an antihistamine, Dimebon was later found to ameliorate AD symptoms in initial human trials. Although subsequent trials have reportedly failed to replicate these finding, there is a growing body of evidence that Dimebon might be neuroprotective in certain models of neurodegeneration. The precise mechanism by which Dimebon is thought to act in AD is unclear, though changes in receptor activity, mitochondria function, and autophagy activity have been proposed. It is thus necessary to test Dimebon in transgenic animal model systems to determine if and how the drug affects development and manifestation of pathology, and which pathogenic processes are altered. In the present study we treated mice harboring five familial mutations associated with hereditary AD (5xFAD line) with a chronic regime of Dimebon. The compound was not found to improve the general health or motor behavior of these mice, nor prevent accumulation of Aβ peptides in the brain. Modest changes in response to an anxiogenic task were, however, detected, suggesting Dimebon might improve behavioral abnormalities and cognition in disease in a mechanism independent of protecting against amyloidosis

Chronic Administration of Dimebon does not Ameliorate Amyloid-β Pathology in 5xFAD Transgenic Mice

Dimebon has been tested as a potential modifier of Alzheimer's disease (AD), resulting in mixed clinical trial outcomes. Originally utilized as an antihistamine, Dimebon was later found to ameliorate AD symptoms in initial human trials. Although subsequent trials have reportedly failed to replicate these finding, there is a growing body of evidence that Dimebon might be neuroprotective in certain models of neurodegeneration. The precise mechanism by which Dimebon is thought to act in AD is unclear, though changes in receptor activity, mitochondria function, and autophagy activity have been proposed. It is thus necessary to test Dimebon in transgenic animal model systems to determine if and how the drug affects development and manifestation of pathology, and which pathogenic processes are altered. In the present study we treated mice harboring five familial mutations associated with hereditary AD (5xFAD line) with a chronic regime of Dimebon. The compound was not found to improve the general health or motor behavior of these mice, nor prevent accumulation of Aβ peptides in the brain. Modest changes in response to an anxiogenic task were, however, detected, suggesting Dimebon might improve behavioral abnormalities and cognition in disease in a mechanism independent of protecting against amyloidosis