Knowledge, attitudes, and practices regarding dengue, chikungunya, and Zika in Cali, Colombia.

Dengue fever (DENF), chikungunya (CHIK), and Zika are responsible for the majority of the burden caused by vector-borne diseases (VBDs); which are produced by viruses primarily transmitted by the Aedes mosquito. Aedes have become prolific in urban areas due to a combination of climate change, rapid urbanization, increased human mobility, and globalization, causing the three VBDs to emerge in novel regions. Community knowledge can provide detailed insights about the spatial heterogeneity of disease risk and rates within a particular region, improving public health interventions. Knowledge, Attitude, and Practice (KAP) surveys are used to shed light on at-risk communities' understanding of the vector, the pathogen, prevention and treatment strategies. Little is known how KAP varies among diseases, and among neighborhoods within a city. Understanding KAP variation among co-circulating VBDs at a fine-level, especially differences between endemic and emerging diseases, can improve targeted interventions, education programs, and health policy. We administered KAP surveys to 327 individuals in healthcare centers and selected neighborhoods in Cali, Colombia in June 2019. We utilized generalized linear models (GLMs) to identify significant predictors of KAP. Our findings suggest that knowledge is related to community characteristics (e.g. strata), while attitudes and practices are more related to individual-level factors. Access to healthcare also forms significant predictor of residents participating in preventative practices. The results can be leveraged to inform public health officials and communities to motivate at-risk neighborhoods to take an active role in vector surveillance and control, while improving educational and surveillance resources in Cali, Colombia.

Multiphoton intravital microscopy in small animals: motion artefact challenges and technical solutions.

Since its invention 29 years ago, two-photon laser-scanning microscopy has evolved from a promising imaging technique, to an established widely available imaging modality used throughout the biomedical research community. The establishment of two-photon microscopy as the preferred method for imaging fluorescently labelled cells and structures in living animals can be attributed to the biophysical mechanism by which the generation of fluorescence is accomplished. The use of powerful lasers capable of delivering infrared light pulses within femtosecond intervals, facilitates the nonlinear excitation of fluorescent molecules only at the focal plane and determines by objective lens position. This offers numerous benefits for studies of biological samples at high spatial and temporal resolutions with limited photo-damage and superior tissue penetration. Indeed, these attributes have established two-photon microscopy as the ideal method for live-animal imaging in several areas of biology and have led to a whole new field of study dedicated to imaging biological phenomena in intact tissues and living organisms. However, despite its appealing features, two-photon intravital microscopy is inherently limited by tissue motion from heartbeat, respiratory cycles, peristalsis, muscle/vascular tone and physiological functions that change tissue geometry. Because these movements impede temporal and spatial resolution, they must be properly addressed to harness the full potential of two-photon intravital microscopy and enable accurate data analysis and interpretation. In addition, the sources and features of these motion artefacts are varied, sometimes unpredictable and unique to specific organs and multiple complex strategies have previously been devised to address them. This review will discuss these motion artefacts requirement and technical solutions for their correction and after intravital two-photon microscopy.

Fibrinogen signal transduction in the nervous system.

Fibrinogen is a pleiotropic blood protein that regulates coagulation, inflammation and tissue repair. Fibrinogen extravasates in the nervous system after injury or disease associated with vascular damage or blood-brain barrier (BBB) disruption. Fibrinogen is not merely a marker of BBB disruption, but plays a causative role in neurologic disease as a potent inducer of inflammation and an inhibitor of neurite outgrowth. Fibrinogen mediates functions in the nervous system as a ligand for cell-specific receptors. In microglia, fibrinogen mediates activation of Akt and Rho via the CD11b/CD18 integrin receptor, while in neurons fibrinogen induces phosphorylation of epidermal growth factor (EGF) receptor via the alphavbeta3 integrin. Pharmacologic targeting of the interactions of fibrinogen with its nervous system receptors could provide novel strategies for therapeutic intervention in neuroinflammatory and neurodegenerative diseases.

Fibrinogen signal transduction as a mediator and therapeutic target in inflammation: lessons from multiple sclerosis.

The blood protein fibrinogen as a ligand for integrin and non-integrin receptors functions as the molecular nexus of coagulation, inflammation and immunity. Studies in animal models and in human disease have demonstrated that extravascular fibrinogen that is deposited in tissues upon vascular rupture is not merely a marker, but a mediator of diseases with an inflammatory component, such as rheumatoid arthritis, multiple sclerosis, sepsis, myocardial infarction and bacterial infection. The present article focuses on the recent discoveries of specific cellular targets and receptors for fibrinogen within tissues that have extended the role of fibrinogen from a coagulation factor to a regulator of inflammation and immunity. Fibrinogen has the potential for selective drug targeting that would target its proinflammatory properties without affecting its beneficial effects in hemostasis, since it interacts with different receptors to mediate blood coagulation and inflammation. Strategies to target receptors for fibrinogen and fibrin within the tissue microenvironment could reveal selective and disease-specific agents for therapeutic intervention in a variety of human diseases associated with fibrin deposition.