A qualitative study on loneliness among Filipino elderly

The objective of this study is to understand the experiences of Filipino elderly with loneliness. The study is comprised of 12 Filipino elderly aged 70 to 83 years old who have reportedly experienced loneliness in the latter part of their lives. Through a qualitative approach using the Social Convoy Theory, data collection was executed by conducting personal interviews. Each participant was interviewed twice in order to have a deeper understanding of their answers. The researchers used a coding method wherein they analyzed each transcript to find common themes that describe the experience of loneliness among the Filipino elderly. The data gathered showed three superordinate themes sorrow from aging, losing something valuable, and resilience through coping. The first two are factors that greatly contribute to the overall experience of loneliness among the elderly while the third superordinate theme is the response of the Filipino elderly toward their loneliness. Each superordinate theme has several subordinate themes that support its message

An ultrasonic-based speed sensing system with automatic image-capture using a camera

This thesis is aimed at measuring the speed of cars and if it exceeds the prescribed speed, it would capture an image of the car which violated the speed limit. Nowadays over speeding vehicles can be a cause for accidents and can often be fatal to man. These drivers tend to become reckless because they are not apprehended and eventually repeat the same infraction. Several devices were invented or developed to determine those automobiles that surpass the maximum allowable velocity. There were the speed guns and others that utilize microwave technology but is too costly to build. Instead of the policeman running after or chasing the offender, the traffic enforcers would just wait for the picture of the violator (car) and give him/her the violation when he/she registers the car once again. There is no escape with the offender denying the accusation because there is a captured image which came along with the citation which proves that he/she violated the law on over speeding

Microbiota-driven transcriptional changes in prefrontal cortex override genetic differences in social behavior

Gene-environment interactions impact the development of neuropsychiatric disorders, but the relative contributions are unclear. Here, we identify gut microbiota as sufficient to induce depressive-like behaviors in genetically distinct mouse strains. Daily gavage of vehicle (dH2O) in nonobese diabetic (NOD) mice induced a social avoidance behavior that was not observed in C57BL/6 mice. This was not observed in NOD animals with depleted microbiota via oral administration of antibiotics. Transfer of intestinal microbiota, including members of the Clostridiales, Lachnospiraceae and Ruminococcaceae, from vehicle-gavaged NOD donors to microbiota-depleted C57BL/6 recipients was sufficient to induce social avoidance and change gene expression and myelination in the prefrontal cortex. Metabolomic analysis identified increased cresol levels in these mice, and exposure of cultured oligodendrocytes to this metabolite prevented myelin gene expression and differentiation. Our results thus demonstrate that the gut microbiota modifies the synthesis of key metabolites affecting gene expression in the prefrontal cortex, thereby modulating social behavior

Astrocyte-shed extracellular vesicles regulate the peripheral leukocyte response to inflammatory brain lesions

Brain injury induces a peripheral acute cytokine response that directs the transmigration of leukocytes into the brain. Because this brain-to-peripheral immune communication affects patient recovery, understanding its regulation is important. Using a mouse model of inflammatory brain injury, we set out to find a soluble mediator for this phenomenon. We found that extracellular vesicles (EVs) shed from astrocytes in response to intracerebral injection of interleukin-1β (IL-1β) rapidly entered into peripheral circulation and promoted the transmigration of leukocytes through modulation of the peripheral acute cytokine response. Bioinformatic analysis of the protein and microRNA cargo of EVs identified peroxisome proliferator–activated receptor α (PPARα) as a primary molecular target of astrocyte-shed EVs. We confirmed in mice that astrocytic EVs promoted the transmigration of leukocytes into the brain by inhibiting PPARα, resulting in the increase of nuclear factor κB (NF-κB) activity that triggered the production of cytokines in liver. These findings expand our understanding of the mechanisms regulating communication between the brain and peripheral immune system and identify astrocytic EVs as a molecular regulator of the immunological response to inflammatory brain damage

Astrocyte-shed extracellular vesicles regulate the peripheral leukocyte response to inflammatory brain lesions

Brain injury induces a peripheral acute cytokine response that directs the transmigration of leukocytes into the brain. Because this brain-to-peripheral immune communication affects patient recovery, understanding its regulation is important. Using a mouse model of inflammatory brain injury, we set out to find a soluble mediator for this phenomenon. We found that extracellular vesicles (EVs) shed from astrocytes in response to intracerebral injection of interleukin-1β (IL-1β) rapidly entered into peripheral circulation and promoted the transmigration of leukocytes through modulation of the peripheral acute cytokine response. Bioinformatic analysis of the protein and microRNA cargo of EVs identified peroxisome proliferator–activated receptor α (PPARα) as a primary molecular target of astrocyte-shed EVs. We confirmed in mice that astrocytic EVs promoted the transmigration of leukocytes into the brain by inhibiting PPARα, resulting in the increase of nuclear factor κB (NF-κB) activity that triggered the production of cytokines in liver. These findings expand our understanding of the mechanisms regulating communication between the brain and peripheral immune system and identify astrocytic EVs as a molecular regulator of the immunological response to inflammatory brain damage