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Water is the most vital nutrient in the human body accounting for about 60% of the body weight. To maintain optimal health, it is important for humans to consume a sufficient amount of fluids daily. Therefore, tracking the amount of human daily fluid intake has a myriad of health applications like dehydration prevention. In this paper, we present FluidMeter: a ubiquitous and unobtrusive system to track the amount of fluid intake leveraging the inertial sensors embedded in smartwatches. To achieve this, FluidMeter first separates the drinking activities from other human activities (playing, running, eating, etc.). Thereafter, it analyzes the sampled sensors data during the extracted drinking episodes to recognize the sequence of micro-activities (lift the bottle, sip, release the bottle) that constitute the drinking activity. Finally, it applies some machine learning algorithms on some features extracted from sampled sensor data during the sipping period to gauge the amount of fluid intake in the designated drinking episode. FluidMeter is evaluated by collecting more than 260 hours of different human activities by 70 different participants using different smartwatch models. The results show that FluidMeter can recognize the drinking activity and its micro-activities accurately which is comparable to that achieved by the state-of-the-art techniques. Finally, FluidMeter can estimate the overall amount of fluid intake in grams accurately with a estimation error limited to 15%, highlighting its promise as a ubiquitous health service.

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Neuronal ceroid-lipofuscinoses (NCL) are a group of neurodegenerative diseases and autosomal recessive lysosomal storage disorders. We examined the involvement of cell death, oxidative stress, and glutamate excitotoxicity using immunohistochemistry against Bcl-2, Bcl-x, oxidative products to proteins, lipids and DNA, calcium-binding proteins (calbindin-D28K, parvalbumin, calretinin), and glial glutamate transporters (excitatory amino acid transporters 1 and 2), in addition to terminal deoxynucleotidyl transferase-mediated dUTP-nick end labeling (TUNEL) in the brains from three cases of late infantile form of NCL (LINCL) and one case of juvenile form of NCL (JNCL) to investigate the neurodegenerative mechanisms. In the cerebral and cerebellar cortex, all of three LINCL cases demonstrated neurons with TUNEL-immunoreactive nuclei, whereas the JNCL case did not show TUNEL-immunoreactive nuclei. The coexistence of the nuclear TUNEL-immunoreactivity nuclei and cytoplasmic deposition of 4-hydroxy-2-nonenal-modified protein in the frontal cortex and hypoglossal nucleus may suggest a possible interrelationship between DNA fragmentation and lipid oxidation in LINCL. Additionally, glycoxidation of protein and oxidative stress to DNA seemed to be involved in the cerebellar and cerebral degeneration, respectively. Interneurons immunoreactive for calbindin-D28K and parvalbumin were severely reduced in the cerebral cortex, whereas those for calretinin were comparatively well preserved in LINCL, indicating the possibility of altered GABAergic system. The disturbance of expression of glial glutamate transporters seemed to be heterogeneous and mild. These findings suggest the possibility of new treatments for neurodegeneration in LINCL using antioxidative agents and/or GABAergic medications.

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