Strategies to reduce fishy odor in aquatic products: Focusing on formation mechanism and mitigation means.

Aquatic products, integral to human diets, often bear a distinct fishy odor that diminishes their appeal. Currently, the formation mechanisms of these odoriferous compounds are not fully understood, complicating their effective control. This review aims to provide a comprehensive overview of key fishy compounds, with a focus on their formation mechanisms and innovative methods for controlling fishy odors. Fishy odors in aquatic products arise not only from the surrounding environment but also from endogenous transformations due to lipid autoxidation, enzymatic reactions, degradation of trimethylamine oxide, and Strecker degradation. Methods such as sensory masking, adsorbent and biomaterial adsorption, nanoliposome encapsulation, heat treatment, vacuum treatment, chemical reactions, and biological metabolic transformations have been developed to control fishy odors. Investigating the formation mechanisms of fishy odors will provide solid foundational knowledge that can inspire creative approaches to controlling these unpleasant odors.

α-Synuclein Aggregates in the Nigro-Striatal Dopaminergic Pathway Impair Fine Movement: Partial Reversal by the Adenosine A2A Receptor Antagonist.

Parkinson's disease (PD) is characterized pathologically by abnormal aggregation of alpha-synuclein (α-Syn) in the brain and clinically by fine movement deficits at the early stage, but the roles of α-Syn and associated neural circuits and neuromodulator bases in the development of fine movement deficits in PD are poorly understood, in part due to the lack of appropriate behavioral testing paradigms and PD models without motor confounding effects. Here, we coupled two unique behavioral paradigms with two PD models to reveal the following: (i) Focally injecting α-Syn fibrils into the dorsolateral striatum (DLS) and the transgenic expression of A53T-α-Syn in the dopaminergic neurons in the substantia nigra (SN, PITX3-IRES2-tTA/tetO-A53T mice) selectively impaired forelimb fine movements induced by the single-pellet reaching task. (ii) Injecting α-Syn fibers into the SN suppressed the coordination of cranial and forelimb fine movements induced by the sunflower seed opening test. (iii) Treatments with the adenosine A2A receptor (A2AR) antagonist KW6002 reversed the impairment of forelimb and cranial fine movements induced by α-Syn aggregates in the SN. These findings established a causal role of α-Syn in the SNc-DLS dopaminergic pathway in the development of forelimb and cranial fine movement deficits and suggest a novel therapeutic strategy to improve fine movements in PD by A2AR antagonists.

Antarctic krill (Euphausia superba) oil modulatory effects on ethanol-induced acute injury of the gastric mucosa in rats.

Antarctic krill oil (KO) prepared using supercritical carbon dioxide extraction and characterized using gas chromatography-mass spectrometry was used to investigate its preventive effect on ethanol-induced gastric tissue damage in a rat model in vivo. KO characterization showed that 74.96% of the unsaturated fatty acids consist of oleic acid, eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA). Rats pre-treated with KO (100, 200, and 500 mg/kg) showed mitigated oxidative stress through enhanced antioxidant enzyme superoxide dismutase (SOD) and reducing enzymes malondialdehyde (MDA) and myeloperoxidase (MPO) in gastric mucosal injury induced by ethanol. Additionally, the secretion of pro-inflammatory cytokines (TNF-α, IL-6, and IL-1ß), the expression of the IκBα/NF-κB signaling pathway, and nitric oxide (NO) production was suppressed. The results also demonstrated a significant decrease in histological injury and hemorrhage scores in a dose-dependent manner in the KO range. Therefore, KO has potential as a food supplement to alleviate ethanol-induced acute gastric mucosal injury.

α-Synuclein Selectively Impairs Motor Sequence Learning and Value Sensitivity: Reversal by the Adenosine A2A Receptor Antagonists.

Parkinson's disease (PD) is characterized pathologically by alpha-synuclein (α-Syn) aggregates and clinically by the motor as well as cognitive deficits, including impairments in sequence learning and habit learning. Using intracerebral injection of WT and A53T mutant α-Syn fibrils, we investigate the behavioral mechanism of α-Syn for procedure-learning deficit in PD by critically determining the α-Syn-induced effects on model-based goal-directed behavior, model-free (probability-based) habit learning, and hierarchically organized sequence learning. 1) Contrary to the widely held view of habit-learning deficit in early PD, α-Syn aggregates in the dorsomedial striatum (DMS) and dorsolateral striatum (DLS) did not affect acquisition of habit learning, but selectively impaired goal-directed behavior with reduced value sensitivity. 2) α-Syn in the DLS (but not DMS) and SNc selectively impaired the sequence learning by affecting sequence initiation with the reduced first-step accuracy. 3) Adenosine A2A receptor (A2AR) antagonist KW6002 selectively improved sequence learning by preferentially improving sequence initiation and shift of sequence learning as well as behavioral reactivity. These findings established a casual role of α-Syn in the SN-DLS pathway in sequence-learning deficit and DMS α-Syn in goal-directed behavior deficit and suggest a novel therapeutic strategy to improve sequence-learning deficit in PD with enhanced sequence initiation by A2AR antagonists.

Striatopallidal adenosine A2A receptors in the nucleus accumbens confer motivational control of goal-directed behavior.

The ability to learn the reward-value and action-outcome contingencies in dynamic environment is critical for flexible adaptive behavior and development of effective pharmacological control of goal-directed behaviors represents an important challenge for improving the deficits in goal-directed behavior which may underlie seemingly disparate symptoms across psychiatric disorders. Adenosine A2A receptor (A2AR) is emerging as a novel neuromodulatory target for controlling goal-directed behavior for its unique neuromodulatory features: the ability to integrate dopamine and glutamate signaling, the "brake" constraint of various cognitive processes and the balanced control of goal-directed and habit actions. However, the contribution and circuit mechanisms of the striatopallidal A2ARs in nucleus accumbens (NAc) to control of goal-directed behavior remain to be determined. Here, we employed newly developed opto-A2AR and the focal A2AR knockdown strategies to demonstrate the causal role of NAc A2AR in control of goal-directed behavior. Furthermore, we dissected out multiple distinct behavioral mechanisms underlying which NAc A2ARs control goal-directed behavior: (i) NAc A2ARs preferentially control goal-directed behavior at the expense of habit formation. (ii) NAc A2ARs modify the animals' sensitivity to the value of the reward without affecting the action-outcome contingency. (iii) A2AR antagonist KW6002 promotes instrumental actions by invigorating motivation. (iv) NAc A2ARs facilitate Pavlovian incentive value transferring to instrumental action. (v) NAc A2ARs control goal-directed behavior probably not through NAc-VP pathway. These insights into the behavioral and circuit mechanisms for NAc A2AR control of goal-directed behavior facilitate translational potential for A2AR antagonists in reversal of deficits in goal-directed decision-making associated with multiple neuropsychiatric disorders.

Pharmacological Blockade of Adenosine A2A but Not A1 Receptors Enhances Goal-Directed Valuation in Satiety-Based Instrumental Behavior.

The balance and smooth shift between flexible, goal-directed behaviors and repetitive, habitual actions are critical to optimal performance of behavioral tasks. The striatum plays an essential role in control of goal-directed versus habitual behaviors through a rich interplay of the numerous neurotransmitters and neuromodulators to modify the input, processing and output functions of the striatum. The adenosine receptors (namely A2AR and A1R), with their high expression pattern in the striatum and abilities to interact and integrate dopamine, glutamate and cannabinoid signals in the striatum, may represent novel therapeutic targets for modulating instrumental behavior. In this study, we examined the effects of pharmacological blockade of the A2ARs and A1Rs on goal-directed versus habitual behaviors in different information processing phases of instrumental learning using a satiety-based instrumental behavior procedure. We found that A2AR antagonist acts at the coding, consolidation and expression phases of instrumental learning to modulate animals' sensitivity to goal-directed valuation without modifying action-outcome contingency. However, pharmacological blockade and genetic knockout of A1Rs did not affect acquisition or sensitivity to goal-valuation of instrumental behavior. These findings provide pharmacological evidence for a potential therapeutic strategy to control abnormal instrumental behaviors associated with drug addiction and obsessive-compulsive disorder by targeting the A2AR.

Spatial Measures of Urban Systems: from Entropy to Fractal Dimension.

One type of fractal dimension definition is based on the generalized entropy function. Both entropy and fractal dimensions can be employed to characterize complex spatial systems such as cities and regions. Despite the inherent connection between entropy and fractal dimensions, they have different application scopes and directions in urban studies. This paper focuses on exploring how to convert entropy measurements into fractal dimensions for the spatial analysis of scale-free urban phenomena using the ideas from scaling. Urban systems proved to be random prefractal and multifractal systems. The spatial entropy of fractal cities bears two properties. One is the scale dependence: the entropy values of urban systems always depend on the linear scales of spatial measurement. The other is entropy conservation: different fractal parts bear the same entropy value. Thus, entropy cannot reflect the simple rules of urban processes and the spatial heterogeneity of urban patterns. If we convert the generalized entropies into multifractal spectrums, the problems of scale dependence and entropy homogeneity can be solved to a degree for urban spatial analysis. Especially, the geographical analyses of urban evolution can be simplified. This study may be helpful for students in describing and explaining the spatial complexity of urban evolution.

Association Study between the FTCDNL1 (FONG) and Susceptibility to Osteoporosis.

Osteoporosis is a systemic skeletal disease characterized by a decreased bone mineral density that results in an increased risk of fragility fractures. Previous studies indicated that genetic factors are involved in the pathogenesis of osteoporosis. Polymorphisms of the FONG (FTCDNL1) gene (rs7605378) were reported to be associated with the risk of osteoporosis in a Japanese population. To assess whether polymorphisms of the FTCDNL1 gene contribute to the susceptibility and severity of osteoporosis in a Taiwanese population, 326 osteoporosis patients and 595 controls of a Taiwanese population were included in this study. Our results indicated that rs10203122 was significantly associated with osteoporosis susceptibility among female. Our findings provide evidence that rs10203122 in FTCDNL1 is associated with a susceptibility to osteoporosis.