Ecological features and sozological assessment of Unio crassus in watercourses of the right-bank Ukraine in the context of EU environmental directives implementation.

Betel quid (BQ) is consumed by approximately 600 million people worldwide, ranking as the fourth most widely used self‐administered psychoactive substance, behind only caffeine, alcohol and nicotine [, ]. The usage of BQ is associated with serious health risks, which begin with localized oral damage such as tooth blackening, periodontitis [] and potentially progressing to systemic diseases including cardiovascular and neurological disorders, as well as significantly elevating the risk of precancerous lesions and oral cancer [, , ]. According to the International Agency for Research on Cancer, BQ is classified as a Group 1 human carcinogen []. BQ mainly consists of areca nut, betel leaf and slaked lime []. As the key psychoactive substance in areca nut, arecoline acts as a competitive γ‐aminobutyric acid (GABA) inhibitor, a muscarinic acetylcholine receptor agonist and a monoamine oxidase‐A inhibitor, thereby disinhibiting and enhancing the activity of dopaminergic neurons within the mesolimbic reward pathway [, , , ]. Neuroimaging studies have revealed reward‐related function deficits in betel quid dependence (BQD) individuals []; however, the pathophysiological mechanism underlying the reward circuit is poorly understood. Converging findings from animal models and human neuroimaging studies demonstrated that reward processing was mediated by a neural circuit centred on ventral striatum (VS), extending to ventral segmental area (VTA), ventromedial prefrontal cortex (VMPFC), posterior cingulate cortex (PCC), anterior cingulate cortex (ACC), anterior insula (Ins) and thalamus (Th) [, , ]. This circuit has been validated by a quantitative meta‐analysis conducted by Bartra et al. [], which confirmed the existence of this core reward‐related circuit. The reward circuit originates from dopaminergic projections of VTA and primarily projects to nucleus accumbens (NAc) of VS [] Striatal signals are transmitted via thalamus to medial cortex regions, including VMPFC, ACC and PCC, which in turn project back to basal ganglia []. Considering that the reward circuit has been identified as a crucial determinant for addiction [], investigating its impairments in BQD is of great importance. A growing body of multimodal neuroimaging studies identified significant alterations in brain regions associated with the reward circuit in BQD chewers. For instance, a voxel‐based morphometric analysis of structural magnetic resonance imaging data demonstrated reduced grey matter volume in bilateral VMPFC and Ins []. Using amplitude of low‐frequency fluctuation and regional homogeneity analyses, the study by Liu et al. revealed reduced spontaneous brain activity in ACC and MPFC among individuals with BQD []. In addition, diffusion tensor imaging analyses indicated compromised white matter integrity, specifically revealing that BQD chewers exhibited lower fractional anisotropy and higher mean diffusivity in Tha []. When [18]. F‐2‐fluoro‐2‐deoxy‐D‐glucose‐positron emission tomography was employed to explore metabolic pattern in brain regions of BQD chewers, one study reported reduced metabolism in MPFC and orbitofrontal cortex, along with increased metabolism in Tha []. To date, few studies employed functional connectivity (FC) analysis to elucidate the neurophysiological mechanisms underlying the reward circuit in BQD individuals.