Contamination of textile dyes in aquatic environment: Adverse impacts on aquatic ecosystem and human health, and its management using bioremediation.

Textile dyes are the burgeoning environmental contaminants across the world. They might be directly disposed of from textile industries into the aquatic bodies, which act as the direct source for the entire ecosystem, ultimately impacting the human beings. Hence, it is essential to dissect the potential adverse outcomes of textile dye exposure on aquatic plants, aquatic fauna, terrestrial entities, and humans. Analysis of appropriate literature has revealed that textile dye effluents could affect the aquatic biota by disrupting their growth and reproduction. Various aquatic organisms are targeted by textile dye effluents. In such organisms, these chemicals affect their development, behavior, and induce oxidative stress. General populations of humans are exposed to textile dyes via the food chain and drinking contaminated water. In humans, textile dyes are biotransformed into electrophilic intermediates and aromatic amines by the enzymes of the cytochrome family. Textile dyes and their biotransformed products form the DNA and protein adducts at sub-cellular moiety. Moreover, these compounds catalyze the production of free radicals and oxidative stress, and trigger the apoptotic cascades to produce lesions in multiple organs. In addition, textile dyes modulate epigenetic factors like DNA methyltransferase and histone deacetylase to promote carcinogenesis. Several bioremediation approaches involving algae, fungi, bacteria, biomembrane filtration techniques, etc., have been tested and some other hybrid systems are currently under investigation to treat textile dye effluents. However, many such approaches are at the trial stage and require further research to develop more efficient, cost-effective, and easy-to-handle techniques.

Breaking boundaries: Artificial intelligence for pesticide detection and eco-friendly degradation.

Pesticides are extensively used agrochemicals across the world to control pest populations. However, irrational application of pesticides leads to contamination of various components of the environment, like air, soil, water, and vegetation, all of which build up significant levels of pesticide residues. Further, these environmental contaminants fuel objectionable human toxicity and impose a greater risk to the ecosystem. Therefore, search of methodologies having potential to detect and degrade pesticides in different environmental media is currently receiving profound global attention. Beyond the conventional approaches, Artificial Intelligence (AI) coupled with machine learning and artificial neural networks are rapidly growing branches of science that enable quick data analysis and precise detection of pesticides in various environmental components. Interestingly, nanoparticle (NP)-mediated detection and degradation of pesticides could be linked to AI algorithms to achieve superior performance. NP-based sensors stand out for their operational simplicity as well as their high sensitivity and low detection limits when compared to conventional, time-consuming spectrophotometric assays. NPs coated with fluorophores or conjugated with antibody or enzyme-anchored sensors can be used through Surface-Enhanced Raman Spectrometry, fluorescence, or chemiluminescence methodologies for selective and more precise detection of pesticides. Moreover, NPs assist in the photocatalytic breakdown of various organic and inorganic pesticides. Here, AI models are ideal means to identify, classify, characterize, and even predict the data of pesticides obtained through NP sensors. The present study aims to discuss the environmental contamination and negative impacts of pesticides on the ecosystem. The article also elaborates the AI and NP-assisted approaches for detecting and degrading a wide range of pesticide residues in various environmental and agrecultural sources including fruits and vegetables. Finally, the prevailing limitations and future goals of AI-NP-assisted techniques have also been dissected.

Adrenal MT1 melatonin receptor expression is linked with seasonal variation in social behavior in male Siberian hamsters.

Many animals exhibit pronounced changes in physiology and behavior on a seasonal basis, and these adaptations have evolved to promote survival and reproductive success. While the neuroendocrine pathways mediating seasonal reproduction are well-studied, far less is known about the mechanisms underlying seasonal changes in social behavior, particularly outside of the context of the breeding season. Our previous work suggests that seasonal changes in melatonin secretion are important in regulating aggression in Siberian hamsters (Phodopus sungorus); it is unclear, however, how melatonin acts via its receptors to modulate seasonal variation in social behavior. In this study, we infused a MT1 melatonin receptor-expressing (MT1) or control (CON) lentivirus into the adrenal glands of male Siberian hamsters. We then housed hamsters in long-day (LD) or short-day (SD) photoperiods, administered timed melatonin or control injections, and quantified aggressive and non-aggressive social behaviors (e.g., investigation, self-grooming) following 10 weeks of treatment. LD hamsters infused with the MT1 lentivirus had significantly higher adrenal mt1 expression than LD CON hamsters, as determined via quantitative PCR. While melatonin administration was necessary to induce SD-like reductions in body and relative reproductive mass, only LD hamsters infused with the MT1 lentivirus displayed SD-like changes in social behavior, including increased aggression and decreased investigation and grooming. In addition, SD CON and LD hamsters infused with the MT1 lentivirus exhibited similar relationships between adrenal mt1 expression and aggressive behavior. Together, our findings suggest a role for adrenal MT1 receptor signaling in regulating behavior, but not energetics or reproduction in seasonally breeding species.

Dissociable roles of the nucleus accumbens core and shell subregions in the expression and extinction of conditioned fear.

The nucleus accumbens (NAc), consisting of core (NAcC) and shell (NAcS) sub-regions, has primarily been studied as a locus mediating the effects of drug reward and addiction. However, there is ample evidence that this region is also involved in regulating aversive responses, but the exact role of the NAc and its subregions in regulating associative fear processing remains unclear. Here, we investigated the specific contribution of the NAcC and NAcS in regulating both fear expression and fear extinction in C57BL/6J mice. Using Arc expression as an indicator of neuronal activity, we first show that the NAcC is specifically active only in response to an associative fear cue during an expression test. In contrast, the NAcS is specifically active during fear extinction. We next inactivated each subregion using lidocaine and demonstrated that the NAcC is necessary for fear expression, but not for extinction learning or consolidation of extinction. In contrast, we demonstrate that the NAcS is necessary for the consolidation of extinction, but not fear expression or extinction learning. Further, inactivation of mGluR1 or ERK signaling specifically in the NAcS disrupted the consolidation of extinction but had no effect on fear expression or extinction learning itself. Our data provide the first evidence for the importance of the ERK/MAPK pathway as the underlying neural mechanism facilitating extinction consolidation within the NAcS. These findings suggest that the NAc subregions play dissociable roles in regulating fear recall and the consolidation of fear extinction, and potentially implicate them as critical regions within the canonical fear circuit.

Anterior Cingulate Cortex and Ventral Hippocampal Inputs to the Basolateral Amygdala Selectively Control Generalized Fear.

A common symptom of anxiety disorders is the overgeneralization of fear across a broad range of contextual cues. We previously found that the ACC and ventral hippocampus (vHPC) regulate generalized fear. Here, we investigate the functional projections from the ACC and vHPC to the amygdala and their role in governing generalized fear in a preclinical rodent model. A chemogenetic approach (designer receptor exclusively activated by designer drugs) was used to inhibit glutamatergic projections from the ACC or vHPC that terminate within the BLA at recent (1 d) or remote (28 d) time points after contextually fear conditioning male mice. Inactivating ACC or vHPC projections to the BLA significantly reduced generalized fear to a novel, nonthreatening context but had no effect on fear to the training context. Further, our data indicate that the ACC-BLA circuit supports generalization in a time-independent manner. We also identified, for the first time, a strictly time-dependent role of the vHPC-BLA circuit in supporting remote generalized contextual fear. Dysfunctional signaling to the amygdala from the ACC or the HPC could underlie overgeneralized fear responses that are associated with anxiety disorders. Our findings demonstrate that the ACC and vHPC regulate fear expressed in novel, nonthreatening environments via projections to the BLA but do so as a result of training intensity or time, respectively.SIGNIFICANCE STATEMENT Anxiety disorders are characterized by a common symptom that promotes overgeneralization of fear in nonthreatening environments. Dysregulation of the amygdala, ACC, or hippocampus (HPC) has been hypothesized to contribute to increased fear associated with anxiety disorders. Our findings show that the ACC and HPC projections to the BLA regulate generalized fear in nonthreatening, environments. However, descending ACC projections control fear generalization independent of time, whereas HPC projections play a strictly time-dependent role in regulating generalized fear. Thus, dysfunctional ACC/HPC signaling to the BLA may be a predominant underlying mechanism of nonspecific fear associated with anxiety disorders. Our data have important implications for predictions made by theories about aging memories and interactions between the HPC and cortical regions.

Basolateral amygdala Thy1-expressing neurons facilitate the inhibition of contextual fear during consolidation, reconsolidation, and extinction.

Disrupted fear inhibition is a characteristic of many anxiety disorders. Investigations into the neural mechanisms responsible for inhibiting fear will improve understanding of the essential circuits involved, and facilitate development of treatments that promote their activity. Within the basolateral amygdala (BLA), Thy1-expressing neuron activity has been characterized by us and others as promoting fear inhibition to discrete fear cues by influencing consolidation of cued fear learning or cued fear extinction. Here, we evaluated how activating BLA Thy1-expressing neurons using DREADDs affected the consolidation, expression, reconsolidation, and extinction of contextual fear. Using an inhibitory avoidance paradigm, our present findings indicate a similar involvement of BLA Thy1-expressing neuron activity in the consolidation and extinction, but not expression, of fear. Importantly, our data also provide the first evidence for involvement of these neurons in inhibiting fear reconsolidation. Therefore, these data enhance our understanding of the roles that Thy1-expressing neurons within the BLA play in inhibiting fear when examining avoidance, in addition to the already established role in Pavlovian fear paradigms. Future investigations should further explore the circuits responsible for these contextual effects modulated by BLA Thy1 neuron activation, and could promulgate development of therapies targeting these neurons and their downstream effectors.

A Study of Various Sociodemographic Factors and Plasma Vitamin Levels in Oral and Pharyngeal Cancer in Gujarat, India.

Present study examined various socio-demographic factors, dietary patterns, habit of tobacco consumption and plasma vitamin levels in 56 healthy individuals, 146 patients with oral precancerous conditions (OPC) and 132 untreated oral and pharyngeal cancer patients. The subjects were interviewed with a detailed health, habit and diet questionnaire. Plasma b-carotene, vitamin-A and vitamin-E levels were determined spectrophotometrically. An increased incidence of OPC was observed in the age group of <30 years which was associated with tobacco chewing. Whereas, incidence of cancer was in the age group of 30-60 years where habit of tobacco smoking was more prevalent. Majorities of the subjects were from rural area, poor, unaware about association of diet with cancer. The body mass index was lower (p=0.045) in patients with OPC and cancer patients as compared to the controls. Plasma b-carotene and vitamin-E levels were lower in patients with OPC (p=0.000 and 0.031, respectively) and untreated cancer patients (p=0.000 and 0.071, respectively) than the controls. ROC curve revealed that plasma vitamin levels have ability to discriminate between controls and cancer patients. Lower plasma b-carotene and vitamin-E levels were observed in tobacco consumers as compared to non-consumers. Odds ratio revealed that controls and patients with OPC having tobacco habit and lower plasma levels of b-carotene were at a higher risk (p<0.05) of developing cancer. Regression study and Analysis of Variance revealed that plasma b-carotene levels were inversely associated (r(2)=0.14, p=0.001 and F=0.000, respectively) with increase in the stage of cancer. The data provide interesting clues of potential role of diet, tobacco habits, socio-demographic status and plasma vitamin levels in etiology of oral and pharyngeal cancer in Gujarat, where no such findings are reported.