Prevalence of Depressive Symptoms in a Predominantly Hispanic/Latinx South Texas Community in the Aftermath of the COVID-19 Pandemic.

OBJECTIVE: COVID-19 has a lasting impact on mental health, particularly within the Hispanic/Latinx communities. This paper empirically investigates the post-COVID-19 presence and severities of depression, one of the most common mental health disorders, among adults in a predominantly U.S.-born Hispanic/Latinx community in South Texas composed primarily of Mexican Americans. METHODS: Multiple statistic regression models were applied to data from 515 adults in Nueces County who completed all questions in a survey from convenience sampling between June 2022 and May 2023. Depression was assessed using both standard PHQ-2 and PHQ-9 measurements. RESULTS: Of the 515 participants, 377 (64.5%) were Hispanic, and 441 (85.6%) had a high school education or higher, reflecting the county's demographics. About half of the participants (47%) reported mild/moderate to severe depression. The regression model estimation results reveal that female participants, those not in full-time employment, and individuals with disabilities were more likely to feel depressed after COVID-19. Middle-aged adults demonstrated greater resilience to depression compared to other age groups. Notably, non-Hispanic participants in the study reported higher levels of depression compared to their Hispanic counterparts. Additionally, COVID-19-related experiences, such as testing positive for the virus, being hospitalized, or having a history of depression before COVID-19, were associated with higher levels of reported depression. CONCLUSIONS: COVID-19 has significantly impacted the mental health of this predominantly U.S.-born Hispanic/Latinx community. These findings can assist healthcare providers and policymakers in developing targeted strategies to tailor interventions aimed at enhancing mental health well-being, reducing disparities, and fostering overall improvement within the Hispanic/Latinx community.

Treatment with quercetin mitigates polystyrene nanoparticle-induced reduction in neuron capacity by inhibiting dopaminergic neurodegeneration and facilitating dopamine metabolism in Caenorhabditis elegans.

In organisms, long-term nanopolystyrenes (PS-NPs) exposure can cause toxicity, including neurotoxicity. Quercetin, the flavonol with extensive distribution within plants, possesses diverse biological activities. Nevertheless, the possible effect of quercetin to suppress PS-NPs-induced neurotoxicity and its associated mechanism remains unknown. Thus, in the present work, Caenorhabditis elegans was utilized as the model animal to investigate quercetin's pharmacological effect on suppressing PS-NPs-induced neurotoxicity and the underlying mechanism. PS-NPs exposure at 1-100 µg/L remarkably reduced locomotion behavior, while only PS-NPs exposure at 100 µg/L significantly decrease sensory perception behavior. Meanwhile, the increase in the number of worms with dopaminergic neurodegeneration was detected in nematodes exposed to 100 µg/L PS-NPs and the decreased dopamine content was observed within nematodes exposed to 10-100 µg/L PS-NPs, demonstrating the function of dopaminergic neurodegeneration and disruption of dopamine metabolism in inducing PS-NPs toxicity on neuron capacity. After 100 µg/L PS-NPs exposure, the 25-100 µM quercetin treatment effectively increased the locomotion behavior and the sensory perception behavior. Developmentally, quercetin treatment (100 µM) remarkably enhanced fluorescence intensity while decreasing worm number with neurodegeneration within BZ555 transgenic strains exposed to 100 µg/L PS-NPs. Physiologically, quercetin treatment (100 µM) significantly enhanced dopamine content within nematodes exposed to 100 µg/L PS-NPs. Molecularly, quercetin treatment (100 µM) notably decreased the expressions of genes governing neurodegeneration (mec-4, deg-3, unc-68, itr-1, clp-1, and asp-3) while significantly increasing the expression of genes governing dopamine metabolism (cat-2, cat-1, dop-1, dop-2, dop-3). As revealed by molecular docking results, quercetin might bind to excitotoxic-like ion channels receptors (MEC-4 and DEG-3) and dopamine secreted protein (CAT-2). Consequently, findings in this work demonstrated that long-term PS-NPs exposure within the µg/L range (1-100 µg/L) was toxic to neuron capacity, which was associated with the enhancement in dopaminergic neurodegeneration and disruption of dopamine metabolism. Notably, PS-NPs-mediated neurotoxicity to nematodes is probably suppressed through subsequent quercetin treatment.

BAPID suppresses the inhibition of BRM on Di19-PR module in response to drought.

Drought is one of the most important abiotic stresses, and seriously threatens plant development and productivity. Increasing evidence indicates that chromatin remodelers are pivotal for plant drought response. However, molecular mechanisms of chromatin remodelers-mediated plant drought responses remain obscure. In this study, we found a novel interactor of BRM called BRM-associated protein involved in drought response (BAPID), which interacted with SWI/SNF chromatin remodeler BRM and drought-induced transcription factor Di19. Our findings demonstrated that BAPID acted as a positive drought regulator since drought tolerance was increased in BAPID-overexpressing plants, but decreased in BAPID-deficient plants, and physically bound to PR1, PR2, and PR5 promoters to mediate expression of PR genes to defend against dehydration stress. Genetic approaches demonstrated that BRM acted epistatically to BAPID and Di19 in drought response in Arabidopsis. Furthermore, the BAPID protein-inhibited interaction between BRM and Di19, and suppressed the inhibition of BRM on the Di19-PR module by mediating the H3K27me3 deposition at PR loci, thus changing nucleosome accessibility of Di19 and activating transcription of PR genes in response to drought. Our results shed light on the molecular mechanism whereby the BAPID-BRM-Di19-PRs pathway mediates plant drought responses. We provide data improving our understanding of chromatin remodeler-mediated plant drought regulation network.

Study on the adsorption performance of fly ash loaded on nano-FeS for chromium-containing wastewater treatment.

In view of the problems caused by chromium-containing wastewater, such as environmental pollution, biological toxicity, and human health risks. Based on fly ash adsorption and nano-FeS reduction characteristics, fly ash loaded nano-FeS composite (nFeS-FA) was synthesized using mineral supported modification technology and ultrasonic precipitation method. The effect of adsorbent dosage, initial pH, contact time, and initial concentration of the solution on the adsorption of Cr(VI) and total Cr by nFeS-FA was investigated. The characteristics of Cr(VI) and total Cr adsorption by nFeS-FA were studied using adsorption isotherms, adsorption kinetics principles, as well as XRD, TEM, SEM-EDS, and BET analysis. The results demonstrated that under the conditions of nFeS-FA of 8 g/L, initial pH of 4, contact time of 150 min, and initial concentration of the solution at 100 mg/L, nFeS-FA achieved removal efficiency of 87.85 % for Cr(VI) and 71.77 % for total Cr. The adsorption of Cr(VI) and total Cr by nFeS-FA followed the Langmuir model and pseudo-second-order kinetic model, indicating monolayer adsorption with chemical adsorption as the dominant mechanism. XRD, TEM, SEM-EDS, and BET revealed that the flaky nano-FeS was uniformly distributed on the surface of fly ash, exhibiting good dispersion and thereby increasing the specific surface area. During the adsorption experiments, nFeS-FA reacted with Cr(VI), and the generated Fe3+ mainly existed as FeOOH precipitation, while S2- reacted with Cr(III) to produce Cr2S3 precipitation. Therefore, nFeS-FA exhibited excellent adsorption performance towards Cr(VI) and total Cr. It can serve as a technological reference for the remediation of heavy metal chromium pollution in the field of water treatment.

CYP2E1 deficit mediates cholic acid-induced malignant growth in hepatocellular carcinoma cells.

BACKGROUND: Increased level of serum cholic acid (CA) is often accompanied with decreased CYP2E1 expression in hepatocellular carcinoma (HCC) patients. However, the roles of CA and CYP2E1 in hepatocarcinogenesis have not been elucidated. This study aimed to investigate the roles and the underlying mechanisms of CYP2E1 and CA in HCC cell growth. METHODS: The proteomic analysis of liver tumors from DEN-induced male SD rats with CA administration was used to reveal the changes of protein expression in the CA treated group. The growth of CA-treated HCC cells was examined by colony formation assays. Autophagic flux was assessed with immunofluorescence and confocal microscopy. Western blot analysis was used to examine the expression of CYP2E1, mTOR, AKT, p62, and LC3II/I. A xenograft tumor model in nude mice was used to examine the role of CYP2E1 in CA-induced hepatocellular carcinogenesis. The samples from HCC patients were used to evaluate the clinical value of CYP2E1 expression. RESULTS: CA treatment significantly increased the growth of HCC cells and promoted xenograft tumors accompanied by a decrease of CYP2E1 expression. Further studies revealed that both in vitro and in vivo, upregulated CYP2E1 expression inhibited the growth of HCC cells, blocked autophagic flux, decreased AKT phosphorylation, and increased mTOR phosphorylation. CYP2E1 was involved in CA-activated autophagy through the AKT/mTOR signaling. Finally, decreased CYP2E1 expression was observed in the tumor tissues of HCC patients and its expression level in tumors was negatively correlated with the serum level of total bile acids (TBA) and gamma-glutamyltransferase (GGT). CONCLUSIONS: CYP2E1 downregulation contributes to CA-induced HCC development presumably through autophagy regulation. Thus, CYP2E1 may serve as a potential target for HCC drug development.

Purple sweet potato anthocyanins normalize the blood glucose concentration and restore the gut microbiota in mice with type 2 diabetes mellitus.

Background: This study investigated the effects of purple sweet potato anthocyanins (PSPA) in a type 2 diabetes mellitus (T2DM) mouse model. Methods: Sixty-five male mice were randomly divided into one control group and four experimental groups, which were fed with a high-fat diet and intraperitoneally injected with streptozotocin (STZ) to induce T2DM. The model mice were treated with 0 (M), 227.5 (LP), 455 (MP), or 910 (HP) mg/kg PSPA for ten days. ELISA, 16S rRNA sequencing, and hematoxylin and eosin staining were used to assess blood biochemical parameters, gut microbial composition, and liver tissue structure, respectively. Results: The FBG concentration was significantly decreased in the LP (6.32 ± 1.05 mmol/L), MP (6.32 ± 1.05 mmol/L), and HP (5.65 ± 0.83 mmol/L) groups; the glycosylated hemoglobin levels were significantly decreased in the HP group (14.43 ± 7.12 pg/mL) compared with that in the M group (8.08 ± 1.04 mmol/L; 27.20 ± 7.72 pg/mL; P < 0.05). The PSPA treated groups also increased blood glutathione levels compared with M. PSPA significantly affected gut microbial diversity. The Firmicutes/Bacteroidetes ratio decreased by 38.9 %, 49.2 %, and 15.9 % in the LP, MP, and HP groups compared with that in the M group (0.62). The PSPAs treated groups showed an increased relative abundance of Lachnospiraceae_Clostridium, Butyricimonas, and Akkermansia and decreased abundance of nine bacterial genera, including Staphylococcus. Conclusion: PSPA reduced blood glucose levels, increased serum antioxidant enzymes, and optimized the diversity and structure of the gut microbiota in mice with T2DM.

Analysis of differences in the rumen microbiome and metabolic function in prepartum dairy cows with different body condition scores.

BACKGROUND: The rumen is a crucial digestive organ for dairy cows. The rumen microbiota assists in the digestion of plant feed through microbe-mediated fermentation, during which the plant feed is transformed into nutrients for the cow's use. Variations in the composition and function of the rumen microbiome affect the energy utilization efficiency of dairy cows, which is one of the reasons for the varying body condition scores (BCSs). This study focused on prepartum Holstein dairy cows to analyze differences in rumen microbiota and metabolites among cows with different BCSs. Twelve prepartum dairy cows were divided into two groups, low BCS (LBCS, BCS = 2.75, n = 6) and high BCS (HBCS, BCS = 3.5, n = 6), to explore differences in microbial composition and metabolites. RESULTS: In the HBCS group, the genera within the phylum Firmicutes exhibited stronger correlations and greater abundances. Phyla such as Firmicutes, Patescibacteria, Acidobacteriota, Euryarchaeota, and Desulfobacterota, in addition to most of their constituent microbial groups, were significantly more abundant in the HBCS group than in the LBCS group. At the genus level, the abundances of Anaerovibrio, Veillonellaceae_UCG_001, Ruminococcus_gauvreauii_group, Blautia, Eubacterium, Prevotellaceae_YAB2003_group, Schwartzia, and Halomonas significantly increased in the HBCS group. The citrate cycle, involved in carbohydrate metabolism, exhibited a significant enrichment trend, with a notable increase in the abundance of its key substrate, citrate, in the HBCS group. This increase was significantly positively correlated with the differential bacterial genera. CONCLUSION: In this study, prepartum dairy cows with higher BCS exhibited greater abundance of Firmicutes. This study provides theoretical support for microbiological research on dairy cows with different BCSs and suggests that regulating the rumen microbiome could help maintain prepartum dairy cows within an optimal BCS range.

Antitumor Effect of Apcin on Endometrial Carcinoma via p21-Mediated Cell Cycle Arrest and Apoptosis.

OBJECTIVE: Endometrial carcinoma (EC) is a prevalent gynecological malignancy characterized by increasing incidence and mortality rates. This underscores the critical need for novel therapeutic targets. One such potential target is cell division cycle 20 (CDC20), which has been implicated in oncogenesis. This study investigated the effect of the CDC20 inhibitor Apcin on EC and elucidated the underlying mechanism involved. METHODS: The effects of Apcin on EC cell proliferation, apoptosis, and the cell cycle were evaluated using CCK8 assays and flow cytometry. RNA sequencing (RNA-seq) was subsequently conducted to explore the underlying molecular mechanism, and Western blotting and coimmunoprecipitation were subsequently performed to validate the results. Animal studies were performed to evaluate the antitumor effects in vivo. Bioinformatics analysis was also conducted to identify CDC20 as a potential therapeutic target in EC. RESULTS: Treatment with Apcin inhibited proliferation and induced apoptosis in EC cells, resulting in cell cycle arrest. Pathways associated with apoptosis and the cell cycle were activated following treatment with Apcin. Notably, Apcin treatment led to the upregulation of the cell cycle regulator p21, which was verified to interact with CDC20 and consequently decrease the expression of downstream cyclins in EC cells. In vivo experiments confirmed that Apcin treatment significantly impeded tumor growth. Higher CDC20 expression was observed in EC tissue than in nonmalignant tissue, and increased CDC20 expression in EC patients was associated with shorter overall survival and progress free interval. CONCLUSION: CDC20 is a novel molecular target in EC, and Apcin could be developed as a candidate antitumor drug for EC treatment.

Propensity matched post-transplant survival in durable CF-axial pump BTT patients with and without diabetes: A UNOS database analysis.

Diabetes and post-transplant survival have been linked. However, the impact on post-transplant survival of patients supported on Continuous Flow (CF) axial left ventricular assist devices (LVAD) as a bridge to transplant (BTT) with diabetes has not been widely studied. This study attempts to assess the impact of diabetes type II (DM type II) as a comorbidity influencing survival patterns in the post-cardiac transplant population supported on LVADs and to test if the presence of a pre- transplant durable LVAD acts as an independent risk factor in long-term post-transplant survival. The UNOS database population from 2004 to 2015 was used to construct the cohorts. A total of 21,032 were transplanted during this period. The transplant data were further queried to extract CF-axial flow pumps BTT (HMII-BTT) patients and patients who did not have VAD support before the transplant. A total of 4224 transplant recipients had HMII at the time of transplant, and 13,131 did not have VAD support. Propensity analysis was performed, and 4107 recipients of similar patient characteristics to those in the BTT group were selected for comparison. The patients with a VAD had significantly reduced survival at 2 years post-transplant (p = 0.00514) but this trend did not persist at 5 years (p = 0.0617) and 10 years post-transplant (p = 0.183). Patients with diabetes and a VAD significantly decreased survival at 2 years (p = 0.00204), 5 years (p = 0.00029), and 10 years (p = 0.00193). The presence of a durable LVAD is not an independent risk factor for long-term survival. Diabetes has a longstanding effect on the posttransplant survival of BTT patients.

Magnetic Array-Aided Visualizing PEMFC Degradation Heterogeneity.

Analyzing degradation heterogeneity of proton exchange membrane fuel cell (PEMFC) while maintaining high practicality is consistently challenging, primarily due to the destructive and costly nature of existing techniques relying on material characterization. In this work, a designed magnetic array integrating 16 sensors within 25 cm2 space is used for direct scanning and imaging of PEMFC performance heterogeneity during its degradation. Results are validated through degradation mechanism analysis and material characterization, confirming its potential in guiding the development of durable materials.

Physicochemical, structural and functional properties of low methoxyl pectin­iron (III) complex and its effect on rats with iron deficiency anemia.

Iron deficiency anemia (IDA) is the most common nutritional disease worldwide. In this study, a low methoxyl pectin (LMP)­iron(III) complex was prepared. The physicochemical and structural properties were characterized by HPSEC, HPIC, CV, FTIR, 1H NMR, XRD, SEM and CD. The results showed that iron increased the molecular weight of the LMP­iron(III) from 11.50 ± 0.32 to 12.70 ± 0.45 kDa and improved its crystallinity. Moreover, the findings demonstrated that -OH and -COOH groups in LMP coordinate with Fe3+ to form ß-FeOOH. The water-holding capacity, emulsion stability, and antioxidant activities of the LMP­iron(III) were lower than those of LMP. Furthermore, the therapeutic effects of LMP­iron(III) on IDA were investigated in rats. Following LMP­iron(III) supplementation, compared with the model group, the administration of LMP­iron(III) significantly increased the body weight, hemoglobin concentration, and serum iron concentration as well as decreased free erythrocyte protoporphyrin concentration. Therefore, the LMP­iron(III) can potentially treat IDA in rats experiments, providing a theoretical basis for the development of a promising iron supplement.

A smartphone-based fluorescent biosensor with metal-organic framework biocomposites and cotton swabs for the rapid determination of tetrodotoxin in seafood.

BACKGROUND: Tetrodotoxin (TTX) is a potent neurovirulent marine biotoxin that is present in puffer fish and certain marine animals. It is capable of causing severe neurotoxic symptoms and even death when consumed through contaminated seafood. Due to its high toxicity, developing an effective assay for TTX determination in seafood has significant benefits for food safety and human health. Currently, it remains challenging to achieve on-site determination of TTX in seafood. To facilitate mass on-site assays, more affordable technologies utilizing accessible equipment that require no skilled personnel are needed. RESULTS: A smartphone-based portable fluorescent biosensor is proposed for TTX determination by using metal-organic framework (MOF) biocomposites and cotton swabs. Oriented antibody (Ab)-decorated and fluorescent quantum dot (QD)-loaded MOF biocomposites (QD@MOF*Ab) are rapidly synthesized for binding targets and fluorescent responses by utilizing the tunability of zinc-based MOF. Moreover, facile Ab-immobilized household cotton swabs are utilized as TTX capture tools. TTX forms sandwich immune complexes with QD@MOF*Ab probes, achieving signal amplification. These probes are excited by a portable device to generate bright fluorescent signals, which can be detected by the naked eye, and TTX quantitative results are obtained using a smartphone. When observed with the naked eye, the limit of detection (LOD) is 0.4 ng/mL, while intelligent quantitation presents an LOD of 0.13 ng/mL at logarithmic concentrations of 0.2-400 ng/mL. SIGNIFICANCE: This biosensor is convenient to use, and an easy-to-operate analysis is completed within 15 min, thus demonstrating excellent performance in terms of detection speed and portability. Furthermore, it successfully determines TTX contents in puffer fish and clam samples, demonstrating its potential for monitoring seafood. Herein, this work provides a favorable rapid sensing platform that is easily portable.

General anesthetic agents induce neurotoxicity through oligodendrocytes in the developing brain.

General anesthetic agents can impact brain function through interactions with neurons and their effects on glial cells. Oligodendrocytes perform essential roles in the central nervous system, including myelin sheath formation, axonal metabolism, and neuroplasticity regulation. They are particularly vulnerable to the effects of general anesthetic agents resulting in impaired proliferation, differentiation, and apoptosis. Neurologists are increasingly interested in the effects of general anesthetic agents on oligodendrocytes. These agents not only act on the surface receptors of oligodendrocytes to elicit neuroinflammation through modulation of signaling pathways, but also disrupt metabolic processes and alter the expression of genes involved in oligodendrocyte development and function. In this review, we summarize the effects of general anesthetic agents on oligodendrocytes. We anticipate that future research will continue to explore these effects and develop strategies to decrease the incidence of adverse reactions associated with the use of general anesthetic agents.

Study on the adsorption of Zn(II) and Cu(II) in acid mine drainage by fly ash loaded nano-FeS.

Aiming at the acid mine drainage (AMD) in zinc, copper and other heavy metals treatment difficulties, severe pollution of soil and water environment and other problems. Through the ultrasonic precipitation method, this study prepared fly ash-loaded nano-FeS composites (nFeS-F). The effects of nFeS-F dosage, pH, stirring rate, reaction time and initial concentration of the solution on the adsorption of Zn(II) and Cu(II) were investigated. The data were fitted by Lagergren first and second-order kinetic equations, Internal diffusion equation, Langmuir and Freundlich isotherm models, and combined with SEM, TEM, FTIR, TGA, and XPS assays to reveal the mechanism of nFeS-F adsorption of Zn(II) and Cu(II). The results demonstrated that: The removal of Zn(II) and Cu(II) by nFeS-F could reach 83.36% and 70.40%, respectively (The dosage was 8 g/L, pH was 4, time was 150 min, and concentration was 100 mg/L). The adsorption process, mainly chemical adsorption, conforms to the Lagergren second-order kinetic equation (R2 = 0.9952 and 0.9932). The adsorption isotherms have a higher fitting degree with the Langmuir model (R2 = 0.9964 and 0.9966), and the adsorption is a monolayer adsorption process. This study can provide a reference for treating heavy metals in acid mine drainage and resource utilization of fly ash.

Effects of Individual Essential Amino Acids on Growth Rates of Young Rats Fed a Low-Protein Diet.

To investigate the effects of individual essential amino acids (EAA) on growth and the underlying mechanisms, EAA individually supplemented a low-protein (LP) diet fed to young rats in the present study. Treatments were an LP diet that contained 6% crude protein (CP), a high-protein (HP) diet that contained 18% CP, and 10 LP diets supplemented with individual EAA to achieve an EAA supply equal to that of the HP diet. The CP concentration of the LP diet was ascertained from the results of the first experiment, which examined the effects of dietary CP concentrations on growth rates, with CP ranging from 2% to 26%. Weight gain was increased with the supplementation of His, Ile, Lys, Thr, or Trp as compared to the LP diet (p < 0.05). Feed intake was greater for the His-, Lys-, and Thr-supplemented treatments as compared to the LP group (p < 0.05). Protein utilization efficiency was lower for the HP group than other groups (p < 0.01). The supplementation of Leu, Lys, and Val led to reduced protein utilization efficiency (p < 0.05), but the supplementation of Thr and Trp led to greater efficiency than the LP group (p < 0.05). Compared to the LP group, plasma urea concentrations were elevated with individual EAA supplementation, with the exception of the Thr addition. The added EAA resulted in increased concentrations of the corresponding EAA in plasma, except for Arg and Phe supplementation. The supplementation of Arg, His, Leu, Lys, and Met individually stimulated mTORC1 pathway activity (p < 0.05), and all EAA resulted in the decreased expression of ATF4 (p < 0.05). In summary, the supplementation of His, Ile, Lys, Thr, or Trp to an LP diet improved the growth performance of young rats. Responses to His and Lys additions were related to the activated mTORC1 pathway and feed intake increases. The improved growth performance resulting from the addition of a single EAA is not solely attributed to the increased plasma availability of EAA. Rather, it may be the consequence of a confluence of factors encompassing signaling pathways, the availability of amino acids, and other associated elements. The additivity of these factors results in independent responses to several EAA with no order of limitation, as is universally encoded in growth models for all production animal species.

Long-term exposure to 6-PPD quinone at environmentally relevant concentrations causes neurotoxicity by affecting dopaminergic, serotonergic, glutamatergic, and GABAergic neuronal systems in Caenorhabditis elegans.

6-PPD quinone (6-PPDQ), an emerging environmental pollutant, is converted based on 6-PPD via ozonation. However, a systematic evaluation on possible neurotoxicity of long-term and low-dose 6-PPDQ exposure and the underlying mechanism remain unknown. In the present work, 0.1-10 µg/L 6-PPDQ was added to treat Caenorhabditis elegans for 4.5 days, with locomotion behavior, neuronal development, sensory perception behavior, neurotransmitter content, and levels of neurotransmission-related genes being the endpoints. 6-PPDQ exposure at 0.1-10 µg/L significantly reduced locomotion behavior, and that at 1-10 µg/L decreased sensory perception behavior in nematodes. Moreover, 6-PPDQ exposure at 10 µg/L notably induced damage to the development of dopaminergic, glutamatergic, serotonergic, and GABAergic neurons. Importantly, nematodes with chronic 6-PPDQ exposure at 10 µg/L were confirmed to suffer obviously decreased dopamine, serotonin, glutamate, dopamine, and GABA contents and altered neurotransmission-related gene expression. Meanwhile, the potential binding sites of 6-PPDQ and neurotransmitter synthesis-related proteins were further shown by molecular docking method. Lastly, Pearson's correlation analysis showed that locomotion behavior and sensory perception behavior were positively correlated with the dopaminergic, serotonergic, glutamatergic, and GABAergic neurotransmission. Consequently, 6-PPDQ exposure disturbed neurotransmitter transmission, while such changed molecular foundation for neurotransmitter transmission was related to 6-PPDQ toxicity induction. The present work sheds new lights on the mechanisms of 6-PPDQ and its possible neurotoxicity to organisms at environmentally relevant concentrations.

General anesthetic agents induce neurotoxicity through astrocytes.

ABSTRACT: Neuroscientists have recognized the importance of astrocytes in regulating neurological function and their influence on the release of glial transmitters. Few studies, however, have focused on the effects of general anesthetic agents on neuroglia or astrocytes. Astrocytes can also be an important target of general anesthetic agents as they exert not only sedative, analgesic, and amnesic effects but also mediate general anesthetic-induced neurotoxicity and postoperative cognitive dysfunction. Here, we analyzed recent advances in understanding the mechanism of general anesthetic agents on astrocytes, and found that exposure to general anesthetic agents will destroy the morphology and proliferation of astrocytes, in addition to acting on the receptors on their surface, which not only affect Ca2+ signaling, inhibit the release of brain-derived neurotrophic factor and lactate from astrocytes, but are even involved in the regulation of the pro- and anti-inflammatory processes of astrocytes. These would obviously affect the communication between astrocytes as well as between astrocytes and neighboring neurons, other neuroglia, and vascular cells. In this review, we summarize how general anesthetic agents act on neurons via astrocytes, and explore potential mechanisms of action of general anesthetic agents on the nervous system. We hope that this review will provide a new direction for mitigating the neurotoxicity of general anesthetic agents.

Vascular endothelial growth factor B improves impaired glucose tolerance through insulin-mediated inhibition of glucagon secretion.

BACKGROUND: Impaired glucose tolerance (IGT) is a homeostatic state between euglycemia and hyperglycemia and is considered an early high-risk state of diabetes. When IGT occurs, insulin sensitivity decreases, causing a reduction in insulin secretion and an increase in glucagon secretion. Recently, vascular endothelial growth factor B (VEGFB) has been demonstrated to play a positive role in improving glucose metabolism and insulin sensitivity. Therefore, we constructed a mouse model of IGT through high-fat diet feeding and speculated that VEGFB can regulate hyperglycemia in IGT by influencing insulin-mediated glucagon secretion, thus contributing to the prevention and cure of prediabetes. AIM: To explore the potential molecular mechanism and regulatory effects of VEGFB on insulin-mediated glucagon in mice with IGT. METHODS: We conducted in vivo experiments through systematic VEGFB knockout and pancreatic-specific VEGFB overexpression. Insulin and glucagon secretions were detected via enzyme-linked immunosorbent assay, and the protein expression of phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) was determined using western blot. Further, mRNA expression of forkhead box protein O1, phosphoenolpyruvate carboxykinase, and glucose-6 phosphatase was detected via quantitative polymerase chain reaction, and the correlation between the expression of proteins was analyzed via bioinformatics. RESULTS: In mice with IGT and VEGFB knockout, glucagon secretion increased, and the protein expression of PI3K/AKT decreased dramatically. Further, in mice with VEGFB overexpression, glucagon levels declined, with the activation of the PI3K/AKT signaling pathway. CONCLUSION: VEGFB/vascular endothelial growth factor receptor 1 can promote insulin-mediated glucagon secretion by activating the PI3K/AKT signaling pathway to regulate glucose metabolism disorders in mice with IGT.

A novel nomogram for predicting the prolonged length of stay in post-anesthesia care unit after elective operation.

BACKGROUND: Prolonged length of stay in post-anesthesia care unit (PLOS in PACU) is a combination of risk factors and complications that can compromise quality of care and operating room efficiency. Our study aimed to develop a nomogram to predict PLOS in PACU of patients undergoing elective surgery. METHODS: Data from 24017 patients were collected. Least absolute shrinkage and selection operator (LASSO) was used to screen variables. A logistic regression model was built on variables determined by a combined method of forward selection and backward elimination. Nomogram was designed with the model. The nomogram performance was evaluated with the area under the receiver operating characteristic curve (AUC) for discrimination, calibration plot for consistency between predictions and actuality, and decision curve analysis (DCA) for clinical application value. RESULTS: A nomogram was established based on the selected ten variables, including age, BMI < 21 kg/m2, American society of Anesthesiologists Physical Status (ASA), surgery type, chill, delirium, pain, naloxone, operation duration and blood transfusion. The C-index value was 0.773 [95% confidence interval (CI) = 0.765 - 0.781] in the development set and 0.757 (95% CI = 0.744-0.770) in the validation set. The AUC was > 0.75 for the prediction of PLOS in PACU. The calibration curves revealed high consistencies between the predicted and actual probability. The DCA showed that if the threshold probability is over 10% , using the models to predict PLOS in PACU and implement intervention adds more benefit. CONCLUSIONS: This study presented a nomogram to facilitate individualized prediction of PLOS in PACU for patients undergoing elective surgery.