Mycobacterium marseillense bloodstream infection combined with skin fungal infection: a case report and literature review.

BACKGROUND: Non-tuberculous mycobacteria (NTM) are present widely in the natural environment and can invade the human body through the respiratory tract, gastrointestinal tract, and skin. Immunocompromised patients are particularly prone to infection, which primarily affects multiple organs, including the lungs, lymph nodes, and skin. However, cases of NTM bloodstream infections are rare. Here, we report a rare case of Mycobacterium marseillense bloodstream infection with concurrent skin fungal infection in a patient after kidney transplantation. Related literature was reviewed to enhance the understanding of this rare condition. CASE PRESENTATION: A 58-year-old male with a history of long-term steroid and immunosuppressant use after kidney transplantation presented with limb swelling that worsened over the past two months. Physical examination revealed redness and swelling of the skin in all four limbs, with a non-healing wound on the lower left limb. Skin tissue analysis by metagenomic next-generation sequencing (mNGS) and fungal culture indicated infection with Trichophyton rubrum. Blood culture results suggested infection with Mycobacterium marseillense. After receiving anti-NTM treatment, the patient's symptoms significantly improved, and he is currently undergoing treatment. CONCLUSION: Mycobacterium marseillense is a NTM. Gram staining suffered from misdetection, and the acid-fast staining result was positive. This bacterium was identified by mass spectrometry and mNGS analyses. Antimicrobial susceptibility tests for NTM were performed using the broth microdilution method. The results of the susceptibility test showed that Mycobacterium marseillense was sensitive to clarithromycin, an intermediary between moxifloxacin and linezolid. Bacterial clearance requires a combination of drugs and an adequate course of treatment. NTM bloodstream infections are relatively rare, and early identification and proactive intervention are key to their successful management.

Thalamic cells and pathway for social memory processing and storage.

In this issue of Neuron, Wang et al.1 demonstrate that parvalbumin interneurons in the sensory thalamic reticular nucleus are necessary and sufficient for regulating social memory in mice, identify a novel cortico-reticular thalamic-parafascicular pathway for social cognition, and highlight an essential role of GABAergic inhibitory neurons in social memory engrams.

The "psychiatric" neuron: the psychic neuron of the cerebral cortex, revisited.

Nearly 25 years ago, Dr. Patricia Goldman-Rakic published her review paper, "The 'Psychic' Neuron of the Cerebral Cortex," outlining the circuit-level dynamics, neurotransmitter systems, and behavioral correlates of pyramidal neurons in the cerebral cortex, particularly as they relate to working memory. In the decades since the release of this paper, the existing literature and our understanding of the pyramidal neuron have increased tremendously, and research is still underway to better characterize the role of the pyramidal neuron in both healthy and psychiatric disease states. In this review, we revisit Dr. Goldman-Rakic's characterization of the pyramidal neuron, focusing on the pyramidal neurons of the prefrontal cortex (PFC) and their role in working memory. Specifically, we examine the role of PFC pyramidal neurons in the intersection of working memory and social function and describe how deficits in working memory may actually underlie the pathophysiology of social dysfunction in psychiatric disease states. We briefly describe the cortico-cortical and corticothalamic connections between the PFC and non-PFC brain regions, as well the microcircuit dynamics of the pyramidal neuron and interneurons, and the role of both these macro- and microcircuits in the maintenance of the excitatory/inhibitory balance of the cerebral cortex for working memory function. Finally, we discuss the consequences to working memory when pyramidal neurons and their circuits are dysfunctional, emphasizing the resulting social deficits in psychiatric disease states with known working memory dysfunction.

Prefrontal Regulation of Social Behavior and Related Deficits: Insights From Rodent Studies.

The prefrontal cortex (PFC) is well known as the executive center of the brain, combining internal states and goals to execute purposeful behavior, including social actions. With the advancement of tools for monitoring and manipulating neural activity in rodents, substantial progress has been made in understanding the specific cell types and neural circuits within the PFC that are essential for processing social cues and influencing social behaviors. Furthermore, combining these tools with translationally relevant behavioral paradigms has also provided novel insights into the PFC neural mechanisms that may contribute to social deficits in various psychiatric disorders. This review highlights findings from the past decade that have shed light on the PFC cell types and neural circuits that support social information processing and distinct aspects of social behavior, including social interactions, social memory, and social dominance. We also explore how the PFC contributes to social deficits in rodents induced by social isolation, social fear conditioning, and social status loss. These studies provide evidence that the PFC uses both overlapping and unique neural mechanisms to support distinct components of social cognition. Furthermore, specific PFC neural mechanisms drive social deficits induced by different contexts.

Modulation of a Loop Region in the Substrate Binding Pocket Affects the Degree of Polymerization of Bacillus subtilis Chitosanase Products.

The hydrolytic products of chitosanase from Streptomyces avermitilis (SaCsn46A) were found to be aminoglucose and chitobiose, whereas those of chitosanase from Bacillus subtilis (BsCsn46A) were chitobiose and chitotriose. Therefore, the sequence alignment between SaCsn46A and BsCsn46A was conducted, revealing that the structure of BsCsn46A possesses an extra loop region (194N-200T) at the substrate binding pocket. To clarify the impact of this loop on hydrolytic properties, three mutants, SC, TJN, and TJA, were constructed. Eventually, the experimental results indicated that SC changed the ratio of chitobiose to chitotriose hydrolyzed by chitosanase from 1:1 into 2:3, while TJA resulted in a ratio of 15:7. This experiment combined molecular research to unveil a crucial loop within the substrate binding pocket of chitosanase. It also provides an effective strategy for mutagenesis and a foundation for altering hydrolysate composition and further applications in engineering chitosanase.

ALKBH5 Suppresses Autophagy in Prostate Cancer Cells via Inhibiting m6A-Modification of TSPAN1 mRNA.

BACKGROUND: Activating autophagy promotes the invasion and progression of prostate cancer (PCa). Tetraspanin 1 (TSPAN1) has been found to promote autophagy flux and its up-regulation can enhance the migration of PCa cells. In addition, there is a binding relationship between TSPAN1 and the N6-methyladenosine (m6A) demethylase AlkB homolog 5 (ALKBH5). Therefore, we wanted to know whether ALKBH5 could affect autophagy by regulating TSPAN1 expression, and thereby participate in PCa malignant progression. METHODS: The expression of ALKBH5 and TSPAN1 in PCa was examined by quantitative real-time polymerase chain reaction (qRT-PCR), and the functional tests included cell counting kit-8 and 5-ethynyl-2'-deoxyuridine (EdU) staining assays. The expression of autophagy-related proteins was confirmed by western blot. Detection of the m6A level of TSPAN1 was performed using methylated RNA immunoprecipitation sequencing (MeRIP)-qPCR. RESULTS: ALKBH5 was significantly downregulated in PCa cells (LNCaP, DU145 and PC3 cells; p < 0.001). Overexpression of ALKBH5 inhibited cell viability and the number of EdU-positive cells (p < 0.01, p < 0.001), decreased the ratio of microtubule-associated protein light chain 3B (LC3B)-II/LC3B-I, and promoted P62 protein expression in LNCaP and DU145 cells (p < 0.001). The m6A level of TSPAN1 was high in LNCaP and DU145 cells, but was inhibited by the overexpression of ALKBH5 (p < 0.001). TSPAN1 overexpression promoted cell viability (p < 0.001), increased EdU-positive cells and the LC3B-II/LC3B-I ratio (p < 0.001, p < 0.05), reduced P62 protein expression (p < 0.05, p < 0.001), and reversed the regulation of ALKBH5 overexpression in LNCaP and DU145 cells (p < 0.01, p < 0.001). CONCLUSIONS: Promoting ALKBH5 expression may inhibit PCa autophagy by reducing the m6A level of TSPAN1.

Enhancing the thermostability and catalytic activity of Bacillus subtilis chitosanase by saturation mutagenesis of Lys242.

Catalysis activity and thermostability are some of the fundamental characteristic of enzymes, which are of great significance to their industrial applications. Bacillus subtilis chitosanase BsCsn46A is a kind of enzyme with good catalytic activity and stability, which can hydrolyze chitosan to produce chitobiose and chitotriose. In order to further improve the catalytic activity and stability of BsCsn46A, saturation mutagenesis of the C-terminal K242 of BsCsn46A was performed. The results showed that the six mutants (K242A, K242D, K242E, K242F, K242P, and K242T) showed increased catalytic activity on chitosan. The catalytic activity of K242P increased from 12971 ± 597 U mg-1 of wild type to 17820 ± 344 U mg-1 , and the thermostability of K242P increased by 2.27%. In order to elucidate the reason for the change of enzymatic properties, hydrogen network, molecular docking, and molecular dynamics simulation were carried out. The hydrogen network results showed that all the mutants lose their interaction with Asp6 at 242 site, thereby increasing the flexibility of Glu19 at the junction sites of α1 and loop1. Molecular dynamics results showed that the RMSD of K242P was lower at both 313 and 323 K than that of other mutants, which supported that K242P had better thermostability. The catalytic activity of mutant K242P reached 17820.27 U mg-1 , the highest level reported so far, which could be a robust candidate for the industrial application of chitooligosaccharide (COS) production.

The role of cell adhesion molecule IgSF9b at the inhibitory synapse and psychiatric disease.

Understanding perturbations in synaptic function between health and disease states is crucial to the treatment of neuropsychiatric illness. While genome-wide association studies have identified several genetic loci implicated in synaptic dysfunction in disorders such as autism and schizophrenia, many have not been rigorously characterized. Here, we highlight immunoglobulin superfamily member 9b (IgSF9b), a cell adhesion molecule thought to localize exclusively to inhibitory synapses in the brain. While both pre-clinical and clinical studies suggest its association with psychiatric diseases, our understanding of IgSF9b in synaptic maintenance, neural circuits, and behavioral phenotypes remains rudimentary. Moreover, these functions wield undiscovered influences on neurodevelopment. This review evaluates current literature and publicly available gene expression databases to explore the implications of IgSF9b dysfunction in rodents and humans. Through a focused analysis of one high-risk gene locus, we identify areas requiring further investigation and unearth clues related to broader mechanisms contributing to the synaptic etiology of psychiatric disorders.

[Preparation and quality evaluation of total flavonoids microemulsion of "Pueraria lobata-Hovenia dulcis"].

The effective components of flavonoids in the "Pueraria lobata-Hovenia dulcis" drug pair have low bioavailability in vivo due to their unstable characteristics. This study used microemulsions with amphoteric carrier properties to solve this problem. The study drew pseudo-ternary phase diagrams through titration compatibility experiments of the oil phase with emulsifiers and co-emulsifiers and screened the prescription composition of blank microemulsions. The study used average particle size and PDI as evaluation indicators, and the central composite design-response surface method(CCD-RSM) was used to optimize the prescription; high-dosage drug-loaded microemulsions were obtained, and their physicochemical properties, appearance, and stability were evaluated. The results showed that when ethyl butyrate was used as the oil phase, polysorbate 80(tween 80) as the surfactant, and anhydrous ethanol as the cosurfactant, the maximum microemulsion area was obtained. When the difference in results was small, K_(m )of 1∶4 was chosen to ensure the safety of the prescription. The prescription composition optimized by the CCD-RSM was ethyl butyrate(16.28%), tween 80(9.59%), and anhydrous ethanol(38.34%). When the dosage reached 3% of the system mass, the total flavonoid microemulsion prepared had a clear and transparent appearance, with average particle size, PDI, and potential of(74.25±1.58)nm, 0.277±0.043, and(-0.08±0.07) mV, respectively. The microemulsion was spherical and evenly distributed under transmission electron microscopy. The centrifugal stability and temperature stability were good, and there was no layering or demulsification phenomenon, which significantly improved the in vitro dissolution of total flavonoids.

A novel cuproptosis-related prognostic gene signature in adrenocortical carcinoma.

BACKGROUND: Adrenocortical carcinoma (ACC) is an aggressive and rare malignant tumor associated with poor outcomes. Cuproptosis, a new pattern of cell death, relies on mitochondrial respiration and is associated with protein lipoylation. Increasing evidence has demonstrated the potential roles of cuproptosis in several tumor entities. However, the relationship between cuproptosis and ACC remains unclear. METHODS: In total, 10 cuproptosis-related genes (CRGs) of patients with ACC were obtained from the Gene Expression Omnibus (GEO) and The Cancer Genome Atlas (TCGA) databases and differential expression analysis of CRGs was analyzed. Functional enrichment of the CRGs was performed and protein-protein interaction analysis was utilized to explore the association between the CRGs. Cuproptosis-related risk score (CRRS) was constructed by Lasso Cox regression and validated. RESULTS: In the current study, the alteration and expression patterns of 10 CRGs in TCGA-ACC datasets were analyzed. We identified different expression patterns of CRGs in ACCs, discovered strong associations between CRGs and ACCs, and found that the CRGs were associated with immune infiltration in ACCs. A CRRS was created thereafter to predict overall survival (OS). CRRS = (0.083103718) *FDX1 + (-0.278423862) *LIAS+(0.090985682) *DLAT+(-0.018784047) *PDHA1 + (0.297218951) *MTF1 + (0.310197964) *CDKN2A. Patients were divided into high- and low-risk groups based on their CRRS, and independent prognostic factors were investigated. Finally, CDKN2A and FDX1 were found to be independent prognostic predictors of patients with ACC. CONCLUSIONS: CDKN2A and FDX1 are independent prognostic predictors of patients with ACC. Cuproptosis may play a role in the development of ACC, providing a new perspective on therapeutic strategies related to CRGs for cancer prevention and treatment.

A Novel Fluorescence Sensor for Iodide Detection Based on the 1,3-Diaryl Pyrazole Unit with AIE and Mechanochromic Fluorescence Behavior.

A D-A type of luminophore, TPA-CDP, was designed and synthesized by using triphenylamine (TPA) as D (electron donor), 1,3-diaryl pyrazole with cyano groups (CDP) as A (electron acceptor) and employing a cyanovinyl segment as a recognition group. Firstly, TPA-CDP demonstrates effective fluorescence quenching as a sensor for I- by the nucleophilic addition reaction of the cyanovinyl segment with a high level of sensitivity, selectivity and a low determination limit of 4.43 µM. Interestingly, TPA-CDP exhibited an AIE phenomenon with the fw value reaching 50%. In addition, TPA-CDP displayed distinct mechanochromic fluorescence behavior with 70 nm red shift, which was observed over four repeated cycles. Furthermore, the mechanochromic fluorescence behavior of TPA-CDP, as observed in powder XRD experiments, was found to be associated with the morphological transition from a crystalline state to an amorphous state. These results confirm the significant potential of CDP as a powerful electron-deficient component in the creation of D-A-type mechanochromic fluorescence materials and biosensors for detecting I-.

DNA methylation and the opposing NMDAR dysfunction in schizophrenia and major depression disorders: a converging model for the therapeutic effects of psychedelic compounds in the treatment of psychiatric illness.

Psychedelic compounds are being increasingly explored as a potential therapeutic option for treating several psychiatric conditions, despite relatively little being known about their mechanism of action. One such possible mechanism, DNA methylation, is a process of epigenetic regulation that changes gene expression via chemical modification of nitrogenous bases. DNA methylation has been implicated in the pathophysiology of several psychiatric conditions, including schizophrenia (SZ) and major depressive disorder (MDD). In this review, we propose alterations to DNA methylation as a converging model for the therapeutic effects of psychedelic compounds, highlighting the N-methyl D-aspartate receptor (NMDAR), a crucial mediator of synaptic plasticity with known dysfunction in both diseases, as an example and anchoring point. We review the established evidence relating aberrant DNA methylation to NMDAR dysfunction in SZ and MDD and provide a model asserting that psychedelic substances may act through an epigenetic mechanism to provide therapeutic effects in the context of these disorders.

Enhanced Cerebral Hemodynamics and Cognitive Function Via Knockout of Dual-Specificity Protein Phosphatase 5.

Alzheimer's Disease (AD) and Alzheimer's Disease-Related Dementias (ADRD) are neurodegenerative disorders. Recent studies suggest that cerebral hypoperfusion is an early symptom of AD/ADRD. Dual-specificity protein phosphatase 5 (DUSP5) has been implicated in several pathological conditions, including pulmonary hypertension and cancer, but its role in AD/ADRD remains unclear. The present study builds on our previous findings, demonstrating that inhibition of ERK and PKC leads to a dose-dependent dilation of the middle cerebral artery and penetrating arteriole, with a more pronounced effect in Dusp5 KO rats. Both ERK and PKC inhibitors resulted in a significant reduction of myogenic tone in vessels from Dusp5 KO rats. Dusp5 KO rats exhibited stronger autoregulation of the surface but not deep cortical cerebral blood flow. Inhibition of ERK and PKC significantly enhanced the contractile capacity of vascular smooth muscle cells from both strains. Finally, a significant improvement in learning and memory was observed in Dusp5 KO rats 24 hours after initial training. Our results suggest that altered vascular reactivity in Dusp5 KO rats may involve distinct mechanisms for different vascular beds, and DUSP5 deletion could be a potential therapeutic target for AD/ADRD. Further investigations are necessary to determine the effects of DUSP5 inhibition on capillary stalling, blood-brain barrier permeability, and neurodegeneration in aging and disease models.

Prefrontal modulation of anxiety through a lens of noradrenergic signaling.

Anxiety disorders are the most common class of mental illness in the U.S., affecting 40 million individuals annually. Anxiety is an adaptive response to a stressful or unpredictable life event. Though evolutionarily thought to aid in survival, excess intensity or duration of anxiogenic response can lead to a plethora of adverse symptoms and cognitive dysfunction. A wealth of data has implicated the medial prefrontal cortex (mPFC) in the regulation of anxiety. Norepinephrine (NE) is a crucial neuromodulator of arousal and vigilance believed to be responsible for many of the symptoms of anxiety disorders. NE is synthesized in the locus coeruleus (LC), which sends major noradrenergic inputs to the mPFC. Given the unique properties of LC-mPFC connections and the heterogeneous subpopulation of prefrontal neurons known to be involved in regulating anxiety-like behaviors, NE likely modulates PFC function in a cell-type and circuit-specific manner. In working memory and stress response, NE follows an inverted-U model, where an overly high or low release of NE is associated with sub-optimal neural functioning. In contrast, based on current literature review of the individual contributions of NE and the PFC in anxiety disorders, we propose a model of NE level- and adrenergic receptor-dependent, circuit-specific NE-PFC modulation of anxiety disorders. Further, the advent of new techniques to measure NE in the PFC with unprecedented spatial and temporal resolution will significantly help us understand how NE modulates PFC function in anxiety disorders.

Recent advances in stem cell therapy for erectile dysfunction: a narrative review.

INTRODUCTION: While phosphodiesterase type 5 inhibitors (PDE5is) and others are used to treat Erectile dysfunction (ED), many patients are either unresponsive or resistant to it. Stem cell therapy (SCT) is a promising alternative approach. Numerous preclinical trials have demonstrated improved erectile function in animal models using SCT, although the number of clinical trials investigating SCT for men with ED is limited. Nonetheless, findings from human clinical trials suggest that SCT may be a useful treatment option. AREAS COVERED: Biomedical literature, including PubMed, ClinicalTrials.gov, and European Union Clinical Trials Registry, were analyzed to summarize and synthesize information on stem cell therapy for ED in this narrative review. The achievements in preclinical and clinical evaluations are presented and critically analyzed. EXPERT OPINION: SCT has demonstrated some benefits in improving erectile function, while further studies are urgently needed. Such studies would provide valuable insights into the optimal use of stem cell therapy and its potential as a therapeutic option for ED. Taking advantage of different mechanisms of action involved in various regenerative therapies, combination therapies such as SCT and low-energy shock waves or platelet-rich plasma may provide a more effective therapy and warrant further research.

Pharmacogenetic activation of parvalbumin interneurons in the prefrontal cortex rescues cognitive deficits induced by adolescent MK801 administration.

The cognitive symptoms of schizophrenia (SZ) present a significant clinical burden. They are treatment resistant and are the primary predictor of functional outcomes. Although the neural mechanisms underlying these deficits remain unclear, pathological GABAergic signaling likely plays an essential role. Perturbations with parvalbumin (PV)-expressing fast-spiking (FS) interneurons in the prefrontal cortex (PFC) are consistently found in post-mortem studies of patients with SZ, as well as in animal models. Our studies have shown decreased prefrontal synaptic inhibition and PV immunostaining, along with working memory and cognitive flexibility deficits in the MK801 model. To test the hypothesized association between PV cell perturbations and impaired cognition in SZ, we activated prefrontal PV cells by using an excitatory DREADD viral vector with a PV promoter to rescue the cognitive deficits induced by adolescent MK801 administration in female rats. We found that targeted pharmacogenetic upregulation of prefrontal PV interneuron activity can restore E/I balance and improve cognition in the MK801 model. Our findings support the hypothesis that the reduced PV cell activity levels disrupt GABA transmission, resulting in the disinhibition of excitatory pyramidal cells. This disinhibition leads to an elevated prefrontal excitation/inhibition (E/I) balance that could be causal for cognitive impairments. Our study provides novel insights into the causal role of PV cells in cognitive function and has clinical implications for understanding the pathophysiology and management of SZ.

Thr22 plays an important role in the efficient catalytic process of Bacillus subtilis chitosanase BsCsn46A.

Threonine 22 (Thr22) located in catalytic center near the catalytic amino acid Glu19 was non-conserved in Bacillus species chitosanase. In order to study the function of Thr22, saturation mutagenesis was carried out towards P121N, a mutant previously constructed in our laboratory. Compared with P121N, which was designated as the wild type (WT) in this research, the specific enzyme activity of all mutants was decreased, and that of the T22P mutant was decreased by 91.6 %. Among these mutants, the optimum temperature decreased from 55 °C to 50 °C for 10 mutants and 45 °C for 4 mutants, respectively. The optimum temperature of mutant T22P was 40 °C. In order to analyze the reasons for the changes in enzymatic properties of the mutants, molecular docking analysis of WT and its mutants with substrate were performed. The hydrogen bond analysis around position 22 also conducted. The substitution of Thr22 was found to significantly affect the enzyme-substrate complex interaction. In addition, the hydrogen network near position 22 has undergone obvious changes. These changes may be the main reasons for the changes in enzymatic properties of the mutants. Altogether, this study is valuable for the future research on Bacillus chitosanase.

Modeling net energy partition patterns of growing-finishing pigs using nonlinear regression and artificial neural networks.

The objectives of this study were to evaluate the net energy (NE) partition patterns of growing-finishing pigs at different growing stages and to develop the corresponding prediction models using nonlinear regression (NLR) and artificial neural networks (ANN). Twenty-four pigs with an initial body weight (BW) of ~30 kg were kept in metabolic cages and fed ad libitum and were moved into six respiration chambers in turns until ~90 kg. The NE partition patterns, i.e., NE for maintenance (NEm), NE retained as protein (NEp), and NE retained as lipid (NEl), were calculated based on indirect calorimetry and nitrogen balance techniques. The energy balance data collected through the animal trial was then randomly split into a training data set containing 75% of the samples and a testing data set containing the remaining 25% of the samples. The NLR models and a series of ANN models were established on the training data set to predict the metabolizable energy intake, NE intake, NEm, NEp, and NEl of pigs. The best-fitted ANN models were selected by 5-fold cross-validation in the training data set. The prediction performance of the best-fitted NLR and ANN models were compared on the testing data set. The results showed that the average NE intakes of pigs were 17.71, 23.25, 24.56, and 28.96 MJ/d in 30 to 45 kg, 45 to 60 kg, 60 to 75 kg, and 75 to 90 kg, respectively. The NEm and NEl (MJ/d) kept increasing as BW increased from 30 kg to 90 kg, while the NEp increased to its maximum value and then kept in a certain range of 4.64 to 4.88 MJ/d. The proportion of NEm for pigs at 30 to 90 kg stayed within the range of 42.0% to 48.6%, while the proportion of NEl kept increasing. For the prediction models built based on the animal trial, ANN models exhibited better performance than NLR models for all the target outputs. In conclusion, NE partition patterns changed in different growth stages of pigs, and ANN models are more flexible and powerful than NLR models in predicting the NE partition patterns of growing-finishing pigs.

Net energy (NE) is the most refined energy system in animal nutrition, and understanding the NE partition patterns of pigs can help us to develop suitable feeding strategies to improve the growth performance and carcass traits of pigs. However, it is time-consuming, laborious, and expensive to directly measure the NE; thus, establishing a predicted model is more efficient. In research on the energy nutrition of pigs, regression is the most used tool to develop models, but little literature has focused on the application of artificial neural networks (ANN) models. In this study, we measured the NE partition patterns of pigs, and our results show that the proportion of NE for maintenance stayed within the range of 42.0% to 48.6%, while the proportion of NE retained as a lipid kept increasing as pig grows (pigs body weight: 30 to 90 kg). The value of NE retained as protein increased to its maximum value and then stayed in a certain range of 4.64 to 4.88 MJ/d, but with a decreased proportion of NE intake. Additionally, we applied the corresponding nonlinear regression (NLR) and ANN models and made comparisons between them. The ANN models exhibited better performance than NLR models for all the target outputs.

Prefrontal Cortical Control of Anxiety: Recent Advances.

Dysfunction in the prefrontal cortex is commonly implicated in anxiety disorders, but the mechanisms remain unclear. Approach-avoidance conflict tasks have been extensively used in animal research to better understand how changes in neural activity within the prefrontal cortex contribute to avoidance behaviors, which are believed to play a major role in the maintenance of anxiety disorders. In this article, we first review studies utilizing in vivo electrophysiology to reveal the relationship between changes in neural activity and avoidance behavior in rodents. We then review recent studies that take advantage of optical and genetic techniques to test the unique contribution of specific prefrontal cortex circuits and cell types to the control of anxiety-related avoidance behaviors. This new body of work reveals that behavior during approach-avoidance conflict is dynamically modulated by individual cell types, distinct neural pathways, and specific oscillatory frequencies. The integration of these different pathways, particularly as mediated by interactions between excitatory and inhibitory neurons, represents an exciting opportunity for the future of understanding anxiety.