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Background: Shingles can cause long-term pain and negative emotions, along with changes in brain function. In this study, Granger Causality Analysis (GCA) was used to compare herpes zoster (HZ) and postherpetic neuralgia (PHN) differences in effective connections within the "pain matrix" between patients and healthy controls to further understand patterns of interaction between brain regions and explore the relationship between changes in effective connections and clinical features. Methods: Resting-state functional magnetic resonance imaging (fMRI) scans were performed on 55 HZ; 55 PHN; and 50 age-, sex- matched healthy controls (HCs). The brain regions associated with the pain matrix are used as the seeds of effective connectivity. GCA was used to analyze effective connections in brain regions that differed significantly between groups. Then the correlation between GCA values and clinical indicators was studied. Results: Compared with HC, GCA values between the thalamus and the amygdala, between the thalamus and the precentral gyrus, from the thalamus to the postcentral gyrus, and from the parahippocampal gyrus to the amygdala, anterior cingulate gyrus were significantly reduced in HZ patients. Compared with HC, GCA values between the insular and the postcentral gyrus, from the insular to the inferior parietal lobe, and from the postcentral gyrus to the amygdala were significantly reduced in PHN patients. Compared with HZ, GCA values between the inferior parietal lobe and the parahippocampal gyrus, between the inferior parietal lobe and the anterior cingulate gyrus, and from the anterior cingulate gyrus to the amygdala were significantly increased in PHN patients. The visual analogue scale (VAS) score of PHN patients was positively correlated with the GCA value from the central posterior lobe to the insula. Conclusions: PHN and HZ patients showed a broad reduction in effective connections, mainly reflected in abnormal pain pathway regulation, pain perception, negative emotion and memory production, providing new perspectives to understand the neuroimaging mechanisms of shingles. [ABSTRACT FROM AUTHOR]

Corticosteroids are extensively used in medicine for their powerful anti-inflammatory and immunosuppressive effects. However, their psychiatric side effects—such as mood disturbances, anxiety, and psychosis—are significant yet often underappreciated. This review provides a comprehensive exploration of corticosteroid-induced psychiatric disorders, with a focus on their underlying mechanisms and clinical implications. We examine how corticosteroids influence the hypothalamic–pituitary–adrenal (HPA) axis, leading to the dysregulation of stress responses and alterations in neurotransmitter levels, particularly dopamine, serotonin, and glutamate. These changes are linked to structural abnormalities in key brain areas such as the hippocampus and amygdala, which are implicated in mood and anxiety disorders, psychosis, and conditions like post-traumatic stress disorder (PTSD) and eating disorders. This review highlights the need for healthcare providers to be vigilant in recognizing and managing corticosteroid-induced psychiatric symptoms, especially in vulnerable populations with pre-existing mental health conditions. The complex relationship between corticosteroid type, dose, duration, and mental health outcomes is explored, emphasizing the importance of personalized treatment approaches to mitigate psychiatric risks. Given the widespread use of corticosteroids, there is an urgent need for more focused research on their psychiatric side effects. This review underscores the importance of patient education and careful monitoring to ensure optimal therapeutic outcomes while minimizing mental health risks associated with corticosteroid therapy. [ABSTRACT FROM AUTHOR]

Background and Aims: The rapid expansion of artificial intelligence (AI) within worldwide healthcare systems is occurring at a significant rate. In this context, the Middle East has demonstrated distinctive characteristics in the application of AI within the healthcare sector, particularly shaped by regional policies. This study examined the outcomes resulting from the utilization of AI within healthcare systems in the Middle East. Methods: A systematic review was conducted across several databases, including PubMed, Scopus, ProQuest, and the Cochrane Database of Systematic Reviews in 2024. The quality assessment of the included studies was conducted using the Authority, Accuracy, Coverage, Objectivity, Date, Significance checklist. Following this, a thematic analysis was carried out on the acquired data, adhering to the Boyatzis approach. Results: 100 papers were included. The quality and bias risk of the included studies were delineated to be within an acceptable range. Multiple themes were derived from the thematic analysis including: "Prediction of diseases, their diagnosis, and outcomes," "Prediction of organizational issues and attributes," "Prediction of mental health issues and attributes," "Prediction of polypharmacy and emotional analysis of texts," "Prediction of climate change issues and attributes," and "Prediction and identification of success and satisfaction among healthcare individuals." Conclusion: The findings emphasized AI's significant potential in addressing prevalent healthcare challenges in the Middle East, such as cancer, diabetes, and climate change. AI has the potential to overhaul the healthcare systems. The findings also highlighted the need for policymakers and administrators to develop a concrete plan to effectively integrate AI into healthcare systems. Summary: AI has a substantial potential in mitigating the challenges posed by cancer and diabetes in the Middle East.In situations where the healthcare system is strained, such as during a pandemic, AI can provide an effective solution.AI enhances the analysis of patient data, accelerating early diagnosis and treatment processes, while increasing the efficiency of healthcare delivery and optimal use of resources.AI can be utilized to confront the climate change and other similar challenges.There is a lack of studies concerning the effects of AI utilization in nonclinical facets of healthcare service delivery, encompassing areas such as human resource management and economics [ABSTRACT FROM AUTHOR]

Autism spectrum disorder (ASD) is one of the most prevalent neurodevelopmental disorders. To explore its pathophysiology, we investigated the association between neonatal allergic exposure and behavioral changes. Adult female C57BL/6J mice were immunized with adjuvant (aluminum hydroxide) or ovalbumin emulsified with adjuvant. After immunization, the mice were mated, and offspring were born at full term. The postnatal dams and infants were then simultaneously exposed to an allergen (ovalbumin) or vehicle via inhalation. After weaning, behavioral testing and histopathological analyses were conducted on male offspring. Compared with the vehicle-exposed offspring, the ovalbumin-exposed offspring had decreased sociability and increased repetitive behavior, thus representing an ASD-like phenotype in mice. Moreover, histopathological analyses revealed that the ovalbumin-exposed mice had increased astroglial, microglial, and eosinophilic infiltration in the olfactory bulb, as well as increased eosinophils in the nasal mucosa. The ovalbumin-exposed mice also had decreased dendritic spine density and a lower proportion of mature spines, suggesting the impairment of stimulus-induced synaptogenesis. In conclusion, postnatal allergic exposure induced an ASD-like phenotype, as well as allergic rhinitis, which was followed by glial inflammation in the olfactory bulb parenchyma. [ABSTRACT FROM AUTHOR]

The brainstem has long been recognized as the major respiratory control center, but it has become increasingly appreciated that areas upstream of the brainstem modulate respiration and airway defensive behaviors. This review aims to define the role of the amygdala, a key temporal brain region essential for limbic function, in respiration and airway defenses. We summarize literature describing roles for the amygdala in control of respiration, swallow, cough, airway smooth muscle contraction, and mucus secretion. We emphasize the need to understand how the amygdala regulates these functions both at a local scale and network scale and identify knowledge gaps for current and future investigations. Lastly, we highlight literature suggesting that amygdala dysfunction may contribute to respiratory dysfunction. [ABSTRACT FROM AUTHOR]

Introduction: Asthma is a serious disease that affects not only the respiratory system but also the brain by decreasing oxygen saturation. Despite the numerous neuroimaging studies that have shed light on the effect of asthma on brain volume, there is still a need for new studies to evaluate brain volume in asthmatic patients. Aim: To evaluate the Grey Matter Volume (GMV) of the brain in asthmatic patients using Magnetic Resonance Imaging (MRI) images to detect possible changes. Materials and Methods: This is an observational analytic casecontrol study carried out at Al Amal Hospital in Khartoum State, Sudan, between January 2020 and October 2022. The study included 100 adult participants (50 asthmatic patients and 50 healthy controls) using MRI and automatic brain segmentation through a software program (BrainSuite). Data were analysed using Statistical Package for Social Science (SPSS) software, version 25.0 (IBM SPSS Inc., Chicago, IL), and Microsoft Excel 2013. An independent sample T-test was used to compare the mean of the measurements between controls and asthmatics. Frequencies, means, and standard deviations were taken. A p-value of 0.05 or less was accepted as statistically significant. Results: Out of all participants, 50 were asthmatics and 50 were controls. The mean age of asthmatics was (31±8.53) years and of controls was 32 ± 8.49 years. The mean Grey Matter Volume (GMV) of the asthmatic patients was 575.93 cm³ ±71.46 SD and of controls was 569.55 cm³ ±73.77 SD. There were no statistically significant differences between the groups depending on the GMV of asthmatic and control participants (p>0.05). The mean GMV in asthmatic males was 355.50 cm³ ±53.26 SD and in females 321.65 cm³ ±32.72 SD, while in control males it was 367.63 cm³ ±45.77 SD and in females 318.03 cm³ ±34.16 SD. GMV showed significant statistical differences between asthmatic males and females (p<0.05). Conclusion: There were no statistically significant differences between the groups depending on the GMV of asthmatic and control participants (p>0.05). Asthma disease does not result in noticeable changes in GMV in either male or female brains. [ABSTRACT FROM AUTHOR]

Objective: Although extensive research has explored the link between mental disorders and asthma, the characteristics and patterns of this association are still unclear. Our study aims to examine the genetic causal links between common mental disorders (specifically, anxiety and depression) and asthma. Methods: We conducted genetic analyses including linkage disequilibrium score regression (LDSC) and bidirectional two-sample Mendelian randomization (MR) analyses, and utilized summary statistics from recent large-scale Genome-Wide Association Studies (GWASs) in European populations, covering sensation of anxiety or depression, anxiety sensation, depression sensation, anxiety disorders, major depression disorder (MDD), and asthma. Results: LDSC revealed significant genetic correlations among sensation of anxiety or depression,MDD and asthma (P < 0.017), highlighting potential genetic correlation between anxiety disorders and asthma (P < 0.05 yet > 0.017). In bidirectional twosample MR, inverse-variance weighted (IVW) analyses suggested that genetic liability to asthma was significantly associated with an increased risk of sensation of anxiety or depression (OR = 4.760, 95% CI: 1.645-13.777), and MDD (OR = 1.658, 95% CI: 1.477-1.860). Conversely, IVW analyses indicated that genetic liability to anxiety disorders was not associated with an increased risk of asthma (P > 0.01), nor was genetic liability to asthma associated with an increased risk of anxiety disorders (P > 0.01). Furthermore, no significant genetic causal relationships were observed for other studied traits. Multivariate MR, after adjusting for body mass index and alcohol consumption, further corroborated the independent causal effect of genetic predisposition to MDD on the risk of asthma (OR = 1.460, 95% CI: 1.285-1.660). Conclusion: Our study establishes MDD as a predisposing factor for asthma. Meanwhile, anxiety disorders are not causal risk factors for asthma, nor is the reverse true. It is recommended to closely monitor asthma symptoms in patients with MDD. [ABSTRACT FROM AUTHOR]

The entorhinal cortex (EC) stands out as a critical brain region affected in the early phases of Alzheimer's disease (AD), with some of the disease's pathological processes originating from this area, making it one of the most crucial brain regions in AD. Recent research highlights disruptions in the brain's network activity, characterized by heightened excitability and irregular oscillations, may contribute to cognitive impairment. These disruptions are proposed not only as potential therapeutic targets but also as early biomarkers for AD. In this paper, we will begin with a review of the anatomy and function of EC, highlighting its selective vulnerability in AD. Subsequently, we will discuss the disruption of EC network activity, exploring changes in excitability and neuronal oscillations in this region during AD and hypothesize that, considering the advancements in neuromodulation techniques, addressing the disturbances in the network activity of the EC could offer fresh insights for both the diagnosis and treatment of AD. [ABSTRACT FROM AUTHOR]

As the growth of society and the continuous upgrading of people's living standards increase, people's requirements for indoor environment are also increasing. To optimize the ventilation methods inside buildings, a numerical simulation method was used to construct numerical simulations of airflow organization and aerosol diffusion, and based on this model, better ventilation methods were determined. To optimize the determined better ventilation method, a multi-constraint optimization model was constructed using infection probability, thermal comfort, energy utilization coefficient, and velocity non-uniformity coefficient. The ventilation method was optimized through multi-objective constraints. To solve the optimization model, an optimized particle swarm algorithm was studied and designed. The results showed that under the "air rain" flow field, the maximum values of aerosol particles at the human body, bed surface, and outlet were 171, 769, and 19,973, respectively, while the minimum values were 4, 169, and 2197, respectively. The "air rain" flow field is a better ventilation method. The maximum and minimum values of the original non-uniformity coefficient were 0.44 and 0.08, respectively. After optimization by the particle swarm optimization algorithm, the maximum and minimum predicted non-uniformity coefficients were 0.457 and 0.08, respectively. The original value and predicted value are very close. The numerical model and algorithm constructed by the research institute are effective. The algorithm designed by the research institute can provide technical support for multi-objective optimization of indoor ventilation methods. [ABSTRACT FROM AUTHOR]

Objective: Bronchial Asthma (BA) is a common chronic respiratory disease worldwide. Earlier research has demonstrated abnormal functional connectivity (FC) in multiple cognition-related cortices in asthma patients. The thalamus (Thal) serves as a relay center for transmitting sensory signals, yet the modifications in the thalamic FC among individuals with asthma remain uncertain. This research employed the resting-state functional connectivity (rsFC) approach to explore alterations in thalamic functional connectivity among individuals with BA. Patients and methods: After excluding participants who did not meet the criteria, this study finally included 31 patients with BA, with a gender distribution of 16 males and 15 females. Subsequently, we recruited 31 healthy control participants (HC) matched for age, gender, and educational background. All participants underwent the Montreal Cognitive Assessment (MoCA) and the Hamilton Depression Rating Scale (HAMD) assessment. Following this, both groups underwent head magnetic resonance imaging scans, and resting-state functional magnetic resonance imaging (rs-fMRI) data was collected. Based on the AAL (Automated Anatomical Labeling) template, the bilateral thalamic regions were used as seed points (ROI) for subsequent rsFC research. Pearson correlation analysis was used to explore the relationship between thalamic functional connectivity and neuropsychological scales in both groups. After controlling for potential confounding factors such as age, gender, intelligence, and emotional level, a two-sample t-test was further used to explore differences in thalamic functional connectivity between the two groups of participants. Result: Compared to the HC group, the BA group demonstrated heightened functional connectivity (FC) between the left thalamus and the left cerebellar posterior lobe (CPL), left postcentral gyrus (PCG), and right superior frontal gyrus (SFG). Concurrently, there was a decrease in FC with both the Lentiform Nucleus (LN) and the left corpus callosum (CC). Performing FC analysis with the right thalamus as the Region of Interest (ROI) revealed an increase in FC between the right thalamus and the right SFG as well as the left CPL. Conversely, a decrease in FC was observed between the right thalamus and the right LN as well as the left CC. Conclusion: In our study, we have verified the presence of aberrant FC patterns in the thalamus of BA patients. When compared to HCs, BA patients exhibit aberrant alterations in FC between the thalamus and various brain areas connected to vision, hearing, emotional regulation, cognitive control, somatic sensations, and wakefulness. This provides further confirmation of the substantial role played by the thalamus in the advancement of BA. [ABSTRACT FROM AUTHOR]

Introduction: Alzheimer's disease (AD) causes progressive loss of cognitive function and synaptic plasticity, which is the most common form of dementia. The present study was designed to scrutinize the effects of cacao on passive avoidance memory function and to identify the roles of hippocampal synaptic plasticity and oxidative stress in an AD rat model induced by unilateral intracerebroventricular (UICV) injection of amyloid-beta (Aβ). Methods: Oral administration of cacao (500 mg/kg/day) was given for 2 consecutive months. A memory retention test was conducted 24 h after passive avoidance training was completed. Subsequently, the amplitude of population spike (PS) and slope of field excitatory postsynaptic potentials (fEPSPs) were assessed at hippocampal long-term potentiation (LTP) in perforant pathway-dentate gyrus (PP-DG) synapses. Moreover, total thiol group (TTG) and malondialdehyde (MDA) concentrations were evaluated in the plasma. Furthermore, compact Aβ plaques were detected in the hippocampal DG by performing Congo red staining. Results: As a result of AD induction, passive avoidance memory was impaired; also, reduced fEPSP slopes, PS amplitudes, and content of TTG, and increase in MDA levels in the rats were observed. In contrast, cacao treatment ameliorated passive avoidance memory impairment, improved hippocampal LTP impairment, modulated oxidative-antioxidative status, and delayed Aβ plaques production in AD rats. Disscussion: Conclusively, cacao alleviates Aβ-induced cognitive deficit, probably by the amelioration of hippocampal LTP impairment, modulation of oxidative-antioxidative status, and inhibition of Aβ plaque accumulation. [ABSTRACT FROM AUTHOR]

Introduction: The positive effects of exercise on spatial memory and learning have been demonstrated in research. The olfactory sensory neurons (OSNs) respond to mechanical stimulation induced by nasal airflow which is associated with airflow intensity. Accordingly, nasal breathing can modulate brain oscillations in nonolfactory areas, and respiration-entrained oscillations aid the improvement of cognitive abilities. Given that aerobic exercise increases the rate of respiration and intensity of nasal airflow, this study evaluates the role of OSNs in mediating the effects of aerobic exercise on memory. Methods: We examined spatial memory following exercise in animal models of olfactory sensory neuron impairment (methimazole injection 300 mg/kg/week). Results: Destroying OSNs significantly reduces olfactory bulb (OB) activity at delta and theta frequency bands as well as its coupling to respiration. More importantly, it abolished the positive effect of exercise on spatial memory (P<0.05). Conclusion: The OB activity is one of the probable mechanisms for improving spatial memory following exercise. [ABSTRACT FROM AUTHOR]

This study aimed to investigate the effects of intranasal air-puffing on cognitive impairments and brain cortical activity following one night of partial sleep deprivation (PSD) in adults. A total of 26 healthy adults underwent the numerical Stroop test (NST) and electroencephalography (EEG) before and after one night of PSD. Following PSD, subjects in the treatment group (n = 13) received nasal air-puffs (5 Hz, 3 min) before beginning the NST and EEG recording. Administration of nasal air-puffs in the treatment group restored the PSD-induced increase in error rate and decrease in reaction time and missing rate in the NST. Intranasal air-puffs recovered the PSD-induced augmentation of delta and theta power and the reduction of beta and gamma power in the EEG, particularly in the frontal lobes. Intranasal air-puffing also almost reversed the PSD-induced decrease in EEG signal complexity. Furthermore, it had a restorative effect on PSD-induced alteration in intra-default mode network functional connectivity in the beta and gamma frequency bands. Rhythmic nasal air-puffing can mitigate acute PSD-induced impairments in cognitive functions. It exerts part of its ameliorating effect by restoring neuronal activity in cortical brain areas involved in cognitive processing. [ABSTRACT FROM AUTHOR]

Introduction: Stuttering is a speech disorder characterized by impaired connections between brain regions involved in speech production. This study aimed to investigate functional connectivity and frequency power during rest in adults who stutter (AWS) compared to fluent adults (AWNS) in the dorsolateral prefrontal cortex (DLPFC), dorsolateral frontal cortex (DLFC), supplementary motor area (SMA), motor speech, angular gyrus (AG), and inferior temporal gyrus (ITG). Materials and methods: Fifteen AWS (3 females, 12 males) and fifteen age-and sex-matched AWNS (3 females, 12 males) participated in this study. All participants were native Persian speakers. Stuttering severity in the AWS group was assessed using the Persian version of the Stuttering Severity Instrument Fourth Edition (SSI-4). Resting-state electroencephalography (EEG) was recorded for 5 min while participants sat comfortably with their eyes open. We analyzed frequency band power across various frequency bands and investigated functional connectivity within the specified speech region. Results: Significant between-group differences were found in band powers including alpha, beta, delta, theta, and gamma, specifically in the premotor, SMA, motor speech, and frontal regions. AWS also showed increased coherence between the right motor speech region compared to controls. We demonstrate that the proposed hierarchical false discovery rate (FDR) method is the most effective for both simulations and experimental data. In the expected regions, this method revealed significant synchrony effects at an acceptable error rate of 5%. Conclusion: The results highlight disrupted functional connectivity in AWS at resting state, particularly in speech-related and associated areas. Given the complex neurological basis of developmental stuttering, robust neural markers are closely linked to this phenomenon. These markers include imbalanced activity within brain regions associated with speech and motor functions, coupled with impaired functional connectivity between these regions. The cortico-basal ganglia-thalamo-cortical system governs the dynamic interplay between cortical regions, with SMA as a key cortical site. It is hypothesized that the aberrant resting state functional connectivity will impact the language planning and motor execution necessary for fluent speech. Examining restingstate metrics as biomarkers could further elucidate the neural underpinnings of stuttering and guide intervention. [ABSTRACT FROM AUTHOR]

The article discusses ventilator-associated brain injury (VABI) as a potential complication of mechanical ventilation, presenting evidence from preclinical studies and observational data. It defines VABI as brain injury resulting directly from positive pressure mechanical ventilation, independent of other factors like sedation. It highlights the need for further research to understand the mechanisms of VABI and evaluate potential therapeutic strategies.

The vagus nerve crucially affects emotions and psychiatric disorders. However, the detailed neurophysiological dynamics of the vagus nerve in response to emotions and its associated pathological changes remain unclear. In this study, we demonstrated that the spike rates of the cervical vagus nerve change depending on anxiety behavior in an elevated plus maze test, and these changes were eradicated in stress-susceptible male mice. Furthermore, instantaneous spike rates of the vagus nerve were negatively and positively correlated with the power of 2–4 Hz and 20–30 Hz oscillations, respectively, in the prefrontal cortex and amygdala. The oscillations also underwent dynamic changes depending on the behavioral state in the elevated plus maze, and these changes were no longer observed in stress-susceptible and vagotomized mice. Chronic vagus nerve stimulation restored behavior-relevant neuronal oscillations with the recovery of altered behavioral states in stress-susceptible mice. These results suggested that physiological vagal-brain communication underlies anxiety and mood disorders. Interactions between the brain and the vagus nerve is crucial for expressing emotions. Here, authors show that vagus nerve activity is associated with prefrontal-amygdalar oscillations and restores stress-induced behavior. [ABSTRACT FROM AUTHOR]

Objective Resting-state functional magnetic resonance imaging (rs-fMRI) and Granger causality analysis (GCA) were used to observe the characteristics of amygdala and whole-brain effect connections in patients with herpes zoster (HZ) and post-herpetic neuralgia (PHN) and to determine their relationship with clinical features. Methods Rs-fMRI scans were performed on 50 HZ; 50 PHN; and 50 age-, sex- and education-year-matched healthy controls (HCs). Bilateral amygdala subregions were used as seeds for functional connectivity (FC). GCA was used to analyze the effective connection of brain regions that were significantly different among groups. Then, the correlation between FC, and GCA values and clinical indices was investigated. Results: PHN had impaired FC between the amygdala subregion with the putamen, cortex, anterior cingulate cortex (ACC) to HCs and reduced FC of medial amygdala (MeA) with the parieto-occipital lobe and motor cortex to HZ; HZ had reduced FC of the lateral amygdala (LA) with the insula to HCs. GCA values from the bilateral LA to the bilateral ACC, left MeA to the bilateral ACC and left putamen, and right ACC to the bilateral MeA were reduced in PHN patients compared to HCs. Compared with HCs, the GCA values from the left MeA to the left ACC and right putamen were reduced in HZ. The GCA values from the amygdala subregion to the ACC were positively correlated with HAMA or HAMD scores in PHN. Conclusion: PHN showed reduced FC between the amygdala subregions and cortico-putamen and decreased effective connectivity from the amygdala subregion to the ACC and putamen. Advances in knowledge: HZ and PHN patients had significant changes in effective connectivity in brain regions, including diverse functional areas emanating from and projecting to the amygdala. The current findings will provide a new perspective for understanding the neuropathophysiological mechanism HZ and PHN. [ABSTRACT FROM AUTHOR]

Background: Idiopathic Anaphylaxis (IA) is the most common anaphylactic syndrome in adults. Mental health problems associated with IA are not well recognised. We aimed to assess if patients diagnosed with IA were more likely to experience mental health problems compared to a normative Australian population. We additionally hypothesised that the number of anaphylactic episodes would correlate with symptoms of anxiety. Methods: A total of 34 patients with at least one episode of IA were recruited from an adult immunology clinic. Patients were recruited as part of a separate study evaluating alternative aetiologies in IA. Mental health problems were measured using the Depression, Anxiety and Stress Scale (DASS-21). An extension of the survey included questions specifically focused on the psychological impact of IA. Results: Compared to population norms, those with IA had significantly higher levels of mental health problems. Statistically significant DASS-21 scores were identified for depression 4.24 vs. 2.57 (p < 0.001), anxiety 4.76 vs. 1.74 (p < 0.012), stress 7.35 vs. 3.95 (p < 0.001) and total score 16.35 vs. 8.00 (p < 0.001). There was no association between two or more episodes of anaphylaxis and increased anxiety levels (β = 0.52, CI -2.59–3.62, p = 0.74). Conclusions: This is the first paper to demonstrate that patients living with idiopathic anaphylaxis are more symptomatic for mental illness than those in the community. Screening for mental illness and referral for psychological support should be undertaken in people with IA. [ABSTRACT FROM AUTHOR]

In addition to typical respiratory symptoms, patients with asthma are frequently accompanied by cognitive decline, mood disorders (anxiety and depression), sleep disorders, olfactory disorders, and other brain response manifestations, all of which worsen asthma symptoms, form a vicious cycle, and exacerbate the burden on families and society. Therefore, studying the mechanism of neurological symptoms in patients with asthma is necessary to identify the appropriate preventative and therapeutic measures. In order to provide a comprehensive reference for related research, we compiled the pertinent literature, systematically summarized the latest research progress of asthma and its brain response, and attempted to reveal the possible "lung--brain" crosstalk mechanism and treatment methods at the onset of asthma, which will promote more related research to provide asthmatic patients with neurological symptoms new hope. [ABSTRACT FROM AUTHOR]

Stress is an enormous concern in our culture because it is the root cause of many health issues. Yoga asanas and mindfulness-based practices are becoming increasingly popular for stress management; nevertheless, the biological effect of these practices on stress reactivity is still a research domain. The purpose of this review is to emphasize various biosignals that reflect stress reduction through various yoga-based practices. A comprehensive synthesis of numerous prior investigations in the existing literature was conducted. These investigations undertook a thorough examination of numerous biosignals. Various features are extracted from these signals, which are further explored to reflect the effectiveness of yoga practice in stress reduction. The multifaceted character of stress and the extensive research undertaken in this field indicate that the proposed approach would rely on multiple modalities. The notable growth of the body of literature pertaining to prospective yoga processes is deserving of attention; nonetheless, there exists a scarcity of research undertaken on these mechanisms. Hence, it is recommended that future studies adopt more stringent yoga methods and ensure the incorporation of suitable participant cohorts. [ABSTRACT FROM AUTHOR]

Experiencing chronic stress significantly increases the risk for depression. Depression is a complex disorder with varied symptoms across patients. However, feeling of sadness and decreased motivation, and diminished feeling of pleasure (anhedonia) appear to be core to most depressive pathology. Odorants are potent signals that serve a critical role in social interactions, avoiding danger, and consummatory behaviors. Diminished quality of olfactory function is associated with negative effects on quality of life leading to and aggravating the symptoms of depression. Odor hedonic value (I like or I dislike this smell) is a dominant feature of olfaction and guides approach or avoidance behavior of the odor source. The neural representation of the hedonic value of odorants is carried by the granule cells in the olfactory bulb, which functions to modulate the cortical relay of olfactory information. The granule cells of the olfactory bulb and those of the dentate gyrus are the two major populations of cells in the adult brain with continued neurogenesis into adulthood. In hippocampus, decreased neurogenesis has been linked to development or maintenance of depression symptoms. Here, we hypothesize that chronic mild stress can alter olfactory hedonics through effects on the olfactory bulb neurogenesis, contributing to the broader anhedonia phenotype in stress-associated depression. To test this, mice were subjected to chronic unpredictable mild stress and then tested on measures of depressive-like behaviors, odor hedonics, and measures of olfactory neurogenesis. Chronic unpredictable mild stress led to a selective effect on odor hedonics, diminishing attraction to pleasant but not unpleasant odorants, an effect that was accompanied by a specific decrease in adult neurogenesis and of the percentage of adult-born cells responding to pleasant odorants in the olfactory bulb. [ABSTRACT FROM AUTHOR]

Mechanical ventilation (MV), as a life‐saving procedure in critical patients, is a risk factor to develop of neurocognitive dysfunction and triggers of inflammation and apoptosis in the brain. Since diversion of breathing route to the tracheal tube diminishes brain activity entrained by physiological nasal breathing, we hypothesized that simulating nasal breathing using rhythmic air‐puff (AP) into the nasal cavity of mechanically ventilated rats can reduce hippocampal inflammation and apoptosis in association with restoring respiration‐coupled oscillations. We found that stimulating olfactory epithelium through applying rhythmic nasal AP, in association with reviving respiration‐coupled brain rhythm, mitigates MV‐induced hippocampal apoptosis and inflammation involving microglia and astrocytes. The current translational study opens a window for a novel therapeutic approach to reduce neurological complications induced by MV. [ABSTRACT FROM AUTHOR]

Non-alcoholic fatty liver disease (NAFLD) includes a range of liver conditions ranging from excess fat accumulation to liver failure. NAFLD is strongly associated with high-fat diet (HFD) consumption that constitutes a metabolic risk factor. While HFD has been elucidated concerning its several systemic effects, there is little information about its influence on the brain at the molecular level. Here, by using a high-fat diet (HFD)-feeding of adult zebrafish, we first reveal that excess fat uptake results in weight gain and fatty liver. Prolonged exposure to HFD induces a significant increase in the expression of pro-inflammation, apoptosis, and proliferation markers in the liver and brain tissues. Immunofluorescence analyses of the brain tissues disclose stimulation of apoptosis and widespread activation of glial cell response. Moreover, glial activation is accompanied by an initial decrease in the number of neurons and their subsequent replacement in the olfactory bulb and the telencephalon. Long-term consumption of HFD causes activation of Wnt/β-catenin signaling in the brain tissues. Finally, fish fed an HFD induces anxiety, and aggressiveness and increases locomotor activity. Thus, HFD feeding leads to a non-traumatic brain injury and stimulates a regenerative response. The activation mechanisms of a regeneration response in the brain can be exploited to fight obesity and recover from non-traumatic injuries. [ABSTRACT FROM AUTHOR]

Rationale: Conditions with sustained low-grade inflammation have high comorbidity with depression and anxiety and are associated with social withdrawal. The basolateral amygdala (BLA) is critical for affective and social behaviors and is sensitive to inflammatory challenges. Large systemic doses of lipopolysaccharide (LPS) initiate peripheral inflammation, increase BLA neuronal activity, and disrupt social and affective measures in rodents. However, LPS doses commonly used in behavioral studies are high enough to evoke sickness syndrome, which can confound interpretation of amygdala-associated behaviors. Objectives and methods: The objectives of this study were to find a LPS dose that triggers mild peripheral inflammation but not observable sickness syndrome in adult male rats, to test the effects of sustained mild inflammation on BLA and social behaviors. To accomplish this, we administered single doses of LPS (0–100 μg/kg, intraperitoneally) and measured open field behavior, or repeated LPS (5 μg/kg, 3 consecutive days), and measured BLA neuronal firing, social interaction, and elevated plus maze behavior. Results: Repeated low-dose LPS decreased BLA neuron firing rate but increased the total number of active BLA neurons. Repeated low-dose LPS also caused early disengagement during social bouts and less anogenital investigation and an overall pattern of heightened social caution associated with reduced gain of social familiarity over the course of a social session. Conclusions: These results provide evidence for parallel shifts in social interaction and amygdala activity caused by prolonged mild inflammation. This effect of inflammation may contribute to social symptoms associated with comorbid depression and chronic inflammatory conditions. [ABSTRACT FROM AUTHOR]

The course of bronchial asthma can be accompanied by cognitive impairments. However, the relationship between cognitive dysfunction and asthma has not been fully revealed, nor has it been fully established what causes cognitive impairments in patients with asthma. There is an opinion that transient hypoxia and persistent systemic inflammation with insufficient control of bronchial asthma can be accompanied by neurotoxicity in relation to the hippocampus and indirectly lead to deterioration of cognitive functions. Comorbid conditions, such as obesity, allergic rhinitis, and depressive states can increase cognitive dysfunction in asthmatics. The review considers the pathophysiology of cognitive dysfunction in patients with bronchial asthma, as well as the impact of comorbid conditions on the cognitive status. This information will allow systematizing the available knowledge about the state of cognitive functions in asthma for timely detection and correction of their impairments and, ultimately, optimization of the management of these patients. [ABSTRACT FROM AUTHOR]

Objective: To investigate the changes in dynamic voxel mirror homotopy connection (dVMHC) between cerebral hemispheres in patients with asthma. Methods: Our study was designed using a case-control method. A total of 31 subjects with BA and 31 healthy subjects with matching basic information were examined using rsfMRI. We also calculated and obtained the dVMHC value between the cerebral cortexes. Results: Compared with the normal control group, the dVMHC of the lingual gyrus (Ling) and the calcarine sulcus (CAL), which represented the visual network (VN), increased significantly in the asthma group, while the dVMHC of the medial superior frontal gyrus (MSFG), the anterior/middle/posterior cingulate gyrus (A/M/PCG), and the supplementary motor area (SMA) of the sensorimotor network decreased significantly in the asthma group. Conclusion: This study showed that the ability of emotion regulation and the efficiency of visual and cognitive information processing in patients with BA was lower than in those in the HC group. The dVMHC analysis can be used to sensitively evaluate oxygen saturation, visual function changes, and attention bias caused by emotional disorders in patients with asthma, as well as to predict airway hyperresponsiveness, inflammatory progression, and dyspnea. [ABSTRACT FROM AUTHOR]

Neural oscillations synchronize the activity of brain regions during cognitive functions, such as spatial working memory. Olfactory bulb (OB) oscillations are ubiquitous rhythms that can modulate neocortical and limbic regions. However, the functional connectivity between the OB and areas contributing to spatial working memory, such as the ventral hippocampus (vHPC) and medial prefrontal cortex (mPFC), is less understood. Hence, we investigated functional interaction between OB and the vHPC–mPFC circuit during the spatial working memory performance in rats. To this end, we analyzed the simultaneously recorded local field potentials from OB, vHPC, and mPFC when rats explored the Y-maze and compared the brain activities of correct trials vs. wrong trials. We found that coupling between the vHPC and mPFC was augmented during correct trials. The enhanced coherence of OB activity with the vHPC–mPFC circuit at delta (< 4 Hz) and gamma (50–80 Hz) ranges were observed during correct trials. The cross-frequency analysis revealed that the OB delta phase increased the mPFC gamma power within corrected trials, indicating a modulatory role of OB oscillations on mPFC activity during correct trials. Moreover, the correlation between OB oscillations and the vHPC–mPFC circuit was increased at the delta range during correct trials, exhibiting enhanced synchronized activity of these regions during the cognitive task. We demonstrated a functional engagement of OB connectivity with the vHPC–mPFC circuit during spatial working memory task performance. [ABSTRACT FROM AUTHOR]

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Memory loss and aberrant neuronal network activity are part of the earliest hallmarks of Alzheimer's disease (AD). Electroacupuncture (EA) has been recognized as a cognitive stimulation for its effects on memory disorder, but whether different brain regions or neural circuits contribute to memory recovery in AD remains unknown. Here, we found that memory deficit was ameliorated in 3xTg-AD mice with EA-treatment, as shown by the increased number of exploring and time spent in the novel object. In addition, reduced locomotor activity was observed in 3xTg-AD mice, but no significant alteration was seen in the EA-treated mice. Based on the functional magnetic resonance imaging, the regional spontaneous activity alterations of 3xTg-AD were mainly concentrated in the accumbens nucleus, auditory cortex, caudate putamen, entorhinal cortex (EC), hippocampus, insular cortex, subiculum, temporal cortex, visual cortex, and so on. While EA-treatment prevented the chaos of brain activity in parts of the above regions, such as the auditory cortex, EC, hippocampus, subiculum, and temporal cortex. And then we used the whole-cell voltage-clamp recording to reveal the neurotransmission in the hippocampus, and found that EA-treatment reversed the synaptic spontaneous release. Since the hippocampus receives most of the projections of the EC, the hippocampus-EC circuit is one of the neural circuits related to memory impairment. We further applied diffusion tensor imaging (DTI) tracking and functional connectivity, and found that hypoconnected between the hippocampus and EC with EA-treatment. These data indicate that the hippocampus-EC connectivity is responsible for the recognition memory deficit in the AD mice with EA-treatment, and provide novel insight into potential therapies for memory loss in AD. [ABSTRACT FROM AUTHOR]

Allergic asthma is a chronic inflammatory respiratory disease. Psychiatric disorders, including anxiety are associated with poorer treatment response and disease control in asthmatic patients. To date, there is no experimental evidence describing the role of peripheral inflammation on the oscillatory activities in the anterior cingulate cortex (ACC) and basolateral amygdala (BLA), two major brain structures modulating anxiety. In the present work we evaluated lung and brain inflammatory responses, anxiety-like behavior, in association with oscillatory features of the ACC-BLA circuit in an animal model of allergic inflammation. Our data showed that allergic inflammation induced anxiety-like behavior and reactivation of microglia and astrocytes in ACC and BLA. Allergic inflammation also enhanced neuronal activities and functional connectivity of the ACC-BLA circuit which were correlated with the level of anxiety. Together, we suggest that disruption in the dynamic oscillatory activities of the ACC-BLA circuit, maybe due to regional inflammation, is an underlying mechanism of allergic asthma-induced anxiety-like behavior. Our findings could pave the way for better understanding the neuro-pathophysiology of the psychiatric disorders observed in asthmatic patients, possibly leading to develop novel treatment strategies. [ABSTRACT FROM AUTHOR]

In addition to nasal symptoms, patients with allergic rhinitis (AR) often experience mental and psychological disorders such as depression. Depression not only makes the treatment of AR more difficult and expensive but also poses a serious impact on the patients' daily activities and quality of life, thus bringing additional burden to the families and the society. Here we systematically review the recent research advances in the correlation between AR and depression, analyze the possible causes and mechanisms of depression in AR, summarize the current diagnosis and treatment strategies, and provide our insights into the AR-related depression; in addition, we introduce briefly the basic research status on AR-related depression. We hope that this review article will provide evidence for future studies. [ABSTRACT FROM AUTHOR]

The coriander plant Centipeda minima (L.) A. Braun et Aschers (Compositae) is used for the treatment of allergic rhinitis. Analyze the difference of the C. minima volatile oil from 7 geographic areas and its therapeutic effect on allergic rhinitis. The volatile oils from different geographic areas were extracted and analyzed, the protein and biological pathway for the treatment of allergic rhinitis were predicted by network pharmacology. Established three groups of Sprague-Dawley rat allergic rhinitis models (n = 10). The treatment group was given 100 μL/nostril of 0.1% C. minima volatile oil, the blank and model groups were given the same amount of normal saline. After 15 days, serum inflammatory factors were detected by ELISA. Nasal mucosa tissues were examined by hematoxylineosin staining and immunuhistrochemistry. There are differences in the content of volatile oil in the seven geographic areas. Experiments showed that the concentration of TNF-α in the serum of the administration group decreased from 63.66 ± 2.06 to 51.01 ± 4.10 (pg/mL), IL-4 decreased from 41.90 ± 3.90 to 28.68 ± 3.39 (pg/mL), IgE decreased from 22.18 ± 1.40 to 17.59 ± 1.60 (pg/mL), IL-2 increased from 314.14 ± 10.32 to 355.90 ± 10.01(pg/mL). Immunohistochemistry showed that compared with the model group, the PTGS2 and MAPK3 proteins in the administration group were significantly reduced. C. minima volatile oil is a multi-target and multi-pathway in the treatment of allergic rhinitis, which provides a new research basis and reference for the treatment of allergic rhinitis. [ABSTRACT FROM AUTHOR]

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Traumatic brain injury (TBI) is a leading cause of morbidity and mortality among military service members and civilians in the United States. Despite significant advances in the understanding of TBI pathophysiology, several clinical reports indicate that multiple genetic and epigenetic factors can influence outcome. Homocysteine (HCY) is a non-proteinogenic amino acid, the catabolism of which can be dysregulated by stress, lifestyle, aging, or genetic abnormalities leading to hyperhomocysteinemia (HHCY). HHCY is a neurotoxic condition and a risk factor for multiple neurological and cardiovascular disorders that occurs when HCY levels is clinically > 15 µM. Although the deleterious impact of HHCY has been studied in human and animal models of neurological disorders such as stroke, Alzheimer's disease and Parkinson's disease, it has not been addressed in TBI models. This study tested the hypothesis that HHCY has detrimental effects on TBI pathophysiology. Moderate HHCY was induced in adult male Sprague Dawley rats via daily administration of methionine followed by impact-induced traumatic brain injury. In this model, HHCY increased oxidative stress, upregulated expression of proteins that promote blood coagulation, exacerbated TBI-associated blood–brain barrier dysfunction and promoted the infiltration of inflammatory cells into the cortex. We also observed an increase of brain injury-induced lesion size and aggravated anxiety-like behavior. These findings show that moderate HHCY exacerbates TBI outcomes and suggest that HCY catabolic dysregulation may be a significant biological variable that could contribute to TBI pathophysiology heterogeneity. [ABSTRACT FROM AUTHOR]

Cognitive functions such as working memory require integrated activity among different brain regions. Notably, entorhinal cortex (EC) activity is associated with the successful working memory task. Olfactory bulb (OB) oscillations are known as rhythms that modulate rhythmic activity in widespread brain regions during cognitive tasks. Since the OB is structurally connected to the EC, we hypothesized that OB could modulate EC activity during working memory performance. Herein, we explored OB–EC functional connectivity during spatial working memory performance by simultaneous recording local field potentials when rats performed a Y-maze task. Our results showed that the coherence of delta, theta, and gamma-band oscillations between OB and EC was increased during correct trials compared to wrong trials. Cross-frequency coupling analyses revealed that the modulatory effect of OBs low-frequency phase on EC gamma power and phase was enhanced when animals correctly performed working memory task. The influx of information from OB to EC was also increased at delta and gamma bands within correct trials. These findings indicated that the modulatory influence of OB rhythms on EC oscillations might be necessary for successful working memory performance. [ABSTRACT FROM AUTHOR]