The article presents a narrative review of the recent scientific literature regarding mental disorders in patients diagnosed with pulmonary hypertension (PH). Psychosomatic disorders were considered, first of all, anxiety, depressive, potentially related to the systemic immune-inflammatory process of the underlying disease. Empirical evidence for the high prevalence of these disorders across various forms of PH is discussed, along with an exploration of the biological mechanisms underlying their onset. The findings underscore the necessity for a comprehensive multimodal approach to both diagnosis and treatment of mental disorders in individuals with PH. This approach should incorporate psychopharmacotherapy and the management of neuroinflammatory processes to enhance overall quality of life.

Procalcitonin (PCT)-guided therapy may optimize antibiotic use in respiratory infections and chronic lung diseases. This systematic review aimed to assess the role of PCT-guided protocols in reducing antibiotic duration, length of hospital and ICU stay, and clinical outcomes in patients with community-acquired pneumonia (CAP), hospital-acquired pneumonia (HAP), ventilator-associated pneumonia (VAP), and chronic obstructive pulmonary disease (COPD). A secondary literature search was conducted using the databases PubMed and Google Scholar to identify the relevant studies published between January 2003 and December 2023. Eligible studies included peer-reviewed original research (clinical trials, observational, cohort, and case-control studies) evaluating PCT in CAP, VAP, HAP, or COPD, including viral and/or bacterial lower respiratory tract infections (LRTIs) in humans. The excluded studies were animal studies, studies not involving LRTIs, PCT studies lacking extractable data, and non-peer-reviewed editorials, opinions, and conference abstracts. Inconsistency across studies was assessed by heterogeneity analyses and publication bias using funnel plots. Twenty-four studies involving 16,134 patients were included. Across all conditions, PCT-guided therapy reduced antibiotic duration, particularly in CAP, without increasing mortality. Studies included in the CAP group reported that patients in the PCT group benefited from a shorter duration of therapy, with the treatment period decreasing from an average of 13.3±6.5 days in the control group to 11.7±6.2 days in the PCT group. Similarly, the PCT group had significantly reduced ICU stays. For COPD, hospital stay was significantly reduced, though fewer studies demonstrated ICU benefits. PCT-guided protocols may effectively help in better treatment strategies for CAP and COPD management.

Asthma is a heterogeneous chronic airway inflammatory disease associated with high global prevalence and substantial clinical burden. Conventional therapies remain limited in controlling refractory phenotypes and preventing disease progression. The gut-lung axis has emerged as a fundamental regulatory network connecting intestinal homeostasis with pulmonary immune function, and mounting evidence has established a close mechanistic link between gut dysbiosis and the onset, persistence, and exacerbation of asthma. This review comprehensively integrates evidence from epidemiological investigations, animal models, clinical observational studies, and randomized controlled trials published between 2011 and 2025 to elucidate the crosstalk mechanisms of the gut-lung axis in asthma, characterize compositional and functional alterations of the gut microbiome, evaluate microbiota-targeted interventions such as probiotics, prebiotics, synbiotics, postbiotics, and fecal microbiota transplantation, and discuss current translational challenges. We highlight that the gut microbiota orchestrates airway inflammatory responses through fine-tuning immune cell differentiation, mediating microbial metabolite signaling, and maintaining intestinal barrier function, with discernible microbial signatures evident across allergic versus non-allergic and pediatric versus adult asthma phenotypes. Despite promising preclinical and preliminary clinical findings, causal evidence remains insufficient, and intervention heterogeneity limits clinical application. This review underscores the potential of microbiome-based precision strategies and identifies key directions for future mechanistic research and clinical translation.

ANCA-associated vasculitides (AAV) - granulomatosis with polyangiitis (GPA), eosinophilic granulomatosis with polyangiitis (EGPA), and microscopic polyangiitis (MPA) - are rare small-vessel autoimmune diseases. Liver involvement in AAV is uncommon and generally manifests as biochemical hepatitis; true hepatic granulomatosis is exceedingly rare and diagnostically challenging.

We conducted a systematic scoping review following PRISMA-ScR guidelines and the Arksey & O'Malley framework, searching PubMed, Google Scholar, ScienceDirect, and Scopus without date restriction (through March 2026). A total of 7, 033 records were initially retrieved; after deduplication, title/abstract screening, and full-text review, five articles meeting strict inclusion criteria were included for qualitative synthesis.

Five published cases of hepatic granulomas in AAV patients with no confirmed confounding etiology were identified. All were GPA or EGPA; no case of pure MPA was documented. Three patients were female and two were male, with a mean age of 57.6 years. Liver histology revealed non-necrotizing epithelioid granulomas (n = 2), granulomatous inflammation with necrosis (n = 1), incomplete septal cirrhosis with vasculopathic changes (n = 1), and incidental calcified granulomas (n = 1). Immunosuppressive therapy with corticosteroids and/or cyclophosphamide achieved clinical and biochemical improvement in all treated patients.

Hepatic granulomatosis is a rare but genuine extra-respiratory manifestation of AAV, most frequently reported in GPA. It may antedate the canonical ENT-pulmonary-renal triad, presenting as incidental hepatomegaly or unexplained liver function test elevation. Systematic exclusion of competing etiologies (sarcoidosis, tuberculosis, primary biliary cholangitis, drug-induced hepatitis) is mandatory before attributing granulomas to AAV. Liver biopsy remains pivotal in confirming the diagnosis. Immunosuppression is the therapeutic cornerstone, with generally favourable outcomes.

Toxic shock syndrome (TSS) caused by group A Streptococcus is uncommon but associated with high mortality. In this case report, a 17-year-old girl with influenza A presented with a rash, hypotension, parapneumonic effusion and multiorgan failure. Group A streptococci were identified in the pleural fluid. This case highlights the importance of early recognition of TSS, since treatment with clindamycin and immunoglobulin may improve the prognosis. As rates of meningococcal disease have decreased, TSS likely causes an increasing proportion of cases of septic shock among children in Denmark.

To investigate the regulatory effects of cellular repressor of E1A-stimulated gene (CREG) on autophagy and polarization of alveolar macrophages in sepsis-induced acute respiratory distress syndrome (ARDS) and its clinical value.

1) Cell experiment: Mouse monocyte/macrophage cell line RAW264.7 was cultured in vitro. Cells in logarithmic growth phase were induced to differentiate into alveolar macrophages. The alveolar macrophages were divided into four groups: the blank control group was cultured with complete medium only; the lipopolysaccharide (LPS) group was stimulated with 5 mg/L LPS for 24 hours to establish the sepsis-induced ARDS model; the CREG overexpression group was transfected with 2 mg CREG overexpression plasmid pLNCX2-CREG for 6 hours, followed by 5 mg/L LPS stimulation for 24 hours; the CREG interference group was transfected with 2 μg CREG interference plasmid pSM2-siCREG for 6 hours, followed by 5 mg/L LPS stimulation for 24 hours. Western blotting was used to detect the expression of autophagy markers [autophagy initiation key protein Beclin1, microtubule-associated protein 1 light chain 3 (LC3), and autophagic substrate protein p62]. Flow cytometry was used to detect the expression of macrophage polarization markers [M1-type characteristic marker cluster of differentiation 86 (CD86) and M2-type characteristic marker CD206]. 2) Clinical trial: A prospective case-control study was conducted in patients with sepsis admitted to the respiratory intensive care unit of The First Affiliated Hospital of Hebei North University from January to December 2024. Patients were divided into sepsis with ARDS group and sepsis without ARDS group based on whether they developed ARDS within 72 hours after enrollment. In addition, healthy volunteers who underwent health check-ups at the hospital during the same period were selected as the controls. Demographic data including gender, age, Acute Physiology And Chronic Health Evaluation II (APACHE II) score, oxygenation index (PaO₂/FiO₂), and laboratory parameters were collected for each group, as well as the sites of infection for the septic patients. Serum levels of CREG and inflammatory markers [interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), procalcitonin (PCT), and C-reactive protein (CRP)] were measured using enzyme-linked immunosorbent assay (ELISA). The differences in the above indicators were compared among groups. Multivariate Logistic regression analysis was used to identify independent influencing factors for sepsis complicated with ARDS. Receiver operator characteristic curve (ROC curve) was plotted to evaluate the predictive value of CREG for sepsis complicated with ARDS.

1) Cell experiment results: Compared with the blank control group, the expressions of Beclin1, LC3-II/LC3-I ratio, and CD206 were decreased in each LPS group [Beclin1 protein (Beclin1/β-actin): 0.32±0.05 vs. 0.87±0.09, LC3-II/LC3-I ratio: 0.41±0.06 vs. 1.24±0.11, CD206: (27.14±3.52)% vs. (51.78±5.91)%, all P<0.05], while p62 and CD86 expressions were increased [p62 protein (p62/β-actin): 1.58±0.13 vs. 0.53±0.07, CD86: (38.35±4.67)% vs. (18.26±3.24)%, both P<0.05]. CREG overexpression significantly improved the above autophagy and polarization indicators, whereas CREG interference further exacerbated these indicators (all P<0.05). 2) Clinical trial results: Ultimately, 40 patients were included in the sepsis with ARDS group, 60 in the sepsis without ARDS group, and 20 in the healthy control group. There were no statistically significant differences in gender, age among the three groups, nor in the distribution of infection sites between the sepsis with ARDS and sepsis without ARDS groups (all P>0.05). Compared with the healthy control group, the patients with sepsis showed aggravated systemic inflammatory burden. Compared with the sepsis without ARDS group, the sepsis with ARDS group exhibited more severe disease, with lower PaO₂/FiO₂ and CREG levels, and higher levels of inflammatory markers (all P<0.05). As APACHE II score increased, serum CREG levels decreased progressively while inflammatory marker levels increased progressively. Multivariate Logistic regression analysis showed that elevated APACHE II score and inflammatory markers were independent risk factors for sepsis complicated with ARDS [all odds ratio (OR) >1, all P<0.05], while elevated CREG was a protective factor [OR=0.385, 95% confidence interval (95%CI) was 0.344-0.432, P=0.015]. ROC curve analysis showed that the area under the ROC curve (AUC) of CREG for predicting sepsis complicated with ARDS was 0.806 (95%CI was 0.713-0.899); at the optimal cut-off value of 7.85 μg/L, the sensitivity was 71.43% and the specificity was 78.57%.

CREG exerts a protective role in sepsis-induced ARDS by positively regulating alveolar macrophage autophagy activity and correcting M1/M2 polarization imbalance. Elevated serum CREG is a protective factor for sepsis complicated with ARDS and has early predictive value for sepsis-induced ARDS.

Cough is a vital defensive reflex that safeguards the airways; however, it can become maladaptive and pathological. Chronic cough (>8 weeks in duration) affects up to 10% of the global adult population and is associated with considerable health status impairment. The understanding of cough physiology remains limited. Cough reflex hypersensitivity is conventionally considered to underpin the pathophysiology of chronic cough, primarily mediated by peripheral nerve dysfunction. Whilst this framework has led to important mechanistic insights and effective pharmacotherapies, recent functional neuroimaging studies have demonstrated equally important central mechanisms. Taken together, cough reflex hypersensitivity may not be mediated exclusively by peripheral nerve dysfunction, and the answer may lie within a complex interplay of central and peripheral neural physiology. In the pathophysiology of chronic cough, impaired voluntary suppression also appears to be important. This review will provide an overview of the physiology and pathophysiology of chronic cough and attempts in pharmacotherapy to date.

Cells normally combine glycolysis and oxidative phosphorylation (OXPHOS) to meet energy demands, but this balance shifts under pathological conditions. During SARS-CoV-2 infection, hypoxia, viral entry, and elevated tissue lactate alter cellular metabolism. To explore these effects, we propose a parsimonious mathematical model describing how oxygen levels, viral infiltration, and extracellular lactate jointly regulate metabolic balance through HIF-1 α protein, inside the cell, accounting for lactate's biphasic, non-monotonic influence on glycolysis. Model simulations reveal a single steady state whose position on the glycolysis-OXPHOS phase plane depends on environmental conditions, namely, oxygen concentration, infection, and extracellular lactate. We identify four metabolic regimes, determined by sufficiency of energy production and the driving process (OXPHOS or glycolysis). Decreasing the oxygen shifts cells from OXPHOS to glycolysis dominance in both infected and non-infected states, but infected cells may become energy-deficient even with sufficient oxygen due to virus-induced mitochondrial damage. Rising extracellular lactate initially promotes glycolysis but ultimately suppresses it at high levels, pushing cells into severe energy deficit with inhibited glycolysis. Simulations of reoxygenation exhibit hysteresis: cells pass through an energy-deficient zone during hypoxia onset but return through a safer trajectory when oxygen is restored; a vulnerability is higher in infected cells. Overall, the model clarifies metabolic trajectories during viral infection, suggesting that early hypoxia is particularly dangerous and that severe acidosis can further collapse energy production. Preventing or rapidly reversing hypoxia in respiratory infection may protect cells from energy failure and limit harmful lactate accumulation.

Public health policies are implemented within legal and regulatory environments associated with heterogeneous economic and health related outcomes across regions and time. Existing policy evaluation approaches often have limited capacity to represent regional heterogeneity, temporal policy patterns, and uncertainty in observed policy associated outcome changes. To address this issue, this study proposes a predictive computational framework for estimating subsequent economic outcome changes under observed public health policy, legal, and regulatory conditions.

The empirical task is formulated as supervised temporal regression using region time observations constructed from the Oxford COVID-19 Government Response Tracker and COVID-19 US State Policy datasets. The proposed Counterfactual Policy Optimizer (CPO) represents legal frameworks as policy constraints and regulatory variables, and combines manifold constraint regularization, agent driven policy interaction modeling, and probabilistic outcome forecasting. In this study, the term counterfactual refers to model based scenario comparison within the observed data distribution and feasible policy space, and does not imply causal identification in the econometric or structural causal sense.

The training objective integrates prediction accuracy, uncertainty modeling, utility based policy comparison, and constraint regularization. Experimental results indicate that the proposed framework achieves lower prediction error and stronger trend consistency than traditional econometric, machine learning, and temporal deep learning baselines under the same observational prediction setting. Additional policy related indicators indicate that legal feasibility, implementation conditions, and uncertainty aware forecasting can support structured predictive evaluation of public health policy associated economic outcome changes. The study provides a reproducible framework for examining temporal associations between legally structured public health policy conditions and subsequent economic outcome changes.

Influenza remains a significant public health threat with pandemic potential. Understanding environmental factors influencing virus spread and severity is critical, particularly as wildfires become more frequent and intense. While temperature and humidity's roles in virus seasonality and persistence are well understood, the impacts of air pollution ─ especially wildfire-specific particulate matter (PM_2.5) ─ on respiratory infections are less explored.

This study aimed to investigate the association between wildfire PM_2.5 exposure and influenza or influenza-like illness (ILI) incidence. Specifically, we assessed (1) the long-term impact of PM_2.5 exposure during the preceding wildfire season on influenza/ILI risk in the following flu season, and (2) the effects of short-term PM_2.5 exposure during the active flu season.

We utilized ILI and influenza data from state health departments in six Western U.S. states (Arizona, Colorado, Montana, Nevada, Oregon, and Washington) from 2010 to 2019. We applied generalized linear distributed lag models to assess the impact of PM_2.5 exposure during the preceding wildfire season on influenza or ILI risk in the subsequent flu season, as well as the effect of short-term PM_2.5 exposure during the current flu season.

Long-term exposure to wildfire PM_2.5 was associated with increased influenza risk in states with influenza data: Arizona ([Rate Ratio (RR) = 1.061 (1.026-1.100)]), Colorado [RR = 1.067 (1.056-1.078)], Montana [RR = 1.038 (1.013-1.063)], and Oregon [RR = 1.049 (1.041-1.057)], per 10 μg/m³ PM_2.5 increase. However, the states with only ILI data did not follow this pattern, revealing no observed effect in Nevada [RR = 1.005 (0.920-1.097)] and a negative effect in Washington [RR = 0.884 (0.842-0.919)]. Similarly, but to a lesser degree, short-term PM_2.5 exposure effects were noted in states with only influenza data but not ILI data.

Our findings underscore a positive association between wildfire-specific PM_2.5 and influenza risk in states with influenza data, suggesting a differential effect of PM_2.5 on respiratory infections. This study supports further investigation into the causative mechanisms behind these correlations, particularly considering the increasing frequency of wildfires and the resulting air quality impacts.