BACKGROUND: Children's respiratory health demonstrates particular sensitivity to air pollution. Existing evidence investigating the association between short-term ozone (O₃) exposure and childhood pneumonia remains insufficient and inconsistent, especially in low- and middle-income countries (LMICs). METHOD: To provide more reliable and persuasive evidence, we implemented a multi-city, time-stratified case-crossover design with a large sample size, using data from seven representative children's hospitals across major geographical regions in China. To avoid the impact of the COVID-19 pandemic, individual-level medical records of inpatient children under 6 years of age diagnosed with pneumonia during 2016-2019 were collected. Conditional logistic regression models were fitted for each city, and city-specific estimates were pooled through a meta-analysis using a random-effects model. RESULTS: In total, the study included 137,470 pediatric pneumonia hospital admissions. The highest pooled estimate for O₃ occurred at lag0-1, with a 10 µg/m³ increase in O₃ associated with a 1.57% (95% CI: 0.67%-2.48%) higher risk of pediatric pneumonia hospital admissions. Stratified analyses indicated that the effects of O₃ were robust across different sexes, age groups, and admission seasons. We also observed a statistically significant increase in risk associated with O₃ concentrations exceeding the World Health Organization Air Quality Guidelines (WHO-AQGs). CONCLUSIONS This study revealed a significant positive association between O₃ and pediatric pneumonia hospital admissions. Our findings substantially strengthen the evidence base for the adverse health impacts of O₃, underscoring the importance of O₃ pollution control and management in reducing the public health burden of pediatric pneumonia.
Humans ; Ozone/analysis* ; China/epidemiology* ; Pneumonia/chemically induced* ; Child, Preschool ; Male ; Female ; Infant ; Cross-Over Studies ; Air Pollutants/analysis* ; Hospitalization/statistics & numerical data* ; Child ; Cities/epidemiology* ; Air Pollution/adverse effects* ; Infant, Newborn ; Environmental Exposure/adverse effects*

Because coronavirus disease 2019(COVID-19) is highly contagious and serious, it has posed a major threat to public health worldwide. The curative effects of integrated traditional Chinese medicine and Western medicine in the treatment of COVID-19 have been widely recognized and confirmed. However, medical workers shall pay attention to drug-induced heart injury in clinical application. Based on the guideline from the Diagnosis and Treatment Plans for COVID-19(trial seventh edition), taking the recommended drugs as examples, by Western medicine, traditional Chinese medicine, Chinese herbal injection and integrated traditional Chinese and Western medicine, the study analyzed the basic characteristics of recommended drugs for cardiac injury by means of literature review and bioinformatics methods, and summarized cardiac adverse reactions, toxicity mechanisms, combined pharmacotherapy, special population and drug monitoring, focusing on the clinical manifestations, toxic components, targets and regulatory mechanisms of drug-induced cardiac injury. The findings suggested being vigilant to drug-induced cardiac injury during the treatment of COVID-19, playing the advantages of clinical pharmacists and clinical Chinese pharmacists, improving the knowledge reserve of pharmacovigilance, strengthening the prescription review, medication notification and medication monitoring, promoting rational drug use and paying attention to special populations and high-risk groups. The study aims to provide suggestions and reference for pharmacovigilance and pharmaceutical care for front-line doctors and pharmacists against COVID-19, in order to avoid the occurrence of drug-induced heart injury for patients with COVID-19.
Betacoronavirus ; Cardiotoxicity ; Coronavirus Infections ; drug therapy ; Drugs, Chinese Herbal ; Heart Injuries ; chemically induced ; Humans ; Medicine, Chinese Traditional ; Pandemics ; Pharmacovigilance ; Pneumonia, Viral

BACKGROUND/AIMS: Asthma is characterized by airway hyperresponsiveness, inflammation, and remodeling. Peroxisome proliferator-activated receptors have been reported to regulate inflammatory responses in many cells. In this study, we examined the effects of intranasal rosiglitazone on airway remodeling in a chronic asthma model. METHODS: We developed a mouse model of airway remodeling, including smooth muscle thickening, in which ovalbumin (OVA)-sensitized mice were repeatedly exposed to intranasal OVA administration twice per week for 3 months. Mice were treated intranasally with rosiglitazone with or without an antagonist during OVA challenge. We determined airway inflammation and the degree of airway remodeling by smooth muscle actin area and collagen deposition. RESULTS: Mice chronically exposed to OVA developed sustained eosinophilic airway inflammation, compared with control mice. Additionally, the mice developed features of airway remodeling, including thickening of the peribronchial smooth muscle layer. Administration of rosiglitazone intranasally inhibited the eosinophilic inflammation significantly, and, importantly, airway smooth muscle remodeling in mice chronically exposed to OVA. Expression of Toll-like receptor (TLR)-4 and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kappaB) was increased in the OVA group and decreased in the rosiglitazone group. Co-treatment with GW9660 (a rosiglitazone antagonist) and rosiglitazone increased the expression of TLR-4 and NF-kappaB. CONCLUSIONS: These results suggest that intranasal administration of rosiglitazone can prevent not only air way inf lammation but also air way remodeling associated with chronic allergen challenge. This beneficial effect is mediated by inhibition of TLR-4 and NF-kappaB pathways.
Actins/metabolism ; Administration, Inhalation ; Airway Remodeling/*drug effects ; Animals ; Anti-Asthmatic Agents/*administration & dosage ; Asthma/chemically induced/*drug therapy/metabolism/physiopathology ; Chronic Disease ; Collagen/metabolism ; Disease Models, Animal ; Female ; Lung/*drug effects/metabolism/physiopathology ; Mice, Inbred BALB C ; NF-kappa B/metabolism ; Ovalbumin ; PPAR gamma/agonists/metabolism ; Pneumonia/chemically induced/physiopathology ; Pulmonary Eosinophilia/chemically induced/prevention & control ; Signal Transduction/drug effects ; Thiazolidinediones/*administration & dosage ; Toll-Like Receptor 4/metabolism

OBJECTIVETo study the effect of β-lactamase (BLs) detection and β-lactam/β-lactamase inhibitor (BL/BLI) on the incidence of antibiotic-associated diarrhea (AAD) in children with severe bacterial pneumonia.

METHODSThe clinical data of the children with bacterial severe pneumonia were retrospectively studied. Of all the patients, 248 using amoxicillin/clavulanate but without BLs detection and 323 using amoxicillin (BLs negative) or amoxicillin/clavulanate (BLs positive) were used as the amoxicillin group; 208 patients using piperacillin/tazobactam but without BLs detection and 291 patients using piperacillin (BLs negative) or piperacillin/tazobactam (BLs positive) were used as the piperacillin group; and 191 patients using cefoperazone/sulbactam but without BLs detection and 341 patients using cefoperazone (BLs negative) or cefoperazone/sulbactam (BLs positive) were used as the cefoperazone group. The incidence and clinical symptoms of AAD between the undetected and detected BLs patients were compared.

RESULTSThe incidences of AAD in the amoxicillin, piperacillin and cefoperazone groups without BLs detection groups were significantly higher than those in the corresponding groups with negative or positive results of BLs detection (P<0.01). The durations of diarrhea, antibiotic use and hospitalization stay in AAD patients receiving BLs detection were shorter than in those without receiving BLs detection (P<0.01).

CONCLUSIONSIt is very important to detect BLs for reducing the incidence and relieving symptoms of AAD in children with severe bacterial pneumonia.

Adolescent ; Anti-Bacterial Agents ; adverse effects ; Child ; Child, Preschool ; Diarrhea ; chemically induced ; epidemiology ; prevention & control ; Humans ; Incidence ; Infant ; Pneumonia, Bacterial ; complications ; beta-Lactamases ; analysis

BACKGROUND/AIMS: Amiodarone is one of the most widely used antiarrhythmic agents; however, amiodarone-induced pulmonary toxicity (APT) can be irreversible and sometimes fatal. The aim of this study was to evaluate the feasibility of chest computed tomography (CT) as a diagnostic tool for APT and to assess the utility of the CT APT score as an index for predicting the severity of APT. METHODS: Patients underwent amiodarone treatment for various reasons, most often atrial fibrillation, for more than 2 years, and those that received a cumulative dose > 100 g were enrolled. A total of 34 patients who underwent chest CT between December 2011 and June 2012 were enrolled, whether or not they had clinical symptoms. The APT CT score was defined as the number of involved regions in the lung, which was divided into 18 regions (right and left, upper, middle, and lower, and central, middle, and peripheral). The CT findings were evaluated according to the total dose and duration of amiodarone treatment and the results of a pulmonary function test. Clinical symptoms and outcomes were also evaluated according to APT CT scores. RESULTS: Seven patients had positive APT CT scores (interstitial fibrosis in five, organizing pneumonia in one, and mixed interstitial fibrosis and organizing pneumonia in one), and these patients exhibited significantly lower diffusion capacity for carbon monoxide in the lungs compared with patients without an increased APT CT score (70.2% +/- 6.9% vs. 89.7% +/- 19.4%; p = 0.011). Three of the seven patients experienced overt APT that required hospital admission. CONCLUSIONS: Chest CT is a useful diagnostic tool for APT, and the APT CT score might be a useful index for assessing the severity of APT.
Aged ; Amiodarone/*adverse effects ; Anti-Arrhythmia Agents/*adverse effects ; Atrial Fibrillation/diagnosis/*drug therapy ; Cross-Sectional Studies ; Cryptogenic Organizing Pneumonia/chemically induced/physiopathology/*radiography/therapy ; Feasibility Studies ; Female ; Forced Expiratory Volume ; Hospitalization ; Humans ; Lung/drug effects/physiopathology/*radiography ; Male ; Middle Aged ; Predictive Value of Tests ; Prospective Studies ; Pulmonary Diffusing Capacity ; Pulmonary Fibrosis/chemically induced/physiopathology/*radiography/therapy ; Respiratory Function Tests ; Risk Factors ; Time Factors ; *Tomography, X-Ray Computed ; Vital Capacity

The aim of this study was to investigate the inhibitory effect of Cnidium monnieri fruit (CM) extracts on pulmonary inflammation induced in mice by cigarette smoke condensate (CSC) and lipopolysaccharide (LPS). Pulmonary inflammation was induced by intratracheal instillation of LPS and CSC five times within 12 days. CM extract was administered orally at a dose of 50 or 200 mg·kg(-1). The number of inflammatory cells in the bronchoalveolar lavage fluid was counted using a fluorescence activated cell sorter. Inflammatory mediator levels were determined by enzyme-linked immunosorbent assay. The administration of LPS and CSC exacerbated airway hyper-responsiveness (AHR) and induced an accumulation of inflammatory cells and mediators, and led to histological changes. However, these responses are modulated by treatment with CM, and the treatment with CM extract produces similar or more extensive results than the treatment with cyclosporin A (CSA). CM extract may have an inhibitory effect on pulmonary inflammation related with chronic obstructive pulmonary disease.
Animals ; Anti-Inflammatory Agents ; pharmacology ; therapeutic use ; Bronchoalveolar Lavage Fluid ; Cnidium ; Female ; Fruit ; Lipopolysaccharides ; Mice, Inbred BALB C ; Phytotherapy ; Plant Extracts ; pharmacology ; therapeutic use ; Pneumonia ; chemically induced ; drug therapy ; Pulmonary Disease, Chronic Obstructive ; drug therapy ; pathology ; Smoke ; adverse effects ; Smoking ; adverse effects ; Tobacco Products ; adverse effects

Alkanes ; adverse effects ; Empyema ; chemically induced ; complications ; Humans ; Male ; Middle Aged ; Pneumonia ; chemically induced ; complications

Temozolomide is an oral alkylating agent with clinical activity against glioblastoma multiforme (GM). It is generally well-tolerated and has few pulmonary side effects. We report a case of temozolomide-associated brochiolitis obliterans organizing pneumonia (BOOP) requiring very high-dose corticosteroid treatment. A 56-yr-old woman presented with a 2-week history of exertional dyspnea. For the treatment of GM diagnosed 4 months previously, she had undergone surgery followed by chemoradiotherapy, and then planned adjuvant chemotherapy with temozolomide. After the 1st cycle, progressive dyspnea was gradually developed. Chest radiograph showed diffuse patchy peribronchovascular ground-glass opacities in both lungs. Conventional dose of methylprednisolone (1 mg/kg/day) was begun for the possibility of BOOP. Although transbronchial lung biopsy findings were compatible with BOOP, the patient's clinical course was more aggravated until hospital day 5. After the dose of methylprednisolone was increased (500 mg/day for 5 days) radiologic findings were improved dramatically.
Antineoplastic Agents, Alkylating/*adverse effects/therapeutic use ; Cryptogenic Organizing Pneumonia/*chemically induced/*drug therapy/radiography ; Dacarbazine/adverse effects/*analogs & derivatives/therapeutic use ; Dyspnea/etiology ; Female ; Glioblastoma/drug therapy/radiography ; Glucocorticoids/*therapeutic use ; Humans ; Methylprednisolone/therapeutic use ; Middle Aged ; Tomography, X-Ray Computed

This study is to determine the preventive effect and mechanism of targeting IL-17A on pulmonary inflammation and fibrosis after acute lung injury. Mice were treated with anti-IL-17A antibody on the day 7 and sacrificed on the day 14 after bleomycin lung injury. The pulmonary inflammatory status and the deposition of collagen were measured by HE and Sirius stains staining. The contents of hydroxyproline and collagen were measured by using commercial kits. The survival rate of mice was calculated by Kaplan-Meier methods. The inflammatory cytokines in bronchoalveolar lavage fluid were measured by ELISA and the expressions of inflammation-related molecules were detected by Western blotting assay. Targeting of IL-17A could prevent the development of lung inflammation, decrease collagen deposition and the contents of hydroxyproline, and protect against the development of pulmonary fibrosis, which together led to an increase in the animal survival. Moreover, blocking IL-17A decreased the expression ofpro-fibrotic cytokines such as IL-17A, TGF-beta1 and IL-13; increased the expression of anti-fibrotic or anti-inflammatory factors such as IFN-gamma, COX-2, 5-LOX, 15-LOX. Indeed, IL-17A antagonism suppressed the activation of pro-inflammatory p65NF-kappaB but enhanced the activation of pro-resolving p50NF-kappaB. In conclusion, that blockade of IL-17A prevents the development of pulmonary fibrosis from acute lung injury, is because blocking IL-17A may prevent acute inflammation converting to chronic inflammation.
Acute Lung Injury ; chemically induced ; complications ; Animals ; Bleomycin ; Collagen ; metabolism ; Hydroxyproline ; metabolism ; Interleukin-13 ; metabolism ; Interleukin-17 ; antagonists & inhibitors ; metabolism ; Male ; Mice ; Mice, Inbred C57BL ; NF-kappa B p50 Subunit ; metabolism ; Pneumonia ; etiology ; metabolism ; Pulmonary Fibrosis ; etiology ; metabolism ; prevention & control ; Random Allocation ; Transcription Factor RelA ; metabolism ; Transforming Growth Factor beta1 ; metabolism ; Up-Regulation

OBJECTIVESan'ao Decoction (, SAD), as a representative Chinese medicine (CM) formula, was chosen to evaluate the effect of airway inflammation and hyperresponsiveness on the lipopolysaccharide (LPS) enhanced asthma model.

METHODSThe asthma model was reproduced in the Balb/C mice sensitized by ovalbumin (OVA), challenged by OVA and LPS. After Balb/C mice's administration of a dose (0.0024 g/kg) of dexamethasone acetate, and three doses (2.2 g/kg, 4.4 g/kg and 8.8 g/kg) of SAD, airway inflammation and responsiveness were observed. The airway inflammation was detected by counting bronchoalveolar lavage fluid (BALF) cells and lung histopathology. Also, differential expressions of interferon-r (IFN-γ), interleukin-4 (IL-4), and IL-5 in the supernatants of BALF were examined. The changes in airway responsiveness indicated by lung resistance (R(L)) and stimulated by acetylcholine (Ach) were determined.

RESULTSSmall-dose SAD hardly inhibit airway inflammation or hyperresponsiveness in the LPS-enhanced asthma, while medium-dose and high-dose SAD significantly inhibited the airway hyperresponsiveness, and to some extent, reduced airway inflammation. Meanwhile, the small-dose, medium-dose, and high-dose SAD promoted Th1-type cytokines (IFN-γ) and reduced Th2-type cytokines (IL-4, IL-5) to different extents, which led to a Th1/Th2 balance.

CONCLUSIONSAD has a good therapeutic effect on airway hyperresponsiveness in the LPS-enhanced asthma model, but its definite influence on airway inflammation is not remarkable.

Animals ; Asthma ; chemically induced ; complications ; drug therapy ; physiopathology ; Bronchial Hyperreactivity ; complications ; drug therapy ; pathology ; Bronchoalveolar Lavage Fluid ; cytology ; Cell Count ; Disease Models, Animal ; Drugs, Chinese Herbal ; therapeutic use ; Female ; Interferon-gamma ; metabolism ; Interleukin-4 ; metabolism ; Interleukin-5 ; metabolism ; Lipopolysaccharides ; Lung ; pathology ; physiopathology ; Mice ; Mice, Inbred BALB C ; Pneumonia ; complications ; drug therapy ; pathology