MATERIALS AND METHODS: A cross-sectional study was carried out among 51 cleaners. The respondents' background information and respiratory symptoms were gathered using a series of standardised questionnaires validated by the American Thoracic Society (ATS-DLD-78-A). The 8- hour respirable dust exposure to cleaners was measured using an air sampling pump (Gillian & Sensodyne Gil Air 3).
RESULTS: The mean of respirable dust was lower than permissible exposure limit with 0.63±0.57mg/m3. The respiratory symptoms among the cleaners showed no significant association between cough, phlegm, and breathing difficulties with working tenure. Meanwhile, wheezing and coughing with phlegm have an almost significant association with working tenure among cleaners with (Χ2=1.00, p=0.08) and (Χ2=1.00, p=0.07) respectively. Exposure to respirable dust has exhibited 6 times the prevalence of coughing with phlegm among cleaners (PR=6.28, 95% CI: 0.44, 89.38).
CONCLUSION: The findings of this study demonstrated that the cleaners were significantly affected by the respirable dust. The cleaners' working environment has caused them to be exposed to respirable dust.
MATERIALS AND METHODS: We retrospectively analysed data from 157 patients who underwent FG-TBLB, with the primary outcome being procedure-related pneumothorax. We assessed several risk factors for pneumothorax following FG-TBLB: patient characteristics, location of biopsy, number of biopsies and computed tomography pattern. Univariate and multivariate logistic regression analyses were performed.
RESULTS: One-hundred fifty-seven patients were included [mean (SD) age 57.9 (16.2) years; 60.5% male]. The most common location for FG-TBLB was the right upper lobe (n=45, 28.7%). The mean (SD) number of biopsy samples was 6.7 (2.1). Radiographic evidence of pneumothorax was reported in 12 (7.6%) patients, with 11 of those requiring intercostal chest tube intervention (mean air leak time: 5.7 days and 1 had persistent air leak requiring autologous blood patch pleurodesis. None experienced pneumothorax recurrence. Female gender and upper lobe location of the biopsy were identified as predisposing factors for pneumothorax. In the multivariable analysis, upper lobe biopsies were associated with a higher risk of pneumothorax (OR 0.120; 95% CI 0.015-0.963; p = 0.046).
CONCLUSION: The overall rate of pneumothorax is low. We recognise the increased risk of pneumothorax associated with upper lobe biopsy. These findings suggest that clinicians should exercise caution when performing FGTBLB in this region and consider alternative biopsy locations whenever feasible. We suggest adequate planning and preparation should be implemented to minimise the risk of pneumothorax following FG-TBLB.
MATERIALS AND METHODS: We retrospectively enrolled patients who underwent the procedure from January 2018 to April 2022. Under real time ultrasound (Hitachi Medical ProSound F37), thoracic lesions adjacent to the chest wall were sampled with a full-core biopsy needle (CT Core Single Action Biopsy Device, 18G × 15 cm, Vigeo, Italy). Chest x-ray was performed 30 minutes post procedure ruling out pneumothorax. Patients were discharged home 1-2 hours post biopsy. Data was analysed using Microsoft Excel 2010 and Statistical Package for Social Science (SPSS) Version 26.
RESULTS: A total of 18 patients (14 males, 4 females) underwent USLB for lung tumours. Biopsies were histologically deemed adequate with an overall diagnostic yield of 77.8% (14/18). A total of 57% were positive for thoracic malignancy (21% squamous cell carcinoma, 21% adenocarcinoma, 15% small cell carcinoma) and another 43% were positive for extra thoracic malignancy (1 hepatocellular carcinoma, 2 DLBCL, 1 Hodgkin's lymphoma, 1 seminoma, 1 thymoma). Four patients had inconclusive results but managed to get positive results from surgical or lymph node biopsy (thymoma and adenocarcinoma). Statistical analysis showed more than two passes are needed to achieve a positive HPE yield (p value<0.05). There were nil complications to all the cases done.
CONCLUSIONS: USLB can safely and effectively be performed by trained pulmonologists with excellent accuracy and low complication rate in outpatients.
METHODS: EMPOWER-Lung 1 was a multicentre, open-label, randomised, phase 3 trial. We enrolled patients (aged ≥18 years) with histologically confirmed squamous or non-squamous advanced non-small-cell lung cancer with PD-L1 tumour expression of 50% or more. We randomly assigned (1:1) patients to intravenous cemiplimab 350 mg every 3 weeks for up to 108 weeks, or until disease progression, or investigator's choice of chemotherapy. Central randomisation scheme generated by an interactive web response system governed the randomisation process that was stratified by histology and geographical region. Primary endpoints were overall survival and progression free survival, as assessed by a blinded independent central review (BICR) per Response Evaluation Criteria in Solid Tumours version 1.1. Patients with disease progression on cemiplimab could continue cemiplimab with the addition of up to four cycles of chemotherapy. We assessed response in these patients by BICR against a new baseline, defined as the last scan before chemotherapy initiation. The primary endpoints were assessed in all randomly assigned participants (ie, intention-to-treat population) and in those with a PD-L1 expression of at least 50%. We assessed adverse events in all patients who received at least one dose of their assigned treatment. This trial is registered with ClinicalTrials.gov, NCT03088540.
FINDINGS: Between May 29, 2017, and March 4, 2020, we recruited 712 patients (607 [85%] were male and 105 [15%] were female). We randomly assigned 357 (50%) to cemiplimab and 355 (50%) to chemotherapy. 284 (50%) patients assigned to cemiplimab and 281 (50%) assigned to chemotherapy had verified PD-L1 expression of at least 50%. At 35 months' follow-up, among those with a verified PD-L1 expression of at least 50% median overall survival in the cemiplimab group was 26·1 months (95% CI 22·1-31·8; 149 [52%] of 284 died) versus 13·3 months (10·5-16·2; 188 [67%] of 281 died) in the chemotherapy group (hazard ratio [HR] 0·57, 95% CI 0·46-0·71; p<0·0001), median progression-free survival was 8·1 months (95% CI 6·2-8·8; 214 events occurred) in the cemiplimab group versus 5·3 months (4·3-6·1; 236 events occurred) in the chemotherapy group (HR 0·51, 95% CI 0·42-0·62; p<0·0001). Continued cemiplimab plus chemotherapy as second-line therapy (n=64) resulted in a median progression-free survival of 6·6 months (6·1-9·3) and overall survival of 15·1 months (11·3-18·7). The most common grade 3-4 treatment-emergent adverse events were anaemia (15 [4%] of 356 patients in the cemiplimab group vs 60 [17%] of 343 in the control group), neutropenia (three [1%] vs 35 [10%]), and pneumonia (18 [5%] vs 13 [4%]). Treatment-related deaths occurred in ten (3%) of 356 patients treated with cemiplimab (due to autoimmune myocarditis, cardiac failure, cardio-respiratory arrest, cardiopulmonary failure, septic shock, tumour hyperprogression, nephritis, respiratory failure, [n=1 each] and general disorders or unknown [n=2]) and in seven (2%) of 343 patients treated with chemotherapy (due to pneumonia and pulmonary embolism [n=2 each], and cardiac arrest, lung abscess, and myocardial infarction [n=1 each]). The safety profile of cemiplimab at 35 months, and of continued cemiplimab plus chemotherapy, was generally consistent with that previously observed for these treatments, with no new safety signals INTERPRETATION: At 35 months' follow-up, the survival benefit of cemiplimab for patients with advanced non-small-cell lung cancer was at least as pronounced as at 1 year, affirming its use as first-line monotherapy for this population. Adding chemotherapy to cemiplimab at progression might provide a new second-line treatment for patients with advanced non-small-cell lung cancer.
FUNDING: Regeneron Pharmaceuticals and Sanofi.
METHODS: A literature search was performed following the PRISMA guidelines. Systematic searches were performed in PubMed, Scopus, Cochrane and Embase databases in October 2022. Retrospective and prospective studies on the delta-radiomics model for RT-induced toxicity were included based on predefined PICOS criteria. A random-effect meta-analysis of AUC was performed on the performance of delta-radiomics models, and a comparison with non-delta radiomics models was included.
RESULTS: Of the 563 articles retrieved, 13 selected studies of RT-treated patients on different types of cancer (HNC = 571, NPC = 186, NSCLC = 165, oesophagus = 106, prostate = 33, OPC = 21) were eligible for inclusion in the systematic review. Included studies show that morphological and dosimetric features may improve the predictive model performance for the selected toxicity. Four studies that reported both delta and non-delta radiomics features with AUC were included in the meta-analysis. The AUC random effects estimate for delta and non-delta radiomics models were 0.80 and 0.78 with heterogeneity, I2 of 73% and 27% respectively.
CONCLUSION: Delta-radiomics-based models were found to be promising predictors of predefined end points. Future studies should consider using standardized methods and radiomics features and external validation to the reviewed delta-radiomics model.
OBJECTIVES: This study aimed to investigate the in vitro growth inhibition of genetically engineered human umbilical cord-derived mesenchymal stromal cells (hUCMSC) expressing IL-12 on H1975 human lung adenocarcinoma cells.
MATERIALS AND METHODS: Both adenoviral method and electroporation which used to generate hUCMSC-IL12 were compared. The method with better outcome was selected to generate hUCMSC-IL12 for the co-culture experiment with H1975 or MRC-5 cells. Characterisation of hUCMSC and hUCMSC-IL12 was performed.
RESULTS: Adenoviral method showed superior results in transfection efficiency (63.6%), post-transfection cell viability (82.6%) and hIL-12 protein expression (1.2 x 107 pg/ml) and thus was selected for the downstream experiments. Subsequently, hUCMSC-IL12 showed significant inhibition effect on H1975 cells after 5 days of co-culture. No significant difference was observed for all other co-culture groups, indicating that the inhibition effect was because of hIL-12. Lastly, the integrity of hUCMSC-IL12 remained unaffected by the transduction through examination of their surface markers and differentiation properties.
CONCLUSION: This study provided proof of concept that hUCMSC can be genetically engineered to express hIL-12 which exerts direct growth inhibition effect on human lung adenocarcinoma cells.
METHODS AND ANALYSIS: Scopus, PubMed, Cochrane, Web of Science and ProQuest will be searched from database inception to February 2023 using PEO search strategy (Population: adults with COPD; Exposure: inflammatory markers; Outcomes: lung function, muscle force and exercise capacity). Four reviewers working in pairs will independently screen articles for eligibility and extract data that fulfilled the inclusion criteria. Depending on the design of the included studies, either Cochrane risk-of-bias version 2 or the Newcastle-Ottawa Scale tools will be used to rate the methodological quality of the included studies. Effect sizes reported in each individual study will be standardised to Cohen's d and a random effects model will be used to calculate the pooled effect size for the association.
ETHICS AND DISSEMINATION: Ethical approval is unnecessary as this study will only use publicly available data. The findings will be disseminated through publication in peer-reviewed journals and conferences.
PROSPERO REGISTRATION NUMBER: CRD42022284446.