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Background: Tele-assisted home-based palliative care (THPC) usually fulfills the desire of terminal patients to pass away at home. The overall costs of such a service deserve evaluation. Objectives: This study aims to determine health care utilization and costs for cancer patients at the end of life, stratified by THPC service. Design: Patients who received THPC were matched 1:1 based on age, gender, year of death, and propensity score with those who did not receive THPC. Setting/Subjects: A total of 773 cancer patients passed away in a regional hospital in Taiwan during the period of 2012–2020, of which 293 received THPC. Measurements: We measured the rates and costs of outpatient clinic visits, emergency department (ED) visits, hospitalizations, and intensive care unit (ICU) admissions during the last week, the last two weeks and the last month before death. In addition, we estimated the driving times and expenses required for transportation from each cancer patient's home to the hospital using Google Maps. National Health Insurance (NHI) reimbursements and out-of-pocket expenses were also calculated. Results: In comparison with patients without THPC, those who received THPC had a 50% lower likelihood of visiting the ED or being hospitalized, a more than 90% reduced chance of ICU admission, but were four times more likely to obtain their medicines from outpatient clinics. THPC patients had similar out-of-pocket expenditures, approximately half of the NHI costs, and lower rates and costs for ambulance transportation to the ED. Conclusions: THPC reduced health care costs for terminal cancer patients in the last week, the last two weeks, and the last month before death, while also increasing the likelihood of patients being able to rest and pass away at home. [ABSTRACT FROM AUTHOR]

Our study sought to determine whether the size of the residual apical pleural space in young patients with primary spontaneous pneumothorax (PSP) following video-assisted thoracoscopic surgery is associated with the risk of recurrence. We retrospectively reviewed patients (≤30 years' old) with primary spontaneous pneumothorax following thoracoscopic surgery (2002-2010) in a university-affiliated hospital. The size of residual apical pleural space was estimated by measuring the apex-to-cupola distance on a postoperative chest radiograph at 2 time windows: first between postoperative day (POD) 0 and 3, and second between POD 4 and 14. A total of 149 patients were enrolled with a median follow-up of 11.2 months (interquartile range, 0.95-29.5 months), of whom 141 (94.6%) were male with a mean age of 20 years. The postoperative recurrence rate was 11.4%. Comparing the characteristics between the patients with and without recurrent pneumothorax, the patients with recurrence were younger (18.2 + 2.4 vs 20.7 + 3.7 years, P = 0.008), with a lower rate of pleurodesis (35% vs1 69%, P = 0.037), longer apex-to-cupola distance at POD 0 to 3 (22.41 ± 19.56 vs 10.07 ± 10.83 mm, P 10 mm (P = 0.027, OR: 5.319), and no pleurodesis during VATS (P = 0.022, OR: 5.042) were independent risk factors for recurrent pneumothorax. The recurrence rate was not low (11.4%) in young patients with PSP following VATS. Residual apical pleural space with apex-to-cupola distance of 10 mm or greater at POD 0 to 3, younger age, and no pleurodesis would increase postoperative recurrence of primary spontaneous pneumothorax.

The tumor microenvironment plays an important role in tumor growth and metastasis. However, the mechanism by which tumor cells regulate the cell and non-cell constituents of surrounding stroma remains incompletely understood. Promyelocytic leukemia (PML) is a pleiotropic tumor suppressor, but its role in tumor microenvironment regulation is poorly characterized. PML is frequently downregulated in many cancer types, including lung cancer. Here, we identify a PML ubiquitination pathway that is mediated by WD repeat 4-containing cullin-RING ubiquitin ligase 4 ([CRL4.sup.WDR4]). Clinically, this PML degradation pathway is hyperactivated in lung cancer and correlates with poor prognosis. The WDR4/PML axis induces a set of cell-surface or secreted factors, including CD73, urokinase-type plasminogen activator receptor (uPAR), and serum amyloid A2 (SAA2), which elicit paracrine effects to stimulate migration, invasion, and metastasis in multiple lung cancer models. In xenograft and genetically engineered mouse models, the WDR4/PML axis elevates intratumoral Tregs and M2-like macrophages and reduces [CD8.sup.+] T cells to promote lung tumor growth. These immunosuppressive effects were all reversed by CD73 blockade. Our study identifies WDR4 as an oncoprotein that negatively regulates PML via ubiquitination to promote lung cancer progression by fostering an immunosuppressive and prometastatic tumor microenvironment, suggesting the potential of immune-modulatory approaches for treating lung cancer with aberrant PML degradation., Introduction Lung cancer is one of the most devastating diseases. Despite advances in treatment, the 5-year survival rate is only slightly better than 10%, and the majority of late-stage patients [...]