635 research outputs found

    Endobronchial Lipomatous Hamartoma: An Incidental Finding in a Patient with Atrial Fibrillation—A Case Report

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    Introduction. Lung hamartomas are the most common benign tumors of the lung. Typically, they are located in the peripheral lung, while an endobronchial localisation is rare. Case Presentation. We present a case with the rare diagnosis of an endobronchial hamartoma as incidental finding in a 69-year-old male, caucasian patient with atrial fibrillation. At first admission, the patient's exertional dyspnea was caused by atrial fibrillation. Relapse of exertional dyspnea in the absence of arrhythmia was due to postobstructive pneumonia caused by an endobronchial hamartoma. Conclusion. Endobronchial tumors such as endobronchial lipoma or hamartoma should be considered as potential causes of exertional dyspnea and thus as differential diagnosis of atrial fibrillation. Although endobronchial hamartomas are benign, resection is recommended to prevent postobstructive lung damage

    Trends in age- and sex-specific lung cancer mortality in Europe and Northern America: Analysis of vital registration data from the WHO Mortality Database between 2000 and 2017

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    Background: In the context of new targeted therapies and immunotherapy as well as screening modalities for lung cancer patients, detailed mortality trends in Europe and Northern America are unknown. Methods: Time-trend analysis using vital registration data of Northern America and Europe from the WHO Mortality Database (years 2000/2017). To assess improvements in lung cancer mortality, we performed a population-averaged Poisson autoregressive analysis. The average annual percent change (AAPC) was used as a summary measure of overall and country-specific trends in mortality. Second, we studied time trends of lung cancer incidence and smoking prevalence rates. Findings: In the total population of 872·5 million people between 2015 and 2017, the average annual age-standardised mortality from lung cancer was 54·6 deaths per 100 000, with substantial differences across countries. Lung cancer was reported as the primary cause of death in 5·4 cases per 100 deaths. The age-standardised mortality rate decreased constantly (AAPC –1·5%) between 2000 and 2017. While mortality in men dropped annually by an average of −2·3%, mortality in women decreased by an average of −0·3%. This slight decline was driven exclusively by the USA. In contrast, 21 out of 31 countries registered a significant increase in female lung cancer mortality between 2000 and 2017, with Spain (AAPC 4·1%) and France (AAPC 3·6%) leading the list. Interpretation: Despite overall decreases in lung cancer mortality trends, female mortality remained unchanged or increased significantly in all countries except the USA. National mortality outcomes reflect variabilities in tobacco control, screening, therapeutic advances, and access to health care

    Predictors of poor outcomes after significant chest trauma in multiply injured patients: a retrospective analysis from the German Trauma Registry (Trauma Register DGU (R))

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    Background: Blunt thoracic trauma is one of the critical injury mechanisms in multiply injured trauma victims. Although these patients present a plethora of potential structural damages to vital organs, it remains debated which injuries actually influence outcome and thereby should be addressed initially. Hence, the aim of this study was to identify the influence of critical structural damages on mortality. Methods: All patients in the database of the TraumaRegister DGU (R) (TR-DGU) from 2002-2011 with AIS Chest >= 2, blunt trauma, age of 16 or older and an ISS >= 16 were analyzed. Outcome parameters were in-hospital mortality as well as ventilation time in patients surviving the initial 14 days after trauma. Results: 22613 Patients were included (mean ISS 30.5 +/- 12.6; 74.7% male; Mean Age 46.1 +/- 197 years; mortality 17.5%; mean duration of ventilation 7.3 +/- 11.5; mean ICU stay 11.7 +/- 14.1 days). Only a limited number of specific injuries had a significant impact on survival. Major thoracic vessel injuries (AIS >= 5), bilateral lung contusion, bilateral flail chest, structural heart injury (AIS >= 3) significantly influence mortality in study patients. Several extrathoracic factors (age, blood transfusion, systolic blood pressure and extrathoracic severe injuries) were also predictive of increased mortality. Most injuries of the thoracic wall had no or only a moderate effect on the duration of ventilation. Injuries to the lung (laceration, contusion or pneumothoraces) had a moderate prolonging effect. Cardiac injuries and severe injuries to the thoracic vessels induced a substantially prolonged ventilation interval. Conclusions: We demonstrate quantitatively the influence of specific structural damages of the chest on critical outcome parameters. While most injuries of the chest wall have no or only limited impact in the study collective, injuries to the lung overall show adverse outcome. Injuries to the heart or thoracic vessels have a devastating prognosis following blunt chest trauma

    Tumor-specific T cells signal tumor destruction via the lymphotoxin ÎČ receptor

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    BACKGROUND: Previously, we reported that adoptively transferred perforin k/o (PKO), and IFN-Îł k/o (GKO), or perforin/IFN-Îł double k/o (PKO/GKO) effector T cells mediated regression of B16BL6-D5 (D5) pulmonary metastases and showed that TNF receptor signaling played a critical role in mediating tumor regression. In this report we investigated the role of lymphotoxin-α (LT-α) as a potential effector molecules of tumor-specific effector T cells. METHODS: Effector T cells were generated from tumor vaccine-draining lymph node (TVDLN) of wt, GKO, LT-α deficient (LKO), or PKO/GKO mice and tested for their ability to mediate regression of D5 pulmonary metastases in the presence or absence of LT-ÎČR-Fc fusion protein or anti-IFN-Îł antibody. Chemokine production by D5 tumor cells was determined by ELISA, RT-PCR and Chemotaxis assays. RESULTS: Stimulated effector T cells from wt, GKO, or PKO/GKO mice expressed ligands for LT-ÎČ receptor (LT-ÎČR). D5 tumor cells were found to constitutively express the LT-ÎČR. Administration of LT-ÎČR-Fc fusion protein completely abrogated the therapeutic efficacy of GKO or PKO/GKO but not wt effector T cells (p < 0.05). Consistent with this observation, therapeutic efficacy of effector T cells deficient in LT-α, was greatly reduced when IFN-Îł production was neutralized. While recombinant LT-α1ÎČ2 did not induce apoptosis of D5 tumor cells in vitro, it induced secretion of chemokines by D5 that promoted migration of macrophages. CONCLUSION: The contribution of LT-α expression by effector T cells to anti-tumor activity in vivo was not discernable when wt effector T cells were studied. However, the contribution of LT-ÎČ R signaling was identified for GKO or PKO/GKO effector T cells. Since LT-α does not directly induce killing of D5 tumor cells in vitro, but does stimulate D5 tumor cells to secrete chemokines, these data suggest a model where LT-α expression by tumor-specific effector T cells interacts via cross-linking of the LT-ÎČR on tumor cells to induce secretion of chemokines that are chemotactic for macrophages. While the contribution of macrophages to tumor elimination in our system requires additional study, this model provides a possible explanation for the infiltration of inate effector cells that is seen coincident with tumor regression

    Mold Attacks a Beating Heart

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    SARS‐CoV‐2 receptor ACE 2 and TMPRSS 2 are primarily expressed in bronchial transient secretory cells

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    The SARS-CoV-2 pandemic affecting the human respiratory system severely challenges public health and urgently demands for increasing our understanding of COVID-19 pathogenesis, especially host factors facilitating virus infection and replication. SARS-CoV-2 was reported to enter cells via binding to ACE2, followed by its priming by TMPRSS2. Here, we investigate ACE2 and TMPRSS2 expression levels and their distribution across cell types in lung tissue (twelve donors, 39,778 cells) and in cells derived from subsegmental bronchial branches (four donors, 17,521 cells) by single nuclei and single cell RNA sequencing, respectively. While TMPRSS2 is strongly expressed in both tissues, in the subsegmental bronchial branches ACE2 is predominantly expressed in a transient secretory cell type. Interestingly, these transiently differentiating cells show an enrichment for pathways related to RHO GTPase function and viral processes suggesting increased vulnerability for SARS-CoV-2 infection. Our data provide a rich resource for future investigations of COVID-19 infection and pathogenesis
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