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Destroyed lung can cause mediastinal displacement and asymmetric chest deformity. Reports on bilateral lung transplantation (LT) to treat destroyed lung and asymmetric chest deformity are rare. This study presents our surgical experience of bilateral LT among patients with destroyed lung and asymmetric chest deformity. Six patients with destroyed lung and asymmetric chest deformity who underwent bilateral LT at our center from 2005 to 2020 were included in the study. Demographic data, technical data, perioperative details, and short-term follow-up data were reviewed. Three patients underwent bilateral LT via anterolateral incisions in the lateral position without sternal transection, while three patients underwent bilateral LT via clam-shell incisions in the supine position with sternal transection. Only one patient required intraoperative extracorporeal membrane oxygenation. Four patients underwent size-reduced LT. In the other two patients, we restored the mediastinum by releasing mediastinal adhesions to ensure maximal preservation of the donor lung function. Patients in the lateral position group had a higher volume of blood loss, longer operation time, and longer postoperative in-hospital stay than those in the supine position group. However, these differences were not statistically significant. Postoperative computed tomography in the supine position group revealed that the donor lungs were well expanded and the mediastina were in their original positions. Although bilateral LT in patients with destroyed lung and asymmetric chest deformity is high risk, with sufficient preoperative preparation and evaluation, it is safe and feasible to perform bilateral LT for selected patients. For patients without severe chest adhesions, releasing the mediastinal adhesions and restoring the mediastinum through a clam-shell incision in the supine position is a simple and effective method to maximally preserve the donor lung function without pneumonectomy or lobectomy.
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http://dx.doi.org/10.3389/fsurg.2021.680207 | DOI Listing |
Invest New Drugs
September 2025
Departamento de Química and Institute for Advanced Research in Chemical Science (IAdChem), Facultad de Ciencias, Universidad Autónoma de Madrid, Módulo 13, 28049, Madrid, Spain.
The oncogenic transcription factor MYC drives proliferation, metabolism, and therapy resistance in the majority of human cancers, yet its large, nuclear protein-protein interface has long frustrated direct drug discovery. A pivotal breakthrough was the identification of Tribbles pseudokinase 3 (TRIB3) as a high-affinity scaffold that binds the helix-loop-helix/leucine zipper region of MYC, blocks the E3-ubiquitin-ligase, UBE3B, from tagging critical lysines, and thereby prolongs MYC protein half-life while enhancing MYC-MAX transcriptional output. This review integrates structural, biochemical, and in vivo data to show how genetic deletion or pharmacological eviction of TRIB3 collapses MYC levels, silences its gene program, and suppresses tumor growth in B-cell lymphomas and selected solid tumors.
View Article and Find Full Text PDFJ Artif Organs
August 2025
Department of Cardiovascular Surgery, Kitasato University School of Medicine, 1-15-1 Kitasato, Minami, Sagamihara, Kanagawa, 252-0374, Japan.
To investigate the feasibility of regional oxygen saturation (rSO) monitoring for preventing acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) caused by cardiopulmonary bypass (CPB) in infants undergoing ventricular septal defect (VSD) closure. This study included 49 infants who underwent VSD closure between January 2012 and December 2023. Patients with preoperative pulmonary hypertension were excluded.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
September 2025
Laboratory of Computational Biology, National Heart, Lung, Blood Institute, National Institutes of Health, Bethesda, MD 20892.
Membrane active peptides (MAPs) represent a diverse group of agents that disrupt the integrity of lipid membranes. One class of MAPs, antimicrobial peptides (AMPs), destroy bacteria by transiently porating the bacterial membrane causing leakage of cellular contents. Transient leakage is classified as "graded," where all vesicles in a population leak partially, or "all-or-none," where some vesicles leak completely.
View Article and Find Full Text PDFFront Immunol
August 2025
Department of Biochemistry and Molecular Biology, Shenyang Medical College, Shenyang, China.
The combination of radiation therapy (radiotherapy) with immunotherapy is changing the landscape of cancer treatment. Radiation damage tumor cell DNA through high-energy rays directly causes cell death or growth arrest; Immunotherapy works by boosting a patient's own immune system's ability to recognize and destroy cancer cells. The combination of the two not only enhances the local control of the tumor, but may also activate the systemic anti-tumor immune response, transforming the "cold" tumor into a "hot" tumor, thereby improving the survival rate and quality of life of patients.
View Article and Find Full Text PDFCureus
July 2025
Pulmonology Department, Moulay Youssef Hospital, Centre Hospitalo-Universitaire (CHU) Ibn Sina, Rabat, MAR.
Kartagener syndrome is a rare genetic disorder characterized by the classic triad of situs inversus, bronchiectasis, and chronic sinusitis. The progression to destroyed lung syndrome represents an exceptionally rare complication, with only a few cases reported in the literature. We present the cases of two Moroccan sisters, aged 20 and 26, born from a first-degree consanguineous marriage, presenting with chronic respiratory symptoms but with different phenotypes.
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