ABSTRACT
Contralateral tension pneumothorax is a rare but fatal complication of one-lung ventilation. The life-saving decompression of pleural space was frequently delayed by the difficult confirmation of diagnosis because of general anesthesia that masks specific clinical presentations when the patient is alert. We reported a case of tension pneumothorax in a patient who underwent thoracic spine instrumentation. There were no contralateral tension pneumothorax cases on file from the search of the Anesthesia Quality Institute Closed Claims Database from 2001 to 2017. We systematically searched PubMed, Ovid MEDLINE, Embase, and Google Scholar. Over the past 30 years, there were 21 single case reports and two case series were retrieved. It was a consensus that difficult confirmation of the diagnosis of contralateral tension pneumothorax is the culprit of delayed life-saving intervention. Difficulty of oxygenation with increasing inspiratory pressure was usually the first sign suggesting contralateral pneumothorax; however, earlier presentations of cardiovascular system failure than respiratory failure have significantly increased the incidence of cardiac arrest and death. It is paramount to maintain a high suspicion of tension pneumothorax. The application of esophageal stethoscope, lung ultrasound, and simulator training may improve the chance of early diagnosis and patient outcome.
ABSTRACT
Historically, immunoglobulin (Ig) has been known as an antibody and is expressed only in B lineage cells; importantly, Ig light chains are conjugated to heavy chains to form intact Igs. However, in this study, we found a free Igκ light chain with a unique Vκ4-1/Jκ3 rearrangement (Vκ4-1/Jκ3-FLC) that was widely expressed in different non-B lineages and was overexpressed in cancer cells. Further study indicated that Vκ4-1/Jκ3-FLC was hydrophobic, formed obvious insoluble deposits in the extracellular matrix (ECM) and existed in free form. Functional analyses demonstrated that Vκ4-1/Jκ3-FLC promoted the proliferation, migration and metastasis of colon cancer cells in vitro and in vivo. Mechanistically, Vκ4-1/Jκ3-FLC bound to integrin ß1 and activated the FAK and Src pathways. More importantly, specific antibodies against the variable region of Vκ4-1/Jκ3-FLC significantly inhibited the growth of colon cancer tumors. Our findings suggested that Vκ4-1/Jκ3-FLC is a novel ECM protein and integrin ß1 ligand and that it is involved in cancer progression and is a potential therapeutic target in cancer, particularly colon cancer.
