The respiratory epithelium is lined by mucus, a gel consisting of water, ions, proteins, and macromolecules. The major macromolecular components of mucus are the mucin glycoproteins, which are critical for local defense of the airway. There are three classes of mucins in the airways: those that are secreted but do not polymerize (MUC7), those that are secreted and polymerize to form gels (MUC5AC, MUC5B), and those that have transmembrane domains and are cell surface associated (MUC1, MUC4, MUC16, MUC20). The mucins are regulated at the transcriptional, posttranscriptional, and epigenetic levels, and posttranslational modifications play an important role in mucin binding and clearance of microbes and pollutants. The development of mice deficient in specific mucins, and the cystic fibrosis pig, has greatly advanced our understanding of the role of mucins as innate immune mediators and how mucins and mucus contribute to lung disease. These observations suggest new strategies to ameliorate mucus obstruction by targeting mucociliary clearance and mucin hyperconcentration. Furthermore, a polymorphism in the promoter of MUC5B is strongly associated with risk of developing pulmonary fibrosis, supporting a novel function for MUC5B to influence interstitial lung disease. Exciting new data support the concept not only that mucins and mucus are important for lung homeostasis and protection from environmental threats but also that goblet cells play an important role as regulators of innate immune function. These insights into the innate immune properties of mucins and goblet cells support a shift from the current paradigm of repressing increased mucin expression to targeting regulation of specific mucins and the abnormal airway milieu.

Oxygen supplementation for exercise-induced hypoxemia is a common clinical practice that improves exercise tolerance. However, we know of no standardized exercise oxygen titration protocol using a single walk test. We report our experience with a protocol developed in our laboratory.

Whether the use of rapid on-site cytologic evaluation (ROSE) increases the diagnostic yield of transbronchial needle aspiration (TBNA) remains unclear. This article is a systematic review of studies describing the utility of ROSE in subjects undergoing TBNA.

Guidelines suggest anticoagulation of patients with high pretest probability of pulmonary embolism (PE) while awaiting diagnostic test results (preemptive anticoagulation). Data relevant to the practice of preemptive anticoagulation are not available.

Sleep apnea has major neurocognitive and cardiovascular and metabolic risks. Treatment of sleep apnea is suboptimal because of variable adherence to existing therapies.

Cardiac tamponade is a medical emergency that can be readily reversed with timely recognition and appropriate intervention. The clinical diagnosis of cardiac tamponade requires synthesis of a constellation of otherwise nonspecific features based on an understanding of the underlying pathophysiological characteristics. Although echocardiographic examination is a central component of diagnosis, alone it is insufficient to establish the physiological diagnosis of hemodynamically significant cardiac tamponade. The hemodynamic diagnosis of cardiac tamponade requires clinical evidence of low cardiac output and stroke volume in the setting of elevated cardiac filling pressures, with evidence of increased sympathetic tone (eg, tachycardia, peripheral vasoconstriction), and exclusion of other causes of shock as the primary problem (particularly cardiogenic shock). The hemodynamic features of tamponade are revealed by considering the effects of pericardial constraint. Pulsus paradoxus and loss of the normal "y" descent of a jugular venous pressure waveform may be appreciated on clinical examination. When a pulmonary artery catheter is placed, equalization of diastolic pressures across all chambers is observed. Echocardiographic examination confirms the size, location, and other characteristics of the causal pericardial collection. Several echocardiographic features support the hemodynamic diagnosis of tamponade, including early diastolic collapse of the right ventricle, late diastolic collapse of the right atrium, respiratory variation in mitral valve inflow (akin to pulsus paradoxus), and decreased early filling (E wave) of mitral valve inflow (related to loss of the y descent). Echocardiographic examination then supports decisions about the early treatment and drainage of the tamponading effusion.

Carbon monoxide (CO) testing is considered an easy, noninvasive, and objective contribution to the assessment of smoking behavior, as CO is rapidly absorbed into the bloodstream when lit cigarettes or cigars are inhaled. CO testing is a medically important billable outpatient service that can contribute to sustainability of face to face tobacco use treatment services by clinicians. This article reviews research on the clinical use of CO testing to provide biomedical feedback in assessing smoking behavior, educating smokers on tobacco health effects, assisting with treatment planning, and as a motivational tool to encourage people to become tobacco free. Further research can focus on how to best incorporate CO testing into clinical practice, including more research on outcomes and methods to ensure that insurers reimburse for testing and improved ways to use CO testing to initiate attempts to quit tobacco use, to maintain cessation, and to prevent relapse.

COPD is a leading cause of morbidity and mortality worldwide. Long-term cigarette smoking is the cause of > 90% of COPD cases in Westernized countries. However, only a fraction of chronic heavy smokers develop symptomatic COPD by age 80. COPD is characterized by an abnormal immune response in the lower airways, and its progression is associated with infiltration of the lung by innate and adaptive inflammatory immune cells that form lymphoid follicles. There is growing evidence that both cellular- and antibody-mediated autoimmunity has a fundamental role in the pathogenesis of stable COPD. In particular, carbonyl-modified proteins may help to drive autoimmunity in COPD and cause the characteristic small airways abnormalities and even contribute to the pathogenesis of pulmonary emphysema. Although direct, indirect, and circumstantial evidence of a role for autoimmunity in stable patients with COPD has been identified, no cause-and-effect relationship between autoimmunity and the mechanisms of COPD has been firmly established in man. As such, the potential contribution of an autoimmune response to the pathogenesis of COPD exacerbation is still being investigated and represents an area of active research. Many drugs targeting autoimmune responses are already available, and the results of controlled clinical trials are awaited with great interest. The potential for measuring specific serum autoantibodies as biomarkers to predict clinical phenotypes or progression of stable COPD is promising.

In this report, we describe a male patient who presented with recurrent life-threatening hemoptysis due to the sequential formation of multiple pulmonary aneurysms. Both pulmonary artery coil embolization and right lower lobectomy were performed, with limited success. The patient experienced extensive bilateral femoral DVT extending into the inferior vena cava, with massive hemoptysis, fulfilling the diagnosis of Hughes-Stovin syndrome. A final diagnosis of Behçet disease was made following extensive investigation, and the patient responded well to prednisone 20 mg orally and azathioprine 100 mg orally.

A 47-year-old man with a medical history of hypertension, diabetes, hyperlipidemia, and OSA presented with a 7- to 10-day history of progressively worsening dyspnea on exertion, with a walking distance of 60 feet. He had bilateral lower-extremity swelling and was prescribed furosemide without clinical improvement. At baseline, he used three pillows for sleeping. The patient was noncompliant with his CPAP treatment. He had no smoking history and was retired from working in technology sales. On review of systems, he denied cough, chest pain, hemoptysis, fevers, chills, or weight loss.

A 53-year-old man was admitted with complaints of back pain of 3 months' duration along with numbness and weakness in his left upper and lower extremities. He denied any respiratory complaints or anorexia but did report an 11 kg weight loss over the last 3 months. He had no other significant medical history and denied any history of cigarette smoking or recreational drug use. Family history was significant for prostate cancer in his father.

An 18-year-old woman with no previous medical history presented to an outside hospital facility with acute chest pain. She had mild shortness of breath, particularly with exertion, for the prior 2 months.