Obstructive sleep apnea is increasingly recognized as a comorbidity in many medical illnesses. This has resulted in an increasing need for sleep testing, which is not entirely met by the currently available sleep laboratory facilities. Home, or out-of-center, sleep testing is an alternative to in-laboratory studies. However, coding and billing for home studies is not as straightforward as it is for in-laboratory studies. This article reviews the process of coding and billing for sleep studies done in an unattended setting.

The goal of asthma management is to achieve disease control; however, despite the availability of effective and safe medications, for many patients asthma remains uncontrolled. One reason for this is the fear of long-term side effects from the regular use of inhaled corticosteroids (ICSs). Adverse effects of poorly controlled asthma (for example, obesity, pneumonia, and risks to the fetus) can be perceived as side effects of ICSs. Poorly controlled asthma adversely affects children's cardiovascular fitness, while children with well-controlled asthma perform at the same level as their peers. Children with uncontrolled asthma also have a higher frequency of obesity than children with controlled asthma. Stress can affect asthma control, and children with poorly controlled asthma are more likely to have learning disabilities compared with those with good control. In adults, focused attention and concentration are negatively affected in patients with untreated asthma, and patients with asthma are at greater risk for depression. Also, poorly controlled asthma increases the risks of severe asthma exacerbations following upper respiratory and pneumococcal pulmonary infections. ICSs used to improve asthma control have been demonstrated to improve all of these outcomes. Lastly, the risks of uncontrolled asthma during pregnancy are substantially greater than the risks of recommended asthma medications. Treatments to maintain asthma control are the best approach to optimize maternal and fetal health in the pregnancies of women with asthma. The maintenance of asthma control has significant advantages to patients and greatly outweighs the potential risks of treatment side effects.

Vaccination is the primary strategy for prevention and control of influenza. The surface hemagglutinin (HA) protein of the influenza virus contains two structural elements (head and stalk) that differ in their potential utility as vaccine targets. The head of the HA protein is the primary target of antibodies that confer protective immunity to influenza viruses. The underlying health status, age, and gene polymorphisms of vaccine recipients and, just as importantly, the extent of the antigenic match between the viruses in the vaccine and those that are circulating modulate influenza vaccine protection. Vaccine adjuvants and live attenuated influenza vaccine improve the breadth of immunity to seasonal and pandemic virus strains. Eliciting antibodies against the conserved HA stem region that cross-react with HAs within influenza virus types or subtypes would allow for the development of a universal influenza vaccine. The highly complex network of interactions generated after influenza infection and vaccination can be studied with the use of systems biology tools, such as DNA microarray chips. The use of systems vaccinology has allowed for the generation of gene expression signatures that represent key transcriptional differences between asymptomatic and symptomatic host responses to influenza infection. Additionally, the use of systems vaccinology tools have resulted in the identification of novel surrogate gene markers that are predictors of the magnitude of host responses to vaccines, which is critical to both vaccine development and public health. Identifying associations between variations in vaccine immune responses and gene polymorphisms is critical in the development of universal influenza vaccines.

T helper 17 (Th17) cytokines are now widely believed to be critical for the regulation of various chronic immune diseases. Investigations have revealed a significant role for IL-17 cytokines in regulating inflammation and modulating lung and airway structural cells in asthma and COPD. In this review, our current understanding of the role of Th17-associated cytokines in airway diseases is summarized. Therapeutic approaches targeting IL-17 during asthma and COPD are also discussed.

The survival of patients with HIV infection has improved dramatically over the past 20 years, largely owing to a significant reduction in opportunistic infections and AIDs-defining malignancies, such as lymphoma and Kaposi sarcoma. However, with improved survival, patients with HIV are experiencing morbidity and mortality from other (non-AIDs-defining) complications, such as solid organ malignancies. Of these, the leading cause of mortality in the HIV-infected population is lung cancer, accounting for nearly 30% of all cancer deaths and 10% of all non-HIV-related deaths. Importantly, the average age of onset of lung cancer in the HIV-infected population is 25 to 30 years earlier than that in the general population and at lower exposure to cigarette smoke. This article provides an overview of the epidemiology of lung cancer in the HIV-infected population and discusses some of the important risk factors and pathways that may enhance the risk of lung cancer in this population.

Simulation-based bronchoscopy training is increasingly used, but effectiveness remains uncertain. We sought to perform a comprehensive synthesis of published work on simulation-based bronchoscopy training.

Over the past 10 years, significant strides have been made in therapeutics for sleep disorders. In this second installment of a two-part review series, we discuss the current evidence surrounding the mechanisms of actions, indications, efficacy, and adverse side effects associated with the current over-the-counter and pharmacotherapeutics for hypersomnia, parasomnias, and movement disorders of sleep.

The evidence regarding physician staffing of ICUs does not yet provide a consistent view of the best model to use. Most studies have significant limitations, and this subject is complicated by the fact that optimal ICU staffing may depend on ICU characteristics. The topic with the most data regarding patient outcomes is the intensity of intensivist involvement in care, particularly the value of closed- vs open-model ICUs; however, the evidence is inconsistent here as well. Even if closed-model ICUs produce better outcomes, we do not know which specific elements of that multifaceted organizational paradigm are responsible for improvement. Also, studies of around-the-clock intensivist presence have not consistently shown that it is associated with superior outcomes. Increasingly, nonphysician providers are playing innovative roles in the ICU, and care provided by teams including nurse practitioners or physician assistants appears to be safe and comparable to that provided by other staffing models. Although we do not know the best way to staff ICUs, the conditions of ICU physician coverage will continue to change under the stresses of shortages of intensivists and increasing duty hour limitations for trainees. Nonphysician providers, innovative physician staffing models, telemedicine, and other technologies will be increasingly used to cope with these realities. This evolution makes it more important than ever to study how staffing affects outcomes. Only quantitative evaluation can tell us whether one staffing model is better than another. Accordingly, we need more research from multiple sites to develop a consistent and integrated understanding of this complex topic.

A great deal of excitement and hope has followed the successful trials and US Food and Drug Administration approval of the drug ivacaftor (Kalydeco), the first therapy available that targets the underlying defect that causes cystic fibrosis (CF). Although this drug has currently demonstrated a clinical benefit for a small minority of the CF population, the developmental pathway established by ivacaftor paves the way for other CF transmembrane conductance regulator (CFTR) modulators that may benefit many more patients. In addition to investigating CFTR modulators, researchers are actively developing numerous other innovative CF therapies. In this review, we use the catalog of treatments currently under evaluation with the support of the Cystic Fibrosis Foundation, known as the Cystic Fibrosis Foundation Therapeutics Pipeline, as a platform to discuss the variety of candidate treatments for CF lung disease that promise to improve CF care. Many of these approaches target the individual components of the relentless cycle of airway obstruction, inflammation, and infection characteristic of lung disease in CF, whereas others are aimed directly at the gene defect, or the resulting dysfunctional protein, that instigates this cycle. We discuss how new findings from the laboratory have informed not only the development of novel therapeutics, but also the rationales for their use and the outcomes used to measure their effects. By reviewing the breadth of candidate treatments currently in development, as well as the recent progress in CF therapies reflected by the evolution of the therapeutics pipeline over the past few years, we hope to build upon the optimism and anticipation generated by the recent success of Kalydeco.

COPD is a complex syndrome that poses a serious health threat to >1.1 billion smokers worldwide. The stable disease is punctuated by episodes of acute exacerbation, which are predominantly the result of viral and bacterial infections. Despite their devastating health impact, mechanisms underlying disease exacerbations remain poorly understood. Mounting evidence suggests that cigarette smoke profoundly affects the immune system, compromising the host's ability to mount appropriate immune and inflammatory responses against microbial agents. This review highlights recent advances in our understanding of the impact of cigarette smoke on type 1 interferon and IL-1 signaling cascades. The immune defects caused by cigarette smoke on these two key pathways contribute to the seemingly contradictory nature of cigarette smoke as both a damaging and a proinflammatory factor as well as an immunosuppressive factor. Understanding the impact of cigarette smoke on the immune system may unravel novel targets for therapies that could affect acute exacerbations and COPD pathogenesis.

Over the past 10 years, significant strides have been made in the understanding, development, and availability of sleep disorder therapeutics. In this review series, we discuss the current evidence surrounding the mechanisms of actions, indications, efficacy, and adverse side effects associated with the available armamentarium of sleep over-the-counter and pharmacotherapeutics. This article is the first of a two-part series that covers the therapeutics for insomnia and circadian rhythm disorders.

This article is a review of the pertinent scientific data regarding obstructive sleep apnea (OSA) as presented in the medical literature. Attention regarding the diagnosis of OSA focused on the debate regarding home testing as compared with in-laboratory polysomnography (PSG), with a surprising result of possibly more cost benefit from PSG. New advances abound in the treatment of OSA, including those directed at preventing pharyngeal collapsibility. Multiple studies reviewed the comparative effects of oral appliances in conjunction with CPAP, with little difference between the two noted, especially for mild OSA. Finally, a number of studies evaluated both risks of OSA and outcomes from the use of CPAP, including functional outcomes, direct cardiac benefits, and overall cardiac mortality.

Over the past 15 years, patients with a myriad of pulmonary conditions have been diagnosed and treated with new technologies developed for the pulmonary community. Advanced diagnostic and therapeutic procedures once performed in an operating theater under general anesthesia are now routinely performed in a bronchoscopy suite under moderate sedation with clinically meaningful improvements in outcome. With the miniaturization of scopes and instruments, improvements in optics, and creative engineers, a host of new devices has become available for clinical testing and use. A growing community of pulmonologists is doing comparative effectiveness trials that test new technologies against the current standard of care. While more research is needed, it seems reasonable to provide an overview of pulmonary procedures that are in various stages of development, testing, and practice at this time. Five areas are covered: navigational bronchoscopy, endobronchial ultrasound, endoscopic lung volume reduction, bronchial thermoplasty, and pleural procedure. Appropriate training for clinicians who wish to provide these services will become an area of intense scrutiny as new skills will need to be acquired to ensure patient safety and a good clinical result.

The standard treatment of stage I non-small cell lung cancer (NSCLC) is lobectomy with systematic mediastinal lymph node evaluation. Unfortunately, up to 25% of patients with stage I NSCLC are not candidates for lobectomy because of severe medical comorbidity.

Immunosuppressive pharmacologic agents prescribed to patients with diffuse interstitial and inflammatory lung disease and lung transplant recipients are associated with potential risks for adverse reactions. Strategies for minimizing such risks include administering these drugs according to established, safe protocols; monitoring to detect manifestations of toxicity; and patient education. Hence, an evidence-based guideline for physicians can improve safety and optimize the likelihood of a successful outcome. To maximize the likelihood that these agents will be used safely, the American College of Chest Physicians established a committee to examine the clinical evidence for the administration and monitoring of immunosuppressive drugs (with the exception of corticosteroids) to identify associated toxicities associated with each drug and appropriate protocols for monitoring these agents.

Immunohistochemistry has come to occupy a key position among the armamentarium of tools pathologists apply to the evaluation of lung and pleural neoplasms. This technique uses antibodies that bind to specific antigens, usually proteins, enabling microscopic detection of the antigens. Over the last several decades, an impressive array of antibodies has become commercially available, and many of these antibodies have become integrated into the routine practice of pathology. Evaluation of tissue or cytology samples with these antibodies can facilitate determination of tumor type and site of origin. Comments citing results of immunohistochemical staining with these antibodies frequently appear in pathology reports and may be difficult to translate for those less familiar with the technique. This review presents, in two parts, common diagnostic applications of immunohistochemistry, with information about strategies taken for frequently encountered differential diagnostic scenarios. This, the first of two parts, offers a basic overview of the technique and discusses its applications in the diagnosis of common primary lung carcinomas.

Household air pollution (HAP) from biomass fuels, coal, and kerosene burned in open fires, primitive stoves, and lamps causes at least 2 million deaths per year. Many of these deaths occur in children <5 years of age with pneumonia and in women with COPD, lung cancer, and cardiovascular disease. HAP is inextricably linked to poverty, with activities to obtain fuel consuming a large proportion of the time and financial resources of poor households. Thus, fewer resources used in this way means less is available for basic needs like food, education, and health care. The burden of work and the exposure to smoke, particularly during cooking, are predominantly borne by women and children. Although historically HAP has not received sufficient attention from the scientific, medical, public health, development, and policy-making communities, the tide has clearly changed with the broad-based support and launch of the Global Alliance for Clean Cookstoves in 2010. There is now considerable reason for optimism that this substantial cause of cardiorespiratory morbidity and mortality will be addressed comprehensively and definitively. Drawing on our experience from four continents, we provide background information on the problem of HAP, health impacts of HAP, opportunities for research, and the current best solutions.

The biologic nature of COPD inflammation is not well understood and agents that inhibit inflammation in COPD are a major unmet need. However, a variety of agents that have the potential to be inhibitors of COPD inflammation are in various stages of development. Agents that have been approved for a non-COPD indication but that have potential for inhibiting COPD inflammation include the statins, some phosphodiesterase inhibitors, some long-acting β agonists, tiotropium bromide, the peroxisome proliferator-activated receptor-γ agonist rosiglitazone, and various monoclonal antibodies. New molecular entities that are being developed specifically as antiinflammatory agents for COPD include a variety of chemokine receptor antagonists, inhibitors of matrix metalloproteinases, inhibitors of p38 mitogen-activated protein kinases, and stem cells. Some other novel agents that are in preclinical or early clinical stages are mentioned.

Important cellular processes such as inflammation, apoptosis, differentiation, and proliferation confer critical roles in the pathogenesis of human diseases. In the past decade, an emerging process named "autophagy" has generated intense interest in both biomedical research and clinical medicine. Autophagy is a regulated cellular pathway for the turnover of organelles and proteins by lysosomal-dependent processing. Although autophagy was once considered a bulk degradation event, research shows that autophagy selectively degrades specific proteins, organelles, and invading bacteria, a process termed "selective autophagy." It is increasingly clear that autophagy is directly relevant to clinical disease, including pulmonary disease. This review outlines the principal components of the autophagic process and discusses the importance of autophagy and autophagic proteins in pulmonary diseases from COPD, α1-antitrypsin deficiency, pulmonary hypertension, acute lung injury, and cystic fibrosis to respiratory infection and sepsis. Finally, we examine the dual nature of autophagy in the lung, which has both protective and deleterious effects resulting from adaptive and maladaptive responses, and the challenge this duality poses for designing autophagy-based diagnostic and therapeutic targets in lung disease.