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From sneeze to wheeze: What we know about rhinovirus Cs.

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While the discovery of HRV-Cs is recent, there are no indications that they are new viruses, or that they are emerging in real-time. Genetically, HRV-Cs are most closely related to the members of HRV-A and HRV-B but even a small genetic difference can impart encompass significant changes to their clinical impact, complicated by a diverse human background of prior virus exposure and underlying host immune and disease variability. It is well known that HRVs are a major trigger of asthma exacerbations and HRV-Cs are now under investigation for their potential involvement in asthma inception.

The newly described HRV-Cs account for a large proportion of HRV-related illness, including common colds and wheezing exacerbations. HRV-Cs are genetically diverse and appear to circulate with seasonal variation, exchanging dominance with HRV-A. Whether HRV-Cs are consistently more pathogenic or "asthmagenic" is unproven. Antigenic diversity complicates passive and active prophylactic interventions (i.e. antibodies or vaccines), so further identification and characterisation of individual types (and their neutralising antigens) is likely to inform future preventive strategies. In the meantime, new antivirals should benefit groups at risk of the most severe disease.

Role of T cell immunity in recovery from influenza virus infection.

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Influenza virus infection has the potential to induce excess pulmonary inflammation and massive tissue damage in the infected host. Conventional CD4(+) and CD8(+) as well as nonconventional innate like T cells respond to infection and make an essential contribution to the clearance of virus infected cells and the resolution of pulmonary inflammation and injury.

Emerging evidence in recent years has suggested a critical role of local interactions between lung effector T cells and antigen presenting cells in guiding the accumulation, differentiation and function of effector T cells beyond their initial activation in the draining lymph nodes during influenza infection. As such, lung effector CD4(+) and CD8(+) T cells utilize multiple effector and regulatory mechanisms to eliminate virus infected cells as well as fine tune the control of pulmonary inflammation and injury.

Elucidating the mechanisms by which conventional and nonconventional T cells orchestrate their response in the lung as well as defining the downstream events required for the resolution of influenza infection will be important areas of future basic research which in turn may result in new therapeutic strategies to control the severity of influenza virus infection.

Contemporary topics in pediatric pulmonology for the primary care clinician.

Disorders of the respiratory system are commonly encountered in the primary care setting. The presentations are myriad and this review will discuss some of the more intriguing or vexing disorders that the clinician must evaluate and treat. Among these are dyspnea, chronic cough, chest pain, wheezing, and asthma. Dyspnea and chest pain have a spectrum ranging from benign to serious, and the ability to effectively form a differential diagnosis is critical for reassurance and treatment, along with decisions on when to refer for specialist evaluation.

Chronic cough is one of the more common reasons for primary care office visits, and once again, a proper differential diagnosis is necessary to assist the clinician in formulating an appropriate treatment plan. Infant wheezing creates much anxiety for parents and accounts for a large number of office visits and hospital admissions. Common diagnoses and evaluation strategies of early childhood wheezing are reviewed. Asthma is one of the most common chronic diseases of children and adults. The epidemiology, diagnosis, evaluation, treatment, and the patient/parent education process will be reviewed. A relatively new topic for primary care clinicians is cystic fibrosis newborn screening.

The rationale, methods, outcomes, and implications will be reviewed. This screening program may present some challenges for clinicians caring for newborns, and an understanding of the screening process will help the clinician communicate effectively with parents of the patient.

Targeting apoptosis pathways in lung cancer.

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Targeting apoptosis pathways in lung cancer.

Cancer Lett. 2013 May 28;332(2):359-68

Authors: Pore MM, Hiltermann TJ, Kruyt FA

Abstract
Lung cancer is a devastating disease with a poor prognosis. Non-small cell lung cancer (NSCLC) and small cell lung cancer (SCLC) represent different forms of lung cancer that are associated with distinct genetic causes and display different responses to therapy in the clinic. Whereas SCLC is often sensitive to chemotherapy at start of treatment, NSCLC are less chemo-sensitive. In NSCLC different histological subtypes are distinguished and increasing efforts are made to identify subtypes that respond to specific therapies, such as those harbouring epidermal growth factor receptor (EGFR) mutations that have benefit from treatment with EGFR inhibitors. Targeting of the apoptotic machinery represents another approach that aims to selectively kill cancer cells while sparing normal ones. Here we describe different ways that are currently explored to induce apoptosis in lung cancer cells, specifically pathways controlled by TNF-related apoptosis-inducing ligand (TRAIL), BCL-2 family members and apoptosis inhibitory proteins (IAPs). Preclinical studies are discussed and for some agents results from early clinical studies and future perspectives are considered.

PMID: 20974517 [PubMed - indexed for MEDLINE]

Primary Ciliary Dyskinesia: Recent Advances in Diagnostics, Genetics, and Characterization of Clinical Disease.

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Primary Ciliary Dyskinesia: Recent Advances in Diagnostics, Genetics, and Characterization of Clinical Disease.

Am J Respir Crit Care Med. 2013 Jun 24;

Authors: Knowles MR, Daniels LA, Davis SD, Zariwala MA, Leigh MW

Abstract
Primary ciliary dyskinesia (PCD) is a genetically heterogeneous recessive disorder of motile cilia that leads to oto-sino-pulmonary diseases and organ laterality defects in ~50% of cases. The estimated incidence of PCD is ~1 per 15,000 births, but the prevalence of PCD is difficult to determine, primarily because of limitations in diagnostic methods that focus on testing ciliary ultrastructure and function. Diagnostic capabilities have recently benefitted from 1) documentation of low nasal nitric oxide (nNO) production in PCD, and 2) discovery of biallelic mutations in multiple PCD-causing genes. The use of these complementary diagnostic approaches shows that at least 30% of PCD patients have normal ciliary ultrastructure. More accurate identification of PCD patients has also allowed definition of a strong clinical phenotype, which includes neonatal respiratory distress in >80% of cases, daily nasal congestion and wet cough starting soon after birth, and early development of recurrent/chronic middle-ear and sinus disease. Recent studies, using advanced imaging and pulmonary physiologic assessments, clearly demonstrate early onset of lung disease in PCD, with abnormal air flow mechanics by age 6-8 years that is similar to cystic fibrosis, and age-dependent onset of bronchiectasis. The treatment of PCD is not standardized, and there are no validated PCD-specific therapies. Most PCD patients receive sub-optimal management, which should include airway clearance, regular surveillance of pulmonary function and respiratory microbiology, and use of antibiotics targeted to pathogens. The PCD Foundation is developing a network of clinical centers, which should improve diagnosis and management of PCD.

PMID: 23796196 [PubMed - as supplied by publisher]

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