Patients with MAC Lung Disease Have a Low Visceral Fat Area and Low Nutrient Intake.

Objective: This study aimed to examine the nutritional status and nutrient intake of patients with MAC lung disease with a focus on visceral fat area.

Patients And Methods: Among 116 patients of our hospital with nontuberculous mycobacteriosis who were registered between May 2010 and August 2011, 103 patients with MAC lung disease were included in this study. In all patients, nutritional status and nutrient intake were prospectively examined.

[A CASE OF PULMONARY MYCOBACTERIUM ABSCESSUS INFECTION SUCCESSFULLY TREATED WITH SHORT-TERM CAM, AMK, AND IPM/cs FOLLOWED BY LONG-TERM ORAL CAM AND LVFX].

A 78-year-old woman who had been treated for two years with ITCZ for chronic pulmonary aspergillosis associated with prior pulmonary tuberculosis was admitted to our hospital because of general fatigue and hemosputum along with deterioration of her chest radiographic findings. Mycobacterium abscessus had been isolated once from her sputum one year before admission. We performed fiberoptic bronchoscopy (FOB) in order to help establish a final diagnosis.

Transcriptional events during the recovery from MRSA lung infection: a mouse pneumonia model.

Community associated methicillin-resistant Staphylococcus aureus (CA-MRSA) is an emerging threat to human health throughout the world. Rodent MRSA pneumonia models mainly focus on the early innate immune responses to MRSA lung infection. However, the molecular pattern and mechanisms of recovery from MRSA lung infection are largely unknown.

Linezolid Exerts Greater Bacterial Clearance but No Modification of Host Lung Gene Expression Profiling: A Mouse MRSA Pneumonia Model.

Background: Linezolid (LZD) is beneficial to patients with MRSA pneumonia, but whether and how LZD influences global host lung immune responses at the mRNA level during MRSA-mediated pneumonia is still unknown.

Methods: A lethal mouse model of MRSA pneumonia mediated by USA300 was employed to study the influence of LZD on survival, while the sublethal mouse model was used to examine the effect of LZD on bacterial clearance and lung gene expression during MRSA pneumonia. LZD (100mg/kg/day, IP) was given to C57Bl6 mice for three days.

A Staphylococcus aureus pore-forming toxin subverts the activity of ADAM10 to cause lethal infection in mice.

Staphylococcus aureus is a major cause of human disease, responsible for half a million infections and approximately 20,000 deaths per year in the United States alone. This pathogen secretes α-hemolysin, a pore-forming cytotoxin that contributes to the pathogenesis of pneumonia. α-hemolysin injures epithelial cells in vitro by interacting with its receptor, the zinc-dependent metalloprotease ADAM10 (ref.

Clinical efficacy and safety of cefepime in febrile neutropenic patients with lung cancer.

Fever often occurs along with chemotherapy-induced neutropenia. This condition is referred to as febrile neutropenia (FN). Excellent guidelines for FN treatment have recently been published; however, there has so far been insufficient research concerning FN associated with solid tumors, especially in Japan.

[A case of secondary pulmonary alveolar proteinosis associated with myelodysplastic syndrome, complicated with disseminated M. abscessus infection].

A 27-year-old man was admitted to our hospital complaining of a persistent high fever since August 2007. Chest radiography showed infiltration shadows in the right lower lung field. Chest CT revealed scattered small nodular shadows and patchy consolidations in the right lower lobe.

Amphiregulin attenuates bleomycin-induced pneumopathy in mice.

Amphiregulin, an EGF receptor (EGFR) ligand, is essential for epithelial development in various organs. A recent report suggested that amphiregulin acts as a protective factor in a liver injury model. Little is known about the roles of amphiregulin in lung injury and pulmonary fibrosis.

TNF receptor 1 and 2 contribute in different ways to resistance to Legionella pneumophila-induced mortality in mice.

Legionella pneumophila is one of the most important pathogens which cause community-acquired pneumonia. Although TNF-alpha is considered to play an important role in response to bacteria, the role of the TNF-alpha receptor on L. pneumophila infection remains to be elucidated.

Biphasic effects of free radical scavengers against bleomycin-induced pulmonary fibrosis.

Oxidative stress plays a critical role in the development of pulmonary fibrosis. However, the effects of treatment with anti-oxidant agents against pulmonary fibrosis have not yet been thoroughly investigated. In this study, the effect of MCI-186, a novel free radical scavenger, on bleomycin-induced pulmonary fibrosis was investigated.

Tubulointerstitial nephritis and IgA nephropathy in a patient with advanced lung cancer treated with long-term gefitinib.

A 52-year-old Japanese female was admitted to our hospital for microhematuria, proteinuria and progressive renal dysfunction. Two years prior to admission, she was diagnosed with lung adenocarcinoma and multiple bone and brain metastases, and was treated with gefitinib (250 mg/day). Treatment for 6 months induced partial response with 30% regression of the primary lung tumor, and resolution of metastatic tumors.

Attenuation of pulmonary hypertension, but not emphysematous change, by breeding emphysema model mice at sea level.

Tumor necrosis factor (TNF)-alpha is a key pro-inflammatory cytokine, thought to be important in the pathogenesis of pulmonary emphysema. TNF-alpha overexpression in the lung leads to the phenotypic features of pulmonary emphysema, pulmonary hypertension, and right ventricular hypertrophy in mice bred in Denver, 5240 feet/1600 m of altitude. This study hypothesized that the altitude could affect the development of pulmonary emphysema as well as pulmonary hypertension.

[A case of pulmonary nocardiosis diagnosed five years after hemoptysis].

A 73-year-old man complaining of bloody sputum was admitted to our hospital in August 2000. His giant left lower lung field bulla had been removed in 1997, at which time atelectasis in left S10 was pointed out. Production of bloody sputum was stopped by the emergency bronchial artery embolization, and Nocardia species was found in the sputum.

The role of collagenases in experimental pulmonary fibrosis.

Matrix metalloproteinases (MMPs) expression plays a critical role in extracellular matrix deposition. Although several pieces of evidence have so far indicated that gelatinase contributes to the development of pulmonary fibrosis, the role of collagenase remains uncertain. In this study, we attempted to determine the role of collagenase using a bleomycin-induced pulmonary fibrosis model.

Successful treatment of refractory chronic necrotizing pulmonary aspergillosis with micafungin.

A 63-year-old man was admitted to our hospital because he complained of fever and productive cough; this was associated with cavitary infiltrates on his chest X-ray. Although several antibiotics were given, his symptoms did not improve. Bronchofiberscope investigation yielded Aspergillus fumigatus; thus, he was diagnosed with chronic necrotizing pulmonary aspergillosis.

Doxycycline attenuated lung injury by its biological effect apart from its antimicrobial function.

Antibiotics can have a biological effect apart from their anti-bacterial effect. We hypothesized that doxycycline could attenuate acute lung injury through its biological effect. Lipopolysaccharide or doxycycline-resistant Streptococcus pneumoniae was administered intratracheally into mice with the co-administration of doxycycline.

Doxycycline attenuated pulmonary fibrosis induced by bleomycin in mice.

The administration of doxycycline prior to bleomycin in mice attenuated pulmonary fibrosis. Bronchoalveolar neutrophil influx and gelatinase activity, but not caseinolytic activity, were attenuated by doxycycline. Established fibrosis was not affected by doxycycline.

Gorham's disease of the chest wall: CT and MR characteristics.

We report a case of Gorham's disease of the chest wall in a 29-year-old man. A chest radiograph showed osteolysis of the left first, second, and third ribs. CT and MR images revealed a soft tissue mass around the affected ribs.

[A case of pulmonary mycobacterium intracellulare infection complicated with pneumothorax and pleurisy].

A 74 year-old female complaining of increased cough and sputum was admitted to our hospital on June 14th 2004. She had been diagnosed as Mycobacterium intracellulare (M. intracellurare) infection since 2002 and had been treated from March to October 2003 in the Department of General Medicine in our hospital.

Serum CC-10 in inflammatory lung diseases.

Background: Although Clara cell secretory protein (CC-10) has been ascribed an anti-inflammatory role in lung diseases, its precise role remains unclear.

Objective: To further our understanding of the role of CC-10 in inflammatory lung diseases, CC-10 protein levels were measured.

Methods: Sera or bronchoalveolar lavage (BAL) fluids were collected from patients with different inflammatory lung diseases including bronchial asthma, chronic obstructive lung disease (COPD), sarcoidosis, idiopathic interstitial pneumonia (IIP), chronic eosinophilic pneumonia (CEP), pneumonia and lung cancer.

Anti-monocyte chemoattractant protein-1 gene therapy attenuates pulmonary fibrosis in mice.

Monocyte chemoattractant protein-1 (MCP-1) is a proinflammatory chemokine and may play an important role in the development of pulmonary fibrosis. We examined a new therapeutic strategy that comprises the transfection of the mutant MCP-1 gene into skeletal muscles as a biofactory for anti-MCP-1 therapy against bleomycin-induced pulmonary fibrosis in mice. Overexpression of the mutant MCP-1 gene at 10-14 days after intratracheal instillation of bleomycin resulted in decreased DNA damage, apoptosis, and pulmonary fibrosis at 14 days.

Induction of CDK inhibitor p21 gene as a new therapeutic strategy against pulmonary fibrosis.

Alveolar epithelial cells are known to be present at the primary site of lung damage in pulmonary fibrosis. Apoptosis has been implicated as being involved in epithelial cell damage and pulmonary fibrosis. Because the cyclin-dependent kinase inhibitor p21 induces G1 arrest and DNA repair and because it also prevents apoptosis in some cells, we hypothesized that p21 gene transfer may attenuate bleomycin-induced pulmonary fibrosis in mice, the pathogenesis of which likely involves epithelial cell apoptosis.

Mitochondria-mediated apoptosis of lung epithelial cells in idiopathic interstitial pneumonias.

We previously demonstrated that the up-regulation of p53, Fas, and DNA damage are present in lung epithelial cells from patients with idiopathic interstitial pneumonias (IIP). Fas ligation induces apoptosis of lung epithelial cells predominantly through the direct activation of the caspase cascade via caspase-8 activation, whereas the up-regulation of p53 and other cellular stresses can induce mitochondria-mediated apoptosis. In this study, we investigated the incidence of mitochondria-mediated apoptosis of epithelial cells in IIP.

MAP kinase activation and apoptosis in lung tissues from patients with idiopathic pulmonary fibrosis.

Three major MAP kinases (MAPKs), including extracellular signal-regulated kinase (ERK), c-jun N-terminal kinase (JNK), and p38 kinase (p38 MAPK), are involved in the regulation of lung inflammation and injury. This study investigated whether MAPKs are activated and associated with lung injury in lung tissues from patients with idiopathic pulmonary fibrosis (IPF). The expression of the active ERK, JNK, and p38 MAPK was examined using western blot analysis and immunohistochemistry and apoptosis was also examined by the TUNEL method, in lung tissues from ten patients with IPF obtained by thoracoscopic biopsy and in eight normal lung parenchyma specimens obtained by lobectomy for lung cancer.