Two cases of bronchiolitis obliterans organizing pneumonia syndrome after postoperative irradiation for breast cancer

We report two cases of bronchiolitis obliterans organizing pneumonia (BOOP) syndrome that developed after postoperative radiation therapy for breast cancer. In both patients, chest radiographs and computed tomography (CT) showed multiple consolidations outside the irradiation fields after several months of tangential radiation therapy. These patients were diagnosed as having radiation-associated BOOP syndrome, based on their clinical course and the findings on examination. After treatment with a systemic corticosteroid, radiographic consolidations and symptoms improved rapidly. In cases where consolidations appear outside the irradiated field, it is important to consider BOOP syndrome as a pulmonary complication of radiation therapy for breast cancer

Influence of corticosteroid therapy on the serum antibody response to influenza vaccine in elderly patients with chronic pulmonary diseases

Annual influenza vaccination is strongly recommended for patients with chronic pulmonary diseases, such as bronchial asthma, chronic obstructive pulmonary disease (COPD), and interstitial pulmonary diseases. However, many of these patients regularly receive systemic and/or inhaled corticosteroid therapy, and the impact of corticosteroid therapy on influenza vaccine efficacy and safety is unclear. Patients with chronic pulmonary diseases were enrolled in the study and divided into three groups based on their maintenance therapy: (A) without corticosteroid therapy (17 males, three females; mean age, 72.3 ± 7.9), (B) oral corticosteroid therapy (four males, seven females; mean age, 66.1 ± 10.6), and (C) inhaled corticosteroid therapy (eight males, nine females; mean age, 62.4 ± 16.0). All patients received influenza vaccine, and serum hemagglutination inhibition (HI) antibodies against influenza strains A/H1N1, A/H3N2, and B were measured at baseline (before vaccination) and 4-6 weeks after vaccination. Sufficient antibody titers or significant increases were observed after vaccination compared with titers before vaccination in all three groups. No systemic reactions were reported. Long-term oral/inhaled corticosteroid therapy was not associated with vaccination side effects and did not affect the immune response to the influenza vaccine

Enhanced interleukin-10 signaling with 14-member macrolides in lipopolysaccharide-stimulated macrophages

Immunomodulatory effects of 14-member macrolides, namely erythromycin (EM) and clarithromycin (CAM), have been reported in chronic respiratory infectious diseases. It has been suggested that 14-member macrolides have immunomodulatory effects on various lung cells such as alveolar macrophages. Interleukin (IL)-10 is an immunomodulatory cytokine that performs an irreplaceable role in negatively regulating inflammation, primarily via a mechanism that selectively blocks the expression of pro-inflammatory genes. It activates sig-nal transducer and activator of transcription (STAT)-3, and subsequently induces the suppres-sor of cytokine signaling-3 (SOCS-3), resulting in the resolution of inflammatory response in macrophages. However, it has been still unclear whether 14-member macrolides exert immu-nomodulatory effects via IL-10 signaling pathway. We aimed to evaluate whether 14-member macrolides affect the IL-10 signaling pathway. The RAW264.7 macrophage cell line was pre-treated with EM or CAM, and stimulated with lipopolysaccharide (LPS). The levels of IL-10, IL-10 receptor, phosphorylated (p) STAT-3, and SOCS-3 were determined by RT-PCR, ELISA and immunoblotting. We observed increased levels of IL-10, p-STAT-3 and SOCS-3 in the treated cells. In addition, while the levels of tumor necrosis factor-α 6 h after LPS stimulation was equal between vehicle-treated and CAM-treated macrophage cells, those of CAM-treated cells were repressed 36 h following LPS stimulation, compared with those of the control cells. Therefore, the 14-member macrolides may initiate an early resolution of inflammation, in part, via the enhancement of the IL-10/STAT-3/SOCS-3 pathway

Management of ostium secundum atrial septal defect in the era of percutaneous trans-catheter device closure: 7-Year experience at a single institution

AbstractObjectivesThis study aimed to review the single institutional experience of the repair of secundum atrial septal defect (ASD) after the initiation of percutaneous trans-catheter device closure, to confirm the current management strategy and outcomes.MethodsFrom August 2005 to December 2012, a total of 1026 (659 females, age 27±21 years) consecutive patients underwent the repair of ASD. Including eight patients who converted to surgical repair, 317 patients (31%) underwent surgical repair and 709 (69%) underwent trans-catheter device closure.ResultsAn embolized device into the left atrium was surgically retrieved in one patient soon after trans-catheter device closure without any postoperative complications. The other patient developed left atrium to aorta fistula due to late erosion, and required the removal of implanted device and patch closure of fistula and ASD 3 months after trans-catheter device closure. Whereas serious central nerve system complications occurred in three patients after the surgical repair including a 75-year-old patient with postoperative transient atrial fibrillation who subsequently developed aspiration pneumonia and died; there were no mortalities and no morbidities associated with cranial nerve function after trans-catheter device closure. A number of patients approached through partial sternotomy with limited skin incision have increased per year, and the length of skin incision was 5.1±1.2cm in pediatric patients weighing less than 15kg (n=40), 6.9±1.9cm in the remaining pediatric patients (n=91), and 10.0±2.5cm in young adult females (n=10).ConclusionPercutaneous trans-catheter ASD closure was safely performed under the support of a surgical team. The cosmetic outcome of surgical closure is improving after initiation of partial sternotomy via limited skin incision for the pediatric population and young adult females. Prior to the treatment, the physicians must thoroughly inform patients and families of the advantages and disadvantages of both treatment options

Spectral Analysis of Epicardial 60-lead Electrograms in Dogs during Acute Myocardial Ischemia

急性心筋虚血が心全サイクルにわたる各周波数の要素に及ぼす効果を分析した.7犬について冠動脈閉塞前後に60誘導心外膜心電図を記録し,単一平均と高速フーリエ変換を行い,逆変換を5周波数レンジで行った.心サイクル中の再構築した波形の絶対値を積分し,フィルターQRST面積地図として表示した.心筋虚血では初期QRSにおいてのみ低周波数(0-25Hz)の要素が有意に感じるが,これら要素はQRSの後半部とSTで著明に増加した.逆に心筋虚血はQRSの中間部の早期に中および高周波(25-250Hz)の要素を有意に減じるが,終末期QRSでの高周波数(80-250Hz)の要素を著明に増加した急性心筋虚血が心全サイクルにわたる各周波数の要素に及ぼす効果を分析した.7犬について冠動脈閉塞前後に60誘導心外膜心電図を記録し,単一平均と高速フーリエ変換を行い,逆変換を5周波数レンジで行った.心サイクル中の再構築した波形の絶対値を積分し,フィルターQRST面積地図として表示した.心筋虚血では初期QRSにおいてのみ低周波数(0-25Hz)の要素が有意に感じるが,これら要素はQRSの後半部とSTで著明に増加した.逆に心筋虚血はQRSの中間部の早期に中および高周波(25-250Hz)の要素を有意に減じるが,終末期QRSでの高周波数(80-250Hz)の要素を著明に増加した急性心筋虚血が心全サイクルにわたる各周波数の要素に及ぼす効果を分析した.7犬について冠動脈閉塞前後に60誘導心外膜心電図を記録し,単一平均と高速フーリエ変換を行い,逆変換を5周波数レンジで行った.心サイクル中の再構築した波形の絶対値を積分し,フィルターQRST面積地図として表示した.心筋虚血では初期QRSにおいてのみ低周波数(0-25Hz)の要素が有意に感じるが,これら要素はQRSの後半部とSTで著明に増加した.逆に心筋虚血はQRSの中間部の早期に中および高周波(25-250Hz)の要素を有意に減じるが,終末期QRSでの高周波数(80-250Hz)の要素を著明に増加した急性心筋虚血が心全サイクルにわたる各周波数の要素に及ぼす効果を分析した.7犬について冠動脈閉塞前後に60誘導心外膜心電図を記録し,単一平均と高速フーリエ変換を行い,逆変換を5周波数レンジで行った.心サイクル中の再構築した波形の絶対値を積分し,フィルターQRST面積地図として表示した.心筋虚血では初期QRSにおいてのみ低周波数(0-25Hz)の要素が有意に感じるが,これら要素はQRSの後半部とSTで著明に増加した.逆に心筋虚血はQRSの中間部の早期に中および高周波(25-250Hz)の要素を有意に減じるが,終末期QRSでの高周波数(80-250Hz)の要素を著明に増加し

Effect of antibiotic therapy on the inflammatory responses during streptococcal pneumonia in emphysematous mice

Background and objective: Bacterial infection is one of the most important causes of acute exacerbation of respiratory failure in patients with chronic obstructive pulmonary disease (COPD). There were few studies evaluating the effects of early intervention by antibiotic on respiratory bacterial infection in COPD subjects. We investigated the effect of early intervention by respiratory quinolone antibiotic on the systemic inflammatory responses induced by streptococcal pneumonia using a mouse model of experimental emphysema. Methods: Experimental pulmonary emphysema was developed by a single intratracheal instillation of porcine pancreatic elastase in ICR mice. Three weeks later, lethal doses of Streptococcus pneumoniae were intratracheally inoculated, followed by oral administration of 50 mg/kg body weight of Grepafloxacin (GPFX) every day from a day after tracheal inoculation. Results: While all emphysematous mice without GPFX treatment died within 8 days, all emphysematous mice with GPFX treatment survived. Seventy two hrs after infection, serum levels of tumor necrosis factor alpha, chemokine (C-X-C motif) ligand 1, and CXCL2 (Macrophage inflammatory protein-2) in emphysematous mice with antibiotic therapy were significantly lower than those without therapy. Conclusions: Thus, the early intervention using a respiratory quinolone antibiotic prevents emphysematous mice with pneumonia from severe systemic inflammation, and rescues these mice from death. These results suggest that early intervention using a respiratory quinolone may improve the outcome of the exacerbated COPD patients

The Relation of Prostate Tissue Protein Content, Nd : YAG Laser Transmissibility and Thermal Effect on Prostatic Hyperplasia

As our society ages, safe and minimally invasive treatment for the frequent occurrence of prostatic hyperplasia have been sought. We have performed prostatic hightemperature treatment for prostatic hyperplasia with the Prostalase using neodymium : yattriumaluminum garnet (Nd : YAG) laser for patients suffering from a bladder outlet obstruction secondary to benign prostatic hyperplasia (BPH). We used agars which included various densities of protein and skim milk as test materials to determine whether the exothermic mechanism of the Nd : YAG laser irradiation has an effect on protein molecules. By measuring the temperature inside the test materials and the irradiation transmissibility, we verified that in tissues with the same degree of color, the higher the protein content, the stronger the exothermic action of the Nd : YAG laser. In addition, in three human prostates obtained through pathological autopsy, the measurement of the protein content and the temperature inside the prostatic tissue in which prostatic thermal treatment had been performed showed that the exothermic action of the Nd : YAG laser varied according to the protein content: the higher the protein content, the stronger was the exothermic action. The present findings suggest that the temperature inside prostatic tissue reaches at least 60-65邃・with intissues with a protein content more than 23g/100g

Senescence marker protein 30 inhibits angiotensin II-induced cardiac hypertrophy and diastolic dysfunction

AbstractBackground and objectiveSenescence marker protein 30 (SMP30) is assumed to behave as an anti-aging factor. Recently, we have demonstrated that deficiency of SMP30 exacerbates angiotensin II-induced cardiac hypertrophy, dysfunction and remodeling, suggesting that SMP30 may have a protective role in the heart. Thus, this study aimed to test the hypothesis that up-regulation of SMP30 inhibits cardiac adverse remodeling in response to angiotensin II.MethodsWe generated transgenic mice with cardiac-specific overexpression of SMP30 gene using α-myosin heavy chain promoter. Transgenic mice and wild-type littermate mice were subjected to continuous angiotensin II infusion (800ng/kg/min).ResultsAfter 14days, heart weight and left ventricular weight were lower in transgenic mice than in wild-type mice, although blood pressure was similarly elevated during angiotensin II infusion. Cardiac hypertrophy and diastolic dysfunction in response to angiotensin II were prevented in transgenic mice compared with wild-type mice. The degree of cardiac fibrosis by angiotensin II was lower in transgenic mice than in wild-type mice. Angiotensin II-induced generation of superoxide and subsequent cellular senescence were attenuated in transgenic mouse hearts compared with wild-type mice.ConclusionsCardiac-specific overexpression of SMP30 inhibited angiotensin II-induced cardiac adverse remodeling. SMP30 has a cardio-protective role with anti-oxidative and anti-aging effects and could be a novel therapeutic target to prevent cardiac hypertrophy and remodeling due to hypertension

Diacylglycerol kinase ζ inhibits myocardial atrophy and restores cardiac dysfunction in streptozotocin-induced diabetes mellitus

<p>Abstract</p> <p>Background</p> <p>Activation of the diacylglycerol (DAG)-protein kinase C (PKC) pathway has been implicated in the pathogenesis of a number of diabetic complications. Diacylglycerol kinase (DGK) converts DAG to phosphatidic acid and acts as an endogenous regulator of PKC activity. Akt/PKB is associated with a downstream insulin signaling, and PKCβ attenuates insulin-stimulated Akt phosphorylation.</p> <p>Methods and Results</p> <p>We examined transgenic mice with cardiac-specific overexpression of DGKζ (DGKζ-TG) compared to wild type (WT) mice in streptozotocin-induced (STZ, 150 mg/kg) diabetic and nondiabetic conditions. After 8 weeks, decreases in heart weight and heart weight/body weight ratio in diabetic WT mice were inhibited in DGKζ-TG mice. Echocardiography at 8 weeks after STZ-injection demonstrated that decreases in left ventricular end-diastolic diameter and fractional shortening observed in WT mice were attenuated in DGKζ-TG mice. Thinning of the interventricular septum and the posterior wall in diabetic WT hearts were blocked in DGKζ-TG mice. Reduction of transverse diameter of cardiomyocytes isolated from the left ventricle in diabetic WT mice was attenuated in DGKζ-TG mice. Cardiac fibrosis was much less in diabetic DGKζ-TG than in diabetic WT mice. Western blots showed translocation of PKCβ and δ isoforms to membrane fraction and decreased Akt/PKB phosphorylation in diabetic WT mouse hearts. However in diabetic DGKζ-TG mice, neither translocation of PKC nor changes Akt/PKB phosphorylation was observed.</p> <p>Conclusion</p> <p>DGKζ modulates intracellular signaling and improves the course of diabetic cardiomyopathy. These data may suggest that DGKζ is a new therapeutic target to prevent or reverse diabetic cardiomyopathy.</p

Cardio-protective effects of pentraxin 3 produced from bone marrow-derived cells against ischemia/reperfusion injury

AbstractBackgroundInflammation is one of major mechanisms contributing to the pathogenesis of myocardial ischemia/reperfusion (I/R) injury. Pentraxin 3 (PTX3), produced in response to inflammatory signals, acts as a humoral arm of the innate immunity. Here we investigated the role of PTX3 produced from bone marrow-derived cells in myocardial I/R injury using PTX3-deficient (PTX3KO) mice.Methods and resultsPTX3KO mice and wild-type littermate (WT) mice were lethally irradiated and injected with bone marrow (BM) cells, generating four types of mice (WTWT-BM, WTPTX3KO-BM, PTX3KOWT-BM and PTX3KOPTX3KO-BM). Six weeks after BM transplantation, the myocardial I/R procedure (45min of left descending coronary artery ligation followed by 48h of reperfusion) was performed. Infarct size was greater in WT and PTX3KO mice with BM from PTX3KO donor (WTPTX3KO-BM and PTX3KOPTX3KO-BM) compared with WT and PTX3KO mice with BM from WT donor (WTWT-BM and PTX3KOWT-BM). Localization of PTX3 was observed in neutrophils and macrophages in WT and PTX3KO mice with BM from WT donor (WTWT-BM and PTX3KOWT-BM), while only in endothelial cells in WT mice with BM from PTX3KO donor (WTPTX3KO-BM). Infiltration of neutrophils and generation of reactive oxygen species (ROS) at ischemic border zones were greater in PTX3KO mice with BM from PTX3KO donor (PTX3KOPTX3KO-BM) than PTX3KO mice with BM from WT donor (PTX3KOWT-BM). Plasma levels and cardiac expressions of interleukin-6 were higher in PTX3KO mice with BM from PTX3KO donor (PTX3KOPTX3KO-BM) than PTX3KO mice with BM from WT donor (PTX3KOWT-BM). However, no significant differences in infarct size, infiltration of neutrophils, generation of ROS and plasma and cardiac levels of interleukin-6 were observed between WT and PTX3KO mice with BM from WT donor and between WT and PTX3KO mice with BM from PTX3KO donor. These results indicated that the lack of PTX3 produced from BM-derived cells, and not from cardiac resident cells, exacerbated myocardial injury after I/R.ConclusionPTX3 produced from bone marrow-derived cells plays a crucial role in cardiac protection against myocardial I/R injury by attenuating infiltration of neutrophils, generation of ROS and inflammatory cytokine