Clinical characteristics of acute respiratory deterioration in pulmonary fibrosis associated with lung cancer following anti-cancer therapy

Background and objective: To clarify the clinical characteristics and risk factors for acute respiratory deterioration following anti‐cancer therapy in patients with pulmonary fibrosis (PF) and lung cancer. Methods: Patients with primary lung cancer and PF were identified by review of medical records. Of the 865 consecutive patients with primary lung cancer who had been treated between June 1999 and September 2007, 53 were diagnosed as having PF. This retrospective study analysed the prevalence of and risk factors for acute respiratory deterioration after treatment of lung cancer in these patients. Results: Acute respiratory deterioration was found in 10 (24%) of the 41 patients who received anti‐cancer therapy, and six (60%) of these patients died of respiratory failure. The incidence of acute respiratory deterioration was 28% (8/29) after chemotherapy and 16% (2/12) after surgery. Mortality after acute respiratory deterioration was 50% (4/8) among patients with idiopathic PF and 100% (2/2) among the patients with PF associated with rheumatoid arthritis. Logistic regression analysis revealed that a higher smoking index (cigarettes smoked per day × years of smoking) was a significant risk factor for acute respiratory deterioration (odds ratio: 1.002, P = 0.025). Conclusions: Patients with lung cancer who have pre‐existing PF should be carefully managed because of their high risk for developing acute respiratory deterioration after anti‐cancer therapy.     

A New Instrument for Measurement of Gastrointestinal Mucosal Color

Abstract: We designed and produced a new instrument that measures the color of the gastrointestinal mucosa during conventional endoscopic examination. The instrument consists fundamentally of an optical fiber sensor and a light source. One end of the optical fiber sensor is connected to the light source and a commercially available spectrophotometric colorimeter, while the other end is passed through the biopsy channel of a commercially available endoscope and placed in contact with the gastrointestinal mucosa. The color of the mucosa is then measured. To evaluate the accuracy of color measurement, the instrument was used to measure the color of 108 color chips belonging to the color range of the gastrointestinal mucosa or surrounding regions, selected from the Munsell Book of Color. The instrument correctly determined the relative hue, chroma and value of all 108 color chips tested. It also had the advantages of consistently measuring the color chips under standardized conditions and of promptly displaying the color readings during endoscopic examination. This instrument was also used to measure the color of the mucosa at different sites of the upper gastrointestinal tract in 20 patients. There were no noteworthy problems in using the instrument clinically. Mucosal color (hue, value and chroma) of the upper gastrointestinal tract was demonstrated to have specific characteristics according to the region measured. The instrument provided highly accurate, objective information that facilitated the distinction of slight differences in mucosal color, an important factor in the endoscopic diagnosis of gastrointestinal diseases.     

小鼠骨髓基质细胞Kusa-A1成骨分化中CBF1的作用

目的揭示CBF1在骨髓基质细胞Kusa-A1成骨分化过程中的作用。方法采用基因转染法建立CBF1稳定过表达细胞系Kusa-A1/CBF1,检测其成骨活性。指标包括细胞钙沉积能力、碱性磷酸酶活性、体外钙化结节(CN)形成、实时PCR测定细胞骨钙素(OC)和骨桥蛋白(OPN)基因表达、蛋白印迹检测细胞RANKL蛋白。最后用报告基因法检测CBF1对HES1启动子活性的影响。结果经RT-PCR和Western blot鉴定,Kusa-A1/CBF1细胞建立成功。与对照细胞系Kusa-A1/host相比,Kusa-A1/CBF1细胞的钙沉积能力、CN形成能力均显著提高;Kusa-A1/CBF1细胞OC和OPN基因表达和RANKL蛋白水平明显高于对照细胞。瞬时转染Notch的细胞内结构域NICD促进HES1的启动子活性,这一作用被CBF1强烈抑制。结论CBF1可以促进Kusa-A1的成骨分化,该作用至少部分是通过影响Notch信号实现的。     

Double Ventricular Responses to a Single Atrial Depolarization in a Patient with Dual AV Nodal Pathways

Electrophysiological study was performed in a patient with atrioventricular nodal reentrant tachycardia (AVNRT). Double ventricular responses through dual AV nodal pathways were observed by atrial extrastimulus technique followed by initiation of AVNRT. The difference in conduction time between the slow and fast AV nodal pathways was longer than 320 msec. A ventricular extrastimulus delivered during sinus rhythm, which was not followed by ventriculoatrial conduction, also induced AVNRT. These findings indicated the presence of an antegrade critical delay and retrograde block in the slow AV nodal pathway, criteria necessary for the occurrence of a double ventricular response.