Pyrimethamine-sulfadoxine treatment of uncomplicated Plasmodium falciparum malaria in Lao PDR

A 28-day in vivo treatment trial to evaluate the efficacy of pyrimethamine/sulfadoxine (Fansidar, PS) was conducted in 21 Lao patients with uncomplicated Plasmodium falciparum malaria. Sixteen patients (76%) were completely cured with PS without any reappearance of asexual stage parasitemia during the follow-up examination. On the other hand, 5 patients (24%) failed to respond to this trial medication, resulting in recrudescence of asexual stage P. falciparum malaria. PS resistance resulted in higher prevalence of post-treatment gametocytemia, 25% gametocyte carriers among PS sensitive cases versus 75% of the resistant cases. These findings suggest that although the level of PS resistance is still valid for treatment of malaria in the study area of Lao PDR, post-treatment induction of gametocytemia among resistant cases may result an increase in transmission rate of PS resistant falciparum malaria.     

Amino acid sequence of the T4 DNA helix-destabilizing protein.

The primary structure of the T4 single-stranded DNA-binding protein coded by gene 32 has been determined by manual and autoated sequencing of peptides derived from partial proteolysis, cyanogen bromide cleavage, and digestion with trypsin, chymotrypsin, and staphylococcal protease. Tryptic digestion of citraconylated or succinylated gene 32 protein yields five peptides containing 4, 27, 42, 65, and 163 residues, which can be separated by Sephadex chromatography. Each of the tryptic peptides was subjected to automated sequencing and, if necessary, more extensive cleavage. The intact protein contains 301 amino acids, has a molecular weight of 33,487, and can be specifically cleaved at lysines 21 and 253 by limited trypsin digestion. Previous studies have shown that the "B" region (residues 1-21), which has a charge of +4, is important for the protein-protein interactions involved in gene 32 protein self-association and cooperaive binding to single-stranded DNA. The "A" region (residues 254-301) has been implicated in controlling the helix-destabilizing "activity" of gene 32 protein and in interacting with other T4 DNA replication proteins. The A region has a charge of -10 and, in addition, contains two unusual stretches of four serine residues separated by glycine 284. The region between positions 73 and 115 contains 75% of the tyrosine residues and may be important for DNA binding.     

Survey to determine the efficacy and safety of guideline-based pharmacological therapy for chronic obstructive pulmonary disease patients not previously receiving maintenance treatment

Objective: To investigate the potential beneficial effects of guideline-based pharmacological therapy on pulmonary function and quality of life (QOL) in Japanese chronic obstructive pulmonary disease (COPD) patients without prior treatment.

Research design and methods: Multicenter survey, open-label study of 49 Japanese COPD patients aged ≥ 40 years; outpatients with >10 pack years of smoking history; ratio of forced expiratory volume in 1 s (FEV₁)/forced vital capacity (FVC) < 70%; predicted FEV₁ < 80%; treated with bronchodilators and/or inhaled corticosteroids as maintenance therapy until week 48.

Main outcome measures: The primary endpoint was change in pulmonary function (trough FEV₁, trough FVC); secondary endpoints were QOL and physical activity at 48 weeks after initiation of therapy.

Results: Airway reversibility was confirmed in untreated patients. Significant changes over time were not observed for FEV₁ and FVC, indicating lung function at initiation of treatment was maintained during the observation period. COPD assessment test scores showed statistical and clinical improvements. Cough, sputum, breathlessness, and shortness of breath were significantly improved.

Conclusions: Lung function and QOL of untreated Japanese COPD patients improved and improvements were maintained by performing a therapeutic intervention that conformed to published guidelines.     

Impact of air-conditioner outlet layout on the upward airflow induced by forced air warming in operating rooms

BackgroundPreviously, we found that an upward air current in the head area, induced by forced air warming (FAW), was completely counteracted by downward laminar airflow. However, this study did not include any consideration of the air-conditioner outlet layout (ACOL); hence, its impact remains unclear.MethodsThis study was performed in 2 operating rooms (ORs)—ISO classes 5 and 6, which are denoted as OR-5 and OR-6, respectively. Both ORs have distinct ACOLs. The cleanliness, or the number or ratio of shifting artificial particles was evaluated.ResultsDuring the first 5 minutes after particles generation, significantly more particles shifted into the surgical field in OR-5 when compared to OR-6 (13,587 [4,341-15,913] and 106 [41-338] particles/cubic foot, P < .0001). Notably, FAW did not increase the number of shifting particles in OR-6. The laminar airflow system fully counteracted the upward airflow caused by FAW in OR-6, where the ACOL covered the operating bed. However, this did not occur in OR-5, where the ACOL did not fully cover the operating bed.ConclusionsRegardless of cleanliness ability of OR, an ACOL that fully covers the operating bed can prevent upward airflow in the head area and reduce the number of artificial particles shifting into the surgical field, which are typically caused by FAW.     

F(ab')2 fragments of anti-Mo1 (904) monoclonal antibodies do not prevent myocardial stunning

To determine if inhibition of leukocyte adhesion and aggregation could improve postischemic ventricular dysfunction ("stunning"), a monoclonal antibody (904) that binds to the adhesion-promoting Mo1 glycoprotein on the cell surface of leukocytes was administered intravenously (0.5 mg/kg) to open-chest dogs before a 15-minute coronary occlusion. Ultrasonic crystals placed in ischemic and control myocardium were used to measure systolic wall thickening during a 15-minute occlusion of the left anterior descending artery and for 3 hours after reperfusion. Myocardial blood flow was measured with tracer-labeled microspheres before occlusion, after 10 minutes of occlusion, 3 minutes of reperfusion, and at 1 and 3 hours after reperfusion. Six animals receiving anti-Mo1 antibody had antibody excess demonstrated with immunofluorescence techniques at 5 minutes and 3 hours of reperfusion; this finding indicated saturation of binding sites. Five animals served as controls and received an antibody (murine immunoglobulin G) that does not influence neutrophils. The two groups did not differ hemodynamically during ischemia and reperfusion. Risk areas and myocardial blood flow were also not significantly different between the two groups. The main parameter used to define regional myocardial stunning, percentage systolic wall thickening in the ischemic/reperfused area, did not differ significantly between the two groups. Specimens from nonischemic myocardium were compared with ischemic specimens for myeloperoxidase content. There were no significant differences within or between groups. These data indicate that the anti-Mo1 monoclonal antibody (904) is not effective in improving the profound myocardial dysfunction that persists for 3 hours of reperfusion after 15 minutes of ischemia.     

A case of pulmonary squamous cell carcinoma coexisting with pulmonary actinomycosis]

A 71-year-old man was referred to our hospital complaining of cough. Chest radiography revealed a mass opacity in the right upper lung field. A transbronchial biopsy specimen revealed non-specific inflammatory changes. Percutaneous lung aspiration biopsy under ultrasound guidance demonstrated gram-positive rods, suggesting actinomyces. On the diagnosis of pulmonary actinomycosis, the patient was treated with penicillin-G and his symptoms were relieved. In a three-month follow-up, the mass shadow in the right upper lung field was found to have increased in size. Squamous cell lung cancer was diagnosed on the basis of repeated transbronchial tumor biopsies, and right upper lobectomy was performed. Most cases of pulmonary actinomycosis have been diagnosed from post-surgical tumor specimens taken on suspicion of the presence of lung cancer. However, the lung cancer in this case was difficult to diagnose because the lung cancer was co-existent with pulmonary actinomycosis.