Catheter-based radiotherapy to inhibit restenosis after coronary stenting

BACKGROUND: In animal models of coronary restenosis, intracoronary radiotherapy has been shown to reduce the intimal hyperplasia that is a part of restenosis. We studied the safety and efficacy of catheter-based intracoronary gamma radiation plus stenting to reduce coronary restenosis in patients with previous restenosis. METHODS: Patients with restenosis underwent coronary stenting, as required, and balloon dilation and were then randomly assigned to receive catheter-based irradiation with iridium-192 or placebo. Clinical follow-up was performed, with quantitative coronary angiographic and intravascular ultrasonographic measurements at six months. RESULTS: Fifty-five patients were enrolled; 26 were assigned to the iridium-192 group and 29 to the placebo group. Angiographic studies were performed in 53 patients (96 percent) at a mean (+/-SD) of 6.7+/-2.2 months. The mean minimal luminal diameter at follow-up was larger in the iridium-192 group than in the placebo group (2.43+/-0.78 mm vs. 1.85+/-0.89 mm, P=0.02). Late luminal loss was significantly lower in the iridium-192 group than in the placebo group (0.38+/-1.06 mm vs. 1.03+/-0.97 mm, P=0.03). Angiographically identified restenosis (stenosis of 50 percent or more of the luminal diameter at follow-up) occurred in 17 percent of the patients in the iridium-192 group, as compared with 54 percent of those in the placebo group (P= 0.01). There were no apparent complications of the treatment. CONCLUSIONS: In this preliminary, short-term study of patients with previous coronary restenosis, coronary stenting followed by catheter-based intracoronary radiotherapy substantially reduced the rate of subsequent restenosis.     

Monoclonal antibodies to the alpha-subunit of the putative human H+,K+-ATPase encoded by the atp1al1 gene

The N-terminal fragment of ATP1AL1, the possible catalytic subunit of human ouabain-sensitive H+,K(+)-ATPase, was expressed in Escherichia coli cells as two recombinant proteins: the Ser14-Ile104 fragment or the same fragment containing His6 sequence at its N-end. The second protein was purified by metal-affinity chromatography and used as an antigen to construct two hybridoma lines producing antibodies of the IgM class. These monoclonal antibodies were shown to recognize not only the starting antigen but also the full-size recombinant ATP1AL1 protein and do not react with Na+,K(+)-ATPase.     

Surface enhanced Raman spectroscopy for characterization of structural characteristics of carbon chains in alpha1-acid glycoprotein and pseudoglycoproteins]

Surface-enhanced Raman scattering (SERS) spectroscopy was used to study the structure of carbohydrate chains in glycosylated forms of alpha 1-acid glycoprotein (AGP) and in pseudoglycoproteins obtained by transferring the carbohydrate chains of AGP to a polyacrylamide carrier. It was found that AGP-D glycoform and pseudoglycoproteins containing three or more glycans per molecule, which possess high immunomodulating activity, have a specific spatial organization of carbohydrate chains. This organization is maintained by the interaction of neighboring glycans with each other and does not depend on the nature of the carrier (whether it is polypeptide or polyacrylamide).     

Preliminary validation of the MMPI-A for a male delinquent sample: an investigation of clinical correlates and discriminant validity

Bacterial strains of Aeromonas salmonicida included in the recognized subsp. acromogenes, subsp. masoucida, and subsp. smithia in addition to the large number of strains not included in any of the described subspecies are referred to as atypical A. salmonicida. The atypical strains form a very heterogeneous group with respect to biochemical characteristics, growth conditions, and production of extracellular proteasess. Consequently, the present taxonomy of the species A. salmonicida is rather ambiguous. Atypical A. salmonicida has been isolated from a wide range of cultivated and wild fish species, non-salmonids as well as salmonids, inhabiting fresh water, brackish water and marine environments in northern and central Europe, South Africa, North America, Japan and Australia. In non-salmonid fish species, infections with atypical strains often manifest themselves as superficial skin ulcerations. The best known diseases associated with atypical A. salmonicida are carp Cyprinus carpio erythrodermatitis, goldfish Carassius auratus ulcer disease, and ulcer disease of flounder Platichthys flesus, but atypical strains are apparently involved in more disease outbreaks than previously suspected. Macroscopical and microscopical studies of ulcerated fish indicate internal organs are infrequently invaded by atypical A. salmonicida. This view is supported by the fact that atypical strains are irregularly isolated from visceral organs of ulcerated fish. High mortality caused by atypical A. salmonicida has been observed in populations of wild non-salmonids and farmed salmonids, although the association between the mortality in the wild fish stocks and atypical A. salmonicida has not always been properly assessed. In injection experiments the pathogenicity of the atypical strains examined showed large variation. An extacellular A-layer has been detected in different atypical strains, but virulence mechanisms different from those described for (typical) A. salmonicida subsp. salmonicida, for example an extracellular metallo-protease and a different iron utilization mechanism, have been described. Limited information is available about the ecology, spread and survival of atypical strains in water. The commonly used therapeutic methods for the control of diseases in farmed fish caused by atypical A. salmonicida are generally effective against the atypical strains. Resistance to different antibiotics and transferable plasmid encoding multiple drug resistance have been observed in atpical A. salmonicida. Studies aimed at producing a vaccine against atypical strains are in progress.     

Long-term results of surgical management of sleep disordered breathing: are our patients really benefiting?

The etiology of sleep disordered breathing is collapse or obstruction of the upper airway during sleep. This obstruction may be localized to one or two areas or may encompass the entire upper airway passages to include the nasal cavity, nasopharynx, oropharynx, hypopharynx, and larynx. The presurgical evaluation, which includes polysomnography, a comprehensive head and neck physical examination, fiberoptic nasopharyngoscopy, and lateral cephalometric analysis is essential in directing surgical therapy in a site specific approach. The surgical procedures available to address hypopharyngeal and base of the tongue collapse include inferior sagittal mandibular osteotomy and gengioglossus advancement, hyoid myotomy and suspension, laser midline glossectomy, lingualplasty, partial glossectomy, and maxillomandibular advancement surgery. The Riley-Powell-Stanford Surgical Protocol has proven to be an effective and safe method for controlling upper airway collapse in sleep disordered breathing.     

Bronchial ruptures are rare and should be surgically treated

Bronchial rupture in blunt trauma is caused by sudden compression of the chest with dislocation of the lungs. The less pliant bronchi may thus rupture. Bronchial rupture is rare in patients admitted alive. Bronchial rupture has been diagnosed in two of the last 275 severe chest traumas admitted to Ullev?l hospital since 1993 (0.7%). A 19-year-old male had total atelectasis of the lung 19 days after the trauma. A four-year-old boy experienced total collapse of the lung and became critically ill the fourth day after initial normalisation of the chest X-ray. Both patients were successfully operated on, with reconstruction of the left main bronchus in both cases, after 29 and seven days, respectively. In the child an upper lobectomy was necessary. These patients illustrate that with expectative treatment in bronchial rupture, serious complications may be experienced.     

Nuclear detection of cellular retinoic acid binding proteins I and II with new antibodies

Apart from the retinoic acid nuclear receptor family, there are two low molecular weight (15 kD) cellular retinoic acid binding proteins, named CRABPI and II. Mouse monoclonal and rabbit polyclonal antibodies were raised against these proteins by using as antigens either synthetic peptides corresponding to amino acid sequences unique to CRABPI or CRABPII, or purified CRABP proteins expressed in E. coli. Antibodies specific for mouse and/or human CRABPI and CRABPII were obtained and characterized by immunocytochemistry and immunoblotting. They allowed the detection not only of CRABPI but also of CRABPII in both nuclear and cytosolic extracts from transfected COS-1 cells, mouse embryos, and various cell lines.