A BRIEF OVERVIEW OF COMPARTMENTAL MODELING FOR INTAKE OF PLUTONIUM VIA WOUNDS.

The aim of this study is to present several approaches that have been used to model the behavior of radioactive materials (specifically Pu) in contaminated wounds. We also review some attempts by the health physics community to validate and revise the National Council on Radiation Protection and Measurements (NCRP) 156 biokinetic model for wounds, and present some general recommendations based on the review. Modeling of intake via the wound pathway is complicated because of a large array of wound characteristics (e.g. solubility and chemistry of the material, type and depth of the tissue injury, anatomical location of injury). Moreover, because a majority of the documented wound cases in humans are medically treated (excised or treated with chelation), the data to develop biokinetic models for unperturbed wound exposures are limited. Since the NCRP wound model was largely developed from animal data, it is important to continue to validate and improve the model using human data whenever plausible.

Potential of phage cocktails in the inactivation of Enterobacter cloacae--An in vitro study in a buffer solution and in urine samples.

The objective of this study was to compare the dynamics of three previously isolated phages for Enterobacter cloacae in order to evaluate their ability to treat urinary tract infections (UTI). The phages genomes, survival, host range, were characterized, and the host-phage dynamics was determined in culture medium and urine samples. The presence of prophages in bacteria, host recovery and development of resistance to phage after treatment was also evaluated. The growth of the E. cloacae was inhibited by the three phages, resulting in a decrease of ≈3 log. The use of cocktails with two or three phages was significantly more effective (decrease of ≈4 log). In urine, the inactivation was still effective (≈2 log). Both phages were considered safe to inactivate the bacteria (no integrase and toxin codifying genes). Some bacteria remained viable in the presence of the phages, but their colonies were smaller than those of the non-treated control and were visible only after 5 days of incubation (visible after 24h in the control). A high bacterial inactivation efficiency with phage cocktails combined with the safety of the phages and their long periods of survival, even in urine samples, paves the way for depth studies, especially in vivo studies, to control urinary tract infection and to overcome the development of resistances by the nosocomial bacterium E. cloacae.

First detection of Klebsiella variicola producing OXA-181 carbapenemase in fresh vegetable imported from Asia to Switzerland.

BACKGROUND: The emergence and worldwide spread of carbapenemase-producing Enterobacteriaceae is of great concern to public health services. The aim of this study was to investigate the occurrence of carbapenemase-producing Enterobacteriaceae in fresh vegetables and spices imported from Asia to Switzerland. FINDINGS: Twenty-two different fresh vegetable samples were purchased in March 2015 from different retail shops specializing in Asian food. The vegetables included basil leaves, bergamont leaves, coriander, curry leaves, eggplant and okra (marrow). Samples had been imported from Thailand, the Socialist Republic of Vietnam and India. After an initial enrichment-step, carbapenemase-producing Enterobacteriaceae were isolated from two carbapenem-containing selective media (SUPERCARBA II and Brilliance CRE Agar). Isolates were screened by PCR for the presence of bla KPC, bla NDM, bla OXA-48-like and bla VIM. An OXA-181-producing Klebsiella variicola was isolated in a coriander sample with origin Thailand/Vietnam. The bla OXA-181 gene was encoded in a 14'027 bp region flanked by two IS26-like elements on a 51-kb IncX3-type plasmid. CONCLUSIONS: The results of this study suggest that the international production and trade of fresh vegetables constitute a possible route for the spread of carbapenemase-producing Enterobacteriaceae. The presence of carbapenemase-producing organisms in the food supply is alarming and an important food safety issue.

Complete genome sequence of the novel Escherichia coli phage phAPEC8.

Bacteriophage phAPEC8 is an Escherichia coli-infecting myovirus, isolated on an avian pathogenic Escherichia coli (APEC) strain. APEC strains cause colibacillosis in poultry, resulting in high mortality levels and important economic losses. Genomic analysis of the 147,737-bp double-stranded DNA phAPEC8 genome revealed that 53% of the 269 encoded proteins are unique to this phage. Its closest relatives include the Salmonella phage PVP-SE1 and the coliphage rv5, with 19% and 18% similar proteins, respectively. As such, phAPEC8 represents a novel, phylogenetically distinct clade within the Myoviridae, with molecular properties suitable for phage therapy applications.

Inhalation scintigraphy with an ultrafine aerosol in infants with functional bronchial stenoses.

Evaporation of Tc-99m pertechnetate at about 2500 degrees C on a carbon surface generates an ultrafine aerosol of Tc-99m-labeled carbon clusters (Technegas). The small particle size of about 100 nm enables the aerosol to behave similarly to a gas in its ability to penetrate. After inhalation, the radioactive particles adhere to the walls of the respiratory bronchioles and alveoli, or to the greater bronchial tubes if the airflow is not laminar. The high concentration of radioactivity in the argon carrier gas makes it possible to perform inhalation scintigraphy after only a few breaths. The authors investigated 24 infants with multiple events of bronchitis, most of whom had pneumonia. Seventeen patients had inhalation scintigraphy and bronchoscopy. Of these, 11 had scans diagnostic of bronchial stenosis and 6 had normal scans. Except for two pathologic scans, all scintigraphic findings matched well with the results of bronchoscopy. Seven patients had scintigraphy only, of which four were normal. Inhalation scintigraphy with Technegas is a reliable, nonhazardous procedure to preselect young patients for directed bronchoscopy.

Plasma growth hormone-releasing hormone levels in type 1 (insulin-dependent) diabetic children following a mixed meal.

Following a mixed meal, plasma hormone responses were measured in four type 1 diabetic children and in eight short normal children. Between 60 and 150 min after ingestion of the mixed meal there was a significant increase in circulating growth hormone-releasing hormone values both in diabetic and in normal children. Mean plasma GHRH peak values were not different between diabetic patients (27.0 +/- 3.9 ng/l) and controls (24.6 +/- 4.9 ng/l). No time relationship to spontaneous growth hormone peaks was observed. Whereas normal children showed a characteristic biphasic plasma somatostatin response, somatostatin plasma levels in diabetic children did not change. In normal children plasma insulin values increased between 30 and 150 min, but remained unchanged in type 1 diabetic patients. Blood glucose response was more pronounced in diabetic children than in short normal children. These results indicate that circulating growth hormone-releasing hormone does not play a dominant role in the regulation of insulin and somatostatin.

Plasma levels of growth hormone-releasing hormone and somatostatin in response to a mixed meal and during sleep in children.

Following a mixed meal, plasma levels of GHRH, GH, SRIH and insulin were measured in 7 prepubertal children with constitutional delay of growth and adolescence (CDGA) and in 3 children with proven GH-deficiency which responded to GHRH-injection. In children with CDGA, plasma levels of GHRH increased between 60 and 120 min (10.1 +/- 1.2 ng/l vs 25.5 +/- 4.4 ng/l; P less than 0.01). Although no GH increase occurred in patients with GH-deficiency, their plasma GHRH increases were comparable to those in CDGA children. No time relationship was present between circulating GHRH and GH, SRIH, or insulin, nor was there any correlation between their integrated hormone response areas. Sleep-induced plasma GHRH, GH and SRIH values were determined in 10 prepubertal children with CDGA. Spontaneous variations of plasma GHRH and GH values occurred with no temporal or quantitative relationship. SRIH values did not change during nocturnal sleep. In one child with GH-deficiency, comparable GHRH plasma fluctuations occurred, although GH values were all below 1 microgram/l. Our results support the concept that circulating GHRH does not only represent hypothalamic GHRH, but derives mainly from extrahypothalamic sources, possibly from the gastrointestinal tract.

Insulinhypoglycemia but not arginine infusion stimulates circulating plasma growth hormone-releasing hormone (GHRH) concentrations in children.

The effect of insulinhypoglycemia and arginine infusion on circulating concentrations of plasma growth hormone-releasing hormone (GHRH) and growth hormone (GH) has been studied in 24 children (4.4 to 14.3 years). Plasma GH and GHRH concentrations were determined by RIA. Basal plasma GHRH levels were detectable in the plasma of all patients ranging from 6.8 to 27.1 pg/ml. Injection of 0.1 U/kg body wt. insulin i.v. resulted in an increase of plasma GHRH levels (11.1 +/- 1.4 pg/ml vs. 18.8 +/- 2.6 pg/ml; P less than 0.01) preceding that of plasma GH (1.5 +/- 0.4 ng/ml vs. 13.6 +/- 1.3 ng/ml; P less than 0.01). Infusion of 0.5 gm/kg body wt. arginine hydrochloride did increase GH concentrations (2.0 +/- 0.6 ng/ml vs. 13.9 +/- 2.3 ng/ml; P less than 0.01) but did not change circulating plasma GHRH levels. Since the source of peripheral GHRH concentrations is not known the importance of these findings remains to be determined.

Effect of insulin-induced hypoglycemia on circulating levels of plasma growth hormone-releasing hormone and somatostatin in children.

In response to insulin-induced hypoglycemia (0.1 U insulin/kg body weight, i.v.) plasma levels of growth hormone-releasing hormone (GHRH), somatostatin (SLI), and growth hormone (GH) were measured by radioimmunoassay in 10 children with short stature. Insulin injection resulted in a significant increase in plasma GHRH values at 15 min (10.0 +/- 0.5 vs. 17.1 +/- 3.1 pg/ml; p less than 0.05) preceding the increase in plasma GH levels (1.5 +/- 0.4 vs. 13.6 +/- 1.2 ng/ml; p less than 0.001). SLI concentrations peaked between 15 and 60 min after insulin injection (20.9 +/- 1.2 vs. 47.1 +/- 6.2 pg/ml; p less than 0.01). No correlation was present between plasma GHRH or SLI levels and plasma GH concentrations. A significant negative correlation could be established between maximum increments of plasma GHRH and SLI levels (r = -0.843; p less than 0.01) in response to insulin injection. This finding suggests a possible relationship between these two hormones at peripheral level.

Serum level monitoring of a new slow release theophylline formulation in patients with chronic lung disease.

1 Serum theophylline levels were performed in 26 patients with chronic lung disease receiving rapid release theophylline (125 mg 6 hourly) and 28 patients receiving slow release theophylline (250 mg 12 hourly) under steady state conditions. 2 For rapid release theophylline the mean +/- s.d. serum theophylline levels at 0 and 2 h were 41.0 +/- 21.7 and 52.3 +/- 20.9 mumol l-1 respectively and for slow release theophylline at 0, 4 and 6 h 43.7 +/- 25.5, 50.9 +/- 23.0 and 51.7 +/- 26.4 mumol l-1 respectively. 3 Serum theophylline monitoring with slow release theophylline was performed in 70 patients with chronic lung disease. The initial dose was 250 mg administered 12 hourly. 4 The mean +/- s.d. steady state serum theophylline level achieved was 76.0 +/- 18.8 mumol l-1 and the mean +/- s.d. dose to produce this level was 9.4 +/ 2.3 mg kg-1 day-1. There was no correlation between dosage and serum theophylline level. 5 Sixty percent of patients required a dosage change for stabilization (375 to 1000 mg/day). Seventeen patients reported unwanted effects (nausea or tremor), which either settled quickly or resolved with dosage reduction. 6 Serum theophylline levels were obtained at different dosages in 44 patients and 18 patients demonstrated dose-dependent kinetics. 7 An initial dose of 500 mg/day is recommended and dosage increments should not exceed 125 mg/day with monitoring by serum theophylline levels.