Nosocomial Pseudomonas pickettii colonization associated with a contaminated respiratory therapy solution in a special care nursery.

Pseudomonas pickettii caused respiratory tract colonization in five infants in the special care nursery of a Chicago hospital. All organisms had the same antimicrobial susceptibilities. Endotracheal suctioning with saline from 5-ml unit-dose vials was identified by epidemiologic investigation as a risk factor for colonization. The vials of saline were contaminated with a strain of P. pickettii having the same antimicrobial susceptibility pattern as the isolates from patients. As part of an investigation of the manufacturing plant where the saline solution was produced, P. pickettii was recovered from deionized water used to make the product and from several sites in the processing line. Bypassing of a 180 degrees F (ca. 82 degrees C) water-holding tank appeared to be temporally related to product contamination. The ability of P. pickettii to survive and grow in this solution has been demonstrated in the laboratory. This outbreak demonstrates that, despite pertinent Food and Drug Administration regulations and company programs for identifying such contamination, intrinsically contaminated solutions can occasionally reach the bedside of the patient.     

Adherence of Streptococcus pneumoniae to Human Bronchial Epithelial Cells (BEAS-2B)

Pneumococcal adherence to alveolar epithelial cells and nasopharyngeal epithelial cells has been well characterized. However, the interaction of Streptococcus pneumoniae with bronchial epithelial cells has not been studied. We have now shown that pneumococci bind specifically to a human bronchial epithelial cell line (BEAS-2B cells). Pneumococci adhered to BEAS-2B cells in a time- and dose-dependent manner. These results suggest that the bronchial epithelium may serve as an additional site of attachment for pneumococci and demonstrate the utility of the BEAS-2B cell line for studying mechanisms of pneumococcal infection.     

Behavioral and hormonal responses to stress in the newborn mouse: Effects of maternal deprivation and chlordiazepoxide

These studies investigated behavioral and hormonal responses to stress in developing mice. Experiment 1 examined the effects of 24-hr maternal deprivation on corticosterone (CORT) secretion and ultrasonic vocalization (UVZ) rate in 4-, 8-, and 12-day-old mice. At these ages, exposure to a novel environment resulted in minimal changes in CORT secretion. Maternal deprivation increased pups′ CORT secretion in an age-dependent fashion but did not affect their UVZ rate. The aim of experiment 2 was to test the effects of cholordiazepoxide (CDP), an anxyolytic compound, on CORT secretion and UVZ in both normally reared and in maternally deprived 8-day-old mice. CDP administration elevated CORT increases in deprived (DEP) animals. CDP affected UVZ only in nondcprived (NDEP) animals: UVZ ratewas decreased by high CDP doses Overall, these findings demonstrate that the infant mouse shows a period of stress hyp9oresponsiveness similar to the rat and that maternal presence contributes to inhibit adrenocorticalactivity. CDP administration, butnot novelty exposure, increased CORT secretion in 8-day- old normally reared mice suggesting that during the stress hyporesponsive period, the HPA axis is capable of responding only to specific stimuli. Changes in HPA axis activity and UVZ rateresulting from maternal deprivation and/or CDP challenge do not seem to be directly related. ©1994 John Wiley & Sons, Inc.     

Effect of atropine and vagotomy on response of transplanted pancreas.

It is well established that atropine and vagotomy inhibit pancreatic enzyme secretion in response to intestinal stimulants such as fat or amino acids. These effects are usually attributed to interference with hypothetical vagal cholinergic mechanisms that facilitate release of cholecystokinin. To determine whether atropine or vagotomy interferes with release of humoral stimulants of pancreatic enzyme secretion, we studied their effect on protein secretion from an autotransplanted portion of pancreas in response to intestinal stimulants in dogs. The transplanted pancreas was as sensitive as the intact pancreas to stimulation by exogenous caerulein, a cholecystokinin-like peptide, and this response was not altered by atropine or vagotomy. Therefore, if vagotomy or atropine interferes with release of humoral pancreatic stimulants, they would be expected to reduce the response of the transplanted pancreas just as they do of the intact pancreas. Truncal vagotomy caused no significant change in protein secretion from the transplant in response to intestinal perfusion with sodium oleate or tryptophan. Atropine was tested only against sodium oleate and caused no change in response. We conclude that release of humoral pancreatic excitants of protein secretion in response to intestinal stimulants is not significantly changed by atropine or vagotomy.     

A quantitative approach to the design of antitumor drug dosage schedule via cell cycle kinetics and systems theory

A discrete-time kinetic model for chemotherapy was developed to deal with the effects of antitumor drugs on the cell cycle and proliferation kinetics of experimental tumor cell populations in which cell kinetic responses of chemotherapy are represented in terms of perturbation of cell kinetic parameters—cell age, cell size and DNA content distributions. The time-course behavior of these cell kinetic parameters was predicted by solving the discrete-time state equations which characterize the dynamics of tumor-drug interactions. The amount of antitumor drug administered was expressed to be the control function of the state equations and the transition matrix representing two modes of drug action, namely, cell kill and progression delay or accumulation of cells due to drug, was derived. The performance of the model, assessed by examining the effects of cell cycle stage-specific agents such as cytosine arabinoside on spontaneous AKR leukemia, compared favorably with experimental data. Utilizing an optimization scheme in engineering systems studies, an analytical method is described for optimizing the regimen of drug administration so as to maximize the effectiveness of drug dosage schedules and minimize the use of toxic amounts of the drug. The superiority of the schedule designed by an optimization scheme was evident at the termination of therapy, although the schedule designed by experimental trials reduced the number of surviving tumor cells more effectively than the one designed by an optimization scheme during the earlier therapy period. In the model, the proposed schedule will function more effectively for the entire therapy period when additional parameters of drug characteristics, such as the toxicity to the host and drug resistance, are encompassed.     

Exclusion of the alpha 1(II) cartilage collagen gene as the mutant locus in type IA osteogenesis imperfecta.

Using two restriction site polymorphisms within the structural gene coding for human type II collagen we have examined the segregation of this gene in three pedigrees with dominantly inherited osteogenesis imperfecta (Sillence type IA). We have demonstrated that the gene does not segregate with clinical expression of the disease and cannot, therefore, contain the mutation responsible for osteogenesis imperfecta in these families.     

Oral infections and systemic disease—an emerging problem in medicine

The relationship between oral and general health has been increasingly recognised during the past two decades. Several epidemiological studies have linked poor oral health with cardiovascular disease, poor glycaemic control in diabetics, low birth-weight pre-term babies, and a number of other conditions, including rheumatoid arthritis and osteoporosis. Oral infections are also recognised as a problem for individuals suffering from a range of chronic conditions, including cancer and infection with human immunodeficiency virus, as well as patients with ventilator-associated pneumonia. This review considers the systemic consequences of odontogenic infections and the possible mechanisms by which oral infection and inflammation can contribute to cardiovascular disease, as well as the oral conditions associated with medically compromised patients. A large number of clinical studies have established the clinical efficacy of topical antimicrobial agents, e.g., chlorhexidine and triclosan, in the prevention and control of oral disease, especially gingivitis and dental plaque. The possible risks of antimicrobial resistance are a concern, and the benefits of long-term use of triclosan require further evaluation. Oral infections have become an increasingly common risk-factor for systemic disease, which clinicians should take into account. Clinicians should increase their knowledge of oral diseases, and dentists must strengthen their understanding of general medicine, in order to avoid unnecessary risks for infection that originate in the mouth.