A school microepidemic of tuberculosis.

BACKGROUND: Microepidemics of tuberculosis continue to occur in countries with a low incidence of tuberculosis. METHODS AND RESULTS: A microepidemic of tuberculosis in a secondary school with 604 girls in Cork city, Ireland, in 1986 with follow up to 1990 is described. Neonatal BCG vaccination was discontinued in the city in December 1972 so most of the 342 pupils who had received BCG were aged 14 years or more. Six active cases and 75 tuberculin positive cases were found. Four of the six girls with active disease had had neonatal BCG. The 75 pupils with a positive (grade 3 or 4) Heaf test response were given chemoprophylaxis with rifampicin and isoniazid for six months; none had developed active tuberculosis four years later. The brother of the girl who was the probable index case, however, developed active tuberculosis in 1988 despite similar chemoprophylaxis. CONCLUSION: The episode highlights the fact that children who have had neonatal BCG can develop active tuberculosis as teenagers.     

Regulation of muscarinic receptors by intrahippocampal injections of gallamine.

Multiple intrahippocampal injections of gallamine impair performance of a representational memory task in rats. The binding of [3H]-(-)-quinuclidinyl benzilate (QNB) to rat brain sections was measured to determine if changes in receptor binding were associated with the deleterious effects of gallamine. [3H]-(-)-QNB binding to sections taken from gallamine-injected animals was compared with binding in saline-injected control animals. Autoradiographic analyses indicated an increase in [3H]-(-)-QNB binding sites within all layers of the cerebral cortex and in the superior colliculus in gallamine-treated animals as compared to saline-injected controls. Significant increases were noted in cortical layers IV and V (P less than 0.025) in gallamine-treated animals. No significant changes (P greater than 0.05) in the number of binding sites were observed in the hippocampus, neostriatum or various thalamic nuclei. The ability of unlabeled pirenzepine, gallamine and carbamylcholine to inhibit 0.2 nM [3H]-(-)-QNB binding also was measured to determine changes in the distribution of receptor subtypes. No significant changes were observed in any brain region for the binding of the selective antagonists pirenzepine and gallamine or the agonist carbamyl-choline. Although other possibilities are considered, the data suggest that an increase in the number of muscarinic receptors may contribute to the observed behavioral deficits associated with long-term gallamine treatment.     

Does antenatal identification of small-for-gestational age fetuses significantly improve their outcome?

OBJECTIVES: Most obstetric clinics have a program for the identification of small-for-gestational age (SGA) fetuses because of the increased risk of fetal complications that they present. We have a structured model for the identification and follow-up of SGA pregnancies. We aimed to determine whether the recognition of SGA antepartum improves fetal outcome. METHODS: All pregnancies at Malm? University Hospital from 1990 to 1998 (n = 26 968) were reviewed. SGA fetuses identified prior to delivery (n = 681) were compared with those not identified (n = 573). Also, all pregnancies with SGA fetuses were compared with those appropriate-for-gestational age (AGA) (n = 24 585). The risk of serious fetal complications (hypoxic encephalopathy grade 2 or 3, intracranial hemorrhage, Apgar score <4 at 5 min, neonatal convulsions, umbilical pH <7.0, cerebral palsy, mental retardation, stillbirth, intrapartum or infant death) was assessed with cross-tabulation and logistic regression analysis, adjusted for gestational age and degree of SGA. RESULTS: When compared with SGA fetuses identified before delivery (54%), SGA fetuses not identified before delivery were characterized by a four-fold increased risk of adverse fetal outcome (odds ratio, 4.1; 95% CI, 2.5-6.8). Similarly, compared with AGA fetuses, SGA fetuses were associated with a four-fold increased risk of serious fetal complications. CONCLUSIONS: A structured antenatal surveillance program for fetuses identified as SGA results in a lower risk of adverse fetal outcome, compared with cases of SGA fetuses not identified antepartum.     

Reengineering transfusion and cellular therapy processes hospitalwide: ensuring the safe utilization of blood products

Efforts to make blood transfusion as safe as possible have focused on making the blood in the bag as disease-free as possible. The results have been dramatic, and the costs have been correspondingly high. Although blood services will have to continue to deal with emerging pathogens, efforts to reduce the transfusion of infectious agents presently posing a risk will require high incremental costs and result in only improvements of a small magnitude.
The other aspect of safe blood transfusion, the actual transfusion process performed primarily in hospitals, has been accorded considerably less interest. We should turn our attention to enhancing overall blood safety by focusing on improving the process of blood transfusion. Errors involving patient, specimen, and blood product identification put transfused patients at risk, increasing the mortality risk for some. Solutions that could improve the transfusion process are discussed as a focus of this article.     

Botulinum toxin and medical liability: is the patient sufficiently informed?]

INTRODUCTION: The use of botulinum toxin injection therapy is soaring significantly today, with an ever-wider field of applications despite well-known side effects of the treatment. This article aims at analysing the medicolegal practices of practitioners who use this therapy, especially the information given to patients and finding a common practice for providing that information. METHODS: We sent a questionnaire to 340 practitioners who might use the therapy (physiatrists, neurologists, ophthalmologists, ENT specialists, plastic surgeons) working in hospitals and in physical therapy and rehabilitation centres in France. Besides mentioning the possible side effects of the therapy, the questionnaire focused on how such information was transmitted before the injection. RESULTS: Data collection and analysis were performed by use of a spreadsheet software programme. A total of 124 questionnaires were analysed. We did not analyse the items dealing with side effects. Sixty-five percent of the responders said they did not seek statutory authorisation for injections. Only 31% provided written, detailed information and 12% required a signed consent form. Complaints were rare, approximately 12%, were written or verbal, and were always dismissed. DISCUSSION: Side effects after botulinum toxin injection are clearly described in the medical literature. Therefore, it is of utmost importance for this product to be used therapeutically and only by experienced therapists who will carefully respect the product's standard rules of use and inform their patients to the best of their ability. Issuing a detailed letter of information describing all the side effects seems necessary. We suggest a model information letter such as that provided to the patients in our facility. CONCLUSION: Botulinum toxin is a very worthwhile product for numerous abnormalities but has side effects, often brief, at the site of the injection. Therefore it is our duty to inform patients effectively.     

Quantitatively distinct requirements for signaling-competent cell spreading on engineered versus natural adhesion ligands.

To design synthetic microenvironments that elicit desired cell behaviors, we must better understand the molecular mechanisms by which cells interact with candidate biomaterials. Using cell lines with distinct alpha5beta1 integrin expression profiles, we demonstrate that this integrin mediates cell spreading on substrata coated with genetically engineered artificial extracellular matrix (aECM) proteins containing the RGD sequence (RGD-containing aECM protein [aRGD]) but lacking the PHSRN synergy site. Furthermore, aRGD-mediated adhesion stimulates an intracellular focal adhesion kinase (FAK) signal that is indicative of integrin tethering. Although both aRGD and the natural ECM protein fibronectin (FN) support alpha5beta1 integrin-mediated cell spreading, quantitative single-cell analysis revealed that aRGD-mediated spreading requires ten-fold greater threshold amount of integrin expression than FN-mediated spreading. Our analysis demonstrates that aRGD-based substrata mediate both biophysical (cell spreading) and biochemical (FAK signaling) events via the alpha5beta1 integrin, albeit with efficacy quantitatively distinct from that of natural ECM proteins that possess the full spectrum of adhesion and synergy domains.