Race and Pulse Oximetry in Infants With Single Ventricles Undergoing Stage 1 Palliation.

This cross-sectional study investigates perioperative oxygen saturation differences in Black and White infants with single ventricles undergoing stage 1 palliation.

Field testing of an enzymatic quorum quencher coating additive to reduce biocorrosion of steel.

Microbial colonization can be detrimental to the integrity of metal surfaces and lead to microbiologically influenced corrosion. Biocorrosion is a serious problem for aquatic and marine industries in the world and severely affects the maritime transportation industry by destroying port infrastructure and increasing fuel usage and the time and cost required for maintenance of transport vessels. Here, we evaluate the potential of a stable quorum quenching lactonase enzyme to reduce biocorrosion in the field. Over the course of 21 months, steel samples coated with lactonase-containing acrylic paint were submerged at two different sites and depths in the Duluth-Superior Harbor (Lake Superior, MN, USA) and benchmarked against controls, including the biological biocide surfactin. In this experiment, the lactonase treatment outperformed the surfactin biocide treatment and significantly reduced the number of corrosion tubercles (37%; P < 0.01) and the corroded surface area (39%; P < 0.01) as compared to the acrylic-coated control coupons. In an attempt to evaluate the effects of signal disruption of surface microbial communities and the reasons for lower corrosion levels, 16S rRNA sequencing was performed and community populations were analyzed. Interestingly, surface communities were similar between all treatments, and only minor changes could be observed. Among these changes, several groups, including sulfate-reducing bacteria (SRB), appeared to correlate with corrosion levels, and more specifically, SRB abundance levels were lower on lactonase-treated steel coupons. We surmise that these minute community changes may have large impacts on corrosion rates. Overall, these results highlight the potential use of stable quorum quenching lactonases as an eco-friendly antifouling coating additive. IMPORTANCE Biocorrosion severely affects the maritime transportation industry by destroying port infrastructure and increasing fuel usage and the time and cost required to maintain transport vessels. Current solutions are partly satisfactory, and the antifouling coating still largely depends on biocide-containing products that are harmful to the environment. The importance of microbial signaling in biofouling and biocorrosion is not elucidated. We here take advantage of a highly stable lactonase that can interfere with N-acyl homoserine lactone-based quorum sensing and remain active in a coating base. The observed results show that an enzyme-containing coating can reduce biocorrosion over 21 months in the field. It also reveals subtle changes in the abundance of surface microbes, including sulfate-reducing bacteria. This work may contribute to pave the way for strategies pertaining to surface microbiome changes to reduce biocorrosion.

Validation of the Normalized Laryngeal Constriction Ratio in Normal and Disordered Swallowing.

PURPOSE: The timing of laryngeal vestibule closure (LVC) is important for airway protection during swallowing. However, it is unknown whether the extent of LVC contributes to airway protection. The goal of this study is to validate the extent of LVC via a measure called laryngeal constriction ratio (LCR). METHODS: A retrospective analysis of videofluoroscopic swallows was conducted on 38 stroke participants and 40 healthy controls. The LCR was calculated by deriving a size-normalized area of airspace from a 1) maximum closed laryngeal vestibule and a 2) maximum open laryngeal airspace (at rest). Airway invasion severity was derived via the Penetration-Aspiration Scale score. RESULTS: Six hundred forty-nine videofluoroscopic swallows were analyzed. A mixed model analysis revealed a statistically significant mean difference between the normalized laryngeal constriction ratios of healthy individuals (mean (m) = 0.003) versus older dysphagic patients (m = .026) (P = 0.001), quantifying less closure in older patients with dysphagia. Additionally, swallows with airway compromise had a statistically worse LCR when compared to swallows without airway compromise (P = 0.001). CONCLUSION: The normalized LCR might be a valid fluoroscopic surrogate measure for LVC and, furthermore, airway compromise during swallowing. By investigating spatial measurements in the laryngeal vestibule during safe and unsafe swallows, the LCR provides a direction for further research to allow for critical examination of the physiology relating to closure degree in order to precisely detect and treat abnormalities during swallowing. LEVEL OF EVIDENCE: 4 Laryngoscope, 130:E190-E198, 2020.

Association of Interstage Home Monitoring With Mortality, Readmissions, and Weight Gain: A Multicenter Study from the National Pediatric Cardiology Quality Improvement Collaborative.

BACKGROUND: Daily home monitoring of oxygen saturation and weight has been reported to improve outcomes for patients with single-ventricle heart disease during the period between stage I palliation and stage II palliation. However, these studies have been limited to single institutions and used historical control subjects. Our objective was to determine the association of various interstage home monitoring strategies with outcomes using a multicenter cohort with contemporary control subjects. METHODS AND RESULTS: We performed a retrospective cohort study using prospectively collected data from the National Pediatric Cardiology Quality Improvement Collaborative from 2008 to 2012. We compared interstage mortality, unscheduled readmissions, and change in weight-for-age Z score for various home monitoring strategies of oxygen saturation (n=494) or weight (n=472), adjusting for sex, syndrome, tricuspid regurgitation, arch obstruction, and shunt type. Overall interstage mortality was 8.1%, and 47% had ≥1 unscheduled readmission. We did not find any associations of home oxygen saturation or weight monitoring with mortality or readmission. Although there was no difference in weight-for-age Z score for daily (0.33±0.12) versus weekly (0.34±0.18, P=0.98) weight monitoring, daily home weight monitoring was superior to no home weight monitoring (-0.15±0.18; P<0.01). CONCLUSIONS: Home weight monitoring is associated with improved weight gain during the interstage period, but we did not find any benefits in other clinical outcomes for either home oxygen saturation monitoring or home weight monitoring.

Is Clinic Visit Frequency Associated with Weight Gain During the Interstage Period? A Report from the Joint Council on Congenital Heart Disease National Pediatric Cardiology Quality Improvement Collaborative (JCCHD-NPCQIC).

Growth problems are prevalent among infants with congenital heart disease. We sought to determine whether frequency of outpatient clinic visits correlated with weight gain in patients with hypoplastic left heart syndrome or variant during the interstage period between discharge from stage I palliation and presentation for stage II palliation (SIIP). Using prospectively collected data from the JCCHD NPC-QIC database from June 2008 to July 2013, we performed a retrospective cohort study assessing the association of days between clinic visits (DBV) with the change in weight-for-age z-score (WAZ) during the interstage period. Eligible subjects were those who survived to a SIIP performed at <270 days of age and had at least two outpatient clinic visits. There were 561 patients from 49 centers who fulfilled inclusion criteria. The average interstage change in WAZ was +0.22. The mean number of DBV was 16.1 days, and the average number of clinic visits was six. There was no correlation of change in WAZ with either DBV (r = 0.02, P = 0.62) or the number of visits (r = 0.03, P = 0.44). Subjects within this cohort are seen about every 2 weeks averaged over the interstage period. There is no correlation between interstage visit frequency and change in WAZ in this patient population. Further research is needed to describe differences in visit frequency as the patient progresses through the interstage period and to elucidate whether patient factors such as growth velocity are influencing visit frequency. The optimal visit frequency remains unknown.

Are study strategies related to medical licensing exam performance?

OBJECTIVE: To examine the relationship between study strategies and performance on a high stakes medical licensing exam entitled the United States Medical Licensing Examination Step 1. METHODS: The action research project included seventy nine student participants at the Texas A & M Health Science Center College of Medicine during their pre-clinical education. Data collection included pre-matriculation and matriculation academic performance data, standardized exam data, and the Learning and Study Strategies Instrument. Multiple regression analyses were conducted. For both models, the dependent variable was the Step 1 score, and the independent variables included Medical College Admission Test, Undergraduate Grade Point Average, Year 1 Average, Year 2 Average, Customized National Board of Medical Examiners Average, Comprehensive Basic Science Exam score, and Learning and Study Strategy Instrument sub-scores. Model 2 added Comprehensive Basic Science Self-Assessment average. RESULTS: Concentration (Model 1 - ß = .264; Model 2 - ß = .254) was the only study strategy correlated with Step 1 performance. The other statistically significant predictors were Customized National Board of Medical Examiners Average (ß = .315) and Year 2 Average (ß = .280) in Model 1 and Comprehensive Basic Science Self-Assessment Average (ß = .338) in Model 2. CONCLUSIONS: There does appear to be a relationship between the study strategy concentration and Step 1 licensing exam performance. Teaching students to practice and utilize certain techniques to improve concentration skills when preparing for and taking exams may help improve licensing exam scores.

Complement deposition and microglial activation in the outer retina in light-induced retinopathy: inhibition by a 5-HT1A agonist.

PURPOSE: Increasing evidence supports a role for complement in the pathogenesis of age-related macular degeneration (AMD). This study evaluated retinal microglia, T-lymphocytes, and complement deposition in a light-induced retinopathy model. The effect of a serotonin (5-hydroxytryptamine, 5-HT(1A)) agonist on these processes was investigated. METHODS: Rats were dark adapted for 24 hours before a 6-hour blue light exposure. Some animals were predosed subcutaneously with AL-8309A. Retinas were evaluated at different times after light exposure. Paraffin sections were stained with antibody for a microglial marker (Iba1), a T-lymphocyte marker (CD3), and complement components C1q, C3, factor B, factor H, and membrane attack complex (MAC). RESULTS: Light exposure resulted in substantial photoreceptor and RPE loss. Robust microglia activation and migration to the outer retina occurred rapidly. Substantial T-lymphocyte recruitment did not occur. Complement alternative pathway was strongly activated, resulting in the deposition of C3, factor B, factor H, and MAC in the area of photic lesions. Dosing with AL-8309A prevented retinal lesions and decreased microglia activation/recruitment and complement deposition in the outer retina. CONCLUSIONS: In blue light exposed retinas, microglia were activated and migrated toward the outer retina, whereas a T-lymphocyte response was minimal. The innate immune system was markedly activated, with substantial complement deposition in the outer retina after light exposure. This complement deposition was prevented by AL-8309A. This model may be useful in the evaluation of complement inhibitors and other neuroprotectants intended for ocular use. AL-8309 is under evaluation in the clinic and may be useful in the treatment of AMD.

Electroclinical features of absence seizures in sleep.

PURPOSE: To analyze electroclinical features of absence seizures during sleep. PRINCIPAL RESULTS: 30 children with genetic generalized epilepsy had 52 paroxysms of GSW >2s during sleep. 18/52 (35%) demonstrated a clinical sign. Ictal GSW lasted an average of 6.5s. CONCLUSION: Motor manifestations are seen during GSW>2s in sleep. 72% likely represent true ictal motor features while the rest may be serendipitous sleep phenomenon.

Electrocorticography and seizure outcomes in children with lesional epilepsy.

PURPOSE: The use of electrocorticographically (ECoG)-guided cortical resection in children with lesional epilepsy is controversial. Given the important developmental issues associated with recurrent childhood seizures, sustained seizure control is a key therapeutic goal. We therefore evaluated the effect of the decision to perform lesionectomy or ECoG-guided cortical resection on seizure outcome and surgical morbidity in the pediatric population. METHODS: We retrospectively analyzed seizure outcomes in 67 patients between the ages of 3 months and 16 years who underwent surgery for lesional epilepsy at British Columbia Children's Hospital. Thirty-four patients underwent ECoG, and 33 patients had lesionectomy without ECoG. RESULTS: One year post-operatively, 80% of patients who had ECoG-guided cortical resection or lesionectomy were seizure free. However, there was a trend toward improved seizure freedom in patients who had ECoG at most recent follow-up (79% patients with ECoG seizure free, vs. 61% with lesionectomy only; mean follow-up time 5.8 year, P=0.078). There was no increase in neurological morbidity in patients who had ECoG-guided cortical resection, and these patients were less likely to experience repeat epilepsy surgery. CONCLUSIONS: Overall, using ECoG to guide additional cortical resection may lead to more robust seizure freedom in children with lesional epilepsy without increasing their risk of surgical morbidity.

gammadelta T cells: the overlooked T-cell subset in demyelinating disease.

gammadelta T cells represent a small subpopulation of T cells expressing a restricted repertoire of T-cell receptors and, unlike alphabeta T cells, function more as cells of the innate immune system. These cells are found in skin and mucosal sites as well as secondary lymphoid tissues and frequently act as first line of defense sentinels. gammadelta T cells have been implicated in the pathogenesis of demyelinating disease, although little was known regarding their trafficking and effector functions. In this Mini-Review, we highlight recent studies demonstrating that gammadelta T cells migrate rapidly to the CNS during experimental autoimmune encephalomyelitis (EAE), the animal model for multiple sclerosis. gammadelta T-cell trafficking to the CNS is independent of beta(2)-integrins and occurs well before onset of clinical signs of disease, peaking early during the acute phase of disease. gammadelta T-cell-mediated production of inflammatory cytokines, including interferon-gamma and tumor necrosis factor-alpha, appears critical for EAE development, suggesting that these cells may set the stage for activation of other subsets of infiltrating effector cells. These data suggest that gammadelta T cells or subsets of gammadelta T cells may represent a new therapeutic target in demeylinating disease.

Clonal composition of Escherichia coli causing community-acquired urinary tract infections in the State of Rio de Janeiro, Brazil.

Recent studies from North America and Europe have demonstrated community-wide clonal spread of uropathogenic Escherichia coli (UPEC). To investigate if a similar pattern of spread occurs in Brazil, we characterized UPEC from women with community-acquired urinary tract infection (UTI) in Rio de Janeiro. E. coli isolates from women with UTI in one public outpatient clinic were evaluated for antibiotic susceptibility, E. coli phylogenetic grouping, enterobacterial repetitive intergenic consensus (ERIC) 2 PCR and pulsed-field gel electrophoresis fingerprinting, and multilocus sequence typing. From March 2005 to November 2006, 344 patients were studied. Of these, 186 (54%) had confirmed UTI, 118 (63.4%) of which were caused by E. coli. More than 50% of these isolates were resistant to ampicillin and trimethoprim/sulfamethoxazole. Of these, 96 (81%) belonged to 19 ERIC2 clonal groups. The largest group included 15 isolates, all belonging to multilocus sequence typing group ST69 and phylogenetic group D; they had pulsed-field gel electrophoresis patterns sharing at least 89% similarity compared with the CgA reference strain ATCC BAA-457. CgA strains have been found to be widespread in the United States in the early 2000s. Clonal group E. coli strains accounted for a large proportion (52%) of all UTIs and 82% of the trimethoprim/sulfamethoxazole-resistant E. coli UTIs. Thus, as in North America and Europe, UPECs that cause UTI in Rio de Janeiro also show clonal distribution, and a substantial proportion of drug-resistant UTI is caused by a small set of genetically related E. coli strains.

Automatisms in absence seizures in children with idiopathic generalized epilepsy.

BACKGROUND: Automatisms are well recognized to occur in complex partial seizures; however, their occurrence in generalized epilepsies is not always appreciated. There has been considerable debate regarding the nature, triggers, and timing of automatisms in absence seizures. OBJECTIVES: To examine the frequency and nature of automatisms in new-onset absence seizures and assess the influence of the state of arousal, provocation, age, and epilepsy syndrome on the presence and type of automatisms. DESIGN: Analysis of absence seizures through video electroencephalogram (EEG) recordings. SETTING: British Columbia's Children's Hospital, Vancouver, British Columbia, Canada. PATIENTS: Seventy consecutive children with new-onset untreated absence seizures in idiopathic generalized epilepsy recruited between January 1, 1992, and June 30, 1997. MAIN OUTCOME MEASURES: Each seizure was analyzed for the presence and characteristics of automatisms. The influence of the following variables on the presence of automatisms was statistically analyzed: state of arousal (awake, drowsy, asleep), provocation (hyperventilation, photic stimulation), age, and epilepsy syndrome. RESULTS: Automatisms occurred in 163 of 405 seizures (40%) in 53 of 70 children (76%). Automatisms were more likely in longer seizures and hyperventilation. Only 23% of spontaneous awake seizures had automatisms. Automatisms were similar for an individual child; however, automatisms were not present in all their seizures. Age, epilepsy syndrome, or state of alertness had no effect on the presence of automatisms. CONCLUSIONS: Automatisms are frequently seen during childhood absence seizures. The high frequency of automatisms during EEG recordings is predominantly due to the effect of hyperventilation. Their preponderance during longer seizures may relate to opportunity for automatisms to occur. The characteristic pattern of automatisms suggests a reactive phenomenon to internal and external stimuli.

Gammadelta T cells in EAE: early trafficking events and cytokine requirements.

We have previously shown that gammadelta T cells traffic to the CNS during EAE with concurrently increased expression of beta(2)-integrins and production of IFN-gamma and TNF-alpha. To extend these studies, we transferred bioluminescent gammadelta T cells to WT mice and followed their movement through the acute stages of disease. We found that gammadelta T cells rapidly migrated to the site of myelin oligodendrocyte glycoprotein peptide injection and underwent massive expansion. Within 6 days after EAE induction, bioluminescent gammadelta T cells were found in the spinal cord and brain, peaking in number between days 10 and 12 and then rapidly declining by day 15. Reconstitution of gammadelta T cell(-/-) mice with gammadelta T cells derived from beta(2)-integrin-deficient mice (CD11a, -b or -c) demonstrated that gammadelta T-cell trafficking to the CNS during EAE is independent of this family of adhesion molecules. We also examined the role of gammadelta T-cell-produced IFN-gamma and TNF-alpha in EAE and found that production of both cytokines by gammadelta T cells was required for full development of EAE. These results indicate that gammadelta T cells are critical for the development of EAE and suggest a therapeutic target in demyelinating disease.

EEG features of absence seizures in idiopathic generalized epilepsy: impact of syndrome, age, and state.

PURPOSE: Factors influencing the electroencephalography (EEG) features of absence seizures in newly presenting children with idiopathic generalized epilepsy (IGE) have not been rigorously studied. We examined how specific factors such as state, provocation, age, and epilepsy syndrome affect the EEG features of absence seizures. METHODS: Children with untreated absence seizures were studied using video-EEG recording. The influence of state of arousal, provocation (hyperventilation, photic stimulation), age, and epilepsy syndrome on specific EEG features was analyzed. RESULTS: Five hundred nine seizures were evaluated in 70 children with the following syndromes: childhood absence epilepsy (CAE) 37, CAE+ photoparoxysmal response (PPR) 10, juvenile absence epilepsy (JAE) 8, juvenile myoclonic epilepsy (JME) 6, and unclassified 9. Polyspikes occurred in all syndromes but were more common in JME. They were brought out by drowsiness and sleep in fragments of generalized spike and wave (GSW). Polyspikes were more likely to occur during photic stimulation, but were not influenced by age independently. GSW was more likely to be disorganized in JME than JAE, and in JAE than CAE. Increasing age and levels of arousal were more likely to result in organized GSW. Factors specific to each child independently influenced EEG features; the nature of these factors has not been identified. DISCUSSION: The EEG features of absence seizures are influenced by a complex interaction of age, epilepsy syndrome, level of arousal, provoking factors, and other intrinsic factors. Epilepsy syndrome alone cannot predict specific features of GSW; however, JME is more frequently associated with polyspikes and disorganization of the paroxysm.

Deletion of the G2A receptor fails to attenuate experimental autoimmune encephalomyelitis.

Lysophosphatidylcholine (LPC) is a chemotactic lysolipid produced during inflammation by the hydrolytic action of phospholipase A(2) enzymes. LPC stimulates chemotaxis of T cells in vitro through activation of the G protein-coupled receptor, G2A. This has led to the proposition that G2A contributes to the recruitment of T cells to sites of inflammation and thus promotes chronic inflammatory autoimmune diseases associated with the generation and subsequent tissue infiltration of auto-antigen-specific effector T cells. However, one study suggests that G2A may negatively regulate T cell proliferative responses to antigen receptor engagement and thereby attenuates autoimmunity by reducing the generation of autoreactive T cells. To address the relative contribution of these G2A-mediated effects to the pathophysiology of T cell-mediated autoimmune disease, we examined the impact of G2A inactivation on the onset and severity of murine experimental autoimmune encephalomyelitis (EAE), a model of multiple sclerosis (MS). Wild type (G2A(+/+)) and G2A-deficient (G2A(-/-)) C57BL/6J mice exhibited a similar incidence and onset of disease following immunization with MOG(35-55) peptide. Disease severity was only moderately reduced in G2A(-/-) mice. Similar numbers of MOG(35-55) specific T cells were generated in secondary lymphoid organs of MOG(35-55)-immunized G2A(+/+) and G2A(-/-) mice. Comparable numbers of T cells were detected in spinal cords of G2A(+/+) and G2A(-/-) mice. We conclude that the proposed anti-proliferative and chemotactic functions of G2A are not manifested in vivo and therefore therapeutic targeting of G2A is unlikely to be beneficial in the treatment of MS.

Group mentoring: a transition-to-work strategy.

Current financial constraints and workplace staffing shortages challenge the viability of using one-on-one mentoring models to support new graduate nurses. This article describes an innovative strategy for mentoring a large cohort of new nurses. Using a Group Mentoring Team, education specialists in a small rural hospital implemented a cost-effective program to help new nurses gain confidence and competence in the first year of nursing practice.

Factors influencing clinical features of absence seizures.

PURPOSE: The clinical features of absence seizures in idiopathic generalized epilepsy have been held to be syndrome-specific. This hypothesis is central to many aspects of epilepsy research yet has not been critically assessed. We examined whether specific factors such as epilepsy syndrome, age, and state determine the features of absence seizures. METHODS: Children with newly presenting absence seizures were studied using video electroencephalography (EEG) recording. We analyzed whether a child's epilepsy syndrome, age, state of arousal, and provocation influenced specific clinical features of their absence seizures: duration, eyelid movements, eye opening, and level of awareness during the seizure. RESULTS: Seizures (509) were evaluated in 70 children with the following syndromes: Childhood absence epilepsy (CAE), 37; CAE plus photoparoxysmal response (PPR), 10; juvenile absence epilepsy (JAE), 8; juvenile myoclonic epilepsy (JME), 6; unclassified, 9. Seizure duration was associated with epilepsy syndrome as children with JME had shorter seizures than in other syndromes, independent of age. Age independently influences level of awareness and eye opening. Arousal or provocation affected all features except level of awareness. Specific factors unique to the child independently influenced all features; the nature of these factors has not been identified. DISCUSSION: The view that the clinical features of absence seizures have syndrome-specific patterns is not supported by critical analysis. We show that confounding variables profoundly affect clinical features and that syndromes also show marked variation. Variation in clinical features of absence seizures results from a complex interaction of many factors that are likely to be genetically and environmentally determined.

Deletion of both ICAM-1 and C3 enhances severity of experimental autoimmune encephalomyelitis compared to C3-deficient mice.

Multiple sclerosis (MS) is an autoimmune disease characterized by central nervous system (CNS) inflammation and leukocyte infiltration, demyelination of neurons, and blood-brain barrier breakdown. The development of experimental autoimmune encephalomyelitis (EAE), the animal model for MS is dependent on a number of components of the immune system including complement and adhesion molecules. Previous studies in our lab have examined the role of C3, the central complement component, and intercellular adhesion molecule-1 (ICAM-1) a key cell adhesion molecule involved in leukocyte trafficking to sites of inflammation including the CNS. In these studies we demonstrated that myelin oligodendrocyte glycoprotein (MOG)-induced EAE is markedly attenuated in both ICAM-1(-/-) and C3(-/-) mice. Given the pivotal role that these proteins play in EAE, we hypothesized that EAE in ICAM-1(-/-) and C3(-/-) double mutant mice would likely fail to develop. Unexpectedly, EAE in ICAM-1(-/-)xC3(-/-) mice was only modestly attenuated compared to wild type mice and significantly worse than C3(-/-) mice. Leukocyte infiltration was commensurate with disease severity between the three groups of mice. Spinal cord T cells from ICAM-1(-/-)xC3(-/-) mice produced the highest levels of IFN-gamma and TNF-alpha, despite reduced disease severity compared to wild type mice. The mechanisms behind the elevated EAE severity in ICAM-1(-/-)xC3(-/-) mice may relate to altered homing of leukocytes or processing of self-antigens in the double mutant background.

Temporal changes in the prevalence of community-acquired antimicrobial-resistant urinary tract infection affected by Escherichia coli clonal group composition.

BACKGROUND: The changing prevalence of drug-resistant community-acquired urinary tract infection (UTI) is often attributed to local antimicrobial drug use or prescribing practices. However, recent molecular epidemiologic studies of community-acquired UTI suggest that other factors may play a greater role. METHODS: We conducted a multiyear, cross-sectional study to characterize temporal changes in the prevalence of drug-resistant community-acquired UTI at a university community in California. During four 3.5-month sampling periods, urine samples from patients consecutively presenting to the university health service with symptoms of UTI were cultured for Escherichia coli. Antimicrobial susceptibility and genotyping tests of the E. coli isolates were performed. RESULTS: We recovered 780 E. coli isolates from 1667 patients with UTI. The prevalence of trimethoprim-sulfamethoxazole, ciprofloxacin, and nitrofurantoin resistance showed no trend over the 4 periods. The prevalence of ampicillin resistance decreased significantly over the last 2 study periods. A single clonal group accounted for 75% of this decrease. Enterobacterial repetitive intergenic consensus 2 PCR-based genotyping revealed that only 4 large clonal groups accounted for 52% of the UTIs resistant to trimethoprim-sulfamethoxazole, ciprofloxacin, or nitrofurantoin. No initially pansusceptible clonal groups gained resistance over time. CONCLUSIONS: This study revealed no obvious trend in the prevalence of drug-resistant community-acquired UTI in a single community. Prevalence at any time was influenced by a small number of E. coli clonal groups. This observation suggests that the introduction of strains that are drug resistant into a community plays a greater role in changing the prevalence of drug-resistant UTI than does the drug use or prescribing habits in that community.

Differential expression of beta 2-integrins and cytokine production between gammadelta and alphabeta T cells in experimental autoimmune encephalomyelitis.

The expression of beta 2-integrins on gammadelta T cells in naïve mice or those with experimental autoimmune encephalomyelitis (EAE) remains poorly characterized. We compared beta 2-integrin expression and cytokine production between gammadelta and alphabeta T cells over the acute course of EAE. We observed that unlike in alphabeta T cells, beta 2-integrin expression on gammadelta T cells increased significantly from baseline, peaked at Day 10, and remained unchanged in the draining lymph nodes or declined in the spleen and CNS by Day 15. In addition, IFN-gamma- and TNF-alpha-producing gammadelta T cells infiltrated the CNS rapidly and produced significantly more of these cytokines than alphabeta T cells throughout the course of EAE. These results suggest unique roles for beta 2-integrins in the trafficking of gammadelta versus alphabeta T cells during EAE and that gammadelta T cells infiltrate the CNS rapidly, producing cytokines, which modulate acute disease.