Insights into the 'healthy immigrant effect': health status and health service use of immigrants to Canada

This paper combines multiple cross-sections of data drawn from the National Population Health Survey and Canadian Community Health Survey to confirm the existence of the 'healthy immigrant effect', specifically that immigrants are in relatively better health on arrival in Canada compared to native-born Canadians, and that immigrant health converges with years in Canada to native-born levels. The paper finds robust evidence that the healthy immigrant effect is present for the incidence of chronic conditions for both men and women, and results in relatively slow convergence to native-born levels. There is only weak evidence in terms of self-assessed health status. The inclusion of controls for region of origin and year of arrival does not account for the observed effects, although region of origin is an important determinants of immigrant health. The paper then considers some alternative explanations for the observed differences, and support is found for the idea that the healthy immigrant effect reflects convergence in physical health rather than convergence in screening and detection of existing health problems.     

A retrospective, comparative evaluation of dysglycemias in hospitalized patients receiving gatifloxacin, levofloxacin, ciprofloxacin, or ceftriaxone

STUDY OBJECTIVES: To compare rates of blood glucose abnormalities in hospitalized patients receiving fluoroquinolones or ceftriaxone, and to describe the characteristics of patients who develop blood glucose abnormalities while receiving these agents. DESIGN: Retrospective chart review. SETTING: Two community-based hospitals in the Houston, Texas, region. PATIENTS: Seventeen thousand one hundred eight patients who received fluoroquinolones or ceftriaxone; of those, 101 received levofloxacin, gatifloxacin, or ceftriaxone and also had serum glucose concentrations above 200 or below 50 mg/dl within 72 hours of receiving the drug. MEASUREMENTS AND MAIN RESULTS: Baseline demographics of patients with glucose abnormalities while receiving gatifloxacin, levofloxacin, or ceftriaxone were similar. Mean +/- SD patient age, weight, and estimated creatinine clearance were 67 +/- 17 years, 79 +/- 21 kg, and 52 +/- 32 ml/minute, respectively. Dysglycemia rates relative to treatment were as follows: gatifloxacin 76 (1.01%) of 7540 patients, levofloxacin 11 (0.93%) of 1179, ceftriaxone 14 (0.18%) of 7844, ciprofloxacin 0 (0%) of 545, and any fluoroquinolone 87 (0.94%) of 9264. Dysglycemia was more likely to occur in patients receiving any fluoroquinolone than in those receiving ceftriaxone (relative risk [RR] 3.32, 95% confidence interval (CI) 2.31-4.78, p < 0.05). The rate of dysglycemia did not differ with gatifloxacin and levofloxacin (RR 1.07, 95% CI 0.62-1.86, p = 0.8). Of the 101 patients with dysglycemias, hypoglycemia occurred in nine (9%) and hyperglycemia in 92 (91%). In a multivariate analysis of patients receiving fluoroquinolones, only concomitant sulfonylurea therapy was identified as an independent risk factor for development of hypoglycemia compared with patients who experienced hyperglycemia. CONCLUSION: In the 17,108 patients receiving a fluoroquinolone or ceftriaxone, the rate of dysglycemia was greater in those receiving levofloxacin or gatifloxacin than in those receiving ceftriaxone. However, no difference was noted in the rate of glucose abnormalities with levofloxacin versus gatifloxacin. Clinicians should be aware of dysglycemic events that may occur in patients receiving fluoroquinolones, especially in those with diabetes mellitus or those receiving sulfonylureas.     

Effect of temporal sparseness and dichoptic presentation on multifocal visual evoked potentials

Multifocal VEP (mfVEP) responses were obtained from 13 normal human subjects for nine test conditions, covering three viewing conditions (dichoptic and left and right monocular), and three different temporal stimulation forms (rapid contrast reversal, rapid pattern pulse presentation, and slow pattern pulse presentation). The rapid contrast reversal stimulus had pseudorandomized reversals of checkerboards in each visual field region at a mean rate of 25 reversals/s, similar to most mfVEP studies to date. The rapid pattern pulse presentation had pseudorandomized presentations of a checkerboard for one frame, interspersed with uniform grey frames, with a mean rate of 25 presentations/s per region per eye. The slow pattern pulse stimulus had six presentations/s per region per eye. Recording time was 5.3 min/condition. For dichoptic presentation slow pattern pulse responses were 4.6 times larger in amplitude than the contrast reversal responses. Binocular suppression was greatest for the contrast reversal stimulus. Consideration of the signal-to-noise ratios indicated that to achieve a given level of reliability, slow pattern pulse stimuli would require half the recording time of contrast reversal stimuli for monocular viewing, and 0.4 times the recording time for dichoptically presented stimuli. About half the responses to the slow pattern pulse stimuli had peak value exceeding five times their estimated standard error. Responses were about 20% smaller in the upper visual field locations. Space-time decomposition showed that responses to slow pattern pulse were more consistent across visual field locations. We conclude that the pattern pulse stimuli, which we term temporally sparse, maintain the visual system in a high contrast gain state. This more than compensates for the smaller number of presentations in the run, and provides signal-to-noise advantages that may be valuable in clinical application.     

Nomenclature proposal to describe vocal fold motion impairment

The terms used to describe vocal fold motion impairment are confusing and not standardized. This results in a failure to communicate accurately and to major limitations of interpreting research studies involving vocal fold impairment. We propose standard nomenclature for reporting vocal fold impairment. Overarching terms of vocal fold immobility and hypomobility are rigorously defined. This includes assessment techniques and inclusion and exclusion criteria for determining vocal fold immobility and hypomobility. In addition, criteria for use of the following terms have been outlined in detail: vocal fold paralysis, vocal fold paresis, vocal fold immobility/hypomobility associated with mechanical impairment of the crico-arytenoid joint and vocal fold immobility/hypomobility related to laryngeal malignant disease. This represents the first rigorously defined vocal fold motion impairment nomenclature system. This provides detailed definitions to the terms vocal fold paralysis and vocal fold paresis.     

Intraperitoneal Instillation of Bupivacaine for Reduction of Postoperative Pain After Laparoscopic Hysterectomy: A Double-Blind Randomized Controlled Trial

Study ObjectiveTo evaluate the effect on postoperative pain of intraperitoneal instillation of dilute bupivacaine at the conclusion of laparoscopic hysterectomy.DesignProspective, randomized, double-blind, placebo-controlled trial (Canadian Task Force classification I).SettingTertiary care, urban, academic teaching hospital.PatientsWomen aged 18 to 65 years undergoing total or supracervical laparoscopic hysterectomy with or without salpingo-oophorectomy.InterventionRandomization to intraperitoneal instillation of bupivacaine vs normal saline solution at the conclusion of laparoscopic hysterectomy performed because of benign indications.Measurements and Main ResultsA total of 160 patients consented to participate in the study and were randomized to receive either intraperitoneal instillation of 100 mg bupivacaine in 100 mL normal saline solution or 100 mL normal saline solution alone, at the conclusion of laparoscopic hysterectomy. Sixty seven of 77 patients (87%) in the treatment group and 73 of 80 patients (91%) in the placebo group completed the study. There were no significant differences in demographic profile, indication for hysterectomy, or number of previous surgeries between the two groups. All patients were prescribed a standardized routine postoperative analgesic regimen. Pain was measured by patient self-report using a 10-cm visual analog scale (VAS) at 1, 2, 4, 6, 12, and 24 hours postoperatively. Mean VAS scores at all time points were between 2.0 and 4.3 and were highest in the first postoperative hour. VAS scores were not significantly different between the two groups at any time point. None of the measured secondary outcomes were significantly different between the bupivacaine and placebo groups, including total postoperative opioid analgesic use in morphine equivalents (23.2 mg vs 27.5 mg; p = .09), length of hospital stay in hours (23.3 vs 23.0; p = .49), patient satisfaction on a 10-cm VAS (9.0 vs 8.2; p = .12), and complication rates (9% vs 15%; p = .35).ConclusionIntraperitoneal instillation of bupivacaine at the conclusion of laparoscopic hysterectomy does not reduce postoperative pain. Opioid analgesic use, length of hospital stay, overall patient satisfaction, and complication rates are also unchanged. Self-reported postoperative pain was low in both groups after this major gynecologic surgery performed laparoscopically.     

Population genetic tests suggest that the epidemiologies of JCV and BKV are strikingly different

The JCV and BKV viruses have been used as markers for the study of human evolution by assuming that these viruses coevolved with their host. However, it is currently unclear whether the details of the population expansion of these viruses and humans agree. To study this in more detail, large numbers of complete genomes were used for population genetic tests to detect evidence for population expansion. Relative to the neutral expectation of no selective forces and no demographic changes, the JCV data set contained a striking excess of synonymous and non-synonymous mutations that occur only once in the data set. The same was found for non-synonymous mutations of BKV, but not at all for synonymous mutations of BKV. The different frequency spectra of mutations in JCV and BKV do not result from the inclusion of patients with clinical symptoms associated with BKV and JCV, such as nephropathy or progressive multifocal leucoencefalopathy, nor from the different numbers of genomes available for JCV and BKV. Instead, the distribution of unique mutations and population genetic models that use older mutation classes indicate a striking difference of the historical demographies of JCV and BKV with only the former virus exhibiting the evidence of demographic expansion. Our analyses expand on recent population genetic analyses that document a global population expansion of JCV by taking into account the impact of deleterious mutations and by comparing both human viruses. The striking difference between the demographics of BKV and JCV suggests that important aspects of their epidemiology remain to be discovered.     

Replicating Adenovirus-Simian Immunodeficiency Virus (SIV) Vectors Efficiently Prime SIV-Specific Systemic and Mucosal Immune Responses by Targeting Myeloid Dendritic Cells and Persisting in Rectal Macrophages,Regardless of Immunization Route

Although priming with replicating adenovirus type 5 host range mutant (Ad5hr)-human immunodeficiency virus (HIV)/simian immunodeficiency virus (SIV) recombinants, followed by HIV/SIV envelope boosting, has proven highly immunogenic, resulting in protection from SIV/simian-human immunodeficiency virus (SHIV) challenges, Ad5hr recombinant distribution, replication, and persistence have not been examined comprehensively in nonhuman primates. We utilized Ad5hr-green fluorescent protein and Ad5hr-SIV recombinants to track biodistribution and immunogenicity following mucosal priming of rhesus macaques by the intranasal/intratracheal, sublingual, vaginal, or rectal route. Ad recombinants administered by all routes initially targeted macrophages in bronchoalveolar lavage (BAL) fluid and rectal tissue, later extending to myeloid dendritic cells in BAL fluid with persistent expression in rectal mucosa 25 weeks after the last Ad immunization. Comparable SIV-specific immunity, including cellular responses, serum binding antibody, and mucosal secretory IgA, was elicited among all groups. The ability of the vector to replicate in multiple mucosal sites irrespective of delivery route, together with the targeting of macrophages and professional antigen-presenting cells, which provide potent immunogenicity at localized sites of virus entry, warrants continued use of replicating Ad vectors.     

Induction of bone loss in DBA/1J mice immunized with citrullinated autologous mouse type II collagen in the absence of adjuvant

Joint damage in rheumatoid arthritis (RA) is characterized by cartilage and bone loss resulting in pain, deformity, and loss of joint function. Anti-citrullinated protein antibody (ACPA) has been implicated in RA pathogenesis and predicts radiographical joint damage and clinical severity. Therefore, the purpose of this study was to assess bone loss by micro-CT, histological joint damage, and ACPA levels using a mouse model of RA. Arthritis was induced by immunizing DBA/1 mice with autologous citrullinated type II mouse collagen (CIT-CII) weekly for 4 weeks. Mice immunized with autologous CII served as controls. At week 5, mice were killed, ACPA levels determined, and micro-CT performed to quantitatively analyze bone damage. Micro-CT analysis revealed significant loss of bone density, volume, and surface (p < 0.05) in bone peripheral to the inflamed joints of CIT-CII animals compared to CII controls. Histological staining demonstrated cartilage, proteoglycan, joint collagen, and bone collagen loss in the CIT-CII group compared to CII. Serum ACPA levels were increased (p = 0.03) in the CIT-CII group compared to CII, and these levels were inversely correlated with bone quantity and quality. In this study, we demonstrate that immunization with autologous CIT-CII initiates significant systemic bone and articular cartilage loss in the absence of adjuvant. Significant inverse correlations of circulating ACPA and bone quality/quantity were present. ACPA levels predict the adverse bone morphological changes in this model of early RA.     

Adrenergic signaling plays a critical role in the maintenance of waking and in the regulation of REM sleep

Many experiments have suggested that the adrenergic system is important for arousal and the regulation of sleep/wake states. Electrophysiological studies have found strong correlations between the firing of adrenergic neurons and arousal state. Lesions of adrenergic neurons have been reported to cause changes in sleep/wake regulation, although findings have been variable and sometimes transient. To more specifically address the role of adrenergic signaling in sleep/wake regulation, we performed electroencephalographic and electromyographic recordings in mice with a targeted disruption of the gene for dopamine beta-hydroxylase, the enzyme that converts dopamine to norepinephrine. These mice are unable to synthesize the endogenous adrenergic ligands norepinephrine and epinephrine. The mutant mice sleep approximately 2 h more each day. The decrease in waking is due to a considerable decrease in the duration of waking bouts in spite of an increase in the number of waking bouts and transitions from sleep to waking. In contrast, the amount of rapid-eye-movement (REM) sleep is only half that in control mice due to a decrease in the number and duration of REM sleep bouts. Delta power is selectively increased in the mutant mice, and there is much less variation in non-REM sleep delta power over 24 h. After 6 h of total sleep deprivation during the first half of the light period, there is no rebound recovery of sleep time in the mutant mice. These results provide genetic evidence that adrenergic signaling acts to maintain waking and is important for the regulation of REM sleep and possibly sleep homeostasis.