An elevational shift facilitated the Mesoamerican diversification of Azure-hooded Jays (Cyanolyca cucullata) during the Great American Biotic Interchange.

The Great American Biotic Interchange (GABI) was a key biogeographic event in the history of the Americas. The rising of the Panamanian land bridge ended the isolation of South America and ushered in a period of dispersal, mass extinction, and new community assemblages, which sparked competition, adaptation, and speciation. Diversification across many bird groups, and the elevational zonation of others, ties back to events triggered by the GABI. But the exact timing of these events is still being revealed, with recent studies suggesting a much earlier time window for faunal exchange, perhaps as early as 20 million years ago (Mya). Using a time-calibrated phylogenetic tree, we show that the jay genus Cyanolyca is emblematic of bird dispersal trends, with an early, pre-land bridge dispersal from Mesoamerica to South America 6.3-7.3 Mya, followed by a back-colonization of C. cucullata to Mesoamerica 2.3-4.8 Mya, likely after the land bridge was complete. As Cyanolyca species came into contact in Mesoamerica, they avoided competition due to a prior shift to lower elevation in the ancestor of C. cucullata. This shift allowed C. cucullata to integrate itself into the Mesoamerican highland avifauna, which our time-calibrated phylogeny suggests was already populated by higher-elevation, congeneric dwarf-jays (C. argentigula, C. pumilo, C. mirabilis, and C. nanus). The outcome of these events and fortuitous elevational zonation was that C. cucullata could continue colonizing new highland areas farther north during the Pleistocene. Resultingly, four C. cucullata lineages became isolated in allopatric, highland regions from Panama to Mexico, diverging in genetics, morphology, plumage, and vocalizations. At least two of these lineages are best described as species (C. mitrata and C. cucullata). Continued study will further document the influence of the GABI and help clarify how dispersal and vicariance shaped modern-day species assemblages in the Americas.

Causes of death and pathogen prevalence in bottlenose dolphins Tursiops truncatus stranded in Alabama, USA, between 2015 and 2020, following the Deepwater Horizon oil spill.

Between 2010 and 2014, an unusual mortality event (UME) involving bottlenose dolphins Tursiops truncatus occurred in the northern Gulf of Mexico, associated with the Deepwater Horizon oil spill (DWHOS). Cause of death (COD) patterns in bottlenose dolphins since then have not been analyzed, and baseline prevalence data for Brucella ceti and cetacean morbillivirus, 2 pathogens previously reported in this region, are lacking. We analyzed records from bottlenose dolphins stranded in Alabama from 2015 to 2020 with necropsy and histological findings to determine COD (n = 108). This period included another UME in 2019 associated with prolonged freshwater exposure. A subset of individuals that stranded during this period were selected for molecular testing for Brucella spp. and Morbillivirus spp. Causes of death for all age classes were grouped into 6 categories, including (1) human interaction, (2) infectious disease, (3) noninfectious disease (prolonged freshwater exposure and degenerative), (4) trauma, (5) multifactorial, and (6) unknown. Two additional categories unique to perinates included fetal distress and in utero pneumonia. Human interaction was the most common primary COD (19.4%) followed closely by infectious disease (17.6%) and noninfectious disease (freshwater exposure; 13.9%). Brucella was detected in 18.4% of the 98 animals tested, but morbillivirus was not detected in any of the 66 animals tested. Brucella was detected in some moderately to severely decomposed carcasses, indicating that it may be beneficial to test a broad condition range of stranded animals. This study provides valuable information on COD in bottlenose dolphins in Alabama following the DWHOS and is the first to examine baseline prevalence of 2 common pathogens in stranded animals from this region.

Hyaluronan promotes the regeneration of vascular smooth muscle with potent contractile function in rapidly biodegradable vascular grafts.

The regeneration of smooth muscle with physiological functions has been a key challenge in vascular tissue engineering. Hyaluronan (HA), as a major component of the extracellular matrix, plays a vital role in regulating tissue injury and repair. In this study, a biomimetic vascular graft was prepared by co-electrospinning of synthetic degradable polymers and native ECM components including collagen type-I as well as low and high molecular weight HA (LMW HA and HMW HA). Upon implantation in the rat abdominal aorta, the grafts exhibited sustained HA release that effectively enhanced the regeneration of vascular smooth muscle. Besides, LMW HA loaded vascular grafts demonstrated rapid endothelialization compared to the other groups. More importantly, HA-loaded poly(L-lactide-co-caprolactone) grafts demonstrated an optimal vascular media layer accompanied by well-organized elastin fibers after long-term implantation (6 months), and they maintained potent physiological function up to 1/3 that of the native artery. In contrast, inadequate smooth muscle regeneration was observed in poly(ε-caprolactone) grafts due to slow degradation restricting the regeneration. The mechanism was further investigated and explained by the HA-induced migration of smooth muscle cell (SMC) via CD44-mediated signaling. Besides, low molecular weight HA can promote the migration of vascular progenitor cells that further differentiate into SMCs. These results highlight the importance of HA in the regeneration of functional vascular smooth muscle, and provide a new insight into the fabrication of tissue engineering vascular grafts (TEVGs) via combining rapidly degradable polymers and bioactive ECM components that hold great translational potential.

DKK3 (Dickkopf 3) Alters Atherosclerotic Plaque Phenotype Involving Vascular Progenitor and Fibroblast Differentiation Into Smooth Muscle Cells.

OBJECTIVE: DKK3 (dickkopf 3), a 36-kD secreted glycoprotein, has been shown to be involved in the differentiation of partially reprogrammed cells and embryonic stem cells to smooth muscle cells (SMCs), but little is known about its involvement in vascular disease. This study aims to assess the effects of DKK3 on atherosclerotic plaque composition. APPROACH AND RESULTS: In the present study, we used a murine model of atherosclerosis (ApoE-/-) in conjunction with DKK3-/- and performed tandem stenosis of the carotid artery to evaluate atherosclerotic plaque development. We found that the absence of DKK3 leads to vulnerable atherosclerotic plaques, because of a reduced number of SMCs and reduced matrix protein deposition, as well as increased hemorrhage and macrophage infiltration. Further in vitro studies revealed that DKK3 can induce differentiation of Sca1+ (stem cells antigen 1) vascular progenitors and fibroblasts into SMCs via activation of the TGF-ß (transforming growth factor-ß)/ATF6 (activating transcription factor 6) and Wnt signaling pathways. Finally, we assessed the therapeutic potential of DKK3 in mouse and rabbit models and found that DKK3 altered the atherosclerotic plaque content via increasing SMC numbers and reducing vascular inflammation. CONCLUSIONS: Cumulatively, we provide the first evidence that DKK3 is a potent SMC differentiation factor, which might have a therapeutic effect in reducing intraplaque hemorrhage related to atherosclerotic plaque phenotype.

Vascular Stem/Progenitor Cell Migration Induced by Smooth Muscle Cell-Derived Chemokine (C-C Motif) Ligand 2 and Chemokine (C-X-C motif) Ligand 1 Contributes to Neointima Formation.

Recent studies have shown that Sca-1(+) (stem cell antigen-1) stem/progenitor cells within blood vessel walls may contribute to neointima formation, but the mechanism behind their recruitment has not been explored. In this work Sca-1(+) progenitor cells were cultivated from mouse vein graft tissue and found to exhibit increased migration when cocultured with smooth muscle cells (SMCs) or when treated with SMC-derived conditioned medium. This migration was associated with elevated levels of chemokines, CCL2 (chemokine (C-C motif) ligand 2) and CXCL1 (chemokine (C-X-C motif) ligand 1), and their corresponding receptors on Sca-1(+) progenitors, CCR2 (chemokine (C-C motif) receptor 2) and CXCR2 (chemokine (C-X-C motif) receptor 2), which were also upregulated following SMC conditioned medium treatment. Knockdown of either receptor in Sca-1(+) progenitors significantly inhibited cell migration. The GTPases Cdc42 and Rac1 were activated by both CCL2 and CXCL1 stimulation and p38 phosphorylation was increased. However, only Rac1 inhibition significantly reduced migration and p38 phosphorylation. After Sca-1(+) progenitors labeled with green fluorescent protein (GFP) were applied to the adventitial side of wire-injured mouse femoral arteries, a large proportion of GFP-Sca-1(+) -cells were observed in neointimal lesions, and a marked increase in neointimal lesion formation was seen 1 week post-operation. Interestingly, Sca-1(+) progenitor migration from the adventitia to the neointima was abrogated and neointima formation diminished in a wire injury model using CCL2(-/-) mice. These findings suggest vascular stem/progenitor cell migration from the adventitia to the neointima can be induced by SMC release of chemokines which act via CCR2/Rac1/p38 and CXCR2/Rac1/p38 signaling pathways. Stem Cells 2016;34:2368-2380.

Hyaluronan Is Crucial for Stem Cell Differentiation into Smooth Muscle Lineage.

Deciphering the extracellular signals that regulate SMC differentiation from stem cells is vital to further our understanding of the pathogenesis of vascular disease and for development of cell-based therapies and tissue engineering. Hyaluronan (HA) has emerged as an important component of the stem cell niche, however its role during stem cell differentiation is a complicated and inadequately defined process. This study aimed to investigate the role of HA in embryonic stem cell (ESC) differentiation toward a SMC lineage. ESCs were seeded on collagen-IV in differentiation medium to generate ESC-derived SMCs (esSMCs). Differentiation coincided with increased HA synthase (HAS) 2 expression, accumulation of extracellular HA and its assembly into pericellular matrices. Inhibition of HA synthesis by 4-methylumbelliferone (4MU), removal of the HA coat by hyaluronidase (HYAL) or HAS2 knockdown led to abrogation of SMC gene expression. HA activates ERK1/2 and suppresses EGFR signaling pathways via its principle receptor, CD44. EGFR inactivation coincided with increased binding to CD44, which was further augmented by addition of high molecular weight (HMW)-HA either exogenously or via HAS2 overexpression through adenoviral gene transfer. HMW-HA-stimulated esSMCs displayed a functional role in vascular tissue engineering ex vivo, vasculogenesis in a matrigel plug model and SMC accumulation in neointimal lesions of vein grafts in mice. These findings demonstrate that HAS2-induced HA synthesis and organization drives ESC-SMC differentiation. Thus, remodeling of the HA microenvironment is a critical step in directing stem cell differentiation toward a vascular lineage, highlighting HA as a potential target for treatment of vascular diseases. Stem Cells 2016;34:1225-1238.

Results of the California Healthy Homes Indoor Air Quality Study of 2011-2013: impact of natural gas appliances on air pollutant concentrations.

This study was conducted to assess the current impact of natural gas appliances on air quality in California homes. Data were collected via telephone interviews and measurements inside and outside of 352 homes. Passive samplers measured time-resolved CO and time-integrated NOX , NO2 , formaldehyde, and acetaldehyde over ~6-day periods in November 2011 - April 2012 and October 2012 - March 2013. The fraction of indoor NOX and NO2 attributable to indoor sources was estimated. NOX , NO2 , and highest 1-h CO were higher in homes that cooked with gas and increased with amount of gas cooking. NOX and NO2 were higher in homes with cooktop pilot burners, relative to gas cooking without pilots. Homes with a pilot burner on a floor or wall furnace had higher kitchen and bedroom NOX and NO2 compared to homes without a furnace pilot. When scaled to account for varying home size and mixing volume, indoor-attributed bedroom and kitchen NOX and kitchen NO2 were not higher in homes with wall or floor furnace pilot burners, although bedroom NO2 was higher. In homes that cooked 4 h or more with gas, self-reported use of kitchen exhaust was associated with lower NOX , NO2 , and highest 1-h CO. Gas appliances were not associated with higher concentrations of formaldehyde or acetaldehyde.

Formaldehyde and acetaldehyde exposure mitigation in US residences: in-home measurements of ventilation control and source control.

Measurements were taken in new US residences to assess the extent to which ventilation and source control can mitigate formaldehyde exposure. Increasing ventilation consistently lowered indoor formaldehyde concentrations. However, at a reference air exchange rate of 0.35 h(-1), increasing ventilation was up to 60% less effective than would be predicted if the emission rate were constant. This is consistent with formaldehyde emission rates decreasing as air concentrations increase, as observed in chamber studies. In contrast, measurements suggest acetaldehyde emission was independent of ventilation rate. To evaluate the effectiveness of source control, formaldehyde concentrations were measured in Leadership in Energy and Environmental Design (LEED)-certified/Indoor airPLUS homes constructed with materials certified to have low emission rates of volatile organic compounds (VOC). At a reference air exchange rate of 0.35 h(-1), and adjusting for home age, temperature and relative humidity, formaldehyde concentrations in homes built with low-VOC materials were 42% lower on average than in reference new homes with conventional building materials. Without adjustment, concentrations were 27% lower in the low-VOC homes. The mean and standard deviation of formaldehyde concentration was 33 µg/m(3) and 22 µg/m(3) for low-VOC homes and 45 µg/m(3) and 30 µg/m(3) for conventional.

The application of medical informatics to the veterinary management programs at companion animal practices in Alberta, Canada: a case study.

Companion animals closely share their domestic environment with people and have the potential to, act as sources of zoonotic diseases. They also have the potential to be sentinels of infectious and noninfectious, diseases. With the exception of rabies, there has been minimal ongoing surveillance of, companion animals in Canada. We developed customized data extraction software, the University of, Calgary Data Extraction Program (UCDEP), to automatically extract and warehouse the electronic, medical records (EMR) from participating private veterinary practices to make them available for, disease surveillance and knowledge creation for evidence-based practice. It was not possible to build, generic data extraction software; the UCDEP required customization to meet the specific software, capabilities of the veterinary practices. The UCDEP, tailored to the participating veterinary practices', management software, was capable of extracting data from the EMR with greater than 99%, completeness and accuracy. The experiences of the people developing and using the UCDEP and the, quality of the extracted data were evaluated. The electronic medical record data stored in the data, warehouse may be a valuable resource for surveillance and evidence-based medical research.

Medical management of inflammatory bowel disease among Canadian gastroenterologists.

BACKGROUND: Little is known about physician perceptions of and practices in using infliximab - a biological agent that was approved in Canada for the treatment of Crohn's disease in 2001, and for ulcerative colitis in 2006. OBJECTIVES: To describe Canadian gastroenterologists' use and perceptions of infliximab in the treatment of refractory inflammatory bowel disease (IBD), and to identify factors that may influence a gastroenterologist's decision to initiate infliximab therapy. METHODS: A postal questionnaire was distributed to all practicing clinicians captured in the 2007 membership of the Canadian Association of Gastroenterology. Each physician was contacted up to a maximum of three times. RESULTS: Of 466 questionnaires mailed out, responses were received from 336 (72%), with 292 respondents (63%) returning fully completed surveys. For 80% of respondents, IBD patients comprised less than 30% of their clinical practice. Most prescribed infliximab at an initial dose of 5 mg/kg (97%), prescribed loading doses at 0, 2 and 6 weeks (88%), premedicated with corticosteroids (74%), administered maintenance infusions at eight-week intervals (89%), co-administered immunosuppressive agents (81%) and continued infliximab 'indefinitely' as long as it was effective and well tolerated (76%). Most gastroenterologists (>70%) identified lack of drug insurance coverage and provincial funding criteria as important barriers to prescribing infliximab. CONCLUSIONS: Most Canadian gastroenterologists exhibited similar practice patterns with respect to the use of infliximab for induction and maintenance therapy of IBD. Common barriers to the initiation of infliximab therapy were identified.

Aging fibroblasts resist phenotypic maturation because of impaired hyaluronan-dependent CD44/epidermal growth factor receptor signaling.

Fibroblast differentiation into myofibroblasts is a key event during normal wound repair. We have previously demonstrated an age-related defect in this process associated with impaired synthesis of hyaluronan (HA) synthase (HAS) 2 but failed to prescribe its role in a mechanistic sense. Here we demonstrate that in addition to HAS2, there is loss of EGF receptor (EGF-R) in aged cells, and both are required for normal fibroblast functionality. Analysis of molecular events revealed that in young cells, transforming growth factor (TGF)-beta1-dependent phenotypic activation uses two distinct but cooperating pathways that involve TGF-beta receptor/Smad2 activation and EGF-mediated EGF-R/extracellular signal-regulated kinase (ERK) 1/2 signaling, and the latter is compromised with in vitro aging. Pharmacological inhibition of any of the five intermediates (TGF-beta receptor, Smad2, EGF, EGF-R, and ERK1/2) attenuated TGF-beta1 induction of alpha-smooth muscle actin. We present evidence that the HA receptor CD44 co-immunoprecipitates with EGF-R after activation by TGF-beta1. This interaction is HA-dependent because disruption of HA synthesis abrogates this association and inhibits subsequent ERK1/2 signaling. In aged fibroblasts, this association is lost with resultant suppression of ERK1/2 activation. Forced overexpression of EGF-R and HAS2 in aged cells restored TGF-beta1-mediated HA-CD44/EGF-R association and alpha-smooth muscle actin induction. Taken together, these results demonstrate that HA can serve as a signal integrator by facilitating TGF-beta1-mediated CD44-EGF-R-ERK interactions and ultimately fibroblast phenotype. We propose a model to explain this novel mechanism and the functional consequence of age-dependent dysregulation.

Age-related changes in pericellular hyaluronan organization leads to impaired dermal fibroblast to myofibroblast differentiation.

We have previously demonstrated that transforming growth factor-beta1 (TGF-beta1)-mediated fibroblast-myofibroblast differentiation is associated with accumulation of a hyaluronan (HA) pericellular coat. The current study demonstrates failure of fibroblast-myofibroblast differentiation associated with in vitro aging. This is associated with attenuation of numerous TGF-beta1-dependent responses, including HA synthesis and induction of the HA synthase enzyme HAS2 and the hyaladherin tumor necrosis factor-alpha-stimulated gene 6 (TSG-6), which led to an age-related defect in pericellular HA coat assembly. Inhibition of HAS2-dependent HA synthesis by gene silencing, removal of the HA coat by hyaluronidase digestion, or gene silencing of TSG-6 or cell surface receptor CD44 led to abrogation of TGF-beta1-dependent induction of alpha-smooth muscle actin in "young" cells. This result supports the importance of HAS2-dependent HA synthesis and the HA coat during phenotypic activation. Interleukin-1beta stimulation, however, failed to promote phenotypic conversion despite coat formation. A return to basal levels of HA synthesis in aged cells by HAS2 overexpression restored TGF-beta1-dependent induction of TSG-6 and pericellular HA coat assembly. However, this did not lead to the acquisition of a myofibroblast phenotype. Coordinated induction of HAS2 and TSG-6 facilitation of pericellular HA coat assembly is necessary for TGF-beta1-dependent activation of fibroblasts, and both components of this response are impaired with in vitro aging. In conclusion, the HA pericellular coat is integral but not sufficient to correct for the age-dependent defect in phenotypic conversion.

Health disparities in chickenpox or shingles in Alberta?

OBJECTIVE: Exploring for evidence of socio-economic health disparities in chickenpox and shingles in Alberta, Canada. METHODS: Chickenpox and shingles cases were identified from administrative data from Alberta's universal health care insurance system for 1994-2002. Incident cases were those with the earliest dated utilization of a health service (chickenpox: ICD9-CM 052/ICD10-CA B01; shingles: ICD9-CM 053/ ICD10-CA B02). Crude and age-specific rates were estimated for each year by an indicator of socio-demographic status based upon the nature of the payer and eligibility for health care premium subsidy (SES-proxy) for the provincial health care insurance system. RESULTS: Among young children there is a gradient of disparity in chickenpox rates prior to the year in which publicly funded vaccination programs were implemented. After this point, disparities decline but less so for First Nations children than for others. There was no evidence of disparity by SES-proxy for shingles. CONCLUSION: Publicly funded vaccination programs may effectively contribute to reduction in disease disparities for vaccine-preventable diseases. Further study is required to ascertain why disparities continue for First Nations children.

Secular trends in the epidemiology of shingles in Alberta.

Varicella vaccine was licensed in Canada in 1998, and a publicly funded vaccination programme introduced in the province of Alberta in 2001. In theory the vaccination programme might increase the burden of disease from shingles, making it important to develop baseline data against which future comparisons can be made. The study's aim was to describe the epidemiology of non-fatal cases of shingles for which publicly funded health services were utilized for the period 1986-2002. Shingles cases were identified from the records of Alberta's universal, publicly funded health-care insurance system for 1986-2002. The earliest dated health service utilizations for ICD-9-CM codes of 053 or ICD-10-CA codes of B02 were classified as incident. Diagnostic codes at least 180 days after the first were classified as recurrent episodes. Denominators for rates were estimated using mid-year population estimates from the Alberta Health Care Insurance Plan Registry. Annual age- and sex-specific rates were estimated. We explored the pattern of rates for sex, age and year effects and their interactions. Shingles rates increased between 1986 and 2002. There was a sex effect and evidence of an age-sex interaction. Females had higher rates than males at every age; however, the difference between females and males was greatest for the 50-54 years age group and declined for older age groups. The increased rate of shingles in Alberta began before varicella vaccine was licensed or publicly funded in Alberta, and thus cannot be attributed to vaccination.

Duration and distance of exposure are important predictors of transmission among community contacts of Ontario SARS cases.

We report attack rates and contact-related predictors among community contacts of severe acute respiratory syndrome (SARS) cases from the 2003 Toronto-area outbreak. Community contact data was extracted from public health records for single, well-defined exposures to a SARS case. In total, 8662 community-acquired exposures resulted in 61 probable cases; a crude attack rate of 0.70% [95% confidence interval (CI) 0.54-0.90]. Persons aged 55-69 years were at higher risk of acquiring SARS (1.14%) than those either younger (0.60%) or older (0.70%). In multivariable analysis exposures for at least 30 min at a distance of

The changing epidemiology of chickenpox in Alberta.

BACKGROUND: Varicella vaccine was licensed in Canada in 1998. The province of Alberta introduced a universal publicly funded varicella vaccination program in 2001. PURPOSE: To describe the epidemiology of non-fatal cases of chickenpox for which publicly funded health services were utilized for the period 1986-2002. METHODS: We used the records of Alberta's universal, publicly funded health care insurance system to identify cases of chickenpox for the period 1986-2002. The earliest dated utilization of a health service for which there was an ICD9-CM code of 052.xx or an IC10-CA code of B01.xx was used as the date of illness onset. Denominators for rates were estimated using mid-year population estimates from the Alberta Health Care Insurance Registry. Age-specific rates were estimated for each year. RESULTS: The crude incidence of chickenpox significantly declined over the period 1994-2002, most steeply after the year 2000. The incidence of chickenpox varied by age group and year and there was evidence of age-group-year interaction. Among those aged 5-19 years, chickenpox incidence began to decline prior to vaccine licensure in Canada. Among those aged less than one year and those aged 1-4 years, the incidence increased until 1999 when a decline began. Over the period 0.8% of cases were hospitalized. CONCLUSION: Chickenpox rates began to decline prior to the introduction of the publicly funded vaccination program; however the declines in rates among the youngest age-groups are consistent with a vaccination program effect.

Doctors, patients and influenza-like illness: clinicians or patients at risk?

BACKGROUND: Healthcare providers can transmit influenza and influenza-like illness (ILI) to patients and vice versa. However, the magnitude of this problem in the healthcare system as a whole is unknown. Using population-based administrative health data, we tested the hypothesis of a temporal association of ILI diagnosis among clinicians and their patients. METHODS: Healthcare providers under study included physicians (85%) and a variety of other medical professionals (such as chiropractors, dentists and optometrists). Cases of ILI were defined as having an ICD-9 code of influenza (487), pneumonia (480-486) or bronchitis (466 and 490) in a province-wide healthcare-provider billing system. Rates of ILI among persons who saw a sick (case) and non-sick (control) doctor were calculated and compared. RESULTS: The rate of ILI was lower among providers than among patients for every year of the study. The mean number of exposures to patients diagnosed with ILI was higher among case providers than among control providers (P = 0.044). However, exposure to case providers did not significantly increase the risk of ILI diagnosis among patients (OR=1.11; 95% confidence intervals 0.85-1.36). INTERPRETATION: Our findings are consistent with the hypothesis of patient-to-provider transmission. However, we may have underestimated the association and magnitude of this effect. Our results do not support the hypothesis that infectious doctors transmit disease to their patients, although this may be partly accounted for by the lower rates of ILI among the provider population in general.

Response rates for surveys of chiropractors.

BACKGROUND: Survey response rates may vary by type of practitioner studied and may have declined over time. Response rates for surveys of complementary practitioners have not been studied. OBJECTIVE: To describe the response rates in published surveys of chiropractors and explore for secular trends in response rates and for methodologic and geographic correlates of response rates. METHODS: Secondary analysis of data extracted from published English language reports of surveys of chiropractors. Response rates were calculated as the total number of persons from whom a questionnaire was returned divided by the total number of persons who were sent a questionnaire. RESULTS: Sixty-two surveys represented by 79 articles published in the interval 1980 to 2000 met inclusion criteria for analysis. We were able to calculate a response rate for 46 postal surveys. The mean response rate was 52.7%. There was no significant association between geographic setting and response rate, and there was no evidence of secular trend in response rates. None of the studies employed incentives. The strongest predictor of response rate was number of contacts with the target population. CONCLUSION: Response rates for surveys of chiropractors are similar to those observed for surveys of medical doctors. The key to obtaining high response rates is the use of evidence-based methods in design and conduct of the surveys.