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PubMed2005

Genetic professionals' reports of nondisclosure of genetic risk information within families.

Patients attending genetic clinics are often the main gatekeepers of information for other family members. There has been much debate about the circumstances under which professionals may have an obligation, or may be permitted, to pass on personal genetic information about their clients but without their consent to other family members. We report findings from the first prospective study investigating the frequency with which genetics professionals become concerned about the failure of clients to pass on such information to their relatives. In all, 12 UK and two Australian regional genetic services reported such cases over 12 months, including details of actions taken by professionals in response to the clients' failure to disclose information. A total of 65 cases of non-disclosure were reported, representing <1% of the genetic clinic consultations in the collaborating centres during the study period. These included 39 cases of the failure of parents not passing full information to their adult offspring, 22 cases where siblings or other relatives were not given information and four cases where information was withheld from partners -- including former and prospective partners. Professionals reported clients' reasons for withholding information as complex, more often citing concern and the desire to shield relatives from distress rather than poor family relationships. In most cases, the professionals took further steps to persuade their clients to make a disclosure but in no instance did the professional force a disclosure without the client's consent.

Attitude of Health Personnel↗
PubMed2001

Glucosensing neurons do more than just sense glucose.

The brain regulates energy homeostasis by balancing energy intake, expenditure and storage. To accomplish this, it has evolved specialized neurons that receive and integrate afferent neural and metabolic signals conveying information about the energy status of the body. These sensor-integrator-effector neurons are located in brain areas involved in homeostatic functions such as the hypothalamus, locus coeruleus, basal ganglia, limbic system and nucleus tractus solitarius. The ability to sense and regulate glucose metabolism is critical because of glucose's primacy as a metabolic substrate for neural function. Most neurons use glucose as an energy substrate, but glucosensing neurons also use glucose as a signaling molecule to regulate neuronal firing and transmitter release. There are two types of glucosensing neurons that either increase (glucose responsive, GR) or decrease (glucose sensitive, GS) their firing rate as brain glucose levels rise. Little is known about the mechanism by which GS neurons sense glucose. However, GR neurons appear to function much like the pancreatic beta-cell where glycolysis regulates the activity of an ATP-sensitive K(+) (K(ATP)) channel. The K(ATP) channel is composed of four pore-forming units (Kir6.2) and four sulfonylurea binding sites (SUR). Glucokinase (GK) appears to modulate K(ATP) channel activity via its gatekeeper role in the glycolytic production of ATP. Thus, GK may serve as a marker for GR neurons. Neuropeptide Y (NPY) and pro-opiomelanocortin (POMC) neurons in the hypothalamic arcuate nucleus are critical components of the energy homeostasis pathways in the brain. Both express Kir6.2 and GK, as well as leptin receptors. They also receive visceral neural and intrinsic neuropeptide and transmitter inputs. Such metabolism-related signals can summate upon K(ATP) channel activity which then alters membrane potential, neuronal firing rate and peptide/transmitter release. The outputs of these neurons are integral components of effector systems which regulate energy homeostasis. Thus, arcuate NPY and POMC neurons are probably prototypes of this important class of sensor-integrator-effector neurons.

Animals↗
PubMed2004

Recognition and management of overweight and obesity in primary care in Germany.

BACKGROUND: In contrast to the well-documented high prevalence of overweight and obesity in the general population, the prevalence, recognition rates and management by primary care physicians--as the core gatekeeper in the health care system--remains poorly studied. PURPOSE OF THE STUDY: To examine (1) the point prevalence of overweight (BMI 25.0-29.9 kg/m(2)) and obesity (BMI> or =30 kg/m(2)) in primary care patients, (2) prevalence patterns in patients with high-risk constellations (diabetes, hypertension, cardiovascular disease, etc.), (3) doctors' recognition and interventions, as well as patients' use and perceived effectiveness of weight-loss interventions and (4) factors associated with non-treatment. METHODS: Cross-sectional point prevalence study of 45 125 unselected consecutive primary care attendees recruited from a representative nationwide sample of 1912 primary care practices. MEASURES: (1) standardized clinical appraisal of each patient by the physician (diagnostic status and recognition, severity, comorbidity, current and past interventions). (2) Patient self-report questionnaire: height and weight, illness history, past and current treatments and their perceived effectiveness, health attitudes and behaviors. RESULTS: (1) In all, 37.9% of all primary care attendees were overweight, 19.4% obese. (2) Rates for overweight and obesity were highest in patients with diabetes (43.6 and 36.7%) and hypertension (46.1 and 31.3%), followed by patients with cardiovascular disorders. Rates of overweight/obesity increased steadily by the number of comorbid conditions. (3) Doctors' recognition of overweight (20-30%) and obesity (50-65%) was low, patients' actual use of weight control interventions even lower (past 12 months: 8-11%, lifetime: 32-39%). Patient success rates were quite limited. (4) Co- and multimorbidity in particular as well as other patient and illness variables were identified as predictors for recognition, but prediction of patients' actual use of weight loss interventions was limited. CONCLUSIONS: Primary care management of overweight and obesity is largely deficient, predominantly due to four interrelated factors: doctors' poor recognition of patients' weight status, doctors' inefficient efforts at intervention, patients' poor acceptance of such interventions and dissatisfaction with existing life-style modification strategies.

Age Distribution↗
PubMed2005

New targets for PPARgamma in the vessel wall: implications for restenosis.

Peroxisome proliferator-activated receptor {gamma} (PPARgamma), the nuclear receptor that binds the insulin-sensitizing thiazolidinediones (TZDs), is prominently upregulated in intimal vascular smooth muscle cells (VSMC) after mechanical injury to the vessel wall. Several TZD PPARgamma ligands have been shown to inhibit neointima formation in both normal and insulin-resistant vasculature. The suppression of intimal hyperplasia by TZD PPARgamma ligands probably results from their activity to inhibit VSMC growth and promote apoptosis. TZDs prevent VSMC proliferation by blocking the activity of regulatory proteins, such as phosphorylation of the retinoblastoma protein (Rb). Rb functions as a G(1) gatekeeper by controlling S phase gene expression mediated by the E2F transcription factor. Consistent with their effect on Rb phosphorylation, PPARgamma ligands inhibit the mitogenic induction of minichromosome maintenance (MCM) proteins 6 and 7, two E2F-regulated S phase genes essential for DNA replication. PPARgamma ligands also induced apoptosis in VSMC, which correlated with a potent induction of GADD45, a gene implicated in controlling cell growth and survival. A constitutively active form of PPARgamma targeted the same cell cycle regulators as did PPARgamma ligands, consistent with a nuclear-receptor-dependent mechanism of action. This review will summarize mechanisms through which PPARgamma modulates VSMC proliferation and apoptosis suggesting that PPARgamma itself is a novel important regulator of cell cycle and apoptosis and may provide a new therapeutic approach to prevent restenosis.

Animals↗
PubMed2006

Coordinated control of renal Ca2+ handling.

Ca2+ homeostasis is an important factor, which is underlined by the numerous clinical symptoms that involve Ca2+ deficiencies. The overall Ca2+ balance is maintained by the concerted action of Ca2+ absorption in the intestine, reabsorption in the kidney, and exchange from bone, which are all under the control of the calciotropic hormones that are released upon a demand for Ca2+. In the kidney, these calciotropic hormones affect active Ca2+ reabsorption, which consists of TRPV5 as the apical entry gate for Ca2+ influx, calbindin-D28K as an intracellular ferry for Ca2+ and, NCX1 and PMCA1b for extrusion of Ca2+ across the basolateral membrane. This review highlights the action of hormones on renal Ca2+ handling and focuses on the coordinated control of the renal Ca2+ transport proteins. Parathyroid hormone stimulates renal Ca2+ handling by regulating active Ca2+ reabsorption on both the genomic and non-genomic level. Estrogens harbor calciotropic hormone characteristics positively regulating the expression of TRPV5, independently of vitamin D. Besides having a strong regulatory effect on the expression of the intestinal Ca2+ transport proteins, vitamin D contributes to the overall Ca2+ balance by enhancing the expression of the Ca2+ transport machinery in the kidney. Dietary Ca2+ is involved in regulating its own handling by controlling the expression of the renal Ca2+ transport proteins. Thus, the magnitude of Ca2+ entry via TRPV5 controls the expression of the other Ca2+ transport proteins underlining the gatekeeper function of this Ca2+ channel in the renal Ca2+ handling.

Absorption↗
PubMed1997

Bcl-2 inhibits p53 nuclear import following DNA damage.

Bcl-2 is an integral membrane oncoprotein that localizes to membranes of the mitochondria, endoplasmic reticulum, and nuclear envelope. Bcl-2 is a member of a family of cell death regulators and functions to inhibit apoptosis. Using confocal microscopy and immunoblotting we show that the ability of bcl-2 to suppress cell death following genotoxic damage can be a consequence of inhibiting nuclear import of induced wild-type p53 protein. Our data suggests that the ability of bcl-2 to modulate trafficking events is not cell type specific. These data support a 'gatekeeper' mechanism for cell death suppression by bcl-2.

3T3 Cells↗
PubMed1999

Bcl-2 overexpression results in reciprocal downregulation of Bcl-X(L) and sensitizes human testicular germ cell tumours to chemotherapy-induced apoptosis.

Testicular germ cell tumours are hypersentive to chemotherapy and cell lines derived from these tumours are chemosensitive in vitro. We have previously shown that these cell lines express undetectable levels of the suppressor of apoptosis Bcl-2 and relatively high levels of the apoptosis inducer Bax (Chresta et al., 1996). To determine whether the absence of Bcl-2 in these cell lines makes them highly susceptible to drug-induced apoptosis, Bcl-2 was expressed ectopically in the 833K testicular germ cell tumour cell line. Stable overexpressing clones were isolated and three clones were studied further. Surprisingly, Bcl-2 overexpressing cells were sensitized to chemotherapy-induced apoptosis compared to the parental and vector control cells. Analysis of potential mechanisms of sensitization revealed there was a reciprocal downregulation of the endogenously expressed Bcl-X(L) in the Bcl-2 overexpressing clones. Downregulation of Bcl-X(L) to the same extent using antisense oligonucleotides enhanced etoposide-induced apoptosis by twofold. Our results indicate that Bcl-2 and Bcl-X(L) have different abilities to protect against chemotherapy-induced apoptosis in testicular germ cell tumours. In contrast to findings in some tumour cell types, Bcl-2 did not act as a gatekeeper to prevent entry of p53 to the nucleus.

Antineoplastic Agents↗
PubMed2001

The pVHL-associated SCF ubiquitin ligase complex: molecular genetic analysis of elongin B and C, Rbx1 and HIF-1alpha in renal cell carcinoma.

The VHL gene product (pVHL) forms a multimeric complex with the elongin B and C, Cul2 and Rbx1 proteins (VCBCR complex), which is homologous to the SCF family of ubiquitin ligase complexes. The VCBCR complex binds HIF-1alpha and HIF-2alpha, transcription factors critically involved in cellular responses to hypoxia, and targets them for ubiquitin-mediated proteolysis. Germline mutations in the VHL gene cause susceptibility to haemangioblastomas, renal cell carcinoma (RCC), phaeochromocytoma and other tumours. In addition somatic inactivation of the VHL gene occurs in most sporadic clear cell RCC (CC-RCC). However, the absence of somatic VHL inactivation in 30-40% of CC-RCC implies the involvement of other gatekeeper genes in CC-RCC development. We reasoned that in CC-RCC without VHL inactivation, other pVHL-interacting proteins might be defective. To assess the role of elongin B/C, Rbx1 and HIF-1alpha in RCC tumorigenesis we (a) mapped the genes to chromosomes 8q(cen) (elongin C), 16p13.3 (elongin B) and 22q11.2 (Rbx1) by FISH, monochromosomal somatic cell hybrid panel screening and in silico GenBank homology searching; (b) determined the genomic organisation of elongin C (by direct sequencing of PAC clones), Rbx1 and elongin B (by GenBank homology searching); and (c) performed mutation analysis of exons comprising the coding regions of elongins B, C and Rbx1 and the oxygen-dependent degradation domain of HIF-1alpha by SSCP screening and direct sequencing in 35 sporadic clear cell RCC samples without VHL gene inactivation and in 13 individuals with familial non-VHL clear cell RCC. No coding region sequence variations were detected for the elongin B, elongin C or Rbx1 genes. Two amino acid substitutions (Pro582Ser and Ala588Thr) were identified in the oxygen-dependent degradation/pVHL binding domain of HIF-1alpha, however neither substitution was observed exclusively in tumour samples. Association analysis in panels of CC-RCC and non-neoplastic samples using the RFLPs generated by each variant did not reveal allelic frequency differences between RCC patients and controls (P>0.32 by chi-squared analysis). Nevertheless, the significance of these variations and their potential for modulation of HIF-1alpha function merits further investigation in both other tumour types and in non-neoplastic disease. Taken together with our previous Cul2 mutation analysis these data suggest that development of sporadic and familial RCC is not commonly contributed to by genetic events altering the destruction domain of HIF-1alpha, or components of the HIF-alpha destruction complex other than VHL itself. Although (a) activation of HIF could occur through mutation of another region of HIF-a, and (b) epigenetic silencing of elongin B/C, Cul2 or Rbx1 cannot be excluded, these findings suggest that pVHL may represent the sole mutational target through which the VCBR complex is disrupted in CC-RCC. HIF response is activated in CC-RCC tumorigenesis.

Carcinoma, Renal Cell↗
PubMed2002

The TRC8 hereditary kidney cancer gene suppresses growth and functions with VHL in a common pathway.

VHL is part of an SCF related E3-ubiquitin ligase complex with 'gatekeeper' function in renal carcinoma. However, no mutations have been identified in VHL interacting proteins in wild type VHL tumors. We previously reported that the TRC8 gene was interrupted by a t(3;8) translocation in a family with hereditary renal and non-medullary thyroid cancer. TRC8 encodes a multi-membrane spanning protein containing a RING-H2 finger with in vitro ubiquitin ligase activity. We isolated the Drosophila homologue, DTrc8, and studied its function by genetic manipulations and a yeast 2-hybrid screen. Human and Drosophila TRC8 proteins localize to the endoplasmic reticulum. Loss of either DTrc8 or DVhl resulted in an identical ventral midline defect. Direct interaction between DTrc8 and DVhl was confirmed by GST-pulldown and co-immunoprecipitation experiments. CSN-5/JAB1 is a component of the COP9 signalosome, recently shown to regulate SCF function. We found that DTrc8 physically interacts with CSN-5 and that human JAB1 localization is dependent on VHL mutant status. Lastly, overexpression of DTrc8 inhibited growth consistent with its presumed role as a tumor suppressor gene. Thus, VHL, TRC8, and JAB1 appear to be linked both physically and functionally and all three may participate in the development of kidney cancer.

3T3 Cells↗
PubMed2002

RecQ family helicases: roles as tumor suppressor proteins.

RecQ family DNA helicases are defined as proteins sharing a homologous region with Escherichia coli RecQ and are basically regarded as enzymes involved in recombination. Humans have five RecQ family members, and deficiencies in three of them, BLM, WRN, and RTS, cause Bloom's, Werner's, and Rothmund-Thomson syndromes, respectively, each characterized by genomic instability and cancer predisposition. In this context, an important function of the RecQ homologs appears to be the unwinding of intermediates of recombination, thereby preventing its uncontrolled execution. As a consequence, their deficiencies give rise to elevated levels of recombination (the hyper-recombination phenotype), which result in chromosomal aberrations including loss of heterozygosity, a common chromosomal change associated with malignancies. Thus, those helicases qualify as caretaker-type tumor suppressor proteins. In addition, BLM and WRN deficiencies have been shown to attenuate p53-mediated apoptosis, suggesting that they also belong to the gatekeeper class of tumor suppressor proteins.

Adenosine Triphosphatases↗
PubMed2003

Emerging roles of DNA tumor viruses in cell proliferation: new insights into genomic instability.

The small DNA virus proteins E1A and E1B from human Adenovirus, E6 and E7 from human papillomavirus, and large T and small T antigens from SV40, are multifaceted molecular tools that can carry out an impressive number of tasks in the host cell. These viral factors, collectively termed 'oncoproteins' for their ability to induce cancer, can be viewed as paradigmatic oncogenic factors which can disrupt checkpoint controls at multiple levels--they interfere with both 'gatekeeper' cellular functions, including major control pathways of cell cycle and apoptosis, and with 'caretaker' functions, thereby inducing mitotic abnormalities and increasing genomic instability. Both E1A and E7 have been recently found to interact physically with the Ran GTPase. This interaction is key in uncoupling the centrosome cycle from the cell cycle, highlighting a direct link between viral infection and the induction of genomic instability. Further expanding our current knowledge in this field will be crucial to elucidate viral strategies leading to cellular transformation and cancer progression, as well as design novel preventive or therapeutic approaches to human cancer.

Adenovirus E1A Proteins↗
PubMed2005

Wild-type p53 stimulates homologous recombination upon sequence-specific binding to the ribosomal gene cluster repeat.

p53 plays a central role in the maintenance of the genome integrity, both as a gatekeeper and a caretaker. Sequence-specific recognition of DNA is underlying the ability of p53 to transcriptionally transactivate target genes during checkpoint control and to regulate DNA replication at the TGCCT repeat from the ribosomal gene cluster (RGC). In contrast, suppression of recombination by p53 has been observed with nonconsensus DNA sequences. In this study, we discovered that wild-type p53 stimulates homologous recombination adjacent to the RGC repeat, whereas downregulation is seen with a mutated version thereof and with a microsatellite repeat sequence. Analysis of the causes possibly underlying the enhancement of homologous recombination revealed that p53 binding to the RGC element delays DNA synthesis. This was demonstrated after integration of the corresponding DNA fragments into our Simian virus 40-based model system, which was used to study recombination on replicating minichromosomes. Differently, with plasmid-based substrates, p53 did not stimulate recombination at the RGC sequence. Thus, in combination with our previous findings, p53 may promote homologous recombination by two separate mechanisms involving either molecular interactions with topoisomerase I or/and by specific binding to certain genomic regions, thereby causing replication fork stalling and recombination.

DNA↗
PubMed2006

PTEN and GSK3beta: key regulators of progression to androgen-independent prostate cancer.

Prostate cancer (PrCa) is characterized by progression from an androgen-dependent phenotype to one that is inevitably androgen independent (AI) and lethal. Recent evidence strongly suggests that the phosphatidylinositol-3-kinase/Akt (PI3K/Akt) and androgen receptor (AR) signalling pathways provide prostatic epithelium with the necessary signalling events to escape the apoptotic response associated with androgen withdrawal therapy. Silencing of phosphatase and tensin homologue deleted on chromosome 10 (PTEN) and glycogen synthase kinase beta (GSK3beta) are frequently associated with advanced PrCa systems and likely serve critical roles in promoting AR and PI3K/Akt gain-of-function. That PTEN negatively regulates AR and is sufficient to promote metastatic PrCa in murine models strongly implies its role as a gatekeeper of progressive PrCa. In human PrCa, PTEN loss is correlated with substantial increases in Akt(Ser473) and integrin-linked kinase expression, both of which promote Ser(9) phospho-inhibition of GSK3beta and inactivation of apoptotic factors. Sufficient evidence also suggests that GSK3beta is not only a critical regulator of proproliferative signalling but also a promiscuous one as PI3K/Akt pools of GSK3beta are, at least in part, functionally interchangeable with those of the Wnt/beta-catenin pathway. Thus, GSK3beta may serve not only as a mediator of PI3K/Akt activation but may also regulate the potent transactivation and proproliferative effects that Wnt3a and beta-catenin confer upon AR. These data suggest that prostate-specific activation of GSK3beta may serve as a viable pharmacological option. Thus, in this review, we emphasize that temporal changes in GSK3beta and PTEN expression during progression to AI PrCa are important factors when considering the potential for therapies targeting the oncogenic contributions of PI3K/Akt and AR signalling pathways.

Androgens↗
PubMed2005

Studying the consequences of immediate loss of gene function in the intestine: APC.

The use of mouse models to study neoplasia is proving particularly powerful in dissecting the mechanisms underlying disease initiation and progression. However, the majority of these models have been somewhat limited in studying the very early effects of loss of gene function, as tumour initiation relies upon either constitutive loss of gene function or spontaneous somatic loss of function. We have therefore adopted a strategy of using an inducible Cre-lox-based system to analyse the effects of loss of gene function, the use of which is reviewed here for the intestinal tumour suppressor APC (adenomatous polyposis coli). Using this approach, we have conditionally and synchronously inactivated APC in virtually all the epithelial cells of the adult murine small intestine. After 5 days following induction of Cre-mediated recombination, mice show grossly altered crypt/villus architecture. Deficiency in APC perturbs migration, alters the normal programme of differentiation and results in increased proliferation and apoptosis. Microarray analysis reveals the transcriptome to be significantly altered; reflecting both gross phenotypic changes and changes in transcriptional activation. These findings demonstrate that APC is indeed the critical determinant of cell fate in the intestinal epithelium, explaining its role as the cellular 'gatekeeper' in preventing neoplasia.

Adenomatous Polyposis Coli↗
PubMed2007

Concerted action of associated proteins in the regulation of TRPV5 and TRPV6.

Ca(2+) is an essential ion in all organisms and many physiological functions in the body rely on the exact maintenance of the Ca(2+) balance. The epithelial Ca(2+) channels TRPV5 [TRP (transient receptor potential) vanilloid 5] and TRPV6 are the most Ca(2+)-selective members of the TRP superfamily and are generally considered as the gatekeepers of Ca(2+) entry across epithelia. TRPV5 is involved in Ca(2+) reabsorption from pro-urine, while TRPV6 has an essential role in intestinal Ca(2+) uptake. These channels are the prime targets of calciotropic hormonal regulation, including vitamin D and parathyroid hormone. In addition, extra- and intra-cellular signalling by associated proteins and Ca(2+) itself play key roles in TRPV5 and TRPV6 regulation. In this paper, we describe the present understanding of the concerted action of calbindin-D(28k), klotho and BSPRY (B-box and SPRY-domain-containing protein) at different levels throughout the epithelial cell to control Ca(2+) influx at the luminal entry gate.

Animals↗
PubMed2002

Parental substance use as a modifier of adolescent substance use risk.

AIMS: A major question in national substance use prevention efforts is how much influence parents have on their children's substance use, answers to which could determine whether current school-based prevention programs that address peer pressure are sufficient or whether parents need to be involved. The present study examines whether parents act as gatekeepers by testing the moderator effects of parents' substance use on the relationships of friends' substance use to adolescent substance use (cigarettes, alcohol and marijuana). DESIGN: A longitudinal school-based trial for prevention of substance use in adolescents. SETTING: Indianapolis, Indiana, USA. PARTICIPANTS: As part of a large substance use prevention trial, entering middle school students were surveyed prospectively at baseline, 6 months and 18 months (n = 1807 from 57 schools). MEASUREMENTS: A self-reported survey was used to measure behaviors, attitudes and social influences related to adolescent substance use. FINDINGS: Results of logistic regression analyses and multiple group structural equation modeling showed that increasing numbers of parents and friends using substances were associated with greater risk of adolescent substance use, as were more substance offers and lower levels of refusal self-efficacy. Additionally, refusal self-efficacy mediated the effects of baseline use and substance offers on subsequent use. However, non-using parents had a buffering effect on friends' influences to use substances, such that friends' use did not affect adolescent use when parents were non-users, and the effects of substance offers on refusal self-efficacy were weaker. CONCLUSIONS: The findings suggest that parent substance use should be addressed in adolescent substance use prevention programs, and that continuing non-use by parents should be reinforced.

Adolescent↗
PubMed2003

Determining small bowel integrity following drug treatment.

Intestinal integrity is maintained by a delicate balance between mucosal defence and luminal aggressors that cause damage if exposed to the mucosa. The intestinal barrier function appears to be the gatekeeper for controlling this balance. It is becoming increasingly clear that if the intestinal barrier is disrupted the consequences are low grade intestinal inflammation which carry with it the risk of significant blood and protein loss both of which may cause clinical management problems. We review the strength and weaknesses of methods for assessing small bowel function that are useful for assessing drug-induced intestinal toxicity. There are a number of imaging methods for assessing intestinal integrity but these do not provide functional information. Intestinal permeability measurements have been optimized for specificity and there are now ways of measuring intestinal permeability regionally, but marker analyses continue to be cumbersome. Recent developments of faecal inflammatory markers make it a matter of routine to assess this in any routine chemical pathology laboratory. Bleeding, protein loss and other complications of inflammation can also be measured with good specificity, but again the methods are cumbersome. Using a combination of functional and imaging techniques it is now possible to characterize and define with precision, the small bowel side-effects of drugs, the best example being the small bowel side-effects of nonsteroidal anti-inflammatory drugs (NSAIDs).

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed2003

Recruitment issues in healthcare research: the situation in home care.

A global shift in the setting of healthcare from hospitals and long-term care institutions to homes and communities has been accompanied by the growth of interest in the home as a site of healthcare research. Home care researchers have identified the recruitment of research subjects as a significant concern. The present descriptive, exploratory study used qualitative, semi-structured interviews with home care researchers (n = 9) to illuminate the challenges related to recruitment. The results suggest that while home care research shares recruitment issues common to other forms of health research, it has unique concerns. Factors affecting recruitment in home care studies include non-dedicated recruiters, the current context of healthcare restructuring, and gatekeeper and participant feelings about the home as a setting for care and research. Reasons for refusal to participate may be more complex in home care research given the meanings care recipients attribute to their 'homes'. Home care researchers may also face unique ethical and/or moral dilemmas. This paper recommends the routine reporting of recruitment problems, increased inclusion of minority subjects to ensure sample representativeness and further studies of the subjective meanings of 'home' as it is associated with healthcare treatment.

Communication↗