Although the patient-centered medical home is a well-established model of care for primary care providers, adoption by specialty providers has been relatively limited. Recently, there has been particular interest in developing specialty medical homes in medical oncology because of practice variation, care fragmentation, and high overall costs of care. In 2012, the Center for Medicare and Medicaid Innovation awarded Innovative Oncology Business Solutions a 3-year grant for their Community Oncology Medical Home (COME HOME) program to implement specialty medical homes in seven oncology practices across the country. We report our early experience and lessons learned.Through September 30, 2014, COME HOME has touched 16,353 unique patients through triage encounters, patient education visits, or application of clinical pathways. We describe the COME HOME model and implementation timeline, profile use of key services, and report patient satisfaction. Using feedback from practice sites, we highlight patient-centered innovations and overall lessons learned.COME HOME incorporates best practices care driven by triage and clinical pathways, team-based care, active disease management, enhanced access and care, as well as financial support for the medical home infrastructure. Information technology plays a central role, supporting both delivery of care and performance monitoring. Volume of service use has grown steadily over time, leveling out in second quarter 2014. The program currently averages 1,265 triage encounters, 440 extended hours visits, and 655 patient education encounters per month.COME HOME offers a patient-centered model of care to improve quality and continuity of care.

6587 Background: Unplanned hospitalizations (UH) during cancer care have been identified as a poor outcome that may significantly increase costs of care. We hypothesized that poor quality of care p...

e17673 Background: Health care costs are an increasing burden for payers, providers and for patients. There is growing evidence that patient centered medical homes (PCMH) can be successful in achieving the Triple Aim of improved quality, lower cost, and higher patient satisfaction in primary care settings. We have developed a related Oncology Medical Home (OMH) model that provides patients with enhanced access by extending practice hours into the evenings and weekends, active disease management via symptom specific triage pathways and evidence-based clinical pathways. We have implemented this model at seven independent community oncology practices in six states. Methods: Implementation was rolling, with the first practice going live September 14, 2012, an additional three practices launching January 1, 2013 and the remaining three practices on April 1, 2013. The initial roll out included triage pathways for symptom management and a gradual roll out of extended hours services in the evenings and weekends. By October 6, 2013, all seven practices were offering at least two hours of extended service on weeknights and at least four hours on the weekends. Results: From the beginning of the grant, through the end of 2013, there were 22,650 calls to the triage lines at the COME HOME practices, resulting in 6,360 triage nursing phone encounters and 1,836 face to face encounters. System utilization varied from 1.1 calls/month/1,000 active patients to 7.6 calls/month/1,000 active patients. Maximum triage nurse capacity seems to be four calls per day, per nurse, with a median phone encounter length of 45 minutes. Conclusions: Patients who utilized COME HOME services tended to be younger (64.2 vs 68.9 years of age, p=0.013), were more likely female (68.1% of COME HOME patients are female vs. 58.9% of the non-COME HOME patients, p<0.001) and had been diagnosed more recently (79.9% of COME HOME patients had been diagnosed within the preceding 6 months vs. 53.1% of the non-COME HOME patients, p<0.001). There was not a significant difference in race or ethnicity. The final outcomes analysis will include ED visit rate, inpatient hospitalization rate, all-cause mortality and total episodic cost of care.

Purpose: The aim of this study was to develop, operationalize, and pilot test a transparent, reproducible, and evidence-informed method to determine when to report incidental findings from next-generation sequencing technologies. Methods: Using evidence-based principles, we proposed a three-stage process. Stage I “rules out” incidental findings below a minimal threshold of evidence and is evaluated using inter-rater agreement and comparison with an expert-based approach. Stage II documents criteria for clinical actionability using a standardized approach to allow experts to consistently consider and recommend whether results should be routinely reported (stage III). We used expert opinion to determine the face validity of stages II and III using three case studies. We evaluated the time and effort for stages I and II. Results: For stage I, we assessed 99 conditions and found high inter-rater agreement (89%), and strong agreement with a separate expert-based method. Case studies for familial adenomatous polyposis, hereditary hemochromatosis, and α1-antitrypsin deficiency were all recommended for routine reporting as incidental findings. The method requires <3 days per topic. Conclusion: We establish an operational definition of clinically actionable incidental findings and provide documentation and pilot testing of a feasible method that is scalable to the whole genome. Genet Med 15 9, 721–728.

Deanna Cross1, Alanna Rahm2, Anh Le2, Jennifer Webster3, Arnold Potosky4, Heather Feigelson2, Gwen Alexander5, Pamala Pawolski6, Andrew Williams7, Yihe Daida7, Stacey Honda7, Adedayo Onitilo1, Catherine McCarty8 and Katrina Goddard3 1Marshfield Clinic 2Kaiser Permanente Colorado 3Kaiser Permanente Northwest 4Georgetown University 5Henry Ford Health System 6HealthPartners 7Kaiser Permanente Hawaii 8Essentia Health

Methods We identified 119,732 HMO members with chronic musculoskeletal pain from electronic medical records data. Patients were contacted by mail and invited to complete an online survey. Those not responding were either contacted by email or mailed a paper copy of the survey. Survey questions included items related to diagnosis, acu/ chiro utilization and payment, and communication about acu/chiro use with HMO clinicians.

INTRODUCTION:Human epidermal growth factor receptor 2 (HER2) expression is amplified in about 20% of breast cancer tumors, and evaluation of HER2 status should influence therapy selection. A critical gap in our knowledge is the real-world implementation of HER2 testing and its impact on treatment decisions for women diagnosed with breast cancer.OBJECTIVES:To assess use of HER2 testing, to describe characteristics of patients who do or do not receive HER2 testing, to describe which HER2 tests were used (fluorescence in situ hybridization or immunohistochemistry), and to evaluate trastuzumab use as a function of HER2 results.STUDY DESIGN:The population included 6460 women diagnosed with invasive breast cancer between 1999 and 2007 at 8 geographically distributed Cancer Research Network healthcare delivery systems in the United States.METHODS:Electronic records were used to identify patient and tumor characteristics and treatment with trastuzumab. Chart abstraction was performed for 400 women (50 per site) to identify receipt of HER2 testing and results.RESULTS:More than 90% of study participants received HER2 testing. Everyone who received trastuzumab had a HER2 test, and nearly all (>95%) who received trastuzumab had a positive HER2 test result recorded in their medical chart. Most (77%) eligible patients with a positive HER2 test result diagnosed after 2005 received trastuzumab. This study expands upon previous work in individual health plans.CONCLUSIONS:HER2 status has been successfully incorporated into medical practice to guide treatment decisions for breast cancer patients in diverse integrated healthcare delivery settings.

Background/Aims Colorectal cancer is the third most common cancer diagnosis in the US, with a lifetime risk of 5.1%. It is the second leading cause of cancer death, and is predicted to cause approximately 50,000 deaths in 2011. With a five year survival rate of less than 25%, the majority of patients diagnosed with metastatic colorectal cancer face decisions about end of life care. This study seeks to understand what influences hospice utilization among metastatic colorectal cancer patients who are part of the Comparative Effectiveness in Genomics and Personalized Medicine for Colon Cancer (CERGEN) population. Methods Electronic medical record (EMR) data was collected, through database queries and manual chart review, for 1220 subjects diagnosed with stage III or stage IV colorectal cancer progressing to metastatic disease between 2006 and 2009, at seven Managed Care Organizations (MCOs) from the Cancer Research Network (CRN). Hospice use is defined as a binary outcome indicating whether there was at least one hospice referral or admission recorded in the subject’s EMR. Descriptive statistics (mean, median, variance) and logistic modeling were used to summarize the demographic, health status, and system factors that influenced hospice use. Results Overall, 59% of subjects utilized hospice services. Patients utilizing hospice care were significantly older (69 vs. 63, p < 0.0001), with a lower average family income (63% for family income <$60,000 vs. 56% for family income = $60,000, p = 0.01), and with longer follow up time after colorectal cancer diagnosis (follow up interval of 639 days vs. 499 days, p = 0.01) than those not utilizing hospice care. We also saw significant variation by site across the seven MCOs studied (p = 0.01, range = 47% to 65%). Race, ethnicity, gender, stage at diagnosis, year of diagnosis, Medicare status, alcohol and/or tobacco use, use of chemotherapy and use of KRAS testing were not significantly associated with hospice utilization. Discussion Health status, demographic and system characteristics all influence the use of hospice services by metastatic colorectal cancer subjects in the CERGEN population.

Pamala Pawloski1, Jennifer Webster2, Tia Kaufman2, Brian Owens1, Clara Hwang3, Adedayo Onitilo4, Heather Feigelson5, Andrew Williams6, Gwen Alexander3, Ajay Behl1, Jessica Engel4 and Katrina Goddard2 1HealthPartners 2Kaiser Permanente Northwest 3Henry Ford Health System 4Marshfield Clinic 5Kaiser Permanente Colorado 6Kaiser Permanente Hawaii

Background Substantial recent research examines the efficacy of many types of complementary and alternative (CAM) therapies. However, outcomes associated with the "real-world" use of CAM has been largely overlooked, despite calls for CAM therapies to be studied in the manner in which they are practiced. Americans seek CAM treatments far more often for chronic musculoskeletal pain (CMP) than for any other condition. Among CAM treatments for CMP, acupuncture and chiropractic (A/C) care are among those with the highest acceptance by physician groups and the best evidence to support their use. Further, recent alarming increases in delivery of opioid treatment and surgical interventions for chronic pain--despite their high costs, potential adverse effects, and modest efficacy--suggests the need to evaluate real world outcomes associated with promising non-pharmacological/non-surgical CAM treatments for CMP, which are often well accepted by patients and increasingly used in the community. Methods/Design This multi-phase, mixed methods study will: (1) conduct a retrospective study using information from electronic medical records (EMRs) of a large HMO to identify unique clusters of patients with CMP (e.g., those with differing demographics, histories of pain condition, use of allopathic and CAM health services, and comorbidity profiles) that may be associated with different propensities for A/C utilization and/or differential outcomes associated with such care; (2) use qualitative interviews to explore allopathic providers' recommendations for A/C and patients' decisions to pursue and retain CAM care; and (3) prospectively evaluate health services/costs and broader clinical and functional outcomes associated with the receipt of A/C relative to carefully matched comparison participants receiving traditional CMP services. Sensitivity analyses will compare methods relying solely on EMR-derived data versus analyses supplementing EMR data with conventionally collected patient and clinician data. Discussion Successful completion of these aggregate aims will provide an evaluation of outcomes associated with the real-world use of A/C services. The trio of retrospective, qualitative, and prospective study will also provide a clearer understanding of the decision-making processes behind the use of A/C for CMP and a transportable methodology that can be applied to other health care settings, CAM treatments, and clinical populations. Trial registration ClinicalTrials.gov: NCT01345409

By using homozygosity mapping in a consanguineous Pakistani family, we detected linkage of nonsyndromic hearing loss to a 7.6 Mb region on chromosome 3q13.31-q21.1 within the previously reported DFNB42 locus. Subsequent candidate gene sequencing identified a homozygous nonsense mutation (c.1135G>T [p.Glu379X]) in ILDR1 as the cause of hearing impairment. By analyzing additional consanguineous families with homozygosity at this locus, we detected ILDR1 mutations in the affected individuals of 10 more families from Pakistan and Iran. The identified ILDR1 variants include missense, nonsense, frameshift, and splice-site mutations as well as a start codon mutation in the family that originally defined the DFNB42 locus. ILDR1 encodes the evolutionarily conserved immunoglobulin-like domain containing receptor 1, a putative transmembrane receptor of unknown function. In situ hybridization detected expression of Ildr1, the murine ortholog, early in development in the vestibule and in hair cells and supporting cells of the cochlea. Expression in hair cell- and supporting cell-containing neurosensory organs is conserved in the zebrafish, in which the ildr1 ortholog is prominently expressed in the developing ear and neuromasts of the lateral line. These data identify loss-of-function mutations of ILDR1, a gene with a conserved expression pattern pointing to a conserved function in hearing in vertebrates, as underlying nonsyndromic prelingual sensorineural hearing impairment.

Objectives/Hypothesis: To determine the cause of autosomal dominant hearing loss segregating in an American family.Study Design: Family study.Methods: Otologic and audiometric examination was performed on affected family members. Genome wide parametric multipoint linkage mapping using a dominant model was performed with Affymetrix 50K GeneChip data. Direct sequencing was used to confirm the causative mutation.Results: In American family 467, segregating autosomal dominant nonsyndromic hearing loss, a novel heterozygous missense mutation (c.362T>C; p.F121S) was identified in the COCH gene. This mutation was also associated with vestibular dysfunction typical of other DFNA9 families. However, affected family members also exhibited memory loss and night blindness.Conclusions: The novel COCH mutation affects the functionally important limulus factor C, Coch-5b2 and Lgl1 domain where most DFNA9 mutations have been localized. The onset of the hearing loss, in the 2nd or 3rd decade of life,. is earlier than in most DFNA9 families. The progression of hearing loss and vestibular dysfunction in the American family is typical of other DFNA9 families with mutations in this domain. Memory loss and night blindness have not been previously reported in DFNA9 families.

In a genome-wide association study of structural brain degeneration, we mapped the 3D profile of temporal lobe volume differences in 742 brain MRI scans of Alzheimer's disease patients, mildly impaired, and healthy elderly subjects. After searching 546,314 genomic markers, 2 single nucleotide polymorphisms (SNPs) were associated with bilateral temporal lobe volume (P<5×10−7). One SNP, rs10845840, is located in the GRIN2B gene which encodes the N-methyl-d-aspartate (NMDA) glutamate receptor NR2B subunit. This protein – involved in learning and memory, and excitotoxic cell death – has age-dependent prevalence in the synapse and is already a therapeutic target in Alzheimer's disease. Risk alleles for lower temporal lobe volume at this SNP were significantly over-represented in AD and MCI subjects vs. controls (odds ratio=1.273; P=0.039) and were associated with mini-mental state exam scores (MMSE; t=−2.114; P=0.035) demonstrating a negative effect on global cognitive function. Voxelwise maps of genetic association of this SNP with regional brain volumes, revealed intense temporal lobe effects (FDR correction at q=0.05; critical P=0.0257). This study uses large-scale brain mapping for gene discovery with implications for Alzheimer's disease.

For late onset Alzheimer's disease (LOAD), the only confirmed, genetic association is with the apolipoprotein E (APOE) locus on chromosome 19. Meta-analysis is often employed to sort the true associations from the false positives. LOAD research has the advantage of a continuously updated meta-analysis of candidate gene association studies in the web-based AlzGene database. The top 30 AlzGene loci on May 1(st), 2007 were investigated in our whole genome association data set consisting of 1411 LOAD cases and neuropathoiogicaiiy verified controls genotyped at 312,316 SNPs using the Affymetrix 500K Mapping Platform. Of the 30 "top AlzGenes", 32 SNPs in 24 genes had odds ratios (OR) whose 95% confidence intervals that did not include 1. Of these 32 SNPs, six were part of the Affymetrix 500K Mapping panel and another ten had proxies on the Affymetrix array that had >80% power to detect an association with α=0.001. Two of these 16 SNPs showed significant association with LOAD in our sample series. One was rs4420638 at the APOE locus (uncorrected p-value=4.58E-37) and the other was rs4293, located in the angiotensin converting enzyme (ACE) locus (uncorrected p-value=0.014). Since this result was nominally significant, but did not survive multiple testing correction for 16 independent tests, this association at rs4293 was verified in a geographically distinct German cohort (p-value=0.03). We present the results of our ACE replication aiongwith a discussion of the statistical limitations of multiple test corrections in whole genome studies.

Myosin VIIA mutations have been associated with non-syndromic hearing loss (DFNB2; DFNA11) and Usher syndrome type 1B (USH1B). We report clinical and genetic analyses of a consanguineous Iranian family segregating autosomal recessive non-syndromic hearing loss (ARNSHL). The hearing impairment was mapped to the DFNB2 locus using Affymetrix 50K GeneChips; direct sequencing of the MYO7A gene was completed. The Iranian family (L-1419) was shown to segregate a novel homozygous missense mutation (c.1184G>A) that results in a p.R395H amino acid substitution in the motor domain of the myosin VIIA protein. As one affected family member had significantly less severe hearing loss, we used a candidate approach to search for a genetic modifier. This novel MYO7A mutation is the first reported to cause DFNB2 in the Iranian population and this DFNB2 family is the first to be associated with a potential modifier. The absence of vestibular and retinal defects, and less severe low frequency hearing loss, is consistent with the phenotype of a recently reported Pakistani DFNB2 family. Thus, we conclude this family has non-syndromic hearing loss (DFNB2) rather than USH1B, providing further evidence that these two diseases represent discrete disorders.

Objectives: We investigated the cause of autosomal recessive nonsyndromic hearing loss (ARNSHL) that segregated in 2 consanguineous Iranian families.Methods: Otologic and audiometric examinations were performed on affected members of each family. Genome-wide parametric multipoint linkage mapping using a recessive model was performed with Affymetrix 50K GeneChips or short tandem repeat polymorphisms. Direct sequencing was used to confirm the causative mutation in each family.Results: In 2 Iranian families, L-1651 and L-8600606, with ARNSHL that mapped to the DFNB7/11 locus, homozygosity for a reported splice site mutation (c.776+1G>A), and a novel deletion (c.1589_1590delCT; p.S530*) were identified in the TMC1 gene, respectively.Conclusions: Consistent with the previously reported phenotype in DFNB7/11 families, the 2 Iranian families had segregated congenital, profound hearing impairment. However, in family L-1651, one affected family member (IV:3) has milder hearing impairment than expected, suggesting a potential genetic modifier effect. These results indicate that DFNB7/11 is a common form of genetic hearing loss in Iran, because this population is the source of 6 of the 29 TMC1 mutations reported worldwide.

We recently reported evidence for an association between the individual variation in normal human episodic memory and a common variant of the KIBRA gene, KIBRA rs17070145 (T-allele). Since memory impairment is a cardinal clinical feature of Alzheimer's disease (AD), we investigated the possibility of an association between the KIBRA gene and AD using data from neuronal gene expression, brain imaging studies, and genetic association tests. KIBRA was significantly over-expressed and three of its four known binding partners under-expressed in AD-affected hippocampal, posterior cingulate and temporal cortex regions (P<0.010, corrected) in a study of laser-capture microdissected neurons. Using positron emission tomography in a cohort of cognitively normal, late-middle-aged persons genotyped for KIBRA rs17070145, KIBRA T non-carriers exhibited lower glucose metabolism than did carriers in posterior cingulate and precuneus brain regions (P<0.001, uncorrected). Lastly, non-carriers of the KIBRA rs17070145 T-allele had increased risk of late-onset AD in an association study of 702 neuropathologically verified expired subjects (P=0.034; OR=1.29) and in a combined analysis of 1026 additional living and expired subjects (P=0.039; OR=1.26). Our findings suggest that KIBRA is associated with both individual variation in normal episodic memory and predisposition to AD.

American Journal of Medical Genetics Part AVolume 149A, Issue 3 p. 555-558 Research Letter A novel splice site mutation in the RDX gene causes DFNB24 hearing loss in an Iranian family† A. Eliot Shearer, A. Eliot Shearer Department of Otolaryngology, Head and Neck Surgery, University of Iowa, Iowa City, Iowa These authors contributed equally to this work.Search for more papers by this authorMichael S. Hildebrand, Corresponding Author Michael S. Hildebrand michael-hildebrand@uiowa.edu Department of Otolaryngology, Head and Neck Surgery, University of Iowa, Iowa City, Iowa These authors contributed equally to this work.Department of Otolaryngology, Head and Neck Surgery, University of Iowa, 5270 CBRB Building, Iowa City, IA 52242.Search for more papers by this authorCatherine J. Bromhead, Catherine J. Bromhead Bioinformatics Division, The Walter and Eliza Hall Institute of Medical Research, Melbourne, Australia Department of Mathematics and Statistics, The University of Melbourne, Melbourne, AustraliaSearch for more papers by this authorKimia Kahrizi, Kimia Kahrizi Genetics Research Center, University of Social Welfare and Rehabilitation Sciences, Tehran, IranSearch for more papers by this authorJennifer A. Webster, Jennifer A. Webster Neurogenomics Division, Translational Genomics Research Institute, Phoenix, ArizonaSearch for more papers by this authorBatool Azadeh, Batool Azadeh Welfare Institution, Esfahan, IranSearch for more papers by this authorWilliam J. Kimberling, William J. Kimberling Department of Genetics, Boys Town National Research Hospital, Omaha, NebraskaSearch for more papers by this authorAli Anousheh, Ali Anousheh Genetics Research Center, University of Social Welfare and Rehabilitation Sciences, Tehran, IranSearch for more papers by this authorArash Nazeri, Arash Nazeri Genetics Research Center, University of Social Welfare and Rehabilitation Sciences, Tehran, IranSearch for more papers by this authorDietrich Stephan, Dietrich Stephan Neurogenomics Division, Translational Genomics Research Institute, Phoenix, Arizona Arizona Alzheimer's Consortium, Phoenix, Arizona Banner Alzheimer's Institute, Phoenix, ArizonaSearch for more papers by this authorHossein Najmabadi, Hossein Najmabadi Genetics Research Center, University of Social Welfare and Rehabilitation Sciences, Tehran, IranSearch for more papers by this authorRichard J.H. Smith, Richard J.H. Smith Department of Otolaryngology, Head and Neck Surgery, University of Iowa, Iowa City, Iowa Interdepartmental PhD Program in Genetics, Department of Otolaryngology, University of Iowa, Iowa City, IowaSearch for more papers by this authorMelanie Bahlo, Melanie Bahlo Bioinformatics Division, The Walter and Eliza Hall Institute of Medical Research, Melbourne, AustraliaSearch for more papers by this author A. Eliot Shearer, A. Eliot Shearer Department of Otolaryngology, Head and Neck Surgery, University of Iowa, Iowa City, Iowa These authors contributed equally to this work.Search for more papers by this authorMichael S. Hildebrand, Corresponding Author Michael S. Hildebrand michael-hildebrand@uiowa.edu Department of Otolaryngology, Head and Neck Surgery, University of Iowa, Iowa City, Iowa These authors contributed equally to this work.Department of Otolaryngology, Head and Neck Surgery, University of Iowa, 5270 CBRB Building, Iowa City, IA 52242.Search for more papers by this authorCatherine J. Bromhead, Catherine J. Bromhead Bioinformatics Division, The Walter and Eliza Hall Institute of Medical Research, Melbourne, Australia Department of Mathematics and Statistics, The University of Melbourne, Melbourne, AustraliaSearch for more papers by this authorKimia Kahrizi, Kimia Kahrizi Genetics Research Center, University of Social Welfare and Rehabilitation Sciences, Tehran, IranSearch for more papers by this authorJennifer A. Webster, Jennifer A. Webster Neurogenomics Division, Translational Genomics Research Institute, Phoenix, ArizonaSearch for more papers by this authorBatool Azadeh, Batool Azadeh Welfare Institution, Esfahan, IranSearch for more papers by this authorWilliam J. Kimberling, William J. Kimberling Department of Genetics, Boys Town National Research Hospital, Omaha, NebraskaSearch for more papers by this authorAli Anousheh, Ali Anousheh Genetics Research Center, University of Social Welfare and Rehabilitation Sciences, Tehran, IranSearch for more papers by this authorArash Nazeri, Arash Nazeri Genetics Research Center, University of Social Welfare and Rehabilitation Sciences, Tehran, IranSearch for more papers by this authorDietrich Stephan, Dietrich Stephan Neurogenomics Division, Translational Genomics Research Institute, Phoenix, Arizona Arizona Alzheimer's Consortium, Phoenix, Arizona Banner Alzheimer's Institute, Phoenix, ArizonaSearch for more papers by this authorHossein Najmabadi, Hossein Najmabadi Genetics Research Center, University of Social Welfare and Rehabilitation Sciences, Tehran, IranSearch for more papers by this authorRichard J.H. Smith, Richard J.H. Smith Department of Otolaryngology, Head and Neck Surgery, University of Iowa, Iowa City, Iowa Interdepartmental PhD Program in Genetics, Department of Otolaryngology, University of Iowa, Iowa City, IowaSearch for more papers by this authorMelanie Bahlo, Melanie Bahlo Bioinformatics Division, The Walter and Eliza Hall Institute of Medical Research, Melbourne, AustraliaSearch for more papers by this author First published: 12 February 2009 https://doi.org/10.1002/ajmg.a.32670Citations: 10 † How to cite this article: Shearer AE, Hildebrand MS, Bromhead CJ, Kahrizi K, Webster JA, Azadeh B, Kimberling WJ, Anousheh A, Nazeri A, Stephan D, Najmabadi H, Smith RJH, Bahlo M. 2009. A novel splice site mutation in the RDX gene causes DFNB24 hearing loss in an Iranian family. Am J Med Genet Part A 149A:555–558. Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Citing Literature Volume149A, Issue3March 2009Pages 555-558 RelatedInformation