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BackgroundPatients with limited English proficiency (LEP) experience worse outcomes following hospital discharge. Care transition programs are common, yet little is known about the disparities in quality (process and outcome measures) experienced by patients with LEP.MethodsWe conducted a retrospective cohort study to determine the association of LEP and care transition quality at an urban, US academic hospital. We examined all adults discharge home from the hospital from May 2018 through April 2019. All patients received a multilingual, automated telephone call three days after discharge to assess and address patient-reported issues. We determined care transition quality using process measures (reach rate, time to resolve reported issue) and outcome measures (discharge instructions questions, difficulty obtaining prescriptions, medication concerns, follow up care questions, new or worsening symptoms, any other clinical issues). All results were adjusted for measured confounders; we used predicted probabilities and average marginal effect (AME) to describe associations.Results13,860 patients were included in the study; 11% had LEP. The program reached most patients regardless of LEP status but was less likely to reach patients with LEP (AME 3.3%; 95% CI, 1.4% to 5.1%). After adjustment, patients with LEP reported high rates of all measured patient-reported outcomes: discharge instruction (AME 4.8%; 95% CI, 2.7% to 6.9%), obtaining prescriptions (AME 2.9%; 95% CI, 0.6% to 5.1%), medications concerns (AME 2.3%; 95% CI, 0.0% to 4.6%), follow up questions (AME 2.8%; 95% CI, 0.3% to 5.3%), new or worsening symptoms (AME 3.2%; 95% CI, 0.7% to 5.8%), and any other clinical issues (AME 3.6%; 95% CI, 1.1% to 6.1%). When issues were identified, the association between LEP and time to resolution of an issue was statistically, but not clinically, significant.Conclusion and RelevanceAmong patients with LEP, substantial disparities exist in patient-reported post-discharge outcome measures indicating a need for better discharge processes that focus on quality and health equity. Following discharge, relatively minor disparities were observed in the processes of a care transitions program that supports non-English languages.

Background Advocacy is a core value of the medical profession. However, patient advocacy (advocacy) is not uniformly assessed and there are no studies of the behaviors clinical supervisors consider when assessing advocacy. Objective To explore how medical students and supervisors characterize advocacy during an internal medicine clerkship, how assessment of advocacy impacted students and supervisors, and elements that support effective implementation of advocacy assessment. Design A constructivist qualitative paradigm was used to understand advocacy assessment from the perspectives of students and supervisors. Participants Medical students who completed the internal medicine clerkship at UCSF during the 2018 and 2019 academic years and supervisors who evaluated students during this period. Approach Supervisor comments from an advocacy assessment item in the medicine clerkship and transcripts of focus groups were used to explore which behaviors students and supervisors deem to be advocacy. Separate focus groups with both students and supervisors examined the impact that advocacy assessment had on students’ and supervisors’ perceptions of advocacy and what additional context was necessary to effectively implement advocacy assessment. Key Results Students and supervisors define advocacy as identifying and addressing social determinants of health, recognizing and addressing patient wishes and concerns, navigating the health care system, conducting appropriate evaluation and treatment, and creating exceptional therapeutic alliances. Effective implementation of advocacy assessment requires the creation of non-hierarchical team environments, supervisor role modeling, and pairing assessment with teaching of advocacy skills. Inclusion of advocacy assessment reflects and dictates institutional priorities, shapes professional identity formation, and enhances advocacy skill development for students and their supervisors. Conclusions Students and supervisors consider advocacy to be a variety of behaviors beyond identifying and addressing social determinants of health. Effectively implementing advocacy assessment shapes students’ professional identity formation, underscoring the critical importance of formally focusing on this competency in the health professions education.

Background Chronic idiopathic musculoskeletal pain (CIMSKP) has become increasingly recognised as a major cause of morbidity in adolescents. In view of increasing referrals to a paediatric rheumatology centre, the Learning and Exercise to Avert Pain (LEAP) intervention was designed as an approach to pain management within a group setting, led by an occupational therapist and a physiotherapist. It involves 2 hour weekly sessions for 6 weeks and includes education, gym activities and relaxation sessions with routine collection of Pain VAS, CHAQ, Bath Pain questionnaires (adolescent BAPQ and parent BAPQ-p forms) at baseline, end of LEAP and 3 months follow-up. We aim to assess the feasibility and impact of LEAP for adolescents with CIMSKP. Methods Young people who had been referred for the LEAP programme were identified (n = 46). Basic demographics and questionnaire scores were collected from electronic patient records and therapy notes. Feasibility was assessed by delivery of programme and percentage completion of questionnaires at three time-points. Semi-structured interviews were conducted with healthcare professionals involved in the programme and analysed using thematic analyses as were any free text comments on the BAPQ from adolescents and parents. Statistical analysis of the outcome data was performed using paired t-tests and SPSS software (v22). Results 46 adolescents were identified: 85% female, median age 16 years (range 10 to 19). 34 participated in LEAP, 12 received 1:1 therapy. Feasibility of programme delivery was achieved with completion of all six sessions. Completion rates for all 3 measures for adolescents/parents at baseline, end of programme review and follow up were 78.6/71.4%, 64.3/71.4%, and 45.5/36.4% respectively. Adolescent scores indicated a significant increase in impairment in the development subscale scores on BAPQ from baseline to programme end (p = 0.021) although not at follow up. Parent scores for adolescent anxiety and pain-specific anxiety on BAPQ-p increased significantly from end of programme to follow-up (p = 0.017, p = 0.034 respectively). Parents scored higher than adolescents for most outcomes. The qualitative data (available for 11 adolescents, 12 parents) revealed that parents and adolescents appreciated learning coping techniques and gaining a greater understanding of chronic pain. The intervention was perceived to be socially beneficial in particular but imperfect in terms of data collection by the professionals interviewed (n = 2). Conclusion Baseline demographics of the LEAP participants echoed current literature. Delivery of the programme was feasible and the programme was positively received by young people, their parents and professionals alike. The increase in adolescent development subscale scores following the programme could represent increased self-reflection and/or peer to peer observations as a result of the group setting but needs longer term follow-up data to clarify further. The increase in parental anxiety highlights the need for a concurrent session for parents. Routine collection of objective measures remains challenging in non-research setting. Conflicts of Interest The authors declare no conflicts of interest.

ObjectiveVariation in the fat mass and obesity-associated (FTO) gene influences susceptibility to obesity. A variant in the FTO gene has been implicated in genetic risk to osteoarthritis (OA). We examined the role of the FTO polymorphism rs8044769 in risk of knee and hip OA in cases and controls incorporating body mass index (BMI) information.Methods5409 knee OA patients, 4355 hip OA patients and up to 5362 healthy controls from 7 independent cohorts from the UK and Australia were genotyped for rs8044769. The association of the FTO variant with OA was investigated in case/control analyses with and without BMI adjustment and in analyses matched for BMI category. A mendelian randomisation approach was employed using the FTO variant as the instrumental variable to evaluate the role of overweight on OA.ResultsIn the meta-analysis of all overweight (BMI?25) samples versus normal-weight controls irrespective of OA status the association of rs8044769 with overweight is highly significant (OR[CIs] for allele G=1.14 [01.08 to 1.19], p=7.5×10?7). A significant association with knee OA is present in the analysis without BMI adjustment (OR[CIs]=1.08[1.02 to 1.14], p=0.009) but the signal fully attenuates after BMI adjustment (OR[CIs]=0.99[0.93 to 1.05], p=0.666). We observe no evidence for association in the BMI-matched meta-analyses. Using mendelian randomisation approaches we confirm the causal role of overweight on OA.ConclusionsOur data highlight the contribution of genetic risk to overweight in defining risk to OA but the association is exclusively mediated by the effect on BMI. This is consistent with what is known of the biology of the FTO gene and supports the causative role of high BMI in OA.

Objective: to compare the combined role of genetic variants loci associated with risk of knee or hip osteoarthritis (OA) in post-traumatic (PT) and non-traumatic (NT) cases of clinically severe OA leading to total joint replacement.\ud \ud Methods: A total of 1590 controls, 2168 total knee replacement (TKR) cases (33.2% PT) and 1567 total hip replacement (THR) cases (8.7% PT) from 2 UK cohorts were genotyped for 12 variants previously reported to be reproducibly associated with risk of knee or hip OA. A genetic risk score was generated and the association with PT and NT TKR and THR was assessed adjusting for covariates.\ud \ud Results: For THR, each additional genetic risk variant conferred lower risk among PT cases (OR=1.07, 95% CI 0.96 to 1.19; p=0.24) than NT cases (OR 1.11, 95% CI 1.06 to 1.17; p=1.55×10−5). In contrast, for TKR, each risk variant conferred slightly higher risk among PT cases (OR 1.12, 95% CI 1.07 to 1.19; p=1.82×10−5) than among NT cases (OR 1.08, 95% CI 1.03 to 1.1; p=0.00063).\ud \ud Conclusions: Based on the variants reported to date PT TKR cases have at least as high a genetic contribution as NT cases.

Objective To assess if a coding variant in the gene\ud encoding transient receptor potential cation channel,\ud subfamily V, member 1 ( TRPV1 ) is associated with\ud genetic risk of painful knee osteoarthritis (OA).\ud Methods The Ile585Val TRPV1 variant encoded by\ud rs8065080 was genotyped in 3270 cases of symptomatic\ud knee OA, 1098 cases of asymptomatic knee OA and\ud 3852 controls from seven cohorts from the UK, the USA\ud and Australia. The genetic association between the\ud low-pain genotype Ile–Ile and risk of symptomatic and\ud asymptomatic knee OA was assessed.\ud Results The TRPV1 585 Ile–Ile genotype, reported to\ud be associated with lower thermal pain sensitivity, was\ud associated with a lower risk of symptomatic knee OA\ud in a comparison of symptomatic cases with healthy\ud controls, with an odds ratio (OR) of 0.75 (95% CI 0.64\ud to 0.88; p=0.00039 by meta-analysis) after adjustment\ud for age, sex and body mass index. No difference was\ud seen between asymptomatic OA cases and controls\ud (OR=1.02, 95% CI 0.82 to 1.27 p=0.86) but the Ile–Ile\ud genotype was associated with lower risk of symptomatic\ud versus asymptomatic knee OA adjusting for covariates\ud and radiographic severity (OR=0.73, 95% CI 0.57 to 0.94\ud p=0.0136). TRPV1 expression in articular cartilage was\ud increased by infl ammatory cytokines (tumour necrosis\ud factor α and interleukin 1). However, there were no\ud differences in TRPV1 expression in healthy and arthritic\ud synovial tissue.\ud Conclusions A genotype involved in lower peripheral\ud pain sensitivity is signifi cantly associated with a\ud decreased risk of painful knee OA. This indicates a role for\ud the pro-nociceptive gene TRPV1 in genetic susceptibility\ud to symptomatic knee OA, which may also be infl uenced\ud by a role for this molecule in cartilage function.

In November 1999, the Queensland Health (QH) Transition to Practice Nurse Education Program - Intensive Care (TPNEP-IC) was initiated in QH Intensive Care Units (ICUs) across Queensland. This 12-month, state-wide, workplace based education program has set minimum standards for intensive care nursing education and therefore minimum standards for intensive care nursing practice in QH. In the 12 years of operation, 824 nurses have completed TPNEP-IC, 761 achieving academic credit status and 453 utilising this academic credit status to undertake postgraduate study in critical/intensive care nursing at three Queensland universities. These outcomes were achieved through the appointment of nurse educators within ICUs who, through a united and strong commitment to this state-wide approach formed collaborative professional networks, which resulted in the development, implementation and maintenance of the program. Furthermore, these networks enabled a framework of support for discussion and dissemination of evidence based practice, to endorse quality processes for TPNEP-IC and to nurture leadership potential among educators. Challenges to overcome included obtaining adequate resources to support all aspects of the program, gaining local management and administrative support, and embedding TPNEP-IC within ICU culture. The 12 years of operation of the program have demonstrated its long term sustainability. The program is being launched through a new blended learning approach utilising e-learning strategies. To capitalise on the current success, a strong commitment by all stakeholders will be required to ensure the ongoing sustainability of the program.

Background: Variants in the growth differentiation factor 5 ( GDF5 ) and in the double von Willebrand factor A ( DVWA ) have recently been reported to be associated with osteoarthritis (OA) in Asian populations. Objective: To assess the role of such variants in OA susceptibility in two independent UK samples of Caucasian origin. Methods: Polymorphisms rs11718863 and rs7639618 ( DVWA ) and rs143383 ( GDF5 ) were genotyped in 999 patients with knee OA, 843 patients with hip OA and 1166 controls from two UK studies from Nottingham and Chingford. Results: In agreement with previous reports, the major allele at rs143383 ( GDF5 ) was associated with a higher risk of knee OA in our samples (OR MH = 1.29, 95% CI 1.14 to 1.47 p = 8×10 −5 ). Conversely, the major allele at the DVWA SNP rs7639618, which increased risk in Asians, was not associated with a risk of knee OA, (OR MH = 0.88, 95% CI 0.74 to 1.04; p = 0.12). A meta-analysis of Asian and UK knee OA data indicated highly significant heterogeneity ( I 2 = 92%, Q = 48.5, p = 7×10 −10 ) and no significant association with knee OA using a random effects meta-analysis (OR DL = 1.18, 95% CI 0.86 to 1.63; p = 0.309). Conclusions: These data confirm that the GDF5 variant is consistently associated with the risk of knee OA. Considerable ethnic variation in allele frequencies at the DVWA gene was found and no significant association was found in UK samples or by combining UK and Asian samples. The results suggest that the effect of DVWA amino acid changes on tubulin binding is unlikely to influence the risk of OA in Caucasians.

Summary The care of the mechanically ventilated patient is a fundamental component of a nurse's clinical practice in the intensive care unit (ICU). Published work relating to the numerous nursing issues of the care of the mechanically ventilated patient in the ICU is growing significantly, yet is fragmentary by nature. The purpose of this paper is to provide a single comprehensive examination of the evidence related to the care of the mechanically ventilated patient. In part one of this two-part paper, the evidence on nursing care of the mechanically ventilated patient was explored with specific focus on patient safety: particularly patient and equipment assessment. This article, part two, examines the evidence related to the mechanically ventilated patient's comfort : patient position, hygiene, management of stressors (such as communication, sleep disturbance and isolation), pain management and sedation.

There is extensive literature reporting discordance between the presence and severity of symptoms and the degree of radiographic structural osteoarthritis (OA).1–⇓⇓⇓5 Genetic differences may account for some of this discordance. Indeed, certain genetic variants implicated in pain sensitivity have been shown to be significantly different between asymptomatic radiographic cases of OA and symptomatic cases.6–9 The catechol-O-methyltransferase, encoded by the COMT gene, is a major degrading enzyme in the metabolic pathways of catecholaminergic neurotransmitters.10 Genetic variation at the COMT gene has been shown to result in differential pain sensitivity.10–12 Carriers of the Val158Met COMT variant have been reported to have a higher risk (OR=2.9, 95% CI 1.2 to 6.1) of hip pain as compared with carriers of the Val/Val genotype among those with hip OA.9 This result has not been replicated in independent cohorts, nor for OA in other joints. We assessed whether the Met allele in the COMT gene is involved in increased risk of symptomatic knee OA in seven cohorts: five cohorts from the UK, …

Osteoarthritis (OA) of the hip is a major cause of pain, disability and use of healthcare resources.1 Although OA is multifactorial, it is known to have significant genetic contribution and a number of studies have attempted to dissect such contribution (see2 for review). The DOT1L gene encodes the DOT1-like histone H3 methyltransferaseis, a potentially dedicated enzyme for Wnt target gene activation in leukaemia recently shown to be associated with endochondral bone formation.3 A polymorphism (rs12982744) in DOT1L has been found to be strongly associated with minimum joint space width (minJSW) at the hip. This exact same single nucleotide polymorphism (SNP) was previously identified to be associated with increased height.4 ,5 The C allele associated with lower minJSW and lower height was associated with hip OA, although this association did not reach genome-wide significance (GWS) (OR 1.14, CI 1.06 to 1.22; p=1.5 × 10−4).3 The GWS level of p

Objective Knee osteoarthritis (OA) has a significant genetic component. The authors have assessed the role of three variants reported to influence risk of knee OA with p

Osteoarthritis (OA) is the most common form of arthritis and a major cause of disability. This study evaluates the association\ud in Caucasian populations of two single nucleotide polymorphisms (SNPs) mapping to the Human Leukocyte Antigen (HLA)\ud region and deriving from a genome wide association scan (GWAS) of knee OA in Japanese populations. The frequencies for\ud rs10947262 were compared in 36,408 controls and 5,749 knee OA cases from European-descent populations. rs7775228 was\ud tested in 32,823 controls and 1,837 knee OA cases of European descent. The risk (major) allele at rs10947262 in Caucasian\ud samples was not significantly associated with an odds ratio (OR) = 1.07 (95%CI 0.94 -1.21; p = 0.28). For rs7775228 the metaanalysis\ud resulted in OR = 0.94 (95%CI 0.81-1.09; p = 0.42) for the allele associated with risk in the Japanese GWAS. In Japanese\ud individuals these two SNPs are in strong linkage disequilibrium (LD) (r2 = 0.86) with the HLA class II haplotype DRB1*1502\ud DQA1*0103 DQB1*0601 (frequency 8%). In Caucasian and Chinese samples, using imputed data, these SNPs appear not to\ud be in LD with that haplotype (r2,0.07). The rs10947262 and rs7775228 variants are not associated with risk of knee OA in\ud European descent populations and they do not appear tag the same HLA class II haplotype as they do in Japanese\ud individuals.

Objective: To clarify the role of common genetic variation in the Interleukin-1 beta (IL1B) and Interleukin-1R antagonist (IL1RN) genes on risk of knee and hip osteoarthritis (OA) and severity of knee OA by means of large-scale meta-analyses. Methods: We searched PubMed for articles assessing the role of IL1B and IL1RN polymorphisms/haplotypes on the risk of hip and/or knee OA. Novel data were included from eight unpublished studies. Meta-analyses were performed using fixed- and random-effects models with a total of 3595 hip OA and 5013 knee OA cases, and 6559 and 9132 controls respectively. The role of ILRN haplotypes on radiographic severity of knee OA was tested in 1918 cases with Kellgren-Lawrence (K/L) 1 or 2 compared to 199 cases with K/L 3 or 4. Results: The meta-analysis of six published studies retrieved from the literature search and eight unpublished studies showed no evidence of association between common genetic variation in the IL1B or IL1RN genes and risk of hip OA or knee OA (P > 0.05 for rs16944, rs1143634, rs419598 and haplotype C-G-C (rs1143634, rs16944 and rs419598) previously implicated in risk of hip OA). The C-T-A haplotype formed by rs419598, rs315952 and rs9005, previously implicated in radiographic severity of knee OA, was associated with reduced severity of knee OA (odds ratio (OR) = 0.71 95% CI 0.56-0.91; P = 0.006, I(2) = 74%), and achieved borderline statistical significance in a random-effects model (OR = 0.61 95% CI 0.35-1.06 P=0.08). Conclusion: Common genetic variation in the Interleukin-1 region is not associated with prevalence of hip or knee OA but our data suggest that IL1RN might have a role in severity of knee OA. (C) 2010 Osteoarthritis Research Society International. Published by Elsevier Ltd. All rights reserved. Osteoarthritis and Cartilage

Osteoarthritis of the knee is a major cause of pain, disability and the use of healthcare resources among middle-aged and older people.1 Although osteoarthritis is multifactorial, it is known to have a significant genetic contribution and a number of studies have attempted to dissect such a contribution (see Valdes and Spector2 for review). The GDF5 gene encodes the growth differentiation factor 5, a bone morphogenetic protein involved in joint formation, expressed in different joint structures, which has been shown to ameliorate tendon, ligament and bone healing after trauma in mice.3 4 A promoter polymorphism (rs143383) in GDF5 has been found to be strongly associated with both hip and knee osteoarthritis in Asian individuals,4 and is the most widely replicated genetic association with knee osteoarthritis, although much less so for hip and hand osteoarthritis.5 This variant is functional, with the lower gene expression variant having increased genetic risk.4 A large-scale meta-analysis reported the association of the major (T) allele with knee osteoarthritis achieved OR 1.15 p=9.7×10−7 and achieved p=9×10−5 (OR 1.13, 95% CI 1.06 to 1.20) when Asian subjects were excluded.5 The genome-wide statistical significance level of p

Objective Smad3 (or, MADH3) is a key intracellular messenger in the transforming growth factor β signaling pathway. In mice, Smad3 deficiency accelerates growth plate chondrocyte maturation and leads to an osteoarthritis (OA)–like disease. We undertook this study to investigate the role of genetic variation in SMAD3 in the risk of large-joint OA in humans. Methods Ten tag single-nucleotide polymorphisms (SNPs) in the SMAD3 gene region were tested in a discovery set: 313 patients who had undergone total knee replacement, 214 patients who had undergone total hip replacement, and 520 controls from the UK. The SNP associated with both hip and knee OA was subsequently genotyped in 1,221 controls and 1,074 cases from 2 cohorts of patients with hip OA and 2,537 controls and 1,575 cases from 4 cohorts of patients with knee OA. Results A SNP (rs12901499) mapping to intron 1 of SMAD3 was associated with both knee and hip OA (P < 0.0022 and P < 0.021, respectively) in the discovery set. In all study cohorts, the major allele (G) was increased among OA patients relative to controls. A meta-analysis for knee OA yielded an odds ratio (OR) of 1.22 (95% confidence interval [95% CI] 1.12–1.34), P < 7.5 × 10−6. For hip OA, the OR was 1.22 (95% CI 1.09–1.36), P < 4.0 × 10–4. No evidence for heterogeneity was found (I2 = 0%). Conclusion Our data indicate that genetic variation in the SMAD3 gene is involved in the risk of both hip OA and knee OA in European populations, confirming the results from animal models on the potential importance of this molecule in the pathogenesis of OA.

Chronic nursing shortages have placed increasing pressure on many nursing schools to recruit greater numbers of students with the consequence of larger class sizes. Larger class sizes have the potential to lead to student disengagement. This paper describes a case study that examined the strategies used by a group of nursing lecturers to engage students and to overcome passivity in a Bachelor of Nursing programme. A non-participant observer attended 20 tutorials to observe five academics deliver four tutorials each. Academics were interviewed both individually and as a group following the completion of all tutorial observations. All observations, field notes, interviews and focus groups were coded separately and major themes identified. From this analysis two broad categories emerged: getting students involved; and engagement as a struggle. Academics used a wide variety of techniques to interest and involve students. Additionally, academics desired an equal relationship with students. They believed that both they and the students had some power to influence the dynamics of tutorials and that neither party had ultimate power. The findings of this study serve to re-emphasise past literature which suggests that to engage students, the academics must also engage.

Objective To quantify the differences in risk factors influencing total hip replacement (THR) and total knee replacement (TKR) based on the presence versus absence of multiple interphalangeal nodes in 2 or more rays of the fingers of each hand in patients with large joint osteoarthritis (OA). Methods A group of 3,800 patients with large joint OA who underwent total joint replacement (1,201 of whom had the nodal phenotype) and 1,906 control subjects from 2 case–control studies and a population-based cohort in the UK were studied. Odds ratios (ORs) and 95% confidence intervals (95% CIs) were calculated for the risk of total joint replacement in association with age, sex, body mass index (BMI), height, and prevalence of the T allele in the GDF5 rs143383 polymorphism. ORs for total joint replacement were compared between cases of nodal OA and cases of non-nodal OA and between patients who underwent TKR and those who underwent THR. Results Age, sex, and BMI had significantly higher ORs for an association with total joint replacement in nodal OA cases than in non-nodal OA cases. The GDF5 polymorphism was significantly associated with THR in cases of nodal OA, but not in cases of non-nodal OA, and increased height was a risk factor for THR in non-nodal OA cases only. Female sex was a protective risk factor for TKR in non-nodal OA cases (OR 0.60, 95% CI 0.52–0.70) but was predisposing for TKR in the nodal form of OA (OR 1.83, 95% CI 1.49–2.26). The nodal phenotype was associated with a significantly higher risk of undergoing both THR and TKR (OR 1.46, 95% CI 1.09–1.94) and also a significantly higher risk of bilateral TKR (OR 1.70, 95% CI 1.37–2.11), but, paradoxically, was associated with a lower risk of bilateral THR (OR 0.72, 95% CI 0.56–0.91). Conclusion Nodal and non-nodal forms of large joint OA have significantly different risk factors and outcomes, indicating a different etiology for the 2 forms of OA. With regard to the likelihood of undergoing THR, this appears to be, at least in part, genetically determined.

Margaret Wheeler discusses the benefits that moving to a vertical house system has had in her inner city school

The isolation, characterization and an efficient synthesis of 4-hydroxyisoxazole 1 , a plant growth regulator isolated from an African plant is reported. It is a new compound, which despite the simple structure, had eluded synthesis.

The distribution of X-ray induced aberrations between trypsin-banded regions within human chromosomes has been studied in over a thousand cells from normal and abnormal individuals. An analysis of this data has been performed for each type of aberration separately, taking into account the relative amount of material at risk in reach region. A number of significant deviations from expectation were detected but many of these could be explained in terms of the failure of detection of some aberrations.

Ideograms of chromosomes obtained by the trypsin/Leishman method are presented in which the size and position of the bands of chromosomes at different stages of contraction have been defined by measurement. A hypothesis is suggested which could explain the changes observed in the banding pattern between stages of condensation.