Transforming Piecemeal Social Engineering into Grand Crime Prevention Policy: Toward a New Criminology of Social Control

This Article focuses on the Situational Crime Prevention (SCP) approach in criminology, which expands the crime reduction role well beyond the justice system. SCP sees criminal law in a more restrictive sense, as only part of the anticrime effort in governance. We examine the “general” and “specific” responses to crime problems in the SCP approach. Our review demonstrates that the most serious barrier to converting SCP techniques into policy remains the gap that exists between problem identification and problem response. We discuss past large-scale SCP interventions and explore the complex links between them and SCP’s better known specificity and piecemeal approach. We develop a graded framework for selecting responses that acknowledge the local, political, and organizational issues involved in identifying and choosing them. This framework determines when SCP interventions and policies can be crafted on the macro level to eliminate or greatly reduce the problem everywhere, and when interventions should be limited to a piecemeal, local approach to eliminate only the specific problem. Finally, we situate this analysis within the general context of the relationship between science and policy, noting the challenges in converting scientific observations into broad social policy and the expansion of crime control beyond criminal justice into the realm of government regulation and partnerships with nongovernmental agencies

Transforming Piecemeal Social Engineering into Grand Crime Prevention Policy: Toward a New Criminology of Social Control

This Article focuses on the Situational Crime Prevention (SCP) approach in criminology, which expands the crime reduction role well beyond the justice system. SCP sees criminal law in a more restrictive sense, as only part of the anticrime effort in governance. We examine the “general” and “specific” responses to crime problems in the SCP approach. Our review demonstrates that the most serious barrier to converting SCP techniques into policy remains the gap that exists between problem identification and problem response. We discuss past large-scale SCP interventions and explore the complex links between them and SCP’s better known specificity and piecemeal approach. We develop a graded framework for selecting responses that acknowledge the local, political, and organizational issues involved in identifying and choosing them. This framework determines when SCP interventions and policies can be crafted on the macro level to eliminate or greatly reduce the problem everywhere, and when interventions should be limited to a piecemeal, local approach to eliminate only the specific problem. Finally, we situate this analysis within the general context of the relationship between science and policy, noting the challenges in converting scientific observations into broad social policy and the expansion of crime control beyond criminal justice into the realm of government regulation and partnerships with nongovernmental agencies

Self-management for osteoarthritis of the knee: Does mode of delivery influence outcome?

Background Self-management has become increasingly popular in the management of chronic diseases. There are many different self-management models. Meta analyses of arthritis self-management have concluded that it is difficult to recommend any one program in preference to another due to inconsistencies in the study designs used to evaluate different programs. The Stanford Arthritis Self-Management Program (ASMP), most commonly delivered by trained lay leaders, is a generic program widely used for people with rheumatological disorders. We have developed a more specific program expressly for people with osteoarthritis of the knee (OAKP). It includes information designed to be delivered by health professionals and results in improvements in pain, function and quality of life. Aim: To determine whether, for people with osteoarthritis (OA) of the knee, the OAKP implemented in a primary health care setting can achieve and maintain clinically meaningful improvements in more participants than ASMP delivered in the same environment. Methods/Design The effectiveness of the programs will be compared in a single-blind randomized study. Participants: 146 participants with established OA knee will be recruited. Volunteers with coexistent inflammatory joint disease or serious co-morbidities will be excluded. Interventions: Participants will be randomised into either OAKP or ASMP groups and followed for 6 months. Measurements: Assessments will be immediately before and after the intervention and at 6 months. Primary outcome measures will be WOMAC and SF-36 questionnaires and a VAS for pain. Secondary outcomes will include balance, tested using a timed single leg balance test and a timed step test and self-efficacy. Data will be analysed using repeated measures ANOVA. Discussion With an aging population the health care costs for people with arthritis are ever increasing. Although cost analysis is beyond the scope of this study, it is reasonable to expect that costs will be greater when health professionals deliver self-management programs as opposed to lay leaders. Consequently it is critical to examine the relative effectiveness of the primary care management strategies available for OA

Crop Updates 2000 Cereals - part 4

This session covers twelve papers from different authors: BREEDING 1.Response to subsoil acidity of wheat genotypes differing in Al-tolerance, C. Tang, Z. Rengel, E. Diatloff and B. McGann, Soil Science and Plant Nutrition/CLIMA, University of Western Australia 2. Application of molecular markers in Barley Improvement, Mehmet Cakir1, Nick Galwey1 and David Poulsen2, 1Plant Sciences, Faculty of Agriculture, University of Western Australia, 2Queensland Department of Primary Industries, Hermitage Research Station, Queensland 3. Implementation of molecular markers for wheat improvement in the Western Region, M. Carter1, A. Briney1, R. Wilson2, R.H. Potter1 and M.G.K. Jones1, 1Western Australian State Agricultural Biotechnology Centre, Murdoch University, 2Crop Industries, Agriculture Western Australia 4. Performance in 1999 of recently released wheat varieties in Western Australia, Robin Wilson, Iain Barclay, Robyn McLean, Dean Diepeveen and Robert Loughman, Agriculture Western Australia ECONOMICS 5. Outlook for prices and implications for rotations, Ross Kingwell1 2, Michael O’Connell1, Simone Blennerhasset1 1Agriculture Western Australia, 2University of Western Australia 6. Price Risk Management and the Western Australian Grain Producer, Benjamin Michael Tiller, Muresk Institute of Agriculture FORECASTING 7. Can we forecast wheat yields in Western Australia, Senthold Asseng1, Holger Meinke2, and Bill Bowden3, 1CSIRO Plant Industry, 2 APSRU/DPI, 3Agriculture Western Australia ON FARM TESTING 8. On-farm testing, the quiet revolution continues, Jeff Russell1, Ivan Lee2 1Agriculture Western Australia, 2 Farmer Kunjin TopCrop group, Corrigin GRAIN STORAGE 9. CD-ROM tool for growers and advisers: Managing on-farm grain storage – effective practices for the delivery of quality assured products, Clare Johnson1, Chris Newman2 1Quality Wheat CRC Ltd, 2Production Resource Protection Services, Agriculture Western Australia 10. The Internet as a tool for managing grain insects, Robert Emery, Romolo Tassone and Ernestos Kostas, Agriculture Western Australia SUMMER CROPS AND WINDBREAK EFFECT ON YIELD 11. Summer crop Update and agronomic considerations, Graeme Ralph, Pioneer Hi-Bred Australia Pty Ltd 12. The effect of tree windbreaks on grain yield in the medium and low rainfall areas in Western Australia, Robert Sudmeyer, David Hall and Harvey Jones, Agriculture Western Australi

Heimler Syndrome is Caused by Hypomorphic Mutations in the Peroxisome-Biogenesis Genes PEX1 and PEX6

Heimler syndrome (HS) is a rare recessive disorder characterized by sensorineural hearing loss (SNHL), amelogenesis imperfecta, nail abnormalities and occasional or late onset retinal pigmentation. We ascertained eight families with HS, and - using a whole exome sequencing approach - identified biallelic mutations in PEX1 or PEX6 in six of them. Loss of function mutations in both genes are known causes of a spectrum of autosomal recessive peroxisome biogenesis disorders (PBDs), including Zellweger syndrome. PBDs are characterized by leukodystrophy, hypotonia, SNHL, retinopathy, and skeletal, craniofacial, and liver abnormalities. We demonstrate that each HS family has at least one hypomorphic allele that results in extremely mild peroxisomal dysfunction. Although individuals with HS share some subtle clinical features found in PBDs, the overlap is minimal and the diagnosis was not suggested by routine blood and skin fibroblast analyses used to detect PBDs. In conclusion, our findings define Heimler syndrome as a mild PBD, expanding the pleiotropy of mutations in PEX1 and PEX6

Voting on sustainable transport: communication and governance challenges in Greater Manchester's ‘congestion charge’ referendum

In December 2008, the Greater Manchester electorate voted to reject a £3 billion package of transport measures that would have included investment in the conurbation's bus, tram and rail networks and walking and cycling infrastructure, together with, and partially funded by, the introduction of a congestion charge. The proposals followed a successful bid to the UK Government Transport Innovation Fund (TIF). High levels of car use present challenges to cities, and the TIF bid can be seen as an attempt to address these by promoting and facilitating a modal shift. The paper reflects on the debates surrounding the proposals, which led to a referendum. In particular, it explores the challenges of communicating complex, controversial plans in a fragmented and contested political arena

Cause of Death and Predictors of All-Cause Mortality in Anticoagulated Patients With Nonvalvular Atrial Fibrillation : Data From ROCKET AF

M. Kaste on työryhmän ROCKET AF Steering Comm jäsen.Background-Atrial fibrillation is associated with higher mortality. Identification of causes of death and contemporary risk factors for all-cause mortality may guide interventions. Methods and Results-In the Rivaroxaban Once Daily Oral Direct Factor Xa Inhibition Compared with Vitamin K Antagonism for Prevention of Stroke and Embolism Trial in Atrial Fibrillation (ROCKET AF) study, patients with nonvalvular atrial fibrillation were randomized to rivaroxaban or dose-adjusted warfarin. Cox proportional hazards regression with backward elimination identified factors at randomization that were independently associated with all-cause mortality in the 14 171 participants in the intention-to-treat population. The median age was 73 years, and the mean CHADS(2) score was 3.5. Over 1.9 years of median follow-up, 1214 (8.6%) patients died. Kaplan-Meier mortality rates were 4.2% at 1 year and 8.9% at 2 years. The majority of classified deaths (1081) were cardiovascular (72%), whereas only 6% were nonhemorrhagic stroke or systemic embolism. No significant difference in all-cause mortality was observed between the rivaroxaban and warfarin arms (P=0.15). Heart failure (hazard ratio 1.51, 95% CI 1.33-1.70, P= 75 years (hazard ratio 1.69, 95% CI 1.51-1.90, P Conclusions-In a large population of patients anticoagulated for nonvalvular atrial fibrillation, approximate to 7 in 10 deaths were cardiovascular, whereasPeer reviewe

Multiple novel prostate cancer susceptibility signals identified by fine-mapping of known risk loci among Europeans

Genome-wide association studies (GWAS) have identified numerous common prostate cancer (PrCa) susceptibility loci. We have fine-mapped 64 GWAS regions known at the conclusion of the iCOGS study using large-scale genotyping and imputation in 25 723 PrCa cases and 26 274 controls of European ancestry. We detected evidence for multiple independent signals at 16 regions, 12 of which contained additional newly identified significant associations. A single signal comprising a spectrum of correlated variation was observed at 39 regions; 35 of which are now described by a novel more significantly associated lead SNP, while the originally reported variant remained as the lead SNP only in 4 regions. We also confirmed two association signals in Europeans that had been previously reported only in East-Asian GWAS. Based on statistical evidence and linkage disequilibrium (LD) structure, we have curated and narrowed down the list of the most likely candidate causal variants for each region. Functional annotation using data from ENCODE filtered for PrCa cell lines and eQTL analysis demonstrated significant enrichment for overlap with bio-features within this set. By incorporating the novel risk variants identified here alongside the refined data for existing association signals, we estimate that these loci now explain ∼38.9% of the familial relative risk of PrCa, an 8.9% improvement over the previously reported GWAS tag SNPs. This suggests that a significant fraction of the heritability of PrCa may have been hidden during the discovery phase of GWAS, in particular due to the presence of multiple independent signals within the same regio

Whole Exome Sequencing Reveals the Major Genetic Contributors to Nonsyndromic Tetralogy of Fallot

Rationale: Familial recurrence studies provide strong evidence for a genetic component to the predisposition to sporadic, nonsyndromic Tetralogy of Fallot (TOF), the most common cyanotic congenital heart disease phenotype. Rare genetic variants have been identified as important contributors to the risk of congenital heart disease, but relatively small numbers of TOF cases have been studied to date. Objective: We used whole exome sequencing to assess the prevalence of unique, deleterious variants in the largest cohort of nonsyndromic TOF patients reported to date. Methods and Results: Eight hundred twenty-nine TOF patients underwent whole exome sequencing. The presence of unique, deleterious variants was determined; defined by their absence in the Genome Aggregation Database and a scaled combined annotation-dependent depletion score of ≥20. The clustering of variants in 2 genes, NOTCH1 and FLT4, surpassed thresholds for genome-wide significance (assigned as P<5×10−8) after correction for multiple comparisons. NOTCH1 was most frequently found to harbor unique, deleterious variants. Thirty-one changes were observed in 37 probands (4.5%; 95% CI, 3.2%–6.1%) and included 7 loss-of-function variants 22 missense variants and 2 in-frame indels. Sanger sequencing of the unaffected parents of 7 cases identified 5 de novo variants. Three NOTCH1 variants (p.G200R, p.C607Y, and p.N1875S) were subjected to functional evaluation, and 2 showed a reduction in Jagged1-induced NOTCH signaling. FLT4 variants were found in 2.4% (95% CI, 1.6%–3.8%) of TOF patients, with 21 patients harboring 22 unique, deleterious variants. The variants identified were distinct to those that cause the congenital lymphoedema syndrome Milroy disease. In addition to NOTCH1, FLT4 and the well-established TOF gene, TBX1, we identified potential association with variants in several other candidates, including RYR1, ZFPM1, CAMTA2, DLX6, and PCM1. Conclusions: The NOTCH1 locus is the most frequent site of genetic variants predisposing to nonsyndromic TOF, followed by FLT4. Together, variants in these genes are found in almost 7% of TOF patients

Genetic mechanisms of critical illness in COVID-19.

Host-mediated lung inflammation is present1, and drives mortality2, in the critical illness caused by coronavirus disease 2019 (COVID-19). Host genetic variants associated with critical illness may identify mechanistic targets for therapeutic development3. Here we report the results of the GenOMICC (Genetics Of Mortality In Critical Care) genome-wide association study in 2,244 critically ill patients with COVID-19 from 208 UK intensive care units. We have identified and replicated the following new genome-wide significant associations: on chromosome 12q24.13 (rs10735079, P = 1.65 × 10-8) in a gene cluster that encodes antiviral restriction enzyme activators (OAS1, OAS2 and OAS3); on chromosome 19p13.2 (rs74956615, P = 2.3 × 10-8) near the gene that encodes tyrosine kinase 2 (TYK2); on chromosome 19p13.3 (rs2109069, P = 3.98 ×  10-12) within the gene that encodes dipeptidyl peptidase 9 (DPP9); and on chromosome 21q22.1 (rs2236757, P = 4.99 × 10-8) in the interferon receptor gene IFNAR2. We identified potential targets for repurposing of licensed medications: using Mendelian randomization, we found evidence that low expression of IFNAR2, or high expression of TYK2, are associated with life-threatening disease; and transcriptome-wide association in lung tissue revealed that high expression of the monocyte-macrophage chemotactic receptor CCR2 is associated with severe COVID-19. Our results identify robust genetic signals relating to key host antiviral defence mechanisms and mediators of inflammatory organ damage in COVID-19. Both mechanisms may be amenable to targeted treatment with existing drugs. However, large-scale randomized clinical trials will be essential before any change to clinical practice