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When a heavy atomic nucleus splits (fission), the resulting fragments are observed to emerge spinning1; this phenomenon has been a mystery in nuclear physics for over 40 years2,3. The internal generation of typically six or seven units of angular momentum in each fragment is particularly puzzling for systems that start with zero, or almost zero, spin. There are currently no experimental observations that enable decisive discrimination between the many competing theories for the mechanism that generates the angular momentum4–12. Nevertheless, the consensus is that excitation of collective vibrational modes generates the intrinsic spin before the nucleus splits (pre-scission). Here we show that there is no significant correlation between the spins of the fragment partners, which leads us to conclude that angular momentum in fission is actually generated after the nucleus splits (post-scission). We present comprehensive data showing that the average spin is strongly mass-dependent, varying in saw-tooth distributions. We observe no notable dependence of fragment spin on the mass or charge of the partner nucleus, confirming the uncorrelated post-scission nature of the spin mechanism. To explain these observations, we propose that the collective motion of nucleons in the ruptured neck of the fissioning system generates two independent torques, analogous to the snapping of an elastic band. A parameterization based on occupation of angular momentum states according to statistical theory describes the full range of experimental data well. This insight into the role of spin in nuclear fission is not only important for the fundamental understanding and theoretical description of fission, but also has consequences for the γ-ray heating problem in nuclear reactors13,14, for the study of the structure of neutron-rich isotopes15,16, and for the synthesis and stability of super-heavy elements17,18.

Background & Aims:: Crohn's disease is a common inflammatory disorder of the gut characterized by variation in both location and behavior. Chromosome 16 and the HLA region on chromosome 6 have been implicated in susceptibility to disease. Mutations in the NOD2/ CARD15 gene, recently identified on chromosome 16, have been associated with disease overall but are found in only 25% of patients. No data regarding their contribution to specific disease subtypes exist. Here we report a detailed genotype-phenotype analysis of 244 accurately characterized patients. Methods:: A total of 244 white patients with Crohn's disease recruited from a single center in the United Kingdom were studied. All patients were rigorously phenotyped and followed-up for a median time of 16 years. By using linkage disequilibrium mapping we studied 340 polymorphisms in 24 HILA genes and 3 NOD2/CARD15 polymorphisms. Results:: We show that NOD2/CARD15 mutations determine ileal disease only. We confirm that alleles on specific long-range HLA haplotypes determine overall susceptibility and describe novel genetic associations with susceptibility, location, and behavior of Crohn's disease. Conclusions:: The clinical pattern of Crohn's disease may be defined by specific genotypes. This study may provide the basis for a future molecular classification of disease.

ABSTRACTCytotoxic T-lymphocyte (CTL) activity plays a central role in control of viral replication and in determining outcome in cases of human immunodeficiency virus type 1 (HIV-1) infection. Incorporation of important CTL epitope sequences into candidate vaccines is, therefore, vital. Most CTL studies have focused upon small numbers of adult Caucasoid subjects infected with clade-B virus, whereas the global epidemic is most severe in sub-Saharan African populations and predominantly involves clade-C infection in both adults and children. In this study, sensitive enzyme-linked immunospot (elispot) assays have been utilized to identify the dominant Gag-specific CTL epitopes targeted by adults and children infected with clade-B or -C virus. Cohorts evaluated included 44 B-clade-infected Caucasoid American and African American adults and children and 37 C-clade-infected African adults and children from Durban, South Africa. The results show that 3 out of 46 peptides spanning p17Gagand p24Gagsequences tested contain two-thirds of the dominant Gag-specific epitopes, irrespective of the clade, ethnicity, or age group studied. However, there were distinctive differences between the dominant responses made by Caucasoids and Africans. Dominant responses in Caucasoids were more often within p17Gagpeptide residues 16 to 30 (38 versus 12%; P< 0.01), while p24Gagpeptide residues 41 to 60 contained the dominant Gag epitope more often in the African subjects tested (39 versus 4%;P< 0.005). Within this 20-mer p24Gag, an epitope presented by both B42 and B81 is defined which represents the dominant Gag response in >30% of the total infected population in Durban. This epitope is closely homologous with dominant HIV-2 and simian immunodeficiency virus Gag-specific CTL epitopes. The fine focusing of dominant CTL responses to these few regions of high immunogenicity is of significance to vaccine design.

&lt;it>Objective&lt;/it>. To identify HLA class II associations with anti &lt;it>β&lt;/it>&lt;inf>2&lt;/inf>&hyphen;glycoprotein I &lpar;&lt;it>β&lt;/it>2GPI&rpar; antibodies in a cohort of Caucasian patients with systemic lupus erythematosus &lpar;SLE&rpar; and to determine whether these &lt;it>HLA&lt;/it> genotypes act as restriction elements for lymphocyte proliferation to native human &lt;it>β&lt;/it>2GPI &lt;it>in vitro&lt;/it>. &lt;it>Methods&lt;/it>. Anti&hyphen;&lt;it>β&lt;/it>2GPI antibodies were detected in patient sera using enzyme&hyphen;linked immunosorbent assays &lpar;ELISAs&rpar;. &lt;it>HLA&lt;/it> class II alleles &lpar;&lt;it>DRB1&lt;/it>, &lt;it>DQB1&lt;/it>&rpar; were determined by polymerase chain reaction&hyphen;based DNA genotyping. &lt;it>In vitro&lt;/it> peripheral blood mononuclear cell &lpar;PBMC&rpar; responses to native human &lt;it>β&lt;/it>2GPI were measured in a 7&hyphen;day proliferation assay. &lt;it>Results&lt;/it>. We identified three groups of Caucasian SLE patients using these ELISAs. In group 1, 16 out of 18 SLE patients &lpar;89&percnt;&rpar; with anti&hyphen;&lt;it>β&lt;/it>2GPI antibodies were positive for HLA&hyphen;DRB1*0401&sol;4&sol;8, DR11 or DRB1*1302 &lpar;&lt;it>P&lt;/it>&equals;0.001 &lt;it>vs&lt;/it> controls&rpar; compared with 23 out of 53 patients &lpar;43&percnt;&rpar; in group 2 with anti&hyphen;cardiolipin antibodies only, 57 out of 151 patients &lpar;38&percnt;&rpar; in group 3 &lpar;SLE patients without anticardiolipin antibodies&rpar; and 109 out of 225 controls &lpar;48&percnt;&rpar;. Fourteen patients with anti&hyphen;&lt;it>β&lt;/it>2GPI antibodies had greater median stimulation indices to &lt;it>β&lt;/it>2GPI &lt;it>in vitro&lt;/it> compared with the 15 controls studied &lpar;&lt;it>P&lt;/it>&equals;0.04&rpar;. &lt;it>Conclusion&lt;/it>. The &lt;it>HLA&lt;/it> class II and PBMC proliferation data suggest that &lt;it>β&lt;/it>2GPI may be both a T&hyphen; and B&hyphen;cell autoantigen in SLE.