New technique for replica symmetry breaking with application to the SK-model at and near T=0

We describe a novel method which allows the treatment of high orders of replica-symmetry-breaking (RSB) at low temperatures as well as at T=0 directly, without a need for approximations or scaling assumptions. It yields the low temperature order function q(a,T) in the full range $0\leq a <\infty$ and is complete in the sense that all observables can be calculated from it. The behavior of some observables and the finite RSB theory itself is analyzed as one approaches continuous RSB. The validity and applicability of the traditional continuous formulation is then scrutinized and a new continuous RSB formulation is proposed

Risk of basal cell carcinoma after Hodgkin's disease

Background: Basal cell cancer is a common skin cancer, yet studies of second tumors after Hodgkin's disease tend to exclude basal cell cancers as second malignant tumors from analysis. Basal cell carcinomas (BCC) are possibly more common in immunosuppressed patients and were recently implicated as indicators of subsequent malignancies. Materials and Methods: Our database of 1,120 patients with Hodgkin's disease (derived from the tumor registry) was investigated for the occurrence of later BCCs. Kaplan-Meier curves were calculated. Results: A total of 9 cases of BCC were observed 0-20 years after the diagnosis of Hodgkin's disease, One case relapsed after excision. The probability of second BCC was 2.1% after 15 years of follow-up and 7.1% after 20 years. Statistically, the risk for second BCC was increased only in younger patients and with prolonged follow-up, but not in the total group of patients with Hodgkin's disease. Conclusion: BCC is not a major threat: for the survivors of Hodgkin's disease, but continued follow-up is necessary

Genetics of subcortical vascular dementia

AbstractSubcortical vascular dementia or cerebral small vessel disease is a common cause of disability in the elderly. On magnetic resonance imaging the disease is manifested as white matter lesions, lacunes and microbleeds. Its etiology is complex, with age and hypertension as established risk factors. The heritability of white matter lesions is constantly high over different populations. Linkage studies identified several loci for these lesions however no genes responsible for the linkage signals had been identified so far. Results from genetic association studies using the candidate gene approach support the role of APOE, the renin–angiotensin system, as well as the Notch3 signaling pathway in the development of subcortical vascular dementia. The recent genomegenome wide association study on white matter lesions identified a novel locus on chromosome 17q25 harboring several genes such as TRIM65 and TRIM47 which pinpoints to possible novel mechanisms leading to these lesions

Angiotensinogen gene promoter haplotype and microangiopathy-related cerebral damage: results of the Austrian Stroke Prevention Study

BACKGROUND AND PURPOSE: Microangiopathy-related cerebral damage (MARCD) is a common finding in the elderly. It may lead to cognitive impairment and gait disturbances. Arterial hypertension and age are the most important risk factors. We assessed the association between MARCD and sequence alterations in the promoter region of the angiotensinogen (AGT) gene. METHODS: We studied 410 randomly selected community-dwelling individuals aged 50 to 75 years. MARCD was defined as early confluent or confluent white matter hyperintensities or lacunes on a 1.5-T MRI. The AGT promoter was analyzed by temporal temperature gradient gel electrophoresis and automated sequencing. RESULTS: We detected 4 polymorphic sites, at positions -6, -20, -153, and -218. They created 5 haplotypes, which we coded as A (-6:g, -20:a, -153:g, -218g), B (-6:a, -20:c, -153:g, -218:g), C (-6:a, -20:c, -153:a, -218:g), D (-6:a, -20:a, -153:g, -218:g), and E (-6:a, -20:a, -153:g, -218:a). MARCD was seen in 7 subjects (63.6%) carrying 2 copies of the B haplotype (B/B), in 12 subjects (38.7%) carrying 1 copy of the B haplotype in the absence of the A haplotype (B+/A-), but in only 70 subjects (19.0%) in the remaining cohort (P:<0.001). The odds ratios for the B/B and the B+/A- genotypes were 8.0 (95% CI, 2.1 to 31.1; P:=0.003) and 1.8 (95% CI, 0.8 to 4.2; P:=0.14) after adjustment for possible confounders. CONCLUSIONS: The B haplotype of the AGT promoter in the absence of the wild-type A haplotype might represent a genetic susceptibility factor for MARCD