After being involved in an accident where I was hit from behind my insurance company (swiftcover) put me in touch with Albany Assistance for a courtesy car. When I received my own vehicle back after being repaired I contacted my insurance co to let them know the hire car was no longer required.
This was Friday afternoon, I received a voicemail on Monday asking me to phone Albany to arrange collection, I tried over and over to phone them but no one was answering the phone. Tuesday arrives and I try to phone again, no joy. After returning home I find a letter from Albany saying they tried to take the car today but as no one was home they couldn’t and if I don’t call them ASAP they would have to inform the police. I ring the number on the letter, yes, you’ve guessed it – no reply.

So I ring the insurance co and tell them I want this car collecting and I am peeved off. The car is collected the next day, Wednesday.

25 days later I receive a letter from Albany informing me they are taking

Hi, I had an fault accident last year on my husbands car. I was a named driver on his policy.

Our car rewnewal is in a month and I just need to ask when looking for a quote do i add the accident under his name as it was his policy or do i add it under my name because I was driving.

thanks

MAP3K7 and GSTZ1 are associated with human longevity: a two-stage case-control study using a multilocus genotyping.
Age (Dordr). 2012 May 11;
Authors: Di Cianni F, Campa D, Tallaro F, Rizzato C, De Rango F, Barale R, Passarino G, Canzian F, Gemignani F, Montesanto A, Landi S, Rose G
Abstract
The pathways that regulate energy homeostasis, the mechanisms of damage repair, and the signaling response to internal environmental changes or external signals have been shown to be critical in modulating lifespan of model organisms and humans. In order to investigate whether genetic variation of genes involved in these pathways contribute to longevity, a two-stage case-control study in two independent sets of long-lived individuals from Calabria (Italy) was performed. In stage 1, 317 SNPs in 104 genes were analyzed in 78 cases (median age 98 years) and 71 controls (median age 67 years). In stage 2, 31 candidate SNPs identified in stage 1 (π (markers) = 0.1) were analyzed in an independent sample composed by 288 cases (median age 92 years) and 554 controls (median age 67 years). Two SNPs, rs282070 located in intron 1 of the MAP3K7 gene, and rs2111699 located in intron 1 of the GSTZ1 gene, were significantly associated (after adjustment for multiple testing) with longevity in stage 2 (p = 1.1 × 10(-3) and p = 1.4 × 10(-3), respectively). Interestingly, both genes are implicated in the cellular response to internal and external environmental changes, playing a crucial role in the inflammation processes that accompany aging. Our data confirm that long-lived subjects are endowed with genetic variants that allow them to optimize these cellular responses and to better deal with environmental and internal stresses.
PMID: 22576335 [PubMed - as supplied by publisher]

 STANDARD LIFE EQUITY INCOME TRUST PLC Standard Life Equity Income Trust PLC announces the following unaudited net asset values (NAVs) as at close of business on 11 May 2012. Unless otherwise disclosed, …

 STANDARD LIFE EQUITY INCOME TRUST PLC Investment Objective The objective of Standard Life Equity Income Trust is to provide shareholders with an above average income from their equity investment while …

I have high excess insurance which makes me pretty much liable to pay for an accident where it’s my fault. I hit a car and did very minor damage to the rear wing – the repair was less than

Hiya,

New here so not sure this is even the right forum!

Basically November 07 I was pulling out of my parking spot and my car was a foot on to the road when a car I had seen at the top of the road in my mirror came whizzing down the road at approx 40 mph (in a 25 mph home zone) and smashed into my wing.

This was seen by 2 witnesses, she also admitted she shouldnt be on the road as she had just had an accident on the M1 – We swapped details and a week later I filled in a form my insurers sent me detailing what had happened, havnt heard anything since.

Moved out with my partner a year later but my parents still live at the address I had the accident, I have since changed insurers and have heard nothing about the accident at all untill I visited my parents house today….

Longevity of Neonatal Ductal Stenting for Congenital Heart Diseases with Duct-dependent Pulmonary Circulation.
Congenit Heart Dis. 2012 Apr 30;
Authors: Sivakumar K, Bhagyavathy A, Coelho R, Satish R, Krishnan P
Abstract
Introduction.  Ductal stent (DS) in duct-dependent pulmonary circulation is less morbid than neonatal Blalock-Taussig shunt. However, there is concern if DS provides an adequately long palliation before definitive repair. Methods.  This is a retrospective review of clinical follow-up of all consecutive infants after successful DS performed by a single operator. They were divided into three anatomic groups. Group A neonates had balloon valvotomy for critical pulmonary stenosis or pulmonary atresia with intact ventricular septum, who needed DS patency until the right ventricle was adequate to provide antegrade pulmonary flows. Group B patients with tetralogy of Fallot and pulmonary atresia suited for later biventricular repair needed ductal patency until conduit surgery was completed. Group C patients with functionally univentricular hearts needed DS patency until bidirectional Glenn shunt completion. Results.  Among 22 infants, four Group A patients followed for 26-54 months after balloon pulmonary valvotomy had adequate oxygen saturation and needed only short-term DS patency. In six out of nine Group B patients, corrective biventricular repair using conduits was performed after 5-14 months at a body weight of 5-7.5 kg. Bidirectional Glenn shunt and confluence repair were performed in seven of nine Group C patients weighing 6-8.5 kg after 8-15 months. The hilar pulmonary artery growth in B and C groups was adequate for surgical repair. No patient needed stent redilatations or additional shunts on follow-up for hypoxia. Four patients had sudden death. Conclusions.  The short-term patency of DS was adequate after balloon valvotomy for critical pulmonary stenosis or pulmonary atresia with intact ventricular septum. Duration of palliation by DS was also sufficient in univentricular hearts to allow adequate somatic growth before Glenn surgery. In patients with biventricular anatomy treated by DS, conduit repair had to be performed at a relatively early age. Interstage mortality was 18%.
PMID: 22548982 [PubMed - as supplied by publisher]

Genetic variation and human longevity.
Dan Med J. 2012 May;59(5):B4454
Authors: Soerensen M
Abstract
The overall aim of the PhD project was to elucidate the association of human longevity with genetic variation in major candidate genes and pathways of longevity. Based on a thorough literature and database search we chose to apply a pathway approach; to explore variation in genes composing the DNA damage signaling, DNA repair, GH/IGF-1/insulin signaling and pro-/antioxidant pathways. In addition, 16 genes which did not belong to the core of either pathway, however recurrently regarded as candidate genes of longevity (e.g. APOE), were included. In this way a total of 168 genes were selected for investigation. We decided to explore the genetic variation in the form of single nucleotide polymorphisms (SNPs), a highly investigated type of genetic variation. SNPs having potential functional impact (e.g. affecting binding of transcription factors) were identified, so were specific SNPs in the candidate genes previously published to be associated with human longevity. To cover the majority of the common genetic variation in the 168 gene regions (encoding regions plus 5,000 bp upstream and 1,000 downstream) we applied the tagging SNP approach via the HapMap Consortium. Consequently 1,536 SNPs were selected. The majority of the previous publications on genetic variation and human longevity had employed a case-control study design, e.g. comparing centenarians to middle-aged controls. This type of study design is somehow prone to bias introduced by for instance cohort effects, i.e. differences in characteristics of cases and controls, a kind of bias which is avoided when a prospective cohort is under study. Therefore, we chose to investigate 1,200 individuals of the Danish 1905 birth cohort, which have been followed since 1998 when the members were 92-93 years old. The genetic contribution to human longevity has been estimated to be most profound during the late part of life, thus these oldest-old individuals are excellent for investigating such effect. The follow-up survival data enabled performance of longitudinal analysis, which is quite unique in the field of genetic epidemiology of human longevity. Since the cohort was nearly extinct when initiating the PhD study we were able to conduct the longitudinal analyses as regression analyses enabling the estimation of the quantitative effects of the associated SNPs. However, this study explores the genetic contribution to survival during the ninth decade of life, hence, in order to investigate the genetic contribution to survival in younger elderly we also included 800 individuals of the Study of Middle-aged Danish twins (MADT). MADT was initiated in 1998 by random selection of 2,640 intact twin pairs from 22 consecutive birth years (1931-1952) via the Danish Central Person Registry. Only one twin from each twin pair was included in the PhD study. The inclusion of these 800 middle-aged individuals enabled the performance of case-control analysis. Consequently DNA was purified from 2,000 blood samples, genotyping was carried out via the GoldenGate genotyping platform (Illumina Inc.), quality control and data cleaning were conducted, leading to genotype data on 1,394 SNPs in 1,089 oldest-old and 736 middle-aged individuals. The genotype data were analysed at the single-SNP and haplotype levels, and for the 16 candidate genes also at the gene level. The analyses of the data set verified the association of a few of the 16 candidate genes not being part of the candidate pathways under study: SNPs in the APOE, CETP and IL6 genes, while the analyses of the 152 pathway-related genes pointed to new candidate genes of human longevity: especially SNPs in the INS, RAD52 and NTHL1 genes appeared promising. As part of these investigations, replication studies of the single-SNP level findings were conducted in German case-control samples of 1,613 oldest-old (ages 95-110) and 1,104 middle-aged individuals and in a Dutch prospective cohort of 563 oldest-old (age 85+). The Dutch oldest-old have been followed for approximately the same number of years as the Danish oldest-old. Interesting aspects of the study were that the majority of the rare alleles of the identified SNPs were longevity variants, not mortality variants, indicating that at least in our study population, longevity is primarily affected by positively acting minor alleles. Moreover, we observed sex-specific differences in the association of the genetic variation with survival during old age. Furthermore, the genotype data generated were used for a number of replication studies on variation in the FOXO3A, TERT and TERC genes. These studies were performed in response to new data being published on the association of genetic variation in the genes with longevity (FOXO3A and TERT) and with telomere length (TERT and TERC). Our studies verified a role of TERC in human telomere length and of FOXO3A in human longevity (survival from middle age to old age), while a novel role of TERC in human longevity was found. Finally, in addition to the literature and database searches, the genotype data generation and the data analyses mentioned here, RNA purification and qPCR experiments have been initiated in order to investigate gene expression of some of the genes holding SNPs found to be associated with human longevity. Data on one of these genes (IL6) have been included in a manuscript.
PMID: 22549493 [PubMed - as supplied by publisher]

 STANDARD LIFE EQUITY INCOME TRUST PLC Standard Life Equity Income Trust PLC announces the following unaudited net asset values (NAVs) as at close of business on 3 May 2012. Unless otherwise disclosed, …