However, the survival benefits of AVR over conservative treatment have not been convincingly demonstrated in AS patients aged above 80.
Aim: To investigate the outcomes of patients aged 80 and over with symptomatic, severe AS and by analyzing the effects of patients
choice in either agreeing or refusing to undergo AVR, determine the survival benefits afforded by AVR.
Design: Cohort study.
Methods: Subjects aged 80 and over with severe symptomatic AS, diagnosed between 2001 and 2006 were segregated into three groups: subjects who underwent AVR (Group A); patients who were fit for AVR but declined surgery due to personal find more choice (Group B) and those who were not fit for surgery and were managed conservatively (Group C). Follow-up was conducted by out-patient attendances, review of medical records and telephone interviews. The primary endpoint was all-cause mortality.
Results: A total of 103 patients (86.0 +/- 4.2
years, 41 male) were identified and no patient was lost during follow-up. In Group A (n = 17), all 15 patients who underwent AVR were alive after 3.6 +/- Verteporfin in vivo 1.4 years follow-up and 2 died whilst awaiting AVR. Seventy-four percent of Group B (n = 24) and 76% of Group C (n = 62) died during follow-up. Group A had significantly better survival than B and C. (P 0.01) Amongst patients fit for AVR with similar operative risks (Groups A and B), refusal to undergo surgery (hazard ratio 12.61, P= 0.001)
was the only predictor of mortality in a multivariate model.
Conclusions: For elderly AS patients fit for surgery, the patients decision to refuse AVR is associated with a >12-fold increase in mortality risk. These findings have significant implications for informed decision-making when managing the fit, elderly patient with AS.”
“Singapore grouper iridovirus (SGIV), a major pathogen Dichloromethane dehalogenase of concern for grouper aquaculture, has a double-stranded DNA (dsDNA) genome with 162 predicted open reading frames, for which a total of 62 SGIV proteins have been identified. One of these, ORF158L, bears no sequence homology to any other known protein. Knockdown of orf158L using antisense morpholino oligonucleotides resulted in a significant decrease in virus yield in grouper embryonic cells. ORF158L was observed in nuclei and virus assembly centers of virus-infected cells. This observation led us to study the structure and function of ORF158L. The crystal structure determined at 2.2-angstrom resolution reveals that ORF158L partially exhibits a structural resemblance to the histone binding region of antisilencing factor 1 (Asf1), a histone H3/H4 chaperon, despite the fact that there is no significant sequence identity between the two proteins. Interactions of ORF158L with the histone H3/H4 complex and H3 were demonstrated by isothermal titration calorimetry (ITC) experiments.
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