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To investigate the impact of Interleukin-16 (IL- 16) and Adiponectin (ANP) gene single nucleotide polymorphisms (SNPs), gene- gene interactions and haplotype on late-onset Alzheimer’s disease (LOAD) risk.
Hardy-Weinberg equilibrium (HWE), haplotype and pairwise linkage disequilibrium (LD) analysis were investigated by using SNPstats (available online at http://bioinfo.iconcologia.net/SNPstats). Generalized multifactor dimensionality reduction (GMDR) was used to examine interaction among 4 SNPs, odds ratio (OR) and 95% confident interval (95%CI) were calculated by logistic regression model.
LOAD risk was significantly higher in carriers of rs266729- G allele than those with CC genotype (CG+ GG versus CC), OR (95%CI) =1.61 (1.26-1.96), and higher in carriers of rs1501299- T allele, OR (95%CI) = 1.62 (1.32-2.12), lower in carriers of rs4072111- T allele, adjusted OR (95%CI) =0.65 (0.44-0.93). We also found a significant gene- gene interaction between rs266729 and rs4072111. Participants with CG or GG of rs266729 and CC of rs4072111 genotype have the highest LOAD risk, OR (95%CI) = 2.62 (1.64 -3.58). Haplotype containing the rs266729- G and rs1501299- T alleles were associated with increased LOAD risk, OR (95%CI)= 1.83 (1.32- 2.43), and haplotype containing the rs1131445- C and rs4072111- T alleles were associated with decreased LOAD risk, OR (95%CI)= 0.53 (0.18- 0.95).
We concluded that rs266729 and rs1501299 minor alleles were associated with increased LOAD risk, but rs4072111 minor allele was associated with decreased LOAD risk. We also found that interaction involving rs266729 and rs4072111, and haplotype combinations were associated with LOAD risk.
interleukin-16, adiponectin, single nucleotide polymorphism, interaction, haplotype
Relationship of polymorphisms and haplotype in interleukin-16 and adiponectin gene with late-onset Alzheimer’s disease risk
Honglei Yin,1 Yuzhen Zhang,1 Linlin Hua,2 Jinfeng Li,1 Zhilei Zeng,2 Xiaopeng Yang,2 Bin Gong,1 Shuang Geng,1 Yajun Liu,1 Hui Zhang,1 Yanqiu Liu,1 Jing Zhao,1 and Yunliang Wang2,1
2017 Oct 3
In humans, mutations in the genes encoding components of the dystrophin-glycoprotein complex cause muscular dystrophy. Specifically, primary mutations in the genes encoding α-, β-, γ-, and δ-sarcoglycan have been identified in humans with limb-girdle muscular dystrophy. Mice lacking γ-sarcoglycan develop progressive muscular dystrophy similar to human muscular dystrophy. Without γ-sarcoglycan, β- and δ-sarcoglycan are unstable at the muscle membrane and α-sarcoglycan is severely reduced. The expression and localization of dystrophin, dystroglycan, and laminin-α2, a mechanical link between the actin cytoskeleton and the extracellular matrix, appears unaffected by the loss of sarcoglycan. We assessed the functional integrity of this mechanical link and found that isolated muscles lacking γ-sarcoglycan showed normal resistance to mechanical strain induced by eccentric muscle contraction. Sarcoglycan-deficient muscles also showed normal peak isometric and tetanic force generation. Furthermore, there was no evidence for contraction-induced injury in mice lacking γ-sarcoglycan that were subjected to an extended, rigorous exercise regimen. These data demonstrate that mechanical weakness and contraction-induced muscle injury are not required for muscle degeneration and the dystrophic process. Thus, a nonmechanical mechanism, perhaps involving some unknown signaling function, likely is responsible for muscular dystrophy where sarcoglycan is deficient.
Muscle degeneration without mechanical injury in sarcoglycan deficiency
A. A. Hack,*† L. Cordier,‡ D. I. Shoturma,‡ M. Y. Lam,† H. L. Sweeney,‡ and E. M. McNally†§
1999 Sep 14;
Providers of psychological therapies are encouraged to offer patients choice about their treatment, but there is very little information about what preferences people have or the impact that meeting these has on treatment outcomes.
Cross-sectional survey of people receiving psychological treatment from 184 NHS services in England and Wales. 14,587 respondents were asked about treatment preferences and the extent to which these were met by their service. They were also asked to rate the extent to which therapy helped them cope with their difficulties.
Most patients (12,549-86.0 %, 95 % CI: 85.5-86.6) expressed a preference for at least one aspect of their treatment. Of these, 4,600 (36.7 %, 95 % CI: 35.8-37.5) had at least one preference that was not met. While most patients reported that their preference for appointment times, venue and type of treatment were met, only 1,769 (40.5 %) of the 4,253 that had a preference for gender had it met. People who expressed a preference that was not met reported poorer outcomes than those with a preference that was met (Odds Ratios: appointment times = 0.29, venue = 0.32, treatment type = 0.16, therapist gender = 0.32, language in which treatment was delivered = 0.40).
Most patients who took part in this survey had preferences about their treatment. People who reported preferences that were not met were less likely to state that treatment had helped them with their problems. Routinely assessing and meeting patient preferences may improve the outcomes of psychological treatment
Psychological treatment, Choice behaviour, Patient preference, Psychotherapy, Treatment outcome
Patient preference in psychological treatment and associations with self-reported outcome: national cross-sectional survey in England and Wales
Ryan Williams, Lorna Farquharson, Lucy Palmer, Paul Bassett, Jeremy Clarke, David M. Clark, and Mike J. Crawfordcorresponding author