Τρίτη 12 Ιουλίου 2016

What Factors Predict Who Will Have a Strong Social Network Following a Stroke?

Purpose
Measures of social networks assess the number and nature of a person's social contacts, and strongly predict health outcomes. We explored how social networks change following a stroke and analyzed concurrent and baseline predictors of social networks 6 months poststroke.
Method
We conducted a prospective longitudinal observational study. Participants were assessed 2 weeks (baseline), 3 months, and 6 months poststroke. Measures comprised the Stroke Social Network Scale (Northcott & Hilari, 2013), Medical Outcomes Study Social Support Survey (Sherbourne & Stewart, 1991), National Institutes of Health Stroke Scale (Brott et al., 1989), Frenchay Aphasia Screening Test (Enderby, Wood, Wade, & Langton Hewer, 1987), Frenchay Activities Index (Wade, Legh-Smith, & Langton Hewer, 1985), and Barthel Index (Mahoney, Wood, & Barthel, 1958). Analyses of variance and standard multiple regression were used to analyze change and identify predictors.
Results
Eighty-seven participants (37% with aphasia) were recruited; 71 (16% with aphasia) were followed up at 6 months. Social network scores declined poststroke (p = .001). Whereas the Children and Relatives factors remained stable, the Friends factor significantly weakened (p R 2 = .42). There were 2 baseline predictors: premorbid social network and aphasia (adjusted R 2 = .60).
Conclusions
Social networks declined poststroke. Aphasia was the only stroke-related factor measured at the time of the stroke that predicted social network 6 months later.

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What Factors Predict Who Will Have a Strong Social Network Following a Stroke?

Purpose
Measures of social networks assess the number and nature of a person's social contacts, and strongly predict health outcomes. We explored how social networks change following a stroke and analyzed concurrent and baseline predictors of social networks 6 months poststroke.
Method
We conducted a prospective longitudinal observational study. Participants were assessed 2 weeks (baseline), 3 months, and 6 months poststroke. Measures comprised the Stroke Social Network Scale (Northcott & Hilari, 2013), Medical Outcomes Study Social Support Survey (Sherbourne & Stewart, 1991), National Institutes of Health Stroke Scale (Brott et al., 1989), Frenchay Aphasia Screening Test (Enderby, Wood, Wade, & Langton Hewer, 1987), Frenchay Activities Index (Wade, Legh-Smith, & Langton Hewer, 1985), and Barthel Index (Mahoney, Wood, & Barthel, 1958). Analyses of variance and standard multiple regression were used to analyze change and identify predictors.
Results
Eighty-seven participants (37% with aphasia) were recruited; 71 (16% with aphasia) were followed up at 6 months. Social network scores declined poststroke (p = .001). Whereas the Children and Relatives factors remained stable, the Friends factor significantly weakened (p R 2 = .42). There were 2 baseline predictors: premorbid social network and aphasia (adjusted R 2 = .60).
Conclusions
Social networks declined poststroke. Aphasia was the only stroke-related factor measured at the time of the stroke that predicted social network 6 months later.

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What Factors Predict Who Will Have a Strong Social Network Following a Stroke?

Purpose
Measures of social networks assess the number and nature of a person's social contacts, and strongly predict health outcomes. We explored how social networks change following a stroke and analyzed concurrent and baseline predictors of social networks 6 months poststroke.
Method
We conducted a prospective longitudinal observational study. Participants were assessed 2 weeks (baseline), 3 months, and 6 months poststroke. Measures comprised the Stroke Social Network Scale (Northcott & Hilari, 2013), Medical Outcomes Study Social Support Survey (Sherbourne & Stewart, 1991), National Institutes of Health Stroke Scale (Brott et al., 1989), Frenchay Aphasia Screening Test (Enderby, Wood, Wade, & Langton Hewer, 1987), Frenchay Activities Index (Wade, Legh-Smith, & Langton Hewer, 1985), and Barthel Index (Mahoney, Wood, & Barthel, 1958). Analyses of variance and standard multiple regression were used to analyze change and identify predictors.
Results
Eighty-seven participants (37% with aphasia) were recruited; 71 (16% with aphasia) were followed up at 6 months. Social network scores declined poststroke (p = .001). Whereas the Children and Relatives factors remained stable, the Friends factor significantly weakened (p R 2 = .42). There were 2 baseline predictors: premorbid social network and aphasia (adjusted R 2 = .60).
Conclusions
Social networks declined poststroke. Aphasia was the only stroke-related factor measured at the time of the stroke that predicted social network 6 months later.

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The effect of microphone wind noise on the amplitude modulation of wind turbine noise and its mitigation

Microphone wind noise can corrupt outdoor recordings even when wind shields are used. When monitoring wind turbine noise, microphone wind noise is almost inevitable because measurements cannot be made in still conditions. The effect of microphone wind noise on two amplitude modulation (AM) metrics is quantified in a simulation, showing that even at low wind speeds of 2.5 m/s errors of over 4 dBA can result. As microphone wind noise is intermittent, a wind noise detection algorithm is used to automatically find uncorrupted sections of the recording, and so recover the true AM metrics to within ±2/±0.5 dBA.



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Release from masking for small spatial separations: Effects of age and hearing lossa)

Spatially separating target and masking speech can result in substantial spatial release from masking (SRM) for normal-hearing listeners. In this study, SRM was examined at eight spatial configurations of azimuth angle: maskers co-located with the target (0°) or symmetrically separated by 2°, 4°, 6°, 8°, 10°, 15°, or 30°. Results revealed that different listening groups (young normal-hearing, older normal-hearing, and older hearing-impaired) required different minimum amounts of spatial separation between target and maskers to achieve SRM. The results also indicated that aging was the contributing factor predicting SRM at smaller separations, whereas hearing loss was the contributing factor at larger separations.



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Beam diffraction effects in sound transmission of a fluid-embedded viscoelastic plate at normal incidence

The characteristics of a sound beam transmitted through a fluid-embedded viscoelastic plate at normal incidence can deviate significantly from those of a plane-wave. Phenomena such as frequency shift, signal amplification or reduction, and changed beam properties, are observed for resonance peaks associated with specific leaky Lamb modes. When interpreting measurements using plane-wave theory, such deviations will influence the measurement of material parameters and plate thickness. The finite-element-based models used in this study describe the signal chain from the electrical voltage excitation at the piezoelectric transducer terminals to the sound pressure propagated through the plate and fluid to the position at which it is measured by a hydrophone. The measured phenomena are described at a quantitative level.



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A polymorphism in human estrogen-related receptor beta (ESRRβ) predicts audiometric temporary threshold shift.

A polymorphism in human estrogen-related receptor beta (ESRRβ) predicts audiometric temporary threshold shift.

Int J Audiol. 2016 Jul 11;:1-9

Authors: Bhatt I, Phillips S, Richter S, Tucker D, Lundgren K, Morehouse R, Henrich V

Abstract
OBJECTIVE: A non-synonymous single nucleotide polymorphism (rs61742642; C to T, P386S) in the ligand-binding domain of human estrogen-related receptor beta (ESRRβ) showed possible association to noise-induced hearing loss (NIHL) in our previous study.
DESIGN: This study was conducted to examine the effect of the ESRRβ rs61742642 T variant on temporary threshold shift (TTS). TTS was induced by 10 minutes of exposure to audiometric narrow-band noise centered at 2000 Hz. Hearing thresholds and distortion product otoacoustic emissions input output function (DP IO) at 2000, 3000, and 4000 Hz were measured before and after the noise exposure.
STUDY SAMPLE: Nineteen participants with rs61742642 CT genotype and 40 participants with rs61742642 CC genotype were recruited for the study.
RESULTS: Participants with the CT genotype acquired a significantly greater TTS without convincing evidence of greater DP IO temporary level shift (DPTLS) compared to participants with the CC genotype.
CONCLUSION: The results indicated that the ESRRβ polymorphism is associated with TTS. Future studies were recommended to explore molecular pathways leading to increased susceptibility to NIHL.

PMID: 27399974 [PubMed - as supplied by publisher]



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A polymorphism in human estrogen-related receptor beta (ESRRβ) predicts audiometric temporary threshold shift.

A polymorphism in human estrogen-related receptor beta (ESRRβ) predicts audiometric temporary threshold shift.

Int J Audiol. 2016 Jul 11;:1-9

Authors: Bhatt I, Phillips S, Richter S, Tucker D, Lundgren K, Morehouse R, Henrich V

Abstract
OBJECTIVE: A non-synonymous single nucleotide polymorphism (rs61742642; C to T, P386S) in the ligand-binding domain of human estrogen-related receptor beta (ESRRβ) showed possible association to noise-induced hearing loss (NIHL) in our previous study.
DESIGN: This study was conducted to examine the effect of the ESRRβ rs61742642 T variant on temporary threshold shift (TTS). TTS was induced by 10 minutes of exposure to audiometric narrow-band noise centered at 2000 Hz. Hearing thresholds and distortion product otoacoustic emissions input output function (DP IO) at 2000, 3000, and 4000 Hz were measured before and after the noise exposure.
STUDY SAMPLE: Nineteen participants with rs61742642 CT genotype and 40 participants with rs61742642 CC genotype were recruited for the study.
RESULTS: Participants with the CT genotype acquired a significantly greater TTS without convincing evidence of greater DP IO temporary level shift (DPTLS) compared to participants with the CC genotype.
CONCLUSION: The results indicated that the ESRRβ polymorphism is associated with TTS. Future studies were recommended to explore molecular pathways leading to increased susceptibility to NIHL.

PMID: 27399974 [PubMed - as supplied by publisher]



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A polymorphism in human estrogen-related receptor beta (ESRRβ) predicts audiometric temporary threshold shift

10.1080/14992027.2016.1192693<br/>Ishan Bhatt

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Allele-specific PCR for detecting the deafness-associated mitochondrial 12S rRNA mutations.

Allele-specific PCR for detecting the deafness-associated mitochondrial 12S rRNA mutations.

Gene. 2016 Jul 7;

Authors: Ding Y, Xia BH, Liu Q, Li MY, Huang SX, Zhuo GC

Abstract
Mutations in mitochondrial 12S rRNA (MT-RNR1) are the important causes of sensorineural hearing loss. Of these mutations, the homoplasmic m.1555A>G or m.1494C>T mutation in the highly conserved A-site of MT-RNR1 gene has been found to be associated with both aminoglycoside-induced and non-syndromic hearing loss in many families worldwide. Since the m.1555A>G and m.1494C>T mutations are sensitive to ototoxic drugs, therefore, screening for the presence of these mutations is important for early diagnosis and prevention of deafness. For this purpose, we recently developed a novel allele-specific PCR (AS-PCR) which is able to simultaneously detect these mutations. To assess its accuracy, in this study, we employed this method to screen the frequency of m.1555A>G and m.1494C>T mutations in 200 deafness patients and 120 healthy subjects. Consequently, four m.1555A>G and four m.1494C>T mutations were identified; among these, only one patient with the m.1494C>T mutation had an obvious family history of hearing loss. Strikingly, clinical evaluation showed that this family exhibited a high penetrance of hearing loss. In particular, the penetrances of hearing loss were 80% with the aminoglycoside included and 20% when excluded. PCR-Sanger sequencing of the mitochondrial genomes confirmed the presence of the m.1494C>T mutation and identified a set of polymorphisms belonging to mitochondrial haplogroup A. However, the lack of functional variants in mitochondrial and nuclear modified genes (GJB2 and TRMU) in this family indicated that mitochondrial haplogroup and nuclear genes may not play important roles in the phenotypic expression of the m.1494C>T mutation. Thus, other modification factors, such as environmental factor, aminoglycosides or epigenetic modification may have contributed to the high penetrance of hearing loss in this family. Taken together, our data showed that this assay is an effective approach that could be used for detection the deafness-associated MT-RNR1 mutations.

PMID: 27397648 [PubMed - as supplied by publisher]



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A polymorphism in human estrogen-related receptor beta (ESRRβ) predicts audiometric temporary threshold shift

10.1080/14992027.2016.1192693<br/>Ishan Bhatt

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A polymorphism in human estrogen-related receptor beta (ESRRβ) predicts audiometric temporary threshold shift

10.1080/14992027.2016.1192693<br/>Ishan Bhatt

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A polymorphism in human estrogen-related receptor beta (ESRRβ) predicts audiometric temporary threshold shift.

A polymorphism in human estrogen-related receptor beta (ESRRβ) predicts audiometric temporary threshold shift.

Int J Audiol. 2016 Jul 11;:1-9

Authors: Bhatt I, Phillips S, Richter S, Tucker D, Lundgren K, Morehouse R, Henrich V

Abstract
OBJECTIVE: A non-synonymous single nucleotide polymorphism (rs61742642; C to T, P386S) in the ligand-binding domain of human estrogen-related receptor beta (ESRRβ) showed possible association to noise-induced hearing loss (NIHL) in our previous study.
DESIGN: This study was conducted to examine the effect of the ESRRβ rs61742642 T variant on temporary threshold shift (TTS). TTS was induced by 10 minutes of exposure to audiometric narrow-band noise centered at 2000 Hz. Hearing thresholds and distortion product otoacoustic emissions input output function (DP IO) at 2000, 3000, and 4000 Hz were measured before and after the noise exposure.
STUDY SAMPLE: Nineteen participants with rs61742642 CT genotype and 40 participants with rs61742642 CC genotype were recruited for the study.
RESULTS: Participants with the CT genotype acquired a significantly greater TTS without convincing evidence of greater DP IO temporary level shift (DPTLS) compared to participants with the CC genotype.
CONCLUSION: The results indicated that the ESRRβ polymorphism is associated with TTS. Future studies were recommended to explore molecular pathways leading to increased susceptibility to NIHL.

PMID: 27399974 [PubMed - as supplied by publisher]



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A polymorphism in human estrogen-related receptor beta (ESRRβ) predicts audiometric temporary threshold shift.

A polymorphism in human estrogen-related receptor beta (ESRRβ) predicts audiometric temporary threshold shift.

Int J Audiol. 2016 Jul 11;:1-9

Authors: Bhatt I, Phillips S, Richter S, Tucker D, Lundgren K, Morehouse R, Henrich V

Abstract
OBJECTIVE: A non-synonymous single nucleotide polymorphism (rs61742642; C to T, P386S) in the ligand-binding domain of human estrogen-related receptor beta (ESRRβ) showed possible association to noise-induced hearing loss (NIHL) in our previous study.
DESIGN: This study was conducted to examine the effect of the ESRRβ rs61742642 T variant on temporary threshold shift (TTS). TTS was induced by 10 minutes of exposure to audiometric narrow-band noise centered at 2000 Hz. Hearing thresholds and distortion product otoacoustic emissions input output function (DP IO) at 2000, 3000, and 4000 Hz were measured before and after the noise exposure.
STUDY SAMPLE: Nineteen participants with rs61742642 CT genotype and 40 participants with rs61742642 CC genotype were recruited for the study.
RESULTS: Participants with the CT genotype acquired a significantly greater TTS without convincing evidence of greater DP IO temporary level shift (DPTLS) compared to participants with the CC genotype.
CONCLUSION: The results indicated that the ESRRβ polymorphism is associated with TTS. Future studies were recommended to explore molecular pathways leading to increased susceptibility to NIHL.

PMID: 27399974 [PubMed - as supplied by publisher]



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