The Family’s Voice: Caregiving for an Older Adult

The purpose of this research was to explore the family as a unit, in particular the effects on the multigenerational family when at least one person is giving care to an adult over the age of 65. While, most prior research focused on the caregiver, this study looked at family as a whole single unit. The respondents were asked to describe how the caregiving affected them personally as well as how it affected the family. The sample for this study included 16 adult family members of caregivers for a person over age 65. Data was collected utilizing an online survey. Respondents were recruited with the assistance of local senior assisted living and apartment communities and by some postings in local social work groups. Respondents voiced that life was now stressful and frustrating. Although some revealed there were benefits, many stated the caregiving affected the family in an adverse way. This study confirmed the idea that having a family member caring for an older adult member does affect the dynamics of the whole family

The Family’s Voice: Caregiving for an Older Adult

The purpose of this research was to explore the family as a unit, in particular the effects on the multigenerational family when at least one person is giving care to an adult over the age of 65. While, most prior research focused on the caregiver, this study looked at family as a whole single unit. The respondents were asked to describe how the caregiving affected them personally as well as how it affected the family. The sample for this study included 16 adult family members of caregivers for a person over age 65. Data was collected utilizing an online survey. Respondents were recruited with the assistance of local senior assisted living and apartment communities and by some postings in local social work groups. Respondents voiced that life was now stressful and frustrating. Although some revealed there were benefits, many stated the caregiving affected the family in an adverse way. This study confirmed the idea that having a family member caring for an older adult member does affect the dynamics of the whole family

Does protein kinase R mediate TNF-α- and ceramide-induced increases in expression and activation of matrix metalloproteinases in articular cartilage by a novel mechanism?

We investigated the role of the proinflammatory cytokine TNF-α, the second messenger C(2)-ceramide, and protein kinase R (PKR) in bovine articular cartilage degradation. Bovine articular cartilage explants were stimulated with C(2)-ceramide or TNF-α for 24 hours. To inhibit the activation of PKR, 2-aminopurine was added to duplicate cultures. Matrix metalloproteinase (MMP) expression and activation in the medium were analysed by gelatin zymography, proteoglycan release by the dimethylmethylene blue assay, and cell viability by the Cytotox 96(® )assay. C(2)-ceramide treatment of cartilage explants resulted in a significant release of both pro- and active MMP-2 into the medium. Small increases were also seen with TNF-α treatment. Incubation of explants with 2-aminopurine before TNF-α or C(2)-ceramide treatment resulted in a marked reduction in expression and activation of both MMP-2 and MMP-9. TNF-α and C(2)-ceramide significantly increased proteoglycan release into the medium, which was also inhibited by cotreatment with 2-aminopurine. A loss of cell viability was observed when explants were treated with TNF-α and C(2)-ceramide, which was found to be regulated by PKR. We have shown that C(2)-ceramide and TNF-α treatment of articular cartilage result in the increased synthesis and activation of MMPs, increased release of proteoglycan, and increased cell death. These effects are abrogated by treatment with the PKR inhibitor 2-aminopurine. Collectively, these results suggest a novel role for PKR in the synthesis and activation of MMPs and support our hypothesis that PKR and its activator, PACT, are implicated in the cartilage degradation that occurs in arthritic disease

Considerations for accurate gene expression measurement by reverse transcription quantitative PCR when analysing clinical samples

Reverse transcription quantitative PCR is an established, simple and effective method for RNA measurement. However, technical standardisation challenges combined with frequent insufficient experimental detail render replication of many published findings challenging. Consequently, without adequate consideration of experimental standardisation, such findings may be sufficient for a given publication but cannot be translated to wider clinical application. This article builds on earlier standardisation work and the MIQE guidelines, discussing processes that need consideration for accurate, reproducible analysis when dealing with patient samples. By applying considerations common to the science of measurement (metrology), one can maximise the impact of gene expression studies, increasing the likelihood of their translation to clinical tools

Familial 4;18 chromosome translocation resulting in trisomy 4p and monosomy 18p: affected individuals with discordant phenotype

No Abstract.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/62156/1/2225_ftp.pd

Odds of Autism at 5 to 10 Years of Age for Children Who Did Not Pass Their AABR Newborn Hearing Screen, But Were Diagnosed with Normal Hearing

Background: Research has found atypical Auditory Brainstem Response (ABR) activity in some children with Autism Spectrum Disorder (ASD). The current study examined whether an association may also be found between ASD and pass/refer results obtained via Automated Auditory Brainstem Response (AABR) screening. As stewards of large-scale AABR data, an AABR – ASD association may be of interest to EHDI programs. Methods: State EHDI data for 29,350 children born in Maine between 2003 and 2005 were linked with education records, including special education status, for the 2010/2011 and 2013/2014 school years. Results: Children who did not pass their AABR screen but were later documented to have typical hearing were at more than eight times the odds of being identified with ASD at 5 to 7 years of age, and over six times the odds at 8 to 10 years of age. Conclusion: Newborns who did not pass their AABR screen but were subsequently diagnosed with typical hearing, experienced higher rates of ASD five to 10 years later. With further research evidence, this may create opportunities for EHDI programs to support and facilitate the work of colleagues in the ASD community, as well as further assist families already touched by EHDI systems

Exogenous sphingomyelinase increases collagen and sulphated glycosaminoglycan production by primary articular chondrocytes: an in vitro study

We previously established a role for the second messenger ceramide in protein kinase R (PKR)-mediated articular cartilage degradation. Ceramide is known to play a dual role in collagen gene regulation, with the effect of ceramide on collagen promoter activity being dependent on its concentration. Treatment of cells with low doses of sphingomyelinase produces small increases in endogenous ceramide. We investigated whether ceramide influences articular chondrocyte matrix homeostasis and, if so, the role of PKR in this process. Bovine articular chondrocytes were stimulated for 7 days with sphingomyelinase to increase endogenous levels of ceramide. To inhibit PKR, 2-aminopurine was added to duplicate cultures. De novo sulphated glycosaminoglycan and collagen synthesis were measured by adding [(35)S]-sulphate and [(3)H]-proline to the media, respectively. Chondrocyte phenotype was investigated using RT-PCR and Western blot analysis. Over 7 days, sphingomyelinase increased the release of newly synthesized sulphated glycosaminoglycan and collagen into the media, whereas inhibition of PKR in sphingomyelinase-treated cells reduced the level of newly synthesized sulphated glycosaminoglycan and collagen. Sphingomyelinase treated chondrocytes expressed col2a1 mRNA, which is indicative of a normal chondrocyte phenotype; however, a significant reduction in type II collagen protein was detected. Therefore, small increments in endogenous ceramide in chondrocytes appear to push the homeostatic balance toward extracellular matrix synthesis but at the expense of the chondrocytic phenotype, which was, in part, mediated by PKR