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Patient-led perspectives on ehealth: How might hyperpersonal data inform design?
Pam Briggs,Claire Hardy,Peter R. Harris,Elizabeth Sillence 한국HCI학회 2014 한국HCI학회 학술대회 Vol.2014 No.12
Patients and carers frequently get their health information and advice from websites containing patient-led, shared health experiences. This means that they often engage in a very idiosyncratic selection process in order to determine which websites have personally resonant material. In this paper we used a Repertory Grid (repgrid) technique to elicit the very personal constructs that individuals use to discriminate between websites. We recruited patients with chronic asthma and carers of people with multiple sclerosis (MS), presenting each patient/carer with a set of health websites relevant to their condition and asking them to sort them using a standard repgrid procedure. We were then able to generate hyperpersonal representations of those constructs associated with liked and trusted vs. disliked and mistrusted sites, giving us new insights into the ways individual patients can navigate the health web.
Yolanda R. Totten,Bonnie M. Hardy,Berry Bennett,Marie-Claire Rowlinson,,Susanne Crowe, 대한진단검사의학회 2019 Annals of Laboratory Medicine Vol.39 No.4
In Florida, where syphilis is a reportable disease, the number of primary and secondary (P&S) syphilis cases has increased from 3,266 in 2008–2010 to 5,340 in 2013–2015, a 63% increase. The objective of this study was to compare the performance and sensitivity of the syphilis reverse algorithm with the traditional algorithm for detecting P&S (infectious) syphilis cases. Clinical specimens from individuals who self-referred for syphilis testing at public health clinics were processed using the traditional algorithm (non-treponemal rapid plasma reagin (RPR) test followed by a confirmatory treponemal (EIA) test) and then further tested with the Architect Syphilis TP (ASTP) immunoassay (Abbott Diagnostics, Chicago, IL, USA) or by RPR confirmation, if needed (reverse algorithm). Of 1,079 specimens, 59 were positive for syphilis. The sensitivity of the reverse algorithm was 98.3% (58/59) and of the traditional algorithm was 72.9% (43/59). Based on clinical evidence, of the 16 traditional algorithm-negative but reverse algorithm-positive cases, 68.8% (11/16) were classified as missed P&S infections (treatment naïve) and 31.2% (5/16) were classified as missed past syphilis (latent or infections with documented linkage to care). The reverse algorithm enables the detection of additional P&S syphilis cases missed by our current traditional algorithm.
SIRT2 directs the replication stress response through CDK9 deacetylation
Zhang, Hui,Park, Seong-Hoon,Pantazides, Brooke G.,Karpiuk, Oleksandra,Warren, Matthew D.,Hardy, Claire W.,Duong, Duc M.,Park, So-Jeong,Kim, Hyun-Seok,Vassilopoulos, Athanassios,Seyfried, Nicholas T.,J National Academy of Sciences 2013 PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF Vol.110 No.33
<P>Sirtuin 2 (SIRT2) is a sirtuin family deacetylase that directs acetylome signaling, protects genome integrity, and is a murine tumor suppressor. We show that SIRT2 directs replication stress responses by regulating the activity of cyclin-dependent kinase 9 (CDK9), a protein required for recovery from replication arrest. SIRT2 deficiency results in replication stress sensitivity, impairment in recovery from replication arrest, spontaneous accumulation of replication protein A to foci and chromatin, and a G2/M checkpoint deficit. SIRT2 interacts with and deacetylates CDK9 at lysine 48 in response to replication stress in a manner that is partially dependent on ataxia telangiectasia and Rad3 related (ATR) but not cyclin T or K, thereby stimulating CDK9 kinase activity and promoting recovery from replication arrest. Moreover, wild-type, but not acetylated CDK9, alleviates the replication stress response impairment of SIRT2 deficiency. Collectively, our results define a function for SIRT2 in regulating checkpoint pathways that respond to replication stress through deacetylation of CDK9, providing insight into how SIRT2 maintains genome integrity and a unique mechanism by which SIRT2 may function, at least in part, as a tumor suppressor protein.</P>