Miracle-dz/UniFAR-FTUs huggingface dataset:
The Acceptability and Efficacy of Using iPads in Music Therapy to Support Wellbeing with Older Adults: A Pilot Study

Portable technology has the potential to help support the wellbeing of older adults living in the community, particularly when targeting the health risk factors of social isolation and low self-esteem. This mixed-method feasibility study investigated the acceptability and efficacy of using iPads1 compared to traditional music instruments (TMI) with older adults living privately in the community. Five women, 71 - 96 years old, were recruited from a community-based day respite centre in Brisbane. Participants were randomly assigned to either the TMI or iPad group, and engaged in five sessions of activity-based music therapy. Participants completed journal entries following each session to detail their experiences, and were assessed for levels of perceived social isolation and global self-esteem pre- and post-intervention. Five themes were found for acceptability of iPads: learning was inherent to all sessions, differences in mood outcomes, differences in emotional communications, playing on an iPad resulted in greater creativity and freedom, and the importance of the environmental and structural considerations. There were no significant differences on scores of social isolation or self-esteem either between (TMI vs. iPad) or within (pre- vs. post-test) the treatment groups, however themes of developing social cohesion, group identity, and enhanced positive self-concepts suggest both iPads and TMIs contributed towards factors of wellbeing for the participants. Collectively, the encouraging findings present an entry point in illustrating that technology can be an acceptable and potentially successful tool for use in music therapy with older people living in the community.
RecruitmentModulating Pulmonary Neutrophil Lung Infection by Streptococcus pneumoniae Reverses Age-Associated Susceptibility to -Tocopherol Form of Vitamin E a The

Streptococcus pneumoniae infections are an important cause of morbidity and mortality in older patients. Uncontrolled neutrophil-driven pulmonary inﬂammation exacerbates this disease. To test whether the a -tocopherol ( a -Toc) form of vitamin E, a regulator of immunity, can modulate neutrophil responses as a preventive strategy to mitigate the age-associated decline in resistance to S. pneumoniae , young (4 mo) and old (22–24 mo) C57BL/6 mice were fed a diet containing 30-PPM (control) or 500-PPM (supplemented) a -Toc for 4 wk and intratracheally infected with S. pneumoniae . Aged mice fed a control diet were exquisitely more susceptible to S. pneumoniae than young mice. At 2 d postinfection, aged mice suffered 1000-fold higher pulmonary bacterial burden, 2.2-fold higher levels of neutrophil recruitment to the lung, and a 2.25-fold higher rate of lethal septicemia. Strikingly, a -Toc supplementation of aged mice resulted in a 1000-fold lower bacterial lung burden and full control of infection. This a -Toc– induced resistance to pneumococcal challenge was associated with a 2-fold fewer pulmonary neutrophils, a level comparable to S. pneumoniae –challenged, conventionally fed young mice. a -Toc directly inhibited neutrophil egress across epithelial cell monolayers in vitro in response to pneumococci or hepoxilin-A 3 , an eicosanoid required for pneumococcus-elicited neutrophil trans epithelial migration. a -Toc altered expression of multiple epithelial and neutrophil adhesion molecules involved in including CD18/CD11b, and ICAM-1. These ﬁndings suggest that a -Toc enhances resistance of aged mice to bacterial pneumonia by modulating the innate immune response, a ﬁnding that has potential clinical signiﬁcance in combating infection in aged individuals through nutritional intervention. The Journal of Immunology , 2015, 194: 000–000.
Preprocessing PPG and ECG Signals to Estimate Blood Pressure Based on Noninvasive Wearable Device

Accurate systolic and diastolic blood pressure measurement is still an open problem in biomedical engineering. This paper introduced a method how to preprocess the PPG and ECG signals to get a series of parameters to estimate blood pressure. It developed a threshold detector to extract characteristic points of PPG and ECG waves and calculated several useful features such as pulse wave velocity. The paper also introduced a BP-feature based model by using those features to estimate SBP and DBP. The accuracy of detection algorithm reached 98.2% by comparing with SFM database. The estimation results were validated by a large-scale dataset we acquired by strict experiment procedures. The average deviation error in estimating SBP and DBP was 0.25 and 2.24 mmHg respectively. The standard deviation between the measured and predicted blood pressure was 8.92 mmHg for systolic pressure and 8.13mmHg for diastolic pressure, which met the standard of AAMI. The results indicated that the BP-feature based model has a reliable estimation of blood pressure.
Cell Surface Externalization of Annexin A1 as a Failsafe Mechanism Preventing Inflammatory Responses during Secondary Necrosis1

The engulfment of apoptotic cells is of crucial importance for tissue homeostasis in multicellular organisms. A failure of this process results in secondary necrosis triggering proinflammatory cytokine production and autoimmune disease. In the present study, we investigated the role of annexin A1, an intracellular protein that has been implicated in the efficient removal of apoptotic cells. Consistent with its function as bridging protein in the phagocyte synapse, opsonization of apoptotic cells with purified annexin A1 strongly enhanced their phagocytic uptake. A detailed analysis, however, surprisingly revealed that annexin A1 was hardly exposed to the cell surface of primary apoptotic cells, but was strongly externalized only on secondary necrotic cells. Interestingly, while the exposure of annexin A1 failed to promote the uptake of these late secondary necrotic cells, it efficiently prevented induction of cytokine production in macrophages during engulfment of secondary necrotic cells. Our results therefore suggest that annexin A1 exposure during secondary necrosis provides an important failsafe mechanism counteracting inflammatory responses, even when the timely clearance of apoptotic cells has failed.
SurvivalCell Maturation, Cytokine Production, and The Tec Kinases Itk and Rlk Regulate NKT

The Tec kinases Itk and Rlk are required for efﬁcient positive selection of conventional CD4 (cid:1) and CD8 (cid:1) T cells in the thymus. In contrast, recent studies have shown that these Tec kinases are dispensable for the development of CD8 (cid:1) T cells with characteristics of innate T cells. These ﬁndings raise questions about the potential role of Itk and Rlk in NKT cell development, because NKT cells represent a subset of innate T cells. To address this issue, we examined invariant NKT cells in Itk (cid:2) / (cid:2) and Itk/Rlk (cid:2) / (cid:2) mice. We ﬁnd, as has been reported previously, that Itk (cid:2) / (cid:2) mice have reduced numbers of NKT cells with a predominantly immature phenotype. We further show that this defect is greatly exacerbated in the absence of both Itk and Rlk, leading to a 7-fold reduction in invariant NKT cell numbers in the thymus of Itk/Rlk (cid:2) / (cid:2) mice and a more severe block in NKT cell maturation. Splenic Itk (cid:2) / (cid:2) and Itk/Rlk (cid:2) / (cid:2) NKT cells are also functionally defective, because they produce little to no cytokine following in vivo activation. Tec kinase-deﬁcient NKT cells also show enhanced cell death in the spleen. These defects correlate with greatly diminished expression of CD122, the IL-2R/IL-15R (cid:3) -chain, and impaired expression of the T-box transcription factor, T-bet. These data indicate that the Tec kinases Itk and Rlk provide important signals for terminal maturation, efﬁcient cytokine production, and peripheral survival of NKT cells. The Journal of Immunology, 2008, 180: 3007–3018.
Case Study: Evaluating Road Performance and Sediment Generation during Simulated Wet Weather Hauling

Aggregate roads are the primary means of access to managed forestlands in western Oregon, but may facilitate sediment transport during rainfall, especially with traffic from heavy trucks. This transported sediment, typically in the means of suspended sediment or turbid effluent, may have detrimental effects on aquatic ecosystems, especially when roads are in proximity to creeks, streams and rivers. However, due to past construction practices and difficult terrain, many existing roads are stream-adjacent, and may require retrofitting to address potential delivery of fine sediment from its surface during rainfall. To evaluate a potential treatment to this problem, a heavily-instrumented field test was performed on a reconstructed aggregate forest road in Western Oregon which sought to test the potential of geosynthetic materials to sequester road sediment and improve road performance during wet-weather hauling. A sand filter berm wrapped with a non-woven geotextile provided 70% and more reduction in turbidity when tested under idealized laboratory conditions. Additionally, a geogrid reinforcement placed on the native road subgrade material prior to placing the aggregate layer reduced subgrade pressures experienced during loading, improving mechanical performance. When applied to well-graded aggregate, the geogrid reinforcement reduced rutting, a potential channel for flow of turbid runoff. When applied to a poorly-graded aggregate the geogrid reinforcement reduced relative breakage. Aggregate degradation and road performance may be improved with use of the geogrid reinforcement and road sediment may be effectively sequestered with use of a geotextile-wrapped filter sand berm when applied correctly. Targeted applications of these approaches are recommended where desired levels of road performance and water quality improvement may justify the additional labor and materials required. However, more replicates and larger scale application may address some levels of variability that are difficult to address under the constraints of an intensive field test.
Endosomal Compartments of B Cells Shuttle Cargo between the Cell Surface and CD22 Is a Recycling Receptor That Can

CD22 is a member of the sialic acid-binding Ig-like lectin (Siglec) family that is known to be a regulator of B cell signaling. Its B cell-speciﬁc expression makes it an attractive target for immunotoxin-mediated B cell depletion therapy for the treatment of B cell lymphomas and autoimmune diseases. Although CD22 is well documented to be an endocytic receptor, it is believed that after internalization, it is targeted for degradation. We show in this study that CD22 is instead constitutively recycled to the cell surface. We also ﬁnd that glycan ligand-based cargo is released from CD22 and accumulates intracellularly as CD22 recycles between the cell surface and endosomal compartments. In contrast, Abs to CD22 do not accumulate but remain bound to CD22 and recycle to the cell surface. The results have implications for development of agents that target CD22 as an endocytic receptor for delivery of cytotoxic cargo to B cells. The Journal of Immunology , 2011, 186: 000–000.
Physiological Autoantigen the Fate of B Cells that Recognize a Anergy and not Clonal Ignorance Determines

2 Autoantibodies to insulin arise spontaneously in the insulin autoimmune syndrome and in type I diabetes. In addition, administration of insulin to individuals without autoimmune disease routinely results in Abs that bind autologous hormone. These observations and ﬁndings in transgenic models of tolerance led to an inference that physiological levels of hormones and growth factors, such as insulin, are not sufﬁcient to induce tolerance in B cells, a state termed clonal ignorance. In contrast, we have discovered that virtually all conventional B cells expressing a low afﬁnity anti-insulin transgene interact with endogenous insulin and are effectively silenced for Ig production and for T cell-dependent immune responses. A fraction of transgenic B cells escapes silencing and functions autonomously to produce insulin Abs that may lower fasting blood sugars similar to an insulin autoimmune syndrome. These B cells have characteristics of a B1-like subset and are depleted by hypotonic peritoneal lysis. These ﬁndings question the concept of clonal ignorance and show that physiological concentrations of Ag may effectively silence conventional B cells even when the afﬁnity for autoantigen is low. Self-reactivity may arise in the repertoire because of compartmental differences that govern the fate of B cells and not as a result of true clonal ignorance. The Journal of Immunology, 2001, 166: 3194–3200. The V H and V k regions derived from the HyHEL10 mAb were removed and replaced with the 5 9 untranslated and L-VDJ or L-VJ DNA segments cloned from anti-insulin mAb125. The nucleotide sequences of the engineered 125V H and 125V k chains were conﬁrmed and the constructs tested for expression by in vitro transfection of B cells lines, as previously described (23). For microinjection, gene constructs were linearized with Sal I and puriﬁed chro- matographically. To avoid the possible complications of anti-insulin Abs on gestation, V H 125- m heavy chain and V k 125-C k founder mice were initially generated individually from microinjection of B6 3 DBA2 single cell oocytes (27). Founders were originally identiﬁed by Southern blot hybridization using cDNA probes on tail DNA digested with Bgl II and Pst for 125VH and with Hin dIII for 125V k genes. Based on hybridization signals relative to endogenous V genes, the number of transgene copies is estimated to be low ( , 3). Founder mice were backcrossed to C57BL/6 mice, and subsequent progeny were monitored for transgene transmission using PCR to identify V H and V k transgenes or by ﬂow cytometry to identify IgMa 1 B cells. Mice were intercrossed to obtain offspring that express both 125V H and 125V k transgenes, 125Tg. 125Tg mice were sub- sequently found to mate and reproduce normally. All animals used in the current study were backcrossed . 10 times to C57BL/6.
Novel Autocrine Loop in Inflammation Endogenous Danger Signal Tenascin-C: A Transcriptional Regulation of the

Inappropriate expression of proinﬂammatory mediators underpins the pathogenesis of autoimmune disease and tumor metastasis. The extracellular matrix glycoprotein tenascin-C is an endogenous activator of innate immunity that promotes the synthesis of inﬂammatory cytokines via activation of TLR4. Little tenascin-C is observed in most healthy adult tissues, but expression is speciﬁcally upregulated at sites of inﬂammation. Moreover, high levels of tenascin-C are associated with chronic inﬂammation and found in the tumor stroma. In this study, we show that the expression of tenascin-C is induced in immune myeloid cells activated by a varietyofinﬂammatory stimuli, including speciﬁc TLR ligands. Its synthesis is transcriptionally regulated and requires the speciﬁc activation of AKT/PI3K and NF- k B signaling pathways. Using a bioinformatic approach, we identiﬁed a large number of conserved noncoding regions throughout the tenascin-C genomic locus that may contribute to its transcriptional regulation during inﬂammation. We also demonstrate that tenascin-C expression is transient during acute inﬂammation. In contrast, persistently high levels of expression occur in the inﬂamed synovium of joints from rheumatoid arthritis patients. Thus, misregulated expression of this endogenous danger signal may promote an autocrine loop of inﬂammation and contribute to the persistence of inﬂammation in autoimmune diseases or to tumor egress and invasion during metastasis. The Journal of Immunology , 2010, 184: 2655–2662. These data as a key mediator in the RA joint. However, the origin of the high levels of tenascin-C in the joint is not known, and it is not clear how synovial tissue levels of this DAMP are regulated during inﬂammation. In this study, we show that tenascin-C expression correlates with disease activity in human rheumatoid joints. We also demonstrate thatthehighleveloftenascin-Csynthesisobservedindiseasedjointsisdrivenbyspeciﬁcsubsetsofsynovialcells,includingimmunecells ofthemyeloidlineage.Weshowthatalthoughtenascin-Cexpressionispersistentlyactivatedinchronicinﬂammation,itissubjecttotighttranscriptionalcontrolduringacuteinﬂammation;expressionis induced upon immune cell activation and then is effectively and rapidly downregulated. Finally, we provide the ﬁrst insights into the molecular machinery that exerts this control over endogenous tenascin-C expression in human myeloid cells during inﬂammation. Understanding how tenascin-C expression is regulated during an tissue levels of this
Inhibitor Inhibits DNA Repair Vitro.

COH29, a novel antimetabolite drug developed at City of Hope Cancer Center, has anticancer activity that stems primarily from the inhibition of human ribonucleotide reductase (RNR). This key enzyme in deoxyribonucleotide biosynthesis is the target of established clinical agents such as hydroxyurea (HU) and gemcitabine because of its critical role in DNA replication and repair. Herein we report that BRCA-1-defective human breast cancer cells are more sensitive than wild-type BRCA-1 counterparts to COH29 in vitro and in vivo . Microarray gene expression profiling showed that COH29 reduces expression of DNA repair pathway genes, suggesting that COH29 interferes with these pathways. It is well-established that BRCA1 plays a role in DNA damage repair, especially homologous recombination (HR) repair, to maintain genome integrity. In BRCA1-defective HCC1937 breast cancer cells, COH29 induced more double-strand breaks (DSB) and DNA-damage response (DDR) than in HCC1937+BRCA1 cells. By EJ5- and DR-GFP reporter assay, we found COH29 could inhibit NHEJ efficiency and that no HR activity was detected in HCC1937 cells, suggesting the repression of the NHEJ repair pathway may be involved in COH29-induced DSB in BRCA1-deficient HCC1937 cells. Furthermore, we observed accumulation of nuclear Rad51 foci in COH29-treated HCC1937+BRCA1 cells, suggesting BRCA1 plays a crucial role in repairing/recovering drug-induced DNA damage by recruiting Rad51 to damage sites. In summary, we have described additional biological effects of the RNR inhibitor COH29 that potentially strengthen its utility as an anticancer agent. NHEJ repair efficiency in a concentration-dependent manner. In the setting of the BRCA1-defective HCC1937 cells, which we also show are HR-deficient, this inhibition of NHEJ by COH29 dramatically reduced repair of DNA lesions. Indicative of this is that after COH29 treatment fewer Rad51 nuclear foci were observed in HCC1937 than in HCC1937+BRCA1 cells. In addition, our microarray results revealed that COH29 downregulated various DNA repair genes. These data suggest defective HR and NHEJ DNA repair pathways may contribute to the cytotoxicity of COH29 in BRCA1-deficient cells, and as a corollary that BRCA1 status plays a central role in determining the cytotoxicity of COH29 in cancer cells.
Accuracy and Usability of a Novel Algorithm for Detection of Accuracy and Usability of a Novel Algorithm for Detection of Irregular Pulse Using a Smartwatch Among Older Adults: Irregular Pulse Using a Smartwatch Among Older Adults: Observational Study Observational Study

Background: Atrial fibrillation (AF) is often paroxysmal and minimally symptomatic, hindering its diagnosis. Smartwatches may enhance AF care by facilitating long-term, noninvasive monitoring. Objective: This study aimed to examine the accuracy and usability of arrhythmia discrimination using a smartwatch. Methods: A total of 40 adults presenting to a cardiology clinic wore a smartwatch and Holter monitor and performed scripted movements to simulate activities of daily living (ADLs). Participants’ clinical and sociodemographic characteristics were abstracted from medical records.
Comparison of Aqueous Flare Values after Micropulse Transscleral Laser Treatment and Continuous Wave Transscleral Cyclophotocoagulation

ABSTRACT Purpose The purpose of this study was to analyse the changes in flare values after Micropulse Transscleral Laser Treatment for Glaucoma (MP-TLT) in patients with refractory glaucoma and to compare with the outcomes of patients who underwent continuous wave (CW) diode laser cyclophotocoagulation (CW-TSCPC). Methods In this single-centre study, we reviewed the medical records of 54 patients who underwent MP-TLT and 35 patients who underwent CW-TSCPC at Ankara University Faculty of Medicine, Department of Ophthalmology. Aqueous flare values were measured by laser flare photometry. Results The mean laser flare values in both groups (MP-TLT/CW-TSCPC) increased after surgery from 20.85 ± 8.74/22.14 ± 7.39 ph/ms at baseline to 48.52 ± 18.23/57.38 ± 20.08 ph/ms (P = .001) on day 1 and then progressively decreased to 44.13 ± 18.32/52.24 ± 20.56 in week 1, 40.5 ± 18.5/48.24 ± 19.23 week 2 and 35.28 ± 17.09/41.11 ± 16.7 month 1 (all p < .05) and returned to similar levels to baseline at month 3 and month 6 (both p > .05). Patients who achieved treatment success had significantly higher flare values than patients who failed on post-operative day 1, week 1 and week 2 in both groups. The flare values were significantly lower in the MP-TLT group than the CW-TSCPC group on post-operative day 1, week 1, week 2 and month 1 (all p < .05). There were no cases of prolonged post-operative inflammation or serious complications in both groups. Conclusion Intraocular inflammation, quantified by aqueous flare, may be a contributing factor to the IOP lowering effect of transscleral diode laser cyclophotocoagulation in the early post-operative period.