Notes

Free-space eye communications utilizing orbital-angular-momentum multiplexing combined with MIMO-based spatial multiplexing.
ROC analyses showed the PPST is effective in discriminating "cases" versus "non-cases" on pain-related disability, pain-fear and catastrophizing. Results reveal the PPST is effective for rapidly screening youth with acute pain for pain and psychosocial symptomatology. An important next step will be to examine the validity of the PPST in predicting recovery outcomes of acute pain samples. PERSPECTIVE This article presents the Pediatric Pain Screening Tool (PPST) as a measure for rapidly screening youth with acute pain for pain and psychosocial symptomatology. The tool categorizes youth into low, moderate or high-risk groups and discriminates among those with versus without clinically significant levels of disability, pain-related fear and catastrophizing.
Actigraphy-based measurements of physiologic parameters may enable design of patient-centric heart failure (HF) clinical trials. Recently, the Heart Failure Collaboratory focused on recommendations for meaningful change and use of actigraphy as an end point in HF clinical trials. We aimed to evaluate randomized controlled trials (RCTs) that have quantified the impact of HF interventions using actigraphy.

Using a scoping review strategy, we evaluated the use of actigraphy in HF RCTs. Studies were identified through electronic searches of Embase, OVID Medline, PubMed, and Cochrane Review. Data on trial characteristics and results were collected.

We identified 11 RCTs with a total of 1,455 participants. The risk of bias across the included trials was high overall. All trials had the primary outcomes reflecting measures of either physical activity (n=8), sleep (n=2), or both (n=1). Five trials evaluated response to pharmacologic therapies compared with placebo, 3 evaluated physical activity interventions, 2 evaluated group or cognitive therapy, and 1 evaluated sleep-ventilation strategy. Sample sizes ranged from 30 to 619 participants. There was significant heterogeneity relating to device type, body placement site, and handling of missing actigraphy data. Duration of monitoring ranged from 48 hours to 12 weeks. None of the studies evaluating pharmacologic therapies (n=5) demonstrated a significant improvement of actigraphy-based primary end point measurements.

There is significant heterogeneity in the use, methodology, and results of actigraphy-based HF RCTs. Our results highlight the need to develop, standardize, and validate actigraphy-specific outcomes for use in HF clinical trials.
There is significant heterogeneity in the use, methodology, and results of actigraphy-based HF RCTs. Our results highlight the need to develop, standardize, and validate actigraphy-specific outcomes for use in HF clinical trials.
Blood-brain barrier (BBB) damage is closely related to various neurological disorders, including bacterial meningitis (BM). Determining a reliable strategy to prevent BBB damage in the context of infection would be highly desirable. In the present study, we investigated the implications of the long non-coding RNA (lncRNA) nuclear paraspeckle assembly transcript 1 (NEAT1) in moderating BBB damage.

In vitro BBB models were developed by co-culturing hCMEC/D3 cells with glioma cells, whereupon the glioma-exposed endothelial cells (GECs) were treated with a series of mimics, inhibitors, overexpression plasmids, and shRNAs for evaluating whether NEAT1, microRNA-135a (miR-135a) and hypoxia-inducible factor 1α (HIF1α) mediated BBB integrity and permeability. Furthermore, the in vivo biological function of NEAT1 was validated in a mouse model of BBB damage.

NEAT1 and HIF1α were determined to be up-regulated, while miR-135a was under-expressed in GECs. As demonstrated by chromatin immunoprecipitation and dual-luciferase reporter assays, NEAT1 could bind to miR-135a, and HIF1α was confirmed as a target of miR-135a. Either overexpression of NEAT1 or depletion of miR-135a impaired the integrity and augmented the permeability of BBB. However, HIF1α silencing could reverse the BBB damage induced by NEAT1 overexpression or by inhibition of miR-135a. In vivo experiments substantiated that knockdown of NEAT1 could alleviate BBB damage in living mice.

Hence, NEAT1 knockdown prevents BBB disruption and exerts promise as a potential target for BM treatment.
Hence, NEAT1 knockdown prevents BBB disruption and exerts promise as a potential target for BM treatment.
We assessed the utility of EndoPAT, a device that measures reactive hyperemia index (RHI) as a clinical screening tool for identifying low coronary flow reserve (CFR). Distinguishing normal from low CFR aids assessment for coronary microvascular dysfunction (CMD) or large vessel coronary artery disease (CAD).

From June 2014-May 2019, in a convenience sample, we measured RHI in adults undergoing clinically indicated cardiac Rubidium-82 positron emission tomography/computed tomography (PET/CT) at a single center. Exclusion criteria were inability to consent, lack of English proficiency, and physical limitation. We defined low RHI as <1.67 and low CFR as <2.5. Distribution of RHI was skewed so we used its natural logarithm (LnRHI) to calculate Pearson correlation and area under the curve (AUC).

Of 265 patients with PET/CT, we enrolled 131, and 100 had adequate data. Patients had a mean age of 61years (SD=12), 46% were female, 29% non-white. see more Thirty-six patients had low RHI, and 60 had depressed CFR. LnRHI did not distinguish patients with low from normal CFR (AUC=0.53; 95% Cl, 0.41-0.64) and did not correlate with CFR (r=-0.021, p=0.83). Low RHI did not distinguish patients with traditional CAD risk factors, presence of calcification, or perfusion defect (p>0.05). Conversely, mean augmentation index, a measure of arterial stiffness, was higher with low RHI (p=0.005) but not CFR (p=0.625). RHI was lower in patients we identified as CMD (low CFR, no perfusion defect and calcium score of 0) (1.88 versus 2.21, p=0.35) although we were underpowered (n=12) to meet statistical significance.

Peripheral RHI is insufficient as a clinical screening tool for low CFR as measured by cardiac PET/CT. Differences in vascular pathology assessed by each method may explain this finding.
Peripheral RHI is insufficient as a clinical screening tool for low CFR as measured by cardiac PET/CT. Differences in vascular pathology assessed by each method may explain this finding.
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