Interest is growing in the creation of wearable sweat sensors for continuous, lowcost, and noninvasive health diagnosis at the molecular level. The biofouling phenomenon leads to degradation of sweat sensors' performance over time, further limiting the successive monitoring of human health status. However, to date, the mechanism of sweat fouling is still unclear, with the inability to provide effective guidance on antifouling strategies. This study clarifies chemical compositions in sweat fouling and fouling distributions on the surface of sensors. Gold film electrodes were prepared on glass and poly(ethylene terephthalate) (PET) substrates and contaminated by human facial sweat (from eccrine sweat glands and apocrine sweat glands) and palm sweat (only from eccrine sweat glands). A scanning electron microscope (SEM), an optical microscope (OM), and an atomic force microscope (AFM) were employed to study the surface morphology of biofouling electrodes. The existence of sweat fouling was characterized by AFM adhesion force, a Fourier transform infrared spectrometer (FTIR), and Xray photoelectron spectra (XPS). FTIR along with XPS was adopted to analyze the biofouling components, and differential reflectance spectroscopy (DRS) was undertaken to observe the distribution of biofouling on the surface of the electrodes. As a result, we found that neither skin cell pieces nor recognized protein adsorption is the dominant source of biofouling, but the lipids in sweat form an inhomogeneous fouling layer on the electrode surface to reduce the electrochemical reactivity of sensors. This study provides deeper insights into sweat biofouling components and distributions and points out the right direction for resolving the problem of limited continuity in wearable sweat sensors.
IntroductionRecent studies have indicated that the dosage of LMWH in patients with specific weights may be controversial. Therefore, we conducted a meta-analysis to explore an appropriate dosage of LMWH for the prevention and treatment of venous thromboembolism (VTE) in patients with obesity.Materials and methodsWe searched the PubMed, EMBASE, and Cochrane Library databases up to July 23, 2022. Study selection, bias analysis, and information extraction were performed by three independent reviewers. The occurrence or recurrence of VTE and bleeding events were the primary outcomes we assessed.ResultsEleven studies (a total of 6266 patients) were included in the prevention group, and 6 studies (a total of 3225 patients) were included in the treatment group. For VTE prophylaxis, compared with the standard-dosage group, the high-dosage group had a lower incidence of VTE (OR: 0.47, 95% CI: 0.27-0.82, P=0.007) and a similar incidence of bleeding events (OR: 0.86, 95% CI: 0.69-1.08, P=0.020). For VTE therapy, compared to the standard-dosage group, the reduced-dosage group had a similar incidence of VTE recurrence (OR: 0.86, 95% CI: 0.11-6.84, P=0.89) but a lower incidence of bleeding events (OR: 0.30, 95% CI: 0.10-0.89, P=0.03).ConclusionIn patients with obesity, increasing the dosage of LMWH is a more appropriate option for the prevention of VTE. Due to the limited evidence, reducing the therapeutic dosage of LMWH requires careful consideration. Larger-scale, well-designed randomized controlled trials are necessary.Systematic Review Registrationhttps://www.crd.york.ac.uk/prospero/display_record.php?, identifier ID=CRD42022298128.
Neovascularization and re-endothelialization rely on endothelial progenitor cells (EPCs). However, the recruitment and angiogenic roles of EPCs are subject to regulation through the vascular microenvironment, which remains largely unknown. Platelet-derived growth factor D (PDGF-D) is a new member of the PDGF family that binds the PDGFR-β homodimer. However, it remains unknown whether and how it affects the angiogenic capacity of EPCs and participates in tube-like formation. EPCs were derived from rat bone marrow cells, and the gain-of-function approach was used to study the effects of PDGF-D on the biological activities of EPCs. EPCs that stably express PDGF-D were generated by lentiviral-mediated transduction, and the expression levels were evaluated by western blotting and reverse transcription, followed by real-time quantitative polymerase chain reaction (RT-qPCR). The biological activities of EPCs evaluated in the present study included proliferation, adhesion, migration, tube formation and senescence. Furthermore, the downstream signaling of PDGF-D was explored by western blot analysis. The results revealed that the lentiviral-mediated expression of PDGF-D in the microenvironment promoted the migration, proliferation, adhesion and tube formation of EPCs. In addition, PDGF-D suppressed the senescence of EPCs. Mechanistically, PDGF-D induced the phosphorylation of several signaling molecules, including STAT3, AKT, ERK1/2, mTOR and GSK-3β, suggesting that PDGF-D enhanced the angiogenic function of EPCs through PDGF receptor-dependent and -independent signaling pathways. In conclusion, PDGF-D promotes the angiogenic capacity of EPCs, including proliferation, migration, adhesion and tube formation, and thereby contributes to angiogenesis.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.