Objective Autonomic imbalance is considered a psychopathological mechanism underlying major depressive disorder (MDD). Heart rate variability (HRV) is an index for autonomic activation. Poor sleep quality is common among patients with MDD. HRV biofeedback (BF) has been used for regulating autonomic balance among patients with physical illness and mental disorders. The purpose of present study was to examine the effects of HRV-BF on depressive symptoms, sleep quality, pre-sleep arousal, and HRV indices, in patients with MDD and insomnia. Methods In this case-controlled study, patients with MDD and Pittsburgh Sleep Quality Index (PSQI) score higher than 6 were recruited. The HRV-BF group received weekly 60-minute protocol for 6 weeks, and the control group who have matched the age and sex received medical care only. All participants were assessed on Beck Depression Inventory-II, Back Anxiety Inventory, PSQI, and Pre-Sleep Arousal Scale. Breathing rates and electrocardiography were also performed under resting state at pre-testing, and post-testing conditions and for the HRV-BF group, also at 1-month follow-up. Results In the HRV-BF group, symptoms of depression and anxiety, sleep quality, and pre-sleep arousal were significantly improved, and increased HRV indices, compared with the control group. Moreover, in the HRV-BF group, significantly improved symptoms of depression and anxiety, decreased breathing rates, and increased HRV indices were detected at post-testing and at 1-month follow-up, compared with pre-testing values. Conclusion This study confirmed that HRV-BF is a useful psychosocial intervention for improving autonomic balance, baroreflex, and symptoms of depression and insomnia in MDD patients.

Thermoresponsive poly(N-isopropyl acrylamide) (PNIPAM) microgels were patterned on polystyrene substrates via dip coating, creating cytocompatible substrates that provided spatial control over cell adhesion. This simple dip coating method, which exploits variable substrate withdrawal speeds form particle suspension formed stripes of densely-packed PNIPAM microgels, while spacings between the stripes contained sparsely-distributed PNIPAM microgels. The assembly of three different PNIPAM microgel patterns, namely patterns composed of 50 μm stripes/50 μm spacings, 50 μm stripes/100 μm spacings, and 100 μm stripes/100 μm spacings was verified using high-resolution optical micrographs and ImageJ analysis. PNIPAM microgels existed as monolayers within stripes and spacings, as revealed by atomic force microscopy (AFM). Upon cell seeding on PNIPAM micropatterned substrates, NIH3T3 fibroblast cells preferentially adhered within spacings to form cell patterns. Three days after cell seeding, cells proliferated to form confluent cell layers. The thermoresponsiveness of the underlying PNIPAM microgels was then utilized to recover fibroblast cell sheets from substrates simply by lowering the temperature, without disrupting the underlying PNIPAM microgel patterns. Harvested cell sheets similar to these have been used for multiple tissue engineering applications. Also, this simple, low cost, template-free dip coating technique can be utilized to micropattern multifunctional PNIPAM microgels, generating complex stimuli-responsive substrates to study cell-material interactions and allow drug delivery to cells in a spatially and temporally-controlled manners.

In patients with PACG, the long-term IOP-lowering effect and surgical complications of combined trabeculectomy and cataract extraction are comparable with those of trabeculectomy alone. However, the combined surgery incurred fewer subsequent surgical interventions.

Plants are an invaluable source of potential new anti-cancer drugs. Momordica charantia is one of these plants with both edible and medical value and reported to exhibit anticancer activity. To explore the potential effectiveness of Momordica charantia, methanol extract of Momordica charantia (MCME) was used to evaluate the cytotoxic activity on four human cancer cell lines, Hone-1 nasopharyngeal carcinoma cells, AGS gastric adenocarcinoma cells, HCT-116 colorectal carcinoma cells, and CL1-0 lung adenocarcinoma cells, in this study. MCME showed cytotoxic activity towards all cancer cells tested, with the approximate IC50 ranging from 0.25 to 0.35 mg/mL at 24 h. MCME induced cell death was found to be time-dependent in these cells. Apoptosis was demonstrated by DAPI staining and DNA fragmentation analysis using agarose gel electrophoresis. MCME activated caspase-3 and enhanced the cleavage of downstream DFF45 and PARP, subsequently leading to DNA fragmentation and nuclear condensation. The apoptogenic protein, Bax, was increased, whereas Bcl-2 was decreased after treating for 24 h in all cancer cells, indicating the involvement of mitochondrial pathway in MCME-induced cell death. These findings indicate that MCME has cytotoxic effects on human cancer cells and exhibits promising anti-cancer activity by triggering apoptosis through the regulation of caspases and mitochondria.

Wurtzite CdS nanoparticles have been lightly deposited on Cu2O cubes, octahedra, and rhombic dodecahedra to examine facet effects on the interfacial charge transfer in a photocatalytic reaction. Instead of an expected photocatalytic activity enhancement on the basis of a favorable band alignment at the heterojunction, CdS-decorated Cu2O octahedra and rhombic dodecahedra show drastically reduced photocatalytic activities. Further increasing the CdS deposition amount leads to complete suppression of photocatalytic activity. Cu2O cubes remain inactive even after CdS deposition. Transmission electron microscopy analysis reveals epitaxial growth of the (101) planes of CdS on the (110) planes of a Cu2O rhombic dodecahedron, whereas the (110) planes of CdS align parallel to the (111) planes of a Cu2O octahedron. Because facet-dependent photocatalytic activity can be understood from different degrees of band bending at the crystal surfaces, significantly upward bending for the CdS-contacting planes can explain the observed photocatalytic inactivity. This work demonstrates that strong facet effects tuning the band energies of both semiconductors at the heterojunctions make the predictions of an enhanced photocatalytic activity, simply through bulk band energy alignment analysis, highly unreliable.

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Aldehyde dehydrogenase 2 (ALDH2) is an enzyme that detoxifies reactive oxygen species (ROS)-generated aldehyde adducts such as 4-hydroxy-trans-2-nonenal (4-HNE). Previous meta-analyses have shown an increase in the risk of atrial fibrillation (AF) in patients with chronic alcohol consumption. ALDH2*2, a common dysfunctional polymorphism in the ALDH2 gene, has been linked to an increased risk of cancer and heart disease. We tested the effect of ALDH2 deficiency on alcohol-induced AF in a murine model of chronic-binge ethanol feeding, with ALDH2*2 knock-in (KI) mice generated by a CRISPR/CAS9 system. In addition, right atrial appendages were obtained from eight patients with AF undergoing open heart surgery. The results showed that burst atrial pacing induced a greater susceptibility to AF in ALDH2*2 KI mice exposed to chronic ethanol intoxication than in wild-type mice, resulting from a higher degree of 4-HNE accumulation and collagen deposition in their atria. Alda-1 attenuated transforming growth factor beta 1 (TGF-β1) expression and collagen deposition in the atria and reduced AF inducibility. Patients with AF and the ALDH2*2 allele exhibited greater oxidative stress and substrate remodeling in their atria than non-carriers. In conclusion, ALDH2 deficiency may increase the risk of chronic alcohol and tachypacing-induced AF through the accumulation of 4-HNE and increased ROS production.

Cancer stem cells (CSCs) are subpopulations of tumor masses with unique abilities in self-renewal, stemness maintenance, drug resistance, and the promotion of cancer recurrence. Recent studies have suggested that breast CSCs play essential roles in chemoresistance. Therefore, new agents that selectively target such cells are urgently required. Reactive oxygen species (ROS)-producing enzymes are the reason for an elevated tumor oxidant status. The nuclear factor erythroid 2-related factor 2 (Nrf2) is a transcriptional factor, which upon detecting cellular oxidative stress, binds to the promoter region of antioxidant genes. By triggering a cytoprotective response, Nrf2 maintains cellular redox status. Cripto-1 participates in the self-renewal of CSCs. Herein, luteolin, a flavonoid found in Taraxacum officinale extract, was determined to inhibit the expressions of stemness-related transcriptional factors, the ATP-binding cassette transporter G2 (ABCG2), CD44, aldehyde dehydrogenase 1 activity as well as the sphere formation properties of breast CSCs. Furthermore, luteolin suppressed the protein expressions of Nrf2, heme oxygenase 1 (HO-1), and Cripto-1 which have been determined to contribute critically to CSC features. The combination of luteolin and the chemotherapeutic drug, Taxol, resulted in enhanced cytotoxicity to breast cancer cells. These findings suggest that luteolin treatment significantly attenuated the hallmarks of breast cancer stemness by downregulating Nrf2-mediated expressions. Luteolin constitutes a potential agent for use in cancer stemness-targeted breast cancer treatments.