The propensity to use more repetitive negative thinking and less positive reappraisal is theorized to play an important role in depression. To date, little is known about the presumed enduring nature of these emotion regulation habits. Therefore, this study examined individual longitudinal trajectories and within-person sources of change in the habitual use of repetitive negative thinking and positive reappraisal.

Participants (N=320) completed twenty waves of data collection separated by one-week time intervals. At each wave, participants completed measures of habitual repetitive negative thinking, habitual positive reappraisal, perceived stress, and depression symptoms.

Growth curve modeling revealed that the prototypical longitudinal trajectories of habitual repetitive negative thinking and positive reappraisal were relatively stable over time. Yet, substantial variation occurred around the prototypical change trajectories. Perceived stress and depressive symptom severity emerged as within-person factors modulating concurrent levels of emotion regulation habits. Moreover, within-person cross-lagged analysis revealed that changes in repetitive negative thinking both predicted and were predicted by changes in perceived stress. No such within-person reciprocal relations were found for positive reappraisal.

This study covered only a period of five months, used self-report measures, and was conducted in a community sample. Furthermore, 25% of the participants did not complete all 20 waves of data collection.

These findings help to understand the enduring trait-like processes and within-person factors that may contribute to the longitudinal course of habitual repetitive negative thinking and positive reappraisal.

These findings help to understand the enduring trait-like processes and within-person factors that may contribute to the longitudinal course of habitual repetitive negative thinking and positive reappraisal.Biomimetic materials are often capable of subtly affecting tissue development, regeneration and carcinogenesis due to their high similarity to natural tissues. Despite the benefit of using such materials in tissue engineering, their prospective use in cancer therapy has been neglected, particularly the functions and mechanisms by which biomimetic materials mediate tumor suppression. Here, we prepare hierarchically constructed bone-mimetic selenium-doped hydroxyapatite nanoparticles (B-SeHANs), which recapitulate the uniaxially oriented hierarchical structure of bone HA and can potentially play a dual role in the postoperative treatment of bone tumors via the chemotherapy from selenium and the promotion of bone repair by hydroxyapatite, to systematically investigate the influence of bone-mimetic hierarchical structure in bone tumor inhibition by SeHANs in vivo and in vitro. We found that, compared to the non-biomimetic SeHANs, the B-SeHANs exhibited highly enhanced cellular internalization and intracellular degradation, and induced subsequent autophagy and caspase-dependent apoptosis via the ROS-mediated activation of the JNK pathway and inhibition of the Akt/mTOR pathway. We further verified that the B-SeHANs promoted autophagy and apoptosis to inhibit tumor growth while profoundly reducing bone destruction in a well-designed orthotopic tibial tumor model. The current work presents a feasible strategy for the development, evaluation and fundamental study of biomimetic mineral nanoparticles to inhibit tumor growth.Cisplatin resistance is a daunting obstacle in cancer therapy and one of the major causes for treatment failure due to the inadequate drug activity and apoptosis induction. To overcome cisplatin resistance, we proposed a multifunctional nanogel (designated as Valproate-D-Nanogel) capable of reactivating cisplatin and enhancing early apoptosis. This Valproate-D-Nanogel was prepared through copolymerizing carboxymethyl chitosan with diallyl disulfide and subsequent grafting with valproate to reverse the drug-resistance in cisplatin-resistant human lung adenocarcinoma cancer. It can significantly increase the proportion of G2/M phase (up to 3.2-fold enhancement) to reactivate cisplatin via high level of G2/M arrest induced by valproate. Meanwhile, the intracellular ROS-P53 crosstalk can be upregulated by diallyl disulfide (up to 8-fold increase of ROS) and valproate (up to 18-fold increase of P53) to enhance early apoptosis. The synchronization of enhanced G2/M arrest and ROS-P53 crosstalk devotes to reverse the cisplatin resistance with a high level of resistance reversion index (50.22). As a result, improved in vivo tumor inhibition (up to 15-fold higher compared to free cisplatin) and decreased systemic toxicity was observed after treatment with Valproate-D-Nanogels. Overall, this nanogel can effectively inhibit cisplatin-resistance cancer through combined pathways and provides an effective approach for overcoming cisplatin-resistance in cancer treatment.Porous synthetic grafts made of poly (glycerol sebacate) (PGS) can transform into autologous vascular conduits in vivo upon degradation of PGS. A long-held doctrine in tissue engineering is the necessity to match degradation of the scaffolds to tissue regeneration. Here, we tested the impact of degradation of PGS and its derivative in an interposition model of rat common carotid artery (CCA). Previous work indicates a complete degradation of PGS within approximately 2 weeks, likely at the fast end of the spectrum. Thus, the derivation of PGS focuses on delay degradation by conjugating the free hydroxy groups in PGS with a long chain carboxylic acid palmitic acid, one of the most common lipid components. We evaluated two of the resultant palmitate-PGS (PPGS) in this study one containing 9% palmitate (9-PPGS) and the other16% palmitate (16-PPGS). 16-PPGS grafts had the highest patency. Ultrasound imaging showed that the lumens of 16-PPGS grafts were similar to CCA and smaller than 9-PPGS and PGS grafts 12 weeksweeks results in vascular conduits closer to arteries in a rat carotid artery interposition model over a 12-week observation period.Polymeric nanoparticles provide a non-invasive strategy for enhancing the delivery of labile hydrophilic enzymatic cargo for neurological disease applications. One of the most common polymeric materials, poly(lactic-co-glycolic acid) (PLGA) copolymerized with poly(ethylene glycol) (PEG) is widely studied due to its biocompatible and biodegradable nature. Although PLGA-PEG nanoparticles are generally known to be non-toxic and protect enzymatic cargo from degradative proteases, different formulation parameters including surfactant, organic solvent, sonication times, and formulation method can all impact the final nanoparticle characteristics. We show that 30s sonication double emulsion (DE)-formulated nanoparticles achieved the highest enzymatic activity and provided the greatest enzymatic activity protection in degradative conditions, while nanoprecipitation (NPPT)-formulated nanoparticles exhibited no protection compared to free catalase. However, the same DE nanoparticles also caused significant toxicity on excitotoxicity-induced brain tissue slices, but not on healthy or neuroinflammation-induced tissue. We narrowed the culprit of toxicity to specifically sonication of PLGA-PEG polymer with dichloromethane (DCM) as the organic solvent, independent of surfactant type. We also discovered that toxicity was oxidative stress-dependent, but that increased toxicity was not enacted through increasing oxidative stress. Furthermore, no PEG degradation or aldehyde, alcohol, or carboxylic acid functional groups were detected after sonication. We identified that inclusion of free PEG along with PLGA-PEG polymer during the emulsification phases or replacing DCM with trichloromethane (chloroform) produced biocompatible polymeric nanoparticle formulations that still provided enzymatic protection. This work encourages thorough screening of nanoparticle toxicity and cargo-protective capabilities for the development of enzyme-loaded polymeric nanoparticles for the treatment of disease.Peri-implant aseptic inflammation and osteolysis can cause aseptic loosening, leading to the failure of implants. Therefore, aseptic loosening of orthopedic implants remains an imminent problem for the development of durable and effective implants. In this work, a common anti-inflammatory drug (aspirin, ASA) was loaded in poly(lactic-co-glycolic acid) (PLGA) to construct nanofiber coatings on titanium (Ti) via electrospinning. The adhesion of the nanofiber coatings to Ti was ensured by polydopamine (PDA) modification. A stable and sustainable release of aspirin from the nanofiber coatings could last up to 60 days. Such electrospun PLGA@ASA nanofiber coatings could promote proliferation and osteogenic differentiation of bone mesenchymal stem cells (BMSCs) as well as inhibit M1 polarization and RANKL-induced osteoclast differentiation of macrophages in vitro. These results indicated that this facile formulation of the PLGA@ASA nanofiber coatings for long-term drug release could be expected to address the problem of aseptic loosening effectively in dual directions of both anti-inflammation and improving osseointegration simultaneously. Notably, the in vivo experiments demonstrated that PLGA@ASA nanofiber coatings did promote osseointegration ability of Ti implants significantly, even in challenging condition with wear particles, and also effectively inhibited Ti particle induced osteolysis around the implants. This work indicates a promising way for the development of durable and effective implants by using PLGA@ASA-PDA-Ti to address the problem of aseptic loosening in dual directions.Recent years have witnessed the blooming of gas therapy nanoplatforms, which emerged as a promising area for cancer therapy. However, uncontrolled or inadequate generation of gas and unclear therapeutic mechanisms, which were still regarded as big challenges to apply gas therapy into clinical. Here in, a gas treatment based on sulfur dioxide (SO2) prodrug doped nanorattles was explored, which could not only inhibit superficial tumor but also deep tumor. A Benzothiazole sulfinate (BTS, a water-soluble SO2 prodrug) doped rattle-structured rough nanocapsule with high drug payload (~80%) composed of gold nanorods cores and polydopamine (PDA) shell (GNRs@PDA-BTS, GPBRs) has been prepared. Taking advantages of excellent photothermal conversion ability as well as acidic condition in the tumor sites, SO2 gas release could be precisely controlled by both photothermal and pH, thus realizing „collusion inside” gas therapy and „outside” photothermal therapy. In addition, the cytotoxic SO2 was found to induce cell apoptosis accompanied by the upregulation of intracellular reactive oxygen species (ROS) levels and modulation of apoptosis-relative proteins such as p53, bcl-2, Bax and caspase-3. Such photothermal/pH triggered SO2 gas therapy may provide an effective strategy to stimulate further development of deep tumor therapy.Radiotherapy (RT) is one of the most commonly employed approaches in the treatment of malignant tumors and is often combined with radiosensitizers to enhance the therapeutic efficacy for clinical use. For developing a smart therapeutic strategy leveraging local tissue response to photo-mediated reactions and the combination of multiple treatment modalities involving ROS-induced sensitization of RT, a novel nanophototherapeutic system has been developed. The nanotherapeutics prepared from the assembly of poly (thiodiethylene malonate) (PSDEM) and PEG-PSDEM-PEG and loaded with suberoylanilide hydroxamic acid (SAHA) employed as the RT sensitizer and indocyanine green (ICG) as the photothermal/photodynamic agent, demonstrated the capability of undergoing structural change and releasing therapeutic payloads in response to near-infrared irradiation and X-ray radiotherapy. With highly localized and controllable reactions within the tumor site, the reactive oxygen species (ROS)-triggered SAHA unloading and the hyperthermia-induced vascular permeability of oxygen led to a significant sensitization of the target tissue in RT, which, in turn, led to the promotion of therapeutic effect in conjunction with photodynamic/photothermal therapies (PDT/PTT).