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The role of fibronectin (FN) in tumorigenesis and malignant progression has been highly controversial. Cancerous FN plays a tumor-suppressive role, whereas it is pro-metastatic and associated with poor prognosis. Interestingly, FN matrix deposited in the tumor microenvironments (TMEs) promotes tumor progression but is paradoxically related to a better prognosis. Here, we justify how FN impacts tumor transformation and subsequently metastatic progression. Next, we try to reconcile and rationalize the seemingly conflicting roles of FN in cancer and TMEs. Finally, we propose future perspectives for potential FN-based therapeutic strategies.

Osteoporosis is the second most-prevalent epidemiologic disease in the aging population worldwide. Cross-sectional and retrospective evidence indicates that tea consumption can mitigate bone loss and reduce risk of osteoporotic fractures. Tea polyphenols enhance osteoblastogenesis and suppress osteoclastogenesis in vitro. Previously, we showed that (−)-epigallocatechin-3-gallate (EGCG), one of the green tea polyphenols, increased osteogenic differentiation of murine bone marrow mesenchymal stem cells (BMSCs) by increasing the mRNA expression of osteogenesis-related genes, alkaline phosphatase activity and, eventually, mineralization. We also found that EGCG could mitigate bone loss and improve bone microarchitecture in ovariectomy-induced osteopenic rats, as well as enhancing bone defect healing partially via bone morphogenetic protein 2 (BMP2). The present study investigated the effects of EGCG in human BMSCs. We found that EGCG, at concentrations of both 1 and 10 µmol/L, can increase mRNA expression of BMP2, Runx2, alkaline phosphatase (ALP), osteonectin and osteocalcin 48 h after treatment. EGCG increased ALP activity both 7 and 14 days after treatment. Furthermore, EGCG can also enhance mineralization two weeks after treatment. EGCG without antioxidants also can enhance mineralization. In conclusion, EGCG can increase mRNA expression of BMP2 and subsequent osteogenic-related genes including Runx2, ALP, osteonectin and osteocalcin. EGCG further increased ALP activity and mineralization. Loss of antioxidant activity can still enhance mineralization of human BMSCs (hBMSCs).

Current harmonics in six-phase permanent magnet synchronous motors (PMSMs) arise from inherent asymmetries caused by manufacturing tolerances and nonlinear characteristics in the inverter output. Additionally, magnetic saturation and slight imbalances in the windings introduce flux linkage asymmetries, resulting in both fundamental current imbalance and low-order harmonics. Although these imbalances are minor and do not indicate fault conditions, they can cause uneven copper loss and eventually reduce the overall service life of the motor. This paper proposes a harmonic suppression strategy for mitigating imbalance current harmonics in non-ideal six-phase PMSMs. The method integrates back-electromotive force harmonic feedforward compensation (BEMF-HFC) with harmonic synchronous reference frame current control (HSRF-CC). An imbalance flux linkage harmonic model is developed in simulations to replicate the measured imbalance phase currents and to validate the effectiveness of the proposed strategy. The experimental setup is built using a microcontroller from Texas Instruments (TI), which generates six-phase complementary PWM signals for the power stage and receives feedback signals including phase currents, DC bus voltage, and rotor position. Rotor position is acquired through a 12-pole resolver and a 12-bit resolver-to-digital converter (RDC). The six-phase PMSM used in the tests is specified with 12 poles, a rated DC bus voltage of 600 V, a rated current of 200 Arms, and a rated rotor speed of 1200 rpm. Compared with conventional harmonic suppression strategies that do not target imbalance current harmonics, the proposed method achieves a better current balance and lower total harmonic distortion (THD). At 1200 rpm, the magnitude deviation of the fundamental, third, and fifth current harmonics is reduced from 8.61%, 2.88%, and 2.94% to 1.19%, 1.02%, and 0.5%, respectively.

This paper investigates a back-electromotive force (EMF) harmonic compensation strategy for six-phase permanent-magnet synchronous motors (PMSMs) to reduce current harmonics and improve system performance. Ideally, the back-EMF waveform should be perfectly sinusoidal. However, manufacturing imperfections such as suboptimal magnetic circuit design, uneven winding distribution, and mechanical eccentricity introduce low-order spatial harmonics, particularly the 5th, 7th, 11th, and 13th orders, which distort the back-EMF, increase current harmonics, complicate control, and reduce efficiency. To address these issues, this study proposes a compensation strategy utilizing common-mode and differential-mode current control. By injecting the 6th and 12th harmonics into the decoupled voltage commands along the d-axis and q-axis, the strategy significantly reduces current harmonic distortion. Experimental validation was conducted using a TMS320F28386D microcontroller, which controlled dual inverters via PWM signals and processed real-time current feedback. Rotor position feedback was provided by a resolver to ensure precise and responsive motor control. At a rotational speed of 900 rpm, with a peak phase current Im of 200 A and an IGBT switching frequency of 10 kHz, the phase-a current total harmonic distortion (THD) was reduced from 11.86% (without compensation) to 6.83% (with compensation). This study focused on mitigating harmonics below the 14th order. The experimental results demonstrate that the proposed back-EMF harmonic compensation strategy effectively minimizes current THD, highlighting its potential for improving the performance and efficiency of multi-phase motor systems.

This paper proposes a current harmonic suppression strategy that combines harmonic synchronous rotating frame (HSRF) current feedback control and back-electromotive force harmonic (BEMFH) feedforward compensation to suppress the fifth and seventh current harmonics of a six-phase permanent magnet synchronous motor (PMSM). The current harmonics of six-phase PMSMs vary with the current due to manufacturing imperfections and the inverter nonlinearity effect. Using fixed-parameter BEMFH feedforward compensation cannot completely eliminate current harmonics. This paper integrates a closed-loop harmonic current control strategy, using HSRF in the differential mode of the six-phase PMSM rotor rotating frame to effectively mitigate current harmonic variations caused by load changes. The controller adapts a Texas Instrument microcontroller featuring encoder interfaces, complementary pulse width modulation (PWM), and analog–digital converters (ADC) to simplify the board design. The rotor angle feedback is provided by a 12-pole resolver in conjunction with an Analog Device resolver-to-digital converter (RDC). The specifications of the six-phase PMSM are as follows: 12 poles, 1200 rpm, 200 A (rms), and 600 V DC bus. The total harmonic distortion (THD) of the phase current for harmonics below the 21st order was reduced from 31.71% to 4.84% under the test conditions of 1200 rpm rotor speed and 200 A peak phase current. Specifically, the fifth and seventh harmonics were reduced from 29.98% and 9.72% to 2.74% and 1.21%, respectively. These results validate the feasibility of the proposed current harmonic suppression strategy.

PurposeThe purpose of this paper is to summarize the findings from focus group interviews conducted with librarians and library staff, faculty and students. It highlights the significance of implementing inclusive teaching and culturally responsive strategies in instructional settings and interactions with library patrons and seeks to emphasize the importance of developing guidelines, best practices and effective strategies.Design/methodology/approachUsing focus groups, this study interviewed librarians and library staff, faculty and students. This research approach identified, reviewed and assessed existing programs and practices in instruction and library interactions.FindingsThe findings from this paper indicate that while faculty and librarians are making individual efforts to promote inclusivity in teaching and interacting with patrons, many participants expressed the necessity for institutional-level training, guidelines and good practices on how to achieve and implement culturally responsive and inclusive teaching strategies.Originality/valueThe methodology utilized in this study can be adapted by other libraries or institutions aiming to explore the practice of inclusive pedagogy and culturally responsive teaching within their own context. The insights from the study inform the development of strategies that librarians, faculty and staff can employ to integrate inclusive and culturally responsive teaching into their instruction and services for the wider academic community.

Background Pathologic scars, including keloids and hypertrophic scars, represent a common form of exaggerated cutaneous scarring that is difficult to prevent or treat effectively. Additionally, the pathobiology of pathologic scars remains poorly understood. We aim at investigating the impact of TEM1 (also known as endosialin or CD248), which is a glycosylated type I transmembrane protein, on development of pathologic scars. Methods To investigate the expression of TEM1, we utilized immunofluorescence staining, Western blotting, and single-cell RNA-sequencing (scRNA-seq) techniques. We conducted in vitro cell culture experiments and an in vivo stretch-induced scar mouse model to study the involvement of TEM1 in TGF-β-mediated responses in pathologic scars. Results The levels of the protein TEM1 are elevated in both hypertrophic scars and keloids in comparison to normal skin. A re-analysis of scRNA-seq datasets reveals that a major profibrotic subpopulation of keloid and hypertrophic scar fibroblasts greatly expresses TEM1, with expression increasing during fibroblast activation. TEM1 promotes activation, proliferation, and ECM production in human dermal fibroblasts by enhancing TGF-β1 signaling through binding with and stabilizing TGF-β receptors. Global deletion of Tem1 markedly reduces the amount of ECM synthesis and inflammation in a scar in a mouse model of stretch-induced pathologic scarring. The intralesional administration of ontuxizumab, a humanized IgG monoclonal antibody targeting TEM1, significantly decreased both the size and collagen density of keloids. Conclusions Our data indicate that TEM1 plays a role in pathologic scarring, with its synergistic effect on the TGF-β signaling contributing to dermal fibroblast activation. Targeting TEM1 may represent a novel therapeutic approach in reducing the morbidity of pathologic scars.

Osteoporosis is the second most common disease only secondary to cardiovascular disease, with the risk of fracture increasing with age. Osteoporosis is caused by an imbalance between osteoblastogenesis and osteoclastogenesis processes. Osteoclastogenesis may be enhanced, osteoblastogenesis may be reduced, or both may be evident. Inflammation and high reactive oxygen enhance osteoclastogenesis while reducing osteoblastogenesis by inducing osteoblast apoptosis and suppressing osteoblastic proliferation and differentiation. Catechins, the main polyphenols found in green tea with potent anti-oxidant and anti-inflammatory properties, can counteract the deleterious effects of the imbalance of osteoblastogenesis and osteoclastogenesis caused by osteoporosis. Green tea catechins can attenuate osteoclastogenesis by enhancing apoptosis of osteoclasts, hampering osteoclastogenesis, and prohibiting bone resorption in vitro. Catechin effects can be directly exerted on pre-osteoclasts/osteoclasts or indirectly exerted via the modulation of mesenchymal stem cells (MSCs)/stromal cell regulation of pre-osteoclasts through activation of the nuclear factor kB (RANK)/RANK ligand (RANKL)/osteoprotegerin (OPG) system. Catechins also can enhance osteoblastogenesis by enhancing osteogenic differentiation of MSCs and increasing osteoblastic survival, proliferation, differentiation, and mineralization. The in vitro effects of catechins on osteogenesis have been confirmed in several animal models, as well as in epidemiological observational studies on human subjects. Even though randomized control trials have not shown that catechins provide anti-fracture efficacy, safety data in the trials are promising. A large-scale, placebo-controlled, long-term randomized trial with a tea regimen intervention of optimal duration is required to determine anti-fracture efficacy.

Aortic wall inflammation, abnormal oxidative stress and progressive degradation of extracellular matrix proteins are the main characteristics of abdominal aortic aneurysms (AAAs). The nucleotide-binding oligomerization domain-like receptor family pyrin domain containing 3 (NLRP3) inflammasome dysregulation plays a crucial role in aortic damage and disease progression. The first aim of this study was to examine the effect of baicalein (5,6,7-trihydroxy-2-phenyl-4H-1-benzopyran-4-one) on AAA formation in apolipoprotein E-deficient (ApoE−/−) mice. The second aim was to define whether baicalein attenuates aberrant vascular smooth muscle cell (VSMC) proliferation and inflammation in VSMC culture. For male ApoE−/− mice, a clinically relevant AAA model was randomly divided into four groups: saline infusion, baicalein intraperitoneal injection, Angiotensin II (Ang II) infusion and Ang II + baicalein. Twenty-seven days of treatment with baicalein markedly decreased Ang II-infused AAA incidence and aortic diameter, reduced collagen-fiber formation, preserved elastic structure and density and prevented smooth muscle cell contractile protein degradation. Baicalein inhibited rat VSMC proliferation and migration following the stimulation of VSMC cultures with Ang II while blocking the Ang II-inducible cell cycle progression from G0/G1 to the S phase in the synchronized cells. Cal-520 AM staining showed that baicalein decreased cellular calcium in Ang II-induced VSMCs; furthermore, a Western blot assay indicated that baicalein inhibited the expression of PCNA and significantly lowered levels of phospho-Akt and phospho-ERK, along with an increase in baicalein concentration in Ang II-induced VSMCs. Immunofluorescence staining showed that baicalein pretreatment reduced NF-κB nuclear translocation in Ang II-induced VSMCs and furthered the protein expressions of NLRP3 while ASC and caspase-1 were suppressed in a dose-dependent manner. Baicalein pretreatment upregulated Nrf2/HO-1 signaling in Ang II-induced VSMCs. Thus, 2′,7′-dichlorodihydrofluorescein diacetate (DCFH-DA) staining showed that its reactive oxygen species (ROS) production decreased, along with the baicalein pretreatment. Our overall results indicate that baicalein could have therapeutic potential in preventing aneurysm development.

Working memory (WM) is a cognitive function important for guiding the on‐going or upcoming behavior. A memory‐related protein Arc (activity‐regulated cytoskeleton‐associated protein) is implicated in long‐term memory consolidation. Recent evidence further suggests the involvement of hippocampal Arc in spatial WM. The medial prefrontal cortex (mPFC) is a key brain region mediating WM. However, the role of mPFC Arc in WM is still uncertain. To investigate whether mPFC Arc protein is involved in WM performance, delayed non‐match to sample (DNMS) T‐maze task was performed in rats with or without blocking new synthesis of mPFC Arc. In DNMS task, a 10‐s or 30‐s delay between the sample run and the choice run was given to evaluate WM performance. To block new Arc protein synthesis during the DNMS task, Arc antisense oligodeoxynucleotides (ODNs) were injected to the bilateral mPFC. The results show that, in rats without surgery for cannula implantation and subsequent intracerebral injection of ODNs, WM was functioning well during the DNMS task with a delay of 10 s but not 30 s, which was accompanied with a significantly increased level of mPFC Arc protein, indicating a possible link between enhanced Arc protein expression and the performance of WM. After preventing the enhancement of mPFC Arc protein expression with Arc antisense ODNs, rat's WM performance was impaired. These findings support enhanced mPFC Arc protein expression playing a role during WM performance.