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An investigation of comprehensive service requirements and their importance across various stakeholders is needed to develop systematic swallowing healthcare services. The present study examined the service requirements and their importance in developing comprehensive swallowing healthcare services from diverse stakeholders, including healthy seniors, individuals at risk, patients, guardians, and medical professionals, within the context of dysphagia. A series of survey-based interviews with 35 participants from the 5 stakeholder groups identified a comprehensive array of requirements pertinent to swallowing healthcare. Subsequently, a larger survey of 125 participants was administered using a 7-point Likert scale to evaluate the perceived importance of the identified requirements. A total of 46 distinct requirements were identified across the prevention/screening, evaluation/diagnosis, and treatment/training stages of swallowing healthcare. Accessibility, customization, usability, practicality, and information availability were features commonly identified across the three stages. Evaluation of the importance of these requirements yielded ratings ranging from 5.0 to 6.6. Significantly higher ratings were found for requirements associated with the evaluation/diagnosis and treatment/training stages, underscoring the stakeholder groups’ pronounced preference for services directed at these specific stages of the healthcare continuum. The study offers insights into the multifaceted requirements of stakeholders in swallowing healthcare, emphasizing the necessity for personalized, easily accessible, and comprehensive services. These findings serve as a foundational framework on targeted interventions and tailored services designed to address the diverse requirements of stakeholders for swallowing healthcare.

Existing swallowing evaluation methods using X-ray or endoscopy are qualitative. The present study develops a swallowing monitoring and assessment system (SMAS) that is nonintrusive and quantitative. The SMAS comprises an ultrasonic Doppler sensor array, a microphone, and an inertial measurement unit to measure ultrasound signals originating only from swallowing activities. Ultrasound measurements were collected for combinations of two viscosity conditions (water and yogurt) and two volume conditions (3 mL and 9 mL) from 24 healthy participants (14 males and 10 females; age = 30.5 ± 7.6 years) with no history of swallowing disorders and were quantified for 1st peak amplitude, 2nd peak amplitude, peak-to-peak (PP) time interval, duration, energy, and proportion of two or more peaks. The peak amplitudes and energy significantly decreased by viscosity and the PP time interval and duration increased by volume. The correlation between the time measures were higher (r = 0.78) than that of the amplitude measures (r = 0.30), and the energy highly correlated with the 1st peak amplitude (r = 0.86). The proportion of two or more peaks varied from 76.8% to 87.9% by viscosity and volume. Further research is needed to examine the concurrent validity and generalizability of the ultrasonic Doppler sensor-based SMAS.

Sushi domain-containing protein 2 (SUSD2), a transmembrane protein containing a sushi motif, has been reported to have tumor-promoting functions in various types of cancer, including breast cancer. However, the regulatory mechanism of SUSD2 and its function in HER2-positive (HER2+) breast cancer have not been fully identified as yet. In this study, we explored the potential of targeting SUSD2 to overcome trastuzumab (TRZ) resistance in HER2+ breast cancer. SUSD2 expression was found to be significantly increased in HER2-overexpressing cells. Endogenous SUSD2 expression was observed in HER2+ breast cancer cells but not in estrogen receptor-positive or triple-negative breast cancer cells. We also found that SUSD2 expression was positively correlated with HER2 expression in a publicly available human primary breast cancer dataset. Although SUSD2 expression was associated with HER2, its expression levels were not affected by TRZ. Through kinase array experiments, we found that SUSD2 expression was modulated downstream of STAT3-dependent signaling in breast cancer cells overexpressing HER2. STAT3 activity was increased in EGFR+ HER2+ breast cancer cells compared to EGFR+ cells. Furthermore, we observed that SUSD2 expression was decreased by C188-9, a STAT3-specific inhibitor. Finally, we analyzed the association between patient survival and SUSD2 expression in breast cancer. Our results showed that SUSD2 expression had a negative correlation with the relapse-free survival of patients with EGFR+ HER2+ breast cancer when compared to EGFR+ breast cancer patients. Collectively, our results demonstrate that SUSD2 expression is mediated by STAT3 and imply the potential of using SUSD2 as a biomarker to stratify HER2+ breast cancer.

Tumor necrosis factor (TNF)-α is one of the pro-inflammatory cytokines highly expressed in Helicobacter pylori that inhibits gastric acid secretion. In this study we determined the effect of silibinin on TNF-α-induced MMP-9 expression in gastric cancer cell lines. MMP-9 mRNA and protein expression was dose-dependently increased by TNF-α in SNU216 and SNU668 gastric cancer cells. On the other hand, TNF-α-induced MMP-9 expression was dose-dependently suppressed by silibinin. To verify the regulatory mechanism of silibinin on TNF-α-induced MMP-9 expression, the gastric cancer cell lines were pretreated with silibinin prior to TNF-α. TNF-α-induced MMP-9 expression was inhibited by the MEK1/2 specific inhibitor, UO126. Finally, we investigated the effect of adenoviral constitutively active (CA)-MEK and CA-Akt on MMP-9 expression. The expression of MMP-9 was significantly increased by CA-MEK overexpression, but not by CA-Akt overexpression. Taken together, we suggest that silibinin down-regulates TNF-α- induced MMP-9 expression through inhibition of the MEK/ERK pathway in gastric cancer cells.

Invasion of cancer cell induced by matrix metalloproteinase-9 (MMP-9) is one of pivotal steps in cancer metastasis. Herein, we investigated how cell invasion was regulated by berberine (BBR), an isoquinoline derivative alkaloid compound, in MDA-MB-231 human breast cancer cells. The basal level of MMP-9 activity and expression was dose-dependently increased by TNF-α, while TNF-a-induced MMP-9 gelatinase activity and expression was decreased by BBR. To investigate regulatory mechanism of TNF-α-induced MMP-9 expression, we pretreated cells with UO126 (MEK inhibitor), SB203580 (p38 inhibitor) and SP600125 (JNK inhibitor), respectively. Interestingly, TNF-α-induced MMP-9 activity and expression was decreased by UO126 and SB203580, but not by SP600125. Therefore, we further examined the effects of BBR on TNF-α-induced AP-1 DNA binding activity which is a downstream target of ERK and p38. Our data showed that TNF-α-induced AP-1 DNA binding activity was inhibited by BBR. Finally, we investigated the effect of BBR on TNF-α-induced cell invasion. TNF-α-induced cell invasion was significantly decreased by BBR treatment. Taken together, we suggest that TNF-α-induced MMP-9 expression and cell invasion are decreased by BBR through the suppression of AP-1 DNA binding activity in MDA-MB-231 human breast cancer cells.

Anthraquinone (9,10-anthraquinone) and several hydroxy derivatives, including purpurin (1,2,4-trihydroxyanthraquinone), anthrarufin (1,5-dihydroxyanthraquinone), and chrysazin (1,8-dihydroxyanthraquinone), were evaluated for antioxidative and anti-inflammatory activities in chemical assays and mammalian cells (murine macrophage RAW 264.7 cells). Several tests were used to assess their activities: 1,1-diphenyl-2-picrylhydrazyl (DPPH) free radical; ABTS radical cation; hydrogen peroxide scavenging; reduction of potassium ferricyanide; chelation of ferrous ions; inhibition of lipid peroxidation; inhibition of nitric oxide generation; scavenging of the intracellular hydroxyl radical; expression of NLRP3 polypeptide for inflammasome assembly; and quantitation of proinflammatory cytokine interleukin 1β (IL-1β) for inflammasome activation. The results show that purpurin, from the root of the madder plant (Rubia tinctorum L.), exhibited the highest antioxidative activity in both chemical and cultured cell antioxidant assays. The antioxidative activities of the other three anthraquinones were lower than that of purpurin. In addition, purpurin could down-regulate NLRP3 inflammasome assembly and activation, suggesting that it might protect foods against oxidative damage and prevent in vivo oxidative stress and inflammation. Structure-activity relationships and the significance of the results for food quality and human health are discussed.

Four types of undulated cylinders with streamwise undulation, transverse undulation, in-phase undulation and antiphase undulation are employed to investigate the undulation-axis effect on the structure of heat transfer around wavy cylinders. The flows around these undulated cylinders are numerically simulated by large eddy simulation at Re = 3000. The force coefficients and Nusselt numbers of the cylinders with transverse undulation and in-phase undulation are significantly influenced by wavelength and wave amplitude. On the other hand, the cylinders with streamwise undulation and antiphase undulation show a very weak dependence of the force coefficients and Nusselt numbers on the combinations of wavelength and wave amplitude. It is noted that the cylinder with antiphase undulation, under certain wavy conditions, provides about the same Nusselt number as the smooth cylinder, even though the force coefficients are considerably decreased. The thermal characteristics, according to the combination of wavy geometric parameters, are supported by the surface distribution of the Nusselt numbers. In addition, the isothermal distribution, which depends on the wake flow, explains the variation in the Nusselt numbers. The present results suggest that a proper modification of geometry can improve both heat transfer and aerodynamic performances.

Interleukin-1 (IL1) is a proinflammatory cytokine and promotes cancer cell proliferation and invasiveness in a diversity of cancers, such as breast and colon cancer. Here, we focused on the pharmacological effect of Entelon® (ETL) on the tumorigenesis of triple-negative breast cancer (TNBC) cells by IL1-alpha (IL1A). IL1A enhanced the cell growth and invasiveness of TNBC cells. We observed that abnormal IL1A induction is related with the poor prognosis of TNBC patients. IL1A also increased a variety of chemokines such as CCL2 and IL8. Interestingly, IL1A expression was reduced by the ETL treatment. Here, we found that ETL significantly decreased the MEK/ERK signaling pathway in TNBC cells. IL1A expression was reduced by UO126. Lastly, we studied the effect of ETL on the metastatic potential of TNBC cells. Our results showed that ETL significantly reduced the lung metastasis of TNBC cells. Our results showed that IL1A expression was regulated by the MEK/ERK- and PI3K/AKT-dependent pathway. Taken together, ETL inhibited the MEK/ERK and PI3K/AKT signaling pathway and suppressing the lung metastasis of TNBC cells through downregulation of IL1A. Therefore, we propose the possibility of ETL as an effective adjuvant for treating TNBC.