The purpose of the present study was to examine 1) characteristics and attitudes of oncologists toward exercise and toward recommending exercise to their patients, 2) association among oncologists’ own physical activity levels, exercise recommendations, and their attitudes toward recommending exercise. A total of 167 oncologists participated in this survey study (41 surgeons, 78 medical oncologists, 25 radiation oncologists, and 21 others). Most oncologists included in the study treat more than one type of cancer, including colorectal, gastric, breast, lung, and liver cancer. To analyze the data, the one-way ANOVA, and t-test were used. All data were indicated for mean, SD, and proportions. Most oncologists agreed that exercise is beneficial (72.8%) and important (69.6%), but only 39.2% of them agreed that exercise is safe, and only 7.2% believed that cancer patients manage to exercise during cancer treatment. Forty-six percentage of the surveyed oncologists recommended exercise to their patients during the past month. The average amount of participation in physical activity by oncologists who participated in the study was 139.5 ± 120.3 min per week, and 11.4% of the study participants met the American College of Sports Medicine (ACSM) guidelines. Oncologists’ own physical activity levels were associated with their attitudes toward recommending exercise. Belief in the benefits of exercise in the performance of daily tasks, improvement of mental health, and the attenuation of physical decline from treatment were the three most prevalent reasons why oncologists recommend exercise to their patients. Barriers to recommending exercise to patients included lack of time, unclear exercise recommendations, and the safety of patients. Oncologists have favorable attitudes toward exercise and toward recommending exercise to their patients during treatment. However, they also experience barriers to recommending exercise, including lack of time, unclear exercise guidelines for cancer patients, and concerns regarding the safety of exercise.

Astaxanthin (AST) is related to apoptosis but the details of the mechanism of how AST makes apoptosis is not clear. The present study investigated apoptotic effects of AST to SKBR3, a breast cancer cell line in detail. Cell viability assay showed cellular proliferation and morphological changes of the cells were observed under AST treatment. FACS analysis indicated that AST blocked cell cycle progression at G0/G1, suppressed proliferation dose-dependently, and induced apoptosis of the cells. The apoptosis of the cells by AST was further demonstrated through the decreased expression level of mutp53 and cleaved a PARP-1 fragment, respectively. In addition, AST induced the intrinsic apoptosis of the cells by activation of Bax/Bcl2, cleaved caspase-3, and cleaved caspase-9 as well as the phosphorylation of ERK1/2, JNK, and p38. Furthermore, AST decreased production of intracellular reactive oxygen species as well as modulated expressions of superoxide dismutases and Pontin, an anti-apoptotic factor. Co-immunoprecipitation assay revealed AST reduced interaction between Pontin and mutant p53. Taken together, these studies proved that AST regulates the expression of apoptotic molecules to induce intrinsic apoptosis of the cells, suggesting AST therapy might provide an alternative for improving the efficacies of other anti-cancer therapies for breast cancer.

Background/Objectives: Mobile health applications are essential for improving healthcare access and promoting healthy lifestyles. This study investigates the roles of perceived ease of use, usefulness, and satisfaction in shaping behavioral intentions using the Technology Acceptance Model. Methods: A survey of 329 mobile health application users in Korea was analyzed using confirmatory factor analysis and structural equation modeling to test hypothesized relationships. Results: The findings indicate that perceived ease of use positively influences perceived usefulness (H1). Customer satisfaction is positively influenced by both the perceived ease of use and perceived usefulness (H2 and H3). Furthermore, behavioral intention is affected by perceived ease of use, perceived usefulness, and customer satisfaction (H4 through H6). Conclusions: The findings from this study elucidate how mobile health applications can enhance users’ perceptions of ease of use and usefulness, thereby influencing their behavioral intentions through increased satisfaction. This research also advances our understanding of application services and informs the development of effective operational and marketing strategies.

Pelargonium sidoides (PS) and Coptis chinensis root (CR) have traditionally been used to treat various diseases, including respiratory and gastrointestinal infections, dysmenorrhea, and hepatic disorders. The present study was conducted to evaluate the anti-inflammatory effects of a combination of PS and CR in vitro and in vivo. The in vitro effects of PS + CR on the induction of inflammation-related proteins were evaluated in lipopolysaccharide (LPS)-stimulated RAW 264.7 cells. The levels of nitric oxide (NO) and of inflammatory cytokines and prostaglandin E2 (PGE2) were measured using the Griess reagent and enzyme-linked immunosorbent assay (ELISA) methods, respectively. The expression of inflammation-related proteins was confirmed by Western blot. Additionally, the effects of PS + CR on paw edema volume, skin thickness, and numbers of infiltrated inflammatory cells, mast cells, COX-2-, iNOS-, and TNF-α-immunoreactive cells in dorsum and ventrum pedis skin were evaluated in a rat model of carrageenan (CA)-induced paw edema. PS + CR significantly reduced production of NO, PGE2 and three pro-inflammatory cytokines (tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, and IL-6) and also decreased levels of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2). Treatment with PS + CR significantly reduced the protein expression levels of LPS-stimulated nuclear factor kappa B (NF-κB) and phosphorylated inhibitor of NF-κB (p-I-κBα). Additionally, PS + CR significantly inhibited the increases in paw swelling, skin thickness, infiltrated inflammatory cells, mast cell degranulation, COX-2-, iNOS-, and TNF-α-immunoreactive cells in the rat model of CA-induced acute edematous paw. These results demonstrate that PS + CR exhibits anti-inflammatory properties through decreasing the production of pro-inflammatory mediators (NO, PGE2, TNF-α, IL-1β, and IL-6), suppressing NF-κB signaling in LPS-induced RAW 264.7 cells. Additionally, the results of the CA-induced rat paw edema assay revealed an anti-edema effect of PS + CR. Furthermore, it is suggested that PS + CR also inhibits acute edematous inflammation by suppressing mast cell degranulation and inflammatory mediators (COX-2, iNOS, and TNF-α). Thus, PS + CR may be a potential candidate for the treatment of various inflammatory diseases, and it may also contribute to a better understanding of the molecular mechanisms underlying inflammatory response regulation.

Pulmonary hypertension (PH) is a progressive and serious disease, where exacerbated inflammatory response plays a critical role. Isoliquiritigenin (ISL), an important flavonoid isolated from Glycyrrhizae radix, exhibits a wide range of pharmacological actions including anti-inflammation. Previously we found ISL alleviated hypoxia-induced PH; in the present study, to extend this, we evaluated the effects of ISL on monocrotaline (MCT)-induced PH and the relevant mechanisms. Rats received a single intraperitoneal injection of MCT, followed by intragastric treatments with ISL (10 mg/kg/d or 30 mg/kg/d) once a day for 28 days. The MCT administration increased the right ventricular systolic pressure (RVSP) (p< 0.001), the median width of pulmonary arteries (p< 0.01), and the weight ratio of the right ventricular wall/left ventricular wall plus septum (Fulton index) (p< 0.01) in rats; however, these changes were inhibited by both doses of ISL (p< 0.05). In addition, treatment with ISL suppressed the upregulated production of serum interleukin-6 (p< 0.01) and tumor necrosis factor-α(p< 0.05) by MCT and reversed the increases in the numbers of proliferating cell nuclear antigen (PCNA)-positive cells (p< 0.01) in the medial wall of pulmonary arteries. In in vitro experiments, ISL (10μM, 30μM, and 100μM) inhibited excessive proliferation of cultured primary pulmonary artery smooth muscle cells (PASMCs) (p< 0.05,p< 0.01, andp< 0.001) in a dose-dependent manner and prevented an increase in the expressions of PCNA (p< 0.01) and phospho-Akt (p< 0.05) in PASMCs induced by hypoxia. These results suggest that ISL can attenuate MCT-induced PH via its anti-inflammatory and antiproliferative actions.

Acupuncture improves ethanol withdrawal‐induced anxiety in rats in an acupoint‐dependent manner. Thus, the present study investigated the effects of acupuncture on acute restraint stress‐ (ARS‐) induced anxiety. Male rats were exposed to ARS for 3 h followed by acupuncture at either PC6 (Neiguan), HT7 (Shenmen), or a nonacupoint (tail) once a day for three consecutive days. Five minutes after the third acupuncture treatment, anxiety‐like behavior was evaluated in an elevated plus maze (EPM). Additionally, plasma corticosterone (CORT) levels were measured by radioimmunoassay and the concentrations of norepinephrine (NE) and 3‐methoxy‐4‐hydroxy‐phenylglycol (MHPG) in the central nucleus of the amygdala (CeA) were determined using high‐performance liquid chromatography. Acupuncture at PC6, but not HT7 or a nonacupoint, attenuated anxiety‐like behavior, but this attenuation was abolished by a postacupunctural intra‐CeA infusion of NE. Acupuncture at PC6 also reduced the oversecretion of plasma CORT and inhibited increases in amygdaloid NE and MHPG induced by ARS. Further, Western blot analyses and real‐time polymerase chain reaction assays revealed that acupuncture at PC6 prevented ARS‐induced enhancements in the protein and mRNA expressions of tyrosine hydroxylase in the CeA. These results suggest that acupuncture performed specifically at acupoint PC6 reduces ARS‐induced anxiety‐like behavior by dampening amygdaloid noradrenergic responses.