Purpose: Cancer patients need ongoing care from healthcare providers to maintain continuity of treatment. Much research has been conducted on digital health services for providing continuous management of discharged cancer patients. This review aimed to identify nurse-led digital health interventions for discharged cancer patients. Methods: This scoping review was conducted using JBI methodology. The population was post-discharge adult cancer patients, the concept was nurse-led digital health intervention, and the context was open. Databases including PubMed, Embase, CINAHL, Cochrane Library, KoreaMed, and RISS were searched.Data were summarized about the general characteristics of the article, participants, interventions, and outcomes. Results: Fifty-seven studies were included, with ten studies that focused on the elderly. One third of the participants included in this review had colorectal cancer (32.7%). Telephone was the most frequently used format, while the others were applications, the internet, and telemonitoring. The nurses’ main roles consisted of counseling, symptom monitoring, and education. Conclusion The development of nurseled digital health intervention for the elderly will be necessary, and studies using more diverse technologies will need to be conducted. Digital health interventions for post-discharge colorectal cancer patients could be applied in practice. Nurses should provide emotional support while providing digital health interventions.

Dysregulation of fibroblast growth factor (FGF)-receptor (FGFR) signaling, which is implicated in various oncogenic processes, including tumor proliferation, survival, migration, invasion, and angiogenesis, has been identified as a critical factor in urothelial bladder cancer (UBC) progression. This has led to the development of novel FGFR-targeted therapies. Erdafitinib is an oral selective pan-FGFR tyrosine kinase inhibitor approved for locally advanced or metastatic urothelial cancer in patients with FGFR3 alterations who progress on both platinum-based chemotherapy and immunotherapy. The approval of FGFR inhibitors (FGFRis), such as erdafitinib, and ongoing research into combination therapies with immune checkpoint inhibitors (ICIs) signify a promising shift in the treatment paradigm for advanced/metastatic UBC despite challenges such as the variable efficacy of FGFRis and treatment-related toxicity. In this study, we review the FGFR signaling pathway and the impact of altered FGFR signaling on UBC tumorigenesis, the clinical development of FGFRis, the rationale for FGFRi-ICI combinations, and future directions.

Dysregulation of fibroblast growth factor (FGF)-receptor (FGFR) signaling, which is implicated in various oncogenic processes, including tumor proliferation, survival, migration, invasion, and angiogenesis, has been identified as a critical factor in urothelial bladder cancer (UBC) progression. This has led to the development of novel FGFR-targeted therapies. Erdafitinib is an oral selective pan-FGFR tyrosine kinase inhibitor approved for locally advanced or metastatic urothelial cancer in patients with FGFR3 alterations who progress on both platinum-based chemotherapy and immunotherapy. The approval of FGFR inhibitors (FGFRis), such as erdafitinib, and ongoing research into combination therapies with immune checkpoint inhibitors (ICIs) signify a promising shift in the treatment paradigm for advanced/metastatic UBC despite challenges such as the variable efficacy of FGFRis and treatment-related toxicity. In this study, we review the FGFR signaling pathway and the impact of altered FGFR signaling on UBC tumorigenesis, the clinical development of FGFRis, the rationale for FGFRi-ICI combinations, and future directions.

Dysregulation of fibroblast growth factor (FGF)-receptor (FGFR) signaling, which is implicated in various oncogenic processes, including tumor proliferation, survival, migration, invasion, and angiogenesis, has been identified as a critical factor in urothelial bladder cancer (UBC) progression. This has led to the development of novel FGFR-targeted therapies. Erdafitinib is an oral selective pan-FGFR tyrosine kinase inhibitor approved for locally advanced or metastatic urothelial cancer in patients with FGFR3 alterations who progress on both platinum-based chemotherapy and immunotherapy. The approval of FGFR inhibitors (FGFRis), such as erdafitinib, and ongoing research into combination therapies with immune checkpoint inhibitors (ICIs) signify a promising shift in the treatment paradigm for advanced/metastatic UBC despite challenges such as the variable efficacy of FGFRis and treatment-related toxicity. In this study, we review the FGFR signaling pathway and the impact of altered FGFR signaling on UBC tumorigenesis, the clinical development of FGFRis, the rationale for FGFRi-ICI combinations, and future directions.

Dysregulation of fibroblast growth factor (FGF)-receptor (FGFR) signaling, which is implicated in various oncogenic processes, including tumor proliferation, survival, migration, invasion, and angiogenesis, has been identified as a critical factor in urothelial bladder cancer (UBC) progression. This has led to the development of novel FGFR-targeted therapies. Erdafitinib is an oral selective pan-FGFR tyrosine kinase inhibitor approved for locally advanced or metastatic urothelial cancer in patients with FGFR3 alterations who progress on both platinum-based chemotherapy and immunotherapy. The approval of FGFR inhibitors (FGFRis), such as erdafitinib, and ongoing research into combination therapies with immune checkpoint inhibitors (ICIs) signify a promising shift in the treatment paradigm for advanced/metastatic UBC despite challenges such as the variable efficacy of FGFRis and treatment-related toxicity. In this study, we review the FGFR signaling pathway and the impact of altered FGFR signaling on UBC tumorigenesis, the clinical development of FGFRis, the rationale for FGFRi-ICI combinations, and future directions.

OBJECTIVE: To investigate the prevalence and characteristics of musculoskeletal pain (MSK) pain in Korean farmers using initial survey data of Farmers' Cohort for Agricultural Work-Related MSK pain (FARM) study. METHODS: Farmers (534 females and 479 males; mean age 57.2±7.5 years) who owned or rented a farm and belonged to an agricultural cooperative unit were recruited. Presence of pain for each body part (neck, shoulder, arm/elbow, wrist/hand/finger, low back, leg/foot), and characteristics of MSK pain (prevalence, location, duration, severity, and frequency) during the last year was assessed. Additionally, demographic data such as farming duration, history of prior injury, and workload (low, moderate, somewhat hard, or hard) were collected using structured questionnaires. RESULTS: Almost all subjects (n=925; 91.3%) complained of pain in more than one body part. The frequency order was low back (63.8%), leg/foot (43.3%), shoulder (42.9%), wrist/hand/finger (26.6%), arm/elbow (25.3%), and neck (21.8%). Low back pain was more frequent in those with over 30 years of farming experience (odds ratio [OR], 1.40; 95% confidence interval, 1.08-1.81). MSK pain was related to history of prior injury (OR, 2.18-5.24; p<0.05) in all body parts except for leg/foot, and very hard workload was associated with low back, leg/foot, neck, shoulder, and wrist/hand/finger pain (OR, 2.88-10.83; p<0.05). CONCLUSION: Most Korean farmers experience MSK pain; furthermore, there is a significant association between pain, history of prior injury, and workload, suggestive of the necessity of coping and preventive strategies to reduce injury or workload.
Agriculture ; Cohort Studies ; Female ; Human Body ; Humans ; Low Back Pain ; Male ; Musculoskeletal Pain* ; Neck ; Prevalence* ; Shoulder

BACKGROUND: Postoperative nausea and vomiting (PONV) is one of the major concerns after anesthesia and surgery, and it may be more frequent in orthopedic patients receiving patient-controlled epidural analgesia (PCEA). The purpose of this study was to compare the effect of palonosetron and dexamethasone on the prevention of PONV in patients undergoing total joint arthroplasty and receiving PCEA. METHODS: Patients scheduled for total hip or knee arthroplasty under spinal anesthesia/PCEA were randomly allocated to receive either intravenous palonosetron (0.075 mg, n = 50) or dexamethasone (5 mg, n = 50). Treatments were administered intravenously to the patients 30 min before the beginning of surgery. The total incidence of PONV and incidence in each time period, severity of nausea, need for rescue anti-emetics, pain score, and adverse effects during the first 48 h postoperatively were evaluated. RESULTS: The total incidence of PONV was lower in the palonosetron group compared with the dexamethasone group (18.4% vs. 36.7%, P = 0.042), but there were no statistically significant differences in incidence between the groups at all time points. No significant intergroup differences were observed in the severity of nausea, use of rescue anti-emetics, pain score, and adverse effects. CONCLUSIONS: Although there were no significant differences in the incidence of PONV between the treatment groups at all time points, intravenous palonosetron reduced the total incidence of PONV in orthopedic patients receiving PCEA compared with dexamethasone.
Analgesia, Epidural* ; Analgesia, Patient-Controlled ; Anesthesia ; Antiemetics ; Arthroplasty ; Arthroplasty, Replacement, Knee ; Dexamethasone* ; Hip ; Humans ; Incidence ; Joints ; Nausea ; Orthopedics* ; Postoperative Nausea and Vomiting*

Purpose: Melanoma-associated antigen C2 (MAGEC2) is an oncogene associated with various types of cancers. However, the biological function of MAGEC2 in circulating tumor cells remains unclear. In this study, we investigated the role of MAGEC2 using adapted suspension cells (ASCs), which were previously developed to study circulating tumor cells (CTCs). Methods: Differential gene expression in adherent cells (ADs) and ASCs was examined using RNA-seq analysis. MAGEC2 expression was assessed using reverse transcription quantitative polymerase chain reaction (RT-qPCR), immunoblotting, and ChIP-seq analysis. Depletion of MAGEC2 expression was performed using siRNA. MAGEC2-depleted ADs and ASCs were used to investigate changes in the proliferation rate and cell cycle. Then, the protein levels of signal transducer and activator of transcription 3 (STAT3), phosphorylated STAT3, and downstream of STAT3 were measured using control and MAGEC2-depleted ADs and ASCs. In ASCs, the direct effect of active STAT3 inhibition with Stattic, a STAT3 inhibitor, was assessed in terms of proliferation and apoptosis. Finally, an Annexin V/7-AAD assay was performed to determine the percentage of apoptotic cells in the Stattic-treated cells. Results: MAGEC2 was highly expressed in ASCs when compared with ADs. Depletion of MAGEC2 reduced the proliferation rate and viability of ASCs. To elucidate the underlying mechanism, the level of STAT3 was examined owing to its oncogenic properties. Tyrosinephosphorylated active STAT3 was highly expressed in ASCs and decreased in MAGEC2-depleted ASCs. Furthermore, on treating ASCs with Stattic, an active STAT3 inhibitor, the cells were markedly sensitive to intrinsic pathway-mediated apoptosis. Conclusions High MAGEC2 expression may play an important role in the survival of ASCs by maintaining the expression of activated STAT3 to prevent apoptotic cell death.

Purpose: Melanoma-associated antigen C2 (MAGEC2) is an oncogene associated with various types of cancers. However, the biological function of MAGEC2 in circulating tumor cells remains unclear. In this study, we investigated the role of MAGEC2 using adapted suspension cells (ASCs), which were previously developed to study circulating tumor cells (CTCs). Methods: Differential gene expression in adherent cells (ADs) and ASCs was examined using RNA-seq analysis. MAGEC2 expression was assessed using reverse transcription quantitative polymerase chain reaction (RT-qPCR), immunoblotting, and ChIP-seq analysis. Depletion of MAGEC2 expression was performed using siRNA. MAGEC2-depleted ADs and ASCs were used to investigate changes in the proliferation rate and cell cycle. Then, the protein levels of signal transducer and activator of transcription 3 (STAT3), phosphorylated STAT3, and downstream of STAT3 were measured using control and MAGEC2-depleted ADs and ASCs. In ASCs, the direct effect of active STAT3 inhibition with Stattic, a STAT3 inhibitor, was assessed in terms of proliferation and apoptosis. Finally, an Annexin V/7-AAD assay was performed to determine the percentage of apoptotic cells in the Stattic-treated cells. Results: MAGEC2 was highly expressed in ASCs when compared with ADs. Depletion of MAGEC2 reduced the proliferation rate and viability of ASCs. To elucidate the underlying mechanism, the level of STAT3 was examined owing to its oncogenic properties. Tyrosinephosphorylated active STAT3 was highly expressed in ASCs and decreased in MAGEC2-depleted ASCs. Furthermore, on treating ASCs with Stattic, an active STAT3 inhibitor, the cells were markedly sensitive to intrinsic pathway-mediated apoptosis. Conclusions High MAGEC2 expression may play an important role in the survival of ASCs by maintaining the expression of activated STAT3 to prevent apoptotic cell death.