Effectiveness of Electrical Heating for Improved Thermal Insulation of a Multi-layered Winter Clothing System

This paper investigated the impact of the distance of the heating unit from the body in a multi-layered winter clothing system on effective thermal insulation and heating efficiency. To identify changes in the thermal insulation and heating efficiency of electrical heating in different layers inside a winter clothing ensemble, a series of thermal manikin tests was conducted. A multi-layered winter ensemble with and without activation of a heating unit was tested on the thermal manikin under two different ambient temperature conditions (10°C and 5°C). Results show that the effective thermal insulation of test ensembles increased by 5-7 percent with the activation of the heating unit compared to that without the activation. The closer the heating unit to the body, the higher the effective thermal insulation was in both ambient temperature conditions. This trend was more significant at lower ambient temperature

Effect of the submandibular push exercise using visual feedback from pressure sensor: an electromyography study

We developed a new exercise method called the submandibular push exercise that can strengthen the suprahyoid muscle by inducing only the motion of the hyoid bone without neck flexion. In this study, we aimed to investigate and compare the muscle activity of the suprahyoid and infrahyoid muscles in the course of performing three different swallowing exercises. Twenty healthy participants and fifteen patients with dysphagia were recruited. Each participant consecutively performed three exercises: Shaker, CTAR, and submandibular push exercises. To investigate muscle activation, surface electromyography was performed on the suprahyoid, infrahyoid, and SCM muscles, during the exercises. Root mean square (RMS) was measured. In healthy participants, the submandibular push exercise showed a significantly higher RMS value in the suprahyoid and infrahyoid muscles than the Shaker and CTAR exercises using repeated ANOVA with Tukey's post hoc test (p<0.05). In patients with dysphagia, the submandibular push and Shaker exercises showed significantly higher RMS value in the suprahyoid and infrahyoid muscles than the CTAR exercise. However, no significant difference was found between the submandibular push and Shaker exercises. In both healthy and patients with dysphagia, the mean RMS values of the SCM muscles during the submandibular push exercise were significantly lower than those during the Shaker exercise using repeated ANOVA with Tukey's post hoc test (p<0.05). In conclusion, considering the relatively superior selectiveness in suprahyoid and infrahyoid muscle contraction, the submandibular push exercise using visual feedback from pressure sensor could be an efficient supplementary exercise to the conventional swallowing muscle exercises. However, further studies may be necessary to confirm the improvement in swallowing difficulty

Cordycepin promotes apoptosis by modulating the ERK-JNK signaling pathway via DUSP5 in renal cancer cells

Constitutive activation of extracellular signal regulated kinase (ERK)-Jun NH2-terminal kinase (JNK) signaling commonly occurs in tumors. The activation of ERK promotes cell proliferation, whereas that of JNK induces cell apoptosis. However, the apoptotic mechanism of ERK-JNK signaling in cancer is not well understood. Recently, we identified that apoptosis and activation of the JNK signaling pathway were induced after cordycepin treatment in human renal cancer, suggesting that JNK signaling might contribute to TK-10 cell apoptosis. We investigated the apoptotic effects of cordycepin by evaluating the activation of the ERK-JNK signaling pathway in renal cancer TK-10 cells. We found that cordycepin downregulated ERK and DUSP5, upregulated phosphorylated-JNK (p-JNK), and induced apoptosis. Moreover, we showed that siRNA-mediated inhibition of ERK downregulated DUSP5, whereas ERK overexpression upregulated DUSP5, and that DUSP5 knockdown by siRNA upregulated p-JNK. The JNK-specific inhibitor SP600125 upregulated nuclear translocation of β-catenin, and downregulated Dickkopf-1 (Dkk1), which has been shown to be a potent inhibitor of Wnt signaling. Dkk1 knockdown by siRNA upregulated nuclear β-catenin, suggesting the involvement of the Wnt/β-catenin signaling pathway. DUSP5 overexpression in TK-10 cells decreased p-JNK and increased nuclear β-catenin. The decreased Bax activation markedly protected against cordycepin-induced apoptosis. Bax subfamily proteins induced apoptosis through caspase-3. Taken together, we show that JNK signaling activation by cordycepin mediated ERK inhibition, which might have induced Bax translocation and caspase-3 activation via regulation of DUSP5 in TK-10 cells, thereby promoting the apoptosis of TK-10 cells. Targeting ERK-JNK signaling via the apoptotic effects of cordycepin could be a potential therapeutic strategy to treat renal cancer

Cordycepin induces apoptosis by caveolin-1-mediated JNK regulation of Foxo3a in human lung adenocarcinoma

Forkhead transcription factor (Foxo3a) is a downstream effector of JNK-induced tumor suppression. However, it is not clear whether the caveolin-1 (CAV1)-mediated JNK/Foxo3a pathway is involved in cancer cell apoptosis. We found that cordycepin upregulates CAV1 expression, which was accompanied by JNK phosphorylation (p-JNK) and subsequent Foxo3a translocation into the nucleus, resulting in the upregulation of Bax protein expression. Furthermore, we found that CAV1 overexpression upregulated p-JNK, whereas CAV1 siRNA downregulated p-JNK. Additionally, SP600125, a specific JNK inhibitor, significantly increased Foxo3a phosphorylation, which downregulated Foxo3a translocation into the nucleus, indicating that CAV1 mediates JNK regulation of Foxo3a. Foxo3a siRNA downregulated Bax protein and attenuated A549 apoptosis, indicating that the CAV1-mediated JNK/Foxo3a pathway induces the apoptosis of A549 lung cancer cells. Cordycepin significantly decreased tumor volume in nude mice. Taken together, these results indicate that cordycepin promotes CAV1 upregulation to enhance JNK/Foxo3a signaling pathway activation, inducing apoptosis in lung cancer cells, and support its potential as a therapeutic agent for lung cancer

Case Series of an Intraoral Balancing Appliance Therapy on Subjective Symptom Severity and Cervical Spine Alignment

Objective. The objective of this study was to investigate the effect of a holistic intraoral appliance (OA) on cervical spine alignment and subjective symptom severity. Design. An observational study on case series with holistic OA therapy. Setting. An outpatient clinic for holistic temporomandibular joint (TMJ) therapy under the supervision of the Pain Center, CHA Biomedical center, CHA University. Subjects. Ambulatory patients presenting with diverse chief complaints in the holistic TMJ clinic. Main Measures. Any immediate change in the curvature of cervical spine and the degree of atlantoaxial rotation was investigated in the images of simple X-ray and computed tomography of cervical spine with or without OA. Changes of subjective symptom severity were also analyzed for the holistic OA therapy cases. Results. A total of 59 cases were reviewed. Alignment of upper cervical spine rotation showed an immediate improvement (). Changes of subjective symptom severity also showed significant improvement (). Conclusion. These cases revealed rudimentary clinical evidence that holistic OA therapy may be related to an alleviated symptom severity and an improved cervical spinal alignment. These results show that further researches may warrant for the holistic TMJ therapy

CTCF cooperates with CtIP to drive homologous recombination repair of double-strand breaks

The pleiotropic CCCTC-binding factor (CTCF) plays a role in homologous recombination (HR) repair of DNA double-strand breaks (DSBs). However, the precise mechanistic role of CTCF in HR remains largely unclear. Here, we show that CTCF engages in DNA end resection, which is the initial, crucial step in HR, through its interactions with MRE11 and CtIP. Depletion of CTCF profoundly impairs HR and attenuates CtIP recruitment at DSBs. CTCF physically interacts with MRE11 and CtIP and promotes CtIP recruitment to sites of DNA damage. Subsequently, CTCF facilitates DNA end resection to allow HR, in conjunction with MRE11-CtIP. Notably, the zinc finger domain of CTCF binds to both MRE11 and CtIP and enables proficient CtIP recruitment, DNA end resection and HR. The N-terminus of CTCF is able to bind to only MRE11 and its C-terminus is incapable of binding to MRE11 and CtIP, thereby resulting in compromised CtIP recruitment, DSB resection and HR. Overall, this suggests an important function of CTCF in DNA end resection through the recruitment of CtIP at DSBs. Collectively, our findings identify a critical role of CTCF at the first control point in selecting the HR repair pathway

Cordycepin induces apoptosis of human ovarian cancer cells by inhibiting CCL5-mediated Akt/NF-κB signaling pathway

The chemokine, CCL5, is a key mediator for the recruitment of immune cells into tumors and tissues. Akt/NF-κB signaling is significantly activated by CCL5. However, the role of NF-κB inactivation in apoptosis induced by negative regulation of CCL5 remains unclear. Here, we analyzed the effect of cordycepin on NF-κB activity in SKOV-3 cells and found that cordycepin-mediated inhibition of NF-κB signaling induced apoptosis in SKOV-3 cells via the serial activation of caspases. In addition, immune-blotting analysis showed that CCL5 is highly expressed in SKOV-3 cells. In addition to activating caspases, we show that, cordycepin prevents TNF-α-induced increase in CCL5, Akt, NF-κB, and c-FLIPL activation and that CCL5 siRNA could inhibit Akt/NF-κB signaling. Moreover, cordycepin negatively regulated the TNF-α-mediated IκB/NF-κB pathway and c-FLIPL activation to promote JNK phosphorylation, resulting in caspase-3 activation and apoptosis. Also, we show that c-FLIPL is rapidly lost in NF-κB activation-deficient. siRNA mediated c-FLIP inhibition increased JNK. SP600125, a selective JNK inhibitor, downregulated p-JNK expression in cordycepin-treated SKOV-3 cells, leading to suppression of cordycepin-induced apoptosis. Thus, these results indicate that cordycepin inhibits CCL5-mediated Akt/NF-κB signaling, which upregulates caspase-3 activation in SKOV-3 cells, supporting the potential of cordycepin as a therapeutic agent for ovarian cancer