• Journal of Life Science
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• v.32 no.11
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• pp.833-840
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• 2022

Chronic inflammation has been shown to be closely associated with tumor development and progression. Nuclear factor kappa B (NF-κB) is composed of a family of five transcription factors. NF-κB signaling plays a crucial role in the inflammatory response and is often found to be dysregulated in various types of cancer, making it an attractive target in cancer therapeutics. In this study, CDC-like kinase 3 (CLK3) was identified as a novel kinase that regulates the NF-κB signaling pathway. Our data demonstrate that CLK3 inhibits the canonical and non-canonical NF-κB pathways. Luciferase assays following the transient or stable expression of CLK3 indicated that this kinase inhibited NF-κB activation mediated by Tumor necrosis factor-alpha (TNFα) and Phorbol 12-myristate 13-acetate (PMA), which are known to activate NF-κB signaling via the canonical pathway. Consistent with data on the ectopic expression of CLK3, CLK3 knockdown using shRNA constructs increased NF-κB activity 1.5-fold upon stimulation with TNFα in HEK293 cells compared with the control cells. Additionally, overexpression of CLK3 suppressed the activation of this signaling pathway induced by NF-κB-inducing kinase (NIK) or CD40, which are well-established activators of the non-canonical pathway. To further examine the negative impact of CLK3 on NF-κB signaling, we performed Western blotting following the TNFα treatment to directly identify the molecular components of the NF-κB pathway that are affected by this kinase. Our results revealed that CLK3 mitigated the phosphorylation/activation of transforming growth factor-α-activated kinase 1 (TAK1), inhibitor of NF-κB kinase alpha/beta (IKKα/α), NF-κB p65 (RelA), NF-κB inhibitor alpha (IκBα), and Extracellular signal-regulated kinase 1/2-Mitogen-activated protein kinase (ERK1/2-MAPK), suggesting that CLK3 inhibits both the NF-κB and MAPK signaling activated by TNFα exposure. Further studies are required to elucidate the mechanism by which CLK3 inhibits the canonical and non-canonical NF-κB pathways. Collectively, these findings reveal CLK3 as a novel negative regulator of NF-κB signaling.

• Journal of Life Science
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• v.32 no.4
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• pp.325-330
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• 2022

While swimming is a very popular competitive sports activity, swimming injuries are unique due to the repetitive nature of the swimming stroke and demanding training programs that can result in upper limb overuse. Therefore, the primary objective of this review was to analyze swimmers' injury areas, injury types by stroke type, and swimming rehabilitation, as well as to discuss safety management for improving swimming performance. In this study, the injuries incurred in swimming events were discussed in the order of upper limb injuries (neck, shoulder, arm, and wrist), lower limb injuries (knee and ankle), and waist injuries. An analysis by stroke type found that shoulder injuries occurred most often with freestyle, backstroke, and butterfly strokes, followed by rotator cuff injury, impingement syndrome, and SLAP (superior labral tear from anterior to posterior) lesions. Knee injuries were associated with the breaststroke, whereas spinal cord injuries occurred with the breaststroke and butterfly stroke. Finally, back injuries were associated with the butterfly stroke. During the freestyle stroke, the shoulder undergoes repetitive overhead movement; hence, shoulder and musculoskeletal pain are the most common and well-documented complaints of swimmers. For safety management, coaches and instructors must ensure that athletes do sufficient warm-up and cool-down exercises to avoid injuries. In case of an injury, they should be familiar with first aid measures so that secondary damage can be prevented with its quick application. In addition, coaches and instructors need to be trained in injury prevention and treatment so that they can provide appropriate rehabilitation treatment for athletes. Although swimming-related injuries cannot be completely eliminated, to reduce them to a minimum, leaders need the knowledge to apply scientific and systematic training principles and methods individualized for each athlete.

• Proceedings of The Korean Society of Health Promotion Conference
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• 2004.10a
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• pp.17-58
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• 2004

뉴저지주 보건교육/건강 증진정책을 논하기전에 건강증진과 보건 교육사의 뜻을 먼저 기술하기로 한다. 건강증진이란 일상 사회생활과 행동과학의 응용에서 시작하며 교육의 효율적 작전 및 기술, 질병 역학 조사, 개인 및 가족단위 건강 위해 행위 절감, 사회연관 구축망 조성, 그리고 적게는 이웃, 더 나아가 조직체계 및 지역 사회의 네트웍 실시등을 실시한다. 보건교육 및 건강증진 전문가란 ' 전국 보건교육 인증 위원회(NCHEC) ' 에서 채택된 다음 7개 활동 영역에서 개인적, 그룹, 각주단위, 그리고 범 국가적 조직에서 종사하는자로 한다. 개인 및 지역사회 보건 교육 필요성 분석- 계회, 실행, 효율성 평가, 사업 진행 조정, 자문, 컴뮤니케이션 등의 활동범위를 들 수 있다. 공인 보건 교육사(CHES)란 대학 및 대학원에서 보건 교육학 소정의 필수 과목을 이수하고 학.석사 소지자로서 ' 전국 보건 교육 인증 위원회 ' 에서 그 자격을 인정 받고 공인 자격 시험에 합격한자로 한다. 합격자는 자기 성명뒤에 CHES란 칭호를 부치며 매 5년마다 75단위이상 인정된 전문 직업 보수 교육을 받아야 한다. 보건 교육사 고용 분야는 연방, 주, 지방 정부의 보건 교육사(10-15%) 및 건강 증진 전문가로 종사하며; 이들은 지역 사회 조직화, 프로그람 기획, 공공사업 마켓팅, 메디아, 컴뮤니케이션 자질을 갓추어야 하며; 상해 예방, 학교 보건, 지역 사회 영양 실태 향상, 그 외 모든 건강 증진과 질병 예방에 일익을 담당 하여; 의사, 간호사, 약사, 영양사,환경 위생사드의 전문분야종사자들괴 한팀이 되어 지역 사회 보건 사업에 기여한다. 쥬저지 보건 교육사들은 주법령 8조 '||'&'||' 보건행정 표준 시행령 ' 에 따라 포괄적 보건교육/건강증진 프로그램을 개발하여 총체적으로 조절 관장한다. 특희 ' 미국 학술원 의료 연구원 ' 에서 제정한 ' 10대 필수 공중 보건 사업 ' 에 기준을 두고; 1) 개인 및 지역사회 필수 보건 여건 분석 평가, 2) 보건 교육 이론에 따른 사업 계획 설정, 3) 교육 전략과 보건문제 발굴에 따라 일반 대중 대상 보건 교육 실행 (프로그람 기획, 연수 교육, 미디어 캠페인, 공중보건 향상책 옹호), 4) 사업 진행 과정 정리, 그 결과에 대한 영향력과 결과 평가, 5) 프로그램진행, 인사 및 예산관리 참여, 6) 근무향상을 위한 보수교육 프로그램 개발, 7) 보건 의료 업무 종사자 상호 협조성 향상 훈련, 8) 지역 사회자원 밭굴, 9) 적절한 고객 의뢰 체제 시행, 10) 위기 관리 컴뮤니케이션 체제 개발실시, 11) 일반 대중에게 공중 보건 향상 고취, 12) 각종 협력 지원금 신청서 작성 제출, 13) 문화/인종적으로 적절한 시청각 교재 발굴, 15) 질적 및 양적 보건교육/건겅증진책 연구 실시, 16) 비 보험 가담자, 저 보험자, 빈곤자, 이민자 색출 선도, 17) 관활 구역내 상재하는 각 건강증진 프로그램 밝혀 내서 불필요한 중복 회피등이다. 그 외에도 보건 교육사들은 사회 복지 단체인 미국 암 협회, 미국 심장 협회,미국 폐장 협회 등 각종 사회 복지 비영리단체 와 자선 사업 단체들과 긴밀희 협조하거나 그 단체 임직원으로서 건강 증진 사업에 종사한다. 병원 및 의료기관에선 임직원 보수 교육, 환자의 질병 예방및 건강증진 교육, 그리고 의료 사업장내 건장 증진업무에 종사한다. 건강 유지 의료 기관(HMO)에선 예방주사, 정기검진 촉진등을 통한 입원일수 절감, 응급실 사용도 절감등으로 의료비 감축, 삶의질 향상상에 종사한다. 사업장 보건 교육사는 스트레스 관리, 금연 및 흡연 중단선도, 체중 절감, 종업원 건강증진 생활화참여 유치, 컴뮤니케이션 개발, 마켓팅, 질병 예방등에 그 전문 직업적 노하우를 사업체 건강 증진 프로그램 개발에 접목한다. 뉴저지 2010년대 건강 증진책은 5대 목표 설정하여 현재 시행하고 있다. 특이한점은 2001년 9.11사태 이후 연방정부와 주정부의 상당한 예산 지원을 그랜트 지원금 형식으로 받아 연방, 주정부, 지방 정부, 의료 기관등에서 일사 불란하게 생물/화학/방사성 테러에 대비하는데 보건 교육사들은 시민 인지도 향상과 위기관리 컴뮤니케이션 영역에서 활약한다. 총체적인 보건 교육/건강 증진책은 다음 천년간 뉴저지 건강증진 백서와 미연방 정부 건강증진 2010에 준하여 설립한 뉴저지 건강 증진 2010 에 의한다. 그 모델을 보면; 1) 생활 습관 향상으로 위해 행위 절제; 적절한 영양 섭취 와 과체중화 차단 불필요한 투약 절제와 그 관리 흡연 탐익 절감, 금연, 흡연관련 신체/정신적 피해 관리/치료 습관성 약물 중독 조기발견 예방 낙상 예방 폭력, 의도적/비의도적 상해 예방 2) 심장질환, 암, 뇌졸중, 당뇨, 폐염, 인프루엔자등 주사망원인 질병 조기 발견 예방 책 마련; 독감.폐렴 예방 주사 실시 3) 보건 교육 대상과 표적 설정 특히 보건사업 참여 동반자 발굴하여 그 동참과 책임분담 책려; 주. 지방 정부기관, 의료 종사자, 의료 보험 업자, 대학 등 교육 기관, 연구 기관, 교육자, 지방 보건소, 지역 사회 비 영리단체, 종교 단체 및 교역자 등의 참여 촉구., 지역 사회 비 영리단체, 종교 단체 및 교역자 등의 참여 촉구.

• Journal of Life Science
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• v.33 no.1
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• pp.15-24
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• 2023

To examine the antitumor effect of proso millet grains, whether proso millet grains exert apoptotic activity against human cancer cells was investigated. When the cytotoxicity of 80% ethanol (EtOH) extract of proso millet grains was tested against various cancer cells using MTT assay, more potent cytotoxicity was observed against human breast cancer MDA-MB-231 cells than against other cancer cells. When the EtOH extract was evaporated to dryness, dissolved in water, and then further fractionated by sequential extraction using four organic solvents (n-hexane, methylene chloride, ethyl acetate, and n-butanol), the BuOH fraction exhibited the highest cytotoxicity against MDA-MB-231 cells. Along with the cytotoxicity, TUNEL-positive apoptotic nucleosomal DNA fragmentation and several apoptotic responses including BAK/BAX activation, mitochondria membrane potential (Δψm) loss, mitochondrial cytochrome c release into the cytosol, activation of caspase-8/-9/-3, and degradation of poly (ADP-ribose) polymerase (PARP) were detected. However, human normal mammary epithelial MCF-10A cells exhibited a significantly lesser extent of sensitivity compared to malignant MDA-MB-231 cells. Irrespective of Fas-associated death domain (FADD)-deficiency or caspase-8-deficiency, human T acute lymphoblastic leukemia Jurkat cells displayed similar sensitivities to the cytotoxicity of BuOH fraction, excluding an involvement of extrinsic apoptotic mechanism in the apoptosis induction. These results demonstrate that the cytotoxicity of BuOH fraction from proso millet grains against human breast cancer MDA-MB-231 cells is attributable to intrinsic apoptotic cell death resulting from BAK/BAX activation, and subsequent mediation of mitochondrial damage-dependent activation of caspase cascade.

• Journal of Life Science
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• v.33 no.2
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• pp.149-157
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• 2023

Transforming growth factor-β (TGF-β) is a multifunctional cytokine that affects not only the survival and growth of cancer cells but also the activity of immune cells. Although it has been generally accepted that cancer cell-derived TGF-β could promote the survival and growth of early cancer cells and have immunosuppressive roles, it has been known that TGF-β has differential effects according to the type or stage of cancer cells. Therefore, it is hard to clearly define its role in cancer progression and immune responses. This study investigated the effects of TGF-β signaling on the expression of five NKG2D ligands and the NK cell-mediated anticancer immune response in the primary colon cancer cell line KM12C and its two metastatic cell lines, KM12SM and KM12L4A. At the surface protein level, exogenous TGF-β decreased the expression of MICA, MICB, ULBP1, and ULBP2, and galunisertib increased the expression of MICA, MIAB, ULBP1, ULBP2, and ULBP3 in KM12C. However, KM12SM and KM12L4A showed no significant changes in the expression of NKG2DLs after treatment with TGF-β or galunisertib. TGF-β signaling inhibition via galunisertib improved the NK cell-mediated anticancer immune response against KM12C but did not show a significant response to KM12SM and KM12L4A. Therefore, the suppression of TGF-β signaling could improve the NK cell-mediated anticancer immune response against KM12C. However, an increase in NKG2DLs expression and an enhanced NK cell-mediated cancer immune response is hard to expect due to the alteration of TGF-β signaling in KM12SM and KM12L4A.

• Journal of Life Science
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• v.33 no.2
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• pp.169-175
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• 2023

As a protective defensive mechanism against ultraviolet (UV) light exposure in skin tissue, melanocytes produce the pigment melanin. Tyrosinase plays a key role in melanin production in melanocytes. However, the overproduction of melanin can lead to lesions, such as freckles and dark spots. Thus, it is clinically important to find a modulating molecule to control melanogenesis by regulating tyrosinase expression and/or activity. It is known that catechin, a plant flavonoid, can reduce melano- genesis through the downregulation of tyrosinase expression. Here, we tested whether catechin derivatives isolated from the stem bark of Ulmus parvifolia have an effect on melanin production by regulating tyrosinase in mouse melanoma cells and in vitro mushroom tyrosinase. The catechin derivatives used in this study included C5A, C7A, C7G, and C7X. Treatments using these catechin derivatives reduced melanin production in mouse melanoma B16F10 cells in which melanogenesis was stimulated by α-MSH. Notably, the anti-melanogenic effects of catechin derivatives were similar to those of kojic acid, a well-known anti-melanogenic molecule. Both C5A and C7A directly inhibited the activity of tyrosinase isolated from mushrooms in vitro. Furthermore, our in silico computational simulation showed that these two compounds were expected to bind to the active site of tyrosinase, which is similar to kojic acid. In addition, all four catechin derivatives reduced tyrosinase protein expression. In summary, our results showed that catechin derivatives can reduce melanogenesis by regulating tyrosinase activity or expression. Thus, this study suggests that catechin derivatives isolated from U. parvifolia can be novel modulators of melanin production.

• Journal of Life Science
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• v.33 no.4
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• pp.315-324
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• 2023

The underlying action of policosanol in lowering cholesterol level has not yet been clearly elucidated. Several recent studies have suggested that sterol regulatory element-binding proteins (SREBP)-1c play a role in the regulation of cholesterol synthesis via the fatty acid synthesis pathway. To date, no study has evaluated the effects of policosanol on SREBP-1c-mediated fatty acid synthesis. Therefore, this study aimed to investigate whether the SREBP-1c-mediated fatty acid biosynthetic pathway is associated with the cholesterol-lowering effects of policosanol. Seven-week-old C57BL/6 male mice were randomly divided into 7 groups (n=7 per group) and treated for 8 weeks as follows: 1) normal diet (normal control), 2) high-fat diet (HFD), 3) HFD+ethanol (Pol-0), 4) HFD+policosanol 1 mg/kg (Pol-1), 5) HFD+policosanol 2 mg/kg (Pol-2), 6) HFD+policosanol 4 mg/kg (Pol-4), and 7) HFD+simvastatin 50 ㎍/kg (positive control). Policosanol and simvastatin were administered at the same time every day while maintaining the HFD. Body weight and food intake were measured weekly for 8 weeks. After 8 weeks, serum cholesterol levels were measured, histological analysis was carried out, and the expressions of SREBP-1c and fatty acid synthase (FAS) in the liver tissues were examined. Policosanol reduced body weight and the amount of food intake in a dose-dependent manner. Serum cholesterol levels were significantly lowered in the Pol-1 and Pol-4 groups. The expression of SREBP-1c and FAS was also significantly decreased in the Pol-4 group. These results suggest that the cholesterol-lowering effects of policosanol can occur due to the inhibition of the expression of SREBP-1c and FAS.

• Journal of the Korean Applied Science and Technology
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• v.40 no.2
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• pp.223-232
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• 2023

Oxidative stress plays a significant role in the pathogenesis of various skin conditions, resulting in cellular and tissue damage that can contribute to the development of skin tone unevenness, roughness and wrinkles. In this study, we found that Trifolium pratense L. extract (TE) attenuated oxidative-induced damage in HaCaT cells and elucidated the underlying molecular mechanism. Our finding demonstrated that TE effectively protected HaCaT cells against H₂O₂-induced cell death by inhibiting caspase-3 activation, downregulating Bax and upregulating Bcl-2, and attenuating the activation of three mitogen-activated protein kinases (MAPKs). Our results suggest that TE has remarkable cytoprotective properties against oxidative damage in HaCaT cells and could serve as a complementary or alternative approach to prevent and treat skin damage.

• Journal of Life Science
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• v.33 no.6
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• pp.471-480
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• 2023

This study was designed to evaluate the anti-inflammatory effects of Rumohra adiantiformis extracts fermented with Bovista plumbea mycelium (B-RAE) in LPS-stimulated RAW 264.7 cells. The total polyphenol and total flavonoid content of B-RAE were 379.26±7.77 mg/g and 50.85±3.08 mg/g, respectively. The results of measuring the antioxidant activity of B-RAE showed that it scavenges 2, 2-diphenyl-1-picrylhydrazyl (DPPH), 2, 2'-azino-bis-3-ethylbenzothiazoline-6-sulfonic acid (ABTS), and superoxide anion radical in a dose-dependent manner. B-RAE inhibited nitric oxide (NO) production in a dose-dependent manner without affecting cell viability. The gene expression of pro-inflammatory cytokines such as tumor necrosis factor-α (TNF-α), interleukin-lβ (IL-1β), and IL-6 was measured using real time quantitative reverse transcription PCR (qRT-PCR). We found that, compared to the LPS-treated group, B-RAE significantly reduced the mRNA levels of the pro-inflammatory cytokines in a concentration-dependent manner. The expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), the phosphorylation of transcription factors such as nuclear factor-κB (NF-κB), and the mitogen-activated protein kinase (MAPK) signaling pathway proteins were assessed using Western blot analysis. We found that B-RAE significantly suppressed the expression of iNOS and COX-2, but their expression was increased by LPS treatment. In addition, the phosphorylation of NF-κB and IκB, which was increased by LPS treatment, was reduced with B-RAE treatment. The effect of B-RAE on the phosphorylation of the MAPK signaling pathway proteins was measured, and the phosphorylation of extracellular signal-regulated kinase (ERK) and the p38 MAPK proteins decreased in a dose-dependent manner, while the phosphorylation of c-Jun N-terminal kinase (JNK) increased. These anti-inflammatory effects of B-RAE may thus have been achieved through the high antioxidant activity, the inhibition of NO production through the suppression of iNOS and COX-2 expression, the inhibition of the NF-κB pathway, and the suppression of pro-inflammatory cytokine expression.

• Journal of Chest Surgery
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• v.43 no.6
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• pp.588-595
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• 2010

Background: Base on types of tumor, the types of expressed tumor is diverse and the difference in its expression rate is even more various. Due to such reasons an animal model is absolutely needed for a clinical research of lung cancer. The author attempted oncogenesis by cultivating a cell line of non-small cell carcinoma and then injecting it inside thoracic cavities of nude mice. The author conducted quantitative analyses of HER2/neu tumor gene - an epidermal growth factor receptor (EGFR) related to lung cancer, and TGF-${\beta}_1$, which acts as a resistance to cell growth inhibition and malignant degeneration. In order to investigate achievability of the oncogenesis, histological changes and the expression of cancer gene in case of orthotopic lung cancer is necessary. Material and Method: Among 20 immunity-free male BALB/c, five nude mice were selected as the control group and rest as the experimental group. Their weights ranged from 20 to 25 gm (Orient, Japan). After injection of lung cancer line (SW900 G IV) into the pleural cavity of nude mice, They were raised at aseptic room for 8 weeks. HER2/neu was quantitatively analyzed by separating serum from gathered blood via chemiluminiscent immunoassay (CLIA), and immunosandwitch method was applied to quantitatively analyze TGF-${\beta}_1$. SPSS statistical program (SPSS Version 10.0, USA) was implemented for statistical analysis. Student T test was done, and cases in which p-value is less than 0.05 were considered significant. Result: Even after lung cancer was formed in the normal control group or after intentionally injected lung cancer cell line, no amplification of HER2/neu gene showed reaction. However, the exact quantity of TGF-${\beta}_1$ was $28,490{\pm}8,549pg/mL$, and the quantity in the group injected with lung cancer cell was $42,362{\pm}14,449pg/mL$, meaning 1.48 times highly Significant (p<0.483). It proved that HER2/neu gene TGF-${\beta}_1$ had no meaningful interconnection. Conclusion: TGF-${\beta}_1$ gene expressed approximately 1.48 times amplification in comparison to the control group. The amplification of TGF-${\beta}_1$ meant somatic recuperation inhibition mechanism due to carcinogenesis in nude mice was definitely working. It may be implemented as a quantitative analysis that allows early detection of lung cancer in human body.