• Title/Summary/Keyword: clinical pathway

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Detection and Characterization of PCR-SSCP Markers of the Bovine Lactoferrin Gene for Clinical Mastitis

  • Zhou, Lei;Yang, Yuan-Yuan;Li, Zhong-Hao;Kong, Li-Juan;Xing, Guan-Dong;Di, He-Shuang;Wang, Gen-Lin
    • Asian-Australasian Journal of Animal Sciences
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    • v.19 no.10
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    • pp.1399-1403
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    • 2006
  • A total of 80 cows, including 40 top mastitis resistant and 40 top mastitis susceptible animals as Group I and Group II, were selected from a population of 520 cows based on clinical mastitis occurrence. PCR-SSCP analysis on four fragments within the 5'region and two fragments of Exons 4,15 of bovine lactoferrin (bLF) revealed that four fragments-P1,P4,E4,E15-had polymorphisms which totally included six base mutations, and only two of them had significant differences in allele frequencies between resistant and susceptible groups, P1 (53.7% vs. 70.0%, p<0.05) and P4 (55.0% vs. 68.8%, p<0.05). Further study on these two promising markers combined with the milk performance traits of cows demonstrated that their selection would result in higher fat percentage (p<0.05), lower Somatic Cell Score (SCS) (p<0.05) and Clinical Mastitis Residuals (CMR) (p<0.01) indicating higher mastitis resistance and lower milk yield (p<0.05). The putative transcription factor binding sites in the 5'region were also studied by using MatInspector 7.2.2 software, and two signal pathways regulating the expression of bLF including the NF-${\kappa}B$ pathway and nuclear hormone receptor pathway were predicted.

Pro-inflammatory Cytokine Expression Through NF-${\kappa}B/I{\kappa}B$ Pathway in Lung Epithelial Cells (폐 상피세포에서 NF-${\kappa}B/I{\kappa}B$ 경로에 의한 염증매개 사이토카인의 발현)

  • Park, Gye-Young;Lee, Seung-Hee;HwangBo, Bin;Yim, Jae-Joon;Lee, Choon-Taek;Kim, Young-Whan;Han, Sung-Koo;Shim, Young-Soo;Yoo, Chul-Gyu
    • Tuberculosis and Respiratory Diseases
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    • v.49 no.3
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    • pp.332-342
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    • 2000
  • Background : The importance of pro-inflammatory cytokines, especially tumor necrosis factor $\alpha$ (INF-$\alpha$) and interleukin-1$\beta$ (IL-1$\beta$), have been extensively documented in the generation of inflammatory lung disease. Lung epithelial cells are also actively involved in initiating and maintaining inflammation by producing pro-inflammatory mediators. Understanding the mechanism of pro-inflammatory cytokine expression in lung epithelial cells is crucial to the development of new therapeutic modalities for inflammatory lung disease. Transcription of most pro-inflammatory cytokines is dependent on the activation of NF-${\kappa}B$. However, the relationship between pro-inflammatory cytokine expression and NF-${\kappa}B/I{\kappa}B$ pathway in lung epithelial cells is not clear. Methods : BEAS-2B, A549, Na-H157, NCI-H719 cells were stimulated with IL-$1{\beta}$ or TNF-$\alpha$ at various times, and then IL-8 and TNF-$\alpha$mRNA expressions were assayed by Northern blot analysis. IL-$1{\beta}$ or TNF-$\alpha$-induced NF-${\kappa}B$ activation was assessed by the nuclear translocation of p65 NF-${\kappa}B$ subunit. The degradation of $I{\kappa}B{\alpha}$ and $I{\kappa}B{\beta}$ by IL-$1{\beta}$ or TNF-$\alpha$stimulation was assayed by Western blot analysis. The phosphorylation of $I{\kappa}B{\alpha}$ was evaluated by Western blot analysis after pre-treating cells with proteasome inhibitor followed by IL-$1{\beta}$ or TNF-$\alpha$ stimulation. The basal level of IKK $\alpha$ expression was evaluated by Western blot analysis. Results: $I{\kappa}B{\alpha}$ and $I{\kappa}B{\alpha}$ was rapidly degraded after 5 minutes of incubation with IL-$1{\beta}$ or TNF-$\alpha$ in BEAS-2B, A549, and NCI-H157 cells. The activation of NF-${\kappa}B{\alpha}$ and the induction of IL-8 and TNF-$\alpha$ mRNA expression were observed by IL-$1{\beta}$ or TNF-$\alpha$ stimulation in these cells. In contrast, neither the changes in NF-${\kappa}B/I{\kappa}B$ pathway nor IL-8 and TNF-$\alpha$mRNA expression was induced by IL-$1{\beta}$ or TNF-$\alpha$ stimulation in NCI-H719 cells. IL-$1{\beta}$ and TNF-$\alpha$-induced $I{\kappa}B$ phosphorylation was observed in BEAS-2B, A549, and NCI-H157 cells, but not in NCI-H719 cells. The basal level of IKK$\alpha$ expression was not different between cell. Conclusion : NF-${\kappa}B/I{\kappa}B$ pathway plays an important role in the expression of pro-inflammatory cytokine in most lung epithelial cells. The absence of the effect on NF-${\kappa}B/I{\kappa}B$ pathway in NCI-H719 cells sæms to be due to the defect in the intracellular signal transduction pathway upstream to IKK.

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Countermeasures of Specimens Showing below Reference Value in APTT Result

  • Choi, Hyun Oh;Kim, Seung Gu;Park, Sang Hee;Lee, Jae Ki;Koo, Bon Kyung;Park, Chang Ho
    • Korean Journal of Clinical Laboratory Science
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    • v.45 no.3
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    • pp.87-90
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    • 2013
  • The activated partial thromboplastin time (APTT) is used primarily to evaluate coagulation abnormalities in the intrinsic pathway. The proper specimen is very important factor for precise results of blood coagulation analysis. The objective of this study was to get to the conclusion of whether to analyze again and to collect blood sample over again when APTT result shows below the reference value. We evaluated 126 samples showing a value below 20.0 sec at ATPT result, which consist of 48 males and 78 females candidates during night duty from March 2012 to December 2012. Average comparisons of APTT result between first and retested analysis among study subjects were significantly different in male samples. APTT results comparison of recollected subjects among clotted samples were also significantly different with both sexes (p<0.000). We suggest that we should carefully check the samples to get accurate results and collect samples again in case of only obtaining improper samples; even though the APTT result show below reference value.

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Bufalin Induces Mitochondrial Pathway-Mediated Apoptosis in Lung Adenocarcinoma Cells

  • Ding, Da-Wei;Zhang, Yong-Hong;Huang, Xin-En;An, Qing;Zhang, Xun
    • Asian Pacific Journal of Cancer Prevention
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    • v.15 no.23
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    • pp.10495-10500
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    • 2015
  • Background: To evaluate the effects of bufalin in A549 human lung adenocarcinoma epithelial cells in vitro and assess the underlying mechanisms. Materials and Methods: Human A549 non-small cell lung cancer (NSCLC) cells were treated with various concentrations of bufalin. Cell proliferation was measured by CCK-8 assay, apoptotic cell percentage was calculated by flow cytometry and morphological change was observed by inverted phase contrast microscopy/transmission electron microscopy. In addition, the membrane potential of mitochondria was detected by JC-1 fluorescence microscopy assay, and the related protein expression of cytochrome C and caspase-3 was analyzed by Western blotting. Results: Bufalin could inhibit the proliferation of A549 cells via induction of apoptosis, with the evidence of characteristic morphological changes in the nucleus and mitochondria. Furthermore, bufalin decreased the mitochondrial membrane potential with up-regulation of cytochrome C in the cytosol, and activation of caspase-3. Conclusions: Bufalin inhibits the proliferation of A549 cells and triggers mitochondria-dependent apoptosis, pointing to therapeutic application for NSCLC.

Mammalian Target of Rapamycin Signaling Pathways and Depression (Mammalian Target of Rapamycin 신호전달체계와 우울증)

  • Lee, Jung Goo;Seo, Mi Kyong;Park, Sung Woo;Kim, Young Hoon
    • Korean Journal of Biological Psychiatry
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    • v.23 no.1
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    • pp.18-23
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    • 2016
  • Depression is a complicated psychiatric illness with severe consequences. Despite recent advanced achievements of molecular neurobiology, pathophysiology of depression has not been well elucidated. Among new findings of pathophysiology of depression, the possible fast antidepressant effect by N-methyl-D-asparate receptor antagonist, such as ketamine, is regarded as a promising treatment target of depression. Ketamine stimulates the mammalian target of rapamycin (mTOR) signaling pathway and activation of mTOR signaling pathway may be a key mechanism of the antidepressant effect of ketamine. Thus, this review describes the role of mTOR signaling in the pathophysiology of depression and developing a new treatment target of depression.

The Extract of Pseudomonas aeruginosa Induces the Apoptosis of the Human Colorectal Cancer Cell Line, HCT 116 Cells, via Mitochondrial Pathway

  • Yang, Eun-Ju;Chang, Jeong-Hyun
    • Biomedical Science Letters
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    • v.18 no.1
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    • pp.16-21
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    • 2012
  • Although there are many potential cytotoxic molecules released from bacteria, the role of these molecules on the apoptosis of various cancer cells is not well understood. Pseudomonas aeruginosa (P. aeruginosa) is a Gram-negative, aerobic and rod-shaped bacterium, and has a number of virulence factors. To understand the cytotoxic effect of bacterial extracts on the colorectal cancer cell line, HCT 116 cells, we examined alteration of the cell viability, proliferation, cell cycle and apoptosis of HCT 116 cells after treatment with extract of P. aeruginosa (PaE). These cytotoxicity of PaE occurred in a time- and a dose-dependent manners. In addition, PaE arrested the cell cycle of HCT 116 cell in a time-dependent manner. PaE inhibited the protein levels of Bcl-2 and induced the release of cytochrome c from mitochondria of HCT 116 cells. The decrease of procaspase-3 was induced by the treatment of PaE. These results indicate that PaE has a cytotoxicity in HCT 116 cells via the induction of apoptosis associated with mitochondrial pathway. Therefore, PaE may used as the potential target for the treatment of colorectal cancer.

Acetate decreases PVR/CD155 expression via PI3K/AKT pathway in cancer cells

  • Tran, Na Ly;Lee, In Kyu;Choi, Jungkyun;Kim, Sang-Heon;Oh, Seung Ja
    • BMB Reports
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    • v.54 no.8
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    • pp.431-436
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    • 2021
  • In recent years, restoring anti-tumor immunity has garnered a growing interest in cancer treatment. As potential therapeutics, immune checkpoint inhibitors have demonstrated benefits in many clinical studies. Although various methods have been applied to suppress immune checkpoints to boost anti-tumor immunity, including the use of immune checkpoint inhibitors, there are still unmet clinical needs to improve the response rate of cancer treatment. Here, we show that acetate can suppress the expression of poliovirus receptor (PVR/CD155), a ligand for immune checkpoint, in colon cancer cells. We demonstrated that acetate treatment could enhance effector responses of CD8+ T cells by decreasing the expression of PVR/CD155 in cancer cells. We also found that acetate could reduce the expression of PVR/CD155 by deactivating the PI3K/AKT pathway. These results demonstrate that acetate-mediated expression of PVR/CD155 in cancer cells might potentiate the anti-tumor immunity in the microenvironment of cancer. Our findings indicate that maintaining particular acetate concentrations could be a complementary strategy in current cancer treatment.

Narrative Review on the Mechanism of Whidam's Vibrator Sugi Therapy (휘담식 진동기 수기요법의 기전에 대한 서술적 고찰)

  • Hun Mo Ahn;Dae Sung Jung;Han Joo Kang
    • Journal of Korean Medical Ki-Gong Academy
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    • v.22 no.1
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    • pp.1-27
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    • 2023
  • Objective : This paper provides a narrative review of the research literature on the neurophysiological and neurochemical mechanisms of local vibration while studying the treatment principles and mechanisms of Whidam's vibrator Sugi therapy. Methods : Searches related to vibration therapy research were conducted in PUBMED using "Vibration", "Whole Body Vibration", "Localized Vibration", and "Focal Vibration". The Conditions were limited to review and systematic review. Results : Roberto Casale's paper was selected as an inquiry task and reviewed critically and narratively by referring to other papers. The stimulation process of local vibration (LV) was broadly classified into receptor transmission (pain reception phase), ascending sensory pathway to the spinal cord (segmental phase), and action of the cortex and subcortical structures (systemic control phase) according to the pain pathway. In addition, the role of C-tactile mechanoreceptors, changes in neurotransmitters and neurohormones, LV stimulation below perception threshold (lower threshold), pain control and kinesiologic illusions were specially addressed. In addition, the expression and function of Piezo Channels were added to supplement the human pain and tactile sensing mechanism. Conclusions : LV exerts pain control mechanisms through different interactions that can interfere with pain transmission and pain perception. Since LV provides sufficient neurophysiological reasons for clinical application, it is necessary to expand the use of Whidam's vibrator Sugi therapy to a wider range of clinical applications.

Humic Substances Suppresses the Proliferation of TC-1 Cells, the Lung Cancer Cell

  • Eun Ju Yang;Jeong Hyun Chang
    • Biomedical Science Letters
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    • v.29 no.4
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    • pp.280-286
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    • 2023
  • In humic substances, fulvic acid (FA) is a subclass of diverse compounds known as humic substances, which are by-products of organic degradation from microorganisms. FA can suppress the proliferation of tumor cells. Despite numerous studies, the exact mechanism for the various effects of FA is not clearly understood. Based on results demonstrating anti-proliferation effects on human cancer, we investigated whether FA has similar effects on lung cancer in this study. Firstly, the anti-cancer effect of FA in pulmonary epithelial tumor cell lines (TC-1 cells) was examined by confirming its inhibitory effect on the cell proliferation of TC-1 cells. TC-1 cell proliferation was reduced by FA on a dose-dependent and time-dependent manner. After 24 hours of FA treatment, cell morphological changes such as cell volume decrease, non-adherence and increased number of apoptotic cells were clearly observed. In addition, FA induced a DNA ladder pattern by increased of DNA fragments in TC-1 cells. In the intracellular regulatory pathway by FA, we confirmed that FA induced the reduction of the anti-apoptotic protein, Bcl-2 protein levels. These results indicate that FA has anticancer effect by inducing intracellular apoptotic pathway. Further research on the mechanism of anticancer effects will be basic data for the development of potential anticancer drugs.

D-Limonene mitigate myocardial injury in rats through MAPK/ERK/NF-κB pathway inhibition

  • Younis, Nancy Safwat
    • The Korean Journal of Physiology and Pharmacology
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    • v.24 no.3
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    • pp.259-266
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    • 2020
  • Cardiovascular diseases are the primary reason of mortality, among which myocardial infarction (MI) is the most dominant and prevalent. This study was considered to examine D-Limonene protective action against isoproterenol (ISO) induced MI. Wister male rats were dispersed into four groups. Normal and D-Limonene control group in which rats administered saline or D-Limonene. ISO control animals were administered saline for 21 days then challenged with ISO (85 mg/kg, subcutaneously) on 20th and 21st day for MI induction. D-Limonene pretreated group in which animals were pretreated with D-Limonene 50 mg/kg orally for 21 days then administered ISO on 20th and 21st day. MI prompted variations were assessed by myocardial infarction area determination, blood pressure (BP) alterations, cardiac injury biomarkers and inflammatory mediators measurements. For more depth investigation, both the apoptotic status was evaluated via measuring mRNA expression of Bcl-2 and Bax as well as mitogen-activated protein kinase-extracellular signal-regulated kinase (MAPK-ERK) signal transduction were investigated via Western blotting. MI group revealed significant infarcted area, blood pressure alterations, myocardial injury enzymes intensification together with inflammatory cytokines amplification. MI was associated with activation of MAPK-ERK signal pathway and apoptotic status within the myocardium. On the other hand, pretreated with D-Limonene demonstrated deterred infracted area, reduced myocardial enzymes, improved BP indices, lessened inflammatory levels. Furthermore, D-Limonene pretreatment caused a decline in MAPK proteins pathway and Bax relative mRNA expression, while intensifying Bcl-2 mRNA expression promoting that D-Limonene may constrain MI induced myocardial apoptosis. D-Limonene mitigated MI injury through MAPK/NF-κB pathway inhibition and anti-apoptotic effect.