• 제목/요약/키워드: pre-activation

검색결과 494건 처리시간 0.022초

한국치위생학회지 게재논문(창간호~2015년)의 연구동향 분석 (Trend analysis of research in the journal of Korean society dental hygiene from 2001 to 2015)

  • 장종화;원복연;장계원;김설악;오상환;김윤정;하명옥;이영은;이가령;박성숙;엄숙
    • 한국치위생학회지
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    • 제17권4호
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    • pp.693-704
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    • 2017
  • Objectives: The purpose of study is to investigate trends in dental hygiene research published in the Journal of Korean Society Dental Hygiene. Methods:Total of 992 researches were published between 2001 to 2015 were reviewed using analysis criteria. Results: 23.7% of the researches were supported financially. The most frequent research topics were oral health (40.9%). 3 to 5 researchers per research (38.5%) was most common and 84.1% of principal researchers were professors. 29 researchers were approved by IRB (2011 to 2015). As for the type of research, 87.1% of quantitative studies adapted survey and 9.5% adapted experiment. Convenient sampling was used in 85.6% of the researches. 32.7% of studies searched information in school. Interventions of dental material were the most in pre experimental design (19.2%) and Interventions of activation of oral health program were the most in quasi experimental design (37.5%). Conclusions: The findings of this study suggested the recent trends and the direction in dental hygiene research.

Conditioning-induced cardioprotection: Aging as a confounding factor

  • Randhawa, Puneet Kaur;Bali, Anjana;Virdi, Jasleen Kaur;Jaggi, Amteshwar Singh
    • The Korean Journal of Physiology and Pharmacology
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    • 제22권5호
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    • pp.467-479
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    • 2018
  • The aging process induces a plethora of changes in the body including alterations in hormonal regulation and metabolism in various organs including the heart. Aging is associated with marked increase in the vulnerability of the heart to ischemia-reperfusion injury. Furthermore, it significantly hampers the development of adaptive response to various forms of conditioning stimuli (pre/post/remote conditioning). Aging significantly impairs the activation of signaling pathways that mediate preconditioning-induced cardioprotection. It possibly impairs the uptake and release of adenosine, decreases the number of adenosine transporter sites and down-regulates the transcription of adenosine receptors in the myocardium to attenuate adenosine-mediated cardioprotection. Furthermore, aging decreases the expression of peroxisome proliferator-activated receptor gamma co-activator 1-alpha ($PGC-1{\alpha}$) and subsequent transcription of catalase enzyme which subsequently increases the oxidative stress and decreases the responsiveness to preconditioning stimuli in the senescent diabetic hearts. In addition, in the aged rat hearts, the conditioning stimulus fails to phosphorylate Akt kinase that is required for mediating cardioprotective signaling in the heart. Moreover, aging increases the concentration of $Na^+$ and $K^+$, connexin expression and caveolin abundance in the myocardium and increases the susceptibility to ischemia-reperfusion injury. In addition, aging also reduces the responsiveness to conditioning stimuli possibly due to reduced kinase signaling and reduced STAT-3 phosphorylation. However, aging is associated with an increase in MKP-1 phosphorylation, which dephosphorylates (deactivates) mitogen activated protein kinase that is involved in cardioprotective signaling. The present review describes aging as one of the major confounding factors in attenuating remote ischemic preconditioning-induced cardioprotection along with the possible mechanisms.

시상경색으로 유발된 주시장애 1예에 관한 임상적 고찰 (A Clinical Case Report of Gaze Palsy due to Thalamic Infarction)

  • 정종안;정수미;노영만;전홍렬;안정조;전상윤;김희철;홍석;김성진
    • 대한한방내과학회지
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    • 제27권2호
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    • pp.533-537
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    • 2006
  • The purpose of this study is to present a case of gaze palsy due to thalamic infarction improved by acupuncture and herb medicine. Monocular gaze palsies which result from a supranuclear cerebral lesion are rare clinical manifestations. The pre-frontal cortico-oculomotor pathways travel across the thalamus and mesodienphalic junction terminating directly in oculomotor complexes. The acute disinhibition of these neurons by a posterior thalamic lesion results in a sustained but transient discharge of the medial rectus and tonic activation. Results of this study suggest a role for conservative therapy with herb medicine and acupuncture to treat gaze palsy due to thalamic infarction. Further research into oriental medical treatment for such disorders will be forthcoming.

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Proliferation of Toxoplasma gondii Suppresses Host Cell Autophagy

  • Lee, Youn-Jin;Song, Hyun-Ouk;Lee, Young-Ha;Ryu, Jae-Sook;Ahn, Myoung-Hee
    • Parasites, Hosts and Diseases
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    • 제51권3호
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    • pp.279-287
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    • 2013
  • Autophagy is a process of cytoplasmic degradation of endogenous proteins and organelles. Although its primary role is protective, it can also contribute to cell death. Recently, autophagy was found to play a role in the activation of host defense against intracellular pathogens. The aims of our study was to investigate whether host cell autophagy influences Toxoplasma gondii proliferation and whether autophagy inhibitors modulate cell survival. HeLa cells were infected with T. gondii with and without rapamycin treatment to induce autophagy. Lactate dehydrogenase assays showed that cell death was extensive at 36-48 hr after infection in cells treated with T. gondii with or without rapamycin. The autophagic markers, LC3 II and Beclin 1, were strongly expressed at 18-24 hr after exposure as shown by Western blotting and RT-PCR. However, the subsequent T. gondii proliferation suppressed autophagy at 36 hr post-infection. Pre-treatment with the autophagy inhibitor, 3-methyladenine (3-MA), down-regulated LC3 II and Beclin 1. The latter was also down-regulated by calpeptin, a calpain inhibitor. Monodansyl cadaverine (MDC) staining detected numerous autophagic vacuoles (AVs) at 18 hr post-infection. Ultrastructural observations showed T. gondii proliferation in parasitophorous vacuoles (PVs) coinciding with a decline in the numbers of AVs by 18 hr. FACS analysis failed to confirm the presence of cell apoptosis after exposure to T. gondii and rapamycin. We concluded that T. gondii proliferation may inhibit host cell autophagy and has an impact on cell survival.

장뇌산삼이 Benzopyrene으로 유도된 간조직의 $TNF-{\alpha}$와 COX-2의 면역조직학적 분포에 미치는 영향 (Immunohistochemical Study of Wild Ginseng on Benzopyrene Induced $TNF-{\alpha}$ and COX-2 Expression in Rats)

  • 안상현;조성준;윤창환;조민경;김진택;신흥묵
    • 동의생리병리학회지
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    • 제19권6호
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    • pp.1568-1572
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    • 2005
  • Polycyclic aromatic hydrocarbon (PAH), such as benzo(a)pyrene (B(a)P), are toxic environmental contaminants known to enhance oxidative stress, production of pro-inflammatory and inflammatory cytokines. The present study was designed in order to determine whether wild ginseng (Panax ginseng C. A. Meyer) protect PAH-induced oxidative stress and inflammation. B(a)P (0.5 mg/kg, i.p.) treatment increased the distribution of immunoreactive cells for tumor necrosis factor $(TNF)-\alpha$ and cyclooxygenase (COX)-2 in peri-portal triad region and immunoreaction was shown in the cytoplasm of macrophage. Pre-treatment with wild ginseng significantly decreased immune responses in the rats treated with B(a)p. The rats given 50 mg/kg/day for 4 weeks before B(a)P treatment had 1.39-fold and 1.5-fold inhibition of $TNF-\alpha$ and COX-2 positive reaction, respectively. Wild ginseng extract alone had no effect on the distributional changes. The SOD activity as scavenger enzymes after wild ginseng administration dose-dependantly increased compared with butylated hydroxytoluene, a general radical scavenger. These data likely indicate that wild ginseng extract may act as inflammatory regulator in conjunction with inhibition of oxidant dependent metabolic activation in environmental contaminants-induced hepatic inflammation.

좌금환(左金丸)의 혈관이완과 $K^+$ channel (Role of $K^+$ Channels in the Vasodilation of Jagumhuan)

  • 손창우;이헌재;유가량;신흥묵
    • 동의생리병리학회지
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    • 제19권3호
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    • pp.743-748
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    • 2005
  • This study was performed for the investigation of vasodilatory efficacy and its underlying mechanisms of Jagumhuan(JGH), a herbal remedy. JGH produced completely endothelium-dependent relaxation and relaxed phenylephrine(PE)-precontracted aorta in a concentration dependent manner. The magnitude of relaxation was greater in PE induced contraction than that of KCl, suggesting involvement of $K^+$ channel in the relaxant effect. Both glibenclamide$(10^{-5}M)$, a $K_{ATP}$ channel inhibitor and indometacin, a cyclooxygenase inhibitor, completely prevented this relaxation. The relaxation effects of JGH, involve in part the release of nitric oxide from the endothelium as pretreatment with L-NAME, an NOS inhibitor, and methylene blue, a cGMP inhibitor, attenuated the responses by 62% and 58%, respectively. In addition, nitrite was produced by JGH in human aortic smooth muscle cells and human umbilical vein endothelial cells. The relaxant effect of JGH was also inhibited by 55.41% by tetraethylammonium(TEA; 5mM), a $K_{Ca}$ channel inhibitor. In the absence of extracellular $Ca^{2+}$, pre-incubation of the aortic rings with JGH significantly reduced the contraction by PE, suggesting that the relaxant action of the JGH includes inhibition of $Ca^{2+}$ release from intracellular stores. These results indicate that in rat thoracic aorta, JGH may induce vasodilation through ATP sensitive $K^+$ channel activation by prostacyclin production. However, the relaxant effect of JGH may also mediated in part by NO pathways and $Ca^{2+}$ activated $K^+$ channel.

석탄점화온도의 직접적인 측정에 의한 촤산화 반응율 도출에 대한 연구 (A Study on Char Oxidation Kinetics by Direct Measurement of Coal Ignition Temperature)

  • 권종서;김량균;송주헌;장영준;전충환
    • 에너지공학
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    • 제20권4호
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    • pp.346-352
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    • 2011
  • 본 연구의 목적은 한국화력발전소에서 사용되는 석탄의 촤 산화반응율을 연구하는 것이다. 석탄촤 산화반응율은 입자의 점화온도에 근거한 Semenov의 열착화이론을 활용하여 도출하였다. 석탄촤의 입자를 열전대를 통해 직접 가열 및 온도 측정을 할 수 있으며, 광각기 센서를 통해 석탄촤점화시 발생되는 빛의 강도를 계측함으로써 점화시점을 결정 할 수 있는 실험장치를 제안 하였다. 아역청탄인 Wira와 역청탄인 Yakutugol의 석탄촤 점화온도는 입자 직경의 변화에 따라 측정을했으며, 입자의 직경이 커질수록 석탄촤 점화온도는 상승하였다. 입자 직경에 따른 석탄촤 점화온도의 결과를 통해 활성화에너지 및 빈도인자를 도출하였다. 본 연구를 통해 도출한 석탄촤 산화반응율 값을 기존의 연구 데이터와 비교한 결과 유사함도 확인할 수 있었다.

The effect of melatonin on prevention of bisphosphonate-related osteonecrosis of the jaw: an animal study in rats

  • Yadegari, Afshin;Aminzadeh, Atousa;Seyyedkhamesi, Sam;Aminian, Maedeh
    • Journal of the Korean Association of Oral and Maxillofacial Surgeons
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    • 제46권4호
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    • pp.266-274
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    • 2020
  • Objectives: Melatonin induces human stem cells, converts pre-osteoblasts to mature osteoblasts, and reduces the duration of this transition. However, melatonin itself prevents activation of osteoclasts. Here, we evaluate the role of melatonin in prevention of bisphosphonate-related osteonecrosis of the jaw. Materials and Methods: In this experimental-interventional study, 30 rats were evaluated in 3 groups. The first and second groups received saline and zoledronic acid, respectively, for 4 weeks and the third group received 4 weeks of zoledronic acid and 3 weeks of melatonin simultaneously. First-right-maxillary-molar extraction was performed for all animals, which were sacrificed after 4 weeks of recovery. The extraction sockets were examined histologically for the presence of osteonecrosis, number of osteoclasts and fibroblasts, severity of inflammation, and vascularization. Data were analyzed by chi-square, one-way ANOVA, Tukey, Kruskal-Wallis and Fisher's exact statistical tests (α=0.05). Results: Osteonecrosis was observed in 20%, 90%, and 70% of the first, second and third groups, respectively (P=0.008). The lowest number of osteoclasts and fibroblasts was seen in the third group. Conclusion: Melatonin may effectively prevent some undesirable side effects of bisphosphonates. However, further studies are required to confirm the results of this study.

Preparation and characterization of microporous NaOH-activated carbons from hydrofluoric acid leached rice husk and its application for lead(II) adsorption

  • Hassan, A.F.;Youssef, A.M.
    • Carbon letters
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    • 제15권1호
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    • pp.57-66
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    • 2014
  • Three activated carbons (ACs) were prepared using NaOH (N) as an activating agent. Hydrofluoric acid pre-leached rice husk was used as a precursor. After leaching, the precursor was washed with distilled water, dried, crushed, and then sieved; a size fraction of 0.3-0.5 mm was selected for carbonization in the absence of air at $600^{\circ}C$. The carbonization product (LC) was mixed with NaOH at ratios of 1:2, 1:3, and 1:4 (wt of LC: wt of NaOH) and the produced ACs after activation at $800^{\circ}C$ were designated NLC21, NLC31, and NLC41, respectively. Surface and textural properties were determined using nitrogen adsorption at $-196^{\circ}C$, scanning electron microscopy images, thermogravimetric analysis, and Fourier transform infrared spectra. These ACs were used as adsorbents for lead(II) from aqueous solutions. The effects of the textural properties and the chemistry of the carbon surfaces were investigated and the impact of the operation conditions on the capacity for lead(II) sorption was also considered. Modification of NLC41 with $H_2O_2$ and $HNO_3$ gave two other adsorbents, $H_{NLC41}$ and $N_{NLC41}$ respectively. These two new samples exhibited the highest removal capacities for lead(II), i.e.117.5 and 128.2 mg/g, respectively. The adsorption data fitted the Langmuir isotherm and the kinetic adsorption followed pseudo-second order kinetics. The thermodynamic parameters have been determined and they indicated a spontaneous endothermic process.

Ursodeoxycholic Acid Inhibits Pro-Inflammatory Repertoires, $IL-1{\beta}$ and Nitric Oxide in Rat Microglia

  • Joo, Seong-Soo;Kang, Hee-Chul;Won, Tae-Joon;Lee, Do-ik
    • Archives of Pharmacal Research
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    • 제26권12호
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    • pp.1067-1073
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    • 2003
  • Ursodeoxycholic acid (UDCA) is a non-toxic, hydrophilic bile acid in widespread clinical use mainly for acute and chronic liver disease. Recently, treatment with UDCA in hepatic graft-versus-host disease has been given in immunosuppressive therapy for improvement of the biochemical markers of cholestasis. Moreover, it has been reported that UDCA possesses immunomodulatory effects by the suppression of cytokine production. In the present study, we hypothesized that UDCA may inhibit the production of the pro-inflammatory cytokine, IL-1$\beta$, and nitric oxide (NO) in microglia. In the study, we found that 100 $\mu$ g/mL UDCA effectively inhibited these two pro-inflammatory factors at 24 hand 48 h, compared to the $A\beta$42-pretreated groups. These results were compared with the LPS+UDCA group to confirm the UDCA effect. As microglia can be activated by several stimulants, such as $A\beta$42, in Alzheimers brain and can release those inflammatory factors, the ability to inhibit or at least decrease the production of IL-1$\beta$ and NO in Alzheimers disease (AD) is essential. Using RT-PCR, ELISA and the Griess Reagent System, we therefore found that UDCA in $A\beta$42 pre-treated cultures played a significant role in suppressing the expression or the production of IL-1$\beta$ and NO. Similarly, lipopolysaccharide (LPS) did not activate microglia in the presence of UDCA. Moreover, we found that UDCA exhibits a prolonged effect on microglial cells (up to 48 h), which suggests that UDCA may play an important role in chronic cell damage due to this long effect. These results further imply that UDCA could be an important cue in suppressing the microglial activation stimulated by massive AD peptides in the AD progressing brain.