• Pediatric Infection and Vaccine
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• 제26권2호
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• pp.112-117
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• 2019

Eikenella corrodens는 구강 상재균으로 두경부 감염을 주로 일으키나 면역력이 정상인 소아청소년에게 감염을 일으키는 경우는 흔하지 않다. 저자들은 발열, 두통, 구토를 증상으로 입원한 이전까지 건강하였던 13세 남자에게서 E. corrodens 감염에 의한 중추신경계 경막 외 농양을 진단하여 보고하는 바이다. 초기에 시행한 신체검진에서 경부 강직은 없었으나, 우측 이루가 관찰되었다. 뇌 magnetic resonance imaging (MRI) 영상소견에서 4.5 cm 크기의 경막 외 농양이 우측 측두엽 부근에서 발견되었고, 양측 사골동염 및 접형동염, 우측 유양돌기염과 중이염이 동반되었다. Vancomycin과 cefotaxime 투약 중에도, 임상증상이 호전되지 않고 추적 MRI에서 경막 외 농양의 크기가 증가하고, 우측 접형동에 농양이 형성되어 항균요법과 함께 천두술과 내시경적 접형동 절개술을 시행하였다. 수술 시 경막 외 농양과 접형동에서 악취가 나는 고름이 다량 흡인되었으며 두 부위에서 흡인된 검체 모두에서 E. corrodens가 배양되었다. 수술 이후 3주 동안 cefotaxime 정맥주사로 치료받고 합병증 없이 회복하였다. 결론적으로, E. corrodens는 건강한 소아청소년에서 치료되지 않은 세균성 부비동염에 합병하여 중추신경계 농양의 원인이 될 수 있다.

• Nutrition Research and Practice
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• 제13권4호
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• pp.302-309
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• 2019

BACKGOURND/OBJECTIVES: Vascular inflammation is an important feature in the atherosclerotic process. Recent studies report that leaves and branches of Carpinus turczaninowii (C. turczaninowii) have antioxidant capacity and exert anti-inflammatory effects. However, no study has reported the regulatory effect of C. turczaninowii extract on the arterial inflammatory response. This study therefore investigated modulation of the arterial inflammatory response after exposure to C. turczaninowii extract, using human aortic vascular smooth muscle cells (HAoSMCs). MATERIALS/METHODS: Scavenging activity of free radicals, total phenolic content (TPC), cell viability, mRNA expressions, and secreted levels of cytokines were measured in LPS-stimulated (10 ng/mL) HAoSMCs treated with the C. turczaninowii extract. RESULTS: C. turczaninowii extract contains high amounts of TPC ($225.6{\pm}21.0mg$ of gallic acid equivalents/g of the extract), as well as exerts time-and dose-dependent increases in strongly scavenged free radicals (average $14.8{\pm}1.97{\mu}g/mL$ $IC_{50}$ at 40 min). Cell viabilities after exposure to the extracts (1 and $10{\mu}g/mL$) were similar to the viability of non-treated cells. Cytokine mRNA expressions were significantly suppressed by the extracts (1 and $10{\mu}g/mL$) at 6 hours (h) after exposure. Interleukin-6 secretion was dose-dependently suppressed 2 h after incubation with the extract, at $1-10{\mu}g/mL$ in non-stimulated cells, and at 5 and $10{\mu}g/mL$ in LPS-stimulated cells. Similar patterns were also observed at 24 h after incubation with the extract (at $1-10{\mu}g/mL$ in non-stimulated cells, and at $10{\mu}g/mL$ in the LPS-stimulated cells). Soluble intracellular vascular adhesion molecules (sICAM-1) secreted from non-stimulated cells and LPS-stimulated cells were similarly suppressed in a dose-dependent manner after 24 h exposure to the extracts, but not after 2 h. In addition, sICAM-1 concentration after 24 h treatment was positively related to IL-6 levels after 2 h and 24 h exposure (r = 0.418, P = 0.003, and r = 0.524, P < 0.001, respectively). CONCLUSIONS: This study demonstrates that C. turczaninowii modulates the arterial inflammatory response, and indicates the potential to be applied as a therapeutic use for atherosclerosis.

• 대한두개안면성형외과학회지
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• 제20권2호
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• pp.101-108
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• 2019

Background: To date, a variety of surgical approaches have been used to reconstruct the medial orbital wall fracture. Still however, there is still a controversy as to their applicability because of postoperative scars, injury of anatomical structures and limited visual fields. The purpose of this study was to introduce a useful additional medial subbrow approach for better reduction and securement more accurate implant pocket of medial orbital wall fracture with the subciliary technique. Methods: We had performed our technique for a total of 14 patients with medial orbital wall fracture at our medical institution between January 2016 and July 2017. All fractures were operated through subciliary technique combined with the additional medial subbrow approach. They underwent subciliary approach accompanied by medial wall dissection using a Louisville elevator through the slit incision of the medial subbrow procedure. This facilitated visualization of the medial wall fracture site and helped to ensure a more accurate pocket for implant insertion. Results: Postoperative outcomes showed sufficient coverage without displacement. Twelve cases of preoperative diplopia improved to two cases of postoperative diplopia. More than 2 mm enophthalmos was 14 cases preoperatively, improving to 0 case postoperatively. Without damage such as major vessels or extraocular muscles, enophthalmos was corrected and there was no restriction of eyeball motion. Conclusion: Our ancillary procedure was useful in dissecting the medial wall, and it was a safe method as to cause no significant complications in our clinical series. Also, there is an only nonvisible postoperative scar. Therefore, it is a recommendable surgical modality for medial orbital wall fracture.

• Journal of Ginseng Research
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• 제43권2호
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• pp.272-281
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• 2019

Background: Diabetic sensorineural damage is a complication of the sensory neural system, resulting from long-term hyperglycemia. Red ginseng (RG) has shown efficacy for treatment of various diseases, including diabetes mellitus; however, there is little research about its benefit for treating sensorineural damage. Therefore, we aim to evaluate RG efficacy in alloxan-induced diabetic neuromast (AIDN) zebrafish. Methods: In this study, we developed and validated an AIDN zebrafish model. To assess RG effectiveness, we observed morphological changes in live neuromast zebrafish. Also, zebrafish has been observed to have an ultrastructure of hair-cell cilia under scanning electron microscopy. Thus, we recorded these physiological traits to assess hair cell function. Finally, we confirmed that RG promoted neuromast recovery via nerve growth factor signaling pathway markers. Results: First, we established an AIDN zebrafish model. Using this model, we showed via live neuromast imaging that RG fostered recovery of sensorineural damage. Damaged hair cell cilia were recovered in AIDN zebrafish. Furthermore, RG rescued damaged hair cell function through cell membrane ion balance. Conclusion: Our data suggest that RG potentially facilitates recovery in AIDN zebrafish, and its mechanism seems to be promotion of the nerve growth factor pathway through increased expression of topomyosin receptor kinase A, transient receptor potential channel vanilloid subfamily type 1, and mitogen-activated protein kinase phosphorylation.

• 대한간학회지
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• 제24권4호
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• pp.374-383
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• 2018

Background/Aims: There have been numerous efforts to reduce mother-to-child transmission (MTCT) of hepatitis B virus (HBV) with antiviral agents during pregnancy. However, there are limited data regarding the outcomes of pregnant women after delivery. This study was performed to evaluate the efficacy of antiviral agents in preventing MTCT of HBV and maternal long-term outcomes. Methods: The HBV-infected pregnant women treated with antiviral agents to prevent MTCT were retrospectively reviewed. Forty-one pregnant women who received telbivudine or tenofovir during late pregnancy (28-34 week) were analyzed. Hepatitis B virus surface antibody (HBsAb) positivity was tested in 43 infants after 7 months of birth. Eleven mothers were followed >1 year after delivery. Results: The mean HBV DNA titer before antiviral therapy was 8.67 (6.60-9.49) log copies/mL, and the median age at delivery was 32 years (range, 22-40). Eleven patients were treated with tenofovir and 30 with telbivudine. The median duration was 57 days (range, 23-100), and the median HBV DNA titer at birth was 5.06 log copies/mL (range, 2.06-6.50). Antiviral treatments were associated with significant HBV DNA reduction (P<0.001). Among 43 infants (two cases of twins), HBsAb was not detected in two, subsequently confirmed to have HBV infection. Biochemical flare was observed in two of 11 mothers followed >12 months, and an antiviral agent was administered. Conclusions: Antiviral treatment during late pregnancy effectively reduced MTCT. Long-term follow-up should be required in such cases. In addition, given that maternal biochemical flare occurred in 18% of mothers, re-administration of antiviral agents might be required.

• 생명과학회지
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• 제30권12호
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• pp.1118-1127
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• 2020

알츠하이머병은 점진적인 신경세포의 손상과 이로 인해 인지기능 장애를 유발하는 질병이다. 이 질환은 현재로서는 치료할 수 있는 질환이 아니고 진행을 멈추게 할 수 있는 방법이 없다. 그러나 초기에 알츠하이머병을 치료하는 것이 가장 효과적이므로 초기 진단은 증상을 관리할 수 있는 가장 좋은 기회를 제공할 수 있다. 알츠하이머병을 진단하기 위한 바이오마커로는 아밀로이드 베타(Aβ), 병적인 타우, 그리고 신경퇴화가 있고, Aβ의 축적, 인산화 타우는 뇌척수액이나 양전자 방출 단층촬영술을 통해 분석할 수 있다. 그러나 뇌척수액의 채취는 매우 침습적이고 양전자 방출 단층촬영술은 전문적인 고가의 장비가 필요하다. 지난 수십년 동안 빠르고 최소한의 침습성을 가진 바이오마커 분석법을 개발하기 위하여 혈액에 기반한 바이오마커 분석 기술이 연구되어 왔다. 그 중 주목할 만 한 발견이 혈장에서 Aβ의 주요 원천으로 혈소판과의 관련성이다. 아밀로이드 베타는 혈액-뇌 장벽을 통과 할 수 있고 정상 상태에서는 뇌와 혈액 간 평형을 이루게 된다. 흥미롭게도, 여러 임상시험 결과 혈장에서 Aβ42/Aβ40 비율이 가벼운 인지장애 질환과 알츠하이머병에서 감소되어 있는 것을 증명하였다. 종합하면, 이러한 최근의 발견들은 침습성을 최소화한 알츠하이머병의 초기 진단 기술을 개발하는 데 이용될 수 있다. 본 총설에서, 저자들은 알츠하이머병의 바이오마커에 대한 최근 연구결과들, 특히 말초에서 Aβ를 생산하는 혈소판의 역할과 혈액 기반 바이오마커로서의 개발 가능성에 대해 고찰하였다.

• Molecules and Cells
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• 제44권1호
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• pp.38-49
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• 2021

Airway mucus secretion is an essential innate immune response for host protection. However, overproduction and hypersecretion of mucus, mainly composed of the gel-forming MUC5AC protein, are significant risk factors for patients with asthma and chronic obstructive pulmonary disease (COPD). The transforming growth factor β (TGFβ) signaling pathway negatively regulates MUC5AC expression; however, the underlying molecular mechanism is not fully understood. Here, we showed that TGFβ significantly reduces the expression of MUC5AC mRNA and its protein in NCI-H292 cells, a human mucoepidermoid carcinoma cell line. This reduced MUC5AC expression was restored by a TGFβ receptor inhibitor (SB431542), but not by the inhibition of NF-κB (BAY11-7082 or Triptolide) or PI3K (LY294002) activities. TGFβ-activated Smad3 dose-dependently bound to MUC5AC promoter. Notably, TGFβ-activated Smad3 recruited HDAC2 and facilitated nuclear translocation of HDAC2, thereby inducing the deacetylation of NF-κB at K310, which is essential for a reduction in NF-κB transcriptional activity. Both TGFβ-induced nuclear translocation of Smad3/HDAC2 and deacetylation of NF-κB at K310 were suppressed by a Smad3 inhibitor (SIS3). These results suggest that the TGFβ-activated Smad3/HDAC2 complex is an essential negative regulator for MUC5AC expression and an epigenetic regulator for NF-κB acetylation. Therefore, these results collectively suggest that modulation of the TGFβ1/Smad3/HDAC2/NF-κB pathway axis can be a promising way to improve lung function as a treatment strategy for asthma and COPD.

• Journal of Ginseng Research
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• 제45권2호
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• pp.295-304
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• 2021

Background: Acute promyelocytic leukemia (APL) is a hematopoietic malignancy driven by promyelocytic leukemia-retinoic acid receptor A (PML-RARA) fusion gene. The therapeutic drugs currently used to treat APL have adverse effects. 20(S)-ginsenoside Rh2 (GRh2) is an anticancer medicine with high effectiveness and low toxicity. However, the underlying anticancer mechanisms of GRh2-induced PML-RARA degradation and apoptosis in human APL cell line (NB4 cells) remain unclear. Methods: Apoptosis-related indicators and PML-RARA expression were determined to investigate the effect of GRh2 on NB4 cells. Z-VAD-FMK, LY294002, and C 87, as inhibitors of caspase, and the phosphatidylinositol 3-kinase (PI3K) and tumor necrosis factor-α (TNF-α) pathways were used to clarify the relationship between GRh2-induced apoptosis and PML-RARA degradation. Results: GRh2 dose- and time-dependently decreased NB4 cell viability. GRh2-induced apoptosis, cell cycle arrest, and caspase3, caspase8, and caspase9 activation in NB4 cells after a 12-hour treatment. GRh2-induced apoptosis in NB4 cells was accompanied by massive production of reactive oxygen species, mitochondrial damage and upregulated Bax/Bcl-2 expression. GRh2 also induced PML/PML-RARA degradation, PML nuclear bodies formation, and activation of the downstream p53 pathway in NB4 cells. Z-VAD-FMK inhibited caspase activation and significantly reversed GRh2-induced apoptosis and PML-RARA degradation. GRh2 also upregulated TNF-α expression and inhibited Akt phosphorylation. LY294002, an inhibitor of the PI3K pathway, enhanced the antitumor effects of GRh2, and C 87, an inhibitor of the TNF-α pathway, reversed NB4 cell viability, and GRh2-mediated apoptosis in a caspase-8-dependent manner. Conclusion: GRh2 induced caspase-dependent PML-RARA degradation and apoptosis in NB4 cells via the Akt/Bax/caspase9 and TNF-α/caspase8 pathways.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• 제24권4호
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• pp.357-365
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• 2021

Purpose: A change in diagnosis from ulcerative colitis (UC) to Crohn's disease (CD) has been reported in pediatric inflammatory bowel disease; however, only a few clinical characteristics and predictors of this diagnostic change have been reported. We aimed to describe the clinical characteristics of patients with UC who underwent a change in diagnosis to CD and identify variables associated with the change. Methods: The medical records of pediatric patients with UC who were followed up at the National Center for Child Health and Development between 2006 and 2019 were retrospectively reviewed. Clinical data on disease phenotype, laboratory parameters, endoscopic findings, and treatment of patients whose diagnosis changed to CD (cCD) were compared to those of patients whose diagnosis remained UC (rUC). Results: Among the 111 patients initially diagnosed with UC, 11 (9.9%) patients were subsequently diagnosed with CD during follow-up. There was no significant difference between the cCD and rUC groups in terms of sex, age at initial diagnosis, and the extent and severity of disease at initial diagnosis. Albumin and hemoglobin levels were significantly lower in the cCD group than in the rUC group. The proportion of patients who required biologics was significantly higher in the cCD group than in the rUC group (p<0.05). Conclusion: Approximately 10% children initially diagnosed with UC were subsequently diagnosed with CD. Hypoalbuminemia and anemia at initial diagnosis and use of biologics could be predictors of this diagnostic change.

• Journal of Microbiology and Biotechnology
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• 제31권11호
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• pp.1501-1507
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• 2021

Lagerstroemia ovalifolia Teijsm. & Binn. (LO) (crape myrtle) has reportedly been used as traditional herbal medicine (THM) in Java, Indonesia. Our previous study revealed that the LO leaf extract (LOLE) exerted anti-inflammatory effects on lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages. Based on this finding, the current study aimed to evaluate the protective effects of LOLE in a mouse model of LPS-induced acute lung injury (ALI). The results showed that treatment with LPS enhanced the inflammatory cell influx into the lungs and increased the number of macrophages and the secretion of the inflammatory cytokines in the bronchoalveolar lavage fluid (BALF) of mice. However, these effects were notably abrogated with LOLE pretreatment. Furthermore, the increase of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2) and monocyte chemoattractant protein-1 (MCP-1) expression in the lung tissues of mice with ALI was also reversed by LOLE. In addition, LOLE significantly suppressed the LPS-induced activation of the MAPK/NF-κB signaling pathway and led to heme oxygenase-1 (HO-1) induction in the lungs. Additionally, in vitro experiments showed that LOLE enhanced the expression of HO-1 in RAW264.7 macrophages. The aforementioned findings collectively indicate that LOLE exerts an ameliorative effect on inflammatory response in the airway of ALI mice.