Naringenin inhibited migration and invasion of glioblastoma cells through multiple mechanisms

Glioblastoma (GBM) is the most mortality brain cancer in the world. Due to high invasion and drug resistance cause the poor prognosis of GBM. Naringenin, an ingredient of citrus, exhibits many cellular functions such as antioxidant, anti‐inflammation, and anticancer. Naringenin inhibits the migration of bladder and lung cancer via modulation of MMP‐2 and/or MMP‐9 activities, Naringenin inhibits migration and trigger apoptosis in gastric cancer cells through downregulation of AKT pathway. However, the effects of naringenin in GBM still remain to be elucidated. In this study, we reveal the molecular mechanisms of naringenin in the inhibition of migration and invasion in GBM. No overt alternation of cell proliferation was found in of GBM 8901 cells treated with different concentration of naringenin. Slight decreased cell viability was found in GBM 8401 cell treated with 200 and 300 μM naringenin. Significant reduction of migration and invasion as assayed by Boyden chamber analysis was found in of GBM cells treated with 100, 200, and 300 μM naringenin. Zymography analysis also revealed that the activities of MMP‐2 and MMP‐9 of GBM cells were significantly inhibited in response to 100, 200, or 300 μM naringenin treatment. Proteins of MMP‐2 and MMP‐9 were downregulated in naringenin treated GBM cells. In addition, naringenin also attenuated the activities of ERK and p38. Naringenin decreased mesenchymal markers (snail and slug) expression as revealed by Western blot analysis. Taken together, our findings indicated that naringenin eliminated the migration and invasion of GBM cells through multiple mechanisms including inhibition of MMPs, ERK, and p38 activities and modulation of EMT markers. Our results also suggested that naringenin may be a potential agent to prevent metastasis of GBM.     

Aortic squamous metaplasia in a patient with aortoesophageal fistula secondary to thoracic aortic aneurysm: An autopsy case

Aortoesophageal fistula (AEF) is highly lethal. A 74‐year‐old man presented with hematemesis and consciousness loss. He had a long‐term history of hypertension and gout. Computed tomography revealed an aneurysm of the distal descending thoracic aorta, which was treated by insertion of an aortic stent graft. After 24 days of stenting, endoscopic examination revealed an AEF. After 6 months of stenting, he died owing to mediastinitis. On autopsy, macroscopically, we found a 4 × 2.5‐cm, oval, well‐circumscribed AEF. We identified squamous epithelium in the area surrounding the AEF that covered the thoracic aorta inner cavity. Immunohistochemical analysis revealed that the squamous epithelium in the thoracic aorta was positive for p63 and 34βE12. In conclusion, we encountered a long‐term AEF case with aortic squamous metaplasia. To the best of our knowledge, human aortic metaplasia has never been reported. In the present case, aortic squamous metaplasia retained continuity with the esophageal squamous epithelium; therefore, the migration of the squamous epithelium through the AEF may have been induced by aortic erosion.     

17β-Estradiol Inhibits Mesenchymal Stem Cells-Induced Human AGS Gastric Cancer Cell Mobility via Suppression of CCL5- Src/Cas/Paxillin Signaling Pathway

Gender differences in terms of mortality among many solid organ malignancies have been proved by epidemiological data. Estrogen has been suspected to cast a protective effect against cancer because of the lower mortality of gastric cancer in females and the benefits of hormone replacement therapy (HRT) in gastric cancer. Hence, it suggests that 17β-estradiol (E2) may affect the behavior of cancer cells. One of the key features of cancer-related mortality is metastasis. Accumulating evidences suggest that human bone marrow mesenchymal stem cells (HBMMSCs) and its secreted CCL-5 have a role in enhancing the metastatic potential of breast cancer cells. However, it is not clear whether E2 would affect HBMMSCs-induced mobility in gastric cancer cells. In this report, we show that CCL-5 secreted by HBMMSCs enhanced mobility in human AGS gastric cancer cells via activation of Src/Cas/Paxillin signaling pathway. Treatment with specific neutralizing antibody of CCL-5 significantly inhibited HBMMSCs-enhanced mobility in human AGS gastric cancer cells. We further observe that 17β-estradiol suppressed HBMMSCs-enhanced mobility by down-regulating CCL5-Src/Cas/paxillin signaling pathway in AGS cells. Collectively, these results suggest that 17β-estradiol treatment significantly inhibits HBMMSCS-induced mobility in human AGS gastric cancer cells.     

Repeated bonding of fixed retainer increases the risk of enamel fracture

The aim of this study was to investigate the influences of repeated bonding, using 2 different orthodontic adhesive systems, on the shear bond strength (SBS) and the enamel surface morphology. Sixty premolars were divided into 2 groups (n = 30), and either Transbond XT (T group) or Fuji Ortho LC (F group) adhesives were used. SBS was measured 24 h after bonding, using a universal testing machine. Then, the enamel surfaces were investigated and the mode of failure was described using adhesive remnant index (ARI) scores. After each debonding, 10 teeth from each group were examined by scanning electron microscopy to determine the penetration of adhesives, the length of resin tags, and the state of the enamel surface. The other teeth were subjected to two more bonding/debonding procedures. In T group, the second debonding sequences had significantly higher bond strengths than the other sequences. The length of resin tags was greatest in the second debonding sequence, although there was no significant difference. In F group, the SBS increased with further rebonding and the failure mode tended towards cohesive failure. In both groups, the ARI scores increased with rebonding. Enamel loss could have occurred with both adhesives, although the surfaces appeared unchanged to the naked eye. From this study, we suggest that enamel damage caused by repeated bonding is of concern. To prevent bond failure, we should pay attention to the adhesion method used for bondable retainers.     

Comparison of mesiodistal tooth crown diameters and arch dimensions between modern Mongolians and Japanese

The purposes of this study were to establish normative data for mesiodistal tooth crown diameters and arch dimensions in Mongolian adults and to compare them with those of Japanese adults. The study materials comprised dental casts of 100 modern Mongolian and 100 Japanese subjects (50 males, 50 females for each) with Angle Class I normal occlusion. The mean ages were 20 years 8 months for the Mongolian subjects and 20 years 0 months for the Japanese subjects. On the dental casts, the mesiodistal tooth crown diameters (excluding wisdom teeth) and dental arch dimensions were measured. The following arch dimensions were measured: inter-canine lingual, inter-premolar lingual, inter-molar lingual, inter-molar central, coronal arch length, basal arch length, and basal arch width. In the Mongolian samples, significant sex differences were noted, and most of the items were significantly larger in males than in females. Significant differences between the Mongolian and Japanese samples were mainly noted in the premolar and molar regions, rather than in the anterior region, and were significantly smaller in the Mongolian samples. In the Mongolian samples, the molar section widths and basal arch width and length were significantly larger in males and females compared with the Japanese samples. These results suggest that the tooth crown size and arch dimensions in the Mongolian samples differed from those in the Japanese samples, and that establishment of the clinical norm for Mongolian adults might be helpful in formulating treatment plans for Mongolian patients, given that these parameters are the basic tools for diagnosis.     

Improving self‐care efficacy and quality of life with a self‐management program among patients with chronic obstructive pulmonary disease: A quasi‐experimental study

Self‐management helps patients understand their illnesses and learn about disease‐related skills so they can better manage their situation. However, published studies on the effectiveness of self‐management for chronic obstructive pulmonary disease (COPD) are heterogeneous. Quasi‐experimental design was used to investigate the effectiveness of a self‐management program in self‐care efficacy and quality of life in patients with COPD. Sixty participants who had experienced COPD were assigned to control group (usual care) or experimental group (self‐care program) (1:1 ratio) according to a purposeful sampling at a Medical Center in Taiwan. The Medical Research Council dyspnea scale, the COPD Self‐Efficacy Scale, the Clinical COPD Questionnaire were used to analyze data. The Medical Research Council dyspnea scale was more significant improvement in the 2 months after discharge in the experimental group than in the control group. The COPD Self‐Efficacy Scale and Clinical COPD Questionnaire scores in the experimental group within 3 months after discharge were significantly improved compared with the control group. These findings demonstrate the application and initial effect of this self‐management program.     

活性元素对生物活性陶瓷促成骨作用的影响研究

生物活性陶瓷已被广泛用于骨骼和牙齿的修复,文献回顾表明,一些离子能够诱导干细胞成骨分化,在骨再生医学中具有广阔的前景.鉴于这些离子从可生物降解的陶瓷材料中释放出来,与生长因子相比,更易实现控释.在生物陶瓷中添加生物活性离子,成为开发具有促血管生成和促成骨等功能的新方法.显然,生物陶瓷的生物反应取决于许多参数,例如化学成...     

Two forms of diffuse alveolar damage in the lungs of patients with acute respiratory distress syndrome

Acute respiratory distress syndrome is a severe disease, the treatment and pathophysiology of which are not completely established. The pathology of acute respiratory distress syndrome involves diffuse alveolar damage, which comprises severe alveolar epithelial cell damage, hyaline membrane formation, and festinate myofibroblast proliferation and fibrosis in the intra-alveolar spaces. We performed a clinicopathologic investigation of 26 autopsy cases of diffuse alveolar damage. Three cases of them were diagnosed as acute interstitial pneumonia that is idiopathic illness and resembles pathologically organizing diffuse alveolar damage. Immunohistochemical staining for types I and IV collagen, α-smooth muscle actin, and Ki-67 was carried out, and the sites of myofibroblast proliferation and type I collagen production were examined. All diffuse alveolar damage cases in the proliferative phase showed intra-alveolar myofibroblast proliferation. When diffuse alveolar damage was diagnosed pathologically as being due to severe infection, all 7 patients showed multiple organ dysfunction syndrome, whereas only 2 of 7 patients showed interstitial myofibroblast proliferation. When diffuse alveolar damage was attributed to tumor treatment with chemotherapy or to drug toxicity, 3 of 16 patients showed multiple organ dysfunction syndrome; 15 of 16 showed interstitial myofibroblast proliferation, 3 of 3 acute interstitial pneumonia patients did not show multiple organ dysfunction syndrome; and 3 of 3 acute interstitial pneumonia showed marked interstitial myofibroblast proliferation. These results suggest that the pathophysiologic mechanism of diffuse alveolar damage caused by severe infection is one of systemic circulation disturbance, although the mechanism underlying diffuse alveolar damage due to tumor with chemotherapy or drug toxicity appears to involve interstitial pneumonia-like lesions that are similar to acute interstitial pneumonia.     

妊娠高血压综合征及过期妊娠时胎膜超微结构的观察

报告正常足月产、妊娠高血压综合征及过期妊娠时胎膜在光镜和电镜下的结构及变化特点。观察发现,妊娠高血压综合征时胎膜为缺氧所致的可复性病变,而过期妊娠之胎膜则为不可复性自身老化。胎膜广泛纤维化表明在妊娠高血压综合征和过期妊娠时易发生早破膜。此外,尚讨论了胎膜屏障存在的可能机制及明、暗细胞这一现象。