Alteration of Oral and Perioral Soft Tissue in Mice following Incisor Tooth Extraction

Oral and perioral soft tissues cooperate with other oral and pharyngeal organs to facilitate mastication and swallowing. It is essential for these tissues to maintain their morphology for efficient function. Recently, it was reported that the morphology of oral and perioral soft tissue can be altered by aging or orthodontic treatment. However, it remains unclear whether tooth loss can alter these tissues’ morphology. This study examined whether tooth loss could alter lip morphology. First, an analysis of human anatomy suggested that tooth loss altered lip morphology. Next, a murine model of tooth loss was established by extracting an incisor; micro-computed tomography revealed that a new bone replaced the extraction socket. Body weight was significantly lower in the tooth loss (UH) group than in the non-extraction control (NH) group. The upper lip showed a greater degree of morphological variation in the UH group. Proteomic analysis and immunohistochemical staining of the upper lip illustrated that S100A8/9 expression was higher in the UH group, suggesting that tooth loss induced lip inflammation. Finally, soft-diet feeding improved lip deformity associated with tooth loss, but not inflammation. Therefore, soft-diet feeding is essential for preventing lip morphological changes after tooth loss.     

纳米二氧化钛溶胶的光催化活性及细胞毒性试验

利用低温合成法制备了分散有锐钛矿纳米颗粒的二氧化钛(TiO2)溶胶,该溶胶均一、透明。利用X射线衍射和透射电镜对该溶胶内纳米颗粒的结构和形貌进行研究。结果显示:颗粒呈梭形,分散性良好,其尺寸小于50nm,晶型为锐钛矿型。通过对TiO2溶胶光催化活性和老鼠内皮细胞毒性进行研究,发现该溶胶在日光照射下光催化活性较高,具有良好的生物相容性和安全性。     

Use of Active Salmon-Lecithin Nanoliposomes to Increase Polyunsaturated Fatty Acid Bioavailability in Cortical Neurons and Mice

Omega-3 polyunsaturated fatty acids (n-3 PUFAs) play an important role in the development, maintenance, and function of the brain. Dietary supplementation of n-3 PUFAs in neurological diseases has been a subject of particular interest in preventing cognitive deficits, and particularly in age-related neurodegeneration. Developing strategies for the efficient delivery of these lipids to the brain has presented a challenge in recent years. We recently reported the preparation of n-3 PUFA-rich nanoliposomes (NLs) from salmon lecithin, and demonstrated their neurotrophic effects in rat embryo cortical neurons. The objective of this study was to assess the ability of these NLs to deliver PUFAs in cellulo and in vivo (in mice). NLs were prepared using salmon lecithin rich in n-3 PUFAs (29.13%), and characterized with an average size of 107.90 ± 0.35 nm, a polydispersity index of 0.25 ± 0.01, and a negative particle-surface electrical charge (−50.4 ± 0.2 mV). Incubation of rat embryo cortical neurons with NLs led to a significant increase in docosahexaenoic acid (DHA) (51.5%, p < 0.01), as well as palmitic acid, and a small decrease in oleic acid after 72 h (12.2%, p < 0.05). Twenty mice on a standard diet received oral administration of NLs (12 mg/mouse/day; 5 days per week) for 8 weeks. Fatty acid profiles obtained via gas chromatography revealed significant increases in cortical levels of saturated, monounsaturated, and n-3 (docosahexaenoic acid,) and n-6 (docosapentaenoic acid and arachidonic acid) PUFAs. This was not the case for the hippocampus or in the liver. There were no effects on plasma lipid levels, and daily monitoring confirmed NL biocompatibility. These results demonstrate that NLs can be used for delivery of PUFAs to the brain. This study opens new research possibilities in the development of preventive as well as therapeutic strategies for age-related neurodegeneration.     

Verification of the Impact of Blood Glucose Level on Liver Carcinogenesis and the Efficacy of a Dietary Intervention in a Spontaneous Metabolic Syndrome Model

Metabolic syndrome (MS) is a risk factor for type 2 diabetes mellitus, vascular inflammation, atherosclerosis, and renal, liver, and heart diseases. Non-alcoholic steatohepatitis (NASH) is a progressive representative liver disease and may lead to the irreversible calamities of cirrhosis and hepatocellular carcinoma. Metabolic disorders such as hyperglycemia have been broadly reported to be related to hepatocarcinogenesis in NASH; however, direct evidence of a link between hyperglycemia and carcinogenesis is still lacking. Tsumura Suzuki Obese Diabetic (TSOD) mice spontaneously develop metabolic syndrome, including obesity, insulin resistance, and NASH-like liver phenotype, and eventually develop hepatocellular carcinomas. TSOD mice provide a spontaneous human MS-like model, even with significant individual variations. In this study, we monitored mice in terms of their changes in blood glucose levels, body weights, and pancreatic and liver lesions over time. As a result, liver carcinogenesis was delayed in non-hyperglycemic TSOD mice compared to hyperglycemic mice. Moreover, at the termination point of 40 weeks, liver tumors appeared in 18 of 24 (75%) hyperglycemic TSOD mice; in contrast, they only appeared in 5 of 24 (20.8%) non-hyperglycemic mice. Next, we investigated three kinds of oligosaccharide that could lower blood glucose levels in hyperglycemic TSOD mice. We monitored the levels of blood and urinary glucose and assessed pancreatic lesions among the experimental groups. As expected, significantly lower levels of blood and urinary glucose and smaller deletions of Langerhans cells were found in TSOD mice fed with milk-derived oligosaccharides (galactooligosaccharides and lactosucrose). At the age of 24 weeks, mild steatohepatitis was found in the liver but there was no evidence of liver carcinogenesis. Steatosis in the liver was alleviated in the milk-derived oligosaccharide-administered group. Taken together, suppressing the increase in blood glucose level from a young age prevented susceptible individuals from diabetes and the onset of NAFLD/NASH, as well as carcinogenesis. Milk-derived oligosaccharides showed a lowering effect on blood glucose levels, which may be expected to prevent liver carcinogenesis.     

Hydroxypropylated Tapioca Starch Retards the Development of Insulin Resistance in KKAy Mice, a Type 2 Diabetes Model, Fed a High-Fat Diet

ABSTRACT:  The hypoglycemic and antidiabetic effect of hydroxypropyl tapioca starch (HPTS, degree of substitution = 0.180) was investigated in male KKAy mice. Mice were fed a purified high-fat (20%) diet without or with HPTS (5% or 10%) for 33 d. Gelatinized tapioca starch (TS) was used as a reference. Fasting blood glucose concentrations, days 14 and 28, were significantly lower in the 10% HPTS group compared with the reference. In an oral glucose tolerance test (OGTT), day 28, blood glucose concentrations in the 5% HPTS group, at 60, 90, and 120 min, and in the 10% HPTS group, at 30, 60, and 90 min after oral administration of glucose, were significantly lower compared with the reference. The area under the glucose curve (AUC) for glucose in both HPTS groups was significantly lower compared with the reference. Energy intake was significantly lower in the 10% HPTS group compared with the reference. At the end of the experiment, adiponectin concentrations were significantly higher in the 10% HPTS group compared with the reference. A homeostasis model assessment of insulin resistance (HOMA-IR) tended to be lower in the 10% HPTS group compared with the reference, whereas a quantitative insulin sensitivity check index (QUICKI) was significantly higher in both HPTS groups compared with the reference. These results show that HPTS retards the development of insulin resistance in KKAy mice fed a high-fat diet.     

构建IgG介导的河虾过敏模型的研究

选取7周龄大的BALB／c和昆明鼠。以腹腔注射河虾粗体液及Al（OH）佐剂的方式进行免疫,每周一次,共四次,第五周进行免疫激发。对照组则以相同方式注射生理盐水及Al（OH）3佐剂。免疫激发后,组胺和IgG1的含最显著提高,小鼠的主要过敏原被测定被证明与人类主要过敏原相似。所以本实验建立了一个新的IgG介导的河虾过敏反应的动物模型。该模型可以为研究IgG介导的系统性过敏的机制,治疗手段,以及检测转基因食品的安全性提供有力的工具。     

关于用鼠标笔代替传统鼠标的人体工程学分析

传统鼠标在使用中因为频繁使用食指,手腕支撑面积又较小,很容易会引起鼠标手等问题,长时间使用必然会对使用者造成伤害。鼠标笔因更符合人体工程学设计,使用时手臂有更大的支撑平台,肌肉没有紧张感,受力较小且手指受力均匀,具有笔形的所有优点。对比分析了传统鼠标和鼠标笔在人体工程学方面的优劣,得出后者在使用时更为方便,且能最大限度地减少对使用者的伤害的结论。     

Toward Understanding the Mechanisms of Malignant Peripheral Nerve Sheath Tumor Development

Malignant peripheral nerve sheath tumors (MPNSTs) originate from the neural crest lineage and are associated with the neurofibromatosis type I syndrome. MPNST is an unmet clinical need. In this review article, we summarize the knowledge and discuss research perspectives related to (1) the natural history of MPNST development; (2) the mouse models recapitulating the progression from precursor lesions to MPNST; (3) the role of the tumor microenvironment in MPNST development, and (4) the signaling pathways linked to MPNST development.