β-Sitosterol Attenuates Dexamethasone-Induced Muscle Atrophy via Regulating FoxO1-Dependent Signaling in C2C12 Cell and Mice Model

Sarcopenia refers to a decline in muscle mass and strength with age, causing significant impairment in the ability to carry out normal daily functions and increased risk of falls and fractures, eventually leading to loss of independence. Maintaining protein homeostasis is an important factor in preventing muscle loss, and the decrease in muscle mass is caused by an imbalance between anabolism and catabolism of muscle proteins. Although β-sitosterol has various effects such as anti-inflammatory, protective effect against nonalcoholic fatty liver disease (NAFLD), antioxidant, and antidiabetic activity, the mechanism of β-sitosterol effect on the catabolic pathway was not well known. β-sitosterol was assessed in vitro and in vivo using a dexamethasone-induced muscle atrophy mice model and C2C12 myoblasts. β-sitosterol protected mice from dexamethasone-induced muscle mass loss. The thickness of gastrocnemius muscle myofibers was increased in dexamethasone with the β-sitosterol treatment group (DS). Grip strength and creatine kinase (CK) activity were also recovered when β-sitosterol was treated. The muscle loss inhibitory efficacy of β-sitosterol in dexamethasone-induced muscle atrophy in C2C12 myotube was also verified in C2C12 myoblast. β-sitosterol also recovered the width of myotubes. The protein expression of muscle atrophy F-box (MAFbx) was increased in dexamethasone-treated animal models and C2C12 myoblast, but it was reduced when β-sitosterol was treated. MuRF1 also showed similar results to MAFbx in the mRNA level of C2C12 myotubes. In addition, in the gastrocnemius and tibialis anterior muscles of mouse models, Forkhead Box O1 (FoxO1) protein was increased in the dexamethasone-treated group (Dexa) compared with the control group and reduced in the DS group. Therefore, β-sitosterol would be a potential treatment agent for aging sarcopenia.     

Enchondral cartilage rests collagen-induced autoimmunity: a possible pathogenetic mechanism of otosclerosis

Collagen autoimmunity has been suggested as one etiologic mechanism to otosclerosis. Although substantial studies relating this disease to collagen autoimmunity have been reported, a basic understanding of the pathogenic mechanism involved is lacking. Some otosclerosis patients have a high level of antibody to type II collagen. In addition, complement and antibody were deposited in the stapes from otosclerosis patients. Furthermore, the otic capsule and stapes have been found to contain type II collagen by immunohistologic studies and biochemical analysis. Otospongiosis-like lesions have also been produced in rats by immunizing them with type II collagen. This finding led us to postulate a hypothesis of an autoimmunity to type II collagen as an etiopathogenesis of this illness. Our initial hypothesis has been updated to incorporate new findings in the field of cell biology. The role of interleukin 1, osteoclasts, osteoblasts, bone resorption, and other factors such as minor collagens, calcitonin, vitamin D, parathyroid hormone, collagenase, and prostaglandins are incorporated in this updated hypothesis.     

Ovarian neuroendocrine carcinoma, non-small cell type, associated with serous carcinoma

BACKGROUND: Neuroendocrine carcinoma of the non-small cell type of the ovary is a rare aggressive tumor, interestingly associated with either a surface epithelial tumor or teratoma. CASE: A 71-year-old woman presented with a pelvic mass and underwent a total abdominal hysterectomy with a bilateral salpingo-oophorectomy. Pathology examination showed a 6.5 cm in greatest dimension ovarian tumor composed of neuroendocrine carcinoma of the non-small cell type and serous carcinoma. Immunohistochemical studies including keratin 7, WT-1, and neuroendocrine markers demonstrated differences in the two components. Microsatellite instability (MSI) analysis using five polymorphic markers also showed a different pattern in the two components. CONCLUSION: This is the first report of an ovarian neuroendocrine carcinoma, non-small cell type, associated with a serous carcinoma. Immunohistochemistry and MSI are very helpful in making a definite diagnosis.     

Prenatal diagnosis of a large subchorionic placental cyst with intracystic hematomas. A case report

A large intrauterine cyst containing a heterogenous mass was found by ultrasound in the placenta of a 35-year-old gravida 2 para 1 woman. The cyst, measuring 10.9 x 10.1 cm with a heterogenous mass shadow, was attached near the placental cord insertion site. The woman delivered a healthy female baby weighing 3,330 g by cesarean section without complication. A histopathological examination revealed that the lesion was a subchorionic cyst and contained an internal hematoma. Large subchorionic cysts are extremely rare, and secondary hemorrhage within the cyst has not been reported. In this article, we report the case of a woman with a large subchorionic cyst complicated by an intracystic hematoma and review its clinical significance.     

朝鲜白头翁、人参和甘草的复合水提物的抗血管生成作用

目的：本研究旨在证实朝鲜白头翁、人参和甘草的复合水提物（water extract ofPulsatillakoreana（Yabe ex Nakai）Nakai ex T.Mori.,PanaxginsengC.A.Meyer andGlycyrrhizauralensisFisch,WEPPG）的抗血管生成作用。方法：使用纤维母细胞生长因子致血管生成的人类脐静脉内皮细胞模型衡量细胞的增殖、黏附及迁移,同时进行细管形成实验及纤维母细胞生长因子致鸡胚绒毛尿囊膜血管生成实验检测WEPPG的抗血管生成作用。结果：WEPPG能够显著抑制纤维母细胞生长因子所致血管生成的人类脐静脉内皮细胞的增殖、黏附及迁移。信号蛋白分析显示多种蛋白表达变化,如细胞周期素A、p63、KIP2的上调及nibrin蛋白和黏着斑激酶的下调。与对照组相比,WEPPG显著减少了鸡胚绒毛尿囊膜血管生成。结论：本研究的结果证实了WEPPG的抗血管生成作用,这可能是这种药物具有抗癌功效的原因之一。     

Friction Properties of Solid Lubricants with Different Multiwalled Carbon Nanotube Contents

Bushes are circular bearings that surround a shaft and help it rotate smoothly. In heavy equipment, bushes are coated with solid lubricants to reduce friction. Although the coating layer of the lubricant has a stable coefficient of friction (CoF), it is important that this should last for a long time. In this study, multiwalled carbon nanotubes (MWCNTs), which have a low CoF, were added to the lubricant to improve its performance. When 2.3 wt% MWCNTs were added to the polymer resin, the dynamic CoF (under a 29 N external load) decreased by 78% in relation to that of the resin without MWCNTs. As the MWCNT content increased, the roughness of the coating decreased, which reduced the CoF. Moreover, MWCNT addition increased the overall tensile strength owing to an increase in the bonding force between the resins. Under a high load of 20 tonnes (t), the MWCNT-based solid lubricant had a CoF of 0.05, lower than commercial MoS₂-based solid lubricants; this was maintained for more than 10,000 cycles in a bush and shaft test. With the MWCNT-based solid lubricant, a lubricating polymer film formed, even on worn bush surfaces. The CoF of the solid lubricant was reduced and the number of cycles with a constant CoF increased when MWCNTs were added owing to the formation of the lubricating polymer film.     

Advanced parental age is an independent risk factor for term low birth weight and macrosomia

We aimed to investigate association between parental age and the risks of term low birth weight and macrosomia.This was a retrospective cohort study using a national database including 2,245,785 term singleton live births with complete parental age data. Old parental age was defined as 35 years or older. Odd ratios (OR) for term low birth weight and macrosomia were analyzed using univariate and multivariate logistic regression analysis.Neonatal sex, maternal occupation, parity, nationality, age, and paternal age were significant factors of term low birth weight and macrosomia, in univariate analysis. In multivariate analysis, old maternal age (≥35 years old) showed increased odds of term low birth weight and macrosomia (aOR = 1.122, 95% CI: 1.083 –1.162; and aOR = 1.166, 95% CI: 1.143 – 1.189, respectively). Similarly, old paternal age (≥35 years old) showed increased odds of term low birth weight and macrosomia (aOR = 1.090, 95% CI: 1.058 –1.122; and aOR = 1.101, 95% CI: 1.083 – 1.119, respectively). Maternal education that lasted more than 12 years had reduced odds of term low birth weight and macrosomia (OR = 0.817, 95% CI: 0.792 –0.842; and OR = 0.894, 95% CI: 0.879 – 0.91, respectively). Paternal education that lasted more than 12 years also had reduced odds of term low birth weight and macrosomia (OR = 0.865, 95% CI: 0.84 –0.892; and OR = 0.897, 95% CI: 0.881 – 0.913, respectively).This study suggests that not only maternal age but also paternal age are significantly associated with term low birth weight and macrosomia. In addition, parental education levels are also associated with term low birth weight and macrosomia.     

Fimasartan Ameliorates Deteriorations in Glucose Metabolism in a High Glucose State by Regulating Skeletal Muscle and Liver Cells

PurposeSince diabetes and hypertension frequently occur together, it is thought that these conditions may have a common pathogenesis. This study was designed to evaluate the anti-diabetic function of the anti-hypertensive drug fimasartan on C2C12 mouse skeletal muscle and HepG2 human liver cells in a high glucose state.Materials and MethodsThe anti-diabetic effects and mechanism of fimasartan were identified using Western blot, glucose uptake tests, oxygen consumption rate (OCR) analysis, adenosine 5′-triphosphate (ATP) enzyme-linked immunosorbent assay (ELISA), and immunofluorescence staining for diabetic biomarkers in C2C12 cells. Protein biomarkers for glycogenolysis and glycogenesis were evaluated by Western blotting and ELISA in HepG2 cells.ResultsThe protein levels of phosphorylated 5′ adenosine monophosphate-activated protein kinase (p-AMPK), p-AKT, insulin receptor substrate-1 (IRS-1), and glucose transporter type 4 (Glut4) were elevated in C2C12 cells treated with fimasartan. These increases were reversed by peroxisome proliferator-activated receptor delta (PPARδ) antagonist. ATP, OCR, and glucose uptake were increased in cells treated with 200 µM fimasartan. Protein levels of glycogen phosphorylase, glucose synthase, phosphorylated glycogen synthase, and glycogen synthase kinase-3 (GSK-3) were decreased in HepG2 cells treated with fimasartan. However, these effects were reversed following the addition of the PPARδ antagonist GSK0660.ConclusionIn conclusion, fimasartan ameliorates deteriorations in glucose metabolism as a result of a high glucose state by regulating PPARδ in skeletal muscle and liver cells.