Ordering behaviors and age-hardening in experimental AuCu-Zn pseudobinary alloys for dental applications

Age-hardening mechanisms and related ordering behaviors of the experimental (AuCu)_1−xZn_x alloys with x0.2 were investigated for dental applications. The addition of Zn to equiatomic AuCu greatly increased the age-hardening rate and delayed overaging. It was suggested that the quenched-in excess vacancies were greatly related to the age-hardening rate in the AuCu–Zn pseudobinary alloys. In these alloys, the hardness became maximum during the very initial stage of ordering, and with the development of ordered phase, the hardness began to decrease. Transmission electron microscopy revealed that the age-hardening of AuCu–Zn pseudobinary alloys is caused by lattice distortion that occurred during the very early stage of atomic ordering. The addition of Zn to AuCu effectively increased the density of antiphase boundaries per unit volume of the AuCu II superstructure. This is suggested to be the main cause for the retardation of the overaging in the alloys containing Zn of 5 at% or more. This pronounced effect of Zn addition to AuCu alloy on its age-hardening characteristics may be advantageous for obtaining stable mechanical properties of dental casting gold alloys.     

Non-invasive detection of fecal protein kinase C betaII and zeta messenger RNA: putative biomarkers for colon cancer

We have developed a non-invasive method utilizing feces, containing sloughed colonocytes, as a sensitive technique for detecting diagnostic colonic biomarkers. In this study, we used the rat colon carcinogenesis model to determine if changes in fecal protein kinase C (PKC) expression have predictive value in monitoring the neoplastic process. Weanling rats were injected with saline or azoxymethane (AOM) and 36 weeks later fecal samples and mucosa were collected, poly A+ RNA isolated, and quantitative RT-PCR performed using primers to PKC betaII and zeta. Fecal PKC betaII and zeta mRNA levels were altered by the presence of a tumor, with tumor-bearing animals having a 3-fold higher (P < 0.05) PKC betaII expression as compared with animals without tumors. In addition, AOM-injection increased mucosal PKC betaII mRNA expression compared with saline controls. No effect of tumor incidence on mucosal PKC betaII expression was observed. In contrast, fecal PKC zeta expression was 2.5-fold lower (P < 0.05) in animals injected with azoxymethane versus saline. Since tumor incidence exerts a reciprocal effect on fecal PKC betaII and zeta mRNA expression, data were also expressed as the ratio between PKC betaII and zeta. The isozyme ratio was strongly related to tumor incidence, i.e. ratio for animals with tumors was 2.18 +/- 1.25, animals without tumors was 0.50 +/- 0.16, P = 0.025. We demonstrate that the expression of fecal PKC betaII and zeta may serve as a noninvasive marker for development of colon tumors. A sensitive technique for the detection of colon cancer is of importance since early diagnosis can substantially reduce mortality.      

Advanced adipose-derived stem cell protein extracts with antioxidant activity modulates matrix metalloproteinases in human dermal fibroblasts

Advanced adipose-derived stem cell protein extracts (AAPE) were used instead of live stem cells to investigate their effect on oxidative stress and matrix metalloproteinases (MMPs) related to tissue repair in human dermal fibroblasts (HDFs). In this study, it was observed that AAPE at 2μg/ml specifically exhibited scavenging activity of hydrogen peroxide and reducing power. The inhibitory effect of AAPE at 2μg/ml on MMP-2 activity was increased in the presence of phorbol myristate acetate (PMA). In the absence of PMA, AAPE significantly enhanced activities of MMP-1 and MMP-2 in HDFs, respectively. However, the level of MMP-1 expression was decreased in a dose dependent manner by AAPE. In addition, while the level of extracellular signal-regulated kinases 1 (ERK1) activation was reduced in the presence of AAPE compared to blank, the level that of ERK2 activation was not changed. The expression level of c-Fos, a part of activator protein-1 (AP-1), was increased in nucleus of HDFs. These results reveal that activation of MMPs in the presence of AAPE was increased via AP-1 in HDFs, suggesting that AAPE can be a potential candidate for tissue repair.     

Fibroblast growth factor 23 regulates renal 1,25‐dihydroxyvitamin D and phosphate metabolism via the MAP kinase signaling pathway in Hyp mice

In X‐linked hypophosphatemia (XLH) and in its murine homologue, the Hyp mouse, increased circulating concentrations of fibroblast growth factor 23 (FGF‐23) are critical to the pathogenesis of disordered metabolism of phosphate (P_i) and 1,25‐dihydroxyvitamin D [1,25(OH)₂D]. In this study, we hypothesized that in Hyp mice, FGF‐23‐mediated suppression of renal 1,25(OH)₂D production and P_i reabsorption depends on activation of mitogen‐activated protein kinase (MAPK) signaling. Wild‐type and Hyp mice were administered either vehicle or the MEK inhibitor PD0325901 (12.5 mg/kg) orally daily for 4 days. At baseline, the renal abundance of early growth response 1 (egr1) mRNA was approximately 2‐fold greater in Hyp mice than in wild‐type mice. Treatment with PD0325901 greatly suppressed egr1 mRNA abundance in both wild‐type and Hyp mice. In Hyp mice, PD0325901 induced an 8‐fold increase in renal 1α‐hydroxylase mRNA expression and a 4‐fold increase in serum 1,25(OH)₂D concentrations compared with vehicle‐treated Hyp mice. Serum P_i levels in Hyp mice increased significantly after treatment with PD0325901, and the increase was associated with increased renal Npt2a mRNA abundance and brush‐border membrane Npt2a protein expression. These findings provide evidence that in Hyp mice, MAPK signaling is constitutively activated in the kidney and support the hypothesis that the FGF‐23‐mediated suppression of renal 1,25(OH)₂D production and P_i reabsorption depends on activation of MAPK signaling via MEK/ERK1/2. These findings demonstrate the physiologic importance of MAPK signaling in the actions of FGF‐23 in regulating renal 1,25(OH)₂D and P_i metabolism. © 2011 American Society for Bone and Mineral Research     

假细锥香茶菜新二萜成分——假细锥甲素的结构

从假细锥香茶菜(Rabdosia coetsoides C.Y.Wu)叶分离得到新二萜成分,根据紫外光谱、红外光谱、质谱、核磁共振氢谱及碳谱等分析,推定了化学结构,并经X-射线衍射确证,命名为假细锥甲素。     

肝硬变和肝细胞癌组织中CD54,CD80,CD86和HLA-ABC的表达

目的探讨CD54,CD80,CD86和HLA-ABC在肝硬变的免疫损伤和抗肝癌免疫中的意义.方法用免疫组化方法检测CD54,CD80,CD86和HLA-ABC在肝硬变(n=30)和肝癌(n=48)中的表达、定位和分布.结果在LC中,CD54阳性率为40%(12/30),CD80为50%(15/30),CD86为37%(11/30),HLA-ABC为63%(19/30);在HCC中,CD54阳性率为77%(37/48),CD80为19%(9/47),CD86为13%(6/47),HLA-ABC为30%(12/40);在癌周围组织(PCT)中,CD54为阴性,CD80阳性率为44%(14/32),CD86为47%(15/32),HLA-ABC为53%(17/32).统计学处理显示,在LC中,CD54阳性率显著低于HCC(P＜0.01);CD80(P＜0.01),CD86(P＜0.05)和HLA-ABC(P＜0.01)均显著高于HCC;而与PCT无显著差别.在HCC中,CD80(P＜0.05),CD86(P＜0.01),HLA-ABC(P＜0.05),均显著低于PCT.结论 CD54,CD80,CD86和HLA-ABC在LC和HCC中的同时足量表达有可能引起肝细胞损伤和有效抗肿瘤免疫应答,而CD80,CD86表达的缺失或不足可能是HCC产生免疫逃避的主要原因.