No abstract

Anatase TiO 2 nanoparticles with average particle size ranging between 12 and 23 nm were synthesized by metalorganic chemical vapor deposition. The structure and particle size were determined by x-ray diffraction and transmission electron microscopy. The specific surface areas were measured by Brunauer-Emmett-Teller and ranged from 65 to 125 m 2 / g. The size effects on the stability of TiO 2 in the air were studied by x-ray diffraction and transmission electron diffraction for isochronally annealed samples in the temperature range of 700-800°C. Only anatase to rutile phase transformation occurred. With the decrease of initial particle size the onset transition temperature was decreased. An increased lattice compression of anatase with the raising of temperature was observed by the x-ray peak shifts. Larger distortions existed in samples with smaller particle size. The calculated activation energy for phase transformation decreased from 299 to 180 kJ/mol with the decrease of initial anatase particle size from 23 to 12 nm. The decreased thermal stability in finer nanoparticles was primarily due to the reduced activation energy as the size related surface enthalpy and stress energy increased.

Polycystic ovary syndrome (PCOS) is a common endocrine disorder found in 5-10% of reproductive-age women and 75-80% of anovulatory women. Characteristics of PCOS include amenorrhea/ oligomenorrhea, infertility, hyperinsulinemia from insulin resistance, leutinizing hormone (LH) hypersecretion and hyperandrogenism [1]. The etiology and pathophysiology of PCOS are not clear, so the treatments only scratch the surface of the problem and drugs are needed to ease the symptoms. Some scholars have considered that PCOS is a single autosomal dominant genetic disease [2,3] abstract. although hyperandrogenism is an important condition and is considered the possible pathogenesis behind polycystic ovary syndrome (PCOS), data supporting this is still scarce. We sought to determine whether or not prenatal androgen exposure leads to PCOS and the possible cellular mechanisms involved. To induce prenatal androgen exposure, pregnant rats were treated with daily subcutaneous injections of free testosterone (T) or dihydrotestosterone (dHT) from embryonic days 16 to 19, and their female offspring were studied as adults. The mRna expression of the progesterone receptor (PR) in the preoptic area (POa) hypothalamus was higher in the experimental groups than in the control group after ovariectomy and stimulation with estradiol benzoate. The levels of T, P, leutinizing hormone (LH), and estradiol were higher in the experimental groups than in the control groups. The frequency and magnitude of LH secretion was increased in experimental rats as compared with the control group. The anogenital distance of the experimental groups was prolonged and the nipple number was lower than that of the control group. almost all experimental rats had prolonged or irregular estrous cycles. The experimental groups had fewer corpus luteum and preovulatory follicles and more preantral follicles and antral follicles than the controls. Our findings are consistent with the hypothesis that excess androgen during the prenatal period may cause PCOS. additionally, we show that hyperandrogenic interference in the release of preovulatory LH surges is mediated by the suppressive effects of androgens on PR expression in POa-hypothalamic tissue.

Patients exposed to a surgical safety checklist experience better postoperative outcomes, but this could simply reflect wider quality of care in hospitals where checklist use is routine.

Human trophoblastic cell surface antigen 2 (Trop2) has been suggested as an oncogene, which is associated with the different types of tumors. In this study, a human Fab antibody against Trop2 extracellular domain was isolated from phage library by phage display technology, and characterized by ELISA, FACS, fluorescence staining and Western blotting analysis. MTT, apoptosis assay and wound healing assay were employed to evaluate the inhibitory effects of Trop2 Fab on breast cancer cell growth in vitro, while tumor‐xenograft model was employed to evaluate the inhibitory effects on breast cancer growth in vivo. The results showed that Trop2 Fab inhibited the proliferation, induced the apoptosis and suspended the migration of MDA‐MB‐231 cells in a dose dependent manner. The expression caspase‐3 was activated, and the expression of Bcl‐2 was reduced while that of Bax was elevated in MDA‐MB‐231 cells by treating with Trop2 Fab. In addition, Trop2 Fab inhibited the growth of breast cancer xenografts and the expression of Bcl‐2 was reduced while that of Bax was elevated in xenografts. Trop2 Fab, which was isolated successfully in this research, is a promising therapeutic agent for the treatment of Trop2 expressing breast cancer.