TIPE1 Inhibits Breast Cancer Proliferation by Downregulating ERK Phosphorylation and Predicts a Favorable Prognosis.

TIPE1, which acts as a cell death regulator, has emerged as a tumor suppressor in the process of carcinogenesis. However, our recent research demonstrated that it serves as an oncogene in the pathogenesis of cervical cancer, indicating that the role of TIPE1 in carcinogenesis needs to be further evaluated. In this study, we show that TIPE1 is able to inhibit breast cancer cell growth both in vivo and in vitro. Functionally, TIPE1 inhibits cancer cell proliferation preferentially by downregulating ERK phosphorylation. Furthermore, the expression of TIPE1 is decreased in breast cancer tissues compared to matched adjacent tissues, and its expression is positively correlated with patients' lifespan. These data indicate that TIPE1 suppresses breast cancer proliferation by inhibiting the ERK signaling pathway. This study also suggests that TIPE1 could serve as a potential therapeutic target and a diagnostic biomarker for breast cancer.

Magnolol prevents ovariectomy­induced bone loss by suppressing osteoclastogenesis via inhibition of the nuclear factor­κB and mitogen­activated protein kinase pathways.

Magnolol is the active component of the traditional Chinese medicine Magnolia officinalis, and has antioxidant, anti­inflammatory and anticancer activities, as well as an effect on bone metabolism in vitro. In the present study, it is reported that magnolol suppresses osteoclastogenesis in vivo and in vitro. Magnolol prevented ovariectomy­induced bone loss and osteoclastogenesis in vivo, and decreased the serum levels of C­terminal telopeptide of type 1 collagen, interleukin­6, tumor necrosis factor (TNF)­α and tartrate­resistant acid phosphatase 5B. In vitro, magnolol inhibited the osteoclastogenesis induced by the receptor activator for nuclear factor­κB ligand, and impaired the osteoclast function in bone marrow monocytes and RAW264.7 cells in a dose­dependent manner. Furthermore, magnolol suppressed the expression levels of the osteoclastogenesis markers cathepsin K, calcitonin receptor, matrix metalloproteinase 9, TNF receptor­associated factor 6 and tartrate­resistant acid phosphatase by inhibiting the nuclear factor­κB and mitogen­activated protein kinase pathways. Therefore, magnolol is a promising agent for the treatment of osteoporosis and associated disorders.

Tim-4 Inhibits NO Generation by Murine Macrophages.

OBJECTIVE: T cell immunoglobulin- and mucin-domain-containing molecule-4 (Tim-4) receives much attention as a potentially negative regulator of immune responses. However, its modulation on macrophages has not been fully elucidated so far. This study aimed to identify the role of Tim-4 in nitric oxide (NO) modulation. METHODS: Macrophages were stimulated with 100 ng/ml LPS or 100 U/ml IFN-γ. RT-PCR was performed to detect TIM-4 mRNA expression. Tim-4 blocking antibody and NF-κB inhibitory ligand were involved in the study. NO levels were assayed by Griess reaction. Phosphorylation of NF-κB, Jak2 or Stat1 was verified by western blot. RESULTS: Tim-4 was up-regulated in murine macrophages after interferon-gamma (IFN-γ) stimulation. Tim-4 over-expression decreased NO production and inducible nitric oxide synthase (iNOS) expression in lipopolysaccharide (LPS) or IFN-γ-stimulated macrophages. Consistently, Tim-4 blockade promoted LPS or IFN-γ-induced NO secretion and iNOS expression. Tim-4 over-expression decreased LPS-induced nuclear factor kappa B (NF-κB) p65 phosphorylation in macrophages, which was abrogated by NF-κB inhibitory ligand. On the contrary, Tim-4 blocking increased LPS-induced NF-κB signaling, which was also abrogated by NF-κB inhibition. In addition, Tim-4 blockade promoted Jak2 and Stat1 phosphorylation in IFN-γ stimulated macrophages. CONCLUSION: These results indicate that Tim-4 is involved in negative regulation of NO production in macrophages, suggesting the critical role of Tim-4 in immune related diseases.

[Degradation of beta-naphthol by catalytic wet air oxidation].

A series of MnO(x)/nano-TiO2 catalysts were prepared and their application in degradation of beta-naphthol by catalytic wet air oxidation (CWAO) was investigated. The catalysts preparation conditions, reaction conditions and its stability were tested. The catalysts had been characterized by X-ray diffraction (XRD), X-ray photoelectron spectroscopy (XPS) and temperature-programmed reduction (TPR) measurements. The results showed that the decrease of the COD removal for the degradation of beta-naphthol at high Mn loading was due to the aggregation of the highly dispersed Mn species and the formation of the correlated crystals. The decline of the COD removal at high calcination temperature was probably attributed to the weak electron transfer between Mn2O3 and MnO2 and the formation of the inactive Mn2O3. The COD removal had been falling slightly when the catalyst was used 6 times, and this was likely related to the decrease of the diffraction peaks. The catalyst had a high activity when the Mn loading (mass fraction) was 4% and the calcination temperature was 450 degrees C. The COD removal was up to 96.4% at 110 degrees C and 0.5 MPa with this catalyst. The COD removal of 92.4% could be obtained with the MnO(x)/nano-TiO2 catalyst was recycled 6 times. The Mn leaching at 50, 80, 110 and 150 degrees C were all less than 9.3 mg x L(-1) by means of Atomic Absorption Spectroscopy (AAS). The probable degradation pathway was proposed according to some publications.

[A study of the occupational stress norm and it' s application for the technical group and scientific research group].

OBJECTIVE: A study of the occupational stress norm and it' s application for the technical group and scientific research group. METHODS: In this study, cross-sectional study method is used, and a synthetic way of sorting and randomized sampling is adopted to deal with research targets(235 scientific research group, 857 technical group). RESULTS: Descriptive statistics for OSI-R scale scores for the technical group and scientific research group were modulated. Scale raw score to T-score conversion tables derived from the OSI-R normative sample for technical group and scientific research group were established. OSI-R profile from for technical group and scientific research group were established. For the ORQ and PSQ scales, scores at or above 70T indicate a strong levels of maladaptive stress and strain. Score in the range of 60T to 69T suggest middle levels of maladaptive stress and strain. Score in the range of 40T to 59T indicate normal levels of stress and strain. Score below 40T indicate a relative absence of occupational stress and strain. For the PRQ scales, score below 30T indicate a significant lack of coping resources. Score in the range of 30T to 39T suggest middle deficits in coping resources. Score in the range of 40T to 59T indicate average coping resources. Scores at or above 60T indicate a strong levels of coping resources. CONCLUSION: Different intervention measure should be take to reduce the occupational stress so as to improve the work ability.