Efficacy of transcranial magnetic stimulation and fluoxetine in the treatment of postpartum depression: A protocol for systematic review and meta-analysis.

BACKGROUND: Numerous studies have reported that transcranial magnetic stimulation (TMS) and fluoxetine is used in the treatment of postpartum depression (PPD). Currently, no study has systematically investigated the efficacy and safety of TMS and fluoxetine for the treatment of patients with PPD. Thus, this study will assess the efficacy and safety of TMS and fluoxetine for treating PPD. METHODS: Relevant studies involving TMS and fluoxetine for the treatment of patients with PPD will be comprehensively searched from the electronic databases from inception to the February 1, 2020: Cochrane Library, EMBASE, MEDILINE, CINAHL, AMED, WANGFANG, VIP, and CNKI databases. No language and publication time restrictions will be applied. RevMan 5.3 software will be utilized for data pooling, data analysis, and risk of bias evaluation. If necessary, we will also assess reporting bias using funnel plot and Egger test. RESULTS: This study will comprehensively summarize the existing evidence to assess the efficacy and safety of TMS and fluoxetine for treating PPD. CONCLUSION: The findings of this study may help to establish a better approach to treat PPD using TMS and fluoxetine. DISSEMINATION AND ETHICS: This study will be disseminated through a peer-reviewed journal. This study does not need ethical approval as no primary patient data will be used. SYSTEMATIC REVIEW REGISTRATION: INPLASY202040017.

ERK/MAPK signalling pathway and tumorigenesis.

Mitogen-activated protein kinase (MAPK) cascades are key signalling pathways that regulate a wide variety of cellular processes, including proliferation, differentiation, apoptosis and stress responses. The MAPK pathway includes three main kinases, MAPK kinase kinase, MAPK kinase and MAPK, which activate and phosphorylate downstream proteins. The extracellular signal-regulated kinases ERK1 and ERK2 are evolutionarily conserved, ubiquitous serine-threonine kinases that regulate cellular signalling under both normal and pathological conditions. ERK expression is critical for development and their hyperactivation plays a major role in cancer development and progression. The Ras/Raf/MAPK (MEK)/ERK pathway is the most important signalling cascade among all MAPK signal transduction pathways, and plays a crucial role in the survival and development of tumour cells. The present review discusses recent studies on Ras and ERK pathway members. With respect to processes downstream of ERK activation, the role of ERK in tumour proliferation, invasion and metastasis is highlighted, and the role of the ERK/MAPK signalling pathway in tumour extracellular matrix degradation and tumour angiogenesis is emphasised.

DAXX promotes ovarian cancer ascites cell proliferation and migration by activating the ERK signaling pathway.

BACKGROUND: The death-domain-associated protein (DAXX) was originally identified as a protein that binds to the transmembrane death receptor FAS and enhances both FAS-induced and transforming growth factor-ß-dependent apoptosis. In a previous study, we found that nude mice injected with DAXX-overexpressing cells (ES-2-DAXX) accumulated large concentrations of first-generation ascites cells (I ascites cells). The role of DAXX in the development of ascites is unknown. The aim of this study was to analyze the effect of DAXX on proliferation and migration of ascites cells in ovarian cancer in vitro and in vivo. METHODS: Nude mice were housed in cages with a 14:10 h light:dark cycle; water and food were provided ad libitum. ES-2-DAXX cells (1×106) were injected intraperitoneally into athymic nude mice (8-week-old female mice). After 4 weeks, I ascites cells were collected. The I ascites cells were injected intraperitoneally into athymic nude mice (8-week-old female mice). After 4 weeks, II ascites cells were collected and cultured. Ascites cell survival, migration, and colony formation were measured using colony formation and cell growth assays. Immunofluorescent staining revealed the co-localization of DAXX and promyelocytic leukemia protein (PML) in ascites cell nuclei. Western blotting and immunohistochemistry showed that extracellular signal-related kinase (p-ERK) 1/2 and CEBP-ß were highly expressed in tumor tissues formed by II ascites cells. Through immunoprecipitation, we also found that DAXX can interact with CEBP-ß. RESULTS: DAXX enhanced ascites cell survival, migration, and colony formation. DAXX and PML nuclear foci dramatically increased in a passage-dependent manner in ascites cells, DAXX promoted the tumor growth of ascites cells in vivo, increased ascites cell proliferation in vivo, and enhanced ascites cell survival and migration by activating the ERK signalling pathway and integrating with CEBP-ß. CONCLUSIONS: DAXX can interact with CEBP-ß. DAXX can induce ovarian cancer ascites formation by activating the ERK signal pathway and binding to CEBP-ß.

PML silencing inhibits cell proliferation and induces DNA damage in cultured ovarian cancer cells.

The promyelocytic leukemia (PML) gene is a tumor suppressor gene. It was first identified in acute promyelocytic leukemia, in which it is fused to retinoic acid receptor α by the (15;17) chromosomal translocation. The function of the PML protein is frequently lost or aberrant in human solid tumors. In human ovarian carcinoma tissue, PML detected by immunohistochemistry was highly expressed. A PML-silencing vector, pSRG-shPml, was constructed and used to transfect human ovarian cancer cells. Cells were cultured and selected with puromycin for 10-15 days, and then the PML mRNA expression levels were detected by RT-qPCR and immunofluorescence. Proliferation and clone number of PML-depleted cells were detected using MTT assay and colony-forming assay. The protein expression associated with DNA damage and apoptosis was assessed in PML-depleted cells using western blot analysis and immunofluorescence. The results showed that PML was highly expressed in human ovarian tissue. The proliferation and colony formation of ovarian cancer cells were significantly inhibited after PML was depleted. Western blot analysis and immunofluorescence revealed that p-H2AX and cleaved caspase-3 expression significantly increased after PML silencing. PML was located in the nucleus, and it formed foci after X-ray irradiation. PML foci increased significantly with increasing irradiation doses.

DAXX silencing suppresses mouse ovarian surface epithelial cell growth by inducing senescence and DNA damage.

Mouse ovarian surface epithelium (OSE) is a single layer of cubodial epithelial cells that covers the ovary surface and is involved in regulating the secretion and transport of 17ß-hydroxysteroid dehydrogenase. Recently, OSE cells have attracted particular interest as a major source of ovarian cancer. Death-associated protein DAXX along with PML (promyelocytic leukemia protein) nuclear bodies (PML-NBs) reportedly play roles in transcriptional regulation and apoptosis. However, little is known regarding a role for DAXX in mOSE cells. In this study, we both over-expressed DAXX and depleted DAXX in primary mOSE cells. We found that Daxx deletion accelerated senescence in a p53/p21-dependent manner and promoted DNA damage by interacting with PML bodies without affecting cell cycle progression. These results suggest that DAXX may transform mOSE cells to an ovarian oncogenic phenotype and may be an anti-cancer target.

[Research progress about Wapl gene].

In Drosophila melanogasler,the wings apart-like (wapl) gene encodes a protein that regulates heterochromatin structure. Human wapl gene is human homolognue of wapl,they have same function. HWAPL is a cohesion-binding protein that affect chromosomal segregation. It has a character of oncoproteins and linked to cervical carcinogenesis and tumor progression.

[Relationship between expression of vimentin, type IV collagen and fibronectin in human placenta and pregnancy induced hypertension].

OBJECTIVE: To elucidate the possible relationship between pregnancy-induced hypertension syndrome (PIH) and expression of vimentin, type IV collagen and fibronectin in human placenta. METHODS: Nineteen pregnant women (PIH group) and 15 normal pregnant women (control group) matched for age and gestation were recruited. The expression of vimentin, type IV collagen and fibronectin in the placenta of PIH patients and normal subjects was investigated using immunohistochemical perioxidase-antiperoxidase (PAP) staining technique combined with an analysis through a computer-aided microphotographic system and compared between the two groups. RESULTS: The average grey value difference (GVD) which indicated positive staining of vimentin was 30 +/- 7 in section images of the moderate and severe PIH group, significantly lower than that of normal control group, 42 +/- 6 and mild PIH group, 42 +/- 9 (P < 0.01). The average GVD of type IV collagen in moderate and severe PIH group was 70 +/- 6, significantly higher than 29 +/- 4 of control group and 30 +/- 5 of mild PIH group (P < 0.001). The average GVD of fibronectin in moderate and severe PIH group was 37 +/- 4, significantly higher than that in control group, 31 +/- 4 and mild PIH group, 32 +/- 6 (P < 0. 05). CONCLUSIONS: There is tight relationship between abnormal expression of placental vimentin, type IV collagen, fibronectin and pathogenesis of PIH. Furthermore, the severity of PIH is positively correlated with the abnormal expression levels of those proteins.