Partial hydatidiform mole pregnancy ended in full-term delivery of a normal infant: a case presentation.

BACKGROUND: Twin pregnancy with a partial hydatidiform mole (PHM) and a coexistent live fetus is extremely rare. The fetus usually has a normal karyotype. The surviving rate of the fetus till lung maturity is only about 25-40%. PHM pregnancy almost ends in abortion due to the presence of triploid embryo. Here, we report a case of PHM coexistent with a live fetus resulting in a live baby. CASE PRESENTATION: A PHM pregnancy was diagnosed by ultrasonography in a 28-year-old Chinese woman, with normal fetal morphology and mosaicism as indicated by amniocentesis. After being fully informed of the risks, the woman chose to proceed with the pregnancy and finally gave birth to a baby girl and the infant was delivered at term. A single placenta with vesicular changes and peripheral blood diploid chromosomes were observed. There were no serious maternal complications. In conclusion, the diagnosis, management, and monitoring of this condition, which is very rare in clinical practice, remain challenging. Under proper management, a PHM-combined pregnancy can still end in full-term delivery of a normal living fetus.

Successfully Managing Cornual Heterotopic Pregnancy:A Case Report and Literature Review.

Cornual heterotopic pregnancy is an extremely rare, life-threatening complication during pregnancy. Here, we report a 33-year-old woman who suffered cornual heterotopic pregnancy afterin vitro fertilization embryo transfer. To prevent rupture during heterotopic pregnancy, she received laparoscopic surgery to remove the ectopic gestational sac at 7+2weeks of gestation. Ultimately, she delivered a healthy boy at 38+3 weeks of gestation. Here, we also review the clinical presentations, risk factors, treatment options and outcomes of cornual heterotopic pregnancy.

Deferoxamine-mediated up-regulation of HIF-1α prevents dopaminergic neuronal death via the activation of MAPK family proteins in MPTP-treated mice.

Accumulating evidence suggests that an abnormal accumulation of iron in the substantia nigra (SN) is one of the defining characteristics of Parkinson's disease (PD). Accordingly, the potential neuroprotection of Fe chelators is widely acknowledged for the treatment of PD. Although desferrioxamine (DFO), an iron chelator widely used in clinical settings, has been reported to improve motor deficits and dopaminergic neuronal survival in animal models of PD, DFO has poor penetration to cross the blood-brain barrier and elicits side effects. We evaluated whether an intranasal administration of DFO improves the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced degeneration of dopaminergic neurons in the nigrostriatal axis and investigated the molecular mechanisms of intranasal DFO treatment in preventing MPTP-induced neurodegeneration. Treatment with DFO efficiently alleviated behavioral deficits, increased the survival of tyrosine hydroxylase (TH)-positive neurons, and decreased the action of astrocytes in the SN and striatum in an MPTP-induced PD mouse model. Interestingly, we found that DFO up-regulated the expression of HIF-1α protein, TH, vascular endothelial growth factor (VEGF), and growth associated protein 43 (GAP43) and down-regulated the expression of α-synuclein, divalent metal transporter with iron-responsive element (DMT1+IRE), and transferrin receptor (TFR). This was accompanied by a decrease in iron-positive cells in the SN and striatum of the DFO-treated group. We further revealed that DFO treatment significantly inhibited the MPTP-induced phosphorylation of the c-Jun N-terminal kinase (JNK) and differentially enhanced the phosphorylation of extracellular regulated protein kinases (ERK) and mitogen-activated protein kinase (MAPK)/P38 kinase. Additionally, the effects of DFO on increasing the Bcl-2/Bax ratio were further validated in vitro and in vivo. In SH-SY5Y cells, the DFO-mediated up-regulation of HIF-1α occurred via the activation of the ERK and P38MAPK signaling pathway. Collectively, the present data suggest that intranasal DFO treatment is effective in reversing MPTP-induced brain abnormalities and that HIF-1-pathway activation is a potential therapy target for the attenuation of neurodegeneration.

Intranasal deferoxamine attenuates synapse loss via up-regulating the P38/HIF-1α pathway on the brain of APP/PS1 transgenic mice.

The widely recognized neuroprotective effect of iron chelators is contributed by their ability to prevent reactive oxygen species (ROS) generation via the Fenton reaction, which sequesters redox-active Fe. An additional neuroprotective mechanism of iron-chelating compounds is to regulate the transcriptional activator hypoxia-inducible factor 1α (HIF-1α). In the present study, we observed that intranasal administration of deferoxamine decreased beta-amyloid (Aß) deposition and rescued synapse loss in the brain of Aß precursor protein and presenilin-1 (APP/PS1) double transgenic mice. We found that deferoxamine (DFO) up-regulated HIF-1α mRNA expression and its protein level, and further induced the proteins that are encoded from HIF-1-adaptive genes, including transferrin receptor (TFR), divalent metal transporter 1 (DMT1), and brain-derived neurotrophic factor (BDNF). The effects of DFO on the induction and stabilization of HIF-1α were further confirmed in vitro. This was accompanied by a decrease of Fe in the CA3 region of the hippocampus. Western blotting studies revealed that DFO differentially enhanced the phosphorylation of mitogen-activated protein kinase (MAPK)/P38 kinase in vitro and in vivo. The results suggest that the DFO may up-regulate several HIF-1-dependent neuroprotective-adaptive genes in AD via activating P38/HIF-1α pathway, which may serve as important therapeutic targets to the disease.

Integrin-ß1 regulates chondrocyte proliferation and apoptosis through the upregulation of GIT1 expression.

Chondrocytes play a critical role in the repair process of osteoarthritis, which is also known as degenerative arthritis. Integrins, as the key family of cell surface receptors, are responsible for the regulation of chondrocyte proliferation, differentiation, survival and apoptosis through the recruitment and activation of downstream adaptor proteins. Moreover, G-protein-coupled receptor kinase interacting protein-1 (GIT1) exerts its effects on cell proliferation and migration through interaction with various cytokines. It has been previously suggested that GIT1 acts as a vital protein downstream of the integrin-mediated pathway. In the present study, we investigated the effects of integrin-ß1 on cell proliferation and apoptosis, as well as the underlying mechanisms in chondrocytes in vitro. Following transfection with a vector expressing integrin-ß1, our results revealed that the overexpression of integrin-ß1 enhanced GIT1 expression, whereas the knockdown of integrin-ß1 by siRNA suppressed GIT1 expression. However, no significant effect was observed on integrin-ß1 expression following the enforced overexpression of GIT1, which suggests that GIT1 is localized downstream of integrin-ß1. In other words, integrin-ß1 regulates the expression of GIT1. Furthermore, this study demonstrated that integrin-ß1 and GIT1 increased the expression levels of aggrecan and type II collagen, thus promoting chondrocyte proliferation; however, they inhibited chondrocyte apoptosis. Taken together, our data demonstrate that integrin-ß1 plays a vital role in chondrocyte proliferation, differentiation and apoptosis. GIT1 exerts effects similar to those of integrin-ß1 and is a downstream target of integrin-ß1.

[Chemical constituents from Solanum rostratum].

Ten compounds were isolated from the aerial part of Solanum rostratum by means of various chromatographic techniques such as silica gel, Sephadex LH-20, ODS and preparative HPLC. Their structures were identified as dioscin (1), hypoglaucin H (2), hyperin (3), isoquercitrin (4), isorhamnetin-3-O-beta-D-galactopyranoside (5), kaempferol-3-O-beta-D-glucoside (6), smilaxchinoside A (7), 26-O-beta-D-glucopyranosyl-3beta, 20alpha,26-triol-25 (R) -delta5,22-dienofurostan-3-O-alpha-L-rhamnopyranosyl (1 --> 2) -[ alpha-L-rhamnopyranosyl (1 --> 4)] -beta-D-glucopyranoside (8), beta-sitosterol (9), and daucosterol (10), on the basis of physicochemical properties and spectroscopic data analysis. Among them ,compounds 7 and 8 were isolated from the genus Solanum for the first time, and the remaining compounds were obtained from this plant for the first time.

[Chemical quality of Chrysanthemum morifolium cv. 'Hangju' (HJ) induced by sulfur fumigation processing].

Eight compounds from six Chrysanthemum morifolium cv. 'Hangju' were determined and multivariate statistics, including principle component analysis (PCA) and partial least squares discriminate analysis (PLS-DA) were used to investigate the potential damaging effect of sulfr-fumigating process. Meanwhile, S, Mn, Fe, Cu, Pb were also detected by using ICP-MS and ICP-OES. In this study, dramatic chemical changes were found that the contents of flavonoid aglycones remarkably increased while those of glycosides and hydroxycinnamoylquinic acids were significantly reduced. The PCA score plots showed six samples were clearly classified into the non-fumigated and sulfur-fumigated types. And according to VIP > 1, the most important chemical markers were luteolin, apigenin and luteolin-7-O-glucoside which indicated that the extracted three components might have a marked effect on the discrimination among different group samples. And then, it was found that the residue of sulfur of SHJ were significantly higher than NHJ (P < 0.05). The established approach was applied to rapidly discriminate sulfur-fumigated HJ with combining the quantitative chemical analysis and multivariate statistical analysis, and then the result will provide some evidence to evaluat the quality of HJ and control its processing.

Study on the effects of sulfur fumigation on chemical constituents and antioxidant activity of Chrysanthemum morifolium cv. Hang-ju.

The traditional after-harvesting drying method of C. morifolium cv. Hang-ju (HJ) is sun drying, but recently sulfur fumigation is increasingly used as a cheap and convenient method. However, the effects of sulfur fumigation on chemical constituents and potential activities of HJ were unknown. A comprehensively comparison of the chemical profiles between non-fumigated HJ (NHJ) and sulfur-fumigated HJ (SHJ) was conducted by HPLC fingerprints analysis and the discrepant peaks were identified or tentatively assigned by HPLC-ESI/MS(n). Dramatic chemical changes were found that the contents of 4 flavonoid aglycones remarkably increased while those of 7 glycosides significantly reduced which suggested that sulfur-fumigation induced flavonoid glycosides transformed into aglycons by hydrolysis reaction. A significant loss of hydroxycinnamoylquinic acids showed the sulfur fumigation was a destructive effect on HJ. Principal component analysis (PCA) was employed to rapidly discriminate NHJ and SHJ samples. By ICP-OES analysis, it was found that the residue of sulfur of SHJ were three times higher than NHJ (p<0.05). The antioxidant activity of NHJ and SHJ were evaluated by DPPH and FRAP assay, and the results showed that NHJ had much stronger antioxidant activities than SCF (p<0.05). Combining the results of chemical analysis, residue of sulfur and pharmacological evaluation, it showed that the sulfur fumigation was a destructive effect on HJ.

Highly sensitive fluorescent immunoassay of human immunoglobulin G based on PbS nanoparticles and DNAzyme.

This paper reports a highly sensitive fluorescent immunoassay for the detection of human immunoglobulin G based on PbS nanoparticles and DNAzyme. A sandwich immunoassay format was performed on a microtiter plate. Goat anti-human IgG was coated onto the polystyrene microtiter plate. The human IgG analyte was first captured by the goat anti-human IgG, and then sandwiched by a goat anti-human IgG antibody labeled with PbS nanoparticles. After being dissolved with HNO3, the released Pb(2+) made the substrate chain of the DNAzyme labeled with the fluorophore dissociate from the enzyme strand of the DNAzyme labeled with the quencher, which resulted in fluorescence recovery. Then, the human IgG could be detected indirectly from the fluorescent signals. Under the optimized conditions, the linear range of the developed immunosensor was from 1 ng mL(-1) to 10 µg mL(-1) with a detection limit of 0.8 ng mL(-1). This immunosensor could be used to detect the amount of human IgG in human serum samples.