Sensitive detection of cyanide using bovine serum albumin-stabilized cerium/gold nanoclusters.

A simple, sensitive, and selective fluorescence assay for the detection of CN(-) has been demonstrated using bovine serum albumin-stabilized cerium/gold nanoclusters (BSA-Ce/Au NCs). When excited at 325 nm, BSA-Ce/Au NCs have two fluorescence bands centered at 410 and 658 nm, which are assigned to BSA-Ce/Au complexes and Au NCs, respectively. Each BSA-Ce/Au NC contains 22 Au atoms and 8 Ce ions. Through etching of the Au core in BSA-Ce/Au NCs by CN(-), the fluorescence at 658 nm is quenched, while that at 410 nm enhances during the formation of complexes among BSA, Ce(4+), and [Au(CN)2](-). The circular dichroism spectra reveal that relative to BSA-Au NCs, BSA-Ce/Au NCs have looser structures of the BSA templates. As a result, it is easier for CN(-) to access the Au cores in BSA-Ce/Au NCs, allowing faster (within 15 min) etching of the Au cores by CN(-). At pH 12.0, this assay allows the detection of CN(-) down to 50 nM, with linearity over 0.1-15 µM. This assay has been applied to the determination of the concentrations of CN(-) in spiked drinking water and pond water samples.

Prevention of methylmercury-triggered ROS-mediated impairment of embryo development by co-culture with adult adipose-derived mesenchymal stem cells.

Methylmercury (MeHg) is a potent toxin that exerts deleterious effects on human health via environmental contamination. Significant effects of MeHg on neuronal development in embryogenesis have been reported. Recently, our group demonstrated that MeHg exerts toxic effects on pre- and post-implantation embryonic development processes from zygote to blastocyst stage. Our results showed that MeHg impairs embryo development by induction of apoptosis through reactive oxygen species (ROS) generation that triggers caspase-3 cleavage and activation, which, in turn, stimulates p21-activated kinase 2 (PAK2) activity. Importantly, ROS were identified as a key upstream regulator of apoptotic events in MeHg-treated blastocysts. Data from the current study further confirmed that MeHg exerts hazardous effects on cell proliferation, apoptosis, implantation, and pre- and post-implantation embryo development. Notably, MeHg-induced injury was markedly prevented by co-culture with adipose-derived mesenchymal stem cells (ADMSCs) in vitro. Furthermore, ADMSC injection significantly reduced MeHg-mediated deleterious effects on embryo, placenta, and fetal development in vivo. Further investigation of the regulatory mechanisms by which co-cultured ADMSCs could prevent MeHg-induced impairment of embryo development revealed that ADMSCs effectively reduced ROS generation and its subsequent downstream apoptotic events, including loss of mitochondrial membrane potential and activation of caspase-3 and PAK2. The collective findings indicate that co-culture with mesenchymal stem cells (MSCs) or utilization of MSC-derived cell-conditioned medium offers an effective potential therapeutic strategy to prevent impairment of embryo development by MeHg.

Role of activated p21-activated kinase 2 in methylmercury-induced embryotoxic effects on mouse blastocysts.

Methylmercury (MeHg), a biotransformation product derived from mercury or inorganic mercury compounds in waterways, is a potent toxin that exerts hazardous effects on human health via environmental contamination. Previous studies have reported MeHg-induced impairment of nerve development in embryogenesis and placental development. However, the potential deleterious effects and regulatory mechanisms of action of MeHg on pre- and post-implantation embryo development are yet to be established. Experiments from the current study clearly demonstrate that MeHg exerts toxic effects on early embryonic development processes, including the zygote to blastocyst stage. Induction of apoptosis and decrease in embryo cell number were clearly detected in MeHg-treated blastocysts. Additionally, intracellular reactive oxygen species (ROS) generation and activation of caspase-3 and p21-activated protein kinase 2 (PAK2) were observed in MeHg-treated blastocysts. Importantly, prevention of ROS generation by pre-treatment with Trolox, a potent antioxidant, significantly attenuated MeHg-triggered caspase-3 and PAK2 activation as well as apoptosis. Notably, the downregulation of PAK2 via transfection of specifically targeted siRNA (siPAK2) led to marked attenuation of PAK2 activity and apoptosis and the deleterious effects of MeHg on embryonic development in blastocysts. Our findings strongly suggest that ROS serve as an important upstream regulator to trigger the activation of caspase-3, which further cleaves and activates PAK2 in MeHg-treated blastocysts. Activated PAK2 promotes apoptotic processes that, in turn, cause sequent impairment of embryonic and fetal development.

Focusing on long-term complications of mid-urethral slings among women with stress urinary incontinence as a patient safety improvement measure: A protocol for systematic review and meta-analysis.

BACKGROUND: There are 3 different types of mid-urethral sling, retropubic, transobturator and single incision performed for women with stress urinary incontinence. Prior studies comparing these three surgeries merely focused on the successful rate or efficacy. But nevertheless, what is more clinically important dwells upon investigating postoperative complications as a safety improvement measure. METHODS: A systematic review via PubMed, Ovid, and the Cochrane Database of Systematic Review and studies were applied based on the contents with clearly identified complications. Selected articles were reviewed in scrutiny by 2 individuals to ascertain whether they fulfilled the inclusion criteria: complications measures were clearly defined; data were extracted on study design, perioperative complications, postoperative lower urinary tract symptoms, postoperative pain, dyspareunia, and other specified late complications. RESULTS: A total of 55 studies were included in the systemic review. Perioperative complications encompassed bladder perforation, vaginal injury, hemorrhage, hematoma, urinary tract infection. There were postoperative lower urinary tract symptoms including urine retention and de novo urgency. Furthermore, postoperative pain, tape erosion/ extrusion, further stress urinary incontinence surgery, and rarely, deep vein thrombosis and injury of inferior epigastric vessels were also reported. CONCLUSIONS: Complications of mid-urethral sling are higher than previously thought and it is important to follow up on their long-term outcomes; future research should not neglect to address this issue as a means to improve patient safety.

Urethral large B-cell urethral lymphoma: A case report and literature review.

OBJECTIVE: We report a case of diffuse large B-cell urethral lymphoma initial presenting with non-healing urethra ulcer. CASE REPORT: A 68-year-old woman presented with a non-healing urethral ulcer accompanied with vulvar pruritus, which failed to medical treatment. Her medical history was unremarkable, lacking fever, weight loss or unexplained fatigue. There were no enlarged lymph nodes or palpable liver or spleen upon physical examination. Pelvic examination revealed an ulcerative lesion arising from the posterior wall of the urethral meatus. Cystourethroscopy showed no bladder involvement. Surgical excision of the urethral ulcer was done and immunohistochemical report showed a diffuse large B-cell lymphoma. Bone marrow needle biopsy and computed tomography were done and the diagnosis of primary diffuse large B-cell urethral lymphoma stage IEA was made. She underwent six cycles of cyclophosphamide, doxorubicin, vincristine, prednisone and rituximab and was free of disease for 51 months. CONCLUSION: This report of urethral lymphoma was presented as a non-healing ulcer initially, which was totally different previous reports, presenting with bleeding, either vaginal or urinary, urinary frequency, dysuria, urine retention and self-perceived mass, suggesting that unhealed ulcer on the perineal area should be promptly evaluated and avoidance of unnecessary delayed therapy for possible curable disease.