Inadvertent trypan blue staining of posterior capsule during cataract surgery associated with Argentinian flag event

Trypan blue is common in visualizing the anterior capsule during cataract surgery. Inadvertent staining of the posterior capsule during phacoemulsification is a rare complication and there are few reports in the literature. The proposed mechanism of posterior capsule staining in previous reports includes a compromised zonular apparatus or iris retractors facilitating the posterior flow of trypan blue. We report the first case of trypan blue staining of the posterior capsule associated with the “Argentinian flag” sign. In our case, the “Argentinian flag” allowed the trypan blue to seep between the posterior capsule and the lens, staining the anterior surface of the posterior capsule

Enhancing fracture toughness of carbon fiber/epoxy composites using polyphenylene ether as a modifier

In this study, carbon fiber/epoxy composites (CFRP) were fabricated by vacuum-assisted resin infusion molding (VARIM) with polyphenylene ether (PPE) as a toughening agent. The PPE contained hydroxyl end groups that facilitated chemical bonding with epoxy during curing. PPE was incorporated into the epoxy matrix by dissolution, and spreading in the interlaminar regions. The presence of PPE as a toughener exhibited significant improvement in the Mode-I fracture toughness of the composites. The CFRP samples, which were toughened with 5 wt.% and 10 wt.% PPE, showed about 191% to 380% enhancement, respectively, in the critical energy release rate (GIC) compared to the unmodified sample. Dynamic mechanical analysis (DMA) showed about a 6°C increase in the glass transition temperature of the toughened composites, which is an interesting aspect of this work. These results indicate the potential of using PPE as a toughening agent in CFRP composites

The Bouveret Syndrome: An Unusual Cause of Hematemesis

Gallstones are usually silent. Less commonly, patients with cholelithiasis develop symptoms and/or complications; biliary fistula occurs in 3% to 5% of the cases. When a large stone is passed and occludes the duodenum, gastric outlet obstruction (the Bouveret syndrome) may result. In reported cases, the stones are usually larger than 2.5 cm. The usual presenting symptoms are those of bowel obstruction: abdominal pain, nausea, and vomiting. Less commonly, the patients experience melena and, rarely, hematemesis. We describe a patient who had the largest stone reported to cause hematemesis rather than bowel obstruction and to be diagnosed endoscopically. The 5 X 4 X 3 cm stone was extracted surgically. Endoscopic diagnosis and extraction of stones up to 3 cm in size has been reported, avoiding the need for surgery

Diacylglycerol regulates acute hypoxic pulmonary vasoconstriction via TRPC6

Background: Hypoxic pulmonary vasoconstriction (HPV) is an essential mechanism of the lung that matches blood perfusion to alveolar ventilation to optimize gas exchange. Recently we have demonstrated that acute but not sustained HPV is critically dependent on the classical transient receptor potential 6 (TRPC6) channel. However, the mechanism of TRPC6 activation during acute HPV remains elusive. We hypothesize that a diacylglycerol (DAG)-dependent activation of TRPC6 regulates acute HPV. Methods: We investigated the effect of the DAG analog 1-oleoyl-2-acetyl-sn-glycerol (OAG) on normoxic vascular tone in isolated perfused and ventilated mouse lungs from TRPC6-deficient and wild-type mice. Moreover, the effects of OAG, the DAG kinase inhibitor R59949 and the phospholipase C inhibitor U73122 on the strength of HPV were investigated compared to those on non-hypoxia-induced vasoconstriction elicited by the thromboxane mimeticum U46619. Results: OAG increased normoxic vascular tone in lungs from wild-type mice, but not in lungs from TRPC6-deficient mice. Under conditions of repetitive hypoxic ventilation, OAG as well as R59949 dose-dependently attenuated the strength of acute HPV whereas U46619-induced vasoconstrictions were not reduced. Like OAG, R59949 mimicked HPV, since it induced a dose-dependent vasoconstriction during normoxic ventilation. In contrast, U73122, a blocker of DAG synthesis, inhibited acute HPV whereas U73343, the inactive form of U73122, had no effect on HPV. Conclusion: These findings support the conclusion that the TRPC6-dependency of acute HPV is induced via DAG

Downregulation of uPAR and Cathepsin B Induces Apoptosis via Regulation of Bcl-2 and Bax and Inhibition of the PI3K/Akt Pathway in Gliomas

Glioma is the most commonly diagnosed primary brain tumor and is characterized by invasive and infiltrative behavior. uPAR and cathepsin B are known to be overexpressed in high-grade gliomas and are strongly correlated with invasive cancer phenotypes.In the present study, we observed that simultaneous downregulation of uPAR and cathepsin B induces upregulation of some pro-apoptotic genes and suppression of anti-apoptotic genes in human glioma cells. uPAR and cathepsin B (pCU)-downregulated cells exhibited decreases in the Bcl-2/Bax ratio and initiated the collapse of mitochondrial membrane potential. We also observed that the broad caspase inhibitor, Z-Asp-2, 6-dichlorobenzoylmethylketone rescued pCU-induced apoptosis in U251 cells but not in 5310 cells. Immunoblot analysis of caspase-9 immunoprecipitates for Apaf-1 showed that uPAR and cathepsin B knockdown activated apoptosome complex formation in U251 cells. Downregulation of uPAR and cathepsin B also retarded nuclear translocation and interfered with DNA binding activity of CREB in both U251 and 5310 cells. Further western blotting analysis demonstrated that downregulation of uPAR and cathepsin B significantly decreased expression of the signaling molecules p-PDGFR-β, p-PI3K and p-Akt. An increase in the number of TUNEL-positive cells, increased Bax expression, and decreased Bcl-2 expression in nude mice brain tumor sections and brain tissue lysates confirm our in vitro results.In conclusion, RNAi-mediated downregulation of uPAR and cathepsin B initiates caspase-dependent mitochondrial apoptosis in U251 cells and caspase-independent mitochondrial apoptosis in 5310 cells. Thus, targeting uPAR and cathepsin B-mediated signaling using siRNA may serve as a novel therapeutic strategy for the treatment of gliomas

Co-Depletion of Cathepsin B and uPAR Induces G0/G1 Arrest in Glioma via FOXO3a Mediated p27Kip1 Upregulation

Cathepsin B and urokinase plasminogen activator receptor (uPAR) are both known to be overexpressed in gliomas. Our previous work and that of others strongly suggest a relationship between the infiltrative phenotype of glioma and the expression of cathepsin B and uPAR. Though their role in migration and adhesion are well studied the effect of these molecules on cell cycle progression has not been thoroughly examined.Cathepsin B and uPAR single and bicistronic siRNA plasmids were used to downregulate these molecules in SNB19 and U251 glioma cells. FACS analysis and BrdU incorporation assay demonstrated G0/G1 arrest and decreased proliferation with the treatments, respectively. Immunoblot and immunocyto analysis demonstrated increased expression of p27(Kip1) and its nuclear localization with the knockdown of cathepsin B and uPAR. These effects could be mediated by alphaVbeta3/PI3K/AKT/FOXO pathway as observed by the decreased alphaVbeta3 expression, PI3K and AKT phosphorylation accompanied by elevated FOXO3a levels. These results were further confirmed with the increased expression of p27(Kip1) and FOXO3a when treated with Ly294002 (10 microM) and increased luciferase expression with the siRNA and Ly294002 treatments when the FOXO binding promoter region of p27(Kip1) was used. Our treatment also reduced the expression of cyclin D1, cyclin D2, p-Rb and cyclin E while the expression of Cdk2 was unaffected. Of note, the Cdk2-cyclin E complex formation was reduced significantly.Our study indicates that cathepsin B and uPAR knockdown induces G0/G1 arrest by modulating the PI3K/AKT signaling pathway and further increases expression of p27(Kip1) accompanied by the binding of FOXO3a to its promoter. Taken together, our findings provide molecular mechanism for the G0/G1 arrest induced by the downregulation of cathepsin B and uPAR in SNB19 and U251 glioma cells