Synthesis, characterization and use of Poly (N-isopropylacrylamide-co-N-vinylcaprolactam) crosslinked thermoresponsive microspheres for control release of Ciproflaxin hydrochloride drug.

Poly (N-isopropylacrylamide-co-N-vinyl caprolactam) copolymer was synthesized as an interesting thermoresponsive material possessing a phase transition temperature around 320C in phosphate buffer, pH 7.4 (PB). Thermoresponsive Poly(N-isopropylacrylamide-co-Nvinylcaprolactam) designated as PNIPA-NVC microspheres crosslinked with N,N’–methylene bisacrylamide (NNMBA) have been prepared by dispersion polymerization using varying amounts of NIPA, NVC and NNMBA., ciproflaxin hydrochloride (CFH) an anti- bacterial drug, was loaded into the microspheres during in situ polymerization and in vitro release of CFH has been studied. The microspheres were characterized by Fourier Transform Infrared Spectroscopy (FTIR) Differential Scanning Calorimetry (DSC), X-Ray Diffractometry (X- RD) and Scanning Electron Microscopy (SEM). The in-vitro release of CFH drug from the microspheres was studied in pH 7.4 medium, at the temperatures 250C & 370C. The microspheres consisting of NIPA and NVC provide thermo responsive nature to the microspheres. The system developed in this study showed a thermoresponsive for the controlled release of CFH. FTIR spectroscopy explained the formation of copolymer. The DSC and XRD techniques indicated the uniform distribution of drug in the microspheres. SEM studies indicated surface morphology of the microspheres. Prolonged and controlled release of CFH was achieved in a controlled manner upto 12 h.

Hemostatic alterations in non-cirrhotic portal fibrosis, extrahepatic portal venous obstruction and Budd-Chiari syndrome.

We studied the coagulation function in ten patients each with non-cirrhotic portal fibrosis (NCPF), extrahepatic portal venous obstruction (EHPO) and Budd-Chiari syndrome (BCS), conditions where venous thrombosis in the hepatic vasculature is a common denominator. Prothrombin time, partial thromboplastin time with kaolin (PTTK) and thrombin time were normal in patients with NCPF and EHPO. However, in BCS the PTTK was prolonged, with a mean test/control ratio of 1.68 +/- 0.11. Fibrin degradation products were absent in all patients. Platelet aggregation tests showed hypoaggregability in all patients with NCPF. They were normal in patients with EHPO. However, two of ten BCS patients showed hyperaggregability, coinciding with a recent onset of illness in one patient. In conclusion, coagulation abnormalities appear unlikely to be the cause of thrombosis in patients with NCPF and EHPO. Further studies are required to substantiate the findings of hyperaggregability of platelets in BCS.