Porozne nanočestice metoprolol tartarata dobivene pomoću sušenja sprejanjem: Razvoj, karakterizacija i evaluacija in vitro

The present investigation was undertaken to fabricate porous nanoparticles of metoprolol tartrate by spray-drying using ammonium carbonate as pore former. Prepared nanoparticles were coated with Eudragit S100 polymer in order to prevent the release of metoprolol tartrate in the upper GI tract. It was shown that nanoparticles with low size ranges can be obtained with a low feed inlet rate. Micromeritic studies confirmed that nanoparticle batches are discrete and free flowing. Effects of the pore former on drug loading, porosity and in vitro release were studied. It was found that there was an increase in drug loading and porosity with increased the amount of pore former. In vitro drug release studies showed that an increase in pore former made drug release faster. Release kinetics proved that nanoparticles follow a zero-order release mechanism.U radu je opisana priprava poroznih nanočestica metoprolol tartarata pomoću sušenja sprejanjem, koristeći amonijev karbonat za stvaranje pora. Da bi se spriječilo oslobađanje metoprolol tartarata u gornjem dijelu GI trakta, nanočestice su obložene polimerom Eudragit S100. Nanočestice podjednake veličine mogu se dobiti polaganim uklapanjem ljekovite tvari. Mikromeričke studije potvrdile su da su nanočestice zasebne i tečne. Proučavan je utjecaj sredstva za stvaranje pora na količinu uklopljenog lijeka, poroznost i in vitro oslobađanje. Povećanje količine sredstva za stvaranje pora povećava količinu uklopljenog lijeka, poroznost i brzinu oslobađanja ljekovite tvari. Oslobađanje metoprolola slijedi kinetiku nultog reda

Development and evaluation of porous tablets of sodium alginate for <span style="font-size:15.0pt;font-family:"Times New Roman";mso-fareast-font-family: "Times New Roman";mso-ansi-language:EN-IN;mso-fareast-language:EN-IN; mso-bidi-language:AR-SA">treatment of Enterotoxigenic <i>Escherichia coli </i>infection</span>

179-185Enterotoxigenic Escherichia coli (ETEC) infections result in large mortality rate and usually a frequent cause of diarrhea in infants. To prevent enterotoxigenic escherichia coli infections animal needs an active mucosal immunity at the moment of weaning. In the present study, F4 loaded porous sodium alginate tablets were prepared by direct compression technique for oral vaccination using ammonium carbonate as a pore former. In order to prevent the release the antigen in upper GI tract and to release it at target site nanoparticles were coated with Eudragit S100 which will protect the antigen against the detrimental effects in the gastrointestinal tract. Tablets were evaluated for pharmaco-technical properties and results were found to be satisfactory. SEM studies were conducted in order to show the porous surface of tablets. Ammonium carbonate as a pore forming agent proves to be promising and was successful in creating pores on surface of tablets through which F4 was loaded in tablets. SEM had given a clear picture showing major and minor pore with different pore size. It was found that an increase in pore forming agent leads to decrease in hardness and disintegration time of porous tablets. Mucosal immune response study revealed that, immune response was elicited and animals vaccinated with porous tablets group shows a significant reduction in excretion of F4+ E coli. Studies indicate that a solid vaccine formulation will be more efficient and these systems can contribute to the development of oral vaccines in veterinary as well as in human medicines

Fungal dysbiosis and intestinal inflammation in children with beta-cell autoimmunity

Abstract Although gut bacterial dysbiosis is recognized as a regulator of beta-cell autoimmunity, no data is available on fungal dysbiosis in the children at the risk of type 1 diabetes (T1D). We hypothesized that the co-occurrence of fungal and bacterial dysbiosis contributes to the intestinal inflammation and autoimmune destruction of insulin-producing beta-cells in T1D. Fecal and blood samples were collected from 26 children tested positive for at least one diabetes-associated autoantibody (IAA, GADA, IA-2A or ICA) and matched autoantibody-negative children with HLA-conferred susceptibility to T1D (matched for HLA-DQB1 haplotype, age, gender and early childhood nutrition). Bacterial 16S and fungal ITS2 sequencing, and analyses of the markers of intestinal inflammation, namely fecal human beta-defensin-2 (HBD2), calprotectin and secretory total IgA, were performed. Anti-Saccharomyces cerevisiae antibodies (ASCA) and circulating cytokines, IFNG, IL-17 and IL-22, were studied. After these analyses, the children were followed for development of clinical T1D (median 8 years and 8 months). Nine autoantibody positive children were diagnosed with T1D, whereas none of the autoantibody negative children developed T1D during the follow-up. Fungal dysbiosis, characterized by high abundance of fecal Saccharomyces and Candida, was found in the progressors, i.e., children with beta-cell autoimmunity who during the follow-up progressed to clinical T1D. These children showed also bacterial dysbiosis, i.e., increased Bacteroidales and Clostridiales ratio, which was, however, found also in the non-progressors, and is thus a common nominator in the children with beta-cell autoimmunity. Furthermore, the progressors showed markers of intestinal inflammation detected as increased levels of fecal HBD2 and ASCA IgG to fungal antigens. We conclude that the fungal and bacterial dysbiosis, and intestinal inflammation are associated with the development of T1D in children with beta-cell autoimmunity