Technology transfer for local vaccine production in Argentina

Technology transfer and local production can be an effective and sustainable strategy to access newer vaccines in developing countries. The influenza pandemic in 2009 highlighted the importance of having a steady supply of vaccines to assure a controlled public-health strategy. To address these issues, Sinergium Biotech S.A. developed an innovative public-private partnership to transfer technology from multinational companies for local vaccine manufacturing. In doing so, it aimed to introduce long-lasting technology in Argentina, to support the steady supply of critical vaccines, and to generate regional exporting capacity. To date, the company has built a green field facility and has successfully completed three technology transfers from worldwide recognized technology providers, establishing state-of-the-art formulation and fill-finish capacity. Sinergium Biotech currently supplies Influenza, Pneumococcal and HPV vaccines (approximately 18 million doses per year) from its current facility in the Buenos Aires suburbs to the Argentinian Ministry of Health. In 2016, the company started a technology transfer to produce the FDA approved recombinant Influenza Vaccine Flublok® locally, including the production of the monovalent antigens. To that end, Sinergium recently started the construction of a new facility that will produce recombinant antigens using the baculovirus expression system (BEVS). The Sinergium Biotech development laboratory is currently working on a downscale process manufacturing model and analytical methods which are critical to support the future manufacturing activities

Ulcerated hemosiderinic dyschromia and iron deposits within lower limbs treated with a topical application of biological chelator

The ulcerative haemosiderinic dyschromia of chronic venous insufficiency is difficult to heal and presents a high accumulation of iron. Lactoferrin, a potent natural iron chelator, could help to scar this ulcerative haemosi - derinic dyschromia. The objective of this study was to determine whether the topical application of a liposomal gel with Lactoferrin favors scarring/degradation of the brown colored spot typical of ulcerative haemosiderinic dyschromia. Nine patients with severe chronic venous insufficiency and ulcerative haemosiderinic dyschromia (CEAP-C6), with a natural evolution of over 12 months, were included in the study. Hemo chromatosis gene mutations were investigated. The levels of serum ferritin, transferrin saturation and blood cell counts were analyzed. The presence of hemosiderin was investigated through periulcerous and ulcer fundus biopsies carried out at baseline and 30 days after treatment with Lactoferrin. The severity of the injuries (CEAP classification) was evaluated at the beginning of and throughout the whole 3-month treatment period. No patient had received compression treatment during the three months previous to this therapy. Significant improvement in these injuries, with a reduction in the dimensions of the brown spot (9 of 9) at Day 90, and complete scarring with a closure time ranging from 15 to 180 days (7 of 9) were observed. The use of topical lactoferrin is a non-invasive therapeutic tool that favors clearance of hemosiderinic dyschromia and scarring of the ulcer. The success of this study was not influenced either by the hemochromatosis genetics or the iron metabolism profile observed

Ulcerated hemosiderinic dyschromia and iron deposits within lower limbs treated with a topical application of biological chelator

The ulcerative haemosiderinic dyschromia of chronic venous insufficiency is difficult to heal and presents a high accumulation of iron. Lactoferrin, a potent natural iron chelator, could help to scar this ulcerative haemosi - derinic dyschromia. The objective of this study was to determine whether the topical application of a liposomal gel with Lactoferrin favors scarring/degradation of the brown colored spot typical of ulcerative haemosiderinic dyschromia. Nine patients with severe chronic venous insufficiency and ulcerative haemosiderinic dyschromia (CEAP-C6), with a natural evolution of over 12 months, were included in the study. Hemo chromatosis gene mutations were investigated. The levels of serum ferritin, transferrin saturation and blood cell counts were analyzed. The presence of hemosiderin was investigated through periulcerous and ulcer fundus biopsies carried out at baseline and 30 days after treatment with Lactoferrin. The severity of the injuries (CEAP classification) was evaluated at the beginning of and throughout the whole 3-month treatment period. No patient had received compression treatment during the three months previous to this therapy. Significant improvement in these injuries, with a reduction in the dimensions of the brown spot (9 of 9) at Day 90, and complete scarring with a closure time ranging from 15 to 180 days (7 of 9) were observed. The use of topical lactoferrin is a non-invasive therapeutic tool that favors clearance of hemosiderinic dyschromia and scarring of the ulcer. The success of this study was not influenced either by the hemochromatosis genetics or the iron metabolism profile observed

Ulcerated hemosiderinic dyschromia and iron deposits within lower limbs treated with a topical application of biological chelator

The ulcerative haemosiderinic dyschromia of chronic venous insufficiency is difficult to heal and presents a high accumulation of iron. Lactoferrin, a potent natural iron chelator, could help to scar this ulcerative haemosi - derinic dyschromia. The objective of this study was to determine whether the topical application of a liposomal gel with Lactoferrin favors scarring/degradation of the brown colored spot typical of ulcerative haemosiderinic dyschromia. Nine patients with severe chronic venous insufficiency and ulcerative haemosiderinic dyschromia (CEAP-C6), with a natural evolution of over 12 months, were included in the study. Hemo chromatosis gene mutations were investigated. The levels of serum ferritin, transferrin saturation and blood cell counts were analyzed. The presence of hemosiderin was investigated through periulcerous and ulcer fundus biopsies carried out at baseline and 30 days after treatment with Lactoferrin. The severity of the injuries (CEAP classification) was evaluated at the beginning of and throughout the whole 3-month treatment period. No patient had received compression treatment during the three months previous to this therapy. Significant improvement in these injuries, with a reduction in the dimensions of the brown spot (9 of 9) at Day 90, and complete scarring with a closure time ranging from 15 to 180 days (7 of 9) were observed. The use of topical lactoferrin is a non-invasive therapeutic tool that favors clearance of hemosiderinic dyschromia and scarring of the ulcer. The success of this study was not influenced either by the hemochromatosis genetics or the iron metabolism profile observed

Lrg1p Is a Rho1 GTPase-Activating Protein Required for Efficient Cell Fusion in Yeast

To identify additional cell fusion genes in Saccharomyces cerevisiae, we performed a high-copy suppressor screen of fus2Δ. Higher dosage of three genes, BEM1, LRG1, and FUS1, partially suppressed the fus2Δ cell fusion defect. BEM1 and FUS1 were high-copy suppressors of many cell-fusion-defective mutations, whereas LRG1 suppressed only fus2Δ and rvs161Δ. Lrg1p contains a Rho-GAP homologous region. Complete deletion of LRG1, as well as deletion of the Rho-GAP coding region, caused decreased rates of cell fusion and diploid formation comparable to that of fus2Δ. Furthermore, lrg1Δ caused a more severe mating defect in combination with other cell fusion mutations. Consistent with an involvement in cell fusion, Lrg1p localized to the tip of the mating projection. Lrg1p-GAP domain strongly and specifically stimulated the GTPase activity of Rho1p, a regulator of β(1-3)-glucan synthase in vitro. β(1-3)-glucan deposition was increased in lrg1Δ strains and mislocalized to the tip of the mating projection in fus2Δ strains. High-copy LRG1 suppressed the mislocalization of β(1-3) glucan in fus2Δ strains. We conclude that Lrg1p is a Rho1p-GAP involved in cell fusion and speculate that it acts to locally inhibit cell wall synthesis to aid in the close apposition of the plasma membranes of mating cells