The effects of nitrogen and phosphorus deficiencies and nitrite addition on the lipid content of Chlorella vulgaris (Chlorophyceae)

The effect of 50% N, 100% N, 50% N plus 50% P and 50% P deficiencies and nitrite addition were treated on Chlorella vulgaris (Chlorophyceae) was studied in laboratory conditions with the aim to determine the effects of the deficient nutrient and different nitrogen sources on lipid and protein contents. Proteinand lipid values of the biomass were found as 50.8 and 12.29% for the control group, 20.3 and 17.5% for 50% N(-), 13.01 and 35.6% for 100% N(-), 21.37 and 20.5% for 50% N(-) and 50% P(-), 38.16 and 16.7% for 50% P(-) and 41.03 and 13.04% for the nitrite group that was added. The highest lipid content was recorded with the culture to which 100% N(-) was treated with 0.18 g/L dry-weight.Key words: Chlorella vulgaris, lipid, nitrogen and phosphorus deficiencies, nitrite

Productively Infected Murine Kaposi's Sarcoma-Like Tumors Define New Animal Models for Studying and Targeting KSHV Oncogenesis and Replication

Kaposi's sarcoma (KS) is an AIDS-defining cancer caused by the KS-associated herpesvirus (KSHV). KS tumors are composed of KSHV-infected spindle cells of vascular origin with aberrant neovascularization and erythrocyte extravasation. KSHV genes expressed during both latent and lytic replicative cycles play important roles in viral oncogenesis. Animal models able to recapitulate both viral and host biological characteristics of KS are needed to elucidate oncogenic mechanisms, for developing targeted therapies, and to trace cellular components of KS ontogeny. Herein, we describe two new murine models of Kaposi's sarcoma. We found that murine bone marrow-derived cells, whether established in culture or isolated from fresh murine bone marrow, were infectable with rKSHV.219, formed KS-like tumors in immunocompromised mice and produced mature herpesvirus-like virions in vivo. Further, we show in vivo that the histone deacetylase (HDAC) inhibitor suberoylanilide hydroxamic acid (SAHA/Vorinostat) enhanced viral lytic reactivation. We propose that these novel models are ideal for studying both viral and host contributions to KSHV-induced oncogenesis as well as for testing virally-targeted antitumor strategies for the treatment of Kaposi's sarcoma. Furthermore, our isolation of bone marrow-derived cell populations containing a cell type that, when infected with KSHV, renders a tumorigenic KS-like spindle cell, should facilitate systematic identification of KS progenitor cells