Fermentative preparation of pyrrolo-quinoline-quinone (PQQ) from methanol

Document(en) uit de collectie Chemische Procestechnologie.DelftChemTechApplied Science

Competition between Heterotrophic and Autotrophic Nitrifiers for Ammonia in Chemostat Cultures

Mixed cultures of a heterotrophic nitrifier/aerobic denitrifier, Thiosphaera pantotropha, and an autotrophic nitrifier, Nitrosomonas europaea, were grown in chemostats under dual ammonia-and acetate limitation. Because of simultaneous nitrification and denitrification by T. pantotropha, the activity of the cultures was evaluated from nitrogen balances as complete as possible. Under most conditions studied, no interaction took place between the two bacteria. Only above a critical C/N ratio of 10.4, T. pantotropha was able to outcompete N. europaea for ammonia (dilution rate = 0.04 h−1). At dissolved oxygen concentrations below 10 μM, the autotroph became oxygen-limited and the heterotroph dominated in the culture. Moreover, when the dilution rate was increased to 0.065 h−1, N. europaea could not maintain itself successfully in the chemostat, even when the C/N ratio was as low as 2.2. Nitrification by T. pantotropha was equivalent to that of N. europaea when the cell ratio of heterotrophs/autotrophs was 250. The relevance of these observations to the nitrogen cycle in natural environments is discussed

De novo heterozygous mutations in SMC3 cause a range of Cornelia de Lange syndrome-overlapping phenotypes

Item does not contain fulltextCornelia de Lange syndrome (CdLS) is characterized by facial dysmorphism, growth failure, intellectual disability, limb malformations, and multiple organ involvement. Mutations in five genes, encoding subunits of the cohesin complex (SMC1A, SMC3, RAD21) and its regulators (NIPBL, HDAC8), account for at least 70% of patients with CdLS or CdLS-like phenotypes. To date, only the clinical features from a single CdLS patient with SMC3 mutation has been published. Here, we report the efforts of an international research and clinical collaboration to provide clinical comparison of 16 patients with CdLS-like features caused by mutations in SMC3. Modeling of the mutation effects on protein structure suggests a dominant-negative effect on the multimeric cohesin complex. When compared with typical CdLS, many SMC3-associated phenotypes are also characterized by postnatal microcephaly but with a less distinctive craniofacial appearance, a milder prenatal growth retardation that worsens in childhood, few congenital heart defects, and an absence of limb deficiencies. While most mutations are unique, two unrelated affected individuals shared the same mutation but presented with different phenotypes. This work confirms that de novo SMC3 mutations account for approximately 1%-2% of CdLS-like phenotypes