Release and Consumption of DMSP from Emiliania Huxleyi during grazing by Oxyrrhis Marina

Degradation and release to solution of intracellular dimethylsulfoniopropionate (DMSP) from Emiliania huxleyi 370 was observed during grazing by the heterotrophic dinoflagellate Oxyrrhis marina in 24 h bottle incubations. Between 30 and 70% of the lost algal DMSP was metabolized by the grazers without production of dimethylsulfide (DMS) when grazer densities were 150 to 450/ml. The rest was released to solution and about 30% was converted to DMS by bacteria associated with the grazer culture. These experiments demonstrate that grazing by herbivorous protists may be an important sink for DMSP in marine waters, removing a potential source of DMS. Microzooplankton grazing may also indirectly increase the production of DMS by transferring algal DMSP to the dissolved pool, making it available for bacterial metabolism

Lowest 2\u3csup\u3e+\u3c/sup\u3e, \u3cem\u3eT\u3c/em\u3e = 2 States in \u3csup\u3e20\u3c/sup\u3eMg and \u3csup\u3e20\u3c/sup\u3eF

A recent experiment located the lowest 2+ state in 20Mg and discovered that the corresponding 2+, T = 2 state in 20F does not fit expectations of the isobaric multiplet mass equation without a d term.We have calculated the energies of the ground and 2+ states in 20Mg and the 2+ in 20F in a potential model, using shell-model spectroscopic factors. We conclude that this important 20F state has likely never been observed, and suggest a reaction to find it

The Importance of DNA Repair in Tumor Suppression

The transition from a normal to cancerous cell requires a number of highly specific mutations that affect cell cycle regulation, apoptosis, differentiation, and many other cell functions. One hallmark of cancerous genomes is genomic instability, with mutation rates far greater than those of normal cells. In microsatellite instability (MIN tumors), these are often caused by damage to mismatch repair genes, allowing further mutation of the genome and tumor progression. These mutation rates may lie near the error catastrophe found in the quasispecies model of adaptive RNA genomes, suggesting that further increasing mutation rates will destroy cancerous genomes. However, recent results have demonstrated that DNA genomes exhibit an error threshold at mutation rates far lower than their conservative counterparts. Furthermore, while the maximum viable mutation rate in conservative systems increases indefinitely with increasing master sequence fitness, the semiconservative threshold plateaus at a relatively low value. This implies a paradox, wherein inaccessible mutation rates are found in viable tumor cells. In this paper, we address this paradox, demonstrating an isomorphism between the conservatively replicating (RNA) quasispecies model and the semiconservative (DNA) model with post-methylation DNA repair mechanisms impaired. Thus, as DNA repair becomes inactivated, the maximum viable mutation rate increases smoothly to that of a conservatively replicating system on a transformed landscape, with an upper bound that is dependent on replication rates. We postulate that inactivation of post-methylation repair mechanisms are fundamental to the progression of a tumor cell and hence these mechanisms act as a method for prevention and destruction of cancerous genomes.Comment: 7 pages, 5 figures; Approximation replaced with exact calculation; Minor error corrected; Minor changes to model syste

Hidden in plain sight: The importance of cryptic interactions in marine plankton

Here, we present a range of interactions, which we term “cryptic interactions.” These are interactions that occur throughout the marine planktonic foodweb but are currently largely overlooked by established methods, which mean large‐scale data collection for these interactions is limited. Despite this, current evidence suggests some of these interactions may have perceptible impacts on foodweb dynamics and model results. Incorporation of cryptic interactions into models is especially important for those interactions involving the transport of nutrients or energy. Our aim is to highlight a range of cryptic interactions across the plankton foodweb, where they exist, and models that have taken steps to incorporate these interactions. Additionally, it is discussed where additional research and effort is required to continue advancing our understanding of these cryptic interactions. We call for more collaboration between ecologists and modelers in order to incorporate cryptic interactions into biogeochemical and foodweb models

The Role of Corpus Callosum Development in Functional Connectivity and Cognitive Processing

The corpus callosum is hypothesized to play a fundamental role in integrating information and mediating complex behaviors. Here, we demonstrate that lack of normal callosal development can lead to deficits in functional connectivity that are related to impairments in specific cognitive domains. We examined resting-state functional connectivity in individuals with agenesis of the corpus callosum (AgCC) and matched controls using magnetoencephalographic imaging (MEG-I) of coherence in the alpha (8–12 Hz), beta (12–30 Hz) and gamma (30–55 Hz) bands. Global connectivity (GC) was defined as synchronization between a region and the rest of the brain. In AgCC individuals, alpha band GC was significantly reduced in the dorsolateral pre-frontal (DLPFC), posterior parietal (PPC) and parieto-occipital cortices (PO). No significant differences in GC were seen in either the beta or gamma bands. We also explored the hypothesis that, in AgCC, this regional reduction in functional connectivity is explained primarily by a specific reduction in interhemispheric connectivity. However, our data suggest that reduced connectivity in these regions is driven by faulty coupling in both inter- and intrahemispheric connectivity. We also assessed whether the degree of connectivity correlated with behavioral performance, focusing on cognitive measures known to be impaired in AgCC individuals. Neuropsychological measures of verbal processing speed were significantly correlated with resting-state functional connectivity of the left medial and superior temporal lobe in AgCC participants. Connectivity of DLPFC correlated strongly with performance on the Tower of London in the AgCC cohort. These findings indicate that the abnormal callosal development produces salient but selective (alpha band only) resting-state functional connectivity disruptions that correlate with cognitive impairment. Understanding the relationship between impoverished functional connectivity and cognition is a key step in identifying the neural mechanisms of language and executive dysfunction in common neurodevelopmental and psychiatric disorders where disruptions of callosal development are consistently identified

Climate variability, oceanography, bowhead whale distribution, and Iñupiat subsistence whaling near Barrow, Alaska

Author Posting. © Arctic Institute of North America, 2010. This article is posted here by permission of Arctic Institute of North America for personal use, not for redistribution. The definitive version was published in Arctic 63 (2010): 179-194.The annual migration of bowhead whales (Balaena mysticetus) past Barrow, Alaska, has provided subsistence hunting to Iñupiat for centuries. Bowheads recurrently feed on aggregations of zooplankton prey near Barrow in autumn. The mechanisms that form these aggregations, and the associations between whales and oceanography, were investigated using field sampling, retrospective analysis, and traditional knowledge interviews. Oceanographic and aerial surveys were conducted near Barrow during August and September in 2005 and 2006. Multiple water masses were observed, and close coupling between water mass type and biological characteristics was noted. Short-term variability in hydrography was associated with changes in wind speed and direction that profoundly affected plankton taxonomic composition. Aggregations of ca. 50–100 bowhead whales were observed in early September of both years at locations consistent with traditional knowledge. Retrospective analyses of records for 1984–2004 also showed that annual aggregations of whales near Barrow were associated with wind speed and direction. Euphausiids and copepods appear to be upwelled onto the Beaufort Sea shelf during Eor SEwinds. A favorable feeding environment is produced when these plankton are retained and concentrated on the shelf by the prevailing westward Beaufort Sea shelf currents that converge with the Alaska Coastal Current flowing to the northeast along the eastern edge of Barrow Canyon.This work was supported by NSF Grants OPPPP-0436131 to C. Ashjian (S. Braund Subcontract), OPPPP-0436110 to R. Campbell, OPPPP-0436127 to W. Maslowski, OPPPP-0436009 to C. Nicolson and J. Kruse, OPPPP-043166 to S. Okkonen, and OPPPP-0435956 to Y. Spitz, E. Sherr, and B. Sherr

ARHGEF9 disease: Phenotype clarification and genotype-phenotype correlation.

ObjectiveWe aimed to generate a review and description of the phenotypic and genotypic spectra of ARHGEF9 mutations.MethodsPatients with mutations or chromosomal disruptions affecting ARHGEF9 were identified through our clinics and review of the literature. Detailed medical history and examination findings were obtained via a standardized questionnaire, or if this was not possible by reviewing the published phenotypic features.ResultsA total of 18 patients (including 5 females) were identified. Six had de novo, 5 had maternally inherited mutations, and 7 had chromosomal disruptions. All females had strongly skewed X-inactivation in favor of the abnormal X-chromosome. Symptoms presented in early childhood with delayed motor development alone or in combination with seizures. Intellectual disability was severe in most and moderate in patients with milder mutations. Males with severe intellectual disability had severe, often intractable, epilepsy and exhibited a particular facial dysmorphism. Patients with mutations in exon 9 affecting the protein's PH domain did not develop epilepsy.ConclusionsARHGEF9 encodes a crucial neuronal synaptic protein; loss of function of which results in severe intellectual disability, epilepsy, and a particular facial dysmorphism. Loss of only the protein's PH domain function is associated with the absence of epilepsy

Global services and support for children with developmental delays and disabilities: Bridging research and policy gaps

Summary: 1. The United Nations Sustainable Development Goals and the UN Convention on the Rights of the Child (CRC) envision an inclusive society in which health and education contribute to the well-being of all. To achieve this vision, children with developmental delays and behavioral, cognitive, mental, and neurological disabilities need greater access to health care, early childhood care and development services, and education. 2. Improved population-level detection, alongside screening, assessment, and linkage to evidence-based, intersectoral services in the first years of life, can help maximize capabilities and increase the chances of social inclusion for children with developmental delays and disabilities. 3. Educational programs for children with delays and disabilities whose service delivery structure supports the ability of parents to work should be encouraged so that parents can participate in achieving children’s educational goals while also meeting their financial needs. 4. Parents and caregivers who receive training in psychosocial interventions and ongoing support can help children with delays and disabilities thrive in family contexts. 5. Family mental health influences the developmental trajectory of children. Ensuring that parents and caregivers have access to affordable, quality mental health services helps to prevent poor outcomes for children. 6. Rigorous evaluation, continuous quality improvement, and regular monitoring of the programmatic outcomes of services and policy approaches targeting children and caregivers would inform their implementation and serve to disseminate lessons learned from successful policy and program implementation

p27KIP1 Deletions in Childhood Acute Lymphoblastic Leukemia

AbstractThe p27KIP1 gene, which encodes a cyclin-dependent kinase (CDK) inhibitor, has been assigned to chromosome band 12p12, a region often affected by cytogenetically apparent deletions or translocations in childhood acute lymphoblastic leukemia (ALL). As described here, fluorescence in situ hybridization (FISH) analysis of 35 primary ALL samples with cytogenetic evidence of 12p abnormalities revealed hemizygous deletions of p27KIP1 in 29 cases. Further analysis of 19 of these cases with two additional gene-specific probes from the 12p region (hematopoietic cell phosphatase, HCP and cyclin D2, CCND2) showed that p27KIP1 is located more proximally on the short arm of chromosome 12 and is deleted more frequently than either HCP or CCND2. Of 16 of these cases with hemizygous deletion of p27KIP1, only eight showed loss of HCP or CCND2, whereas loss of either of the latter two loci was uniformly associated with loss of p27KIP1. Missense mutations or mutations leading to premature termination codons were not detected in the coding sequences of the retained p27KIP1 alleles in any of the 16 ALL cases examined, indicating a lack of homozygous inactivation. By Southern blot analysis, one case of primary T-cell ALL had hemizygous loss of a single p27KIP1 allele and a 34.5-kb deletion, including the second coding exon of the other allele. Despite homozygous inactivation of p27KIP1 in this case, our data suggest that haploinsufficiency for p27KIP1 is the primary consequence of 12p chromosomal deletions in childhood ALL. The oncogenic role of reduced, but not absent, levels of p27KIP1 is supported by recent studies in murine models and evidence that this protein not only inhibits the activity of complexes containing CDK2 and cyclin E, but also promotes the assembly and catalytic activity of CDK4 or CDK6 in complexes with cyclin D