Tracing the Arguello Submarine Canyon System from Shelf Origins to an Abyssal Sink

The Arguello submarine canyon/channel system extends over 300 km from the continental shelf off Point Arguello and Point Conception in southern California westward onto the oceanic crust of the Pacific plate. In the northernmost reaches where the canyon system originates, all stages in the evolution of seafloor morphologic fluid flow features—from pockmarks to gullies to converging rills—are observed, similar to what has been described for the Ascension slope, north of Monterey Bay. These features appear to be active today and are linked to fluid leakage from the underlying hydrocarbon basin. The channel dissects a continental slope that exhibits features consistent with large-scale mass wasting. Upslope scarps may be the source of the morphological feature at the base of the slope previously referred to as the "Arguello submarine fan," with topographic expressions (e.g., large channel meanders, ridges) that are more consistent with mass transport deposits than with deep-sea fan depositional lobes. The modern canyon crosscuts these deposits and parallels an older, meandering channel/canyon to the west. Modern seismicity along the shelf and slope may have, and potentially still can, trigger landslides on the slope. Seismicity associated with seamount volcanism, past subduction, and Borderland transrotational and extensional processes most likely played a role in stimulating mass wasting. The presence of abundant nearby petroleum suggests that gas venting and hydrate dissociation cannot be ruled out as a triggering mechanism for the slope destabilization occurring today. The canyon/channel continues due south on a path possibly determined by the structural grain of north–south-aligned abyssal hills underlying oceanic basement. At latitude 33deg 18min N, the channel makes a 90deg turn (bend) to the west at the E–W-striking Arguello transform fault wall and develops into a meandering channel system that crosses over abyssal hill crustal fabric. The system ultimately straightens as it continues west before veering north, curving around a thickened crustal bulge at a corner offset in the Arguello fracture zone in complex basement structure, and then finally empties into an 800-m-deep basin depocenter

Diagnosis of infections in newborns using a new particle-mediated immunoassay for serum C-reactive protein

C-reactive protein (CRP) levels were measured using a new particle-mediated immunoassay. Tests for precision and linearity of this method gave satisfactory results. The minimum sensitivity of the assay was 1 ng/ml. Interference by bilirubin (<220mg/l) and haemoglobin (<20g/l) was not observed. Using this method, CRP was assayed as a means of monitoring for infection in newborns up to 72 h after delivery. The pattern of time course elevation curves was similar for both groups (10 healthy subjects and 26 patients), but the serum CRP (ng/ml) of infected newborns rose significantly higher than in healthy subjects at 24 h after birth. The rate of increase of CRP (∆CRP; ng/ml/h) may be a more useful parameter to detect infection, since a significant change in ∆CRP was apparent only 12 h after birth. The reported method was reliable and the parameters obtained were considered clinically useful for early detection of infection

Tracing the Arguello Submarine Canyon System from Shelf Origins to an Abyssal Sink

The Arguello submarine canyon/channel system extends over 300 km from the continental shelf off Point Arguello and Point Conception in southern California westward onto the oceanic crust of the Pacific plate. In the northernmost reaches where the canyon system originates, all stages in the evolution of seafloor morphologic fluid flow features—from pockmarks to gullies to converging rills—are observed, similar to what has been described for the Ascension slope, north of Monterey Bay. These features appear to be active today and are linked to fluid leakage from the underlying hydrocarbon basin. The channel dissects a continental slope that exhibits features consistent with large-scale mass wasting. Upslope scarps may be the source of the morphological feature at the base of the slope previously referred to as the "Arguello submarine fan," with topographic expressions (e.g., large channel meanders, ridges) that are more consistent with mass transport deposits than with deep-sea fan depositional lobes. The modern canyon crosscuts these deposits and parallels an older, meandering channel/canyon to the west. Modern seismicity along the shelf and slope may have, and potentially still can, trigger landslides on the slope. Seismicity associated with seamount volcanism, past subduction, and Borderland transrotational and extensional processes most likely played a role in stimulating mass wasting. The presence of abundant nearby petroleum suggests that gas venting and hydrate dissociation cannot be ruled out as a triggering mechanism for the slope destabilization occurring today. The canyon/channel continues due south on a path possibly determined by the structural grain of north–south-aligned abyssal hills underlying oceanic basement. At latitude 33deg 18min N, the channel makes a 90deg turn (bend) to the west at the E–W-striking Arguello transform fault wall and develops into a meandering channel system that crosses over abyssal hill crustal fabric. The system ultimately straightens as it continues west before veering north, curving around a thickened crustal bulge at a corner offset in the Arguello fracture zone in complex basement structure, and then finally empties into an 800-m-deep basin depocenter

SINC-seq: correlation of transient gene expressions between nucleus and cytoplasm reflects single-cell physiology

We report a microfluidic system that physically separates nuclear RNA (nucRNA) and cytoplasmic RNA (cytRNA) from a single cell and enables single-cell integrated nucRNA and cytRNA-sequencing (SINC-seq). SINC-seq constructs two individual RNA-seq libraries, nucRNA and cytRNA, per cell, quantifies gene expression in the subcellular compartments, and combines them to create novel single-cell RNA-seq data. Leveraging SINC-seq, we discover distinct natures of correlation among cytRNA and nucRNA that reflect the transient physiological state of single cells. These data provide unique insights into the regulatory network of messenger RNA from the nucleus toward the cytoplasm at the single-cell level

Succinyl-CoA:3-ketoacid coenzyme A transferase (SCOT): development of an antibody to human SCOT and diagnostic use in hereditary SCOT deficiency

AbstractSuccinyl-CoA:3-ketoacid CoA transferase (SCOT) is a key enzyme for ketone body utilization. Hereditary SCOT deficiency in humans (McKusick catalogue number 245050) is characterized by intermittent ketoacidotic attacks and permanent hyperketonemia. Since previously-available antibody to rat SCOT did not crossreact with human SCOT, we developed an antibody against recombinant human SCOT expressed in a bacterial system. The recombinant SCOT was insoluble except under denaturing conditions. Antibody raised to this polypeptide recognized denatured SCOT and proved useful for immunoblot analysis. On immunoblots, SCOT was easily detectable in control fibroblasts and lymphocytes but was detected neither in fibroblast extracts from four SCOT-deficient patients, nor in lymphocytes from two SCOT-deficient patients. These data indicate that immunoblot analysis is useful for diagnosis of SCOT deficiency in combination with enzyme assay

Extensive arterial and venous thrombo-embolism with chemotherapy for testicular cancer: a case report

Germ cell tumours tend to affect young adults and with advanced treatments achieve more than 90% cure rates. Over the years cisplatin has significantly improved the relapse free survival in these patients, hence forming an essential component of chemotherapy regimes. But, the thrombo-embolic complications suffered with cisplatin significantly affect the quality of life in these young patients

Post-coital intra-cerebral venous hemorrhage in a 78-year-old man with jugular valve incompetence: a case report

<p>Abstract</p> <p>Introduction</p> <p>Spontaneous intra-cerebral hemorrhage can occur in patients with venous disease due to obstructed venous outflow.</p> <p>Case presentation</p> <p>We report the case of a 78-year-old Caucasian man with jugular valve incompetence who experienced an intra-cerebral temporo-occipital hemorrhage following sexual intercourse. He had no other risk factors for an intra-cerebral hemorrhage.</p> <p>Conclusions</p> <p>To the best of our knowledge, this is the first case of intra-cerebral hemorrhage due to jugular valve incompetence in association with the physical exertion associated with sexual intercourse.</p

Identification of Novel SNPs in Glioblastoma Using Targeted Resequencing

High-throughput sequencing opens avenues to find genetic variations that may be indicative of an increased risk for certain diseases. Linking these genomic data to other “omics” approaches bears the potential to deepen our understanding of pathogenic processes at the molecular level. To detect novel single nucleotide polymorphisms (SNPs) for glioblastoma multiforme (GBM), we used a combination of specific target selection and next generation sequencing (NGS). We generated a microarray covering the exonic regions of 132 GBM associated genes to enrich target sequences in two GBM tissues and corresponding leukocytes of the patients. Enriched target genes were sequenced with Illumina and the resulting reads were mapped to the human genome. With this approach we identified over 6000 SNPs, including over 1300 SNPs located in the targeted genes. Integrating the genome-wide association study (GWAS) catalog and known disease associated SNPs, we found that several of the detected SNPs were previously associated with smoking behavior, body mass index, breast cancer and high-grade glioma. Particularly, the breast cancer associated allele of rs660118 SNP in the gene SART1 showed a near doubled frequency in glioblastoma patients, as verified in an independent control cohort by Sanger sequencing. In addition, we identified SNPs in 20 of 21 GBM associated antigens providing further evidence that genetic variations are significantly associated with the immunogenicity of antigens

Mitochondrial changes within axons in multiple sclerosis

Multiple sclerosis is the most common cause of non-traumatic neurological impairment in young adults. An energy deficient state has been implicated in the degeneration of axons, the pathological correlate of disease progression, in multiple sclerosis. Mitochondria are the most efficient producers of energy and play an important role in calcium homeostasis. We analysed the density and function of mitochondria using immunohistochemistry and histochemistry, respectively, in chronic active and inactive lesions in progressive multiple sclerosis. As shown before in acute pattern III and Balo’s lesions, the mitochondrial respiratory chain complex IV activity is reduced despite the presence of mitochondria in demyelinated axons with amyloid precursor protein accumulation, which are predominantly located at the active edge of chronic active lesions. Furthermore, the strong non-phosphorylated neurofilament (SMI32) reactivity was associated with a significant reduction in complex IV activity and mitochondria within demyelinated axons. The complex IV defect associated with axonal injury may be mediated by soluble products of innate immunity, as suggested by an inverse correlation between complex IV activity and macrophage/microglial density in chronic lesions. However, in inactive areas of chronic multiple sclerosis lesions the mitochondrial respiratory chain complex IV activity and mitochondrial mass, judged by porin immunoreactivity, are increased within approximately half of large (>2.5 μm diameter) chronically demyelinated axons compared with large myelinated axons in the brain and spinal cord. The axon-specific mitochondrial docking protein (syntaphilin) and phosphorylated neurofilament-H were increased in chronic lesions. The lack of complex IV activity in a proportion of Na+/K+ ATPase α-1 positive demyelinated axons supports axonal dysfunction as a contributor to neurological impairment and disease progression. Furthermore, in vitro studies show that inhibition of complex IV augments glutamate-mediated axonal injury (amyloid precursor protein and SMI32 reactivity). Our findings have important implications for both axonal degeneration and dysfunction during the progressive stage of multiple sclerosis