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

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

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

An NF-κB - EphrinA5-Dependent Communication between NG2+ Interstitial Cells and Myoblasts Promotes Muscle Growth in Neonates

SummarySkeletal muscle growth immediately following birth is critical for proper body posture and locomotion. However, compared with embryogenesis and adulthood, the processes regulating the maturation of neonatal muscles is considerably less clear. Studies in the 1960s predicted that neonatal muscle growth results from nuclear accretion of myoblasts preferentially at the tips of myofibers. Remarkably, little information has been added since then to resolve how myoblasts migrate to the ends of fibers. Here, we provide insight into this process by revealing a unique NF-κB-dependent communication between NG2+ interstitial cells and myoblasts. NF-κB in NG2+ cells promotes myoblast migration to the tips of myofibers through cell-cell contact. This occurs through expression of ephrinA5 from NG2+ cells, which we further deduce is an NF-κB target gene. Together, these results suggest that NF-κB plays an important role in the development of newborn muscles to ensure proper myoblast migration for fiber growth

Oncocytic carcinoma of parotid gland: a case report with clinical, immunohistochemical and ultrastructural features

BACKGROUND: Oncocytic carcinoma is an extremely rare neoplasm of the salivary glands. We report a case of oncocytic carcinoma arising in a parotid gland in a 66-year-old female. METHOD: An excisional biopsy of the parotid tumor was performed. The specimen was submitted for histology and after fixation in formalin solution and inclusion in paraffin, 3–5 μm sections were stained with hematoxylin and eosin for conventional evaluation and Periodic acid Schiff stain. Immunohistochemical studies were performed using antibodies against mitochondrial antigen, keratin, S-100, alpha-actin, vimentin, alpha-1-antichymotrypsin as well as an ultrastructural analysis was performed. RESULTS: Frozen sections revealed an infiltrative growth pattern and the diagnosis of a malignant epithelial lesion was made. Permanent sections stained with haematoxylin and eosin revealed a neoplasm that had replaced a wide area of the parotid gland and had invaded subcutaneous adipose tissue. Perineural invasion was evident, but vascular invasion was not found. Neoplastic elements were large, round or polyhedral cells and were arranged in solid sheets, islands and cords. The cytoplasm was abundant, eosinophilic and finely granular. The nuclei were large and located centrally or peripherally. The nucleoli were distinct and large. Periodic acid Schiff stain demonstrated a granular cytoplasm. Immunohistochemistry demonstrated mithochondrial antigen, keratin, and chymotrypsin immunoreactivity in the neoplastic cells. Ultrastructural analysis revealed numerous mitochondria packed into the cytoplasm of the neoplastic cells. Thus, the final diagnosis was that of oncocytic carcinoma of parotid gland. CONCLUSION: This neoplasm shows clinical, microscopical, histological and ultrastructural features of oncocytic carcinoma and this must be considered in the differential diagnosis of other proliferations in the parotid gland with abundant granular cytoplasm and metastatic oncocytic carcinomas

Observation of isotropic giant magnetoresistance in paramagnetic Au80 Fe20

Magnetization and magnetoresistance were measured at room temperature and above on Au80Fe20 platelets and ribbons obtained by solid-state quenching and melt spinning. The as-quenched samples contain a solid solution of Fe in Au and exhibit a paramagnetic (Curie-Weiss) behavior in the considered temperature range; magnetic data indicate very short-ranged magnetic correlation among adjacent spins, enhanced by local composition fluctuations. The solid solution is very stable. Only a very limited fraction (never exceeding 1%) of nanometer-sized, bcc Fe particles appears after long-time isothermal anneals at suitable temperatures. A negative magnetoresistance was observed at room temperature in all examined samples. The observed effect is anhysteretic, isotropic, and quadratically dependent on magnetic field H and magnetization M. The signal scales with M rather than with H, indicating that it depends on the field-induced magnetic order of the Fe moments, as it does for conventional giant magnetoresistance in granular magnetic systems. This effect derives from spin-dependent scattering of conduction electrons from single Fe spins or very small Fe clusters. The scattering centers are almost uncorrelated at a distance of the order of the electronic mean free path (of the order of 1.5 nm, or a few atomic spacings, at RT

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

Advanced papillary serous carcinoma of the uterine cervix: a case with a remarkable response to paclitaxel and carboplatin combination chemotherapy

Papillary serous carcinoma of the uterine cervix (PSCC) is a very rare, recently described variant of cervical adenocarcinoma. This review, describes a case of stage IV PSCC whose main tumor existed in the uterine cervix and invaded one third of the inferior part of the anterior and posterior vaginal walls. Furthermore, it had metastasized from the para-aortic lymph nodes to bilateral neck lymph nodes. Immnoreactivity for CA125 was positive, whereas the staining for p53 and WT-1 were negative in both the original tumor and the metastatic lymph nodes. Six cycles of paclitaxel and carboplatin combination chemotherapy were administered and the PSCC dramatically decreased in size. The main tumor of the uterine cervix showed a complete response by magnetic resonance imaging (MRI), and on rebiopsy, more than 95% of the tumor cells in the cervix had microscopically disapperared. This is the first report of PSCC in which combination chemotherapy was used and showed a remarkable response