Late Quaternary sedimentation off the western Sahara

Late Quaternary sediments on the West African continental margin between 24°N and 15°N were studied with RV METEOR (1971) and VALDIVIA (1975). Cores on the shelf were taken with a 6-m-vibrocorer, in deeper water mainly with a 12 m Kastenlot corer. During Holocene, and up to the present time, more or less and climatic conditions north of the Senegal River area reduced terrigenous supply. Therefore, the biogenic-carbonate content exceeds about 50%. Wüstenquarz numbers (red + yellow quartz : white quartz x 100) are high (20 to mmore than 200), indicating eolian input. The Senegal River supplied fine grained, green colored, terrigenous material with some plant debris. During Würm, the Mediterranean climatic zone with winter rains was shifted more than 5° to the South and was reaching Banc d'Arguin (at about 20°N). Therefore, the terrigenous supply was increased in this northern part and consequently the carbonate content and the Wüstenquartz numbers dropped below 50% and 10, respectively. The arid zone was also shifted to the south; as a consequence, the Senegal River did not reach the sea, eolian supply diluted the biogenic carbonates, and increased Wüstenquartz numbers to more than 200. Eolian dunes covered parts of the shelf. Ratios of radiolarians/plankonic foraminifera and planktonic/benthonic organisms and sedimentation rates of organic carbon indicate stronger upwelling in the northern region. Turbidity currents were more frequent, eroding as much as a third of the material supplied ba pelagic sedimentation

BNP controls early load-dependent regulation of SERCA through calcineurin

Heart failure is characterised by reduced expression of sarcoplasmic reticulum calcium-ATPase (SERCA) and increased expression of B-type natriuretic peptide (BNP). The present study was performed to investigate causality of this inverse relationship under in vivo conditions in the transversal aortic constriction mouse model (TAC). Left ventricular SERCA-mRNA expression was significantly upregulated in TAC by 32% after 6 h, but not different from sham after 24 h. Serum proANP and BNP levels were increased in TAC after 24 h (BNP +274%, p < 0.01; proANP +60%, p < 0.05), but only proANP levels were increased after 6 h (+182%, p < 0.01). cGMP levels were only increased 24 h after TAC (+307%, p < 0.01), but not 6 h after TAC. BNP infusion inhibited the increase in SERCA expression 6 h after TAC. In BNP-receptor-knockout animals (GC-A), the expression of SERCA was still significantly increased 24 h after TAC at the mRNA level by 35% (p < 0.05), as well as at the protein level by 25% (p < 0.05). MCIP expression as an indicator of calcineurin activity was regulated in parallel to SERCA after 6 and 24 h. MCIP-mRNA was increased by 333% 6 h after TAC, but not significantly different from sham after 24 h. In the GC-A-KO mice, MCIP-mRNA was significantly increased in TAC compared to WT after 24 h. In mice with BNP infusion, MCIP was significantly lower 6 h after TAC compared to control animals. In conclusion, mechanical load leads to an upregulation of SERCA expression. This is followed by upregulation of natriuretic peptides with subsequent suppression of SERCA upregulation. Elevated natriuretic peptides may suppress SERCA expression by inhibition of calcineurin activity via activation of GC-A

Stem cells in liver regeneration and therapy

The liver has adapted to the inflow of ingested toxins by the evolutionary development of unique regenerative properties and responds to injury or tissue loss by the rapid division of mature cells. Proliferation of the parenchymal cells, i.e. hepatocytes and epithelial cells of the bile duct, is regulated by numerous cytokine/growth-factor-mediated pathways and is synchronised with extracellular matrix degradation and restoration of the vasculature. Resident hepatic stem/progenitor cells have also been identified in small numbers in normal liver and implicated in liver tissue repair. Their putative role in the physiology, pathophysiology and therapy of the liver, however, is not yet precisely known. Hepatic stem/progenitor cells also known as “oval cells” in rodents have been implicated in liver tissue repair, at a time when the capacity for hepatocyte and bile duct replication is exhausted or experimentally inhibited (facultative stem/progenitor cell pool). Although much more has to be learned about the role of stem/progenitor cells in the physiology and pathophysiology of the liver, experimental analysis of the therapeutic value of these cells has been initiated. Transplantation of hepatic stem/progenitor cells or in vivo pharmacological activation of the pool of hepatic stem cells may provide novel modalities for the therapy of liver diseases. In addition, extrahepatic stem cells (e.g. bone marrow cells) are being investigated for their contribution to liver regeneration. Hepatic progenitor cells derived from embryonic stem cells are included in this review, which also discusses future perspectives of stem cell-based therapies for liver diseases